2000 Trauma Management

v a d e m e c u m
Trauma Management
Demetrios Demetriades, M.D., Ph.D., F.A.C.S.

University of Southern California
Juan A. Asensio, M.D., F.A.C.S.

University of Southern California
LANDES
BIOSCIENCE
GEORGETOWN, TEXAS U.S.A.
VADEMECUM Trauma Management LANDES BIOSCIENCE Georgetown, Texas U.S.A. Copyright 2000 Landes Bioscience All rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopy, recording, or any information storage and retrieval system, without permission in writing from the publisher. Printed in the U.S.A. Please address all inquiries to the Publisher: Landes Bioscience, 810 S. Church Street, Georgetown, Texas, U.S.A. 78626 Phone: 512/ 863 7762; FAX: 512/ 863 0081 ISBN: 1-57059-641-7
Library of Congress Cataloging-in-Publication Data Trauma management / [edited by] Demetrios Demetriades, Juan A. Asensio. p. ; cm. -- (Vademecum) Includes bibliographical references and index. ISBN 1-57059-641-7 (spiral) 1. Wounds and injuries--Treatment. 2. Traumatology. 3. Surgical emergencies. 4. Emergency medical services. I. Demetriades, Demetrios, 1951- II. Asensio, Juan A. III. Series. [DNLM: 1. Wounds and Injuries--diagnosis. 2. Wounds and Injuries--therapy. 3. Critical care--methods. 4. Emergency Medical Services--methods. 5. Emergency Treatment--methods. WO 700 T77569 2000] RD93.T6892 2000 617.1--dc21 00-031657
While the authors, editors, sponsor and publisher believe that drug selection and dosage and the specifications and usage of equipment and devices, as set forth in this book, are in accord with current recommendations and practice at the time of publication, they make no warranty, expressed or implied, with respect to material described in this book. In view of the ongoing research, equipment development, changes in governmental regulations and the rapid accumulation of information relating to the biomedical sciences, the reader is urged to carefully review and evaluate the information provided herein.
Dedication
To my parents, my wife Elizabeth, my daughters, Alexis and Stephanie, and my son, Nicholas. D. Demetriades
To my family, (E, JC, AA, JAA and HV) and to the memory of AOA, SG, RP and SG, who were instrumental in my life. J.A. Asensio
Contents
Prehospital Care
1. Prehospital Trauma Care .............................................................. 2
Samuel J. Stratton and Mark Eckstein
Emergency Room Care

2. Initial Evaluation and Management in the Emergency Department .................................................... 16
Jack Sava and Juan A. Asensio
3. Ultrasound in Trauma ................................................................ 29

Diku Mandavia
4. Analgesia and Sedation in Trauma .............................................. 39

William K. Mallon, Grace Ting and Maria Rudis
5. Emergency Airway Management in the Trauma Patient ............. 54

Kirsten Robinson and Sean O. Henderson
6. Shock and Resuscitation ............................................................. 69

Fred Bongard
Head
7. Management of Head Injury ...................................................... 84
Peter Gruen
8. Maxillofacial Trauma .................................................................. 94

Dennis-Duke R. Yamashita and Mark M. Urata
Neck
9. Evaluation of the C-Spine ......................................................... 115
George C. Velmahos
10. Penetrating Injuries of the Neck ............................................... 127

Demetrios Demetriades
11. Carotid Artery Injuries ............................................................. 135

S. Ram Kumar and Fred A. Weaver
12. Subclavian and Axillary Vascular Injuries .................................. 141

13. Vertebral Artery Injuries .......................................................... 152

14. Laryngotracheal Injuries ........................................................... 157

Uttam K. Sinha and Dennis M. Crockett
15. Traumatic Brachial Plexus Injuries ............................................ 171

Milan Stevanovic and Frances Sharpe
Chest
16. Blunt Thoracic Trauma ............................................................ 186
George C. Velmahos
17. Penetrating Chest Injuries: Evaluation and Management .......... 195

Arthur Fleming
18. Cardiac Injuries ........................................................................ 200

19. Lung Injuries ............................................................................ 212

William C. Chiu and Aurelio Rodriguez
20. Blunt Aortic Trauma ................................................................ 221

Ismael Navarro Nuo, Juan A. Asensio
21. Penetrating Thoracic Vascular Injuries ...................................... 229

Matthew J. Wall, Jr. and Anthony Estrera
22. Diaphragm Injuries .................................................................. 237

James A. Murray
23. Esophageal Injury ..................................................................... 249

Juan A. Asensio and Esteban Gambaro
24. CT Scan in Chest Trauma ........................................................ 254

Alison Wilcox and Randall Radin
25. Emergency Department Thoracotomy ..................................... 271

Juan A. Asensio and Kuen-Jang Tsai
Abdomen
26. Evaluation of Blunt Abdominal Trauma ................................... 281
Michael Sugrue
27. Evaluation of Penetrating Abdominal Trauma .......................... 293

George C. Velmahos
28. Hepatic Injuries and Bile Duct Injuries .................................... 303

Thomas V. Berne
29. Splenic Injuries ......................................................................... 314

John A. Androulakis and Michael N. Stavropoulos
30. Pancreatic Injuries .................................................................... 326

Juan A. Asensio and Walter Forno
31. Duodenal Injuries ..................................................................... 333

Juan A. Asensio and Walter Forno
32. Colon/Rectal Injuries ................................................................ 340

Claudia E. Goetter and William F. Fallon Jr.
33. Genitourinary Tract Trauma ..................................................... 348

Eila C. Skinner
34. Abdominal Vascular Injury ....................................................... 356

Juan A. Asensio and Matias Lejarraga
35. Abdominal Compartment Syndrome ........................................ 363

36. Damage Control Operations .................................................... 370

Richard J. Mullins and John C. Mayberry
37. CT Scan in Abdominal Trauma ................................................ 380

Sravanthi R. Keesara and Nabil A.Yassa
Orthopedic Injuries
38. Extremity Compartment Syndrome .......................................... 405
George C. Velmahos and Pantelis Vassiliu
39. Penetrating Extremity Injury .................................................... 413

Edward Newton
40. Popliteal Vessel Injuries ............................................................. 420

Michael S. Walsh and John P. Raj
41. Hand Trauma ........................................................................... 426

Christopher Shean and Stephen Schnall
42. Long Bone Fractures and the General Surgeon ......................... 437
Jackson Lee
43. Pelvic Fractures and the General Surgeon ................................. 450

Jackson Lee
44. Spinal Injuries .......................................................................... 458

Larry T. Khoo, Wei-Lee Liao and Gordon Engler
Miscellaneous Topics
45. Pediatric Trauma ...................................................................... 480
M. Margaret Knudson
46. Geriatric Trauma ...................................................................... 492

47. Trauma in Pregnancy ................................................................ 496

John Fildes and Timothy Browder
48. Interventional Radiology in the Care of the Trauma Patient ............................................................... 501
Trevor D. Nelson and M. Victoria Marx
49. Minimally Invasive Surgery in Trauma ..................................... 527

James A. Murray
50. Ballistics of Gunshot Injuries .................................................... 532

Kenneth G. Swan and K.G. Swan, Jr.
51. Blast Injuries ............................................................................. 544

Avraham I. Rivkind and Tal Luria
52. Forensics for Trauma Care Givers ............................................. 553

Thomas T. Noguchi
53. Endocrine Problems in Trauma ................................................. 563

Elizabeth O. Beale
54. MOF Failure: MOF Syndrome ................................................. 577

H. Gill Cryer
55. Surgical Nutrition ..................................................................... 581

Edward E. Cornwell
56. Acute Burn Injury ..................................................................... 585

Jeffrey R. Antimarino and Warren L. Garner
57. Inhalation Injury ...................................................................... 594

John F. Fraser and Michael Muller
58. Management of the Potential Organ Donor Patient ....................................... 602

Bradley J. Roth
59. Hypothermia in Trauma Patients ............................................. 607

Thomas V. Berne
60. Trauma Scores .......................................................................... 610

D. Bowley and Ken Boffard
61. Crush Syndrome ....................................................................... 618

Gail T. Tominaga
62. Anesthesia of the Traumatized Patient ...................................... 623

Michael J Sullivan and Earl Moore-Jefferies
63. Transfusion Therapy ................................................................. 636

Gay Wehrli and Ira A. Shulman
64. Venous Thromboembolism After Injury ................................... 646

George C. Velmahos
65. Trauma Program Manager ........................................................ 655

Kathleen E. Alo and Pamela M.Griffith
66. Fat Embolism ........................................................................... 663

George Androulakis and Demetrios Demetriades
67. Alcohol, Illicit Drugs and Trauma ............................................ 668

Howard Belzberg
Index ........................................................................................ 674
Editors
Demetrios Demetriades, M.D., Ph.D., F.A.C.S.
Professor of Surgery Director of Trauma and Critical Care Division of Trauma and Critical Care University of Southern California Department of Surgery Los Angeles, California, U.S.A. Chapters 10, 12, 13, 18, 35, 46, 66
Juan A. Asensio, M.D., F.A.C.S.

Associate Professor of Surgery Unit Chief, Trauma Surgery Service 'A' Division of Trauma/Critical Care Department of Surgery University of Southern California School of Medicine Los Angeles, California, U.S.A. Chapters 2, 20, 23, 25, 30, 31, 34
Preface
This book has been prepared to serve as a quick and practical guide in the evaluation and management of trauma patients by residents, surgeons, and emergency physicians. The style of the text and the liberal use of figures and algorithms make reading easy and pleasing to the reader. The authors of the various Chapters have been carefully selected for their extensive clinical experience in their fields. We are confident that this handbook will serve as a good and reliable companion of those taking care of trauma patients. D. Demetriades, M.D., Ph.D., F.A.C.S. Juan A. Asensio, M.D., F.A.C.S.
Acknowledgments
We are indebted to Mrs. Reina E. Lopez for overseeing and coordinating the timely submission of all manuscripts and helping with the editing of this book.
PREHOSPITAL CARE
CHAPTER 1
Prehospital Trauma Care

Samuel J. Stratton and Mark Eckstein A. Emergency Medical Service Systems
Emergency medical service (EMS) systems serve to organize out-of-hospital medical components that move ill and injured individuals into the hospital medical system. EMS organization in the US is based on state oversight of smaller regional or local systems. EMS components include: emergency 911 telephone access, 911 communication centers for dispatch of ambulances and other EMS units, EMS responders (first responders, emergency medical technicians, and paramedics), designated medical command centers for radio communication with field personnel, and EMS hospital receiving centers.
Background
The role of prehospital providers in the care of the trauma patient has undergone intense scrutiny over the past several years. The most important steps that prehospital providers can take to minimize morbidity and mortality in the major trauma patient is to secure an airway, protect the cervical spine, and provide rapid transport to a trauma center.
Historical Perspectives
Military EMS systems date back to the time the first armies were organized. Civilian EMS systems originated in the 1960s after it was shown that persons with cardiac disease suffering ventricular tachycardia or fibrillation could be defibrillated in the field with portable equipment. Because civilian EMS systems were initially based on an acute cardiac model, the initial emphasis in out-of-hospital patient care was to stabilize patients in the field and then transport them to receiving hospitals. In the late 1970s, the concept of regional trauma systems was adopted by many local EMS systems. Trauma systems identify trauma-receiving centers that have expertise and dedicated resources for the acute care of trauma victims. As the scope of practice of paramedics expanded and the number of jurisdictions that had paramedics expanded nationwide, the same skills that paramedics successfully applied on cardiac patients were assumed to be of benefit to major trauma patients. With the maturing of trauma systems, it was recognized that trauma patients may better benefit from rapid transport from the field, called load and go,
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Samuel J. Stratton, Los Angeles County EMS Agency and Harbor-UCLA Medical Center Commerce, California, U.S.A. Mark Eckstein, M.D., Los Angeles City Fire Department and Los Angeles-USC Medical Center, Los Angeles, California, U.S.A.
rather than stabilization in the field, called stay and play. Providing advanced life support (ALS) intervention often prolongs the time on-scene, which therefore delays definitive care. This was particularly significant for patients in need of surgical hemostasis, where the time spent establishing intravenous lines, applying military antishock trousers (MAST), or carefully packaging the patient actually increased morbidity and mortality by allowing ongoing internal hemorrhage to continue unchecked. Current trauma management in the out-of-hospital environment emphasizes safe and rapid transport from the field to the appropriate receiving center. Most EMS systems now stress the need to minimize the on-scene time while establishing an airway and protecting the cervical spine where appropriate. Any attempts at establishing IV access should only be done while en route to the trauma center.
Trauma Systems
A trauma system is integrated into an overall EMS system that provides all emergency treatment and transport. A trauma system includes the personnel and transport resources of an EMS system with the addition of recognized trauma centers (Fig. 1.1). Trauma centers are hospitals that have dedicated resources for the acute care of trauma victims. Trauma centers are based on strict national guidelines that describe the types of physicians, support staff, equipment, and facilities needed to provide optimal trauma care. For a comprehensive trauma system, optimal trauma care not only includes the acute medical care of trauma victims but begins with prevention of injury and ends with the best rehabilitation processes for trauma victims. In urban environments, about 7% of the total patients who access the EMS system through 911 require the specialized care of trauma centers.
B. Clinical Presentation and Management of Trauma in the Field

The out-of-hospital setting is less controlled than the hospital environment. Equipment is limited and field personnel are not as highly medically trained as those in the in-hospital setting. For trauma victims, the emphasis in the field is recognition of serious trauma based on field assessment, stabilization within the means available and rapid transport to an appropriate emergency trauma center.
Limitations in the Field

Equipment used in the EMS setting must be portable and durable. Field equipment is generally limited to a hand carried box of essential resuscitation drugs, airway and intubation equipment, and intravenous fluids, a portable defibrillator; portable suction equipment, backboards, and personal items such as stethoscopes and scissors. EMS field personnel in the US are usually maximally trained to the level of a paramedic (1,000 to 3,000 hours of instruction in all EMS skills). Minimal training is at the first responder level, which can be 16-40 hours of instruction. Emergency Medical Technicians or EMTs [often referred to as basic life support (BLS)] receive between 100 and 140 hours of instruction in EMS skills.
Trauma Management
Fig. 1.1. Typical inputs and outputs of a trauma center.
Prehospital care for the major trauma patient always begins with first assessing scene safety. There may be some of the same hazards present on-scene that caused the injury to the patient that can pose a danger to would-be rescuers, including traffic hazards, electrical wires, environmental conditions, or perpetrators in the vicinity. In unsafe environment situations, initial care of a trauma victim may be delayed while the scene is secured. Often trauma victims are entrapped within an auto or other vehicle and must be extricated using heavy equipment (jaws of life). Safe extrication can add considerable time in the field for trauma victims. Often assessment and attempted resuscitation must be done concurrently with extrication. During rapid transport, vehicle motion and the need for safety restraints limits the ability to assess and provide care for trauma victims.
General Management of Trauma in the Field

The primary focus for trauma stabilization or resuscitation in the field is airway, breathing (ventilation), circulation, (the ABCs) and spinal stabilization. Shock, respiratory distress, and altered mental status are associated with high mortality and must be rapidly identified in the field with subsequent rapid transport to the nearest appropriate receiving center.
Observing and reporting to the receiving center the mechanism of injury is an important aspect of field trauma care (Table 1.1).
Airway/Breathing
Ensuring an open airway for ventilation is essential for critically ill trauma victims. Basic first aid maneuvers such as chin lift or jaw thrust can keep the tongue and soft pharyngeal tissues from occluding the airway (Fig. 1.2). If there is concern over possible cervical spine injury, a modified jaw thrust should be used to open the airway while using the bag-valve-mask (BVM). This technique requires at least two rescuers to be performed properly. Vomiting or bleeding can often complicate airway management and require frequent suctioning to prevent aspiration and occlusion of the airway. Particular attention should be paid to the presence of any airway obstruction, which may be the result of copious oral secretions, excess blood pooling in the oropharynx from facial trauma, avulsed teeth, or the tongue falling back in the hypopharynx. These scenarios are particularly common when there is coexistent head trauma resulting in a decreased level of consciousness. Oropharyngeal or nasopharyngeal airways may be helpful in lifting the tongue and occluding pharyngeal soft tissues from the airway in some victims. Although these are basic devices, they must be used with caution as they can cause upper airway injury or secondary vomiting with subsequent aspiration. Nasopharyngeal airways should be avoided in head injured victims because they can cause cerebral spinal fluid contamination by bacteria colonizing the upper airway through open basal skull fractures. For an airway obstructed by a foreign body, direct visualization of the upper airway and removal of the foreign body with Magill forceps is recommended. If the foreign body cannot be removed with Magill forceps, endotracheal intubation should be attempted. In rare circumstances, cricothyroidotomy by properly trained field personnel may be necessary to establish an open airway. There are no controlled studies showing the benefit of prehospital intubation on major trauma patients. The studies in the literature are all retrospective. However the following conclusions can be made. Intubation appears to have a beneficial effect on major trauma patients by lengthening the time that the patient can undergo CPR and be successfully resuscitated. In addition, it appears to improve outcomes in patients with severe head injury. One must be mindful of the time required to perform intubation in the field. If intubation can be performed rapidly with a minimal increase of on-scene time or can be performed while en route, then it has the most potential to decrease morbidity and mortality. It will improve oxygenation and simultaneously protect the patients airway from aspiration. Indications for endotracheal intubation of trauma victims in the field include obstructed airway that cannot be managed with direct laryngoscopy, respiratory failure, depressed mental status with loss of ability to protect the airway, and cardiopulmonary arrest. Intubation success rates are typically much lower in the trauma patient as compared to the medical patient. Trauma patients requiring intubation for respiratory failure or cerebral resuscitation usually have potential cervical spine injury, therefore limiting the amount of movement of the head and neck that can be performed. Vomiting with aspiration is a significant risk during intubation attempts. In addition, these patients usually have a gag reflex or trismus,
Trauma Management
Table 1.2. Revised trauma score: to calculate RTS, add the value code for each one of the three parameters present
GCS 13-15 9-12 6- 8 4- 5 3 SBP > 89 76-89 50-75 1-49 0 RR 10-29 >29 6- 9 1- 5 0 Value Code 4 3 2 1 0
GCS = Glasgow Coma Score, SBP = systolic blood pressure, RR = respiratory rate
Fig. 1.2. Illustration of soft pharyneal tissues occluding the upper airway as can occur with the seriously injured trauma victim with poor muscle tone.
necessitating the use of neuromuscular paralytic agents to facilitate intubation. Although used in some EMS systems, the safety and benefit of paralytic agents in the field setting is currently unproven. Esophageal obturator airways and various types of pharyngeal lumen tubes are commonly used in the out-of-hospital setting as a backup when endotracheal intubation cannot be accomplished. Percutaneous (needle) cricothyroidotomy techniques are preferred in the outof-hospital setting for management of the obstructed airway when basic airway management techniques fail and endotracheal intubation cannot be accomplished (Fig. 1.3). This technique is preferred because it can be rapidly
Fig. 1.3. Cricothyroid membrane, the site for emergency airway access by needle cricothyroidectomy.
performed with a minimum of required training. Field cricothyroidotomy is indicated when no other accepted technique for airway management has been successful and personnel have been trained in the technique. Assisted ventilation is indicated when a patient clinically appears to be hypoventilating, either by shallow breathing or slow rate. Victims with chest trauma may be unable to adequately ventilate and often require airway control with assisted ventilation. For head injured patients, it is generally accepted that ventilation should be assisted at a normal rate and tidal volume to avoid hypocarbia which can decrease cerebral blood flow. For the typical adult, normal rate and tidal volume are about 16 breaths per minute at 800 ml of volume. Needle thoracostomy is indicated for the signs and symptoms of increased intrathoracic pressure associated with a closed tension pneumothorax. Needle thoracostomy is accomplished by insertion into the thoracic cavity of a large bore needle and catheter, allowing release of intrathoracic pressure, through the second or third intercostal space at the midclavicular line. Occasionally, an open pneumothorax (most often presenting as a sucking chest wound) that has been managed in the field with an occlusive dressing will develop tension. To manage this situation, the occlusive dressing should be removed to allow relief of the tension pressure.
Circulation
For victims with signs of circulatory collapse, immediate and rapid transport to a trauma-receiving center is mandatory. For trauma victims in shock, venous access should be attempted during transport to a receiving center rather than prior to transport in order to minimize time spent in the field. For entrapped victims undergoing extrication, venous access can sometimes be established during extrication.
Trauma Management
Field resuscitation fluids are generally limited to isotonic crystalloid (normal saline or Ringers Lactate). The use of hypertonic saline is controversial and investigational. Blood products are generally unavailable in the field. Intravenous (IV) lines have been a mainstay of ALS care for the trauma patient for many years. However, recent studies have found that aggressive administration of IV fluids may actually worsen patient outcome for hypotensive penetrating trauma patients. The pneumatic antishock garment (PASG) or military antishock trousers (MAST) may be useful for management of shock due to pelvic fracture or uncontrolled bleeding of a lower extremity. The device consists of three inflatable compartments that when fully inflated to 60-80 mmHg externally compresses the legs, pelvis, and abdomen. This external compression raises peripheral vascular resistance, potentially supporting the blood pressure of a hypotensive victim. Femur fractures and other long bone fractures can result in significant blood loss in the field. The application of a traction or air splint to a femur fracture in the field can decrease blood loss into the fracture site.
Spinal Stabilization
Spinal stabilization, the securing of a victim to a rigid spine support device (backboard), is an important aspect of the prehospital care of trauma victims. Stabilization of the spine is necessary for limiting potential nervous system damage from unstable spine fractures or dislocations during movement and transport of the spine-injured individual. Spinal immobilization should include the entire spine, not just the cervical spine. Any blunt or penetrating trauma with the potential for disruption of the spine should be considered an indication for spinal stabilization in the field. Highrisk situations for spinal injury include injuries from diving into water, football injuries; falls from horseback or tractors, rear-end auto collisions, and gun shot wounds to the neck or torso. Victims can be cleared from the need for spinal stabilization in the field if they are alert and have no reported or palpable spinal tenderness or pain, are without signs of intoxication, do not have painful injuries that may distract their attention from the pain of a spine injury, and are without acute neurologic deficits including numbness and tingling. Complications of field spinal stabilization include inability of the victim to handle airway secretions or bleeding which leads to aspiration, partial airway obstruction in the unconscious victim, and discomfort.
Head Injury
In the patient with an isolated severe head injury, the emphasis should be on airway control while protecting the cervical spine. Moderate hyperventilation should only be performed for patients exhibiting signs of increased intracerebral pressure (ICP). This is demonstrated by a Glasgow Coma Score of 9 or less. Ideally hyperventilation should be performed after intubation to minimize gastric insufflation which can lead to vomiting and aspiration. In the head injured patient in shock from multiple trauma, fluids should not be withheld. While the goal is not to cause further increases in the ICP, cerebral perfusion pressure must be ensured. Therefore, intravenous fluids should
be administered to achieve normotension in the multiple trauma patient with coexistent head injury.
Trauma Triage
Field recognition of major trauma and appropriate triage to a trauma center is essential for optimal trauma care. Field trauma triage is usually based on a sequential assessment including physiologic parameters, evidence of severe anatomic injury, and mechanism of injury (Fig. 1.4). Regardless of the nature of injury, field presentation with shock, respiratory distress, or altered mental status is associated with high risk of serious injury and the need of specialized trauma center care. Evidence of severe injury is an indicator of the need for high-level trauma care. Severe head, chest, abdominal, or pelvic trauma requires trauma center management. The mechanism of an injury can be helpful in determination of the need for specialized trauma care. This is particularly true for falls greater than 15 feet, motor vehicle accidents with severe passenger compartment damage, and penetrating trauma to the neck or thorax. Some prehospital systems also use the Trauma Score or Revised Trauma Score (RTS) to triage victims in the field. The RTS is based on the respiratory rate, systolic blood pressure, and Glasgow Coma Score (Table 1.2). For multiple-victim incidents it is important to rapidly determine those patients that need immediate care versus delayed care. A common system employed is the simple triage and rapid transport (START) system which uses respiratory status, perfusion parameters, and mental status to triage victims into immediate, delayed and minor groups.
Transport
Rapid transport from the scene to an appropriate trauma center is of utmost importance for the management of trauma. Airway stabilization, insuring adequate ventilation, controlling external hemorrhage, packaging the victim with appropriate spinal stabilization and rapid movement of the victim from the field to a trauma center are the primary steps in efficient prehospital trauma care. Venous access and other field maneuvers should not delay transport. Smooth transfer of the trauma victim from the field to the hospital setting is dependent on ongoing identification of available trauma center resources for field personnel and notification of trauma centers from the field of incoming traffic and the specific types of injuries suffered by the victim(s). Transport under lights and sirens mode is often necessary but dangerous. This type of transport places the prehospital transport unit at risk of collision with other vehicles or obstacles and can cause watershed accidents among other nonemergency vehicles. Ongoing monitoring of patients while transporting is extremely difficult because of movement and noise. Movement during transport or moving a patient from the transport unit to the hospital gurney can inadvertently result in dislodgment of an endotracheal tube from the airway. Helicopter transport has not been shown to offer any advantage over ground transport in an urban setting. Its use should be reserved for areas where ground transport is either unavailable or would result in extremely extended transport
10
Trauma Management
Fig. 1.4. A typical field trauma triage algorithm (Adapted from the American College of Surgeons Field Triage Guidelines).
times. Exceptions to this may be in jurisdictions where helicopter transport is readily available and can provide a higher level of care than ground-based paramedics. This often includes the ability to administer paralytic agents for head injured patients.
11
Table 1.3. Signs of respiratory compromise in the child

Tachypnea (normal rates are age dependent) Shallow breathing with minimal chest movement Head bobbing with each breath Gasping or grunting Flared nostrils (widening of the nares with inspiration) Stridor or snoring Suprasternal, supraclavicular, and intercostal retractions Accessory muscle breathing with neck and abdominal muscles
Prehospital Pediatric Trauma

Injury is the most common cause of death for children in the United States. Prehospital management of the injured child requires an appreciation of the unique characteristics of the growing and developing child. Good pediatric trauma care requires more than applying adult principles. Children have unique physiologic responses to trauma based on their age, size, and psychological development. Multisystem involvement is the rule rather than the exception when dealing with the injured child. All organ systems should be suspected of injury until proven otherwise. The most common causes of immediate death in pediatric trauma are respiratory failure and hypoxia, central nervous system trauma, and hemorrhage. Tachypnea with signs of increased effort or difficulty breathing may be the first manifestations of respiratory distress. Table 1.3 lists other signs of respiratory compromise that are helpful in the prehospital assessment of the child. Injured children can rapidly deteriorate from labored ventilation to an exhausted state of respiratory failure. Brain injury is more common in children than the adult population but for given severity levels of brain injury, children have a lower mortality and higher potential for recovery than do adults. Unlike the adult, the signs of hypovolemia or significant hemorrhage in a child are subtle and difficult to identify. The best early sign of hypovolemia is a weak pulse as opposed to tachycardia, which is often difficult to quantify because the normal resting heart rate in small children is fast; also fear and pain may affect the heart rate. Because of increased physiologic reserve, children sustaining hemorrhagic injury will frequently have minimal signs of impending shock and then rapidly decompensate. When required venous access cannot be obtained for stabilization of a child in the field, intraosseous infusion can be used as an alternative site for volume replacement (Fig. 1.5). As in the adult, Ringers Lactate or normal saline are the best initial resuscitation fluids in the field. Usual fluid resuscitation volumes are 20 ml/kg rapid infusion with reevaluation of circulatory status, up to 60 ml/kg total volume in the field. Young children have disproportionately large heads in comparison to the body and when placing a child in spinal stabilization, padding must be used under the torso to maintain appropriate alignment of the spine.
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Trauma Management
Fig. 1.5. Intraoseous infusion: resuscitation fluids infused into the marrow space are moved into the circulatory system by venous plexuses within the boney stroma.
The skeleton and soft tissues of children are more elastic and flexible than those of the adult. Because of this anatomic flexibility, significant underlying organ and vascular damage can occur without obvious visual signs of injury. Table 1.4 lists signs and types of injuries that can be found in the field that must be considered potentially unstable. A frequent combination of injuries occurring when a car strikes a walking child is Waddells triad. Generally the bumper of the oncoming car strikes the femur while the fender hits the spleen or liver area, the child flies through the air and lands on the opposite side of his head. Anticipate that a child struck by a car will have femur, spleen or liver, and opposite side of the head injuries. A child who is a passenger in a motor vehicle accident and restrained in a car seat may be transported from the field in the car seat with the head taped directly to the back of the seat to provide spinal stabilization. Because of the short stature of a child, automobile airbags can cause fatal or serious injury when deployed. Direct face and chest injury often result, but most important is the potential for cervical spine injury as the childs body is thrown forward by an impact and the head hyperextended backward by a deployed airbag.
C. Common Mistakes and Pitfalls

Trauma is not treated in the field; rather the patient is stabilized for transport for treatment. Safe and rapid transport from the field to an appropriate trauma treatment center is the foremost task in prehospital trauma care.
13
Table 1.4. Signs and mechanisms of injury associated with potential serious injury in the child
Poor environmental response: lack of alertness Difficulty breathing Signs of shock or circulatory instability History of unconsciousness postinjury Significant blunt trauma to the thorax Fractured ribs Significant blunt trauma to the abdomen Pelvic fracture
Considering safe and rapid transport as primary in the field management of trauma, insuring an open airway and adequate ventilation are the primary medical tasks in the field. Prehospital airway management in trauma can be difficult. Some prehospital systems aggressively encourage advanced airway techniques and some use paralytic agents to facilitate endotracheal intubation. Generally, evidence shows that if the airway can be maintained during transport and the victim ventilated by means of basic rescue maneuvers, there is less time spent in the field and a better chance of establishing a secure and timely airway in the emergency center. Intravenous fluid administration in the field is of secondary concern. Time should not be taken to establish venous access or administer field fluids. Again, rapid transport to a trauma center is paramount. Studies have suggested that aggressive administration of fluids in the field setting of hemorrhagic shock may be detrimental for some victims, particularly those with penetrating chest injuries. In general, prehospital fluids should be secondary to moving the patient to the operating room where bleeding sites can be controlled surgically. The use of the PASG in the field is controversial. Little data exists to support the use of the device. It is accepted as useful in the setting of pelvic fractures or for air splinting long bone fractures of the legs. In other settings of hemorrhagic shock the device has not been proven useful and can have detrimental effects by increasing the rate of uncontrolled hemorrhage. In the setting of thoracic trauma, evidence suggests that the use of PASG in the field leads to increased mortality, probably as a result of increased bleeding rates into the thoracic cavity. For children under seven years old and those over 65 years old, the usual methods of field triage for serious trauma are imprecise and clinical evaluation difficult. Trauma victims at the extreme of ages, pediatric and elderly, are at higher risk of poor outcome and should be managed with extreme caution. Mechanism of injury is important information that should be transmitted from the field to the receiving hospital. For example use of seat belts and air bag deployment in the setting of an auto accident are important for the receiving trauma center personnel to know in assessment of a patient. Field trauma triage systems are purposefully designed to over triage victims to trauma centers so that transport of the seriously injured is usually to trauma facilities.
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Trauma Management
References
1.
1
2. 3. 4. 5. 6.
Norcross ED, Ford DW, Cooper ME et al. Application of American College of Surgeons Field Triage Guidelines by prehospital personnel. J Am Coll Surg 1995; 181:539-544. Pepe PE, Eckstein M. Reappraising the prehospital care of the major trauma patient. Emerg Med Clin N Amer 1998; 16:1-15. Bickell WH, Wall MJ, Pepe PE et al. Immediate vs. delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331:1105-1109. Domeier RM, OConnor RF, Delbridge TR et al. Use of pneumatic antishock garment (PASG). Prehospital Emerg Care 1997; 1:32-35. National Association of EMS Physicians. Indications for prehospital spinal immobilization: National Association of EMS Physicians Standards and Practice Committee. Prehospital Emerg Care 1999; 3:251-253. Eckstein M, Suyehara D. Needle thoracostomy in the prehospital setting. Prehospital Emerg Care 1998; 2:132-135.
EMERGENCY ROOM CARE
CHAPTER 2
Initial Evaluation and Management in the Emergency Department

Jack Sava and Juan A. Asensio Introduction
There are approximately 140,000-150,000 deaths resulting from traumatic incidents in the United States each year. It is estimated that approximately one third of these deaths are preventable or potentially preventable. Trauma is the leading cause of death for people under the age of 44. Trauma respects no boundaries, neither age, sex or ethnicity. It clearly affects members of all socioeconomic strata in North America and throughout the world. Trauma deaths occur in a tri-modal distribution.
- The first peak of death occurs at the time of injury. These injuries are usually so devastating that only few patients are able to arrive alive but in extremely critical condition to trauma centers. - The second peak of death occurs in the initial hour from the time of origin of the traumatic incident and has been dubbed the Golden Hour. The most important causes of death in this period are generally exsanguination from injuries to the major components of the cardiovascular system, major abdominal solid visceral injuries, open pelvic fractures and space occupying intracranial hemorrhagic lesions. It is precisely in this period, when a well organized and immediate trauma response can be quite effective in decreasing morbidity and mortality, provided rigid protocols are instituted to evaluate and manage these patients expediently and definitively. - The third peak of death generally occurs days to weeks after the initial traumatic injuries in patients that have sustained serious injuries and experience complications such as sepsis, reperfusion injuries and multiple systems organ failure (MSOF).
Early in the 1970s the Committee on Trauma (COT) of the American College of Surgeons (ACS) began to establish standards for the development of regionalized trauma care systems in the United States. Simultaneously, the implementation of the Advanced Trauma Life Support course (ATLS) was promulgated to provide basic skills in the initial assessment and care of injured patients. This course describes the necessary steps to assess, identify and treat injuries during the Golden Hour. It has become the standard of care nationally and internationally. The key components of a regional trauma system are an efficient EMS program and well-organized regionalized trauma centers. These centers must have trauma teams available 24 hours, staffed by trauma and surgical critical care
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Jack Sava, University of Southern California, Los Angeles, California, U.S.A. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A.
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experts and emergency medicine, as well as a multidisciplinary team including radiologists, nurses, rehabilitation specialists, and surgical specialists.
- Additionally, there must be immediate availability of operating rooms, intensive care units, and burn facilities. It has been consistently shown that in severely injured patients, rapid and direct transportation to a trauma center will avoid preventable deaths. - The American College of Surgeons through its verification program has clearly set forth the standard guidelines for certification and ongoing development of these systems.
The Trauma Team

Patients are triaged both in the field and in the emergency department. When specific criteria suggesting a possible serious injury are met, the trauma team is activated through a trauma alert system. The entire team responds immediately. The USC Trauma Center criteria for the activation of the trauma team include systolic blood pressure of less than 90, heart rate of greater than 120, respiratory rate of less than 10 or greater than 29, multiple trauma patients, patients who are unresponsive to pain (at the scene or in the emergency room), and age >70 years. In addition, the triage officer may activate the trauma alert system at his/her own discretion for any reason.
- Ideally, the team arrives before the patient. The trauma surgery attending physician is the team leader. Each team member must understand their role. Communication is essential, and discussion of potential scenarios prior to the arrival of the patient can be very useful. - The operating room should be notified and made aware of a possible emergent case. - The radiology team should be ready and waiting for patients arrival.
Protecting the Trauma Team

- Needlesticks and splashes are endemic in acute trauma management. - Universal precautions are probably more important here than in any other part of the hospital, given the patient population, use of sharp instruments and needles, number of staff, and accelerated pace of trauma assessment. - Be careful of unexpected sharps such as broken ribs and retained missiles or foreign bodies.
The team leader is responsible for keeping the resuscitation smooth and calm.
Initial Assessment
All trauma patients are assessed by a primary survey, resuscitation, secondary survey, and definitive care. The goals of these phases are as follows:
- Primary survey : Identify injuries that may be life threatening immediately or within minutes - Resuscitation: Stabilize and/or treat these immediately lethal injuries - Secondary survey: Identify injuries that are less rapidly fatal, but still potentially lethal, as well as all other injuries - Definitive care: Treatment (surgical or otherwise) of identified injuries - The more drastic the situation, the more closely this template should be followed. In actual practice many steps will likely proceed simultaneously (i.e., primary survey and resuscitation).
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Trauma Management
Primary Survey
Evaluation of all trauma patients begins with the ABCs:
A: Airway. Establish a patent airway while avoiding cervical spine injury B: Breathing. Ensure effective ventilation C: Circulation. Identify shock and life threatening hemorrhage D: Disability. Briefly assess neurologic status E: Exposure/Environment. Remove all clothing. Keep patient warm.
Airway
Assessing for a patent airway is the highest priority. Ask the patient a question. If they can speak normally, they have a patent airway, can breathe on their own, and have adequate cerebral perfusion for mentation. Look in mouth. Clear the oropharynx. Apply pulse oximeter. Massive facial injuries may cause loss of airway control. Maintain c-spine stabilization while evaluating and managing airway. Endotracheal intubation is indicated for :
- inability to adequately oxygenate or ventilate due to thoracic trauma - GCS < 8. Consider intubation if GCS > 8 but patient will be transported to other areas where emergency airway management will be suboptimal - face or neck injuriesblunt or penetratingthat threaten the stability of the airway - multiple, severe injuries especially in elderly patients - severe shock - very restless, combative patients who put at risk themselves or the care givers.
Rapid sequence intubation is the usual technique of securing the airway. (see Airway Chapter) Verify that ETT is in proper position
- Ambubags are fitted with CO2 sensors that change color when the tube is properly in the airway - Verify that there are bilateral breath sounds and that there are no sounds over the stomach. If breath sounds are heard over the right hemithorax only, the tube is likely in the right mainstem bronchus and should be withdrawn appropriately.
Cricothyroidotomy should be promptly performed if three attempts at intubating a paralyzed patient are unsuccessful or there are massive facial injuries preventing intubation.
- in children less than 12, cricothyroidotomy is generally avoided, due to an increased risk of subglottic stenosis. Needle cricothyroidotomy is used until intubation or tracheostomy can be accomplished
Breathing
Evaluate for effective ventilation
- Assess the chest wall for symmetric rise with inspiration. - Palpate the trachea to ascertain a midline position. Palpate the chest wall for subcutaneous emphysema or chest wall deformity. - Auscultate for breath sounds. If breath sounds are obviously diminished, a chest tube should be placed immediately to evacuate air or blood. If there is a question about symmetry of breath sounds, wait for chest x-ray, provided that the patient is hemodynamically stable and saturating well.
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Several chest injuries may be rapidly fatal and must be immediately identified and treated.
- Tension pneumothorax. This may occur in blunt or penetrating trauma. The diagnosis is clinical, based on decreased breath sounds on the injured side, deviation of the trachea away from the injured side, and signs of respiratory and hemodynamic collapse, including hypotension and elevated neck veins. Traditionally, treatment is with needle thoracostomy, followed by tube thoracostomy. - Open pneumothorax (sucking chest wound) prevents effective ventilation. Treatment is tube thoracostomy at a site away from the chest wound, followed by occlusive dressing. - Flail chest occurs when two or more breaks occur on at least three adjacent ribs, creating an island of chest wall that moves paradoxically. Frequently these patients have severe underlying pulmonary contusion and require ventilatory support.
Circulation and Bleeding

Check heart rate and blood pressure
- Remember that pulse and blood pressure are LATE signs of shock, and will not be observed until there is severe blood loss or circulatory dysfunction. To identify early shock, keep in mind the various derangements that occur before hypotension or tachycardia: - Any trauma patient with cool, clammy skin is in shock until proven otherwise. - Blood flow to the brain may be inadequate, resulting in combativeness or lethargy. - Sympathetic discharge will cause diastolic hypertension and resultant narrowing of pulse pressure, while systolic pressure may be maintained until the patient decompensates. - If available, several monitoring modalities may be used to detect subtle hypoperfusion, including transcutaneous oxygen and CO2 measurement.
Beware of deceptively normal vital signs in the following patients

- Children have a remarkable compensatory ability, and may maintain relatively normal vital signs until they are near death, at which time they experience sudden and often irreversible cardiovascular collapse. - Elderly patients may be unable to mount a compensatory tachycardia, which may mask shock. - Athletes, like children, may compensate for blood loss with increases in stroke volume, until profound hypovolemia causes collapse. - Patients on street or prescription drugs may not mount tachycardia (e.g., betablockers) or may have inappropriate tachycardia (e.g., cocaine).
Check for pulses

- Carotid. A carotid pulse implies a systolic pressure of approximately 60 mm Hg - Femoral = 70 mm Hg - Radial = 90 mm Hg
Establish intravenous access. Frequently patients arrive with intravenous lines in place, but these must be assessed for adequacy.
- Two large (14 or 16 gauge) upper extremity lines are ideal. Avoid lower extremity lines if iliac vein or IVC injury is suspected. If peripheral lines cannot be placed, an 8.5 F introducer (Cordis) is placed, either in the subclavian or femoral vein. If this is not successful, a greater saphenous vein cutdown is performed 1 cm superior and 1 cm anterior to the medial malleolus.
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Trauma Management
In children younger than 6 years, interosseous infusion should be considered in cases with difficult peripheral veins when venous access is difficult. If there is evidence of hemodynamic compromise, consider different types of shock. Hypovolemic/hemorrhagic shock
most common type of shock seen in trauma patients neck veins are typically flat hemorrhage may be internal or external Initial resuscitation is with 2L Ringers Lactate (RL). This solution offers several advantages over normal saline (NS). The pH of RL is 6.5, whereas pH of NS is 5. Use of the more acidic NS contributes to potentially lethal hyperchloremic metabolic acidosis. Also, shock patients recruit fluid from their interstitial space to replace lost intravascular volume. RL most closely approximates the electrolyte composition of the depleted interstitial space. - Colloid solutions (albumin, hetastarch, gelatins) are expensive and have been associated with worse outcomes. They are not used in acute trauma resuscitation. - If still unstable, transfuse O- blood (not typed or crossed). Always use a microfilter and blood warmer. - Rapid transfuser technology is very useful for rapid delivery of warmed blood and crystalloids.
Neurogenic shock
- Caused by disruption of sympathetic chain next to spinal cord, resulting in loss of vasomotor tone - Patients with lesions in the upper cervical cord lose sympathetic innervation of the heart and will not be able to mount a compensatory tachycardia. Lesions below this will be accompanied by appropriate tachycardia. - Treatment is aggressive fluid resuscitation, and alpha agonists such as dopamine may rarely be necessary - Usually, neurogenic shock is associated with serious spinal cord injury. However, rarely, the sympathetic chain may be injured with relatively little injury to the spinal cord.
Cardiogenic shock
- occurs when the heart is unable to eject blood or sustain an adequate cardiac output cardiac contusion causing myocardial akinesia or dyskinesia pericardial tamponade tension pneumothorax causing the SVC to twist on its axis, and preventing venous return via the IVC. air embolism preventing coronary artery perfusion myocardial infarction - The treatment for cardiogenic shock depends on the cause. MI and contusion are treated with close monitoring, as well as inotropic agents and antiarrythmic agents as necessary Pericardial tamponade is treated by emergent surgical decompression Tension pneumothorax is treated by needle or tube thoracostomy Air embolism is treated by placement of the patient in Trendelenburg position, and an attempt should be made to aspirate air from the heart using a pulmonary artery catheter.
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Control of Hemorrhage
External bleeding should be controlled with direct pressure. Attempts at clamping and ligation of individual vessels under suboptimal conditions should be avoided. Remember that blood vessels are frequently found in neurovascular bundles with important nerves. Attempts at clamping may result in iatrogenic injury to other structures. Avoid tourniquets unless a decision to sacrifice a limb to save life has been made. There are several tips for controlling bleeding in the emergency department:
- Foley catheters may be effectively used in certain scenarios to stop or slow bleeding. Usually the catheter is inserted in the tract of a penetrating injury, the balloon inflated, and the catheter withdrawn. A clamp is then placed at the level of the skin to maintain tension. thoracic inletthe catheter may be used to temporarily compress a bleeding subclavian vessel against the clavicle chest/intercostalthe catheter may stop intercostal bleeding, and the lumen allows drainage and measurement of hemothorax facial injuriesmay stop bleeding without resorting to surgery, which is frequently ineffective and often causes additional injuries - scalp lacerations may cause exsanguination. They should be rapidly sutured with a running locking stitch in one layer. - anterior and posterior nasal packing often controls nasal hemorrhage
Disability
The Glasgow Coma Scale remains the gold standard in grading the mental status of all trauma patients. This provides a rapid means for quantifying changes in mentation. It is essential to frequently and quantitatively reevaluate the level of consciousness. Subtle changes in GCS may be missed by a brief or careless exam, especially in comatose patients.
- PITFALL: Failure to notice deterioration in GCS in unresponsive patients.
Check the pupils for size, symmetry, and reactivity to light. Anisocoria or blown pupils may occasionally be diagnosed in patients with previous eye surgery, isolated third cranial nerve injury, or direct ocular impact. Check for motion of extremities. Note any asymmetry. The rectal examination gives important information about potential spinal cord injury. Patients diagnosed with blunt spinal cord injury should be given high dose Methlyprednisolone (30 mg/kg bolus + 5.4 mg/kg/hour) Treatment duration is 24 hours if started within 3 hours of injury, 48 hours if started 3-8 hours after injury. Steroids should not be started more than 8 hours after injury, and are not helpful in brain injury or penetrating spinal injury. Used appropriately, they may lower the spinal level at which neurological function is lost. In the case of high cervical spine injury, this may mean the difference between spontaneous breathing and ventilator dependence. However, when used late or in penetrating injuries, they will result in an increase in septic complications with no neurological benefit. Do as thorough an exam as possible before sedating and paralyzing patient.
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Trauma Management
Exposure/Environment
All clothing is removed to avoid missed injuries. Remove any restrictive jewelry. Hypothermia is one of the biggest enemies of the trauma patient. Decrease in core temperature of just one to two degrees causes severe coagulopathy, respiratory depression, decreased myocardial contractility, decreased renal and gut perfusion, and obtundation. Elderly patients, and patients intubated before arrival at the trauma center are particularly prone to hypothermia:
maintain emergency room and operating room temperature high use warm blankets and circulating air mattresses liberally warm all intravenous fluids and blood use warm humidified air in ventilators
Secondary Survey
The secondary survey involves a thorough head-to-toe physical exam and is accompanied by radiographic studies. The biggest pitfalls in the secondary survey usually result from failure to examine the areas of the patient that are inaccessible: The back, buttocks, and perineum. The importance of a complete and thorough examination cannot be overemphasized. The following are routine parts of examination of the trauma patient:
- Head: Examine for lacerations, hematomas and skull fractures. Frequently the posterior aspect of the head can only be seen when the patient is log-rolled. Examine the face for stability. Note periorbital ecchymosis (Raccoons eyes) and mastoid ecchymosis (Battles sign), which suggest a basilar skull fracture. Also note any clear fluid leaking from nose or ears (rhinorrhea or otorrhea), which may be CSF, also suggesting basilar skull fracture.
- Neck:
Palpate the trachea to look for deviation, suggesting tension pneumothorax. If vascular injury is suspected, listen and feel for bruit or thrill. All patients with potential cervical spine injuries should be immobilized in semirigid collars. The collar may be removed for examination if the neck is stabilized. Missed cervical spine injuries are devastating to the patient, staff, and hospital. Examination in trauma patients may be unreliable for a number of reasons, including intoxication, head injury, and distracting injury. However, in select patients with an intact sensorium, no distracting injuries, and no alcohol or drug use, cervical spine injury may be effectively ruled out by the following exam: - Palpate the spinous processes for step-offs or deformity. - Ask the patient to rotate their head from side to side, and then to flex and extend, lifting their head off the gurney. If there is any posterior neck discomfort, the exam should be terminated and the collar replaced. - Press on the top of the patients head to axially load the cervical spine. Chest - Inspect the chest for any wounds or abrasions. - A seat belt sign over the anterior chest should suggest a forceful thoracic blow, and should raise concern for blunt thoracic injury. - Palpate the thoracic cage for fractures. Flail chest is frequently missed on plain radiography, but may sometimes be seen clinically. - Auscultate for bilateral equal breath sounds.
Initial Evaluation and Management in the Emergency Department -
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Remember that chest wounds below the nipple line are potentially abdominal wounds. Thoracoabdominal wounds are also suspicious for diaphragmatic injury. - Virtually all patients receive a plain chest radiograph. If there is no spinal injury, upright films are better. Abdomen - Look for distention. Most commonly, this will be due to hemoperitoneum, but it may also result from retroperitoneal bleeding, inadvertent esophageal intubation and ventilation, gastric distention, or an undrained bladder. - Evaluate for tenderness and signs of peritoneal irritation. - A full bladder or stomach may be a misleading cause of abdominal/pelvic discomfort. A Foley catheter and nasogastric tube should be placed if not contraindicated. - A seat belt mark over the abdomen is an important sign, and suggests an increased risk for intraabdominal injury.
Pelvis
- The pelvis is examined for anterior/posterior instability, lateral instability, or acetabular disruption. To evaluate AP stability, place one hand on each anterior superior iliac spine and push firmly towards the floor, feeling for any crepitus or instability. Also, press on the sypmphysis pubis, evaluating for motion. For lateral stability, grasp the iliac spines and compress inward, toward the midline. Most unstable pelvic fractures will be identified by this test. Bend each leg and flex the hip, feeling for instability and crepitus in the acetabulum. - If pelvic ring instability is diagnosed, no further examinations should be performed, as rocking the fracture site may increase bleeding. - Rectal and vaginal exams should be performed. Examine for signs of violation of vaginal or rectal mucosa, signifying an open fracture. Inspect the perineum for lacerations. The rectal exam is particularly useful in the following scenarios: suspected rectal injury. Look for gross blood. suspected spinal cord injury. Feel for tone. Have the patient squeeze. If possible, test for perianal sensation, indicative of sacral sparing in spinal injuries. suspected urethral tear. Feel for a high riding prostate. If present, Foley catheter placement is contraindicated.
- Unstable pelvic fractures may bleed massively into the retroperitoneum. There are several techniques for controlling this bleeding: 1. Pelvic angiography with gelfoam or coil embolization. Consider early angiography in the following high risk groups:
have clinical evidence of bleeding associated with pelvic fracture have high-risk fractures (bilateral superior/inferior ramus, sacroiliac separation, or pubic diastasis > 2.5 cm) show a contrast blush on CT pelvis, indicative of active bleeding
2. External fixators may be applied in the emergency department, or in the operating room. They work best on open book fractures with pubic diastasis. 3. A sheet may be tied tightly around the pelvis, which will contain hemorrhage preventing further volume expansion of the pelvis. Back
- Examination of the back is routine in all trauma patients. In any patient with a possible spinal injury, the patient must be log-rolled. One team member must stabilize the head during this procedure.
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Trauma Management - Look for any wounds. Clear skin of broken glass and debris to avoid missing injuries. - Feel all spinous processes for deformity or malalignment, and to assess for tenderness
Extremities
- Look for wounds or deformities. Ecchymosis frequently signals an underlying fracture. External bleeding from extremities is best controlled by direct pressure. A tourniquet is almost never necessary. - In any limb with a possibility of vascular injury (fracture, dislocation, penetrating wound), a complete vascular exam should be performed, documenting the presence and character of the pulse. Furthermore, the Doppler occlusion pressure of the injured limb should be compared to an unaffected extremity. A ratio of affected limb to unaffected limb of less than .95 suggests possible vascular injury and demands further investigation. - Injured extremities should be immediately and frequently evaluated for compartment syndrome. This occurs when bleeding or edema elevates the pressure in a fascial compartment high enough to limit capillary perfusion, resulting in ischemia and necrosis. Clinical exam of relevant compartments should be accompanied by measurement of compartment pressures when there is any concern of compartment syndrome. - All fractures should be immediately immobilized. This drastically reduces pain, helps control bleeding, and prevents further damage to neurovascular structures. Open fractures should be dressed with sterile saline gauze dressings. - Keep in mind that bony fractures may be the source of substantial blood loss femur fractures may result in 1500 cc blood loss humeral or tibial-fibular fracture may result in 750 cc blood loss rib fractures may result in 125 cc blood loss per fracture pelvic fracture may result in 250 cc blood loss per break (i.e., each broken ramus = 250 cc) Motor nerve function in the upper extremity can be rapidly assessed by testing the following five nerves: median: have the patient make an O with their thumb and 2nd finger radial: have the patient extend their wrist ulnar: spread fingers apart axillary: abduct arms musculocutaneous: flex elbow
Adjuncts
The following are routine in evaluation of all trauma patients: Monitors continuous ECG and pulse oximetry, as well as intermittent noninvasive blood pressure measurement, are mandatory Supplemental O2. Inadequate oxygen delivery is characteristic of posttraumatic shock, and oxygen content of blood is directly related to saturation of hemoglobin. 12-lead ECG is used to rule out myocardial contusion or infarction A Foley catheter is placed, unless contraindicated A nasogastric tube is placed, unless contraindicated by:
raccoons eyes rhinorrhea/otorrhea penetrating neck injury
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AMPLE history
Allergies Medications Past illness/Pregnancy Last meal Events of injury
Investigations
The following investigations may be used in the further evaluation of the trauma patient: Plain x-rays are frequently used as adjuncts to the initial evaluation and resuscitation
Prioritize! The first film should be a chest x-ray, followed by an AP pelvis film Chest X-ray identifies pneumo/hemothorax, rib fractures, clavicular fractures, and other chest wall injuries used to assess for signs of aortic injury, i.e., mediastinal widening, tracheal/ nasogastric tube deviation, apical capping, loss of detail of the aortic knob may reveal pulmonary contusion assesses placement of endotracheal tube and thoracostomy tubes AP Pelvic X-ray identifies most fractures, and nearly all unstable fractures. Injuries are best delineated by CT with fine pelvic cuts. Cervical Spine the standard cervical spine series includes lateral, AP, and open-mouth odontoid projections remember that cervical spine x-rays are not life saving and should not delay vital procedures or surgery. If necessary, keep the cervical collar on, maintain precautions, and investigate the cervical spine when the patient is stabilized
Computed Tomography (CT)

CT head identifies operable mass lesions and intracranial hemorrhage indicated in all patients with loss of consciousness, abnormal level of consciousness, or gunshot wound to head CT cervical spine CT of cervical spine is performed in most patients with severe head injury, as they frequently cannot be examined clinically, and they are at risk for spinal injury Remember that CT only shows cross-sectional images and may miss malalignment, dislocation and ligamentous injuries. CT Abdomen/Pelvis may be used when clinical evaluation of the abdomen is equivocal or unreliable Advantages: very sensitive for solid organ injuries and free peritoneal air or fluid. 80-95% sensitive for pancreatic/duodenal injuries. Drawbacks: Frequently misses injuries to mesentery, bowel, and diaphragm. More importantly, takes up to an hour and requires transport. Should not be used on unstable patients.
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Trauma Management CT Chest it may be used to reliably rule out blunt aortic disruption if there is clinical or radiographic suspicion of aortic injury it will accurately identify rib fractures, parenchymal hemorrhages, and flail segments that may be missed on plain radiographs it will identify small pulmonary contusions and retained hemothoraces. for transmediastinal gunshot injuries, the trajectory of the bullet can be traced by visualization of air bubbles or metal fragments in the path of the missile . This allows us to be more selective in further diagnostic studies. CT Spine/Pelvic Bones used to delineate injuries before definitive treatment
Ultrasound: A focussed ultrasonic exam is used on every trauma patient to identify fluid in the abdomen and in the pericardium.
Advantages: Very rapid, reliable in expert hands. Useful when there is a question of which body cavity is bleeding. Drawbacks: User dependent. Only identifies fluid, not specific injuries.
Diagnostic peritoneal lavage (DPL)

used for rapid evaluation of abdomen Advantages: Very fast. Can be used to rule out exsanguinating abdominal bleeding in a few minutes Drawbacks: May be false positives/false negatives depending on which cutoffs are used. May miss bowel injuries. For rapid assessment of gross intraabdominal hemorrhage, the catheter is inserted and a syringe used to aspirate for gross blood. More accurate evaluation may be performed by lavaging abdomen with one liter of saline and evaluating the effluent cytologically. Positive results are: More than 100,000 red blood cells/ml More than 500 white blood cells/ml Fecal or food particles Elevation of amylase in lavage fluid in the absence of serum elevation raises concern for pancreatic or bowel injury
Angiography. An experienced and available angiography team is tremendously helpful in several diagnostic or therapeutic trauma problems in all body areas.
Establishing Management Priorities in Diagnostic and Therapeutic Dilemmas

One of the most challenging aspects of trauma management is the prioritization of various diagnostic and therapeutic procedures. Each case demands judgment and individualization, but the following are examples of common dilemmas. Patient with Low GCS and Possible Multiple Injuries
Use the ABCs to find out if the patient is stable or in shock. If the patient is stable, an emergent CT scan of the brain supersedes all other priorities, because early evacuation of an expanding brain hematoma may prevent irreversible brain damage. Unnecessary procedures must be avoided or postponed, but usually it is worthwhile to perform a quick chest x-ray. The patient must be intubated if the GCS is less than 8 or appears to be worsening. PITFALL: Do not delay head CT to evaluate the cervical spine, place a Foley catheter or perform any other procedure that is not lifesaving. Conversely, if the patient is unstable, do not send them to the CT suite. The
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source of shock must be found and addressed. The patients may need to be operated first, and rushed for a brain CT afterwards. PITFALL: Do not transport unstable patients to the CT scanner. Address lifethreatening hemorrhage before brain injury.
Shock of Unknown Origin

Remember the different types of shock . Identify or exclude sources of cardiogenic shock or neurogenic shock. Usually, if these are not present, the patient is bleeding. Sometimes this will be confirmed by a drop in hematocrit. The goal is to find the source of the lost blood, which can only be in a few places: the chest: This can be ruled out with auscultation and chest radiograph. the abdomen: Blood in the abdomen is usually identified by trauma ultrasound. CT is very helpful, but dangerous in an unstable patient. Diagnostic peritoneal lavage is a quick way to detect intraabdominal bleeding. the pelvis/retroperitoneum: An AP pelvic x-ray will identify any pelvic fracture bad enough to cause significant bleeding. the thighs. Femur fractures may bleed several units into surrounding tissues external bleeding. Ask the paramedics if there was substantial blood loss on scene. Inspect the gurney and floor for evidence of external blood loss. PITFALL: Do not attribute shock to intracranial injury.
Unstable patient with pelvic fracture and unevaluable abdomen. Is the problem in the abdomen or in the pelvis?
Perform a supraumbilical DPL. If grossly positive, the patient should immediately undergo laparotomy. If negative, or only microscopically positive, the bleeding has probably resulted from the pelvic fracture and the patient should have external fixation or angioembolization. ER ultrasound may also be used to rule out exsanguinating intraabdominal bleeding.
Patient with Intraabdominal Hemorrhage and Radiographic Findings Suspicious for Aortic Tear
Proceed with laparotomy. Evaluate aorta with spiral CT or angiogram postoperatively. If the patient has a ruptured aorta but survived to hospital, their aorta is not likely to be bleeding freely. Active hemorrhage in the abdomen or elsewhere should be addressed. Then the aortic injury may be repaired.
Penetrating Thoracoabdominal Injuries (Between Nipple Level and Costal Margin)

Remember that gunshot injuries to the thorax are associated with abdominal injuries in 30-40% of cases. Liver, spleen, stomach, and colon are the most commonly injured abdominal organs. evaluate the abdomen using physical exam and ultrasound or DPL evaluate the chest using auscultation and CXR. Chest tube will drain hemo/ pneumothorax as well as quantifying chest bleeding. if there are indications for both thoracotomy and laparotomy, the surgeon must exercise judgement as to which procedure to choose first. If there is any question, open the abdomen, control any life-threatening bleeding. Then pack the abdomen while you open the chest. When thoracic bleeding is controlled, return to the abdomen for formal exploration.
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Trauma Management
References
1. 2. Cales RH, Trunkey DD. Preventable trauma deaths. A review of trauma care systems development. JAMA 1985; 254:1059. Moore FA, Moore EE. Trauma resuscitation. Chapter 2. In: Care of the Surgical Patient. Wilmore DW, Brennan MF, Harken AH et al, eds. 1998; 1-15. New York: Scientific American I. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Course for Physicians. Manual. Chicago. American College of Surgeons 1997. Krantz BE. Initial assessment. Chapter 9. In: Trauma. Feliciano DV, Moore EE, Mattox KL, eds. 3rd ed., 2000; 153-170 Stamford CT: Appleton and Lange. Nordenholz KE, Rubin MA, Gularte CG et al. Ultrasound in the evaluation and management of blunt trauma. Ann Emer Med 1997; 29:357.
3. 4. 5.
CHAPTER 1 CHAPTER 3
Ultrasound in Trauma
Diku Mandavia Introduction
Ultrasound has been used to evaluate emergency patients since the 1970s but only in the last 10 years has there been significant interest in the United States. At many European centers, ultrasound has essentially replaced diagnostic peritoneal lavage. Many prospective studies done by emergency physicians and surgeons here in the United States confirm that this modality can be used by nonradiologists with the reported sensitivity for free intraperitoneal fluid varying from 80-90% and the specificity 95-100%.
U/S vs. DPL vs. CT

Ultrasound (U/S) has significant advantages over diagnostic peritoneal lavage (DPL) and computed tomography (CT) for the rapid detection of intraperitoneal bleeding in critically injured patients. U/S is a fast technique requiring < 5 minutes for a full exam, is noninvasive, and can be used in unstable patients. DPL is invasive, takes 10-15 minutes to complete and is complicated by pregnancy and previous laparotomy. CT scanning provides excellent organ detail including the retroperitoneum but remains an expensive modality and is not readily available. CT is a relatively slow technique and with transport considered, often takes 45-60 minutes to complete and thus this modality can only be used in stable patients. As each method has its advantages and disadvantages, a combination of techniques may be both necessary and optimal. In many US centers, this has translated into ultrasound replacing DPL as the initial diagnostic study. The main advantages of ultrasound can be summarized: 1. Noninvasive 2. No radiation/contrast agents 3. No adverse effects 4. Portable 5. Rapid 6. Repeatable 7. Cost-effective 8. Accurate
Ultrasound Indications and Limitations

Bedside ultrasound is very useful for the rapid detection of:
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Diku Mandavia, Department of Emergency Medicine, Cedars-Sinai Medical Center, Los Angeles County-USC Medical Center, Los Angeles, California, U.S.A.
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1. hemoperitoneum, 2. pericardial effusions, and 3. pleural effusions. Ultrasounds greatest utility is in the evaluation of blunt abdominal trauma for hemoperitoneum, and in penetrating chest injuries for the detection of pericardial effusions. Ultrasound does have limitations. Notably those patients that are morbidly obese or those with massive subcutaneous emphysema can be difficult to image. Even in these patients you are often able to obtain sufficient views for clinical decision making.
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Incorporating Trauma Ultrasound

Algorithms incorporating ultrasound will vary at different sites reflecting their experience and subsequent reliance on this technology.
Ultrasound Training
Clinicians can reliably learn trauma ultrasonography with a short training period. Though this period is not well defined, it appears that this technique can be taught within a day. For trauma abdominal sonography the focused exam will concentrate on the finding of free intraperitoneal fluid rather than delineation of specific organ injury. Ultrasound will not reliably detect low-grade injuries without hemoperitoneum. For the echocardiographic exam, the focus will be the sole finding of a pericardial effusion. Other echocardiographic findings such as segmental wall abnormalities or valvular lesions as may be done by ultrasound technologists or noninvasive cardiologists will not be part of this focused study.
Ultrasound Equipment
Since the goals for trauma ultrasonography are relatively simple, state of the art expensive ultrasound equipment is not necessary. Low end systems at $30,000-50,000 are sufficient for most all of emergency ultrasonography. Quality hand-held machines starting at $20,000 are available and are especially suited for prehospital applications. Though the initial cost may be steep for some departments, the cost per exam is minimal when the cost is amortized over thousands of exams. The ultrasound machine would ideally have two or more ultrasound probes and a 3.5 MHz probe is a good jack of all trades probe. A small footprint probe that can allow intercostal scanning is ideal for most exams. The exams will need to be recorded so print and/or video capability are necessary. Many new machines include options for digital imaging and ethernet connection allowing images to be transferred via the hospital radiology network. Size, portability and durability of the machine are also important, as it is likely the machine will be moved to different areas on a frequent basis and encounter unusually heavy wear in a busy emergency department.
FAST-Focused Abdominal Sonography for Trauma

Focused Abdominal Sonography for Trauma or FAST is a simple, quick ultrasound screening exam for hemoperitoneum. Again, the exam is a focused exam as our only objective is detection of free intraperitoneal fluid. The goal is not to determine the source of the bleeding such as a ruptured spleen or a liver laceration, as the determination of the actual injury is often difficult and unreliable by ultrasound. If hemoperitoneum is detected by ultrasound, it is a strong predictor for the need of therapeutic laparotomy. If intraperitoneal fluid is seen, most often it will be hemoperitoneum but at times needle aspiration may be necessary to confirm the presence of blood. Ascites can be confused and may need to be differentiated from hemoperitoneum. Intestinal fluid and urine also will have positive findings on ultrasound, but both diagnoses also require operative intervention. FAST consists of focused views of the abdomen including the pericardium and is performed after the primary survey. Multiple views greatly increase the
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Fig. 3.1. Views in trauma scanning.
sensitivity of ultrasonography and standard areas examined include the following: 1. Morisons pouch 2. Pericardium 3. Perispenic space 4. Paracolics 5. Suprapubic view
Morisons Pouch
Morisons pouch (Figs. 3.2, 3.3) is a very useful initial view in the ultrasound evaluation of the trauma victim. The exact amount of free fluid detected in Morisons pouch varies but is as little as 250 cc. This view is easily obtained within 20-30 seconds as the landmarks are easy to find. The probe is placed in the mid to posterior axillary line at the just below the nipple level. The liver is identified and the kidney will be adjacent. The space between these two organs is Morisons pouch and is a potential space that can fill with fluid. Free fluid appears as a anechoic or as a black stripe in this area. With time, hemoperitoneum loses its anechoic consistency and becomes more hyperechoic, thus the fluid will have a grayer color and an inconsistent appearance.
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Hyperechoic (white or gray areas) that surround the kidney represent normal perinephric fat and Gerotas fascia and are not to be confused with free fluid. Patient positioning in Trendelenburg can improve sensitivity by making this area more dependent. Once Morisons pouch is adequately examined, angle the probe cephalad and examine the diaphragm for fluid above or below. This will be evident by black areas and small hemothoraces can easily be detected with a little practice.
Pericardium
The pericardium (Figs. 3.4, 3.5) is especially important to evaluate in penetrating thoracic injuries to rule out a pericardial effusion and tamponade. For this view, the probe is placed in the subcostal area just to the right of the xiphisternum. It is angled toward the patients left shoulder. To view the heart adequately, you will need to increase the depth of penetration at this point. A coronal section of the heart should give you a good four chamber view of the heart. The normal pericardium is seen as a hyperechoic (white) line intimately surrounding the heart. A pericardial effusion is seen as an anechoic (or black area) surrounding the heart within the pericardium. A sagittal view should also be used for confirmation, as pulmonary effusions can be confused with pericardial effusions. Though beyond the scope of this chapter, a long axis parasternal view of the heart is the best view to examine the pericardium to avoid any confusion with pleural fluid.
Perisplenic Area
The perisplenic view (Figs. 3.6, 3.7) is obtained by placing the probe at the posterior axillary line at the 9-10th interspace. A common mistake when doing this view is not placing the probe posterior enough to adequately see the kidney. Once the kidney is found, angle the probe slightly cephalad to find the spleen and carefully look for free fluid surrounding it. Once the spleen and kidney are fully scanned, angle the probe more cephalad to examine the diaphragm. As with Morisons pouch, the diaphragm should be visualized to see a pulmonary effusion or subdiaphragmatic fluid.
Paracolic Views
The paracolic views (Fig. 3.8) can be done in conjunction with Morisons pouch and the perisplenic view. Simply place the probe in the paracolic area and examine for free fluid and/or free floating loops of bowel. Fluid is often detected first on other views limiting the usefulness of the paracolic view and thus this view is eliminated in some protocols.
Suprapubic View
Ideally this exam is done prior to the placement of a foley catheter. The full bladder is easily found by placing the probe just cephalad to the pubis. Once the bladder is found, look for free fluid anterior, posterior and lateral to the bladder. In females, the uterus will be seen posterior to the bladder. The culde-sac is a very dependent area of the peritoneal cavity and should be carefully examined for free fluid (Figs. 3. 9, 3.10).
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Fig. 3.2. Normal Morisons Pouch. Note there is a clean interface between the liver and kidney. There are no anechoic or black areas seen which would represent free fluid.
Fig. 3.3. Positive Morisons Pouch. Note that free fluid appears anechoic or black.
Pitfalls in Trauma Ultrasound

To best utilize clinical ultrasonography the clinician must understand the limitations of the technology. The sensitivity for detection of free fluid varies between 80-98% and is definitely operator dependent. In addition, extremely obese patients and those with extensive subcutaneous emphysema are difficult to examine.
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Fig. 3.4. Normal subcostal pericardium. Note the hyperechoic pericardium closely surrounding the heart.
Fig. 3.5. Positive pericardial effusion. The anechoic area surrounding the heart represents fluid within the pericardial sac.
Common mistakes when performing trauma ultrasound include the following: 1. Failure to do a multiple view examination. Sensitivity is highly dependent on the number of views obtained thus a full exam is necessary. 2. Failure to consider other etiologies of free intraperitoneal fluid. Intestinal fluid and intraperitoneal bladder rupture mimic hemoperitoneum, but both require
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Fig. 3.6. Normal perisplenic view. Note the absence of anechoic areas.
Fig. 3.7. Positive perisplenic view. Note the anechoic area representing a hematoma.
laparotomy. Ascites will mimic hemoperitoneum but is easily differentiated with needle aspiration. 3. Failure to do serial exams when the initial examination is negative. Trauma patients are extremely dynamic and contained injuries may later release causing a positive ultrasound exam. Consider serial exams in those with high clinical suspicion and those with changing vital signs and/or hematocrits.
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Fig. 3.8. Positive paracolic view. Note the free fluid and free floating loops of bowel. Normally no fluid should be visible.
Fig. 3.9. Normal suprapubic view. Note the absence of free fluid outside of the bladder on this transverse suprapubic view.
4. Overreliance on ultrasonography. Use ultrasonography as a single data point in the entire clinical picture. Use it in conjunction with other data such as mechanism of injury, vital signs, hematocrits, radiographs and clinical suspicion.
Recommended Texts
1. 2. Ultrasound in Emergency Medicine by Heller & Jehle, WB Saunders, 1995. Ultrasound in Emergency and Ambulatory Medicine by Simon & Snoey, Mosby, 1996.
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Fig. 3.10. Positive suprapubic view. In this sagittal suprapubic view, free fluid is seen in the cul-de-sac and anterior to the uterus.
References
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. Aaland M, Bryan C, Sherman R. Two-dimensional echocardiogram in hemodynamically stable victims of penetrating precordial trauma. Am Surg 1994; 6:412. Jehle D. Bedside ultrasonographic evaluation of hemoperitoneum: The time has come. Acad Emerg Med 1995; 2:575. Lucciarini P, Ofner D, Weber F et al. Ultrasonography in the initial evaluation and follow-up of blunt abdominal injury. Surgery 1993; 114:506. Ma OJ, Kefer MP, Mateer JR et al. Prospective analysis of a rapid trauma ultrasound examination performed by emergency physicians. J Trauma 1995; 38:879. McKenney M, Martin L, Lentz K et al. 1000 consecutive ultrasounds for blunt abdominal trauma. J Trauma 1996; 40:607-612. Meyer D, Jessen M, Grayburn P. Use of echocardiography to detect occult cardiac injury after penetrating thoracic trauma: A prospective study. J Trauma 1995; 39:902. Plummer D, Brunette D, Asinger R. Emergency department echocardiography improves outcome in penetrating cardiac injury. Ann Emerg Med 1992; 21:709. Rozycki GS, Shackford S. Ultrasound, what every trauma surgeon should know. J Trauma 1996; 40:1. Rozycki GS, Ochsner G, Schmidt J et al. A prospective study of surgeon-performed ultrasound as the primary adjuvant modality for injured patient assessment. J Trauma 1995; 39:492. Rozycki GS, Feliciano D, Ochsner G et al. The role of ultrasound in patients with possible penetrating cardiac wounds: A prospective multicenter study. J Trauma 1999; 46:543-552. Shackford S, Rogers F, Osler T et al. Focused abdominal sonogram for trauma: The learning curve of nonradiologist clinicians in detecting hemoperitoneum. J Trauma 1999; 46:553564. Thomas B, Falcone R, Vasquez D et al. Ultrasound evaluation of blunt abdominal trauma: Program implementation, initial experience, and learning curve. J Trauma 1997; 42:384390. Yoshii H, Sato M, Yamamoto S et al. Usefulness and limitations of ultrasonography in the initial evaluation of blunt abdominal trauma. J Trauma 1998; 45:45-51.
CHAPTER 1 CHAPTER 4
Analgesia and Sedation in Trauma

William K. Mallon, Grace Ting and Maria Rudis Introduction
Pain management, sedation, and the control of psychomotor agitation are important pharmacologic goals in the management of trauma. Existing studies of pain management have revealed poor analgesia and sedation in trauma patients. Oligoanalgesia is widespread in trauma care adding physiologic insult to injury. Oligoanalgesia and inadequate treatment of agitation are known to potentiate the adverse physiologic responses to trauma. There are several possible explanations for oligoanalgesia:
Fear regarding hemodynamic fluctuations and respiratory depression associated with treatment. Lack of knowledge regarding the current treatment options. Under-recognition of pain. Language and communication barriers. Trauma care traditions.
Physiology of Pain
Trauma affects the physiologic process via direct damage to organ systems, via shock states, or via the secondary effects of the neurohumoral stress response. Table 4.1 summarizes some of the ways that pain can exacerbate the trauma patients physiologic state. Furthermore, pain slows down the entire healing process by increasing catabolic metabolism. Increased sympathetic outflow stresses all organ systems, leading to the belief that pain management may potentially improve the recovery process. One of the major consequences of oligoanalgesia and undersedation is the associated delay in care. Critical diagnostic studies cannot be performed while the patient is in agony and exhibiting psychomotor agitation.
The restrained, struggling trauma patient poses a danger to himself and caregivers.
Terms and Definitions

Analgesia does not always yield concomitant sedation, and sedation frequently provides no analgesia. Often analgesia and sedation drugs are used to control psychomotor agitation; however, it is possible to control psychomotor agitation without sedation or analgesia. For example, paralysis will obviously control psychomotor
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. William K. Mallon, LAC + USC Medical Center, Los Angeles, California, U.S.A. Grace Ting, Department of Emergency Medicine, LAC + USC Medical Center, Los Angeles, California, U.S.A. Maria Rudis, USC Schools of Pharmacy and Medicine, Los Angeles, California, U.S.A.
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Table 4.1. Organ system responses to poorly controlled trauma related pain
Organ Systems Pathologic Responses to Trauma Related Pain
Neuroendocrine
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Pulmonary
Increased catecholamines and sympathetic nerve activity Increased cortisol, growth hormone, ACTH, prolactin Increased renin, angiotensin, aldosterone, vasopressin Acute phase reactantsincreased coagualability Altered immune response Decreased pulmonary function Pneumonia ARDS Pneumothorax secondary to barotrauma (yelling, coughing) Increased respiratory rate Acid-base disturbances ICP elevation and herniation Spinal cord injury due to struggling against physical restraints and spinal precautions SVR increases with tissue hypoperfusion, lactic acidosis and ultimately multi-organ system failure Tachycardia which may complicate assessment of resuscitative measures Ectopy and conduction abnormalities Cushings ulcers Decreased gut motility Spasm and immobility Rhabdomyolysis from struggling against physical restraints ATN/renal failure
Central Nervous System
Cardiovascular
Gastrointestinal Musculoskeletal
Genitourologic
Table 4.2. Terms and definitions

Term Definition
Analgesia Cerebral resuscitation Conscious sedation
Defasciculating dose
Blunting the perception of pain locally or centrally. Management of ICP in head trauma patients via drugs, head elevation, or hyperventilation. Light-controlled depression of sensorium, pain perception and anxiolysis. Protective reflexes (gag, respiration) are intact. Deep-profound depression of awareness, necessitating attention of airway, ventilation and vital signs. Protective reflexes may be lost. Small dose of medication given prior to administracontinued on next page
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Depolarizing drugs
General anesthesia Nondepolarizing drugs Oligoanalgesia Pharmacodynamic Pharmacokinetic Pretreatment drugs
tion of a depolarizing paralytic such as succinylcholine to reduce muscle fasciculation. This reduces ICP, reduces IOP and decreases incidences of aspiration. Nicotinic receptor agonists that dissociate slowly and causes muscle to contract/fasciculate. During the time the agonist remains bound to the receptor, other agonist molecules cannot stimulate the receptor. Combined state of unconsciousness, amnesia, analgesia, and muscle relaxation. No response to surgery. Paralytics that are pure antagonist of the nicotinic receptor, causing muscle paralysis without muscle contraction (fasciculation). Failure to provide adequate pain control. The effects of a drug on the bodys different tissues and its receptors. The movement of a medication through the body and its various tissues or compartments. Drugs given to minimize the hemodynamic and intracranial effects of rapid sequence intubation drugs.
Psychomotor agitation Motor agitation due to altered mental status. Concussion, drugs of abuse, pain, and noxious stimuli may all cause it. Rapid sequence induction In anesthesiology, the term rapid-sequence induction is used to describe the initial steps in the delivery of general anesthesia in unprepared patients at risk for aspiration of gastric contents. Induction of a sleep state in preparation for surgery is the goal of treatment. The use of appropriate pharmacologic adjuncts to facilitate endotracheal intubation and to reduce adverse effects. It is an organized approach to emergency intubation comprising rapid sedation and paralysis with minimal or no positive-pressure ventilation. In addition, adjunctive pharmacologic agents and techniques are used to minimize complications such as aspiration, hypoxemia, and sympathomimetic mediated rises in blood pressure and ICP. The production of a restful state of mind, by the use of a drug. A common pain assessment tool used for measuring acute and chronic pain. Patient is asked to make a mark along a 10 cm line with no pain at one end and worst that pain can be at the other end.
Rapid sequence intubation
Sedation Visual analogue scales
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agitation, but in some cases patients receive neither adequate sedation nor analgesia. Paralytics have no analgesic, sedative, anxiolytic or amnesic properties.
The Pharmacopoeia Analgesics (see Table 4.3)

Narcotics (e.g., morphine, meperidine, fentanyl, sufentanyl) NSAID (e.g., ketorolac, ibuprofen)
Sedatives (see Table 4.4)

Benzodiazepines (e.g., diazepam, lorazepam, midazolam) Barbiturates (e.g., methohexital, thiopental, pentobarbital) Etomidate Propofol
Antipsychotic (see Table 4.5)

Haloperidol Droperidol
Dissociative anesthetic (see Table 4.6)

Ketamine
Paralytics (see Table 4.7)

Depolarizing (e.g., succinylcholine) Nondepolarizing (e.g., pancuronium, vecuronium, rocuronium)
Principle of Dosing
Many of the agents listed have fairly wide dose ranges. Once clinical experience with an agent has developed, dosing becomes more accurate. For these reasons it is recommended that clinicians gain experience with a few selected agents rather than attempt to know the entire pharmacopoeia. Drugs used in combination with each other may have both pharmacokinetic and pharmacodynamic interactions, therefore combinations should be kept simple (e.g., fentanyl and midazolam).
Loading doses should be used to achieve the desired effect, then followed by a continuous infusion as needed. Reassess efficacy frequently. Combinations of analgesics and sedatives may be synergistic, which minimizes dosing requirements. Doses may need to be increased in those who are young, previously healthy, or are drug abusers. Doses should be decreased in some patients summarized in the mnemonic CLOCK:
Central nervous system disease Liver disease Older age Children and infants Kidney disease
Table 4.3. Analgesics

Contraindication Side effects Comments
Medications
Dosing
Indication
Narcotics
Morphine Hypotension Nausea and vomiting Respiratory depression Hypotension Histamine release Same as morphine Vagolytic response Accumulation of toxic metabolite (normeperidine may cause seizures and agitation) especially in renal dysfunction and in cumulative doses Same as morphine except less hypotension and less histamine release Wooden chest syndrome with higher dosing, due to dopaminergic stimulation (can be reversed with naloxone)
2.5-15 mg IV q4 hr 5-20 mg IM/SC q4 hr 10-30 mg PO/PR q4 hr 2-5 mg/hr drip
Drug of choice for relief of moderate to severe pain
Onset < 1 min IV, 10-30 min IM Duration 4-5 hr
Meperidine (Demerol) Atrial flutter and SVT (due to vagolytic response) MAO inhibitors use in past 14 days (may cause serotonin syndrome) Respiratory depression
50-150 mg IV/IM/SC q4 hr 10-20 mg/hr drip
Relief of moderate to severe pain
Onset 1min IV, 10-15 min IM Duration 2-4 hr Less smooth muscle spasm, constipation and cough depression than morphine Onset < 1 min IV Duration 0.5-1 hr
Fentanyl
2-150 mcg/kg IV q1-2 hr 25-50 mcg/hr drip
Brief analgesia Short painful procedures Decreasing ICP during intubation
continued on next page
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Table 4.3. continued

Medications
Dosing
Indication
Sufentanyl Same as morphine except less hypotension and less histamine release Wooden chest syndrome with higher dosing, due to dopaminergic stimulation (can be reversed with naloxone)
1-8 mcg/kg IV q1-2 hr
Brief analgesia Short painful procedures
Onset < 1 min IV Duration 0.25-1 hr More expensive
NSAID
Acute renal failure GI bleed associated with > 60 mg/dose GI bleed Reduce dose in elderly
Ketorolac (Toradol) Bleeding disorders Peptic ulcer disease
30 mg IV/IM q6 hr 10 mg PO q4-6 hr
Relief of mildBleeding disorders mod pain, Peptic ulcer disease especially renal colic
Ibuprofen (Motrin)
200-800 mg PO bid-qid
Relief of mild pain
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Table 4.4. Sedatives

Medication
Dosing
Indication
Benzodiazepines
Diazepam (Valium) Hypotension Hypotension if other depressants on board Prolonged effect in elderly and liver/renal dysfunction
2-20 mg IV/IM Treat anxiety or 0.1-0.2mg/kg IV/IM Treat ETOH 2-10 mg PO bid-qid withdrawal Treat seizures acutely
Amnestic in addition to sedation Consider benzodiazepine withdrawal Propylene glycol diluent associated hypotension and phlebitis Onset 1-3 min Duration 1-2 hr Active metabolites Onset 5-15 min, max effect 20-30 min Stacking doses at 45-60 min Duration 1-6 hr No active metabolites
Lorazepam (Ativan)
1-2 mg IV or 0.04 mg/kg IV 0.05/kg up to 4mg IM
Same as diazepam
Hypotension Respiratory depression
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Medication
Dosing
Indication
Midazolam (Versed)
1-5 mg IV or 0.05-0.1 mg/kg IV 5 mg IM or 0.07 mg/kg IM Drip 2-10 mg/hr Peds (6-12yr) 0.025-0.05 mg/kg IV, max 0.4 mg/kg
Conscious sedation for short procedures
Same as lorazepam Very short acting, CNS agitation (from inadequate thus excellent for or excessive dosing) short procedures Onset 1-2 min Duration 1-2 hr Drip required for longer sedation
Barbiturates and related drugs
Thiopental (Pentothal) Porphyria Cardiac disease Epilepsy ETOH withdraw Severe liver disease Asthma
3-5 mg/kg IV
Induction of general anesthesia
Hypotension Laryngospasm Histamine release causing bronchospasm May cause seizure by inducing transient withdrawal Decreases ICP Same as thiopental Less hypotension
Onset 10-20 sec Duration 5-15 min If laryngospasm occurs, give more brevital; decrease ICP Onset 0.2-0.5 seconds Duration 5-15 min
Methohexital (Brevital)
1-2 mg/kg IV 5-8 mg/kg IM
Short procedures Same as thiopental Induce of general anesthesia
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Medication
Dosing
Indication
Pentobarbital (Nembutal) Same as thiopental Same as thiopental
20-150 mg IV/IM/PO/PR tid-qid Drip 1mg/kg/hr Peds 2-6mg/kg/day Not FDA approved for age < 12 Prolonged sedation will inhibit cortisol production Decrease ICP Myoclonic jerks Nausea and vomiting
Short procedures Induction of general anesthesia
Onset < 1min Duration 15 min
Etomidate (Amidate)
0.2-0.4 mg/kg IV Drip 5-10 mcg/kg/min
Induction agent in RSI Induction and maintenance of general anesthesia
Minimal cardiovascular side effects Very useful induction agent in the emergency department Onset < 1min Duration 3-12 min after induction 0.1 mg/kg provide 100 sec of sleep Hypotension Decrease cerebral perfusion Respiratory depression Patients need to be intubated Onset 30 sec Duration 5 min
Propofol (Diprivan) Elderly with cardiopulmonary disease is relatively contraindicated
0.5-2 mg/kg IV Drip 25-100 mcg/kg/min
Induction agent in RSI Induction and maintenance of general anesthesia
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Table 4.5. Antipsychotics

Medication
Dosing
Indication
Haloperidol (Haldol) Theoretical decrease in seizure threshold Enhances actions of CNS depressants May increase QRS and QT intervals Extrapyramidal effect with IM route
2-5 mg IV/IM For rapid neuroleptization: start 5 mg IV, then double dose (10, 20, 40 and so on) until desired response, then repeat dose q 4hr 1-5 mg PO tid to start, usual effective dose 6-20 mg/day
Psychomotor agitation Psychosis Delirium Tourettes syndrome Huntingtons disease
Onset 3-5min Duration 1-12 hr Caution with type Ia agents and tricyclic overdoses
Table 4.6. Dissociative Anesthetics

Medication
Dosing
Indication
Ketamine Age< 3 months URI or pulmonary infection Tracheal stenosis or Cardiovascular disease Psychosis Relative contraindications: stimulation of posterior pharynx, head injury/CNS mass/possible increased ICP, glaucoma, hyperthyroidism, porphyria, asthma (for conscious sedation)
1-2 mg/kg IV 3-4 mg/kg IM For asthmatic intubation: 1.5 mg/kg slow IV then 0.51.0 mg/kg/hr IV
Conscious sedation for brief painful procedure Rapid sequence induction in asthmatics
Increased transient stridor and laryngospasm in age < 3 months Elevates ICP Nystagmus and ataxia (lasting 1-4 hr after administration) Emergence phenomenon (hallucinations and nightmares)
Also analgesic Maintains protective reflexes Onset 1-2 min Duration 10-30 min To decrease salivation and bronchial secretions: atropine 0.01mg/kg, max 0.5 mg or glycopyrrolate 0.005 mg/kg, max 0.25 mg
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Table 4.7. Paralytics

Duration Advantages Disadvantages
Medication
Dosing
Onset
Depolarizing Agent
Succinylcholine Rapid onset Short duration IM dosing possible if no IV access
1.0-1.5 mg/kg IV(for > 10 kg) 15-30 sec 3-12 min 1.0-2.0 mg/kg IV(for < 10 kg)
Contraindications1 Bradycardia Hypotension Dysrhythmia Cardiac arrest Pulmonary edema Increased gastric pressure Increased intraocular pressure Hyperkalemia Myoglobinuria Malignant hyperthermia Masseter spasm
Nondepolarizing Agents
Pancuronium 45-90 min
0.1 mg/kg IV
2-5 min
Little cardiovascular Useful in status asthmaticus Reversible with physostigmine 100-300 mcg/kg or neostigmine 25-75 mcg/kg
Contraindication2 Long action Prolonged paralysis with renal impairment Some histamine release
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Duration Advantages Disadvantages
Medication
Dosing
Onset
Vecuronium 25-60 min Few cardiovascular side effects Low risk for histamine release Shorter duration than pancuronium Reversible Fast onset Reversible
0.1-0.2 mg/kg IV
30-90 sec
Contraindication2 Longer duration than succinylcholine
Rocuronium 25-60 min
0.6-1.0 mg/kg IV
30-60 sec
Contraindication2 Increased heart rate
1. Crush injuries, glaucoma, penetrating eye injuries, significant neuromuscular disease, one week after burn or trauma, history or family history of malignant hyperthermia, pseudocholinesterase deficiency, myotonia, muscular dystrophy, paraplegia, and hyperkalemia. 2. Myasthenia gravis.
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Table 4.8. Local approaches to pain management

Approaches Utility
Fingers: digital, metacarpal nerve block Hand: ulnar, radial, median nerve block Elbow: intra-articular block Shoulder: intra-articular block Femur: femoral nerve block Ankle/foot: saphenous, peroneal, sural nerve block Face and mouth Cornea: topical anesthetics Upper lip and lateral nose: infraorbital nerve block Lower lip: mandibular nerve block Frontal scalp: supraorbital nerve block Miscellaneous Penis: dorsal penile nerve block Vulva/vagina: pudendal nerve block Ribs: intercostal nerve block Rib fractures and flail chest
Finger trauma with severe fractures and lacerations Hand trauma with severe fractures and lacerations Elbow dislocation Shoulder dislocation Hip fractures Ankle and foot fractures and lacerations
Complex and painful facial fractures and lacerations
Genital trauma
Table 4.9. Different causes of pain and agitation in trauma patients

Hypoxia Hypoglycemia Airway obstruction Bladder distension Hypotension Pain Drugs Seizures Intracranial bleeds Fractures Glass Tape Early pulse oximetry, ABG as indicated Early accucheck to rule out this correctable problem Assess in primary survey, check frequently, use respiratory therapists often as adjunct to care Foley catheter early Frequent blood pressure checks and appropriate resuscitation Visual analog scale, treat early Especially sympathomimetics or alcohol Both preictal and postictal states can produce agitation Early CT scan Splinting, reduction and dressings can decrease pain dramatically Check for glass under the patient on a board, in eyes and other sensitive areas Check for taped eyebrows, hair, skin folds
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Local Approaches to Pain Management

Some painful conditions can be rapidly and safely dealt with by using a local approach. Intra-articular injections and nerve blocks may obviate the need for high doses of parenteral opioids. This approach mandates a detail neurovascular exam first, but can be extremely useful. In almost all cases a long acting agent such as bupivicaine should be used.
Rapid Sequence Intubation (RSI)
RSI uses appropriate pharmacologic adjuncts to facilitate endotracheal intubation. It is an organized approach to emergency intubation comprising rapid sedation and paralysis with minimal or no positive-pressure ventilation. Paying attention to sedation and analgesia is essential after intubation because the patient can no longer gesture or verbalize pain. Maintenance of appropriate sedation and analgesia will:
Prevent pulmonary complications (aspiration, ARDS, pneumothorax) Promote ventilation and the correction of acid base disturbances Optimize ICP Blunt the counter regulatory sympathomimetic surge Maximize patient comfort
Pediatrics
The approach to pain control and sedation in the pediatric patient is just as important, if not more important than in the adult. Often the pediatric patient is beyond reassurance and verbal interventions, therefore a pharmacological intervention is essential. When treating pediatric patients, accurate weights are critical to appropriate dosing. Since trauma patients cannot be weighed, a Broselow tape should be used to reach an accurate weight estimate. Age based formulas are less reliable and should be avoided, and may overestimate weights for Asian and Hispanics. Pediatric doses can be either greater or less than adults due to differential pathways of metabolism and elimination rates. Chloral hydrate and the Demerol/Phenergan/Thorazine cocktail have been widely condemned in the pediatric literature and have no role in the management of pediatric trauma patients.
Common Pitfalls
While advocating for appropriate analgesia and sedation in trauma patients, some pitfalls should be recognized.
Even before initiating care, a thorough examination for treatable causes of pain and agitation should be done. Noxious stimuli such as taped hair and glass shards should be sought out and eliminated prior to sedation and analgesia.
Summary
Analgesia and sedation are important elements of trauma care that should be addressed early, usually in the emergency department. Appropriate drug selection and titration will improve the patients physiologic state, prevent diagnostic and treatment delays, and is the only humane approach. The RELIEF mnemonic will help those involved in trauma care to assess and treat pain. The tradition of oligoanalgesia is no longer acceptable in the face of
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an expanded pharmacopioea of titratable short acting and vital signs neutral drugs. Record the pain score on the patients chart before and after treatment. Ease the patients concernsoften the fear of pain is more distressing than the pain itself. Inform the patient that pain control is a goal of the ED patient care team. Look and listen to the patientthey will be the best judge on how much pain they are having and how much relief they have obtained. Inquire: always ask the patient if they need pain medication. Educate ED staff on proper analgesic techniques. Facilitate multi-disciplinary protocols with nursing and other specialties to manage common painful conditions in the ED. An overview of the drugs available leads to the following recommendations:
References
1. 2. 3. 4. 5. Raj PP, Hartrick C, Pither CE. Pain management of the injured. In: Capan LM, Miller SM, Trundort H, eds. Trauma Anesthesia and Intensive Care. New York: JB Lippincott 1991:685-723. Carr DB, Goudas LC. Acute Pain Lancet 1999; 353:2051-58. Wilson JE, Pendleton JM. Oligoanalgesia in the emergency department. Am J Emerg Med 1989; 7:620-623. Pace S. Intravenous morphine for early pain relief in patients with acute abdominal pain. Acad Emerg Med 1996; 3:1086-1092. Acute Pain Management Guideline Panel: Acute Pain Management: Operative or Medical Procedures and Trauma. AHCPR Pub. No. 92-0032. Rockville, MD: Agency for Health Care Policy and Research, Public Health Service, U.S. Department of Health and Human Services. Feb. 1992.
CHAPTER 5
Emergency Airway Management in the Trauma Patient

Kirsten Robinson and Sean O. Henderson Overview of the Trauma Airway
In any patient, securing an adequate airway should be the first priority for the physician. Proper use of medications and procedural techniques will facilitate this task as well as maximize patient comfort, safety, and therapeutic benefits. The trauma patient demands special attention to the airway for many reasons. These include: The possibility of anatomic variables that could make ventilation, intubation, and placement of a surgical airway difficult: facial fractures, neck/laryngeal trauma, local hematoma with mass effect, and direct airway disruption secondary to trauma. Cervical spine (C-spine) immobilization which prevents optimal visualization of airway structures. Combative behavior whether due to intoxication, hypoxia, pain, etc. This can create difficulty in both assessment and management of the airway. Hemodynamic instability. This is of special concern when deciding which medications to use prior to definitive airway procedures. Head trauma or altered level of consciousness (ALOC) where increased intracranial pressure (ICP) may be present. Direct stimulation of the larynx during intubation can elevate ICP placing these patients at higher risk of herniation and secondary brain injury.
Rapid Sequence Intubation

Rapid Sequence Intubation (RSI) refers to use of a sedative followed immediately by a paralytic agent in order to facilitate placement of an oral endotracheal tube and minimize the risk of subsequent aspiration. In addition, RSI allows for administration of medications which may provide therapeutic benefit to the patient by blunting the adverse cardiovascular/cerebrovascular effects that occur with airway manipulation. RSI is the standard of care for the patient who needs emergent intubation in whom the time of most recent food ingestion is unknown (and who, therefore, is at risk for aspiration of gastric contents).
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Kirsten Robinson, Department of Emergency Medicine, LAC+USC Medical Center, Los Angeles, California, U.S.A. Sean O. Henderson, Department of Emergency Medicine, LAC+USC Medical Center, Los Angeles, California, U.S.A.
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Contraindication
Anticipated difficult intubation in which mask ventilation may not be possible if intubation fails (massive facial trauma, expanding neck hematoma, etc). In this case, alternative airway techniques may be mandated (see section D).
Technique
RSI involves the sequential Ps (Table 5.1). Keep in mind that the specifics of each step will vary depending upon the patient and the injuries present. Preparation: All of the necessary airway equipment/medications as well as appropriate staff must be present and the equipment verified to be in working order. Preoxygenation: Placing a patient (with spontaneous respirations) on 100% oxygen for 2-5 minutes will allow for a period of approximately 3-7 minutes of apnea without desaturation. This permits the physician to avoid bag valve mask (BVM) ventilation during pretreatment and paralysis. Use of positive pressure ventilation, as with BVM, can lead to gastric distension which increases the risk of aspiration. Thus, preoxygenation is the key factor towards minimizing aspiration during RSI. Ideally, this step should be begun in the field or during the preparation phase. Pretreatment: In this phase, the patient is given agents to counteract the adverse circulatory effects of intubation. Airway manipulation leads to reflex neural responses which manifest as tachycardia, hypertension, increased myocardial oxygen demand, fasciculations, increased intracranial pressure (ICP), and increased intraocular pressure (IOP). The physician can minimize these sequelae by pretreating with cerebroprotective agents and a defasciculating dose of paralytic. Ideally, pretreatment should precede paralysis by 3 minutes. Paralysis with Induction: It is here that one gives a sedative agent followed immediately by a paralytic. Unless the patient is hypoxic, BVM ventilation should be avoided as noted above. If ventilation is required, the Sellick maneuver should be performed concomitantly in order to minimize air entry into the stomach. Placement of the Tube: After achieving complete relaxation/paralysis, the patient may be intubated. Afterwards, appropriate tube placement should be confirmed via ausculation, end capnography, chest x-ray (CXR), and pulse oximeter.
Pharmacologic Therapy in RSI

In this section, we will cover sedatives, neuromuscular blocking agents (paralytics), and cerebroprotective agents. Generally, those medications with the most rapid onset of action and shortest half-life are preferredin the case of a failed intubation, the need for positive pressure ventilation by BVM is minimized. However, the physician should also consider the side effect profile, efficacy, and personal experience when selecting which drugs to use. With a few exceptions, the specifics of metabolism will not be considered as these drugs are generally for single dose use when used for RSI.
Neuromuscular Blocking Agents

There are two classes of paralytics: a) depolarizing agents which bind with the acetylcholine (ACh) receptor at the motor end plate and lead to sustained
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Trauma Management
Table 5.1. The Ps of RSI

RSI 1. Preparation
2. Preoxygenation 3. Pretreatment 4. Paralysis 5. Pass the tube
depolarizationsuccinylcholine (SCh) is the only agent of this class to consider for use; and b) nondepolarizing agents which bind competitively at the Ach receptor and prevent depolarization. SCh is the paralytic most commonly used for RSI because it has the most rapid onset and the shortest duration of action (Table 5.2). Although rare, there are contraindications to SCh which may mandate use of a longer-acting nondepolarizing agent.
Succinylcholine
Extremely rapid onset of action of 60 seconds which makes SCh the ideal medication to use for RSI. This is especially true for patients receiving a suboptimal period of preoxygenation who may not tolerate even short periods of apnea. SCh is rapidly hydrolyzed by plasma pseudocholinesterase and so has a short duration of action3-10 minutes. The dose varies with age: 2 mg/kg for children less than 10 years of age and 1-1.5 mg/kg for adults and older children. The higher dose of 1.5 mg/kg may be required in patients who receive a defasciculating dose of a nondepolarizing agent. Side Effects
Unlike nondepolarizing agents, SCh may cause muscle fasciculations. After binding at the ACh receptor, the initial depolarization presents as uncoordinated muscle activity or fasciculations. These are possibly linked to muscle soreness, increased intragastric pressure (via fasciculations of the abdominal musculature), and increased ICP/IOP. This side effect may be prevented by giving a defasciculating dose of a nondepolarizing agent during the pretreatment phase. Pediatric patients are less likely to have this side effect. SCh causes cardiovascular changes via its action at ACh receptors in the autonomic ganglia and at muscarinic receptors. These changes may present as hypertension and both tachycardic and bradycardic dysrrhythmias. Pediatric patients are especially likely to experience bradycardia and should receive atropine 0.02 mg/kg during the pretreatment phase. These changes may be of particular concern in the elderly with underlying cardiovascular disease. Mild hyperkalemia ( 0.5 mEq/L) can occur because of a transient release of potassium from the muscle cell after it is depolarized. Even in patients with renal failure, this elevation of K+ is usually mild. This effect may be severe in patients with burns, trauma, intraabdominal sepsis, and denervation syndromes. However, the risk period for dangerous hyperkalemia begins several days after injury or symptom onset. Therefore, a nondepolarizing agent should be used in patients with known preexisting hyperkalemia, subacute burns/major tissue trauma, and subacute/chronic denervation disorders.
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Table 5.2. Neuromuscular blocking agents used in RSI

Agent Time to Onset Duration of Action Dose (mg/kg) Side Effects IOP, ICP, IGP fasciculations K+ (mild) HR, BP histamine release
Succinylcholine (D) Pancuronium (ND) Vecuronium (ND) Rocuronium (ND)
60 sec.
3-10 min.
1-1.5 2 for pediatric patients 0.01 defasciculating dose 0.1-0.15 intubating dose 0.01 defasciculating dose 0.1-0.15 intubating dose 0.5-1.0
1-5 min.
40-80 min.
2-5 min.
20-40 min.
minimal
1-3 min. 20-25 min. (dose dep) (dose dep)
minimal
D, depolarizing; ND, nondepolarizing; IOP, intraocular pressure; ICP, intracranial pressure; IGP, intragastric pressure; HR, heart rate; BP, blood pressure
Malignant hyperthermia characterized by muscle rigidity and hyperpyrexia may occur in those patients who are genetically predisposed (rare). In cases where patients know that they possess this predisposition, a nondepolarizing agent should be used. Decreased metabolism of SCh can occur in patients with genetically abnormal pseudocholinesterase or in those patients with decreased levels of the normal enzyme (seen with liver disease, pregnancy, connective tissue disease, cancer, therapeutic use of cholinesterase inhibitors for myasthenia gravis). This is not a definite contraindication to use of SCh, but the physician should keep in mind that the duration of action may be very prolonged in such cases.
Pancuronium (Pavulon)
Onset of action is 1-5 minutes with a duration of action from 40-80 minutes. Because of the longer duration of action, this agent is most commonly used in the emergency department as a defasciculating medication at a dose of 0.01 mg/kg. However, pancuronium may also be used to maintain paralysis in patients who are already intubated or may be given rather than SCh for intubation (as in the case of hyperkalemia or other contraindication for SCh). In these latter two cases, the dose is 0.1-0.15 mg/kg. Side Effects
The main adverse effects are transient tachycardia and hypertension. This is generally of little consequence except in those patients with severe underlying cardiovascular disease. May also cause histamine release although thought to be minimal. Like other nondepolarizing agents, may result in prolonged paralysis when given to patients in conjunction with aminoglycoside medications, tetracycline, clindamycin, and several other less commonly used medications.
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Trauma Management
Vecuronium
A structural analog of pancuronium. This agent was originally designed to minimize the cardiovascular side effects seen with its parent compound and, in fact, produces little or no cardiovascular changes. Onset of action is two to five minutes with a duration of action from 20-40 minutes (@ half that of pancuronium). Like pancuronium, vecuronium is mainly used for defasciculation and to maintain paralysis after intubation. Defasciculating and intubating doses identical to pancuronium. Minimal side effects other than the prolonged duration of action seen when given with aminoglycosides, etc.
Rocuronium
Nondepolarizing agent which is structurally similar to vecuronium. Designed to be more rapid-acting than other nondepolarizing agents and, thus, serve as an alternative to SCh and its adverse side effects. Onset of action is similar to that of SCh, one to two minutes. Duration of action varies depending upon the dose but ranges from 20-25 minutes. Dose ranges from 0.5-1.0 mg/kg. The higher doses give more rapid onset of action ( SCh) but also lead to longer duration of action. Not used for defasciculation. Minimal side effects.
Sedatives
The necessity of sedating agents in RSI is twofold: 1) to blunt the adverse hemodynamic and cerebrovascular effects of paralysis and intubation as previously noted; and 2) to minimize the negative psychologic sequelae of paralysis. All but the completely unresponsive patient require sedation prior to paralysis, and even the unresponsive patient may warrant the use of a sedating agent if there is any possibility of an intracranial injury. As with the paralytic agents, the ideal sedative for RSI in the trauma patient would have a rapid onset of action, a short half-life, and minimal adverse hemodynamic effects. While numerous sedating agents are available, only a relative few are appropriate for use in RSI (Table 5.3).
Etomidate
This is an imidazole derivative unrelated to other sedative/hypnotic agents and is rapidly becoming the agent of choice for sedation in RSI. Purely hypnotichas no anticonvulsant, analgesic, or amnestic properties. Onset of action is 60 seconds with a duration of action of five minutes. Dosage is 0.3 mg/kg. Benefits:
Decreases IOP, ICP, and cerebral metabolism which makes it ideal for use in patients with intracranial and penetrating globe injuries. Has little to no effect on blood pressure and heart rate which makes it unique among the other sedative agents and ideal for the trauma patient where hypotension and/or shock are often present.
Side effects:
Postprocedural nausea and vomiting.
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Cortisol suppressionwhile initially thought to be a significant adverse effect, now felt to be of little consequence after single dose use.
Midazolam
This is the only benzodiazepine well-suited for use in RSI. While other shortacting benzodiazepines exist, this is the only one available for intravenous use. When adequately dosed, onset of action is 30-120 seconds with a duration of action of 10-20 minutes. Commonly given in doses of 0.02-0.1 mg/kg for procedural sedation but higher doses of 0.1-0.3 mg/kg should be given in RSI as this will produce a much more rapid onset of action. Benefits: in addition to sedation, midazolam also provides amnesia, muscle relaxation, and anticonvulsant activity. Side Effects
Hypotension Respiratory depressionthis is obviously of no concern in the intubated patient, but may be problematic in the case of a failed intubation.
Sodium Thiopental and Methohexital

These are the only two barbiturates which should be considered for use in RSI and are used mainly for the patient with isolated head injury. These agents are extremely lipid soluble which allows for rapid penetration into the central nervous system (CNS) followed by rapid redistribution to lean body tissue. This explains the prompt induction and short-lived duration of anesthesia. Kinetics are similar to that of etomidate. Dose is 2-5 mg/kg for thiopental and 1 mg/kg for methohexital. Benefits
Anticonvulsant properties (thiopental). Reduce ICP and cerebral metabolism.
Side Effects
Respiratory depression. May cause marked hypotension secondary to both myocardial depression and vasodilatation. While decreased doses may minimize the degree of hypotension, use of other agents is warranted in those patients with preexisting hypotension and in the polytrauma patient who is potentially hemodynamically unstable.6 Histamine release which may produce bronchospasm and laryngospasm. Muscle spasm/myoclonus (methohexital). Decreased seizure threshold (methohexital).
Fentanyl
A synthetic narcotic which is 50-100 times more potent than morphine. Onset of action is approximately two minutes with a duration of action 30-40 minutes. Dose is 3-5 mg/kg. Benefits
Decreases ICP. Blunts the cardiovascular changes (tachycardia, hypertension) that may occur with intubation and administration of SCh. Provides analgesia.
5
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Table 5.3. Sedating Agents used in RSI for the trauma patient
Dose Advantages Side Effects
Agent
Time to Onset
Duration of Action
Etomidate 0.3 mg/kg 0.1-0.3 mg/kg.
60 sec.
5 min.
Midazolam
30-120 sec.
10-20 min.
Thiopental 2-5 mg/kg
30-60 sec.
5-10 min.
Methohexital 1 mg/kg
30-60 sec.
5 min.
Trauma Management
Fentanyl (also Alfentamil, Sufentamil) 3-5 g/kg
2 min.
30-40 min.
Adv: IOP, ICP hemodynamic stability SE: cortisol suppression emesis Adv: anticonvulsant/amnestic SE: tachycardia respiratory depression hypotension Adv: anticonvulsant ICP, cerebral metabolism SE: hypotension respiratory depression broncho/larygospasm Adv: ICP SE: hypotension bronch/laryngospasm seizure threshold myoclonus respiratory depression Adv: ICP analgesic blunts CV response hemodynamic stability reversal with naloxone SE: muscle rigidity bradycardia respiratory depression
Dose Advantages Side Effects
Agent
Time to Onset
Duration of Action
Propofol 1-3 min
30 sec.
Ketamine 1-2 mg/kg
30-60 sec.
5-15 min.
1.0-2.5 mg/kg Adv: ICP, IOP SE: hypotension, CO respiratory depression risk - bacterial contamination Adv: airway reflexes intact CO, HR, BP bronchodilation SE: emergence phenomena ICP, IOP mycoardial O2 demand
ICP, intracranial pressure; IOP, intraocular pressure; CV, cardiovascular; CO, cardiac output; HR, heart rate; BP, blood pressure
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62 Minimal effect on blood pressure. Easily reversed with Narcan.
Trauma Management
Side Effects
Respiratory depression. Bradycardia. May see skeletal muscle rigidityinvolvement of the chest wall musculature can interfere with ventilation. This typically occurs after very rapid injection. Treatment is with a neuromuscular blocking agent.
Sufentanil and alfentanil are newer, more potent synthetic narcotic agents which differ from fentanyl mainly in their kinetic profile. Both have an immediate onset of action and a very short duration of action. Dose is 10-25 mg/kg for sufentanil and 8-20 mg/kg for alfentanil.
Propofol
A sedative/hypnotic unrelated to other agents. Like the barbiturates, propofol is highly lipid soluble and so has rapid penetration into the CNS followed by rapid redistribution. Onset of action is 30-40 seconds with a short duration of action of several minutes. Dose is 1.0-2.5 mg/kg for bolus use. Benefits
Decreases cerebral blood flow, ICP, and cerebral oxygen consumption. Decreases IOP.
Side Effects
Respiratory depression. Decreased cardiac output, hypotension. Difficulty of use: propofol is maintained in an oily, organic emulsion consisting of soybean oil, glycerol, and egg lecithin. Although a bacteriostatic agent has been added, but this medication can potentially support the growth of microorganisms. As a result, the use of propofol demands extremely strict adherence to asepsispossibly a concern in the often chaotic setting of a trauma resuscitation.
Ketamine
This is a dissociative anesthetic related to PCP. The patient remains awake, but has deep analgesia and amnesia for the event. The principal setting for use in trauma is for the hemodynamically unstable patient without any possibility of intracranial injury.2 Onset of action is 30-60 seconds with a duration of 5-10 minutes after IV use (dont use the IM route for RSI). Dose is 1-2 mg/kg (IV). Benefits
Protective airway reflexes are maintainedespecially useful in the trauma setting where the time of most recent food ingestion is uncertain. Increases cardiac output, heart rate, and blood pressure. Bronchodilation.
Side Effects
Increases ICP, cerebral oxygen demand, cerebral blood flow, and IOP Increases myocardial oxygen consumption.
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Emergence phenomenon may occur including hallucinations and dysphoria. This is reported to occur mainly in the first few hours after awakening and is possibly less pronounced in pediatric patients.
Lidocaine
Lidocaine is an amide anesthetic whose usefulness as adjunctive therapy during RSI has been studied for decades. The effect of lidocaine (via both topical and IV administration) on heart rate, blood pressure, and ICP has been the subject of numerous investigations. While results of these studies are controversial, the majority of evidence suggests that lidocaine given IV at a dose of 1.0-1.5 mg/kg during the pretreatment phase of RSI can prevent the increased ICP which occurs due to SCh and airway manipulation. Lidocaine should be used for all patients with head injury or in whom the possibility of increased ICP exists (ALOC, etc).
Alternate Airway Techniques

In most cases, the initial approach at securing an airway in the trauma patient should be orotracheal intubation using RSI as described above. Even in potentially difficult airway settings (such as penetrating neck trauma), this is often the preferred and most effective route as many physicians are experienced in the procedure and it allows for direct visualization of the airway. There are times when securing the airway via RSI may not be possible and may even be detrimental: most often this occurs in the setting of severe facial injury or neck trauma. In these instances where it may be difficult to maintain oxygenation with BVM ventilation, the use of paralytics may create disaster as protective airway reflexes and spontaneous respiratory drive will be abolished. It is critical in the trauma patient for the physician to determine whether the potential for a difficult airway exists. It is equally important to recognize when standard techniques such as RSI and BVM ventilation are unsuccessfulthe failed airway. It is in these cases that alternate means of establishing an airway must be employed. The failed airway should be considered in the following situations:
Patients who cant be adequately ventilated by BVM. While a single attempt at orotracheal intubation is often appropriate, these patients demand an airway via other techniques (often surgical) if this attempt is unsuccessful. Further attempts at intubation are likely to increase airway trauma and prolong the duration of hypoxia. Patients who have undergone three unsuccessful attempts at intubation by a physician skilled in the procedure. This applies even to patients who can be adequately ventilated by BVM. If three attempts fail, the fourth is unlikely to succeed.
Many other techniques exist for placement of an effective airwayboth surgical and noninvasive. In general, these techniques should be considered for use only in the setting of the failed airway. However, some methods such as the lighted stylet and fiberoptic intubation may be useful as the primary means of securing the airway when difficulty is anticipated (see following discussion). As with the proper selection of intubation medications, the technique which is used should depend upon physician experience, availability of necessary equipment, and patient presentation.
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Trauma Management
The Surgical Airway Cricothyrotomy

Cricothyrotomy is the definitive mechanism of airway control for the failed airway and for those patients with massive facial trauma which precludes orotracheal intubation or other alternate methods. Cricothyrotomy should be performed in any patient with a failed airway who cant be adequately ventilated by BVM especially if other methods of airway control are not immediately available and appropriate for use. Preferred invasive airway method (vs. tracheostomy) because it is safer and easier to perform. Relative contraindications (considered only relative since this a technique of last resort):
Coagulopathy. Distortion of neck anatomy. Obstruction below the level of the cricothyroid membrane. Preexisting infection.
Absolute Contraindication: Age less than ten years of age. Because of their anatomical differences, smaller children require other invasive methods for the failed airway. Basic Technique
Vertical midline or horizontal skin incision followed by a horizontal incision through the inferior aspect of the cricothyroid membrane. The cricothyroid membrane is ideally cannulated with a cuffed tracheostomy tube, but one can also use small endotracheal tubes.
Complications
Bleeding Airway stenosis Creation of false passage Laceration of neighboring structures Mediastinal emphysema
Percutaneous Transtracheal Ventilation

Specific Indications
The failed airway in pediatric patients less than ten years of age where cricothyrotomy is contraindicated. Possibly as a temporizing measure for surgical cricothyrotomy.
Relative Contraindications
Proximal airway obstruction. Although this greatly increases the risk of pulmonary barotrauma because of failed exhalation, successful oxygenation can still be obtained. Coagulopathy Distortion of neck anatomy Preexisting infection
Basic Technique
Cannulation of the airway via a large-bore Angiocath through the cricothyroid membrane (10-14 g for adults; 18 g for pediatrics). Subsequent ventilation through the Angiocath using 55 psi wall oxygen source. Alternatively, the female end of the Angiocath can be connected to the male end of a 3.0 endotracheal tube and the patient ventilated with BVM.
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Noninvasive Rescue Airway Techniques Laryngeal Mask Airway (LMA)

A soft, silicone mask connected to a ventilation tube that is blindly inserted into the pharynx. The rim of the mask is then inflated which ideally provides a snug fit at the airway and minimizes air entry into the gastrointestinal tract during ventilation (see Fig. 5.1). Indication: For use only as a temporizing measure in patients with failed intubation who cant be adequately ventilated via BVM. Physicians familiar with its use should consider LMA for the failed airway especially if not skilled in cricothyrotomy or other alternate airway techniques. Advantages: Ease of placement. Although use of the LMA requires some instruction, it is easy to useno direct visualization is required and there is a high rate of successful insertion. Disadvantages: The LMA has mainly been used in the elective setting where patients have a known period of preprocedural fasting. The LMA does not provide adequate protection against aspiration. In fact, aspiration is likely to occur if the patient vomits.
Esophageal Tracheal Combitube

Double lumen tube which is placed blindly into either the esophagus (preferred) or the trachea. There is a large balloon located proximally that when inflated prevents the efflux of air through the upper airway (see Fig. 5.2). After determining where the tube has been placed, the appropriate port can be used for tracheal ventilation. Indication: Although mainly studied as an alternate airway management technique for prehospital personnel and persons not skilled in endotracheal intubation, the Combitube can be used in the emergency department. However with the LMA, its main use should be for the failed airway.2
The Lighted Stylet

A semiflexible, lighted stylet which is attached to a battery handle. The stylet is placed through an endotracheal tube which is subsequently attached to the battery handle via a special device. Technique:
The stylet is placed blindly using transillumination from the lighted tip through the midline soft tissues of the neck to guide placement into the airway. With appropriate placement, one should see strong transillumination versus faint as seen with esophageal placement. After proper placement, the endotracheal tube can be advanced over the stylet into the airway.
Indications
The failed airway where previous attempts at intubation have failed. Since paralysis is not necessary, it may be used instead of routine oral intubation in cases where a difficult airway is anticipatedfacial trauma, fixed dental appliances.
Advantages
Reduced concern regarding cervical spine manipulation in those patients with potential injury.
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Trauma Management
Fig. 5.1. Laryngeal Mask Airway (LMA).
High success rate. Ease of use since no direct visualization is required.
Disadvantages
Requires special equipment which may not be as readily available as that for a surgical airway. Also requires operator experience. Difficult to use in brightly lighted settings such as trauma resuscitation rooms.
Fiberoptic Intubation
Bronchoscopy is used to directly visualize the glottis. An endotracheal tube which has been threaded over the end of the bronchoscope can then be advanced into the trachea. Either the nasal or oral approach can be utilized. Indication: While this technique is most useful as an elective procedure, it can be useful in the emergency department setting for anticipated difficult oral intubation especially with distorted neck anatomy where paralysis and a surgical airway may be problematic. Advantage: Allows direct visualization of the airway. Disadvantages
May be difficult to properly identify airway structures in the presence of blood (and other secretions) as with many trauma patients. In fact, this is one of the principal reasons for failure to intubate via bronchoscopy.3 Requires very specialized equipment which is often not readily available and is expensive to maintain Demands a high degree of operator skill and a cooperative patient Time consuming Hypoxemia can occur during bronchoscopy which would mandate abortion of the procedure in order to ventilate the patient.
The Bullard Laryngoscope

A relatively new similar airway modality which employs a long, curved blade with a fiberoptic scope. A stylet may be attached which can be threaded through an endotracheal tube so that the scope and tube can be inserted as a unit.
67
5
Fig. 5.2. Esophogeal Tracheal Combitube.
Retrograde Intubation
Placement of an endotracheal tube via an over-the-wire method. Technique:
Cannulation of the cricothyroid membrane with a large-bore needle directed in a cephalad direction followed by passage of a guidewire through the needle directed toward the oropharynx. Identification of the guidewire in the mouth which can then be secured via forceps. Passage of the endotracheal tube over the guidewire. Once the tube is palpable at the cricothyroid membrane, the guidewire can be removed and the tube advanced to the appropriate level. Rarely used but can be considered for the failed or anticipated difficult airway.
Nasotracheal Intubation
Passage of an endotracheal tube blindly through the naris into the trachea. The tube should be one size smaller than that used for oral intubation. Technique:
Initial placement of the tube into the pharynx through the nose. Advancement of the tube into the trachea during inspiration with negative intrapleural pressure being used to guide accurate placement.
Contraindications
Apnea Midface and basilar skull fractures Combative patient Presence of an upper airway foreign body
Advantages
Used in the awake patient so no paralysis required. High success rate when performed by experienced individuals. Very safe in patients with potential cervical spine injury.
Complications
Epistaxismay be minimized by pretreatment with a topical vasoconstrictor.
68 Trauma to the vocal cords. Increased intracranial pressure. Creation of a false passage.
Trauma Management
Tactile Digital Intubation

Consists of blind placement of an endotracheal tube using the index and long fingers to guide the tube over the dorsum of the tongue and through the glottis. Rarely used but can be used as a last resort when other methods have failed. Advantages:
Minimal special equipment or skill required. Can be done rapidly with little preparation.
Disadvantages:
Higher risk of failure compared to other airway techniques. Operators hand at risk for bite injuries.
References
1. 2. 3. 4. 5. 6. 7. 8. 9. Walls R. Management of the difficult airway in the trauma patient. Emerg Med Clin North Am 1998; 16:45-61. Morris I. Pharmacologic aids to intubation and the rapid sequence induction. Emerg Med Clin North Am 1988; 6:753-768. Kharasch M, Graff J. Emergency management of the airway. Crit Care Clin. 1995; 11:53-66. Walls R. Rapid-sequence intubation in head trauma. Ann Emerg Med. 1993; 22:1008-1013. Schwartz D, Wiener-Kronish J. Management of the difficult airway. Cl Chest Med 1991: 12:483-495. Walls R. Rapid-sequence intubation in head trauma. Ann Emerg Med 1993; 22:1008-1013. Taylor P. Agents acting at the neuromuscular junction and autonomic ganglia. In: Gilman A, Rall T, Nies A, Taylor P, eds. Goodman and Gilmans The Pharmacological Basis of Therapeutics. 8th ed. New York: Pergamon Press, 1990:166-79. Kovac A. Controlling the hemodynamic response to laryngoscopy and endotracheal intubation. J Cl Anes 1996; 8:63-79. Schwartz D, Wiener-Kronish J. Management of the difficult airway. Cl Chest Med 1991; 12:483-495.
CHAPTER 1 CHAPTER 6
Shock and Resuscitation

Fred Bongard
Shock is defined as the inadequate delivery of oxygen and nutrients at the cellular level. It must be understood that shock may be organ specific and that not all organs are underperfused simultaneously. Indeed, as shock progresses, there exists a hierarchy of organ perfusion so that some organs such as the heart and brain may be minimally affected, while other tissues such as skin and muscle may be severely compromised.
Causes of Shock
Hypovolemic
- Hemorrhagic (most common following injury) - Nonsanguinous fluid loss (e.g., diarrhea, fistulas)
Distributive
- Neurogenic (e.g., after high spinal cord injury) - Anaphylactic/Anaphylactoid (e.g., drug reaction) - Sepsis (rarely responsible immediately after injury)
Cardiac
- Cardiac compressive (e.g., pericardial tamponade) - Cardiogenic (e.g., pump failure with congestive heart failure)
Hypovolemic Shock Etiology and Pathophysiology

Hemorrhagic shock is the most common form following injury and results from loss of circulating blood volume either internally or externally. Hallmark is decreased cardiac output, increased systemic vascular resistance, decreased central venous pressure, tachycardia, and hypotension.
- Concealed hemorrhage should always be considered in trauma victims. This represents blood loss into body cavities or tissue plains and generally requires imaging modalities to detect. Hemothorax: Each thoracic cavity can accommodate several liters of blood. A massive hemothorax occurs when more than 1500 mL is contained in the chest. This can severely compromise circulating blood volume. A history of blunt or penetrating chest injury should prompt consideration of a hemothorax. Hemoperitoneum: Intraabdominal bleeding from any source leads to hemoperitoneum. The abdominal cavity forms a capacious potential space and a large volume of blood is required before a change in abdominal girth is readily observed.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Fred Bongard, Division of Trauma and Critical Care, Harbor-UCLA Medical Center, UCLA School of Medicine, Los Angeles, California, U.S.A.
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Trauma Management - Do not be fooled into thinking that a nondistended abdomen does not contain blood. The most common cause of abdominal distention after injury is aerophagia (typically from bag-mask-valve ventilation) resulting in gastric distention. - The intraabdominal organs most commonly injured after blunt trauma leading to hemoperitoneum are: spleen (25%), liver (15%), and kidney (retroperitoneal, 12%). - The intraabdominal organs most commonly injured after penetrating trauma leading to hemoperitoneum are: small bowel (30%), mesentery and omentum (18%), and liver (16%). Retroperitoneal and pelvic hematomas occur following the injury of retroperitoneal structures (such as the kidneys or aorta), or fracture of the pelvis. Pelvic fractures with posterior element involvement (sacro-iliac joint) are particularly likely to cause extensive hemorrhage and hypotension. Orthopedic injuries: Fractures are common causes of concealed hemorrhage. Because of their hematopoetic function and requisite vascular connections, long bones such as the femur and tibia can lead to considerable concealed hemorrhage.
The severity of hypovolemic shock depends not only on the absolute amount of blood lost, but also upon the rate at which it was depleted, the age of the patient, and premorbid status.
Table 6.1. Hemorrhagic shock

Blood loss (mL) Blood loss (% BV) Pulse Rate Blood Pressure Pulse Pressure Respiratory Rate Urine Output (mL/hr) Mental Status Class I Up to 750 Up to 15% < 100 Normal Normal or Increased 14-20 > 30 Anxious Class II 750-1500 15-30% > 100 Normal Decreased 20-30 20-30 Anxious Class III 1500-2000 30-40% >120 Decreased Decreased 30-40 5-15 Confused Class IV > 2000 > 40% >140 Decreased Decreased >35 Nil Lethargic
Adapted from American College of Surgeons, Advanced Trauma Life Support for Physicians, 1993.
Hemodynamic Effects:
- As venous return falls, cardiac output and oxygen delivery decrease. Increased heart rate and peripheral vasoconstriction: These two compensatory reflexes help to maintain blood pressure. As volume falls, peripheral vascular resistance increases. This is apparent clinically by an increase in diastolic blood pressure and a fall in pulse pressure. In the terminal stage of shock, vasoconstriction fails and pulse pressure widens. Patient is cool to palpation. Pulses are difficult to feel. Femoral pulse typically palpable until blood pressure falls below 90 mm Hg. - Venoconstriction displaces pooled blood back toward the heart Neck veins are collapsed
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- As glomerular filtration falls, urine becomes more concentrated and urine output declines. - As intravascular volume (and hence pressure) falls, transvascular flow occurs. This allows the movement of blood-free fluid from the interstitial and intracellular spaces into the intravascular space to refill the vascular volume. Transvascular refill takes about 20 minutes to begin, and is essentially complete by two hours. The extent of transvascular refill is likely limited to a total of 1-2 liters. - This is the mechanism responsible for the decrease in hematocrit observed after blood loss. The red cell free fluid that refills the vascular space dilutes the number of red cells remaining, thereby decreasing the hematocrit.
Metabolic Effects:
- When oxygen delivery is inadequate, ATP must be generated through anaerobic glycolysis. Lactic acid is produced (lactate is also known as the ion of ischemia). Largely responsible for the acidemia which accompanies shock. - Causes a decrease in pH and fall in serum bicarbonate. Increase in the base deficit is observed on arterial blood gas analysis. - The decrease in red blood cell volume and cardiac output produces a decrease in systemic oxygen delivery. - Peripheral oxygen consumption stays constant until systemic oxygen delivery reaches a very low level. - Maintained oxygen consumption in the face of decreased oxygen delivery depends upon increased peripheral oxygen extraction. As more oxygen is removed from the blood delivered, the venous oxygen saturation (and content) declines. This is apparent on mixed venous blood gas testing. A fall in SvO2 (venous oxygen hemoglobin saturation) will be noted. Normal SvO2 is approximately 75%. Even small decreases in SvO2 signify important increases in oxygen extraction due to decreased oxygen delivery.
Neuroendocrine Effects
- Secretion of aldosterone and renin. Together, these two hormones increase renal retention of salt and water, which serve to maintain circulating blood volume - Secretion of epinephrine, glucagon, and cortisol. These stress hormones make energy stores available. They also assist in maintaining hemodynamic homeostasis.
Neurologic Effects
- Sympathetic stimulation increases peripheral vascular resistance to help maintain blood pressure. Sympathetic stimulation has little effect on intracerebral vessels. Autoregulation of the brains blood flow is maintained until mean systemic blood pressure falls below approximately 70 mm Hg.
Gastrointestinal Effects
- Decrease in splanchnic blood flow is one of the early consequences of systemic hypoperfusion. This decrease in oxygen delivery to the gut may permit bacterial translocation and subsequent systemic sepsis.
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Trauma Management
Clinical Findings
Changes in heart rate and blood pressure do not reliably indicate the extent of hypovolemia.
- Younger patients tend to maintain their blood pressure through increased peripheral vascular resistance with only minimal changes in heart rate. Older patients who cannot vasoconstrict as completely may maintain a seemingly normal blood pressure until they decompensate.
Decreased capillary perfusion produces coolness of the skin. The generalized sympathetic discharge responsible for vasoconstriction also causes sweating, leading to a moist or clammy sensation. Absence of jugular venous distention is due to hypovolemia.
- Although jugular venous distention is associated with pericardial tamponade and/or tension pneumothorax, patients who are hypovolemic may have normal appearing jugular veins even in the presence of either of these conditions.
Decreased urine output (< 0.5 mL/kg/hr) is due to decreased renal perfusion. Mental status is an important, and often overlooked, clinical parameter. Patients who are awake and normally responsive are likely to have adequate perfu--sion.
Be wary of the patient who presents with normal mental status and then becomes anxious, confused or lethargic. While this may be due to intracranial pathology (subdural, epidural, or subarachnoid hemorrhage), or to intoxicants, it may also be due to declining perfusion from worsening shock and unrecognized hemorrhage.
Laboratory Examination
There is no single laboratory examination which reliably includes or excludes the diagnosis of shock !! Hematocrit measures the volume percentage of red blood cells in plasma. Patients with hemorrhagic hypovolemic shock may have normal or decreased values of hematocrit. The hematocrit will depend on the amount of blood lost, the time elapsed since the blood loss, and the amounts of nonsanguinous fluid and blood transfused.
- Hematocrit declines after blood loss primarily through capillary refill (described above), in which red cell free fluid moves from the intracellular and interstitial spaces into the intravascular space. This begins approximately 20 minutes after injury. A patient presenting shortly after injury may have a relatively normal hematocrit.
Urine analysis will show concentrated urine with a high specific gravity. Lactic acid is usually elevated as a result of anaerobic metabolism.
- Serial determination of lactic acid is a useful parameter to follow during resuscitation. Progressive decrease in lactic acid is associated with an improved outcome.
Bicarbonate is decreased and base deficit is increased.

- Base deficit is an approximation of base depletion secondary to metabolic causes. It is a calculated value reported as part of a blood gas analysis. The base deficit can be used to calculate the amount of bicarbonate required to correct the acidosis. [HCO3-] required = Base deficit * 0.4 * Body Weight
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- Approximately one half of the calculated dose of bicarbonate should be given as an acute bolus.
Hemodynamic Monitoring
Blood pressure should be monitored by either invasive or noninvasive means. Whichever modality is chosen, values should be checked every several minutes to insure that therapy is efficacious. Pulse rate monitoring should accompany the EKG. Pulse oximetry is useful to ensure that arterial hemoglobin oxygen saturation is optimized.
- Pulse oximeters are perfusion dependent and may not work reliably in patients who are in severe shock or are hypothermic and profoundly vasoconstricted.
If the patient has been orotracheally or nasotracheally intubated, end-tidal carbon dioxide monitoring is helpful to evaluate CO2 excretion. Low values of end tidal CO2 suggest poor systemic perfusion, which prevents carbon dioxide from returning to the lung. Very low values of end tidal CO2 suggest cardiac decompensation or endotracheal tube dislodgement or misplacement. A urinary catheter should be inserted and connected to a calibrated collection device. Urine output less than 0.5 mL/kg/hr is consistent with inadequate renal perfusion and continued shock.
- The amount of urine present in the bladder at the time of initial catheterization is immaterial, as the patient may have had a full bladder prior to the injury. The initial return should be discarded and zero time begun with new urine collection. Although specific gravity testing is required to determine objectively how concentrated the urine is, dark urine suggests hypoperfusion and renal volume conservation. Hemolysis with hemoglobinuria and Rhabdomyolysis with myoglobinuria may also cause dark urine. A dipstick test for blood will be helpful in rapidly excluding either of these etiologies.
Central venous catheters are useful in only a limited number of situations and generally are not needed in the initial evaluation of the trauma patient. Furthermore, their insertion poses real risks such as vascular injury or creation of a pneumothorax. If a suspicion of pericardial tamponade exists and other modalities such as echocardiography are not available, a central venous catheter may be helpful.
Treatment
Resuscitation must follow an organized path. The first priority is ALWAYS assurance of an adequate airway and gas exchange.
- Endotracheal intubation is usually required. - When intubation is not possible or feasible (such as when the patient sustains massive orofacial trauma), cricothyroidotomy is the surgical airway of choice. - After the airway is secured, 100% oxygen should be used initially until adequate hemoglobin oxygen saturation is assured.
Adequate intravenous access is required for fluid replacement. At least two large bore upper extremity intravenous catheters should be placed.
- The rate at which fluid can be infused is directly proportional to the cross sectional area of the intravenous catheter. The resistance of these catheters is inversely proportional to the fourth power of the radius. Hence, a smaller catheter with one-half the radius of another will have 16 times the resistance to flow.
74
Trauma Management - Although access is often gained through a femoral vein, this route should be used only when upper extremity access is not possible. Injuries of the vena cava and/or iliac veins may allow extravasation of fluid infused through the lower extremities. Central venous access in the emergency situation is to be condemned as a modality of last choice. Normally, such catheters are placed with patients positioned in a manner that will open the thoracic inlet and expose the subclavian vein. Hypovolemic patients usually should not have their heads rotated (due to cervical spine precautions) and cannot have towels placed between their scapulae. For these reasons, the subclavian vein is relatively more difficult to cannulate and attempts may result in a simple or tension pneumothorax, a hemothorax, or a vascular injury. Dont do it! Interaosseous needles are effective and safe in children less than six years of age.
Resuscitation in adults should begin with rapid infusion of one to two liters of isotonic electrolyte solution.
- An initial bolus of 20 mL/kg should be used in children. - The total amount of fluid required for resuscitation is difficult to estimate. Using the table above, an approximation of the amount of blood lost can be made. Each 1 mL of blood loss should be replaced with 3 mL of isotonic electrolyte solution. The amount of fluid actually required should be based on the patients overall response rather than on a formula. Improvement in mental status, increased urine output, and decrease in tachycardia are favorable indicators. Some controversy still exists regarding the optimal fluid for resuscitation. Isotonic fluids (such as balanced salt solutions) have the same osmolality as body fluids. - Ringers lactate and normal (0.9%) saline are commonly used. - Some centers prefer normal saline because it can be mixed with blood. - Because the chloride concentration in lactated Ringers solution is less than that found in normal saline, and approximately equal to that of the intravascular space, many prefer lactated Ringers since it does not produce the metabolic hyperchloremic acidosis caused by resuscitation with normal saline. - Electrolytes and water partition themselves in a manner similar to the bodys extracellular water content: 75% extravascular and 25% intravascular. - This partitioning usually takes place within 30 minutes after the fluid is administered. - Within 2 hours, less than 20% of the infused fluid remains within the intravascular space. - Hypertonic saline (3% saline) expands the extracellular space by exerting an osmotic effect that displaces water from the intracellular compartment. May also exert positive inotropic effect. Decreases wound and peripheral edema. Smaller volume required making it attractive as an agent for resuscitation of mass casualties in remote sites. May have other salutary effects. - Colloids are solutions that rely on high molecular weight species to create osmotic effects.
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Colloids tend to stay within the intravascular space for longer periods than crystalloids. Smaller volumes are required. More expensive than crystalloids. No real advantage over crystalloids. - Other resuscitation fluids include albumin, starches, and dextrans. While some modest advantages have been demonstrated for each, they are significantly more expensive than crystalloid and generally should not be used. - Although the decision to institute blood transfusion must be individualized, a general rule is to begin blood infusion when crystalloid infusion exceeds 50 mL/ kg without stabilization or improvement of shock. This usually occurs after the first three liters of crystalloid have been infused. Blood is used primarily to restore oxygen carrying capacity volume resuscitation itself should be accomplished with crystalloids. Fully crossmatched blood is preferable. Type specific blood is usually available within 10 minutes of a patients specimen delivery to the blood bank. This blood is ABO, but not necessarily Rh, compatible. Type O packed cells should be used in the patient with exsanguinating hemorrhage. Type specific blood should be substituted as soon as it is available. Dilutional coagulopathy may follow massive blood transfusion, prompting the need for platelet and factor transfusion. - Hypothermia from the infusion of cold blood may also lead to coagulopathy. Every effort should be made to warm the blood during infusion. - Contrary to popular belief, most patients receiving massive transfusions do not need supplemental calcium.
M.A.S.T. primarily of historic interest

- Military AntiShock Trousers (also called pneumatic antishock garment) was popular for a brief time. - Applied to the lower extremities and abdomen, the garment was used when access to medical care was delayed (as in extended transport from the battlefield). Mechanism of action is still debated but may be related to either increased systemic vascular resistance or an autotransfusion of pooled venous blood. May still have some role in the management of hemorrhage in select patients with compound pelvic fractures in whom fracture stabilization is delayed. - Garment may improve the pelvic geometry and reduce the potential space for hemorrhage.
Pharmacologic agents (such as pressors) are seldom required to treat hypovolemic shock.
- It is imperative that a patient receive adequate volume resuscitation before the use of a pressor is even considered. If a pressor is to be used, the patient should be admitted to an intensive care unit and central venous pressure or pulmonary artery pressure monitoring instituted to ensure that volume replacement has been adequate.
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Trauma Management
There are no uniformly agreed upon endpoints for resuscitation from hypovolemic (hemorrhagic) shock. Return of mental status is useful, but patients may have a head injury or may have ingested alcohol or drugs which confound the situation. Decrease in base deficit and/or lactic acid concentration are associated with improved survival. Increased urine output, in the absence or glucosuria or intravenous dye administration (which produces an obligatory osmotic diuresis), signifies improved renal perfusion. Increased transcutaneous oxygen concentration is impractical in the acute situation as a resuscitation parameter. If a pulmonary artery catheter is in place, increased mixed venous oxygen saturation (SvO 2) and decreased oxygen extraction ratio signal improved systemic oxygen delivery.
Distributive Shock
Occurs when there is inappropriate distribution of blood flow to the viscera.
- An adequate volume of blood may be present, and cardiac output may be sufficient.
Types include septic, neurogenic, and anaphylactic.

- Septic shock rarely occurs in the acute situation.
Neurogenic shock
Preceded by trauma or spinal anesthesia.
Clinical Findings
Hypotension Never assume that a hypotensive patient with a spinal cord injury is in neurogenic shock until all potential causes of blood loss (hemorrhagic shock) have been excluded !
- If the level of spinal cord interruption is below the mid thorax, the proximal sympathetic nervous system is activated and a tachycardia is observed - If the level of interruption is high, sympathetic outflow is affected and bradycardia results.
Signs and symptoms of spinal cord injury and spinal shock are often present. Skin is pink and warm in the denervated areas. Patient is anxious (if awake) with paralysis of the lower body. Loss of the peripheral venous muscular pump may also decrease venous return.
Laboratory and Radiographic Examination

Laboratory studies are nonspecific. Radiographs should be obtained to help determine the level of the spinal injury.
- Computerized axial tomography with saggital reconstruction may be particularly useful. Be sure that the patient is adequately resuscitated before transport to the CT suite. - Never transport a hypotensive patient to CT scan with the sole intention of establishing a diagnosis!
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Treatment
As with all trauma patients, be sure that the airway is patent and that the patient is breathing.
- In very high injuries (above the fourth cervical vertebrae) breathing may be compromised by phrenic nerve interruption, making emergent airway intubation for mechanical ventilation an immediate priority. - Most patients in spinal shock will require airway intubation and mechanical ventilation. Many will have associated head or thoracic/abdominal injuries that will require operative intervention.
Infusion of large amounts of fluid will be required to ensure adequate venous return.
- Blood transfusion is seldom required unless hemorrhage from associated injuries is present. Prior to the use of pressors, a central venous catheter should be inserted to be sure that CVP has risen to a normal range with fluid infusion. - Do not hesitate to continue fluid infusion until CVP has reached 12-15 mm Hg. Phenylephrine or norepinephrine may be used as pressors. - These agents should be started at low doses and titrated to a mean blood pressure of 60-80 mm Hg. - Weaning from pressors can usually be achieved quickly.
Septic Shock
Occurs in association with overwhelming infection. Observed features are likely predominantly due to immune response to bacteria, their components, or their products. Rarely an immediate cause of hypotension in trauma patients.
- Generally occurs days to weeks later after the combination of hypotension and bacterial inoculation have had a chance to evoke an immune response. Mechanism of bacterial translocation has been invoked to explain sepsis in patients without apparent bacterial contamination. Hypotension with resultant hypoperfusion of the intestines may allow bacteria to translocate across compromised mucosa and into the blood stream and lymphatics. - Has been difficult to demonstrate in humans although good animal models exist.
Overall mortality from septic shock is 40-60%. Aerobic gram-negative bacillary infections are the most common cause.
- Long cascade of reactions is initiated by endotoxin contained in bacterial cell wall. - Gram positive organisms and fungi can also causes septic shock.
Clinical Features
Decreased blood pressure with increased heart rate and decreased urine output. Increased cardiac output with decreased systemic vascular resistance produces characteristic physical examination of warm and pink extremities. Underlying signs of infection and/or inflammation usually present.
- In the trauma patient, the chest and abdomen are the most common location. Infection of devitalized tissue in the extremities should also be considered.
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Trauma Management
Mental status is usually depressed. Patients may appear anxious and agitated. Tachypnea usually present. May even manifest as air hunger.
Hemodynamic and Laboratory Findings

Hypotension and tachycardia Oliguria If a pulmonary artery catheter is placed, increased cardiac output and decreased systemic vascular resistance are noted.
- Decreased peripheral consumption of oxygen produces a higher than normal SvO2 ( > 75%) and a lower than normal arteriovenous oxygen content difference ( < 4 mL/dL).
Increased white blood cell count with evidence of increased polymorphonuclear and immature forms. Disseminated intravascular coagulation as evidenced by decreased fibrinogen concentration, increased fibrin split products and fibrin monomers, increased d-dimer concentration, decreased platelet concentration, and increased PT and PTT. Hyperglycemia in the early stages
- Decreased glucose concentration may occur late and is an ominous sign, usually due to failure of hepatic glucose production.
Arterial blood gas determination reveals moderate hypoxemia and metabolic acidosis.
- Increased based deficit. - Increased lactic acid concentration.
Subsequent positive blood cultures are present in 45%.
Treatment
Intravenous crystalloid solution, such as normal saline or lactated Ringers solution, should be infused in sufficient quantity to overcome the maldistribution of total body water.
- Capillary leaks are common in septic shock, and lead to peripheral and pulmonary edema. - Cardiac output and left ventricular filling pressure determinations obtained from a pulmonary artery catheter should guide the amount of fluid infused. If the patient is in profound shock, an initial crystalloid bolus of 500 mL over 10-15 minutes is an appropriate starting point for a 70 kg patient. Pulmonary artery pressure should be increased to between 10-15 mm Hg. - Hemodilution is a common consequence, and may necessitate blood transfusion. - Minimum level of acceptable hemoglobin concentration before blood transfusion is required is not well defined. Many clinicians use a hematocrit of 25% as a transfusion trigger, but a higher hematocrit may be required in older patients with established cardiac disease. - Patients with refractory hypoxemia and decreased arterial oxyhemoglobin saturation will require higher levels of hemoglobin concentration to maintain adequate oxygen delivery.
Endotracheal intubation and mechanical ventilation will be required in most patients.

- Adult respiratory distress syndrome (ARDS) is a typical feature of septic shock.
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ARDS reduces lung compliance and gas exchange. During mechanical ventilation, an Inspiratory: Expiratory (I:E) ratio approaching 1:1, or inverted (i.e., 1.5:1) may be required for adequate gas exchange. Pressure controlled ventilation is a useful mode since it allows the clinician to preset the inspiratory pressure.
Appropriate antibiotics should be infused intravenously

- Broad-spectrum agents, preferably without renal toxicity, are preferred.
Pharmacological Support
- A pulmonary artery catheter should be placed prior to beginning pharmacological support to ensure that adequate fluid infusion has been achieved. The pulmonary artery catheter is also indispensable for monitoring the effects of pressor infusion. - Dopamine is the first choice of pressors Immediate precursor of endogenous epinephrine. - Effect is due to release of norepinephrine from sympathetic nerves and direct stimulation of alpha, beta, and dopaminergic receptors. - Depletion of norepinephrine in septic states may lead to dopamine tachyphylaxis. Effects somewhat dependent on dose. - At lower doses, has inotropic effect without significant increase in heart rate. - Renal blood flow and urine output generally increase in doses less than 5.0 g kg/min. - When dose reaches 10 g/kg/min, has both chronotropic and inotropic effect. - At doses in excess of 10 g/kg/min, alpha-adrenergic stimulation occurs with increase in systemic vascular resistance. - Dobutamine has predominantly B-adrenergic effect. Minor chronotropic effect Does not rely on preformed norepinephrine stores. - Loses effect after prolonged administration due to down-regulation of receptors. - Better choice for long-term infusion than dopamine. May actually decrease peripheral vascular resistance - Pressor of choice in patients with adequate blood pressure but depressed cardiac output. Infusion begun at 2-5 g/kg. Common dosing range is 5-15 g/kg/min. - Increased urine output may occur due to increased cardiac output. - Epinephrine produces dose-dependent increase in both systolic and diastolic pressure. Increase in blood pressure is caused by increase in heart rate and myocardial activity (beta-1 effect) and by an increase in systemic vascular resistance (alpha-1 effect). - Causes an increase in myocardial oxygen consumption. - High potential for arrhythmias. - More useful in the treatment of cardiac shock than in the management of septic shock. - May be of some limited value in hypotensive patients who are unresponsive to other treatment regimens.
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Trauma Management - Be alert for severe hypertension and ventricular arrhythmias, both of which may be transient. - Isoproterenol (Isuprel) is a nonselective -adrenergic agonist that is a positive inotrope and chronotrope. Venous return is increased because of decreased venous compliance. Pulmonary and systemic vascular resistances are decreased and may lead to a fall in blood pressure. Short duration of action. - May be useful in patients who do not respond to dopamine or to dobutamine. - Typical infusion rates are 0.01 g/kg/min and increased until the desired effect is obtained. - Alpha-adrenergic agents. When blood pressure remains depressed despite adequate fluid resuscitation and institution of dopamine and/or dobutamine, one of these agents may be tried. Norepinephrineposes both alpha and beta effects (at low doses). At higher doses, effect is primarily alpha with marked vasoconstriction, which may help to increase blood pressure by increasing systemic vascular resistance. This can decrease renal blood flow and produce mesenteric ischemia. Short half-life of about 2 minutes. Infusion rates are 0.05-0.1 g/kg/min. Usual maximum dose is 1 g/kg/min. Neosynephrine is a synthetic alpha-adrenergic agent that has effects similar to norepinephrine.
Cardiac Shock
Cardiac compressive shock occurs when the pericardial space is compromised and the cardiac chambers cannot fill. Most common with stab wounds to the chest which produce bleeding from a cardiac chamber or from a coronary artery.
Clinical Findings
Hypotension and tachycardia Distended neck veins Unlike tension pneumothorax, is not accompanied by deviation of the mediastinum or by change in breath sounds (unless an associated hemothorax is present)
Laboratory and Diagnostic Findings

Mechanism of injury should prompt suspicion of the diagnosis. Chest radiography seldom is diagnostic and usually wastes time. Ultrasonography (echocardiography) is diagnostic. If echocardiography is unavailable, a central venous catheter will show elevated central venous pressure.
- If an associated injury is present, hemorrhage and volume loss may prevent the expected increase in central venous pressure. While pericardiocentesis was recommended in the past, the availability of echocardiography relegates this modality to one of historic interest only.
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Treatment
Surgical relief of the tamponade with control of the bleeding vessel
- Pericardiocentesis will produce only temporary results and may be dangerous if a ventricular or coronary artery injury occurs as part of the procedure.
Cardiogenic Shock
Also known as pump failure Rarely occurs acutely after trauma except in previously compromised individuals May occasionally occur with myocardial contusion Always suspect hypovolemia as a cause of shock before entertaining cardiogenic shock as a diagnosis.
Clinical Findings
Hypotension, tachycardia (bradycardia in the terminal stages), increased systemic vascular resistance, oliguria, and signs of increased intravascular volume.
- Auscultation may reveal a third heart sound. - Neck veins are often distended, and if left ventricular failure is present. signs and symptoms of pulmonary edema will be apparent.
Chest pain may be present in the acute setting.
Laboratory and Diagnostic Findings

Chest X-ray is seldom diagnostic in the acute situation. Evidence of pulmonary edema and vascular congestion becomes apparent with time. Concentrated urine with high specific gravity, low sodium, and FeNa (fractional excretion of sodium) < 1. If acute myocardial injury is present (infarction or contusion) creatine phosphokine (MB fraction) and troponin will be elevated. Increased serum lactate. If a pulmonary artery catheter is inserted, pulmonary capillary wedge and central venous pressures will be high (unless hemorrhage has reduced circulating blood volume), cardiac output low, and systemic vascular resistance high.
- Note the key differentiating factor between cardiogenic and hypovolemic shock is increased central venous pressure in the former and decreased central venous pressure in the latter. - Decreased mixed venous hemoglobin oxygen saturation (SvO2 < 75%). Increased arterial-venous oxygen content difference ( > 6 gm O2/dl) due to increased peripheral oxygen extraction.
EKG evidence of myocardial infarction or ischemia may be present.
Treatment
Insure that pericardial tamponade is not present as the cause of decreased cardiac output and increased central venous pressure!! Begin supplemental oxygen to insure adequate myocardial oxygen delivery. A small amount of morphine will facilitate sedation and increase venous capacitance. This helps unload the heart. A pulmonary artery flotation catheter should be placed to measure filling pressures, calculate cardiac output, and derive oxygen variables. Intravenous nitroglycerin, nitroprusside, and beta-blockers are useful, but must be titrated with great care to avoid additional hypotension. Several pharmacologic agents (previously detailed) may be of help.
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Trauma Management Dopamine Dobutamine Epinephrine Amrinone and milrinone are phosphodiesterase inhibitors which probably decrease the intracellular breakdown of cyclic AMP. Increase cardiac output and decrease afterload and preload. Does not cause tachycardia or arrhythmias. Particularly useful in the treatment of cardiac, as opposed to, septic shock. - Loading dose of amrinone is 0.75 mg/kg over 3-5 minutes, followed by a maintenance infusion of 5-10 g/kg/min. Initial vasodilator effects may cause marked hypotension with the institution of therapy. - Significant side effect includes thrombocytopenia. - May be used in combination with dobutamine - Milrinone is more potent and has fewer side effects, but also causes pronounced arteriolar and venous dilator activity. Initial loading dose is 50 g/kg over 10 minutes, followed by continuous infusion of 0.375-0.75 g/kg/min. Should be used with extreme caution in patients with decreased afterload (such as septic shock).
Digitalis Vasodilators such as nitroprusside and nitroglycerin may be used to decrease systemic vascular resistance and allow the left ventricle to empty.
- Begin nitroprusside at 5-10 g/min and advance in increments of 2.5-5.0 g/min every ten minutes until an increase in cardiac output is noted. Use for more than 3 days may lead to cyanide toxicity. - Monitor thiocyante levels. Toxic level is > 10 mg/dL. - Begin nitroglycerin at 10 g/min and increase by 10 g/min every 5-10 minutes, until a total dose of 50-100 g/min is administered. Doses as high as 400 g/min can be tolerated for several days.
References
1. 2. 3. 4. Shock. In: American College of Surgeons. Advanced Trauma Life Support Manual. Chicago, IL: American College of Surgeons, 1993. Bongard FS. Shock and resuscitation. In: Bongard FS and Sue DY, eds. Current Critical Care Diagnosis and Treatment. Norwalk, CT: Appleton and Lange 1994. Holcroft JW. Shock: ICU management. In: Wilmore DW, Cheung LY, Harken AH et al, eds. American College of Surgeons Scientific American: Surgery. New York: Scientific American 1998. Holcroft JW. Shock. In: Wilmore DW, Cheung LY, Harken AH et al, eds. American College of Surgeons Scientific American: Surgery. New York: Scientific American 1998.
HEAD
CHAPTER 7
Management of Head Injury

Peter Gruen Nonpenetrating Head Injury Historical Perspectives
Trephination (opening the cranium) is a procedure that was practiced by the ancient Egyptians and precolonial Aztecs. Guidelines for the management of severe head injury published by organized North American neurosurgery (1995).
Incidence
Head injury is the cause of death in about 50% of trauma deaths in the US.
Mechanisms of Injury
The mechanisms of nonpenetrating head injury fall into two major categories: those due to acceleration-deceleration and those due to focal impact.
Acceleration Deceleration Injuries
Brain Contusion
Contusion is bruising of the tissue just below the pial surface that results from impact of brain tissue against the skull. Contusions are most common in cortex overlying the rough bone surface of the floor of the frontal (anterior) and temporal (middle) fossae.
Coup-Contre Coup Injury

Impact injury to the side of the brain contralateral to the head impact (Fig. 7.4)
Tearing of Bridging Veins

Small caliber veins that drain the cortex into the sagittal sinus may be torn. The tearing of bridging veins usually results in formation of a subdural hematoma. Elderly patients have atrophied brains with a larger subdural space separating their cortex from the sagittal sinus. Relatively minor displacements of the head can result in tearing of bridging veins with slow leakage of subdural blood (chronic subdural hematoma) in this age group (Fig. 7.1).
Sheering Forces
Sheering injuries to axons result in disruption and loss of neuronal function. Sheered brain tissue will show evidence of trauma in the form of retraction balls or glial scarring by microscopy. Unfortunately the brain has
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Peter Gruen, LAC + USC Medical Center, Los Angeles, California, U.S.A.
85
Fig. 7.1. Epidural with ipsilateral contusion.
no regenerative capacity so the dysfunction resulting from sheering is irreversible. The poor prognosis of sheer injuries is due not just to irreversibility but also due to the frequent involvement of the brain stem area.
- The brainstem reticular activating system that controls consciousness is situated at a very vulnerable site with respect to sheering injuries which can result in permanent coma in the absence of any cranial imaging abnormalities.
Sheering injuries frequently are not visible on computerized tomography of the head (head CT) and are the presumed diagnosis in the majority of head injured patients who present in coma with a negative head CT scan.
Focal Impact Injuries

A blow with its force focused at one site on the head frequently results in a soft tissue injury of the scalp and the underlying brain parenchyma. Middle meningeal artery laceration and epidural hematoma may occur on the intracranial side of a skull fracture.
Pathophysiology
Ischemia
Ischemia is a well-described consequence of head injury and a major cause of secondary brain damage.
Cerebral Edema
Increased tissue water and volume due to increased permeability of the blood brain barrier associated with a failure in the autoregulatory mechanisms of the cerebral arterial vasculature.
Autoregulation Failure
Normally the systolic and diastolic pressure of the blood in the cerebral vasculature is maintained within a relatively narrow range in spite of larger fluctuations in systemic pressures. This autoregulatory mechanism frequently fails following a cranial injury.
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Increased Intracranial Pressure

Intracranial pressure is the result of the pressure due to three volumes contained within the rigid, nonexpansile skull:
1. the brain parenchyma, 2. the cerebral vasculature, and 3. the cerebrospinal fluid spaces (ventricles, cisterns, sulci).
An increase in any one or more of these volumes will lead to an increase in the intracranial pressure unless there is a compensatory decrease in one or more of the other volumes. Increased intracranial pressure decreases cerebral perfusion according to the equation: CPP (cerebral perfusion pressure) = MAP (mean arterial pressure) ICP (intracranial pressure).
Herniation
Brain swelling can lead to occlusion of the subarachnoid CSF circulation pathways around and through the brain allowing for the occurrence of pressure gradients. Brain tissue in a higher pressure compartment moving down a gradient into a lower pressure compartment results in herniation. Herniation can occur across the midline, from the temporal into the posterior fossa (uncal herniation) or from the posterior fossa into the vertebral canal (cerebellar tonsillar herniation).
Clinical Presentation Neurologic

No Loss of Consciousness
Patients with a focal blow to the head are more likely to have no loss of consciousness than those with an acceleration-deceleration event. The absence of loss of consciousness in an acceleration-deceleration injury is reassuring that there is not significant intracranial pathology. However, nausea, vomiting, focal neurologic deficit are all indications for head CT.
Transient Loss of Consciousness

A transient loss of consciousness is suggestive of a mechanism of injury with enough force applied to the brainstem that it causes transient neurologic dysfunction at the level of the reticular activating formation. Loss of consciousness should, therefore, be an indication for obtaining a head CT scan even if the patient is conscious at the time he is encountered in the field and remains so in the DEM. Concussion is the diagnosis given to patients with a head injury significant enough to cause a transient loss of consciousness, but without traumatic hematoma or cerebral edema detected on head CT.
Seizures
Convulsions are frequent following head injury. They are particularly common in pediatric patients. Seizures are more common in patients who have subdural hematomas or contusions of the frontal or temporal lobes of the brain but can occur in patients with negative head CT who are diagnosed as having concussion.
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Found Down
Until proven otherwise, patients found unconscious with mechanism and time of injury unknown should have a head CT done.
Intoxicated
Intoxication is present in a large number of head trauma victims and in many patients who are found down. All intoxicated patients who are found unconscious, with a focal neurologic deficit, or with a GCS less than 15, with or without external signs of head trauma should have a head CT done.
Lucid Interval
Described as the classic presentation of epidural hematoma, the lucid interval is a period of time postinjury during which the patient is awake and alert (frequently not even complaining of a headache) while blood is accumulating in and expanding the narrow space between the brain and the inner side of the skull, but not yet of sufficient volume to cause impaired consciousness or other neurologic deficit. Once the volume of the clot reaches a critical threshold the patient can rapidly decompensate neurologically and descend into deep coma with focal deficit (such as hemiparesis, aphasia) or signs of brainstem compromise (papillary asymmetry, posturing. abnormal breathing pattern) and even brain death. Any patient who could be in the lucid interval particularly those with a mechanism suggestive of epidural hematoma (temporal blow) should be observed until a head CT has ruled out an expanding intracranial hematoma mass.
Focal Deficit
Focal deficits are those that can be lateralized to one side, or localized to one lobar region of the brain: Weakness (paresis), paralysis (plegia), and hyperreflexia. Language deficits are usually ascribed to a process resulting in dysfunction of the temporal lobe on the dominant (90-plus percent of brains) side. Profound language deficits such as receptive or expressive aphasia (complete inability to understand or speak) or dysphasia (partial but obvious inability) are usually due to dominant temporal and posterior frontal pathways, but nondominant and nontemporal injuries can also cause significant language impairments. Asymmetry, sluggishness, or absence of a pupillary response can be a sign of third nerve compression by a herniated temporal lobe but can also be due to injury to the afferent visual pathway deficit.
Brainstem Findings
The pupillary reflex pathway has an afferent (inward to the midbrain papillary constrictor nucleus) and efferent (outwards from the nucleus) arm. Normally the efferent parasympathetic constrictor innervation to the pupil is opposed by sympathetic innervation with the balance between the two resulting in a pupil midway between fully constricted and fully dilated. Injury to the constrictor (Edinger Westfal) nucleus or the outgoing third cranial nerve results in elimination of the parasympathetic constrictor output and a pupil that remains fixed and dilated by unopposed sympathetics. Posturing is a sign of brainstem dysfunction.
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Extensor posturing, (formerly called decerebrate posturing because of the animal model in which it was experimentally produced) presents as upper extremity extension at the shoulders, elbows, wrists, and fingers. Extensor posturing receives a 2 for Glascow Coma motor score reflecting the severity of the neurologic dysfunction and poor prognosis when this sign is present. Flexor posturing (formerly called decorticate posturing) presents as upper extremity flexion of the shoulders, elbows, wrists, and fingers. Flexor posturing receives a 3 for Glascow Coma motor score reflecting the severity of the neurologic dysfunction and poor prognosis when this sign is presentonly extensor posturing is a clinically more ominous movement.
Brain Death
Brain death is an irreversible neurologic syndrome characterized by absence of any central nervous activity above the level of the foramen magnum (cerebrum, basal ganglia, thalamus, cerebellum, brainstem). The criteria for brain death are discussed in a separate chapter.
Limitations of Clinical Examination

The side of a neurologic deficit does not necessarily predict the side of the brain with pathology. Herniation of the uncal portion of the temporal lobe can displace the brainstem against the opposite tentorial edge causing injury on the side opposite the herniation. Pupillary asymmetry or nonreactivity can also be misleading. Injury to the globe, optic nerve, or tracts can result in a deafferentation pupillary deficit that has a very different significance (not a brainstem injury) than does an afferent deficit of the third nerve at or near the brainstem pupillary constrictor (Edinger Westfal) nucleus or along the course of the nerve.
Management Prehospital Management

Patients with GCS < 8 should be intubated unless there is evidence of severe orofacial or suspected cervical trauma. Every patient should receive supplemental oxygen at the scene of injury and during transportation to the hospital. Intravenous access may be important in order to maintain blood pressure, cardiac output, and cerebral perfusion, and to administer anticonvulsants or sedatives.
Emergency Room Management

Hemodynamic treatment considerations have priority over intracranial. Hypotension and hypoxia are the major factors associated with worse neurologic outcome following head injury. Patients should be hemodynamically stabilized before any cerebral resuscitative or surgical interventions are undertaken. Cerebral resuscitative measures that conflict with hemodynamic stabilization should be deferred (such as administration of mannitol to bring down ICP in a hypovolemic patient). The Glascow Coma Score (GCS) and pupillary reactivity are the most important prognostic indicators. Patients with a GCS of 8 or less are considered to
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have severe head injuries and, due to the high association between increased ICP and low GCS, are candidates for intracranial pressure monitoring. The clinician must assume that every patient with closed head injury and headache, vomiting, focal neurologic deficit, or GCS less than 15 has increased intracranial pressure and/or a lesion requiring evacuation until these are ruled out by a period of hospital observation and/or head CT and/or intracranial pressure monitoring. The optimal angle for head elevation is 30. In the absence of other injuries and with no concern about hypovolemia intravenous fluid administration (normal saline) at 75 ml/hr-1 is adequate. To maintain cerebral perfusion, in the absence of ICP data, euvolemia should be the goal of fluid administration. Central venous pressure monitoring can be helpful in maintaining adequate volume at low hourly infusion rates. Diuresis should be administered only to patients with clinical findings (sensorium, motor system, pupils) suggestive of increased intracranial pressure or its associated epiphenomena (i.e., herniation). Moderate hyperventilation (PC02 32-35 mmHg) should be considered only in patients with clinical findings (sensorium, motor system, pupils) suggestive of increased intracranial pressure or its associated epiphenomena (i.e., herniation).
- Severe hypocapnia may aggravate brain hypoperfusion.
Sedation and paralysis should be administered for the comfort and safety of the patient. Whenever possible agents for sedation and paralysis should be short acting and easily and reliably reversed. Opiates not only decrease agitation, but also blunt some of the sympathetic responses seen in head injury, such as hypertension and tachycardia, and decrease the amount of shivering. Possibly for the preceding reasons but perhaps by other mechanisms as well, opiates frequently decrease intracranial pressure.
- The opiates have the advantage of being readily reversible with naloxone. - Haldol (Haloperidol) interferes little with the neurologic exam, but it may cause extrapyramidal symptoms, and is not pharmacologically reversible.
Benzodiazepines are useful for sedation but are not as readily reversible as opiates. Like opiates they are respiratory depressants and their use may require intubation of the patient who otherwise would not require this intervention. Pharmacological paralysis with long-acting agents (Pancuronium, Vecuronium) make neurologic exam impossible for several hours. The drugs can be useful in the ICU to control ICP but in the ER should be limited to a defasciculating dose administered with a depolarizing agent short-acting (succinylcholine).
- Depolarizing agents (Succinyl-choline) are short acting (usually paralysis wears off within 20 minutes) but because of the associated violent muscular contractions they should be administered with a defasciculating dose of a receptor blocker. - A neurosurgical consultation should be called for every patient with head injury and loss of consciousness if the CT scan is positive for any acute traumatic finding.
Intracranial Pressure Monitoring

The indications for intracranial pressure monitoring are a low GCS (< 8) with an abnormal head CT scan or a GCS 9-12 with abnormal CT scan if the patient will undergo a prolonged operation for extracranial injuries.
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Trauma Management - The Cerebral Perfusion Pressure (CPP) should be kept above 60 mmHg. - Without valves to create differential pressure among the compartments, the ICP is the same in the entire intracranial spaceepidural, subdural, subarachnoid, intraparenchymal, intraventricular. An ICP catheter can be placed in any of these spaces. The advantage of placing an ICP monitor in the ventricular space (when the ventricles are adequately large so that this is technically feasible) is that in addition to measuring ICP, CSF can be drained in cases of intracranial hypertension.
Investigations
A head CT scan should be done on any head injury patient who presents with a history of loss of consciousness, headache, amnesia, GCS< 15, or localizing signs.
- Findings suggestive of increased intracranial pressure include cisternal obliteration and midline shift (Fig. 7.1). - Patients who have a positive finding on an initial CT require a repeat study the next day.
Operating Room Management

Exploratory Burr Holes
Exploratory burr holes are placed in four sites on the side of suspected extraaxial pathology in patients who present with a low GCS when CT scanning is not available within a reasonable time frame (1-2 hours) or in patients whose findings are suggestive of such pathology but who are hemodynamically unstable and must be taken to the operating room for life-saving intrathoracic or intraabdominal surgery.
- The burr holes should be placed over each of the lobes of the brain where hematomas are likely to occur and suboccipitally in the posterior fossa (Fig. 7.2).
Craniostomy
After ten days to two weeks a solid clot in the subdural (or much less frequently, the epidural) space has lysed sufficiently so that it appears on CT scanning as a liquefied collection. Liquid can be drained through a small diameter catheter placed through a twist drill hole made through the skull.
Craniotomy
A craniotomy is necessary for the evacuation of acute hematomas associated with coagulated, solid blood.
Brain Resections
One frontal lobe can be removed (assuming the other is functionally normal) without a detectable neuropsychologic deficit. The anterior 5 cm of the dominant and 7 cm of the nondominant temporal lobes can be resected without a deficit.
Late Complications
Traumatic aneurysms occur at sites where vessels can move against relatively rigid bony or dural structures such as the falx or clinoid processes. These aneurysms are frequently unsuspected until the patient is found to have a subarachnoid hemorrhage. Treatment is the same as for congenital aneurysms: clipping, wrapping, endovascular.
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7
Fig. 7.2. Location of skin incisions for exploratory burr holes.
Fig. 7.3. Hemispheric acute subdural hematoma.
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7
Fig. 7.4. Epidural hematoma with contralateral contusion.
Traumatic aneurysms may present days or months after a head injury with a subarachnoid hemorrhage. Dissections of either the carotid or vertebral artery may take time to become clinically manifest. Carotid cavernous fistulae may occur after trauma, especially penetrating. The treatment of choice for these lesions is endovascular with coils or balloons. Posttraumatic hydrocephalus typically occurs two weeks or more after head injury. It can occur in the absence of subarachnoid hemorrhage and usually presents as a failure to progress in rehabilitation. Delayed seizures (after day 7 postinjury) are most likely in patients with intracranial hematomas or contusions in the temporal or frontal lobes, penetrating trauma (especially gunshot wounds), depressed fractures, and intracranial sepsis. Prophylactic treatment has no effect on the incidence of late seizures. Postconcussive syndrome presents as cognitive impairment (with or without findings on neuropsychologic testing of depression, nightmares, emotional lability, etc.) afflicts a significant number of patients with mild head injury. Postconcussive symptoms can persist for 6 or even 9 months and may require antidepressants and psychotherapy
Penetrating Head Injury

Gunshot wounds to the head are different pathophysiologically from closed injuries. Delayed swelling can result from the shock waves propagated through the brain and account for rapid deterioration and death in patients who present to the DEM shortly after the injury awake and alert. Surgical intervention is urgent only for those gunshot wounds associated with a mass lesion causing increased ICP (subdural, contusion, etc). Debridement of a gunshot wound can be delayed up to 24 hours without significant increased risk of complications.
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Gunshot wounds should be debrided to remove any fragments of bone or skin driven intraparenchymally. These fragments are potential niduses of infection. Bullets can migrate in the brain over time but do not cause increased brain injury when they do so and should not be removed unless impinging on a structure associated with neurologic deficit or pain.
Skull Fractures
A nondisplaced fracture of the skull requires no treatment unless there is an associated injury to a cranial nerve running within a bony canal or through a foramen. Open depressed skull fractures need elevation only if there is an displacement of the outer aspect of the outer table to the level of the inner layer of the inner table. The key surgical challenge in surgery for open depressed skull fractures is identification and closure of dural tears which may require harvesting and placement of a periosteal or other connective tissue graft. Basilar skull fractures do not require treatment.
- There is a high incidence of VIIth and VIIIth never injuries (internal auditory and facial canals run through petrous bone at skull base. Patients with basilar skull fracture clinically or on CT require careful exam for facial movement and hearing and may need temporal bone CT.
CHAPTER 8
Maxillofacial Trauma
Dennis-Duke R. Yamashita and Mark M. Urata
Motor vehicle accidents and personal altercations are responsible for two thirds of all maxillofacial trauma. Fifty to seventy percent of patients with facial injuries will also have injury to other organ systems. In fact, midface fractures are accompanied by injuries to the head 51%, chest 12%, abdomen 5%, and skeletal system 33%. Few patients actually die as a result of their maxillofacial injuries; however, the surgeon must act quickly to rule out those entities which can be fatal. Airway compromise, significant aspiration, and massive hemorrhage as well as brain and cervical spine injuries must be addressed in a timely fashion.
Initial Evaluation Epidemiology

In general, women have a lower impact tolerance than men owing to a lower density and thickness of the facial skeleton. Of the maxillofacial region, the nasal bone has the lowest impact tolerance with the zygomatic arch following close behind. The glabellar region overlying the frontal sinus requires the greatest amount of force amongst the maxillofacial components. The maxilla is typically more sensitive to horizontal forces while the mandible is more susceptible to lateral force.
Blunt Trauma
This is the most common cause of maxillofacial trauma typically a result of motor vehicle accidents, falls, or assaults. Blunt trauma can generate enough force that the crush injury can be similar in nature to a GSW except that there is less obvious and perhaps more occult damage. In fact, a 30 mile/hour collision can result in as much as 80 g of force.
Penetrating Trauma
Gunshot Wounds
Gunshot wounds (GSW) to the maxillofacial region pose a unique situation. In the GSW, the missile dissipates high levels of energy as it enters the soft tissue and then encounters the bone producing many secondary missiles that
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Dennis-Duke R. Yamashita, Division of Oral and Maxillofacial Surgery, Los Angeles County-USC Medical Center, University of Southern California School of Dentistry, Los Angeles, California, U.S.A. Mark M. Urata, Los Angeles County-USC Medical Center, University of Southern California School of Dentistry, Division of Plastic and Reconstructive Surgery, University of Southern California Keck School of Medicine, Los Angeles, California, U.S.A.
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result in tremendous local tissue damage. Our protocol for GSW trauma is to minimally delay treatment for 48-72 hours until all the soft tissue damage has manifested. The length of observation is not absolute but one must allow definitive soft tissue and bony viability to be declared and treat or reconstruct accordingly. GSW injuries deserve careful debridement, initial soft tissue management (immediate closure versus delayed reconstruction) and careful observation. Severe avulsive injuries may be packed open and followed by delayed reconstructive procedures including free and rotational flaps. Early stabilization and space maintenance of bony segments (extraskeletal fixation) is of vital importance to better allow for more ideal reconstruction. Shotgun wounds typically are less deep, but more dispersed. In either situation, missile removal is more hobby than therapeutic unless it impinges on vital structures.
Knife Wounds
The assessment of penetrating knife wounds to the maxillofacial region deserves careful scrutiny. There can be very minimal superficial damage with a great deal of occult damage to vital structures. Careful clinical examination and appropriate imaging are a necessity to evaluate the path and depth of instrument penetration.
Physical Evaluation Primary Survey

Airway
In assessing the A or airway, several factors are related directly to maxillofacial trauma. Firstly, there is an association between maxillofacial trauma and cervical spine injuries of 12-18%. This occurs primarily with frontal impact causing hyperflexion and is usually accompanied by mandibular fractures. For this reason, care must be taken to ensure adequate stabilization of the C-spine while both examining and securing an airway. Six percent of severe maxillofacial injuries require intubation for adequate oxygenation. A bilateral fracture through the mandible often called a bucket handle fracture can lead to airway compromise due to the resultant retraction of the anterior segment and tongue. This also compromises the efficacy of the chin lift or jaw thrust maneuver. With bilateral mandible fractures, it is often more appropriate to grasp the anterior segment of the mandible and hold it anteriorly to displace the tongue from the posterior pharynx while ensuring stabilization of the cervical spine. Maxillofacial trauma can also cause airway compromise by dislodging teeth, dentures, bridgework, or bone into the airway. When assessing the airway, it is prudent to check for newly fractured or avulsed teeth. Penetrating trauma of the maxillofacial region, in particular the floor of the mouth and neck can also lead to loss of the airway due to massive swelling. In Le Fort injuries there is a risk of inappropriate placement of the nasotracheal and nasogastric tubes superiorly into the anterior cranial fossa. These complications may be avoided with fiberoptic intubation techniques. After establishing cervical spine precautions, nasotracheal intubation should be considered particularly in panfacial fractures. In these patients, the mandible is often comminuted or fractured bilaterally allowing the tongue to retrude
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and providing a difficult laryngoscopic intubation. If the patient is taken to the operating room for other concomitant injuries, an elective tracheostomy should be entertained in anticipation of closed reduction maxillomandibular fixation or significant long term edema.
Breathing
During this phase of the Primary Survey, the surgeon should expose the neck and chest for examination. Injuries to the maxilla and mandible can create an environment conducive to aspiration. Neck swelling, pharynx and tongue swelling as well as floor of the mouth swelling must all be considered potential environments for aspiration. Blood, saliva, and gastric contents are often the culprits. Ventilating a maxillofacial trauma patient with a bag-valve mask in the face of blood or loose teeth can be catastrophic. Securing an airway by intubation or tracheostomy with cuff inflation is the safest manner to avoid such a complication.
Circulation
Profuse life threatening bleeding in maxillofacial trauma is usually associated either with nasoorbitalethmoidal (NOE) fractures or upper LeFort injuries. Both of these regions boast a generous vascular supply and placement of petroleum lubricated anterior packs and posterior nasal packs is the initial management if the vessel cannot be easily identified. The anterior packing is placed against the buttress supplied by the posterior nasal packing. Two Foley catheters placed through the nose into the posterior pharynx and inflated can also be effective in a posterior hemorrhage. If these modalities fails to stop the bleeding, repacking the anterior once or twice is indicated. However, direct pressure on the columella should not exceed 2 hours due to the delicacy of is blood supply. Moreover, any packing should be removed within 24-72 hours to avoid masking a CSF leak. Hemorrhage from displaced Lefort fractures will often subside once the patient is placed in maxillomandibular fixation. Continued bleeding may require angiography and embolization. Cranial base fractures can be associated with lacerations of the jugular or carotid which require vascular surgical intervention. Bleeding from the branches of the internal maxillary artery can be reduced by 90% by ligation of the ipsilateral carotid and superficial temporal artery.
Disability
This component of the primary survey evaluates the patients level of consciousness, pupillary size, and reaction. Trauma to the orbits can often cause injury to the optic nerve and thus, a paradoxical pupillary dilatation or Marcus Gunn pupil is noted when a light is swung between the intact and injured eyes. With optic nerve injuries, the briskness of response to light is first affected which is followed next by a loss of visual acuity and the aforementioned Marcus Gunn pupil. A Marcus Gunn pupil is a paradoxical dilation rather than constriction of the pupil when a light is shone in the affected eye. It is indicative of damage to the retina or optic nerve back to the chiasm on the tested side.
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Secondary Survey
It is during the Secondary Survey that the meticulous evaluation of the maxillofacial region is executed. A drivers license or other photograph, dental records, radiographs, or models of the patient prior to trauma may be invaluable in assessing what changes have occurred to the maxillofacial region. As an example, some patients may innately possess a malocclusion. Failure to recognize such preexisting conditions may lead the physician to incorrectly diagnose a traumatic injury to those structures. The authors preferred method at the Los Angeles County/USC Medical Center is to conduct this examination utilizing the acronym HEENON C.
(H)Head
It is appropriate to develop and utilize a standardized examination with each facial trauma patient. Intuitively, one should proceed from superior to inferior, superficial to deep. Examination of the patient for facial distortions, hematomas, contusions, crepitus, ecchymosis, discoloration, and lacerations is the first component of the maxillofacial exam. The face is divided into thirds to evaluate symmetry, shape, and length. The upper third is from the hair line to the nasofrontal or nasion region. The middle third is from this point to the subnasale while the lower third is from the subnasale to the mentum. LeFort fractures can often cause rotation of the maxilla with a resultant flattened and elongated appearance to the face particularly in the lower third. This is due to the inferior displacement of the posterior maxilla which creates an anterior open bite. The origin of any ecchymosis must be determined to demonstrate whether it is the result of direct soft tissue injury or bleeding at a fracture interface or both. Posterior-inferior auricular region ecchymosis also termed Battles sign is an indicator of basilar skull fracture. Bilateral periorbital ecchymosis is termed Owls sign and typically is representative of a Le Fort II or III fracture. A 50% mixture of 3% H202 and saline is used to clean dried blood from the hair and skin. Wounds should be copiously irrigated and obvious necrotic tissue should be debrided. Betadine is recommended; however, it may be detrimental to the taste organs of the tongue and should also be avoided near the globes. Nerves and ducts should be identified, immediately repaired or tagged for delayed reconstruction. The parotid duct or Stensens duct would be in peril in any deep laceration crossing a line drawn from the tragus to the alar base of the nose. Cotton swabs are used delicately in cuts near the eyelids and oral cavity to ensure detection of through and through lacerations. Palpation of the skull and meticulous examination to hair bearing regions may reveal hidden lacerations or fractures. Simultaneous palpation of the facial bones provides an instant tactile comparison for recognition of bony discontinuity. As demonstrated, the examiner stands in front of the patient and begins by palpating the entire frontal bone contour. Next, the supraorbital rims from the medial region sweeping laterally over the zygomaticofrontal suture and then along the infraorbital rim returning to the medial region near the frontal process of the maxilla. The zygoma is palpated from the malar prominence posteriorly along the zygomatic arches over the
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zygomaticotemporal suture to the tragus. The nasal bones and frontal process of the maxilla are palpated, proceeding inferiorly over the anterior maxilla to the region of the anterior nasal spine. The examiner then stabilizes the frontal region with one hand while straddling the index finger and thumb of the other hand across the maxillary dentition. Any dentures or removable prosthodontic devices should be removed prior to the examination. An attempt to mobilize the maxillary complex independent of the skull is attempted. Simultaneous palpation of a step off across the nasofrontal region may indicate a Le Fort II or III fracture.
(E) Eyes
It is our practice to include the examination of the orbit and overlying soft tissues in the (H)ead exam and concentrate on the globe during this section of the maxillofacial survey. We start from the anterior of the globe and proceed posteriorly. Chemosis, hyphema, and subconjunctival hemorrhage are all common in orbital trauma and should be duely recorded. Hyphema should be evaluated for posterior extent by an ophthalmologist. Epiphora is seen clinically as excessive tearing and in the trauma patient may be due to a severe orbital injury with disruption of the nasolacrimal system. Lacerations near the medial canthus are the most likely culprit. Photophobia and pain may indicate a corneal abrasion. Evaluation with ophthalmic anesthetic drops, flourescein eye drops, and ultraviolet light should be conducted to confirm this suspicion. Intraocular pressure should also be measured in the face of obvious orbital trauma given the possibility of vascular disruption. Normal intraocular pressure is 10-22 mm Hg while pressures over 40 mm Hg require immediate intervention by an ophthalmologist. The pupillary size and shape is noted as well as their symmetry. One millimeter of difference between the two pupils is considered within the normal range. Extraocular muscles are checked in the typical H pattern. Restriction in the upper gaze is consistent with the entrapment of the inferior rectus seen in orbital floor fractures. Diplopia or double vision in peripheral gaze is often secondary to the muscular edema and resultant restriction inherent to orbital complex fractures. Finally, visual acuity must be evaluated to further rule out optic nerve or retinal damage in each eye.
(E) Ears
As with the eyes, the examination of the associated soft tissues of the auricles is completed in the (H)ead section. At this juncture, it is our preference to perform an otoscopic examination noting the continuity of the tympanic membrane. Blood in the middle ear may indicate a basilar skull fracture. In mandible fractures, the condyles are often displaced posterior in the glenoid fossa rupturing the anterior bony or cartilaginous wall of the external auditory meatus. Minor lacerations and dried blood on the anterior surface of the canal may be the only clues that this has occurred. Placing both index fingers in the bilateral external auditory meatus and instructing the patient to open his mouth allows the physician to note any un-
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usual excursion of the mandibular condyles. Fractured condyles may have diminished or exaggerated movement. CSF otorrhea may indicate a basilar skull fracture.
(N) Nose
The nose should be examined internally with a speculum. Managing hemorrhage in this arena has previously been discussed under Circulation. Septal hematomas must be drained immediately to prevent avascular necrosis. Once control has been obtained, the packs are removed and the nasal structures should be thoroughly examined. LeFort I fractures violate the piriform aperature and disruption of the lateral nasal walls may be visible. Any violation of the mucosa or displacement of the turbinates, the septum or other cartilaginous structures should be recorded. CSF rhinorrhea is a strong indication that a LeFort II, III or nasoorbitalethmoidal fracture has occurred with disruption of the dura.
(O) Oral Cavity/Oral Pharynx

Again, our examination proceeds in an orderly fashion from the anterior to the posterior, superior to inferior of the oral cavity. The integrity of the lips and in particular the vermillian border are critical. The labial mucosa (abutting the anterior teeth) and the buccal mucosa (abutting the posterior teeth) should be retracted and examined for obvious trauma. Through and through lacerations are common and utilization of cotton swabs to explore is highly recommended. Lacerations near the maxillary second molars at the level of the occlusal plane should increase suspicion for involvement of Stensens duct. Drying the region with gauze and milking the parotid gland from posterior to anterior should produce clear serous saliva. Failure to do so may indicate a disruption of the duct. Ecchymosis or open lacerations of the gingiva may represent an underlying fracture of the alveolus, maxilla, or mandible. The palatal mucosa may be disrupted in a LeFort or alveolar ridge fracture. Including a set of 4 third molars, there are 32 teeth in the average complete dentition of an adult as compared to 20 in the deciduous dentition. Avulsed, subluxated, or fractured teeth as well as a complete or partial dentures should be recorded The teeth are of paramount importance and serve as the infrastructure for the reduction and fixation of many facial fractures. Maximum incisal opening is the distance in millimeters (normal 35-45 mm) between the incisal edge of the maxillary central incisors and the mandibular central incisors. An excessive MIO upon passive examination may represent a fractured mandible. Limited opening can be due to soft tissue swelling, muscle edema, or fracture of the zygoma, maxilla, or mandible. In isolated zygomatic arch fractures, the arch may be collapsed which actually prevents the patient from closing due to interference between the arch and coronoid process of the mandible. The Angle Classification of occlusion (interdigitation of the teeth) was developed in 1890 by Edward Angle, D.D.S. and is based on the position of the maxillary first molar. Class I normal occlusion finds the mesiobuccal cusp of the maxillary first molar occluding in the mesiobuccal groove of the mandibular first molar. In a Class II relationship, the lower first molar is posterior
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to the upper first molar while a Class III occlusion has the lower first molar anterior to the upper first molar. Malocclusion is a deviation from the normal relationship between upper and lower teeth. Accurately recording the occlusion, arch alignment, and dental midline, may all contribute to defining a displaced maxillary or mandibular fracture. The diagnosis of an open bite (premature contact of the molar teeth resulting in a lack of contact in the incisor region) is most often due to the posteriorinferior displacement of the maxilla in Le Fort fractures or the posterior-superior bodily rotation of the mandible in displaced bilateral angle or bilateral condyle fractures. Finally, the gingiva, tongue, and floor of the mouth should be inspected for lacerations or a functional deficit which could be attributable to edema or direct trauma to the muscles or nerves of the region. The submandibular gland empties into the oral cavity on the floor of the mouth via Whartons duct. This should be examined in a similar fashion to the manner in which Stensens was evaluated.
(N) Neck
Evaluation of neck trauma is discussed elsewhere in this book. Notation should be made of any lacerations or the trajectory of bullet or knife wounds into the maxillofacial region. Severe comminution of the maxilla and mandible is common with a seemingly small entrance wound on the neck.
(C) Cranial Nerves

CN I-Olfactory In maxillofacial trauma, this may be disrupted as it passes from the cranial vault through the cribiform plate. Test the sense of smell in each nostril by presenting the patient with familiar available objects such cloves, coffee, or soap. CN II-Optic Test visual acuity and check the optic fundi. CN III, IV, VI-Oculomotor, Trochlear, Abducens Check the extraocular movements in the six cardinal directions of gaze. The mneumonic SO4LR6 reminds us that CN IV trochelar controls the superior oblique while the CN VI abducens is responsible for the lateral rectus. Down and in and lateral movement tests these muscles respectively. CN V-Trigeminal Two muscles of mastication can be palpated while they are activated by opening and closing the mouth. These are the temporalis and masseter while the lateral and medial pterygoids are tested by protrusion and retrusion of the mandible. Sensation over the forehead, cheeks, and jaws on each side represent the trigeminal distribution of its three branches respectively. CN VII-Facial The facial nerve can be damaged almost anywhere along its path from a temporal fracture to a laceration of the cheek. Ask the patient to perform the following tasks to check the muscles of facial expression:
Raise the eyebrows Frown Close both eyes tightly against examiners resistance Show maxillary and mandibular teeth Smile
Maxillofacial Trauma - Puff out cheeks
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CN VIII-Acoustic Check for hearing acuity and if diminished perform Weber and Rhinne for lateralization. CN IX, X-Glossopharyngeal and Vagus Ask the patient to yawn. Check for symmetrical movement of the soft palate. A failure of the palate to rise bilaterally usually indicates a lesion of the X. Unilateral involvement is more consistent with damage to IX. Check the gag reflex (IX or X) and quality of voice (X). CN XI-Spinal Accessory Ask the patient to shrug both shoulders against your hands. CN XII-Hypoglossal Have the patient protrude their tongue and note any asymmetry or deviation from the midline. The hypoglossal nerve can be easily damaged with penetrating wounds in the submandibular region of the neck.
Imaging Plane Films

A modified Townes view, Waters view, and the Caldwell (posteroanterior) comprise the traditional facial series. The submental vertex view should always be ordered in the midface trauma patient as it allows evaluation of the zygomatic arches and malar eminence. The Caldwell, the modified Townes, and the mandibular obliques make up the mandible series. However, the Panorex radiographic exam is often considered the most valuable in lower third face fractures. The entire mandible can be visualized with distortion and blurring evident only in the symphyseal and parasymphyseal portion of the jaw. Often, this can be the only studies available in a timely fashion and can certainly be used for screening and triage purposes.
Computed Tomography (CT) Scans

Most bony discontinuities are best evaluated by computed tomographic studies. An exception to this rule is nondisplaced fractures of the ascending ramus of the mandible. The more finite the area being assessed, the thinner the windows should be made. An example is orbital fractures which are best evaluated with 2-3 mm cuts to accurately demonstrate the thin medial orbital wall (lamina papyracea) and orbital floor. These studies may be made with or without contrast. CT imaging without contrast media can best show pure bony problems, while those images with contrast show the interface and the juxtaposition of hard and soft tissue as well as edema and cellulitis. Recently, three dimensional scans produced by computer compilation of thin cut CTs have been used to plan for surgical approach and possible reconstructive modalities. As an example, this can be of particular benefit in ordering a 3 D generated reconstructive plate for the patient with a frontal bone defect.
Magnetic Resonance Imaging (MRI)

Currently, MRI evaluations are best reserved for soft tissue injuries and are not often used as a primary diagnostic tool unless there is a suspicion of vascular injury.
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General Principles of Treatment of Maxillofacial Injuries

Maxillofacial injuries are most accurately assessed within the first 24-48 hours. Unfortunately, many maxillofacial trauma patients present after this period. Their evaluation is compromised by the soft tissue edema which may exaggerate or mask the severity of their bony displacement. Ideally, these trauma patients should be operated on before the onset of edema. Given those circumstances where this is not possible, one may allow the swelling to subside before deciding whether surgical intervention is required to restore proper functional anatomy and esthetics. On the other hand, delayed treatment of maxillofacial injuries can result in suboptimal fracture reductions making alignment of fractured segments difficult due to fibrosis and osteoclastic activity at the fracture margins. These prolonged delays may require osteotomies and other reconstructive efforts. Waiting up to 1 week allows the edema to resolve and accurate surgical assessment can then be completed. Additionally, operating on an edematous patient makes dissection and placement of incisions challenging. Most maxillofacial injuries involve extensive soft tissue violation. Adequate tetanus vaccination and coverage with oral or intravenous broad spectrum antibiotics is the rule. Violation of the oral cavity necessitates coverage for oral bacterial flora, primarily Penicillin. To ensure the best outcomes for a patient, complex maxillofacial injuries should be managed by a team approach. With the overlap and convergence of the specialties (plastic and reconstructive surgery, otolaryngology/head and neck surgery, oral and maxillofacial surgery, and ophthalmology), one can draw on all the specialties for the comprehensive treatment of the patient.
Soft Tissue Injury Anatomic Considerations

The soft tissues of the maxillofacial region are well perfused. Except for the lips, eyelids, and nose, a rim of tissue may be debrided in lacerations to avoid excessive scarring from a contused wound edge.
Management
Ice compresses to contusions will assist in limiting soft tissue edema during the initial 24-72 hours. As a general rule, facial lacerations should be repaired as soon as possible. They require thorough and meticulous irrigation and debridement producing a wound edge that is perpendicular to the skin surface. Buried absorbable subcutaneous and dermal sutures approximate the edges and produce slight eversion while the skin is closed with nonabsorbable, nonreactive suture. The surface sutures are usually removed 5 days later. In rare instances where repair must be delayed, the wounds are irrigated and debrided and dressed with a moistened saline gauze. Due to an extensive collateral circulation, these wounds can undergo twice a day dressing changes and delayed primary closure 24-36 hours later. Lacerations of the oral cavity, eyelids, lips, ears, and nose require specialty consultation at most institutions. Local anesthesia is the method of choice with general anesthesia reserved for extensive injuries, an uncooperative patient, or special areas of concern such as the parotid duct and facial nerve.
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Facial Series
Caldwell (Posterioanterior) Waters Modified Townes Submental vertex (must be ordered separately)
Mandible Series
Caldwell (Posterioranterior) Modified Townes Mandibular obliques (right and left)
0.5% lidocaine with 1:200,000 epinephrine is used throughout the face except in the regions of the ear and nose. Dog bites can usually be closed primarily after generous irrigation. The patient should be placed on oral or intravenous antibiotics of amoxicillin and clavulonic acid. Human bites pose more of a threat and have been treated with daily dressing changes, IV antibiotics with delayed primary closure 3-4 days later.
Upper 1/3 Facial Fractures Frontal Sinus Fractures

Anatomic Considerations
Frontal sinus is composed of a paired, air filled cavities which are triangular in cross section. The anterior table is thick while the thin posterior table provides a separation between the air cushion and the frontal lobes in the anterior cranial fossa.
Statistical Perspectives
5-15% of all maxillofacial injuries are frontal sinus fractures The anterior table of the frontal sinus is notably thick and requires 2-3 times greater force to fracture than the zygoma, maxilla, or mandible. Due to the energy required to fracture the anterior sinus wall, these are typically associated with other maxillofacial fractures primarily nasoorbitalethmoidal (NOE). The frontal sinus begins pneumatization at age 7 and is completed by age 18-20. The nasofrontal ducts are remnants of the embryonic connection between sinuses. They run from the posteromedial aspect of the sinus, through the ethmoid air cells ending below the middle turbinate of the middle meatus.
Clinical Presentation
Lacerations, contusions, hematoma over the frontal bone, particularly the glabellar region CSF rhinorrhea Palpable bony depression
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Supraorbital paresthesia or anesthesia (V1) Subcutaneous crepitus
Imaging
Plain radiographs-large, displaced frontal sinus walls with air fluid levels, but can miss smaller fractures and cannot delineate nasofrontal duct injury CT scan-best image although it is still difficult to determine nasofrontal duct violation. Fractures near the midline or crossing the midline that are posterior must be presumed to have ductal injury.
Management
Nondisplaced anterior table fractures can be observed with broad spectrum antibiotics.
- Displaced anterior table fractures are managed in accordance with the amount of comminution and displacement and the resultant cosmetic defect. Suspicion of nasofrontal duct violation is an indication for exploratory surgery. - Posterior table fractures displaced more than one wall thickness are managed by removing the lining mucosa of the sinus followed by the obliteration of the nasofrontal duct using autologous bone, pericranium, fascia, and muscle. The remainder of the sinus is obliterated using fat harvested from the lateral thigh or other convenient location.
Middle 1/3 Facial Fractures Orbitozygomatic Fractures (Fig. 8.1)

The orbit is composed of eight bones: zygoma, lesser and greater wings of sphenoid, frontal bone, ethmoid bone, lacrimal bone, palatine bone, and maxilla. The infraorbital nerve (V2) travels along the floor of the orbit exiting at the infraorbital foramen to provide sensation to the anterior cheek. Tripod, triamalar, malar complex, orbital complex, zygoma, zygomaticomaxillary complex (ZMC) fracture are all terms that describe the same entity. It is a fracture through the zygomaticofrontal suture, then into the orbit through the zygomaticosphenoid suture to the inferior orbital fissure to the zygomaticomaxillary suture and buttress and finally the zygomatic arch. Isolated fractures of the zygomatic arch are common with directed lateral force.
The most common orbitozygomatic fracture is the zygomaticomaxillary complex fracture or zygoma fracture. 90-95% demonstrate paresthesia or anesthesia of infraorbital nerve
Pain Flattening of the malar prominence Subcutaneous emphysema Paresthesia or anesthesia of cheek (V2) Palpable step off at zygomaticofrontal, infraorbital rim, zygomaticomaxillary buttress, and zygomatic arch.
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8
Fig. 8.1. The typical orbitozygomatic or zygomaticomaxillary complex fracture involving the orbital floor and lateral wall. In this diagram, the infraorbital nerve is spared, but stretching of the soft tissue drape will often cause parasthesia.
Periorbital ecchymosis and edema Diplopia (due to orbital dystopia or edema) Epiphora (violation of the nasolacrimal system) Enophthalmos Entrapment of orbital contents Superior orbital fissure syndrome-fractures violating the superior orbital fissure can directly (displaced bones) or indirectly (hematoma) cause ptosis, proptosis of the globe, paralysis of CN III, IV, VI, V1 and decreased sensation over the forehead, upper eyelid, cornea, conjunctiva, and sclera. Orbital apex syndrome-consists of everything in superior orbital fissure syndrome with the addition of blindness.
Investigations
CT scan-2-3 mm axial views demonstrate the anterior posterior displacement of the complex as well as isolated zygomatic arch fractures. Coronal views will demonstrate the orbital floor violation and displacement of the ZM and ZF suture. Facial series with submental vertex view-may be able to appreciate the infraorbital rim, orbital floor, zygomaticofrontal suture, and zygomatic arch violations if CT not available. Opacification of the maxillary sinus due to hemorrhage is a common finding.
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Management
Most agree that each fracture must be individually evaluated for stability based on clinical and radiographic findings. Patients with entrapment or enophthalmos due to herniation of orbital contents are obvious candidates for surgical intervention while those with nondisplaced stable complexes are not. Isolated zygomatic arch fractures may be reduced with an intraoral or scalp incision while ZMC fractures may require multiple approaches and complex reconstruction of the orbital floor and walls.
Nasoorbitalethmoidal Fractures (NOE) Anatomic Considerations

The five bones of the nose are: frontal process of the maxilla, the nasal process of the frontal bone, the paired nasal bones, the vomer, and the ethmoid. Orbital fractures that also involve the nasal and ethmoidal bones are sometimes termed nasoorbitalethmoidal or NOE fractures. The medial canthal tendon inserts along the anterior lacrimal crest of the frontal process of the maxilla as well as the nasal bone itself. Traumatic disruption of this region in NOE fractures often leads to telecanthus and saddle nose deformity.
The nasal bones are fractured in 33% of all facial fractures. Nasal bone fractures are classified as:
Plane 1-simple nasal bone fracture Plane 2-complex nasal bone fracture Plane 3-nasoorbitalethmoidal complex fracture
Thirty percent of severe NOE fractures have a CSF leak detected within the first 24 hours. Fifty percent demonstrate CSF by 48 hours.
Isolated nasal bone fractures are most often a clinical diagnosis with bruising, swelling, pain, epistaxis, nasal airway obstruction with a deviated septum or hematoma. Periorbital ecchymosis Saddle nose deformity Paresthesia or anesthesia of the cheek (V2) Ocular dystopia Entrapment CSF rhinorrhea Enophthalmus Telecanthus Diplopia Visual acuity changes Enophthalmos
Imaging
CT scan-axial and coronal scans with 3 mm or less intervals Facial series
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Nasal bone films-including 45 occipitomental view and low density soft tissue views for isolated nasal bone fractures
Management
Nasal fractures are often accompanied by septal hematomas. These are addressed by an incision along the base of the hematoma along with nasal packing. Isolated nasal fractures are often treated with closed reduction in the emergency room with local anesthesia and sedation. Asch forceps are used to realign the septum and overlying nasal bones. Closed reduction can actually be performed up to 3 weeks after the initial insult. Comminuted nasal fractures are treated with intranasal packing and external splinting. NOE fractures typically require a combination of approaches with bony reduction and reestablishment of the position of the medial canthal tendon.
Maxillary Fractures (Fig. 8.2) Anatomic Considerations

The maxilla is considered the cornerstone of the face bridging the cranium with the mandible. LeFort I-a bilateral horizontal transmaxillary fracture preserving the nasal base with lateral extension through the piriform aperature and pterygoid plates separating the maxillary alveolar process from the rest of the maxilla. LeFort II-a pyramidal fracture that extends through the nasofrontal junction, laterally through the lacrimal bones and infraorbital rim (often through the infraorbital nerve foramen causing V2 paresthesia) continuing inferoposteriorly along the zygomaticomaxillary suture through the pterygoid plates. LeFort III-this is complete craniofacial disjunction with separation of the orbits and maxilla from the cranium. The fracture line is through the nasofrontal junction laterally through the medial wall or orbital floor, the zygomaticofrontal suture, the zygomatic arch and through the pterygoids. The floor of the maxillary sinus remains above the floor of the nose until the age of 8 years old.
LeFort fractures in order from least to most frequent: II > I > III Forty percent of all facial fractures involve the middle third of the face not including the nasal bones. LeFort fractures generally occur in older children and adolescents rather than infancy or early adulthood.
Malocclusion Movement elicited by digital manipulation of the maxilla Palpable step off possible at maxillary buttress, nasofrontal junction, zygomaticofrontal suture, zygomatic arch. Owls or bilateral periorbital ecchymosis Bilateral subconjunctival hemorrhage Paresthesia or anesthesia of the cheek (V2) Visual acuity changes
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Fig. 8.2. Maxillary Fractures. This series of diagrams demonstrate the bony involvement of LeFort I, LeFort II, and LeFort III fractures. Reprinted with permission from Dingman RO, Natvig P, eds. Surgery of Facial Fractures Philadelphia: W.B. Saunders Company, 1964.
Enophthalmos Orbital dystopia Diploplia Entrapment of orbital contents Trismus Fractured or avulsed dentition
Imaging
Panorex radiograph-this will demonstrate the condition of the teeth and surrounding bone. CT scan-both axial and coronal films of 3mm or less are mandatory in maxillary fractures.
Management
Oral or IV broad spectrum cephalosporin LE FORT I: Ideally, the teeth are placed into centric occlusion (their normal relationship) via closed reduction maxillomandibular fixation (CRMMF).
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Then, the fractures are fixated with miniplates across the zygomaticomaxillary buttress and nasomaxillary buttress. In LeFort I fractures with multiple pieces and instability, CRMMF alone is the treatment of choice and should be maintained for 4-6 weeks. In edentulous patients with atrophic maxillary and mandibular alveolus, splints are often used in conjunction with wire skeletal fixation. LE FORT II: Disimpaction of the fractured maxillary segment may be required depending upon whether the fracture has telescoped superiorly or posteriorly. This may require the use of minimal traction on arch bars to maximal traction utilizing disimpaction forceps. Following CRMMF, true LeFort II fractures can be rigidly fixated via a bilateral buccal sulcus incision plating both the zygomaticomaxillary buttress and nasomaxillary buttress to preserve height and projection. Unstable infraorbital rim fractures are addressed through an existing laceration, transconjunctival, subciliary, lower lid, or infraorbital incision. LE FORT III: Most often, disimpaction is not required with this type of fracture which is usually more mobile.
Lower 1/3 Facial Fractures Mandible Fractures (Fig. 8.3)

The mandible is the largest and strongest facial bone and is divided into several regions from anterior to posterior: symphysis, parasymphysis, body, angle, ramus, coronoid, and condyle. After location, mandibular fractures can be further divided into favorable and unfavorable. Favorable fractures are those that by their inherent geometry do not allow muscular distraction of the involved segments of bone. Most lateral forces will result in two fractures of the jaw. The discovery of one fracture should lead the examiner to search for another. Anterior force to the symphysis will often result in bilateral condylar fractures.
20% of all facial fractures are mandibular fractures 11% of mandibular fracture patients have cervical spine injuries Causes of mandible fractures
- 47.5% of mandible fractures are due to altercations - 27.3% of mandible fractures are due to automobile accidents
Force to chin is responsible for 72% of condylar neck fractures 50% of mandible fractures are multiple
Frequency of fracture by regions of the mandible

Condyle Angle Symphyseal/Parasymphyseal Body Alveolar ridge Ramus Coronoid 36% 20% 14% 21% 3% 3% 2%
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Fig. 8.3. Mandible Fractures.
Paresthesia or anesthesia of lips due to disruption or avulsion of inferior alveolar or mental nerve (V3) Limited maximum incisal opening (MIO) Anterior open bite (due to bilateral body, angle, or condyle fractures with vertical collapse) Drooling (difficulty managing secretions with limited swallowing capability) Malocclusion Mobility of segments-able to move segments of mandible independently, particularly at angle, body, parasymphyseal, and symphyseal fractures Trismus Floor of the mouth swelling(may be secondary to edema or hematoma from fracture) Splaying between teeth, Fractured or avulsed teeth Investigations: Panorex radiograph-best single exam with disadvantage of poorly visualized symphyseal region Mandible series-can appreciate three dimensional location of fractured segments CT-may be useful in panfacial trauma or for localization of displaced condyles
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Management
Oral suspension or IV penicillin Unless there are other injuries or possible airway compromise, most mandible fractures can be treated on an outpatient basis. Most favorable mandible fractures are amenable to closed reduction maxillomandibular fixation (CRMMF). This is done by applying arch bars to the maxillary and mandibular dentition with circumdental wires and then wiring the jaws together with the teeth in their normal occlusion. Unfavorable fractures can also be placed in CRMMF if manipulation can lock them into a stable alignment. However, unstable reduction is an indication for open reduction and fixation with plates and screws. Rigid fixation can be of great value, including an earlier return to function and better oral hygiene and nutrition. Plates for the symphysis and parasymphyseal region are applied intraorally while the angle, body, and ramus may also be approached extraorally. Edentulous patients may require either intraoral splints with CRMMF or open reduction internal fixation. Condylar fracture are usually treated with CRMMF for 2-4 weeks. However, those patients with condyles displaced from the fossa require open reduction to reacquire vertical height of the ramus. The condyles are most often displaced medially and anteriorly and can be approached through one or a combination of the following incisions: retromandibular, preauricular, buccal sulcus. Condylar fractures in children have special treatment considerations: The total length of closed reduction in children would be less than in adults, usually between two to four weeks. In isolated condylar fractures, early mobilization is favored with closed reductions reserved to eliminate functional pain. External pin fixators or biphasic systems have been used in edentulous mandibles and severely comminuted fractures such as those caused by gunshot or shotgun wounds.
Dentoalveolar Trauma Anatomic Consideration

Dental professionals refer to the surfaces of the teeth visible in the oral cavity as mesial (anterior), distal (posterior), buccal, lingual, and occlusal. In both the maxilla and mandible, from anterior to posterior there are usually a pair of central incisions, lateral incisors, cuspids (canines), 1st bicuspids (1st premolars), 2nd bicuspids (2nd premolars), 1st molars, 2nd molars, and third molars. In the average complete permanent dentition with four third molars, there are 32 teeth. These are assigned with the right maxillary 3rd molar being Tooth #1 proceeding across the maxilla to the left maxillary 3rd molar as #16. The left mandibular 3rd molar is #17 again numbering across the mandibular dentition to the right mandibular 3rd molar #32. The deciduous dentition has 20 teeth which are numbered in the same sequence using the letters A to T. Trauma to the teeth primarily results in fractures, avulsions, and subluxations. Subluxations are classified as intrusion (into the socket) or extrusion (out of the socket).
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Fractures of the teeth are the most common dentoalveolar trauma. Eruption Sequence Deciduous Dentition:
Central incisors Lateral incisors 1st primary molars Cuspids 2nd primary molars 6-7 months 7-9 months 12-14 months 16-18 months 20-24 months 6 yrs 6 yrs 7 yrs 7 yrs 8 yrs 10 yrs 10 yrs 11 yrs 11 yrs 12 yrs 17 yrs
Eruption Sequence Permanent Dentition:

1st molar Mandibular cental incisors Mandibular lateral incisors Maxillary central incisors Maxillary lateral incisors 1st premolars Mandibular cuspids 2nd premolars Maxillary canines Second molars Third molars
3.1% of mandible fractures involve alveolar ridge fractures.
Alveolar ridge fractures are noted when a tooth or multiple teeth move with their supporting alveolus independent of the rest of the maxilla or mandible. Many patients have preexisting fractures to their teeth and this should be elicited in the history.
Imaging
Periapical dental films-highest definition of individual teeth demonstrating fractures and cracks. Panorex radiograph-demonstrates relationship of bony support to teeth.
Management
The level of the fracture of a tooth will determine the mode of therapy. Enamel or partial dentin fractures can often be restored by the dentist with resin while fractures violating the pulp will also require root canal therapy. Subluxation of teeth is ideally treated by repositioning and splinting with acrylic or wires or orthodontic bracketing. Avulsed teeth require immediate stabilization. When a tooth has been avulsed, the patient should be instructed to place the tooth in sterile saline. The ideal medium is actually the socket itself, however, the risk of aspiration is often too great particularly in a child or elderly patient. After 30 minutes out of the socket, the chances for a successful reimplantation are minimal. Fixation is usually in the form of interdental wiring, placement of arch bars, placement of specialized acrylic splints or the placement of orthodontic brackets and wires. Oral and maxillofacial surgery or dental consultation is strongly advised.
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Alveolar ridge fractures are usually treated with CRMMF for 4 weeks. This will simultaneously maintain occlusion and provide stability. In those instances where occlusion is not as critical, stabilization with arch bars and circumdental wires can be performed.
References
1. 2. 3. 4. 5. 6. Dingman RO, Natvig P. Surgery of Facial Fractures. Philadelphia: W.B. Saunders, 1964. Weinzweig J. Plastic Surgery Secrets. Philadelphia, Hanley & Belfus, Inc., 1999. Wolfe SA, Baker S: Facial fractures. New York, Thieme, 1993. Manson PN. Facial fracures. In: Aston SJ, Beasley RW, Thorne CHM, eds. Grabb and Smiths Plastic Surgery, 5th ed. Manson PN, ed. Maxillofacial injuries. In: Siegel J, ed. Management of trauma. New York, Churchill-Livingstone, 1986. Demetriades D, Chahwan S, Gomez H et al. Initial evaluation and management of gunshot wounds to the face. J Trauma 1998; 45:39-41.
NECK
CHAPTER 1 CHAPTER 9
Evaluation of the C-Spine

George C. Velmahos The Magnitude of the Problem
The incidence of cervical spine injuries among blunt trauma survivors is between 1-3%. The sequelae are serious, with 7% direct mortality and 10-40% morbidity due to devastating neurologic injuries. A high rate of missed C-spinal injuries is reported, ranging from 5-30%. Missed C-spinal injuries are a primary cause of litigation. The appropriate methods of evaluating the C-spine are widely debated in the literature. Universal consensus is lacking.
Basic Principles of Initial C-Spinal Precautions

All blunt trauma patients should be placed in spinal precautions and presumed to have a spinal injury before they are evaluated and cleared by clinical examination and/or radiographic tests. Patients with penetrating injuries to the neck are much less likely to have injuries that require spinal immobilization:
1. Stab wounds do not cause spinal fractures, even if the spinal cord is injured. 2. C-spinal fractures may be caused by civilian gunshot wounds but are rarely unstable. This fact, combined with the high incidence of complete cervical spinal-cord injuries related to gunshot wounds, results in a very low incidence of operations to the spine in order to establish stability after such injuries. 3. Small children may be an exception to the above rule due to the small mass of their vertebrae relative to the bullet. 4. High-velocity bullets from military weapons create extensive damage and fragmentation. They may cause unstable C-spinal injuries.
The most common method of C-spinal precautions is a hard C-collar. There are multiple types of C-collar, including the Aspen, Philadelphia, Miami J and NecLoc collars. The type of collar is less important than a proper fit. A C-collar will not offer optimal protection if its size is not appropriate for the patients neck. Even a hard C-collar does not immobilize the neck completely. A properly fitted C-collar still allows an estimated 10-25% of the normal range of lateral, anterioposterior and rotational movements. Taping the head onto the hard board or offering additional manual stabilization is advisable, particularly for patients who are suspected to have incomplete C-spinal cord injuries. A soft C-collar does not offer any immobilization and should not be used at the acute stage. A C-collar should never interfere with complete clinical evaluation of the neck.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. George C. Velmahos, Division of Trauma/Critical Care, University of Southern California School of Medicine, Los Angeles, California, U.S.A.
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9
Fig. 9.1. Atlanto-occipital dislocation indicates major blunt forces have been applied to the area. This patient was thrown from a moving train. The injury is usually fatal.
The collar should be removed, stabilization should be maintained manually and the neck should be thoroughly examined. Removal of the C-collar and manual in-line neck stabilization is used when a patient needs intubation.
Tools to Evaluate the C-Spine

Clinical examination is an important part of the evaluation of the C-spine. It requires an alert, nonintoxicated patient and a reassuring, focused physician. It is simple and can be completed in the following steps:
1. The patient is asked if he or she has any neck pain. A gross motor and sensory neurologic exam is completed. If the patient reports no pain and the neurologic exam is negative, proceed to the next step. 2. The C-collar is removed and neck stabilization is maintained by gentle pressure on the forehead of the patient. Each C-spinal vertebra is palpated, and the patient is asked if there is any tenderness during palpation. It the answer is negative for tenderness, proceed to the next step. 3. Vertical pressure to the patients skull is applied by pushing on it. The patient is asked if this maneuver elicits pain. If the answer is negative, proceed to the final step.
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Fig. 9.2. The C-spine collar provides adequate protection, if it fits properly. For patients with short thick necks, a good collar fit may be difficult. Additional methods, such as sandbags on each side of the head or taping the head to the gurney, should be used in such cases.
4. The patient is asked to move his/her head forward (chin to chest) and laterally (chin to shoulder) and report any neck pain during movement.
Radiographic evaluation consists of plain films, flexion/extension films, computed tomography, magnetic resonance imaging and myelography. Plain films include an anterioposterior view, a lateral view, an odontoid view and two oblique views (five films). The addition of the last two views adds minimal information and is usually not necessary. A lateral swimmers view (arm elevated over head) is useful for visualization of the lower cervical vertebrae when the plain lateral film is not adequate. The plain films should be reviewed systematically. The lateral film provides the majority of relevant information:
1. All seven cervical vertebrae should be visualized as well as the top of the T1. 2. Prevertebral soft-tissue edema (more than half the length of the vertebra in front of C2 or the entire vertebra in front of C6) and loss of normal spinal lordosis are indirect signs of underlying injury. 3. Four lines should be checked for deviation: the anterior and posterior lines (representing the anterior and posterior longitudinal ligaments), the spinolaminar line (joining the laminar junctions) and the spinous process line (joining the spinous processes). 4. Imaginary lines projected from all transverse processes should meet at a single point. The opposite (fanning) is associated with injuries. 5. Each vertebra should be evaluated carefully for fractures or subluxations. The intervertebral spaces should also be evaluated.
Flexion/extension views are plain lateral (and sometimes oblique) films after the patient has extended or flexed his/her neck to the point where pain or
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9
Fig. 9.3. Spinal dislocation of C5/C6 with complete impairment of neurologic function at this level.
discomfort is elicited. Flexion/extension radiographs detect with high sensitivity inappropriate spinal motion (subluxation, dislocation) produced due to ligamentous injuries. For this examination, the patient must be awake and cooperative. Passive flexion/extension views done under fluoroscopic guidance are diagnostic alternatives for certain groups of clinically unevaluable patients (see below), but the validity of the method is still unknown. CT of the C-spine can be focused on suspicious areas suggested by the patients symptoms or radiographic findings on plain films. In certain groups of unevaluable patients (see below), these areas may also include the entire C-spine. CT is highly sensitive for detection of fractures. Nonosseous injuries (ligaments, disks) may be missed on CT. MRI is the ultimate radiographic tool to evaluate the C-spine. It allows complete visualization of osseous and soft-tissue structures from multiple angles. Its disadvantage is that it is expensive and prevents close monitoring of the patient during the exam. Myelography involves the injection of contrast into the spinal canal to evaluate for compression or discontinuation of flow. It is used infrequently because it is invasive.
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Fig. 9.4. Loss of normal lordosis of the cervical spine may be an indirect sign of injury. This patient had an isolated laminar fracture of C3.
Types of Patients
Patients who require C-spine evaluation may be grouped in the following categories:
1. 2. 3. 4. Alert patients without neck pain or neurologic signs. Alert patients with neck pain and/or neurologic signs. Unevaluable patients with minimal trauma. Unevaluable patients with significant trauma.
Each group requires different methods of C-spine evaluation. Protocols that outline the sequence of procedures needed for the C-spine clearance of the four groups of patients are strongly encouraged. A nonsystematic approach to the C-spine is subject to diagnostic omissions and errors. Alert patients without neck pain or neurologic deficits. Asymptomatic patients who are alert and nonintoxicated can be cleared clinically without radiographic evaluation. The C-collar may be removed if the clinical examination is negative for C-spinal trauma. There are multiple studies documenting that this policy is safe. The role of distracting injuries (painful injuries in other areas of the body) is debated. Some authors believe that their presence should be a contraindication for clinical clearance. We believe that a careful neck examinationafter asking a cooperative patient to focus on the neckcan be reliable even in the presence of distracting injuries. Each such case should be individualized based on the type and location of distracting injury and the pain it causes.
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Fig. 9.5. Civilian gunshot wounds to the spine rarely produce unstable fractures. However, high-velocity bullets from military weapons, as shown here, can cause extensive injury with resulting instability.
There are a few case reports on occult C-spinal injuries (in the absence of symptoms). These reports are more likely to result from superficial and careless clinical examination than from a fracture that does not cause even minimal pain.
Alert Patients with Neck Pain and/or Neurologic Deficits

Three initial plain views should be done (anterioposterior, lateral and odontoid). If there is an abnormality, additional tests may be needed. If there is no abnormality, we recommend flexion/extension views to evaluate stability, and a focused CT of the area of pain to screen for fractures. If no injury is revealed and the symptoms persist, the case should be individualized. In the presence of high-risk factors for C-spine injury (osteoporotic spine, significant associated facial or skull injuries), an MRI may be obtained. In the absence of such factors, an MRI is still a reasonable test for persistent neurologic symptoms
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Fig. 9.6. Prolonged application of the C-spine collar may cause skin ulceration at areas of pressure. In some cases, areas with extensive facial or neck skin necrosis require skin grafts or flaps.
Fig. 9.7. Clinical examination is highly accurate for alert, nonintoxicated patients. The spine is palpated with the collar removed, while manual stabilization is provided by the nonexamining hand.
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Fig. 9.8A. The plain radiograph may be unreliable for patients who are not clinically evaluable. This patient with severe head injury has no findings on the imaged vertebrae of the plain lateral film.
Trauma Management
Fig. 9.8B. The CT scan of C1 to T1 revealed a potentially unstable C2 fracture.
but not for pain. In the absence of risk factors and in the presence of pain only, the collar may be removed.
Unevaluable Patients with Minimal Trauma

These are typically intoxicated or head-injury patients with a slightly depressed GCS. Most of these patients are expected to regain full consciousness within a few hours.
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Plain radiography should be performed. Even if it is negative for trauma, the patient should be left in the C-collar. The patient can be evaluated clinically once consciousness is regained. If the clinical examination is negative, the Ccollar is removed. If it is positive, the steps suggested in the evaluation of alert patients with symptoms should be followed.
Unevaluable Patients with Significant Trauma

Complete clinical examination is usually not possible for prolonged periods of time. The evaluation of the C-spine of these patients is a very difficult and thus far unsolveddiagnostic problem. Individualization of care of the C-spine is appropriate. Rates of C-spine injuries of up to 35% have been reported among such patients. A high index of suspicion should be maintained. We recommend adequate three-views plain films and a complete CT from C1 to T1. If there is any evidence of spinal trauma, C-spinal precautions are maintained and additional diagnostic or therapeutic maneuvers are done as appropriate. If no evidence of C-spinal trauma is observed, the C-collar can be removed in the absence of compelling reasons to retain it (e.g., major associated injuries around the neck). An alternative method is to obtain plain films, a CT of C1 and C2 (or any other suspicious area) and passive flexion/extension views under fluoroscopic guidance. This method is time-consuming, labor-intensive, logistically difficult and potentially dangerous. We do not recommend it. At no point during the prolonged hospitalization of these patients should the C-collar interfere with their care. The neck should be used for central-line catheterization if needed. Alternative methods of stabilization (sandbags, temporary manual stabilization, pharmaceutical paralysis) are available when the C-collar must be released. Prolonged C-collar placement is associated with skin breakdowns which, if unattended, may cause significant wound problems. The C-collar should be released and the neck inspected on a daily basis. Skin pressure-release (e.g., a soft piece of cloth between the collar and the skin) is appropriate for areas at risk.
Pitfalls in the Radiologic Evaluation of the C-Spine

Reporting a lateral C-spine film as normal when the entire length of the cervical spine is not visualized. Evaluating the osseous structures only and ignoring indirect signs of C-spinal injury from the soft tissues. Remember that up to 11% of C-spinal injuries will involve only ligamentous structures or disks but not the actual bone. In the presence of a C-collar, a subluxation may be reduced and not be apparent. The C1/C2 area is often difficult to interpret on plain films. Look for subtle signs of injury. The atlanto-dental interval (ADI, the space between the posterior surface of the anterior arch of C1 and the anterior surface of the dens) should be less than 3 mm in adults and 6 mm in children. Widening of this space indicates injuries to the area. There are differences in the radiographic appearance of the C-spine in children due to the increased flexibility of their ligaments and bones:
1. Pseudosubluxation of C1 on C2 and/or C2 on C3 are normal findings in up to 25% of children.
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Fig. 9.9A. Compression fracture of C6 caused by a heavy object that fell on the patients head. The anterior wedging indicates severe fracture.
2. The ADI is normal up to 6 mm. 3. Prevertebral soft tissues may be normally wide. 4. The intervertebral distances (particularly between C1 and C2) may be normally wide.
Pitfalls in the Clinical Examination of the C-Spine

Examining the patient who is been given pain medication. No pain medication is allowed before the C-spine examination is completed. Disregarding minimal pain or attributing it to pressure from the C-collar. Even minimal pain over the C-spine should prevent discontinuation of Cspine precautions. Focusing on pain and ignoring neurologic symptoms (numbness, tingling, decreased strength, etc.).
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Fig. 9.9B. The CT reveals an unstable fracture with significant retropulsion of bony fragments, occupying more than 50% of the spinal canal. The patient had a complete neurologic deficit.
Attempting clinical examination in a chaotic environment while other providers perform different procedures on the patient (blood drawing, examination of other parts, etc.). Clinical examination should be done when the patient is calm and can focus on his/her neck. Intoxication cannot always be assessed easily. The absence of alcohol odor on the breath of an alert and communicative patient would qualify him/her for clinical clearance.
Pitfalls of C-Collar Application

Inadequate clinical examination of the neck due to reluctance to remove the C-collar. The neck should always be examined under manual stabilization after temporary removal of the C-collar. A very tight C-collar can compress an edematous neck and contribute to air-
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way obstruction. It can also compress the jugular veins and increase the intracranial pressure in patients with head injuries. A C-collar should never prevent therapeutic or diagnostic procedures at the neck (line placement, laryngoscopy, etc.). Alternative methods of stabilization should be used temporarily.
References
1. 2. 3. 4. 5. 6. Velmahos GC, Theodorou D, Tatevossian R et al. Radiographic cervical spine evaluation in the alert asymptomatic blunt trauma victim: Much ado about nothing. J Trauma 1996; 40:768-774. Berne JD, Velmahos GC, El-Tawil Q et al. Value of complete cervical helical CT scanning in identifying cervical spine injury in the unevaluable blunt trauma patient with multiple injuries: A prospective study. J Trauma 1999; 47:896-903. Blacksin MF, Lee HJ. Frequency and significance of fractures of the upper cervical spine detected by CT in patients with severe neck trauma. AJR 1995; 165:1201-1204. Reid DC, Henderson R, Saboe L et al. Etiology and clinical course of missed spine fractures. J Trauma 1987; 27:980-986. Williams J, Jehle D, Cottington E et al. Head, facial, and clavicular trauma as a predictor of cervical spine injury. Ann Emerg Med 1992; 21:719-722. Marion DW, Domeier R, Dunham CM et al. Practice management guidelines for identifying cervical spine instability after trauma. J Trauma 1998; 44:945-946. Also available at: http://www.east.org/tpg (Web site of the Eastern Association for the Surgery of Trauma).
CHAPTER 1 CHAPTER 10
Penetrating Injuries of the Neck

Demetrios Demetriades Anatomy
For trauma purposes the neck is divided into three anatomical zones:
Zone I between the clavicle and the cricoid cartilage, Zone II between the cricoid cartilage and the angle of the mandible, and Zone III between the ankle of the mandible and the base of the skull (Fig. 10.1).
Epidemiology
About 20% of stab wounds to the neck have significant injuries and 10% require surgical intervention. About 34% of gunshot wound to the neck have significant injuries and 17% require surgical intervention. About 70% of transcervical gunshot wounds have significant injuries and 20% require surgical repair.
Physical Examination
Highly advisable that physical examination is performed according to a written protocol (Fig. 10.2). Failure to do so may result in missing important signs and symptoms. The physical examination should be systematic according to systems, i.e., vascular structures, aerodigestive tract, spinal cord, cranial nerves, brachial plexus. Hard signs are diagnostic of significant injury, soft signs are suggestive of injury and require further investigation. Vascular Structures
- Hard physical findings: severe active bleeding, large expanding hematoma, unexplained shock, absent or diminished peripheral pulses, bruits. - Soft physical findings: stable hematoma, mild hypotension, unexplained low GCS or hemiplegia.
Aerodigestive Tract
- Hard signs: Air bubbling through the wound, dyspnea. - Soft signs: hemoptysis, subcutaneous emphysema, hoarseness, odynophagia, hematemesis.
Nerves
- Cranial nerves: Examine 7, 9, 10, 11, 12 nerves. - Brachial plexus: Examine axillary, musculocutaneous, radial, medial and ulnar nerves. - Sympathetic chain: check for Horners syndrome (enophthalmos, ptosis, miosis, anhydrosis).
Chest: Check for associated hemothorax or pneumothorax

Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Demetrios Demetriades, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 10.1. Anatomical zones of the neck
Investigations
Investigations should be reserved only for fairly stable patients. Chest and Neck X-rays: Look for hemopneumothorax, subcutaneous emphysema, a widened upper mediastinum, hematomas causing deviation of the trachea or nasogastric tube, an elevated diaphragm, foreign bodies (Figs. 10.3, 10.4).
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- Subcutaneous emphysema may be due to aerodigestive tract injury or associated pneumothorax or air from outside.
Color Flow Doppler: The investigation of choice for vascular evaluation. It should be performed on all stable patients. It has some limitations in the evaluation of the internal carotid artery near the base of the skull, the proximal subclavian vessels in obese patients especially on the left side, and the vertebral artery under the bony part of the vertebral canal. Angiography: It has largely been replaced by color flow doppler, but has an important role in selected cases.
- Diagnostic indications of angiography: Shotgun injuries, zone III injuries with a hematoma, zone I injuries with a widened mediastinum, and inconclusive color flow doppler studies (Fig. 10.5). - Therapeutic indications of angiography: Stable patients with a diminished or absent peripheral pulses or bruit, where angiographically placed stents may be possible. Also, slow bleeding from the vertebral arteries or branches of the external carotid artery may be controlled with angiographic embolization (Fig. 10.6).
Esophageal Evaluation: Esophagography and/or esophagoscopy should be performed in patients with proximity injuries and symptoms (subcutaneous emphysema, odynophagia, hematenesis) or clinically unevaluable patients (Fig. 10.7).
- Esophagography or esophagoscopy alone may miss cervical esophageal injuries. The combination of the two identifies all significant injuries.
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Fig. 10.2. Protocol for physical examination in penetrating injuries of the neck.
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Fig. 10.3. Neck xray showing a large neck hematoma with displacement of the nasogastric tube.
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Fig. 10.4. Chest x-ray showing an elevated left hemidiaphragm due to a phrenic nerve injury.
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Fig. 10.5. Angiogram in a patient with shotgun in-
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Fig. 10.6. Angiogram showing false aneurysms of the facial artery before and after successful embolization.
Laryngotracheal evaluation: Endoscopy should be performed in all patients with proximity injuries who are symptomatic or are clinically unevaluable.

Airway management may be a significant problem in patients with large neck hematomas or major laryngotracheal trauma.
- Pharmacological paralysis for endotracheal intubation in patients with large hematomas may be risky! Inability to visualize the vocal cords and failure to insert the endotracheal tube may be catastrophic!
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- Cricothyroidotomy in the presence of a hematoma, especially anterior, may be very difficult and perhaps dangerous. - Endotracheal intubation without pharmacological paralysis may exacerbate any hemorrhage and make any hematoma larger due to patient straining and coughing. - Awake nasotracheal fiberoptic intubation is the safest way of intubation in patients with large neck hematomas. - No efforts should be made to introduce a nasogastric tube before anesthesia. Patient straining and coughing may aggravate bleeding. Bleeding control may be achieved by direct pressure. If this fails, balloon tamponade is very often effective (Fig. 10.8). In patients with zone I injuries avoid intravenous lines on the side of injury, in order to avoid extravasation of the infused fluids from a proximal subclavian venous injury.
Operation or Observation
The decision to operate or observe should be made on the basis of a good clinical examination according to a protocol and appropriate investigation. The suggested algorithm for the initial evaluation and management is shown in Figure 10.9.
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Fig. 10.7. Esophageal leak following a gunshot wound to the neck.
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Gunshot injuries should be evaluated and managed like stab wounds. Only about 10% of stab wounds and 17% of gunshot wounds require operation. Transcervical gunshot injuries should be managed like the rest of gunshot injuries. Although 70% of these patients have injuries to significant neck structures, only 20% require surgical intervention. Patients selected for nonoperative management are admitted and observed for at least 24 hours.
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Fig. 10.8. Balloon tamponade in a patient with zone III injury and severe bleeding.
Operative Management
The standard incision for neck exploration is one along the anterior border of the sternomastoid muscle. Occasionally a transverse incision may be used for suspected injuries to the larynx or trachea. Bilateral sternomastoid incisions may be necessary for transcervical wounds. A clavicular incision alone or combined with a median sternotomy provide exposure for subclavian vascular injuries.
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Common Mistakes in the Initial Evaluation and Management of Penetrating Injuries of the Neck
Pharmacological paralysis for emergency room intubation in the presence of a large neck hematoma. Danger or airway loss! Attempts to insert a nasogastric tube in the emergency room in the presence of a suspected vascular injury. Straining and coughing may precipitate major hemorrhage. Failure to examine the patient according to a written protocol. Important signs and symptoms may be missed! Insertion of an intravenous line on the same side as the neck injury. Infused fluids may extravasate from a proximal injury to the subclavian vein!
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References
1. 2. 3. 4. Demetriades D, Asensio J, Velmahos G et al. Complex problems in penetrating neck trauma. Surg Clin North Am 1996; 76; 661-684. Demetriades D., Theodorou D, Cornwell EE et al. Evaluation of penetrating injuries of the neck. A prospective study of 223 patients. World J Surg 1997; 21:41-48. Demetriades D, Theodorou D,. Cornwell EE et al. Penetrating injuries of the neck in stable patients: Physical examination, angiography, or color flow doppler. Arch Surg 1995; 130:971-979. Demetriades D, Theodorou D, Cornwell EE et al. Transcervical gunshot injuries: Mandatory operation is not necessary. J Trauma 1996; 40:758-760.
Fig. 10.9. Algorithm for the initial evaluation and management of penetrating injuries of the neck.
Carotid Artery Injuries

S. Ram Kumar and Fred A. Weaver Introduction
Five to ten percent of arterial injuries involve the carotid artery, all but 3-10% of which follow penetrating trauma. A vascular injury is present in approximately 25% of all neck injuries. Mortality rates range between 10-30%. The incidence of permanent neurological deficit varies between 40-80%.
Historical Perspective
In 1522, Ambroise Par reported the first successful management of a bleeding carotid injury by ligation. Ligation was used routinely for many years in the management of carotid artery injuries, resulting in high rates of mortality and hemiplegia. Primary repair of the carotid arteries was attempted during the Korean conflict. In 1973, Bradley challenged the wisdom of primary repair of an injured carotid artery in patients with a neurologic deficit. He reported autopsies of two neurologically compromised patients with hemorrhagic infarctions after repair of a penetrating carotid injury. Later reports have refuted Bradleys contentions and established that primary repair of all carotid injuries regardless of the neurologic status provides a superior neurologic outcome.
Penetrating Carotid Injuries Clinical Findings

Anatomically, injuries are classified into three zones: Iinjuries from the sternal notch to clavicle, IIinjuries between the clavicle and angle of the mandible and IIIinjuries above the angle of mandible (Fig. 11.1). A cervical bruit, thrill, or a rapidly expanding hematoma in the anterior triangle of the neck is highly suggestive of a carotid injury. Pulse deficit in the superficial temporal artery, evidence of active bleeding from the oropharyngeal or neck wounds, widened mediastinum, ipsilateral Horners syndrome or dysfunction of cranial nerves IX-XII are additional findings often associated with a carotid injury. Contralateral neurologic deficits may be present, but can be obscured by an associated head injury, systemic hypotension or the patients use of psychoactive substances prior to the injury.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. S. Ram Kumar, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California, U.S.A. Fred A. Weaver, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 11.1. Anatomical classification of zones of the neck. Reprinted with permission from: Weaver FA, Yellin AE. Vascular System. In: Donovan AJ, ed. Trauma Surgery. 1st ed. 1994:207-62. 1994 Mosby-Year Book, Inc
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Injuries to the esophagus and trachea are frequently associated due to their proximity.
Investigations
Arteriography is advisable for any Zone I and III penetrating injury. Zone I injuries may involve the vessels of the aortic arch and hence planning the proper incision necessitates arteriographic evaluation. Zone III injuries are difficult to expose and treat surgically. Arteriography aids in formulating an operative plan or may be used in many instances to guide endovascular management of mid and distal internal carotid injuries. Arteriography can help recognize unsuspected vertebral, arch, great vessel or contralateral carotid injuries, or aberrant vascular anatomy in patients who require operative management. Zone II injuries with signs and symptoms suggestive of a carotid artery injury may be screened with a duplex exam with arteriography reserved to confirm duplex documented injuries (Fig. 11.2). Head CT scans are important in selected cases to evaluate the presence and extent of parenchymal brain injury, concurrent intracranial hematomas, cerebral edema or cranial vault injuries.
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Fig. 11.2. Algorithmic approach to a patient with penetrating neck trauma. Reprinted with permission from Kumar SR, Weaver FA. Current Diagnostic Techniques in Vascular Trauma. In: Yao, Pearce, eds. Modern Vascular Surgery. 1st ed. 1999:381-92. 1999 McGraw-Hill.
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Management
Low-velocity penetrating injuries that cause intimal defects, pseudoaneurysms less than 5 mm in size, or adherent or downstream nonobstructive intimal flaps with intact distal circulation and without active hemorrhage can be safely observed. Documentation of vessel healing should be obtained by follow-up duplex scanning or arteriography. Arterial repair is the preferred option for most other internal or common carotid injuries regardless of the contralateral neurologic status. However, patients with a dense neurologic deficit and large infarct on CT have a poor outcome irrespective of treatment. Occlusive internal carotid injuries in an asymptomatic patient may also be treated nonoperatively. When this is elected, it is critical to maintain normotension. Anticoagulation, if not contraindicated, is advisable for 3-6 months. Incision
- For Zone II injuries, the carotid artery is exposed by an incision parallel to the anterior border of the sternocleidomastoid muscle.
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Trauma Management - For Zone I injuries, exposure of the proximal portion of the common carotid artery requires a median sternotomy. - The mid to distal internal carotid artery is a challenge to expose. Division of the digastric muscle, osteotomy of the angle of mandible, or anterior subluxation of the mandible may be required.
The injured artery is repaired by lateral arteriorrhaphy for the simpler wounds and excision of the injured area with primary anastomosis or interposition saphenous vein grafts for more complex wounds. Simple injuries to the external carotid arteries can be surgically ligated or embolized by an endovascular approach. Proximal internal carotid artery injuries can be managed by simple repair or interposition vein graft. Another option is to oversew the injury, then ligate the external carotid artery distally and divide it. The distal internal carotid artery is then transposed to the proximal stump of the external carotid artery (Fig. 11.3). Use of Shunts
- Shunts are not necessary for proximal common carotid injuries. - During internal carotid artery repair, intraluminal shunts should be used to reestablish or maintain cerebral perfusion. - Shunts should be passed through the lumen of the graft material before being placed and then the graft sewn in place (Fig. 11.4). The shunt can be removed just prior to the placement of the last few sutures. - Systemic anticoagulation with heparin is necessary when shunts are used.
False aneurysms in the distal internal carotid artery can be embolized with
Fig. 11.3. Repair of proximal internal carotid artery injury by transposition to the external carotid artery. Reprinted with permission from: Weaver FA, Yellin AE. Vascular System. In: Donovan AJ, ed. Trauma Surgery. 1st ed.1994:207-62. 1994 Mosby-Year Book, Inc.
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Fig. 11.4. Use of shunts during interposition graft repair of carotid artery injuries. Reprinted with permission from: Weaver FA, Yellin AE. Vascular System. In: Donovan AJ, ed. Trauma Surgery. 1 st ed. 1994:207-62. 1994 Mosby-Year Book, Inc.
detachable balloons at the time of arteriography. Prior to balloon occlusion, temporary occlusion with monitoring of the neurologic status should be performed. If a contralateral deficit develops an external carotid-internal carotid bypass may be required prior to permanent balloon occlusion. When balloon occlusion is used, anticoagulation for 3-6 months is necessary to inhibit thrombus propagation into the middle cerebral artery. If there is an associated aerodigestive tract injury, vascular repair should be protected by interposing the belly of the sternomastoid muscle between the vascular and aerodigestive tract repairs.
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Complications
Short-term complications include thrombosis of the repair, perioperative hemodynamic instability causing cerebral infarcts and sepsis that may ensue following dehiscence of an aerodigestive tract repair. Early diagnosis and treatment offers best prognosis. Injury due to cerebral ischemia increases with delays in management.
Blunt Carotid Injuries

The mechanism of blunt injury includes direct blows, injuries that cause severe flexion and rotation of the neck and hyperextension injuries with stretch of the vessel over the transverse processes of the cervical vertebra. Blunt injury usually involves the internal carotid artery and produces vessel contusion or intimal tears that lead to dissection, intimal flaps or occlusion.
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Diagnosis
A high index of suspicion is required, especially in patients with neurological deficits and minimal physical findings of cervical trauma. A history of lucid interval of hours to days between the injury and the appearance of neurologic symptoms is the classic presentation. The patient may complain of hearing a buzzing sound. Clinical findings may include Horners syndrome or a bruit. Duplex evaluation has been used to diagnose blunt carotid injuries; however, arteriography remains the gold standard since intimal flaps and dissections of the mid and distal internal carotid artery may be missed by duplex exam.
Management
Blunt injuries to the carotid artery are usually not amenable to definitive surgical repair. Systemic anticoagulation, which limits thrombus propagation and embolization, is the treatment of choice. Pseudoaneurysms may develop in up to 30% of patients treated by anticoagulation therapy. Endovascular stenting has been used to treat pseudoaneurysms with good success. Outcome depends on the initial neurologic deficit, early diagnosis and adequacy of collateral circulation. If the initial neurological deficit is limited, the outcome with anticoagulation is generally good.
References
1. 2. 3. 4. 5. Hood DB, Yellin AE, Weaver FA. Vascular trauma. In: Dean RH, Yao JST, Brewster DC, eds. Current Diagnosis and Treatment in Vascular Surgery. Edition 1 CT: Appleton Lange, 1998: 405-28. Demetriades D, Asensio J, Velmahos G et al. Complex problems in penetrating neck trauma. Surg Clin N Am 1996; 76(4):661-83. Kuehne JP, Weaver FA, Papanicolaou G et al. Penetrating trauma of the internal carotid artery. Arch Surg 1996; 131:942-8. Biffl WL, Moore EE, Ryu RK et al. The unrecognized epidemic of blunt carotid arterial injuries. Ann Surg 1998; 228(4):462-70. Weaver FA, Yellin AE, Wagner WH et al. The role of arterial reconstruction in penetrating carotid injuries. Arch Surg 1988; 123:1106-11.
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Subclavian and Axillary Vascular Injuries

The left subclavian artery originates directly from the aortic arch and the right subclavian from the brachiocephalic artery. The rest of the anatomy is similar in both sides. The first part of the subclavian artery lies behind the sternomastoid muscle and medial to the scalenus anterior muscle. The second part lies behind the anterior scalenus muscle, and the third part lateral to the scalenus muscle. Most of the axillary artery lies underneath the pectoralis minor muscle. The subclavian vein is in front and below the artery. The scalenus anterior muscle separates the two vessels. The axillary vein lies inferior to the artery (Fig. 12.1).
Incidence
In about 3% of all penetrating injuries to the neck. In about 3.5% of all gunshot wounds to the neck. In about 3% of all gunshot wounds to the chest. In about 2% of stab wounds to the neck. In about 1% of stab wounds the chest. In about 14% of patients with fracture of the 1st rib. In about 0.4% of patients with fracture of the clavicle. All patients with scapulothoracic dissociation have vascular injuries.
Many patients are dead or near death on arrival. Hard Signs Diagnostic of Vascular injury: Severe external bleeding, massive hemothorax or significant continuous bleeding in the thoracostomy tube in patients with thoracic inlet injuries, absent or diminished peripheral arm pulses, bruit or murmur. Soft Signs Suspicious of Vascular injury: Hematoma, unexplained anemia or hypotension in the presence of a proximity penetrating injury. Ankle-Brachial Index (ABI) is part of the standard examination. An ABI higher than 0.90 is unlikely to be associated with significant arterial injury. However, small arterial injuries may be associated with a normal ABI. The presence of a peripheral pulse does not exclude a proximal arterial injury. A good physical examination can reliably diagnose or suggest all significant subclavian or axillary vascular injuries.
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Fig. 12.1. Anatomy of the subclavian and axillary vessels. Used with permission: Textbook of Techniques in Complex Trauma Surgery. Asensio J, Demetriades D, eds. W.B. Saunders (in press).
Investigations
No investigations for hemodynamically unstable patients or in the presence of a threatened extremity. Chest X-ray: May show an associated hemopneumothorax, the presence of a missile, a local hematoma (Fig. 12.2). Color Flow Doppler: The investigation of choice; it is not invasive, it can evaluate both arteries and veins, and has a high sensitivity and specificity in experienced hands. However, it is operator dependent and in obese patients it may not be possible to visualize the proximal vessels, especially the left side. Arteriography: a) Diagnostic Indications: Widened mediastinum on chest xray, shotgun injuries, inconclusive color flow doppler (Figs. 12.3-12.6). b) Therapeutic indications: Selected stable patients with bruits or murmurs or decreased peripheral pulses where angiographically placed stents may be possible (Figs. 12.7A-12.7B).
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Note
- The combination of physical examination and color flow doppler by an experienced operator identifies almost all injuries. - The choice of angiography or color flow doppler should be individualized taking into account the capabilities of the trauma center.
Prehospital Management
Control any external bleeding by direct compression. Scoop and run.

No intravenous lines on the injury side
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If direct pressure cannot control the bleeding, balloon tamponade may be effective. A Foley catheter is inserted into the wound and advanced as far as it can go. The balloon is then inflated and in most cases the bleeding is effectively controlled. If the Foley enters into the pleural cavity through a supraclavicular wound, the balloon is again inflated and firm traction is applied on the catheter. The traction is maintained by applying a Kelly forceps on the Foley, just above the skin. The balloon compresses the bleeding subclavian vessel against the first rib or the clavicle and the bleeding is controlled. This technique controls bleeding into the chest. If external bleeding persists a second Foley may be inserted and inflated into the wound tract (Fig. 12.8). Patients with active bleeding, hemodynamic instability, or an ischemic arm, need urgent operation, without any vascular studies. Patients in cardiac arrest or imminent cardiac arrest should have an emergency room thoracotomy. Bleeding from the subclavian vessels can be controlled by direct pressure at the apex of the hemithorax.
Operative Technique
Incision: A clavicular incision provides a good exposure for distal subclavian and proximal axillary vascular injuries. The incision starts at the sternoclavicular joint, extends directly over the medial half of the clavicle and curves downwards into the deltopectoral groove (Fig. 12.9). The medial half of the clavicle may be excised or the sternoclavicular joint is disarticulated and the clavicle retracted. The retroclavicular space is carefully dissected and the subclavian vessels are identified (Fig. 12.10).
- A combination of a clavicular incision and a median sternotomy provides a good exposure for both, left and right proximal subclavian injuries (Fig. 12.11). - A trap door incision (a combination of clavicular, upper median sternotomy and anterior thoracotomy through 3rd intercostal space) has been used for left proximal injuries. This incision is not recommended. - An incision over the deltopectoral groove with division of the pectoralis major muscle about 2 cm from its attachment to the humerous, and division of the underlying pectoralis minor muscle provides good exposure for distal axillary vessels (Fig. 12.12).
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Management of the Vascular injury

- Arterial injuries should be repaired in almost all cases. In critically ill patients a temporary stent should be considered. Ligation of the artery is not desirable because it may cause severe ischemia and aggravate the systemic condition of the patient. - If primary repair of the artery is not possible an autologous venous or PTFE graft should be used. Both types of graft are acceptable. - Venous injuries should be repaired only if it can be done easily with simple suturing and without significant postrepair stenosis. Complex venous reconstruction should be avoided. Ligation is well tolerated and except for transient early edema there are no long-term side effects.
Wound Closure
- Excision of the medial half of the clavicle does not result in permanent disabilities. Regeneration of the bone occurs within a few months. - If disarticulation of the sternoclavicular joint had been performed, the anatomy should be restored by suturing the periosteum and the ligaments over the joint.
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Fig. 12.2. Thoracic inlet injury with hematoma near the proximal left clavicle. The patient had a subclavian venous injury.
Complications
Air embolism may occur in venous injures. It often presents as unexpected cardiac arrest or arrhythmia. Air bubbles may be seen in the vein. The treatment is aspiration of the right ventricle. Venous ligation may result in temporary arm edema.
Therapeutic Interventional Radiology

Selected stable patients with subclavian artery injuries (especially false aneurysms or fistulae) can be managed with angiographically placed stents (Figs. 12.7A, 12.7B).
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Fig. 12.3. Shotgun injury is a strong indication for arteriography.
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Fig. 12.4. Arteriogram showing partial transection of the subclavian artery.
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Fig. 12.5. False aneurysm of the subclavian artery.
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Fig. 12.6. False aneurysm of the axillary artery.
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Fig. 12.7A. Traumatic false aneurysm and arteriovenous fistula of the subclavian vessels.
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Fig. 12.7B. Patient in Figure 12.7A, successfully treated with endovascular stent.
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Fig. 12.8. Foley balloon tamponade of bleeding from the subclavian vessels. Used with permission: Textbook of Techniques in Complex Trauma Surgery. Asensio J, Demetriades D, eds. W.B. Saunders (in press).
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Fig. 12.9. Clavicular incision provides good exposure of distal subclavian and proximal axillary vessels.
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Fig. 12.10. Proximal subclavian vessel exposure after excision of the medial half of the clavicle. Used with permission: Textbook of Techniques in Complex Trauma Surgery. Asensio J, Demetriades D, eds. W.B. Saunders (in press).
Prognosis
The overall survival for patients reaching medical care in about 70%. Survival for patients reaching the operating room alive is about 85%. Venous injuries are associated with a higher mortality than arterial injuries, perhaps due to air embolism or inability of the vein to contract and reduce bleeding.
Scapulothoracic Dissociation
It involves disruption of the shoulder from the chest. The clavicle is fractured or dislocated, the shoulder muscles are avulsed, and the neurovascular structures are severely damaged. If there is significant preservation of the brachial plexus function, vascular reconstruction should be attempted. In the absence of brachial plexus function the arm should be amputated below the shoulder.
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References
1. 2. 3. Demetriades D, Asensio JA, Velmahos G et al. Complex problems in penetrating neck trauma. Surg Clin North Am 1996; 76: 665-683. Demetriades D, Chahwan S, Gomez H et al. Penetrating injuries, to the subclavian and axillary vessels. J Am Coll Surg 1999; 188:290-295. Demetriades D, Rabinowitz B, Pezikis A et al. Subclavian vascular injuries. Br J Surg 1987; 74:1001-1003.
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Fig. 12.11. A median sternotomy combined with a clavicular incision provides satisfactory exposure for proximal subclavian injuries. Used with permission: Textbook of Techniques in Complex Trauma Surgery. Asensio J, Demetriades D, eds. W.B. Saunders (in press).
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Fig. 12.12. Excision or division and retraction of the clavicle and division of the pectoralis major and the underlying pectoralis minor expose the subclavian and axillary vessels. Used with permission: Textbook of Techniques in Complex Trauma Surgery. Asensio J, Demetriades D, eds. W.B. Saunders (in press).
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CHAPTER 13
Vertebral Artery Injuries

The vertebral artery (VA) is the first cephalad branch of the subclavian artery. It enters the vertebral canal at C6 and exits at C1.
Incidence
In about 10% of gunshot wounds to the neck. In about 5% of stab wounds to the neck. It may occur in fractures of the C-spine due to blunt trauma.
About two thirds of patients with VA injury have major associated injuries to other neck structures. Fracture of the spine is the most common associated injury. In about 50% of cases there are hard signs of vascular injury (severe bleeding, large hematoma, bruit). In about 30% there are soft signs of vascular injury (stable hematoma, mild hypotension). In about 20% there are no significant signs of vascular injury.
Investigations
Investigations should be reserved only for hemodynamically stable patients with no severe active bleeding. All patients with gunshot wounds involving the transverse processes of the cervical spine should be evaluated for VA injuries. Overextension injuries to the cervical spine should be evaluated by doppler studies for VA injuries. Color flow doppler may be helpful in selected cases. It can not visualize the parts of the artery underneath the bony vertebral canal. Angiography for selected cases with large neck hematomas, bruits, shotgun injuries, gunshot wounds involving the transverse processes (Fig. 13.1).
Management
Fewer than half of patients with VA injuries require operation. Patients with thrombosed VA do not need any treatment (Fig. 13.2). Angiographic embolization is the treatment of choice for patients with continuous slow bleeding or false aneurysm or arteriovenous fistula (Figs. 13.3, 13.4). Operative management should be reserved only for patients with severe active bleeding or where angiographic embolization had failed.
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Fig. 13.1. Gunshot wound of the C-spine involving the transverse foramen. Angiographic evaluation should be performed in these cases.
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Fig. 13.2. Angiography showing thrombosis of the VA. No treatment is required.
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Fig. 13.3. Vertebral artery arteriovenous fistula, before and after angiographic embolization. (From Demetriades D, Theodorou D, Asensio J et al. Management options in vertebral artery injuries. Br J Surg 1996; 83:83-86, with permission). Fig. 13.4. VA false aneurysm before and after successful angiographic embolization. Reprinted with permission from Demetriades D, Asensio J, Velmahos G, Thal E. Complex problems in penetrating neck trauma. Surg Clin North Am 1996; 76:661-683.
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Fig. 13.5A, B. Surgical exposure of the VA: Following an incision along the anterior border of the sternomastoid muscle, the carotid sheath is retracted laterally or medially. The trachea and esophagus are retracted medially and the longus colli muscle is swept off the vertebra. The anterior rim of the vertebral foramen is then removed with bone rongeurs and the VA is exposed and ligated. Reprinted with permission from Demetriades D, Theodorou D, Asensio J et al. Management options in vertebral artery injuries. Br J Surg 1996; 83:83-86.
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Fig. 13.6. Incision and craniectomy for complex high VA injuries not amenable to angiographic embolization. Reprinted with permission from Demetriades D, Theodorou D, Asensio J et al. Management options in vertebral artery injuries. Br J Surg 1996; 83:83-86.
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The operation for VA injuries is one of the most difficult in trauma surgery and very often involves deroofing of the vertebral canal (Figs. 13.5A,B). For very high lesions a craniectomy may be necessary (Fig. 13.6).
Prognosis
Isolated VA injuries have a mortality of about 7%. Thrombosis or ligation of the VA are very well tolerated and neurological sequelae are extremely rare.
Common Mistakes and Pitfalls

Failure to evaluate for VA injuries in the presence of a fracture of the transverse process of the C-spine. Underestimate the difficulties of the surgical exposure of the VA! Angiographic embolization should be the procedure of choice whenever is possible.
References
1. 2. 3. Demetriades D, Theodorou D, Asensio JA et al. Management options in vertebral artery injuries. Br J Surg 1996; 83:83-86. Demetriades D, Asensio J, Velmahos G et al. Complex problems in penetrating neck trauma. Surg. Clin North Am 1996; 76:661-684. Hatzitheofilou C, Demetriades D, Melissas J et al. Surgical approaches to vertebral artery injuries. Br J Surg 1988; 75:234-237.
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Laryngotracheal Injuries
Uttam K. Sinha and Dennis M. Crockett Introduction
Experience in managing laryngeal trauma is limited because of the relative rarity of this injury. External laryngeal trauma accounts for only 1 in 30,000 emergency room visits. Although these injuries are rare, their initial management has a tremendous impact on the immediate probability of survival of the patient, as well as long-term quality-of-life. Proper management of laryngeal trauma requires a thorough understanding of the complex anatomy of the larynx and hypopharynx (Fig. 14.1).
- The skeletal framework of the larynx is made up of three paired and three unpaired cartilages, a circumferential conus elasticum membrane and two paired vocal ligaments. While the epiglottis, thyroid and cricoid cartilages are unpaired and larger, the arytenoid, corniculate and cuneiform cartilages are paired and smaller. The thyroid cartilage has an anterior angle of approximately 90 in the male and 120 in the female and provides an anterior fulcrum to which the vocal ligaments (vocal cords) are attached. During repair of a fracture of the thyroid cartilage, maintenance of this anterior angle is critical to preserve the proper length of the true vocal cords and to restore optimum phonatory function. - The cricoid is the strongest cartilage and forms a complete ring, surrounding the space immediately inferior to the vocal cords (subglottic space). One of the critical factors in the prevention of subglottic stenosis following trauma is preservation of the shape and diameter of this cartilage. - The paired arytenoid cartilages articulate with the cricoid cartilage through synovial joints. They constitute the posterior one-third of the true vocal cords. Full range of excursion of the vocal cords takes place by the action of intrinsic laryngeal muscles on the arytenoid cartilages. Distortion of the arytenoid cartilage(s) may occur following external laryngeal injury or traumatic intubation, which may result in fixation of the cord with associated breathy dysphonia and aspiration.
The larynx is protected anteriorly by the forward projection of the mandible, and posteriorly by the rigid cervical spine. Nonetheless, injuries occur, and the resultant damage to the larynx is usually characteristic of the mechanism of injury. These mechanisms can be divided into the following:
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Uttam K. Sinha, Department of Otolaryngology Head and Neck Surgery, University of Southern California School of Medicine, Los Angeles, California, U.S.A. Dennis M. Crockett, Department of Otolaryngology Head and Neck Surgery, University of Southern California School of Medicine, Los Angeles, California, U.S.A.
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Fig. 14.1. Normal anatomy of the larynx and hypopharynx at the level of the true vocal cord.
Blunt trauma, including crushing, strangulation, and clothesline type injuries Penetrating trauma Inhalation injuries Injuries caused by caustic ingestion Intubation injuries
Motor vehicle accidents are the most common cause of anterior blunt trauma to the larynx. The incidence of this type of injury is declining for the following reasons:
- Mandatory seat belt laws - Deployment of air bags - Better education regarding drunk driving
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Strangulation injuries occur as a result of compressive forces from assaults with blunt objects or from attempted suicides by hanging. The magnitude of the force sustained to the anterior neck should be critically assessed, as delayed profound edema of the larynx may result in loss of the airway. Clothesline injuries typically occur in motorcyclists or snowmobilists when the riders neck encounters a fixed horizontal object, such as a clothesline (Fig. 14.12). Many of these injuries lead to immediate death resulting from a crushed larynx or laryngotracheal separation. Penetrating trauma commonly occurs as a result of gunshot wounds or knife injuries. High-velocity weapons may cause massive tissue destruction beyond the trajectory of the bullet. Knife injuries do not destroy tissue distant to the path of injury. Inhalation injuries are caused by superheated air, especially steam. This injury is usually associated with burns to other parts of the body. An airway should be secured early in these injuries before fluid resuscitation of the associated burn injury begins because this will lead to marked edema of the injured
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laryngeal mucosa with loss of airway. Inhalation injury causes damage mostly in the supraglottic area, as does caustic ingestion. Both these injuries cause reflex closure of the glottis for protection of the lower airway. Laryngeal trauma in the pediatric population is uncommon and differs from adult laryngeal trauma in several aspects:
Larynx is better protected because of its higher position in the neck Increased soft-tissue damage Decreased incidence and severity of cartilaginous fractures Smaller cross-sectional area of the larynx Higher chance of respiratory embarrassment due to soft-tissue damage in a relatively smaller cross-sectional area of the airway
External Laryngeal Trauma Clinical Presentation

The spectrum of laryngeal trauma varies from obvious laryngeal fracture to subtle aberrations of laryngeal function. Dysphonia is a common symptom of laryngeal trauma.
- Hematoma of the true vocal cord reduces vibratory capacity of the cord. - Unilateral fixation (arytenoid dislocation) or paralysis (recurrent nerve palsy) causes breathy dysphonia. - Any structural alteration in the larynx that changes airflow patterns has the potential to alter the voice. - Patient can be completely aphonic in more severe trauma.
Stridor is an ominous clinical finding as it suggests impending airway obstruction.

- Soft tissue edema, hematoma and displaced fracture of the thyroid cartilage are common causes of stridor. - Fracture of the cricoid cartilage with narrowing of the subglottic area may produce stridor. - Bilateral dislocation of the arytenoid cartilages with fixation of both vocal cords is an uncommon cause of stridor (unilateral fixation or paralysis of the cord usually produces breathy dysphonia, unless there is associated soft-tissue edema or hematoma).
- Bilateral recurrent laryngeal nerve paralysis causing stridor is extremely rare; both nerves are well protected in the tracheo-esophageal grooves deep to the sternocleidomastoid and strap muscles. - Disruption of the laryngeal framework from gunshot injuries or cricotracheal separation causes stridor; in these instances, no attempt should be made to cover, compress, or otherwise manipulate such a wound before securing the airway. Laryngeal injuries can produce dysphagia and odynophagia. Vertical movement of the injured larynx with swallowing may produce pain and difficulty in swallowing. Aspiration is laryngeal dysfunction that may be caused by immobility of one or both vocal folds. Although not clinically apparent immediately postinjury, this may become evident later. Hemoptysis indicates an injury in the upper aerodigestive tract, however this is a nonspecific symptom.
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The skin of the anterior neck may reveal contusions or abrasions from blunt trauma or a line pattern indicative of a strangulation injury. Anterior neck is palpated to elicit crepitance, tenderness and loss of laryngeal prominence. It is very difficult to palpate a step-off of the thyroid cartilage fracture, especially in the presence of anterior cervical soft tissue swelling. Penetrating injuries are assessed initially without exploration of the wound. Manipulation of the wound may cause complete obstruction of the airway, may dislodge a clot causing further bleeding or may further damage the delicate laryngeal structure. The entrance and exit wounds, and trajectory of the bullet are determined.
Investigations
If the patient is stable, flexible laryngoscopic examination is performed carefully, as minor trauma associated with insertion of the flexible laryngoscope may precipitate an airway emergency. The larynx and hypopharynx are assessed for soft tissue edema and hematoma and their location, as well as the presence of mucosal laceration and exposure of cartilage. The arytenoids are evaluated for their position and full range of motion with phonation (asking the patient to say i) and respiration. Failure of the true vocal cords to meet in the same horizontal plane may also be present, indicating a structural change in the laryngeal framework or superior laryngeal nerve injury. Flexible laryngoscopic examination is occasionally impossible to perform in an acutely injured patient because of the patients inability to cooperate. If the patients airway and hemodynamics are stable, a noncontrast thin-cut (3 mm) CT scan of the larynx can be obtained to evaluate the laryngeal skeletal framework in a noninvasive manner (Fig. 14.2). CT allows selecting out the subgroup of patients that do not require surgical intervention. CT adds little to the preoperative evaluation in patients with the obvious surgical indications of exposed cartilage or displaced fractures with overlying mucosal laceration.
Initial Management
The first priority in the management of a laryngeal injury is to establish an airway. The patient is then hemodynamically stabilized, and the cervical spine is kept stable until injury to the spine is ruled out. The most conservative, reliable method of securing an airway in a patient with suspected laryngeal injury is tracheotomy performed under local anesthesia with the patient awake and breathing spontaneously (Fig. 14.3). Endotracheal intubation may further damage the larynx, prove exceedingly difficult, convert an urgent procedure to an emergent one, and interfere with subsequent examination and repair of the larynx. Endotracheal intubation is acceptable when:
- the endolaryngeal mucous membrane is intact - the laryngeal skeleton is minimally displaced - intubation is performed by highly skilled personnel
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Once the patient is stabilized, laryngeal injuries are further assessed to determine whether the patient requires surgical intervention or can be managed conservatively.
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Fig. 14.2. CT findings show fracture of the left lamina of the thyroid cartilage with blunting of the angle of the thyroid cartilage.
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Fig. 14.3. Ideally, tracheotomy should be performed at the level of the second or third tracheal rings, shown by two arrows on right. High tracheotomy (left) has increased incidence of tracheal stenosis.
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Fig. 14.4. Minor mucosal laceration of the left supraglottic without exposure of cartilage does not need surgical repair.
Nonsurgical Management
Patients with laryngeal trauma are extensively evaluated (physical examination, flexible laryngoscopy, CT scan) to select the subgroup who are likely to do well without surgical intervention. Medical management assumes that the patient has an otherwise stable airway and does not require a tracheotomy. The following laryngeal injuries can be managed nonsurgically:
- Minor endolaryngeal mucosal lacerations not involving the anterior commissure (Fig. 14.4) - Single nondisplaced, nonangulated fracture of the thyroid cartilage without overlying mucosal laceration or exposed cartilage - Minor nonexpanding submucosal hematoma not causing respiratory embarrassment - Minimum soft tissue edema without respiratory compromise - Mild abnormal findings upon flexible laryngoscopic examination with normal CT scan
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If a decision for nonsurgical management is made, the following measures should be taken:
- Elevation of the head of the bed (30-45)
Laryngotracheal Injuries - Humidified air - Corticosteroid therapy instituted early after injury
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Surgical Management
Surgical management of laryngeal injuries should be coordinated with all surgical teams involved and with the anesthesiologist. A vast majority of patients who undergo repair of laryngeal injuries will require a tracheotomy performed under local anesthesia. In the noncooperative child, tracheotomy under local anesthesia may not be feasible: the airway is secured via rigid laryngoscopy and bronchoscopy in the operating room, followed by tracheotomy. Following induction of general anesthesia, direct rigid laryngoscopy, bronchoscopy and esophagoscopy are performed for detailed evaluation of the injuries. If a tracheotomy is performed for soft-tissue edema or hematoma, and direct rigid examination and CT scan findings are otherwise normal, no further surgical intervention is required. Although controversy exists as to the optimum time of repair of laryngeal injuries, the best results are obtained with immediate or early repair.
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Fig. 14.5. Fracture of the left thyroid lamina (A) with no endolaryngeal lesion. This type of fracture can be repaired either by miniplate (B) or wire (C); refer to text for details.
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The majority of the laryngeal injuries that require surgical repair can be categorized into three groups:
- Displaced single or comminuted fractures of the thyroid cartilage with intact endolaryngeal mucosa or with minimal mucosal laceration and no exposure of the cartilage (Fig. 14.5) - Fracture of the thyroid cartilage with endolaryngeal injury requiring repair of the endolarynx by a thyrotomy approach (Fig. 14.6) - Massive trauma requiring placement of an endolaryngeal stent (Fig. 14.9)
Displaced single and comminuted fractures are repaired by open reduction and internal fixation (Fig. 14.5A).
- The larynx is completely exposed by raising cutaneous subplatysmal apron flaps. - The strap muscles are divided in the midline and retracted laterally. - The fractures are reduced and their positions are maintained by wire (26 gauge) which is passed through the cartilage by using a curved cutting needle. Care is taken not to penetrate the mucosa. An 18 gauge needle is cut into two segments with optimum length to pass the wire through them. The needle segments are placed on either side of the fracture to prevent the wire from cutting through the cartilage (Fig. 14.5C). If the cartilage is ossified, a drill is used to thread the
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Fig. 14.6. Normal anatomy of the larynx is restored following open reduction and internal fixation of fracture of left thyroid lamina.
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Fig. 14.7. Displaced figure of the lamina with exposed cartilage (right) needs repair through thyrotomy approach (shown by dotted lines on the left).
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Fig. 14.8. Extensive endolaryngeal injuries (right) are repaired through thyrotomy approach (shown by dotted lines on the left).
wire. To avoid further damage to the cartilaginous skeleton, no fracture site sutures are tightened until all fractures have been reduced. - Micro and mini-plates (1.0 mm preferred) can be used instead of wire for internal fixation (Fig. 14.5B). - Endolaryngeal anatomy should be maintained as close to normal as possible during open reduction and internal fixation (Fig. 14.6); failure to achieve this will result in dysphonia.
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Fig. 14.9. A Portex endotracheal tube is fabricated for endolaryngeal stenting. Fourcentimeter long stent extends from the supraglottis to the first tracheal ring. The upper end of the tube is closed with nylon sutures to prevent aspiration. The stent is secured by two monofilament sutures tied to the skin buttons.
When significant endolaryngeal injuries are encountered, a midline thyrotomy is performed after retracting the strap muscles laterally (Fig. 14.7).
- All mucosal lacerations are meticulously repaired. - A dislocated arytenoid, if present, is reduced (Fig. 14.8). - Most mucosal lacerations can be repaired by either simple closure or by using adjacent mucosal advancement flaps. In rare instances in which the soft tissue defect is too large, a pedicled mucosal flap raised from the adjacent pyriform sinus is used to repair the defect. - It is of utmost importance to reconstitute the anterior commissure to maintain the scaphoid shape of this region and to preserve a normal voice. This is achieved by suturing the anterior ends of the true vocal cords to the outer perichondrium of the thyroid cartilage. The thyrotomy is closed using permanent sutures or wire.
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The indications for stenting in laryngeal injuries are controversial. The advantages of using a stent should be balanced against the risk of additional pressure damage to the mucosa. Indications for placement of stents are:
- Injuries involving the anterior commissure - Severe comminuted fractures of the thyroid cartilage, in which the architecture of the larynx is not maintained by open reduction and internal fixation of the fractures
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The advantages of stenting are:

- Reduced chance of web formation at the anterior commissure - Improved support of the laryngeal cartilaginous skeleton during healing - Reduced movement of the larynx during swallowing
Stenting alone without open reduction and internal fixation and closure of lacerations are unsatisfactory. A wide variety of stents are available (Figs. 14.9 and 14.10). All should be roughly in the shape of the laryngeal lumen and made of soft material to prevent further mucosal damage. The stent should extend from the false vocal cord to the first tracheal ring for proper stability and to prevent the formation of adhesions in the laryngeal lumen. The position of the stent can be maintained by two through and through monofilament sutures tied to skin buttons (Fig. 14.9). An Eliachar stent can be introduced into the laryngeal lumen through the tracheostomy by a blunt instrument (Fig. 14.10). The phalanges of the stent are sutured to the skin. Alternatively, it can be introduced by direct laryngoscopy (Fig. 14.11). Early removal of the stent is recommended to minimize mucosal damage. Usually, 10-14 days are adequate, even in severe injuries. A variety of laryngeal injuries can be encountered during repair.
- Small defects in the cricoid and tracheal cartilages can be repaired using pedicled flaps of strap muscle. - Loss of the anterior portion of the thyroid cartilage can be repaired by suturing mucosa over a stent. - Laryngotracheal separation can be repaired by suturing the trachea to the cricoid cartilage, taking care not to injure the recurrent laryngeal nerves near their entrance into the larynx at the cricoarytenoid joints (Fig. 14.12).
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Fig. 14.10. The Eliacher stent (left) can be introduced through the tracheostome and positioned in the endolarynx (right).
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Fig. 14.11. The Eliacher stent can be introduced transorally by direct laryngoscopy.
- Repair of a severed recurrent laryngeal nerve is not gratifying. - In massive trauma where laryngeal reconstruction is not possible, partial or total laryngectomy may be necessary. Fortunately, this is extremely rare.
Postoperative Care
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The patient should receive antibiotics for 5-7 days. Proton pump inhibitors or H2-blockers are routinely given to prevent reflux. Nasogastric feeding tubes are avoided when possible. The head of the bed is kept elevated. Stents are removed as soon as possible. Decannulation is done as soon as the patient tolerates occlusion of the tracheotomy tube. The patients are followed for at least one year to assess the return of true vocal cord movement, and development of stenosis.
Complications
Speech, swallowing and respiration are affected to some degree after repair depending on the severity of the trauma. Granulation tissue formation occurs especially after placement of stents. Meticulous closure of lacerations, postoperative antibiotics and H2blockers and early removal of stents prevent this complication. Profuse granulation tissue may require endoscopic laser debulking.
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Fig. 14.12. Laryngotracheal separation occurs from clothesline injuries, left. Anatomy of a normal cricoid cartilage is shown on right; ant.=anterior.
Laser cordotomy or arytenoidectomy is done for bilateral paralysis or fixation of vocal cords. Glottic/subglottic stenosis is managed by standard techniques of laryngotracheal reconstruction. Tracheal resection and end-to-end anastomosis is performed for stenosis of a short tracheal segment (4-6 cm).
Outcome
Functional outcome depends mostly on the extent of trauma and quality of initial repair. Excellent functional recovery can be expected in patients who do not need surgical repair. Superb recovery is also noted in patients that require repair of the cartilages and no endolaryngeal surgery. Prognosis is poorest among patients who require stent placement.
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Intubation Injuries
The vast majority of endolaryngeal injuries are due to endotracheal intubation. Injuries are sustained as a result of either faulty techniques or prolonged intubation.
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Prevention of intubation trauma is best accomplished by educating personnel who perform intubation as to the correct techniques of intubation, including choosing the correct size of the endotracheal tube. Common injuries encountered following intubation are oropharyngeal, hypopharyngeal or laryngeal mucosal lacerations, and dislocation of the arytenoid cartilage. Superficial mucosal lacerations do not need any surgical intervention. However, deep lacerations are sutured. Through-and-through lacerations at the level of the pyriform sinus require transcervical repair and drainage, and feeding through a nasogastric tube for 7 days along with antibiotic therapy. Endoscopic reduction of cricoarytenoid joint dislocation should be performed urgently.
References
1. 2. 3. 4. 5. Leopold DA. Laryngeal trauma. Arch Otolaryngol Head Neck Surg 1983; 109:106-108. Olson NR, Miles WK. Treatment of acute blunt laryngeal injuries. Ann Otol Rhinol Laryngol 1971; 80:705-709. Schaefer SD. Laryngeal and esophageal trauma. In: Cummings et al. OtolaryngologyHead and Neck Surgery, Third Ed. St. Louis, MO: Mosby Year Book 1999: 2001-2012. Stanley RB, Hanson DG. Manual strangulation injuries of the larynx. Arch Otolaryngol Head Neck Surg 1983; 109:344-346. Whited RE. A prospective study of laryngotracheal sequelae in long term intubation. Laryngoscope 1984; 94:367-377.
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Traumatic Brachial Plexus Injuries

Milan Stevanovic and Frances Sharpe Brachial Plexus Injuries Brachial Plexus
Injuries to the brachial plexus can result in devastating impairment of upper extremity motor and sensory function. Recovery from these injuries is seldom complete and depends on the level, extent, and mechanism of injury.
The first repair of the brachial plexus reported in English literature was performed by William Thoburn in 1896 and published in 1900. Prior to the advent of microsurgical reconstruction, the treatment of brachial plexus injuries focused on late reconstruction. Reconstructive surgeries included joint fusions, tendon transfers, and amputations for painful flail limbs. By the late 1960s, direct microsurgical repair of nerves and the introduction of nerve grafting significantly changed the early treatment of these injuries.
Epidemiology
Minor stretch injuries to the brachial plexus (burners or stingers) can occur frequently in contact sports, most commonly in American-style football. These generally have full spontaneous recovery over a period of minutes. Persistent or recurrent symptoms should be further investigated. Most often, injuries occur as a closed traction injury. Penetrating injuries, either laceration or gun shot wounds account for a smaller percentage of injuries. Over 70% of injuries occur in high-speed accidents. Motorcycle accidents account for a higher percentage of injuries than motor vehicle accidents. About 2% of motorcycle accidents result in brachial plexus injury. Snowmobile accidents are a recently increasing cause of brachial plexus injury. Urban centers have a higher percentage of penetrating injuries to the brachial plexus from knife and gun shot wounds.
Classification of Nerve Injury

Classification by Degree
Two classification systems of nerve injury are commonly used:
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Milan Stevanovic, University of Southern California, Keck School of Medicine, Department of Orthopaedics, Hand and Microsurgery, Los Angeles, California, U.S.A. Frances Sharpe, Department of Orthopaedics, Kaiser Permanente, Fontana, California, U.S.A.
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Seddon Classification
- neuropraxia: temporary disruption of nerve fiber conduction with nerve fibers and axonal sheath remaining intact. Full spontaneous recovery occurs over several weeks. - axonetmesis: disruption of nerve fibers. The axonal sheath remains intact. Spontaneous recovery occurs, but may be incomplete due to scarring within the sheath. - neurotmesis: disruption of nerve fibers and nerve sheath. This usually but not always represents nerve transection. No spontaneous recovery is anticipated.
Sunderland Classification (MacKinnon Modification)

Describes degree of nerve injury based on neural anatomy Six types described based on involved structures. I-V: myelin, axon, endoneurium, perineurium, and epineurium. Type VI represents a mixed injury. Provides a more detailed anatomic understanding of nerve injury.
Classification by Location
Preganglionic lesions are the most devastating injuries. These usually occur as an avulsion from the spinal cord. To date, there is no possibility for primary repair. Postganglionic lesions are described by their location relative to the clavicle (Fig. 15.1).
- Supraclavicular lesions involve the roots and trunks. - Retroclavicular lesions involve the divisions. - Infraclavicular lesions involve the cords and branches.
Closed Injuries to the Brachial Plexus

Most closed injuries to the brachial plexus result from traction to the plexus. They can also result from direct compression or iatrogenic causes. The degree of injury and the location of the plexus injury depend upon the position of the arm at the time of injury, and the direction of the applied force.
- upper plexus injuries occur when the arm is positioned at the side and a downward force is applied to the lateral shoulder girdle. - middle plexus injuries occur when the arm is abducted and sustains a posteriorly directed force. - lower plexus injuries occur when the arm is at extremes of elevation.
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Traction injuries usually are a neurologically mixed injury and involve multiple levels of the plexus.
- Isolated single nerve is rarely seen from traction injuries. When they do occur, it is usually at specific sites, where the nerve is anchored to surrounding structures: suprascapular nerve at the supraspinatus notch axillary nerve at the quandrangular space musculocutaneous nerve at the coracobrachialis muscle.
Open Injuries to the Brachial Plexus

Open injuries to the brachial plexus are more frequently seen in urban centers. They often result from penetration of sharp objects (e.g., knife, glass, chain saw) or from gun shot injuries.
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Fig. 15.1. Figure drawing of the brachial plexus showing the anatomic relationship of the trunks, divisions and cords to surrounding anatomy. The trunks are superior to the clavicle, the divisions are directly behind the clavicle, and cords and branches below the clavicle.
Associated vascular and pulmonary injury are commonly seen. The upper and middle plexus are most vulnerable to stab wounds.
Clinical PresentationPhysical Examination

Once associated injuries are identified and stabilized, evaluation of the brachial plexus involves a detailed neurologic examination, which must be well documented. The neurologic examination should be repeated. Initially this is to evaluate for deterioration which may suggest an unrecognized vascular injury causing compression on the plexus. Later examinations are to confirm the initial examination and to evaluate for recovery or deterioration. Evaluation of the brachial plexus begins with the cervical spine. After radiographic clearance, evaluate for local tenderness and active range of motion. Palpate the clavicle and shoulder girdle for tenderness and/or crepitance suggesting fractures. Examine the entire extremity for any evidence of laceration or fracture. Check for clinical findings associated with preganglionic injury (nerve root avulsion).
- tilting of the cervical spine away from the site of injury suggests complete intradural injury - characteristic preganglionic pain: may begin in first 24 hours (50%), constant crushing, burning, electrical shocks, C8/T1 more painful than C5/C6 - Upper trunk findings: anesthesia above the clavicle, paralysis of the hemidiaphragm, serratus anterior, and/or trapezius - Lower trunk findings: Horners syndrome: ptosis, meiosis, and anhydrosis.
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Perform and record a detailed motor examination to include motor grade. Each muscle need not be tested, but representative muscles from each terminal branch can usually be assessed. The serratus anterior and latissimus dorsi muscles can usually be examined and help in determining the level of the injury. Ipsilateral injuries to the extremity may prevent accurate assessment and grading of function.
- Motor function is graded from 0-5. M0 No contraction M1 Visible contraction only M2 Full active range of motion with gravity eliminated M3 Full active range of motion against gravity M4 Strength against moderate resistance M5 Normal strength - Sensory examination is complicated by the overlap of segmental and peripheral innervation patterns. However, autonomous zones have been described for each spinal root: C5 distal lateral arm (distal deltoid) C6 volar thumb tip C7 volar tip of long finger C8 volar tip of small finger T1 medial distal arm (just above medial epicondyle)
See Table 15.1 and Figures 15.1 and 15.2 for help in localizing the level of injury and involved.

A thorough clinical examination may be limited by the need for emergent transfer of the patient to the operating room to treat life-threatening injuries (vascular, pulmonary, or cardiac). Other factors which may confound the clinical examination include:
- variability in brachial plexus anatomy Pre-fixed and post-fixed brachial plexus are the most common variant. Pre-fixed has significant contribution from C4 root. Post-fixed has significant contribution from T2 root. - associated nerve injuries with neurologic deficits head trauma cervical spine trauma distal nerve injuries
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What you should do:

Perform a thorough neurologic and vascular examination. Record all motor and sensory deficits. Look for other sites of fracture or lacerations which could cause nerve injury Maintain a high level of suspicion. Protect the cervical spine until clinically and radiographically clear.
Investigations
Radiographic Examination
Cervical Spine - Evaluate for unstable injuries to the cervical spine - Look for transverse process fractures. Fracture of the transverse process of
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Fig. 15.2. This describes an easy technique to quickly draw the brachial plexus. Following steps 1 and 2, three lines representing contributions from the first three roots are combined to form the long thoracic nerve, three lines representing the posterior divisions are drawn, and three branches are added to each cord. Courtesy to Dr. George S. Edwards, Jr., M.D., Raleigh North Carolina, who permitted the printing of his technique.
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Table 15.1. Nerves arising from the brachial plexus

Origin Nerve Muscles Sensory Cervical Segments*
Root(s)
Long thoracic Dorsal scapular Phrenic nerve
Serratus anterior Rhomboids, levator scapulae Diaphragm Subclavius Supraspinatus, infraspinatus Pectoralis major (Clavicular head) Subscapularis Latissimus dorsi Subscapularis and teres major Pectoralis major (sternal head) and pectoralis minor medial arm medial forearm
C5, C6, C7 C5 C5 contribution (C3,4,5) C5, C6 C5, C6 C5, C6, C7 C5, C6

C6, C7, C8 C5, C6 C8 and T1 C6, C7, C8
Trunk(s) Division(s) Lateral Cord Posterior Cord
Nerve to Subclavius Suprascapular None Lateral Perctoral Upper subscapular n Thoracodorsal n. Lower subscapular n. Medial pectoral n. Medial Brachial Cutaneous Medial Antebrachial Cutaneous
Medial Cord
C8 and T1 C8 and T1
Terminal Branches (Lateral Cord) Musculocutaneous n Median nerve (lateral cord contribution) Axillary Nerve Radial Nerve
Coracobrachialis, brachialis, biceps
lateral antebrachial cutaneous
C5, C6, C7
(Posterior Cord)
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See below for combined median nerve Deltoid and teres lateral arm minor Triceps, brachialis superficial (lateral 1/3), radial anconeus, brachio- nerve to radialis, extensor dorsoradial carpi radialis hand longus and brevis. Through posterior interosseous nerve: Supinator, extensor digitorum, extensor carpi ulnaris, EDMQ, APL, EPB, EPL, and EIP
C5, C6
C5, C6 C7, C8, T1
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Origin Nerve Muscles Sensory Cervical Segments*
(Medial Cord)
Median nerve (medial cord contribution)
Ulnar Nerve
Pronator teres, flexor carpi radialis, palmaris longus, FDS, FDP (index and long), Thenars (3), lumbricals 1 and 2). Through anterior interosseous nerve: FPL and pronator quadratus Flexor carpi ulnaris, FDP (small and ring), palmaris brevis, hypothenar (3), lumbricals to 4th and 5th, interossei (7), adductor pollicis, and deep head of FPB
Volar radial hand
C5, C6, C7, C8, T1
volar and dorsal ulnar hand
C8 and T1
*Bold indicates dominant segmental innervation when present. EDMQ: extensor minimi digiti quinti; APL: abductor pollicis longus; EPB: extensor pollicis brevis; EPL: extensor pollis longus; EIP: extensor indicis proprius; FDS: flexor digitorum superficialis; FDP: flexor digitorum profundus; FPB: flexor pollicis brevis
C7 or a 1st rib fracture may indicate intradural injury of the lower two roots.
Chest
- Evaluate for pneumothorax, mediastinal widening, rib or clavicle fractures - First rib fractures, especially with posterior displacement are associated with vascular injury. - An inspiratory chest film may demonstrate paralysis of the hemidiaphragm (phrenic nerve injury). This helps localize the level of injury and may affect reconstructive options
Shoulder and Clavicle

- Evaluate for fractures or an unrecognized shoulder dislocation
Angiography
- Normal distal pulses do not preclude the presence of a proximal injury. - Strong indications for angiography include open injuries, absent or abnormal pulses, or if there is any doubt regarding the vascular status of the extremity. - Progressive neurologic deficits following the initial injury may indicate expanding hematoma, pseudoaneurysm, or arteriovenous fistula.
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Myelography
- Not as useful in the acute phase due to local swelling, reactive changes, and intradural blood clots. - Should be done as a CT myelogram to improve diagnostic accuracy.
178 - Pseudomeningocele suggests nerve root avulsion.
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Magnetic Resonance Imaging

- Most useful in closed injuries without associated trauma which mandates immediate exploration. - Will become increasingly useful with gadolinium-enhanced studies, improved software, and 3-D imaging capabilities.
Electrodiagnostic Studies
- Useful in monitoring closed injuries or in examining for recovery after repair of open injuries - Not helpful in the early stages of treatment. - Initial studies should be performed at a minimum of four weeks after the injury. - Useful in determining the level of injury, involved muscle groups, which cannot be easily examined clinically, and in monitoring for recovery of closed injuries prior to recommending surgical exploration. - Sensory nerve conduction velocity preservation in a clinically nonfunctioning nerve suggests root avulsion.
Intradermal Histamine Test

- Used to distinguish preganglionic from postganglionic lesions - One percent histamine is injected into anesthetic skin Production of a flare reaction indicates root avulsion. No reaction suggests postganglionic lesion. - Currently this test is not often used.

The emergency room treatment of brachial plexus injuries is dependent upon the associated injuries. Stabilize the patient. Treat the associated injuries. Protect the patient from iatrogenic injury.
- When patient is stable: Perform a thorough clinical examination Obtain appropriate studies In the stable patient, this should at least include radiographs of: - cervical spine - chest - shoulder and clavicle
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Arteriography should be considered in any patient with an open or closed brachial plexus injury. If immediate surgical intervention is not required, the patient may be transferred to the floor, where definitive work-up can be initiated. Repeated neurologic examinations should be performed routinely. This is done on a daily basis throughout hospitalization. Outpatient examination should be repeated weekly for the first month.
- When the patient is not stable: Treatment should be directed to stablizing the patient and expediting surgical intervention.
Traumatic Brachial Plexus Injuries Crossmatch blood Notify the appropriate consulting services. - Vascular surgery - Microsurgical team
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When the patient requires emergent surgery for associated vascular injury produced by sharp laceration, simultaneous exploration and repair by the microsurgical team is the preferred management of the brachial plexus injury. Emergent surgery for vascular injuries by other mechanisms may produce brachial plexus injuries not amenable to primary nerve repair. However, the microsurgical team should be notified to evaluate the extent of injury, tag disrupted nerve endings, and develop a plan for surgical reconstruction.
Operating Room Managment Emergent Setting

Brachial plexus injuries alone do not require emergent surgery Due to the common association with vascular injury to the subclavian or axillary artery, some brachial plexus injuries are treated emergently.
- Exposure for the vascular injury is parallel to the inferior margin of the clavicle. - The pectoralis major should be identified at is clavicular origin, and meticulously dissected from the clavicle. This preserves the entire muscle and its innervation (Figs. 15.3, 15.4). - Whenever possible, avoid transection of the pectoralis muscle. Although this provides a quicker exposure of the vascular injury, it creates a significant functional deficit in an already compromised extremity.
The microsurgical team should be present at the time of exposure and if the patient is stable, brachial plexus exploration and possible repair can be performed at this time.
Nonemergent Setting
Reconstructive Options
- primary nerve repair; - nerve grafting; (sural or saphenous nerves) - nerve transfer (intercostal nerves, accessory nerve, C4, phrenic nerve, or ulnar nerve) - neurotization; and - use of contralateral C7 (reserved for cases of devastating injury with multiple level root avulsions.) - neurolysis
Operating Room Preparations

- Availability of appropriate equipment: scalp evoked potentials; nerve stimulator; microscope; micorsurgical instruments. - Planning with anesthesia length of surgery blood availability no use of paralytic agents
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Fig. 15.3. The surgical incision for exploration of the brachial plexus is shown. The incision parallels the inferior margin of the clavicle. For supraclavicular lesions, the incision is extended superiorly along the posterior margin of the sternocleidomastoid muscle. For infraclavicular lesions, the incision is extended inferiorly along the deltopectoral groove.
Timing of Surgery
Early Surgery (Immediate to two weeks)
- Surgical treatment directed at nerve repair, using nerve grafts as necessary - Sharp penetrating injury - Injuries associated with vascular trauma - Sharp iatrogenic injuries - Known single level nerve injury (from sharp penetrating trauma).
One month
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- Surgical treatment directed at nerve exploration and repair as possible, nerve grafting and nerve transfer as indicated Blunt penetrating trauma (gunshot wounds) Progressive neurologic or vascular lesions Preganglionic Lesions
- Treatment in these cases is directed at nerve transfer as indicated, with possible use of nerve grafts. Two to Three Months - Surgical treatment directed at nerve exploration, repair, grafting, neurolysis, neurotization, and nerve transfer as indicated. - Closed injuries of C5, C6, and/or C7 without evidence of electrical recovery and with stationary Tinels sign. Six Months
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Fig. 15.4. Supraclavicular exposure of the brachial plexus requires division of the platysma. Below this, the deep cervical fascia covers the jugular vein and scalene muscles. The fascia is opened and the jugular vein is retracted anteriorly. Dividing the omohyoid allows the best exposure of the plexus; however, in most cases, it can be retracted medially and inferiorly. For infraclavicular exposure, the deltopectoral groove is opened. The pectoralis majors is elevated off of its clavicular origin and reflected inferiorly. Occasionally, the clavicle must be divided for exposure of the retroclavicular plexus. This should be plated at the completion of the surgery.
- Generally used as the upper limit for nerve reconstruction. Same treatments as listed above. - Prognosis for recovery for transected or avulsed nerves significantly worse if repair is later than 6 months. More than One Year - Surgical treatment generally limited to salvage procedures, including shoulder fusion, tendon transfers, pedicled and free muscle transfers. - In cases of plexus compression related to extraneural scarring, neurolysis may be beneficial even more than two years after injury, as there is usually sufficient nerve conduction to preserve motor endplates.
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Postoperative Care
Management for brachial plexus injuries following nerve repair or grafting is immobilization in a shoulder immobilizer for two to three weeks, depending on the extent of repair. Occupational therapy for splinting, muscle stimulation, and education in maintaining passive range of motion should begin in the first week after injury. Care should be exercised for the first four weeks to maintain shoulder immobilization and prevent rupture at the repair site. Social services intervention and vocational rehabilitation should be instituted early. Prognosis for return to work is minimal if more than one year has elapsed since the injury
Complex Injuries and Complications

Brachial plexus injuries are frequently associated with serious and potentially life-threatening injuries, which must be recognized in the emergency room. These incude: - head injury - cervical fracture - vascular injury - pulmonary injury - fractures of the chesto and/or shoulder girdle. Associated life-threatening injuries are seen in up to 15% of patients with brachial plexus injuries. Rupture of the subclavian or axilliary artery occurs in 10-20% of injuries, more commonly in infraclavicular injuries.
Scapulothoracic Dissociation
It represents a closed forequarter amputation and indicates a very high energy injury. It is diagnosed radiographically by a laterally displaced scapula, associated with acromioclavicular joint disruption, sternoclavicular joint disruption, or a displaced clavicle fracture. It has a high association with severe life-threatening vascular injury. Associated brachial plexus injuries are common, and usually severe with multiple level root avulsions. It is often a devastating injury with high morbidity and mortality rates.
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Pain
Other than disability from motor and sensory loss, one of the most disabling complications of brachial plexus injuries is pain. Preganglionic injuries have a characteristic pain component, frequently described as constant burning or crushing sensation, experienced day and night.
- Surgical treatments, including amputation, neurolysis, wrapping of the plexus with an omental free flap have not been successful in relieving this pain. - Dorsal root entry zone (DREZ) coagulation, which requires cervical laminectomy and destruction of spinal cord sensory tracts helps with controlling pain in up to two-thirds of patients. However, it may be associated with increased neurologic deficit.
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Postganglionic injuries can be associated with chronic pain.

- It is generally less disabling than pain associated with preganglionic injuries and can usually be controlled with oral pain medications. - There are some reports in the literature of pain control using neurolysis and free omental wrapping of the plexus. - A permanent in-dwelling brachial plexus catheter for delivery of local anesthetic can be useful in the treatment of severe and refractory pain in postganglionic injuries.
Outcomes
Outcome following brachial plexus injuries depends on the level, and mechanism, and extent of injury. Outcome goals are based on restoration of a functional limb. Full function is seldom achieved. Preganglionic Injuries
- Without surgical intervention, preganglionic injuries result in a flail arm. - Functional outcome can be improved with nerve transfer, neurotization, and salvage procedures described above.
Postganglionic Injuries
- Postganglionic injuries have a better prognosis than preganglionic injuries. - Infraclavicular lesions respond better to repair than supra- or retroclavicular injuries. - Postganglionic injuries involving C5, C6, and C7 have better outcome than those involving C8 and T1.
Factors Associated with Improved Outcome

Time to surgery less than four months; Age of patient (younger patients do better); Length of nerve graft required less than 7 cm; Number of strands used for interfascicular repair or cable grafting greater than four; and - Presence of neuroma on the proximal stump.
Factors Adversely Affecting Outcome

Preganglionic injuries; Previous surgery for vascular injury Severe regional trauma C8 and T1 root avulsions
Quality of Life Assessment

- Despite the devastating affect on upper extremity function, one study evaluating quality of life following brachial plexus injury found the following: Only 31% of patients felt that their injury had a significant effect on their quality of life. Quality of life factor most affected by the injury was the patients financial status. 54% of patients who were employed prior to their injury returned to work within one year of the injury. Constant pain (graded as 3/10) was experienced by 75% of patients, with intermittant severe pain up to a level of 7/10. 8% of those patients who had constant pain consistently used pain medications to control their symptoms.
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Common Mistakes and Pitfalls in Brachial Plexus Injuries

The frequency of associated injuries that can affect upper extremity function (head injury, cervical spine injury, and fractures of the ipsilateral extremity) may confuse the diagnosis of brachial plexus injury. Repeated neurologic examination and maintaining a high level of suspicion are the key factors in making an early diagnosis of brachial plexus injury.
References
1. 2. 3. 4. 5. 6. 7. 8. Bentoilila V, Nizard R, Bizot P et al. Complete traumatic brachial plexus palsy. J Bone Joint Surg 1999; 81-A:20-28. Krauker JD, Wood MB. Intercostal nerve transfer for brachial plexopathy. J Hand Surg 1994; 19A:829-35. Millesi H. Surgical management of brachial plexus injuries. J Hand Surg 1977; 2(5):367-379. Narakas AO. The treatment of brachial plexus injuries. Int Orthop 1985; 9:29-36. Terzis JK, Vekris MD, Soucacos PN. Outcomes of brachial plexus reconstruction in 204 patients with devastating paralysis. Plast Reconstr Surg 1999; 104:1221-1240. Doi K, Sakai K, Kuwata N, Ihara K, Kawai S. Reconstruction of finger and elbow function after complete avulsion of the brachial plexus. J Hand Surg 1991; 16A: 796-803. Richards RR, Waddell JP, Hudson AR. Shoulder arthrodesis for the treatment of brachial plexus palsy. Clin Orthop Rel Res 1985; 128: 250-258. Samardzic MM, Grujcic DM, Antunovic V, Joksimovic M. Reinnervation of avulsed brachial plexus using the spinal accessory nerve. Surg Neurol 1990; 33: 7-11.
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CHEST
CHAPTER 16
Blunt Thoracic Trauma

George C. Velmahos The Thoracic Cage
Fractures of the ribs, clavicles, scapulae or sternum, although not life-threatening per se, are associated with significant complications. Fractures of the thoracic cage should always remind the physician of the need to evaluate underlying organs, vessels and nerves for potential injuries. Ribs are usually fractured laterally along the mid-axillary line, but rib fractures can occur at any location. Isolated rib fractures can be caused by relatively small forces. Multiple rib fractures, or fractures of the sternum or scapula, indicate major impact and should increase the level of suspicion for underlying injuries. The thoracic cage in children is elastic. Significant underlying injuries may occur in the absence of thoracic-cage fractures. In contrast, the thoracic cage of elderly patients is rigid and inelastic. Extensive thoracic-cage fractures may occur even with forces that are too weak to cause internal injuries.
Rib Fractures
Rib fractures produce significant pain that may last for many days. They may be diagnosed by palpation, plain chest radiography or special rib views. Chest CT is not a sensitive means of detecting rib fractures. Upper-rib fractures (1st and 2nd) are associated with thoracic aortic injuries. Lower-rib fractures are associated with liver and spleen injuries. All rib fractures are associated with lung contusions, pneumothorax and hemothorax. The patients tend to avoid painful respiratory movements. They splint their diaphragms by taking short and shallow breaths. The lungs are not fully expanded and become vulnerable to infection. Pneumonia is the most common complication after rib fractures. The entire therapeutic philosophy should target the prevention of lung infection rather than the actual treatment of the rib fracture. Therapy consists of adequate treatment of pain in order to allow the patient easy breathing and proper lung expansion. Incentive spirometry and chest physiotherapy are important therapeutic adjuncts. Pain treatment consists of:
- Oral medication for ambulatory patients or patients with minimal-to-moderate pain.
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Fig. 16.1. Severe lung contusion of the left upper lobe. Compare with the normal parenchyma of the lower lobe.
- Parenteral medication for patients who have severe pain that limits respirations: Epidural analgesia is proven to offer the best pain relief. A catheter is inserted into the epidural space of the spine. Disadvantages are that it is invasive and cannot usually be done at the early stages after severe trauma if the patient is coagulopathic and injuries of the thoracolumbar spine are not ruled out. Intercostal nerve block is also an effective form of analgesia. It requires experience, and the analgesic effect is not as reliable as that produced by epidural analgesia. Patient-controlled analgesia is a good method of pain relief. However, it is not the method of choice because it is associated with intravenous injection and therefore all the associated complications of systemic narcotic administration. Continuous intravenous analgesia is reserved for severely injured patients who are ventilated and sedated, and are not expected to recover soon.
Chest physiotherapy is important. The best physiotherapy is mobilization of the patient out of bed. The patients should be encouraged to breath deeply, cough and use incentive spirometry. There is no role for prophylactic antibiotics in this condition.
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Flail Chest
A flail chest is defined by fractures of two or more ribs at two or more sites on each rib. It is an indicator that severe blunt forces have been applied to the chest. Diagnosis is clinical upon observation of paradoxical movement of the thoracic wall: the flail segment moves inwards during inspiration (due to the negative intra-thoracic pressure generated) and outwards during expiration (due to the positive intra-thoracic pressure). Plain films also show the multiple fractures.
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Fig. 16.2. Flail chest on the rib views of a plain film. Observe the multiple and severe rib fractures.
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Fig. 16.3. Elderly patients may have extensive rib fractures without lung contusions, as evident on this CT of the chest.
At least two-thirds of patients with flail chest require intubation. Respiratory failure is a result of two factors
- ineffective movement of the hemithorax due to the flail segment, and - most importantly, associated lung contusion. Almost 100% of patients with flail chest will have significant underlying lung injury.
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Fig. 16.4. Children can have significant lung contusion in the absence of rib fractures, as shown in this plain chest film.
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Fig. 16.5. The adult respiratory distress syndrome is a devastating complication that may follow severe blunt thoracic trauma. It is characterized by bilateral diffuse patchy infiltrates.
Close arterial saturation and blood-gas monitoring are essential in patients with flail chest. Early intubation should always be considered. Although the initial signs and symptoms may not appear significant, normal breathing
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Trauma Management
becomes progressively impaired and lung contusions expand. Respiratory deterioration usually follows in the next few hours. Patients with flail chest are at high risk for prolonged respiratory failure and infectious lung complications. Pain control is of paramount importance. Epidural analgesia is strongly recommended as soon as possible. Old techniques of immobilizing the chest by circular bandages are not only useless but also potentially harmful because they restrict normal breathing even further. Surgical immobilization of flailing ribs by plating or wiring has been advocated by some authors for selected patients. The technique does not seem to offer significant advantages over expectant therapy and is not widely practiced.
Clavicular Fractures
Fractures of the clavicle are usually benign injuries that require minimal or no intervention. Surgical intervention is very rarely required to correct grossly overriding parts of the clavicle. The diagnosis is obvious on plain chest radiography, and often on clinical examination. The association with underlying vascular or neurological structures is weak at best. Routine vascular imaging of the subclavian vessels is not recommended for clavicular fractures alone.
Scapular Fractures
Scapular fractures are indicators of severe injury. It is unusual for isolated scapular fractures to occur. Scapulothoracic dissociation is defined by the avulsion of soft tissues, including muscle, vessels and nerves, and the destruction of the shoulder joint. It is often associated with scapular, distal clavicular and proximal humeral fractures. It is caused by acute hyperextension of the upper extremity. Except for the severe osseous injuries, blunt subclavian artery injuries may occur. Brachial plexus injuries are very common, ranging from simple nerve stretching to root avulsion. The final outcome is determined by the nerve injuries. Because these injuries are usually severe, the prognosis for function of the involved upper extremity is often grave. Amputation due to complete and irreversible denervation is not uncommon.
Sternal Fractures
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Fractures of the sternum indicate significant blunt forces have been imposed on the chest. These fractures are often missed because clinical or radiographical diagnosis is difficult. Such fractures are not apparent on plain chest radiograph. Patients with anterior-chest-wall contusions and pain should be further evaluated with sternal views. Often the sternal fracture is visualized on chest CT. Historically, sternal fractures are associated with blunt myocardial injury. This association has never been proven. It is recommended that patients with sternal fractures be evaluated for blunt myocardial injury. Specific treatment for the sternal fracture is almost never necessary. The healing rate is excellent.
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Blunt Pulmonary Trauma

Lung contusions and lacerations, hemothorax and pneumothorax are frequent events following blunt thoracic trauma. The lung may be injured by either the blunt object, a fractured rib or the acute elevation of alveolar pressures when the glottis is closed. Lung lacerations from fractured ribs mimic lacerations caused by penetrating trauma. Intraparenchymal lung lacerations (usually caused by the acute build-up of intrapulmonary pressures at the time of the accident) may appear as cysts that contain air and/or blood. These cysts are called hemopneumatoceles. Expectant management is successful, and intervention to drain or repair a hemopneumatocele is rarely necessary. Pulmonary contusion is the form of lung injury most frequently encountered after blunt trauma. It involves an area of the lung with acutely distorted alveolar architecture and subsequent dysfunction of gas exchange. The shunt occurring in the contused areas is responsible for low partial-arterial-oxygen tension and decreasing arterial saturation. The initial clinical picture may be misleading. Pulmonary contusion usually progresses with time. Although the patient may compensate initially, ongoing loss of alveolar tissue leads to acute respiratory failure. Additionally, the radiographic picture may not be highly abnormal during the first few posttraumatic hours. The extent of the pulmonary contusion usually is not visible on plain radiography earlier than 12 hours after injury. Chest CT is more sensitive in defining the real extent of the pulmonary injury. Thoracotomy to repair blunt pulmonary injuries should be done after indications similar to those recommended for penetrating trauma, i.e., significant intrathoracic bleeding (more than 1 L immediately or more than 200 ml per hour) causing hemodynamic disturbances. Lung resection after blunt trauma is associated with poor outcome. Traumatic lobectomies or pneumonectomies are followed by acute increases in pulmonary artery pressures and, often, right cardiac decompensation. The use of staplers has facilitated the operative procedure. Stapled wedge resections, lobectomies or even pneumonectomies are done safely and rapidly.
Complications of Blunt Pulmonary Trauma

The extent of pulmonary injury and subsequent complications is proportional to the amount of energy that is dissipated to the pulmonary parenchyma at the time of injury. Complications include the adult respiratory distress syndrome (ARDS) and pulmonary infections. ARDS following blunt pulmonary trauma is a major therapeutic problem. Multiple modes of ventilation, including pressure-control, inverse-ratio, highfrequency percussion and airway-pressure-release ventilation have been used to manage the extreme forms of ARDS. Pulmonary infections, i.e., pneumonia and empyema, are not uncommon. Failure to wean a patient from mechanical ventilation suggests these complications exist. The long-term functional compromise due to fibrosis of injured alveoli after blunt pulmonary trauma is not known but seems to be worse than comparable injuries after penetrating trauma.
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Fig. 16.6. Hemopneumatoceles are associated more frequently with blunt than with penetrating pulmonary trauma. They usually resolve spontaneously. A giant hemopneumatocele is presented on this CT. It resolved without surgical intervention.
Blunt Tracheobronchial Trauma

The trachea and major bronchi may rupture due to acute intraluminal pressure elevation after direct impact, or be lacerated after shear forces usually applied to the level of the carina. Extensive mediastinal emphysema is the dominant sign on plain chest radiography or chest CT. The emphysema usually extends to the soft tissues and often involves the entire chest and neck or even more body areas. Severe air leaks from the chest tube or loss of more than one-third of the delivered tidal volume in mechanically ventilated patients are also strongly suggestive of tracheobronchial injuries. Flexible bronchoscopy is the procedure of choice for definitive diagnosis. Treatment may be expectant (minimal or well-sealed injuries) or surgical. The approach is usually through a high right thoracotomy.
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Blunt Esophageal Trauma

Rupture of the esophagus is extremely rare among survivors of blunt thoracic trauma. These patients are critically injured and clinically unevaluable, and usually have severe injuries to adjacent structures such as the thoracic aorta, bronchi or spine. The diagnosis should be suspected in the presence of air in the mediastinum or hematemesis in the absence of gastroduodenal injury. Because the incidence is low, the diagnosis is often delayed and the outcome is poor.
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Fig. 16.7. Empyema is a complication related to severe thoracic trauma. It should be suspected in patients with persistent infection or inability to wean from the ventilator.
Traumatic Asphyxia
This term is used to indicate respiratory insufficiency due to direct impact on the chest associated with acute elevation of venous pressures. Typically, the syndrome occurs after a heavy object lands suddenly on the upper chest. The acute elevation of venous pressures causes extravasation of red blood cells from capillaries above the level of the injury. These microhemorrhages are obvious on the skin and conjunctivae, which show a characteristic red-blue color. Such micro-hemorrhages may also occur in the brain and cause changes to the level of consciousness. Respiratory function may be compromised due to direct damage to the lungs or the accumulation of edema in the interstitial space around the airway. Ventilatory support may be required in cases with severe chest compression. In its usual form, traumatic asphyxia has a benign course and resolves without major interventions.
Pitfalls in the Evaluation and Management of the Above Injuries

Reliance on the initial clinical and radiographic picture to estimate the severity of pulmonary injury is misleading. Both are not reliable at the acute stage. Associated injuries should serve as indicators of significant trauma. Cautious monitoring is required because clinical deterioration may occur. Failure to provide patients with rib fractures with adequate pain control causes the development of respiratory infections because the patients cannot move sufficient air without pain. The mainstay of management of such patients should be adequate pain control.
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Immobilization of patients in order to let rib fractures heal is conceptually wrong. The best method for fast recovery and prevention of complications is mobilization as soon as possible after the injury. The mechanism that produces ecchymotic areas at the skin and conjunctivae in patients with traumatic asphyxia also occurs in the brain. Careful neurologic monitoring is recommended.
References
1. 2. 3. 4. 5. 6. Hoff SJ, Shotts SD, Eddy VA et al. Outcome of isolated pulmonary contusion in blunt trauma patients. Am Surg 1994; 60:138-142. Johnson JA, Cogbill TH, Winga ER. Determinants of outcome after pulmonary contusion. J Trauma 1986; 26:695-697. Lewis RF. Thoracic trauma. Surg Clin North Am 1992; 69:97-102. Richardson JD, Adams L, Flint LM. Selective management of flail chest and pulmonary contusion. Ann Surg 1982; 196:481-487. Fulton RL, Peter ET. The progressive nature of pulmonary contusion. Surgery 1970; 67:499-506. Clark GC, Schechter WP, Trunkey DD. Variables affecting outcome in blunt chest trauma: Flail chest vs. pulmonary contusion. J Trauma 1988; 28:298-304.
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Penetrating Chest Injuries: Evaluation and Management

Arthur Fleming
Penetrating chest injuries can be separated by mechanism of injury [stab wound (SW) or gunshot wound (GSW)]; or by the patients response to injury (extremis, unstable or stable). The patients response is used as the major focal point.
The first written thoracic operative record in North America appeared in the diary of Cabeza de Vaca in 1635. Operative intervention for penetrating thoracic trauma in the modern era was ushered in by the availability of endotracheal anesthesia and antibiotics, the development of radiology, and greatly facilitated by refinement in the double lumen endotracheal tube. Tube thoracostomy became the mainstay in treatment of traumatic hemothorax during the Vietnam conflict and remains so today.
Incidence
Approximately 90% of penetrating chest injuries miss the heart from a series of 2076 penetrating chest injuries (See Chapter 1, Cardiac Injuries). Of 250 consecutive GSWs to the chest in our institution, 20% had associated injuries to the diaphragm or one or more abdominal viscera1.
Penetrating chest injury patients (in the absence of cardiac injury), may present along an entire spectrum: Extremis unstable (profound shock) completely stable Over 70-85% of patients will bleed less than 1500 cc initially and less than 250 cc per hour thereafter and can be managed by chest tube drainage and/or observation. The 15-30% of patients who bleed greater then 1500 cc initially and more than 250cc per hour require operative intervention.

Absent or decreased breath sounds, hyperresonance on chest percussion, and a penetrating injury to the chest is diagnostic of a tension pneumothorax. It is sometimes difficult to detect these signs in a noisy resuscitation bay. However, when these signs are coupled with respiratory distress, chest pains, and
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Arthur Fleming, Department of Surgery, Martin Luther King Hospital, Los Angeles, California, U.S.A.
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air hunger in association with hypotension and tachycardia, the diagnosis should be complete. Multiple GSWs or SWs and external blood loss prior to arrival make it difficult to determine which site requires the most urgent care or attention.
Investigations
There should be limited investigations for those patients in extremis or profound shock. Rhythm strips and pulse oximetry are both desirable in most patients. Chest x-rays with external radiopaque markers are the mainstays of evaluation in patients with penetrating trauma. Transesophageal echocardiograms, ultrasound studies, CT scans and angiography are required in complex cases that are stable.
A tension hemopneumothorax is the only chest injury requiring intervention in the field. A needle thoracoscopy may be both diagnostic and therapeutic in a rapidly deteriorating patient. Administer oxygen by mask or intubate the moribund patient (Note! An untreated pneumothorax may be made worse with intubation). Intravenous lines may be started en route to a trauma center.

An x-ray should be obtained in patients prior to chest tube insertion except when there is a tension pneumothorax or the patient is rapidly deteriorating (near death). An x-ray plate placed on the gurney prior to transferring the patient from the paramedics stretcher facilitates this approach. The degree of hemo- or pneumothorax can be estimated in a supine film. An upright x-ray film is obtained in the stable patient. Radiopaque markers are placed over entry and exit sites so that the trajectory of missiles and the potential associated injuries can be anticipated. Fracture of ribs along the lower cortex may identify the potential source of significant arterial bleeding (in the absence of a trajectory that might suggest great vessel injuries). Closed tube thoracoscopy and or observation can manage the majority of patients with penetrating injuries (70-85%).
- Appropriate local anesthetic is required. - Patients, who have a massive hemothorax on initial chest x-ray, might benefit from the insertion of the chest tube in the operating room depending on the proximity to the emergency room, and the suspected injury that might require a thoracotomy. Some patients arrest when the tamponading effect is released by placing a chest tube and further rapid bleeding occurs).
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Emergency Room Thoracotomy

Reserved for penetrating trauma victims with witnessed signs of life (at some point). ECG on arrival shows a narrow-complex rhythm. Patients with cardiac arrest or imminent cardiac arrest should undergo emergency room thoracotomy (See Chapter 1, Cardiac Injuries).
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Direct operating room admissions should be considered when such facilities and policies are available. Cross-clamping of the pulmonary hilum is used to control massive hemorrhaging from the lung and to prevent further air emboli. Aortic and great vessels injuries should be controlled with partial occluding vascular clamps or cross-clamping and the patient take to the operating room for definitive surgery. In the absence of a hemo- or pneumothorax, which is confirmed by both inspiratory and expiratory films, patients may be observed in a holding area and discharged if repeat films at six hours are negative.
Management in the Operating Room

The indications for operation in penetrating chest injuries are listed in Table 17.1.
- Thoracotomy Incision An anterolateral thoracotomy is used in the unstable patient with the patient supine. Penetrating injury side is opened first. Transternal extension to the opposite side is an option. A posterolateral thoracotomy incision is used for esophageal and aortic injuries (right side for the esophagus and the left side for the aorta. Note! The esophagus can be visualized from the left side below the aortic arch). - Procedures Pulmonary tractotomy is used for lung injuries, especially in unstable patients (using staples and selective vascular ligation). Pulmonary hilar clamping allows assessment of lung injury and temporary prevention of further air emboli. Pneumonectomy may be required for hilar injuries and especially in the unstable patient. Intercostal vessels are ligated proximall and distal to injuries. Tracheal injuries are repaired directly after guiding the endotracheal tube past the site of injury. Esophageal injuries require appropriate debridement, primary repair, coverage with viable tissue (such as an interiostal muscle flap) and adequate drainage. Two chest tubes are used when there is both bleeding and a significant air leak. - Thoracoscopy Is used to examine the mediastinum, to remove clotted blood, to evaluate the diaphragm in stable patients, and to control selective bleeding from intercostal vessels or lung parenchyma in selected cases.
Complex Injuries
Thoracoabdominal Injury: Defined as an injury that occurs between the 6th and 12th ribs, or appears to pass upward from the subcostal region.
- The intrathoracic portion of the injury is treated as per management indicated for the Emergency Department or Operating Room. The abdominal region should be evaluated and treated as for isolated abdominal injuries.
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Air Embolism
- May occur with through and through lung injuries and collection of blood and air within the tract; and
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Table 17.1. Indications for thoracotomy in penetrating injuries to the chest (excluding hearts)
Aorta, innominate, subclavian, or carotid artery injuries Hilar injury (central pulmonary injury) Endoscopic or radiographic (contrast) study demonstrating injuries to: Bronchus Trachea Esophagus Massive air leak Vascular injury at the thoracic outlet Possibly for mediastinal traverse (diagnostic studies may be required) Greater than 250 ml blood loss per hour for two or more hours Greater than 20 ml/kg initially Massively clotted hemothorax
- May also occur when oversewing entrance and exit wounds to lungs without doing a pulmonary tractotomy. - The left ventricle should be aspirated and attempts made to elevate the diastolic pressure to force the air emboli through the coronary system.
Outcomes
Survival (varies with associated injuries)
Overall survival (all thoracic trauma): 90% Overall hospital survival for emergency thorocotomy: 25% Hospital survival for GSWs to the trachea: 50% Hospital survival for stab wounds to the trachea: 90%
Prognostic factors determining survival

- Mechanism of injury (GSW vs. SW) - Presence of hilar injuries (may be rapidly fatal)
Postoperative Care
Routine chest x-rays and auscultation to determine complete expansion of the lung and evacuation of air and blood from the pleural space. Removal of chest tubes when drainage is less than 75-100 ml per 24 hours. Follow-up in six weeks and six months with chest x-rays and physical examination.
Late Complications
Posttraumatic empyema occurred in 87 of 5,474 patients (in our institution) for incidence of 1.6%.
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Common Mistakes and Pitfalls in Penetrating Trauma to the Chest

Since seven out of ten patients can be managed successfully with closed tube thoracostomy, a cavalier attitude and low index of suspicion for major injuries sometimes exist. The placement of a chest tube before obtaining the initial chest x-ray may obscure the true significance of the degree of injury and delay the need for a thoracotomy.
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The lack of chest drainage may mean that bleeding has stopped or that the chest tube is clotted. Repeat chest x-rays at appropriate intervals are required to prevent misinterpretation.
References
1. 2. 3. 4. 5. Oparah SS, Mandal AK. Penetrating gunshot wounds of the chest in civilian practice: Experience with 250 consecutive cases. Br J Surg 1978; 85:45-51. Liu D, Liu H, Lin PJ et al. Video-assisted thoracic surgery in treatment of chest trauma. J Trauma 1997; 42:670-674 Mandal AK, Thadepalli H, Mandal AK et al. Posttraumatic empyema thoracis: A 24-year experience at a major trauma center. J Trauma 1997; 43:764-771. Stratton SJ, Brickett K, Crammer T. Prehospital pulseless, unconscious penetrating trauma victims: Field assessments associated with survival. J Trauma 1997; 45:96-100. Murray JA, Demetriades D, Cornwell EE et al. Penetrating left thoracoabdominal trauma: The incidence and clinical presentation of diaphragm injuries. J Trauma 1997; 43:624-626.
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CHAPTER 18
Cardiac Injuries
Demetrios Demetriades Penetrating Cardiac Injuries
Penetrating cardiac injuries are the most lethal organ injuries. More than 80% of the victims die at the scene. For those victims reaching the hospital alive early diagnosis and immediate operation is the most critical factor for survival.
The first attempt at repairing a cardiac injury was made by Cappelen in Norway in 1896. The first successful repair of a cardiac wound was performed by Rehn, in Germany, in 1896.
Incidence
About 10% of all penetrating chest trauma (from a series of 2076 penetrating chest injuries). The incidence is similar in both, gunshot wounds and stab wounds.
Many patients are dead or near death on arrival. Those reaching the hospital alive are usually in severe shock. Occasionally, patients with fairly minor cardiac injuries and short prehospital time may be normotensive on admission. The victim is very restless, even with fairly mild hypotension. It is possible that this restlessness might be due to venous stasis in the brain, secondary to tamponade. The neck veins are distended in the presence of cardiac tamponade. However, if there is associated hypovolemia due to blood loss the veins are not distended. Tachycardia, thready peripheral pulse. The classical pulsus paradoxus described in tamponade is found in only about 10% of the patients. The classical Becks triad of cardiac tamponade (hypotension, distant cardiac sounds, distended neck veins) is found in about 90% of cases. Every precordial stab wound or gunshot wound to the chest, especially with hypotension, is a cardiac injury until proven otherwise!

Although in most cases clinical examination is reliable in diagnosing cardiac injuries, in some situations it is not possible or easy to establish the diagnosis. These conditions include: Absence of hypotension on admission (usually in patients with small cardiac wounds and short prehospital time).
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Multiple penetrating injuries in many body areas (i.e., chest, abdomen, extremities). This is not an uncommon scenario in urban trauma centers.
Investigations
Investigations should be reserved only for fairly stable patients where the diagnosis is not certain! Trauma ultrasound performed by the emergency physician or the trauma surgeon in the emergency room is the fastest and most effective way to diagnose cardiac tamponade (Fig. 18.1). It should be part of the standard primary survey and the machine should be located in the emergency room. The technique and role of the trauma ultrasound are discussed elsewhere in this handbook. Chest x-ray may be suspicious of cardiac injury in about 30-50% of patients. Radiological signs suspicious of cardiac injury are:
- Enlarged, globular cardiac shadow (Fig. 18.2) - Widened upper mediastinum (due to dilated major veins as a result of the tamponade and venous stasis) (Fig. 18.3) - Pneumopericardium (air in the pericardium due to a pericardial breach) (Figs. 18.3, 18.4)
ECG may be diagnostic in about 30% of patients. It may show low QRS complexes, elevated or depressed ST segments, inverted T waves (Fig. 18.5). Pericardiocentesis is recommended by ATLS protocols. However, it has very limited value in organized, modern trauma centers. It is associated with a high incidence of false negative results due to clot formation in the pericardium. In addition, it is a potentially dangerous procedure especially if is performed on a restless, hypotensive patient. Subxiphoid window is used by some centers (Fig. 18.6). The author believes that it is the most invasive diagnostic procedure in surgery and has very limited value in modern trauma centers. It might delay the definitive cardiac repair by 10-20 minutes. Transabdominal, transdiaphragmatic window is an excellent approach for patients with penetrating thoracoabdominal injuries requiring laparotomy. The pericardium is grasped and pulled down with a strong forceps and a small pericardiotomy is performed. In the presence of blood in the pericardial sac the laparotomy incision is extended into a median sternotomy for cardiac repair. Central venous pressure might be helpful in some cases. A CVP higher than 12 cm H20 is suspicious of cardiac tamponade. It is important to remember that in the presence of associated hypovolemia the CVP will raise only after restoration of the blood volume. On the other hand an elevated CVP may be due to inappropriate positioning of the tip of the catheter or due to the presence of major hemopneumothorax or a restless patient. In summary, in a modern trauma center the diagnosis of cardiac injury in most cases should be based on the combination of a good clinical examination and an emergency room trauma ultrasound.
No attempts for ALS (Advanced Life Support) should be made! Scoop and run is associated with the best chances of survival! Administer oxygen by mask or intubate patients with imminent cardiac arrest, and transfer to the nearest trauma center. An intravenous line might be attempted in the ambulance en route to the hospital.
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Fig. 18.1. Cardiac tamponade: enlarged cardiac shadow
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Fig. 18.2. Cardiac tamponade: note the pneumopericardium and the widened upper mediastinum.
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Fig. 18.3. Pericardial penetration: Pneumopericardium
Fig. 18.4. ECG in cardiac trauma: Elevated ST segments
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Fig. 18.5. Echocardiogram in ER: Cardiac tamponade
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Fig. 18.6. Subxiphoid window (used with permission: Trinkel et al. Ann Thorac Surg 1974; 17:231-236)
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Remember that every minute counts! No delays for detailed physical examination, unnecessary investigations or administrative paperwork! Patients with cardiac arrest or imminent cardiac arrest: Orotracheal intubation with simultaneous emergency room thoracotomy (ERT).
Technique for ER Thoracotomy:

The left chest is opened with an anterolateral thoracotomy through the 5th intercostal space, just below the nipple in males or below the breast in females (Fig. 18.7). The intercostal muscles are divided and the pleural cavity is entered. If the exposure is not satisfactory extend the thoracotomy into the right chest, through the sternum (clamp the transected internal mammary arteries!). The pericardium is opened longitudinally, above the phrenic nerve. The pericardial clot is evacuated and the bleeding from the heart is controlled with manual pressure between the left thumb and the index finger. A figure of eight suture is placed and tied. Alternatively skin staplers may be applied. The thoracic aorta is cross-clamped just above the diaphragm and the heart is massaged (Fig. 18.8). During this period other members of the trauma team continue with fluid resuscitation, manual ventilation, NaHCO3 and calcium administration. If the heart is full but fails to start, apply internal defibrillation (30-40 Kjoules) or adrenaline through the central line, as indicated. For persistent asystole or fibrillation apply electrodes through the myocardium of the right ventricle and pace the heart with a pacemaker. If air bubbles appear in the coronary veins make the diagnosis of air embolism and aspirate the ventricle. If the heart recovers, the operation is completed in the operating room.
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Fig. 18.7. Incision for ER thoracotomy
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Fig. 18.8. ER thoracotomy with aortic cross-clamping

Incision
- A median sternotomy is the preferred incision for most cases. It provides excellent exposure, is fast and bloodless and is associated with a lower incidence of postoperative pain and respiratory complications than a thoracotomy. - A left thoracotomy is preferred for ER operations and injuries to the posterior chest. Extension into the right thorax through the sternum may be performed if necessary.
Cardiac Repair
- The pericardium is opened and the heart repaired as described above. - No need for routine use of Teflon pledgets for cardiac repairs. They slow down the repair! Reserve pledgets only for friable thin tissues.
Pericardium
- The pericardium should be closed without tension. Leave opening at the top to avoid retamponade. - Leave pericardium open if tension-free closure can not be achieved (i.e., cardiac failure, fluid overloading).
Chest Wall Closure

- Thoracostomy tube in the mediastinum and in open pleural cavities. - Sternum closed with wire. Thoracotomy closed with heavy absorbable sutures around ribs. Closure of the rest of the wound in layers.
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Complex Injuries and Complications

Coronary Vessel Injury (Fig. 18.9)
- In about 3% of all cardiac injuries - Only patients with peripheral coronary injuries reach the hospital alive.
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Fig. 18.9. ECG following injury and ligation of the LADA
- Ligate the injured vessel and observe for a few minutes. If no arrhythmia develops during the observation period, no further treatment is required. If arrhythmia develops after ligation, remove the suture and apply gentle digital pressure while a cardiac team prepares for cardiac bypass and repair of the vessel.
Air Embolism
Fairly common problem with injuries to the low-pressure cardiac chambers. Often unexpected cardiac arrest or arrhythmia. Often air bubbles can be seen in the coronary veins. The treatment is aspiration of the ventricle. The prognosis is extremely poor.
Outcomes
- Survival Overall survival: 10-15% Overall hospital survival: 30-35% Hospital survival for GSWs: 10-15% Hospital survival for stab wounds: 60-65% ER thoracotomy survival: 10-15% - Prognostic Factors Determining Survival Mechanism of injury (GSW vs stab wounds) (Fig. 18.10). Prehospital time. Presence of tamponade (improves survival by preventing exsanguination). Injured cardiac chamber
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Fig. 18.10. High velocity GSW of the heart
Intrapericardial aortic injuries have the worst prognosis. The combination of a thin wall with high pressures causes exsanguination or very tense tamponade. Right ventricular injuries have the best prognosis. The relatively thick myocardium combined with the relatively low pressures prevent rapid exsanguination or tense tamponade. Injuries to multiple chambers decrease the probability of survival. - Experience of the trauma team.
Postoperative Care
Routine ECG evaluation (The ECG may show ischemia during the first few days. It usually returns to normal within a few days). Routine echocardiographic evaluation for anatomical or functional cardiac abnormalities. Late follow up at one month by means of clinical examination, ECG echocardiography.
Late Complications
About 30% of survivors develop late cardiac complications. Possible late complications: Ventricular or atrial septal defects (Fig. 18.11), valvular abnormalities, papillary muscle dysfunction, myocardial dyskinesia, pericarditis. Many of the complications may not show at the early clinical or echocardiographic examinations (small defects may enlarge and manifest at a later stage). It is essential that a late clinical examination should be performed at about one month after the injury.
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Fig. 18.11. Traumatic VSD which was diagnosed many weeks after the injury
Blunt Cardiac Trauma Definition

Blunt cardiac trauma includes a wide range of pathologies: asymptomatic cardiac contusion, symptomatic cardiac contusion, rupture of the pericardium, valves, papillary muscles and septum, and free cardiac rupture.
Mechanism of Injury
Direct compression of the heart between the anterior thoracic wall and the spine. Deceleration injuries, such as in high speed traffic accidents or falls. Tearing of the pericardium or myocardium by a fractured rib or sternum. Major and sudden blunt abdominal trauma. Such trauma may result in a sudden, massive return of venous blood into the heart and rupture of the right atrium or ventricle.
Incidence
The reported incidence of blunt cardiac trauma varies from 10-38% of blunt trauma and depends on the diagnostic criteria used. Cardiac rupture is found in about 5-10% of motor vehicle accident fatalities and about 0.5% of blunt trauma hospital admissions.
Diagnosis
There are no generally accepted criteria for myocardial contusion. Often the victim is clinically asymptomatic but the cardiac enzymes or troponin levels are abnormal. Some patients with myocardial contusion may present with cardiogenic shock or arrhythmias.
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In cardiac rupture death occurs at the scene of the accident within a few minutes. Very few patients reach the hospital alive. The diagnosis should be based on the suspicious mechanism of injury, clinical presentation, and investigations. Seatbelt mark signs over the anterior chest and fractured sternum or anterior ribs should increase the suspicion of blunt cardiac trauma.
Investigations
ECG: It should be performed on all patients with serious blunt trauma. It might show arrhythmia or ischemic patterns. Troponin levels: Significantly more sensitive and specific than cardiac enzymes (CPK-MB). In suspicious injuries the troponin levels should be repeated in about 6 hours. There is no correlation between troponin levels and clinical presentation or the severity of myocardial injury. Cardiac enzymes (CPK-MB): They have been replaced by troponin. Echocardiogram: A trauma ultrasound should be performed by a trauma surgeon or an emergency physician on all major trauma patients in order to look for free blood in the pericardial sac and the peritoneal cavity. A detailed echocardiogram by a cardiologist should be performed in symptomatic patients and in patients with an abnormal ECG or high troponin levels. A transesophageal echocardiogram is much more accurate than a transthoracic. The echocardiogram may demonstrate anatomical or functional abnormalities (i.e., septal or valvular lesions, hypokinesia of the myocardium, etc.)
Management (Fig. 18.12)

All patients with major blunt chest trauma should have a trauma ultrasound, ECG, and troponin levels. Asymptomatic patients with abnormal ECG or troponin levels should be observed with continuous ECG monitoring, serial troponin level measurements, and an echocardiogram performed by a cardiologist. Symptomatic patients should be monitored in an ICU environment and treated with antiarrhythmics or inotropes. Patients with myocardial contusion tolerate surgical procedures well, provided they are closely monitored perioperatively. Patients with cardiac or pericardial rupture need emergent surgical intervention.
Common Mistakes and Pitfalls in Cardial Trauma

Patients with cardiac tamponade are very often restless and confused. The inexperienced surgeon may mistake it for alcohol or drug intoxication! External massage for cardiac arrest due to cardiac trauma has no beneficial effect. In fact, it might reduce the chances of successful resuscitation! The procedure of choice is ER thoracotomy, cardiac repair and internal massage. Do not give adrenaline or defibrillate an empty heart. It reduces the chances of successful resuscitation. These procedures should be considered only after volume restoration! Early postoperative clinical or echocardiographic evaluation may miss significant cardiac defects. Late re-evaluation at about one month is essential.
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Fig. 18.12. Evaluation and management of suspected blunt cardiac trauma
References
1. 2. 3. 4. 5. 6. 7. Asensio JA, Stewart BM, Murray J et al. Penetrating cardiac injuries. Surg Clin Nort Am 1996; 76:605-624. Demetriades D. Cardiac wounds. Experience with 70 patients. Ann Surg 1986; 203:315-317. Demetriades D, Charalambides D, Sareli P et al. Late sequelae of penetrating cardiac injuries. Br J Surg 1990; 77:813-814. Rozycki GS, Feliciano DV, Ochsner MG et al. The role of ultrasound in patients with possible penetrating cardiac wounds: A prospective multicenter study. J Trauma 1999; 46:543-552. Asensio JA, Berne JD, Demetriades D et al. One hundred five penetrating cardiac injuries: A 2-year prospective evaluation. J Trauma 1998;44:1073-1082. Swaanenburg JC, Klaase JM, DeJongste et al. Troponin I, troponin T, CKMBactivity and CKMB-mass as markers for the detection of myocardial contusion in patients who experienced blunt trauma. Clin Chim Acta 1998; 272:171-181. Fulda GJ, Giberson F, Hailstone D et al. An evaluation of serum Troponin T and signal averaged electrocardiography in predicting electrocardiographic abnormalities after blunt chest trauma. J. Trauma 1997; 43:304-312.
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CHAPTER 19
Lung Injuries
William C. Chiu and Aurelio Rodriguez Blunt Pulmonary Trauma
Blunt chest trauma may result in life-threatening injuries that require immediate recognition and treatment. These injuries include tension pneumothorax, open pneumothorax, massive hemothorax and flail chest. The majority of other lung injuries, such as pulmonary contusion, simple pneumothorax and simple hemothorax may be treated expectantly or with tube thoracostomy. The decision to intervene with endotracheal intubation or thoracotomy depends on astute clinical judgment.
The first description of pulmonary trauma without chest wall injury is attributed to Morgagni in 1761. Hooker showed that pulmonary hemorrhage was the predominant pathophysiologic effect of blast injury to the chest in 1924. Traumatic wet lung was described for pulmonary contusion in World War II chest injuries by Burford and Burbank in 1945.
Incidence
Approximately two-thirds of blunt trauma patients sustain a chest injury. Pulmonary contusion is the most common lung injury and accounts for 30-75% of these injuries.
The symptoms of pneumothorax include dyspnea and pleuritic chest pain. Some patients may also experience shoulder or back pain. Typical signs of pneumothorax include tachypnea, hyperresonance to percussion, crepitus from subcutaneous emphysema and decreased or absent breath sounds on the affected side. Tension pneumothorax may be associated with tachycardia, hypotension, tracheal deviation and jugular venous distention. The diagnosis of tension pneumothorax should be made on clinical grounds and treatment by decompression should proceed expeditiously without delaying for chest radiographic results! Progressively worsening dyspnea from pulmonary contusion may appear within minutes or may develop over several days. Some minor lung injuries are clinically silent. Hemothorax is associated with dullness to percussion.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. William C. Chiu, University of Maryland Medical Center, R. Adams Cowley Shock Trauma Center, Baltimore, Maryland, U.S.A. Aurelio Rodriguez, University of Maryland Medical Center, R. Adams Cowley Shock Trauma Center, Baltimore, Maryland, U.S.A.
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Pulse oximetry and arterial blood gas may demonstrate decreased oxygen saturation and hypoxia.

Physical examination of the chest may be hampered by patient and environmental factors: The uncooperative or acutely agitated patient may not allow adequate assessment of lung sounds. The obtunded or unresponsive patient may have globally diminished breath sounds. The noisy setting of the emergency room may interfere with accurate assessment of lung sounds.
Investigations
An anteroposterior chest radiograph should be performed on all blunt trauma patients.
- The most common radiographic finding with pneumothorax is the peripheral radiolucent region without lung markings (Fig. 19.1). Associated findings may include tracheal and mediastinal deviation away from the affected side, depression of the diaphragm or a deep sulcus on the affected side or subcutaneous emphysema. - On supine radiograph, a hemothorax appears as a diffuse radio-opacity of the affected side (Fig. 19.2). On an upright projection, blunting or obscuring of the diaphragm on the affected side is seen. - A pulmonary infiltrate suggests a pulmonary contusion, but radiographic findings may lag behind clinical evolution of injury (Fig. 19.3). - An upright expiratory view may aid detection of a small pneumothorax.
Computed tomography (CT) scan is extremely sensitive in identifying small pulmonary contusions, hemothoraces or pneumothoraces. Clinical judgment should be exercised to determine if a chest tube should be inserted for these small injuries incidentally discovered by CT.
Needle decompression should be performed emergently on unstable, hypoxic or deteriorating patients suspected of having a tension pneumothorax. The procedure is performed using a large-bore (e.g., # 14-gauge) angiocatheter inserted into the second intercostal space, in the midclavicular line on the affected side. A sudden escape of air indicates relief of the tension pneumothorax. The needle is then removed and the catheter is left in place.

Pneumothorax and hemothorax are treated with insertion of a chest tube.
- Technique for chest tube insertion: The usual insertion site is at the nipple level (fifth intercostal space) anterior to the midaxillary line. - Through a small transverse skin incision, blunt dissection of the subcutaneous tissues and intercostal muscles is performed. The parietal pleura is carefully punctured with the tip of the clamp and the clamp is spread. - Digital examination of the thoracostomy is performed to confirm the presence of a free pleural space and to evaluate for pleural adhesions. - A large-bore (e.g., # 36-French in adults) chest tube is then advanced posteri-
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Fig. 19.1. Left tension pneumothorax producing cardiac and mediastinal shift toward the right.
orly toward the apex of the lung. The tube is sutured to the skin and connected to a collection device.
Less than 10% of blunt chest injuries require an operation. Massive hemothorax results from the accumulation of more than 1500 mL of blood in the chest cavity. Autotransfusion of blood drained is desirable. Clinical correlation should facilitate the decision to perform thoracotomy. A continuing blood loss of 200 mL/hour provides additional evidence toward the need for surgery. Operative Methods
- The goals of surgery for lung injury include control of hemorrhage, control of major air leak, and debridement of devitalized tissue. - Many lung lacerations can be treated with the use of stapling devices. Other injuries may be controlled using nonabsorbable vascular sutures. Deep sutures are usually required to achieve hemostasis. - Wedge resection of injured lung parenchyma with a stapler or with the aid of sutures around an atraumatic clamp may be needed. - Anatomic lobectomy is occasionally needed when injury to a segmental bronchus is not reparable. The use of a pleural flap to buttress the bronchial stump may deter bronchopleural fistula formation. - Pneumonectomy is rarely necessary for lung injury and would only be indicated for severe hilar injury in which the mainstem bronchus is irreparable or uncontrolled hemorrhage persists.
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Fig. 19.2A. Increased opacity of the right lung field consistent with pulmonary contusion and hemothorax.
Fig. 19.2B. CT scan of the chest in the same patient confirms the right lower lobe pulmonary contusion and hemothorax.
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Fig. 19.3A. Multiple left-sided rib fractures and bilateral parenchymal contusions: Note the left chest wall subcutaneous emphysema.
Fig. 19.3B. Corresponding CT scan of the chest confirmed extensive bilateral pulmonary contusions, greater on the left, with left subcutaneous emphysema.
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Complications
Retained Hemothorax
- Retained hemothorax develops after inadequately drained blood persists and becomes clotted in the pleural cavity. It results in loss of lung capacity, development of trapped lung or fibrothorax and increases the risk of empyema. - Clotted hemothorax that is unable to be drained with a chest tube may be evacuated by video-assisted thoracoscopic surgery (VATS) if performed within one week of injury. Older lesions tend to be well organized and a limited thoracotomy may be required with manual evacuation of hematoma.
Empyema
- Empyema most often occurs as a pleural infection following hemothorax or pneumothorax. The diagnosis may be made by direct evidence of purulent drainage from a chest tube or by CT evidence of pleural infection. - An attempt at CT-guided percutaneous catheter drainage may be made for simple fluid collections along with intravenous antibiotics. For more established infections that are multiloculated and unsuccessfully drained with a tube, thoracotomy is recommended. At thoracotomy, all infected fluid is evacuated making sure all loculations are entered, and all infected debris is cleared.
Outcome
Long-term disability from hemothorax, pneumothorax, or pulmonary contusion is most commonly from restrictive lung disease and occurs in up to 10% of patients.
Penetrating Pulmonary Trauma

Penetrating injuries to the lung are predominantly from stab wounds and gunshot wounds. The diagnosis of injury is more straightforward than in blunt trauma and may be readily apparent. Since the majority of these injuries can be treated with tube thoracostomy, the need for thoracotomy after penetrating lung injury is declining. Management priorities include not only treatment of the lung injury, but also the detection of associated injuries.
Incidence
Between 10-40% of all patients with penetrating trauma have a chest injury. Following penetrating chest trauma, the incidence of lung parenchymal injury, hemothorax or pneumothorax is between 55-90%. Approximately 40% of patients with penetrating lung injury also suffer a major extrapulmonary injury.
On physical examination, the chest wall defect may be the only obvious sign of injury. High-velocity missiles and shotgun blasts frequently result in greater tissue destruction and patients may present with a large chest wall defect. If the wound is greater than two-thirds the diameter of the trachea, each inspiratory effort would preferentially result in sucking air through the defect rather than through the tracheobronchial tree.
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In this open pneumothorax or sucking chest wound, there is immediate equilibration between intrathoracic and atmospheric pressure and inability to ventilate effectively.

Physical examination of penetrating chest wounds can occasionally be misleading because they only indicate the surface points of injury: Cervicothoracic wounds require careful assessment of the neck and upper extremity vasculature. Central and transmediastinal trajectories require full assessment of the heart, great vessels, esophagus and tracheobronchial tree. Thoracoabdominal wounds require evaluation for diaphragmatic and peritoneal penetration.
Investigations
An anteroposterior chest radiograph is obtained in all patients with a penetrating chest wound (Fig. 19.4). If the patient is not in respiratory distress and hemodynamics are normal, an upright expiratory view aids in detecting a small pneumothorax. Besides pneumothorax and hemothorax, radiographic findings of associated injuries include apical pleural cap, abnormal mediastinum, pneumomediastinum, pneumopericardium or pneumoperitoneum. There have been a few reports on using CT scan to evaluate transmediastinal trajectory of gunshot wounds (Fig. 19.5). Clinical decisions based on this test require careful and accurate interpretation of the findings.
Needle decompression may be necessary in some penetrating chest injuries. A large chest wall defect or open pneumothorax should be covered with a sterile occlusive dressing. This dressing should be taped to the skin on three sides to create a flap-valve effect. During inspiration, the dressing acts as an occlusive flap preventing air from entering into the pleural cavity. During expiration, the same dressing acts as a valve allowing pleural air to escape.

As with blunt chest injuries, pneumothorax and hemothorax should be treated with a chest tube. Patients in hemorrhagic shock require immediate resuscitation and possibly urgent thoracotomy. The potential for extrathoracic injury must be fully assessed. A carefully selected group of patients with a small pneumothorax associated with a small stab wound, normal hemodynamics and no hypoxia without supplemental oxygen may be clinically observed without a chest tube. This patient should be admitted, observed for at least 24 hours, and serial chest radiographs must show resolution or lack of progression of the pneumothorax.
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Patients with a penetrating chest wound arriving in extremis may have a cardiac injury with pericardial tamponade or exsanguination.
- In emergency thoracotomy for penetrating left chest wounds, a left anterolateral
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Fig. 19.4. Gunshot wound of the chest: CT scan reveals a large right lower lobe pulmonary contusion.
thoracotomy is performed. With penetrating right chest wounds, a bilateral thoracotomy is performed for both open cardiac massage and hemorrhage control. - Only the occasional patient with massive hemothorax from penetrating lung injury will require emergency room thoracotomy. - If emergency room thoracotomy is performed, obvious bleeding sources may be controlled with application of long atraumatic clamps until these patients can be brought to the operating room.
Rapid control of massive bleeding may be achieved by application of an atraumatic clamp at the pulmonary hilum. In the hemodynamically stable patient, posterolateral thoracotomy with the patient in the lateral decubitus position is the preferred operative approach for suspected lung injuries. In the hemodynamically unstable patient, anterolateral thoracotomy in the operating room will allow access to most pulmonary injuries. In addition to the operative methods described for blunt pulmonary injuries, a useful technique for hemorrhage control is pulmonary tractotomy.
- This procedure involves dividing or unroofing the path of the bullet tract between atraumatic clamps to expose and accurately identify the bleeding source. Selective ligation of injured vessels may then be performed. - A handy technique is to perform the tractotomy using a linear stapler/cutter to simultaneously control the parenchyma and divide the tract.
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Outcome
After penetrating chest trauma, approximately one-third of patients develops a complication. The incidence of recurrent pneumothorax is 23%, residual hemothorax 16% and empyema 3%. The survival rate is near 100% for patients with isolated penetrating pulmonary injury requiring only tube thoracostomy treatment. Among patients with hilar pulmonary injury, the survival rate is only 30-56%. After thoracotomy for penetrating lung injury, the mortality rate for pneumonorrhaphy is 20%, lobectomy 55% and pneumonectomy near 100%.
Common Mistakes and Pitfalls in Pulmonary Trauma

In the hypoxic or hemodynamically unstable patient, the diagnosis of tension pneumothorax should be made on clinical grounds and treatment by decompression should proceed without delaying for x-ray results. When tubes are malpositioned or clotted, chest tube drainage rate does not reflect actual ongoing hemorrhage in massive hemothorax. Thoracotomy should be considered in the unstable patient with persistent hemothorax on chest radiograph. In the patient with pulmonary contusion, fluid administration should be controlled to achieve adequate resuscitation, but avoid fluid overload.
References
1. 2. 3. 4. 5. Cohn SM. Pulmonary contusion: Review of the clinical entity. J Trauma 1997; 42:973-979. Feliciano DV, Rozycki GS. Advances in the diagnosis and treatment of thoracic trauma. Surg Clin North Am 1999; 79:1417-1429. McSwain NE Jr. Blunt and penetrating chest injuries. World J Surg 1992; 16:924929. Richardson JD, Spain DA. Injury to the lung and pleura. In: Mattox KL, Feliciano DV, Moore EE, eds. Trauma. 4th ed. New York: McGraw-Hill Companies, Inc., 2000: 523-543. Rodriguez A, Thomas MD, Shillinglaw WRC. In: Ivatury RR, Cayten CG, eds. The textbook of penetrating trauma. Philadelphia: Williams & Wilkins, 1996: 531-554.
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Blunt Aortic Trauma

Ismael Navarro Nuo, Juan A. Asensio Introduction
Blunt aortic trauma resulting in aortic disruption and hemorrhage is a life threatening injury that requires emergency diagnosis and treatment. Usually there are a significant number of associated injuries that may also be life threatening making the management of an aortic injury much more complex and challenging. Other than exsanguination, paraplegia is one of the most devastating complications in this type of an injury. A high index of suspicion for an associated aortic injury and its appropriate treatment are key to survival.
Vesalius in 1557 reported the first case of a patient who died of a ruptured aorta after being thrown from a horse. Kuhn collected a series of 75 postmortem cases of blunt aortic injury between 1895 and 1925. Parmley in 1958 collected from the literature over 199 cases of blunt aortic injuries and described its management and the natural history of untreated injuries. In 1952 Henry Bahnson reported an aneurysmorrhaphy for a patient with a chronic posttraumatic thoracic aortic aneurysm. DeBakey and Cooley in 1954 resected a posttraumatic thoracic aneurysm and replaced the aorta with a synthetic graft. Klassen, in 1958, is credited with the first successful primary repair of an acute traumatic thoracic aortic injury.
Epidemiology
Eighty-five percent of patients with aortic rupture die within minutes of the traumatic incident. Fifty percent of survivors die within 48 hrs if injury is not recognized or treated. Of these, 38% survive longer than 30 minutes and 12% survive longer than 4 hours.
Mechanism of Injury
The primary mechanism of injury is rapid deceleration at high speeds.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Ismael Navarro Nuo, University of Southern California, Los Angeles, California, U.S.A. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A.
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The usual site of disruption is located within 2-3 cm distal to the junction of the left subclavian artery and the aorta. The posterior aspect of the aorta is the site most commonly torn. The mediastinal pleura and other mediastinal structures hold the aorta in place above. The descending aorta is fixed at the isthmus by the ligamentum arteriosum, left main bronchus and intercostal arteries. The rapid forces of deceleration, torsion, bending or direct impact associated with cranio-caudal movement and horizontal shear movement against the supportive tissues holding it in place are responsible for the tears of the aorta. Shear forces, compression of the vessel between bony structures and profound intraluminal hypertension during the traumatic event all summarily act in the creation of an aortic rupture. It wasnt until recently that side impacts were recognized as capable of producing aortic ruptures. A contained hematoma around the site of disruption is the reason for most survivors reaching the hospital alive. Blood flow distal to the site of aortic disruption may be interrupted leading to massive ischemia producing lactic acidosis. This metabolic acidosis can easily lead to cardiac arrhythmias and death.
Associated Injuries
Ninety percent of patients with blunt injury of the aorta have associated injuries. Forty-two percent have associated cardiac injuries. Thirty-three percent demonstrate associated lung injuries. Twenty to forty-three percent have a CNS injury. Twenty-five percent have an intra-abdominal or retroperitoneal injury with active bleeding. The triad of significant pelvic fracture, left hemidiaphragmatic rupture and aortic rupture is well described. ONLY 5-10% will have an isolated aortic injury.
Anatomic Location of Injury

The aortic disruption is usually linear, transverse, and in 35-60% of the cases it is located posteriorly. The aortic laceration usually has smooth edges and involves the intima, media and often all three layers. The edges of the transected tissue may be separated by as much as a few centimeters and it may include the entire circumference of the aorta. Occasionally the laceration is longitudinal. The aortic isthmus is involved in 84-100% of the cases. The ascending aorta and arch are involved in 3-7% of the cases. Multiple injury sites throughout the thoracic aorta have been reported in the literature to have a frequency between 13 and 18%. The left carotid artery is the least affected vessel whereas the left subclavian and innominate arteries are occasionally involved.
Diagnosis Clinical Presentation

There must be a high index of suspicion when there are other associated injuries
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Fig. 20.1. CXR showing widened midiastinum and deviated nasogastric tube to the left. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
At initial evaluation, 30% of patients will present with dyspnea, back pain, higher differential blood pressure in the upper extremities compared to the lower. There may be absence of lower extremity pulses. Twenty percent of patients may have a midscapular systolic murmur. The patient may show evidence of left chest wall contusion. The presence of first to third rib fractures, left clavicular fracture or scapular fractures, flail chest, or combinations of the above should raise the index of suspicion for blunt aortic trauma.
Investigations
Chest X-Rays
- Classic radiographic findings in a patient with blunt aortic rupture include a widened (> 8 cm) mediastinum, loss of the acute contour of the aortic knob, left apical cap, left pleural effusion, loss of AP window, rightward deviation of a properly placed nasogastric tube (least frequently seen but highly reliable), displacement of the trachea, depression of the left main bronchus, sternal, clavicular, first rib or multiple rib fractures. - In 25% of the cases the chest X-ray may be initially normal but reveals abnormal findings on a delayed basis. - Only 10-20% of patients with an abnormally widened mediastinum on chest X-ray will actually have a ruptured aorta. - Some patients may have a normal mediastinum and harbor a ruptured thoracic aorta.
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Fig. 20.2. Thoracic Aortogram showing contained rupture of the thoracic aorta. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
CT Scan
- Routine helical CT is an excellent diagnostic tool and has to a greater extent replaced the aortogram for evaluation of the mediastinum in high risk blunt trauma patients. In many centers it has become the first line investigation for suspected aortic injury. - Aortogram is still the gold standard. - Aortograms may have a 6% false positive rate. - An aortogram may be obtained to help in the diagnosis if the patient is stable, or if the CT scan has questionable findings.
MRI
- MRI is helpful but access to the patient during an acute phase of resuscitation may be a problem.
TEE
- Transesophageal echogram (TEE) is a good adjunct to the diagnosis of aortic disruption by blunt trauma. The distal ascending aorta and the aortic arch are difficult to visualize because of the intervening trachea and left main bronchus and an injury in this area may be overlooked.
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Fig. 20.3. Spiral CT scan showing aortic rupture. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
Surgical Management Emergency Department Management

All trauma patients should be evaluated and resuscitated per ATLS protocols. All other major life threatening injuries must be evaluated promptly. All other more life threatening bleeding must be controlled first, if the mediastinal hematoma is deemed to be stable. Pneumothoraces must be evacuated by the insertion of chest tubes as necessary. Systolic blood pressure control should be maintained in a range of 90-110 mm Hg in order to allow target organ perfusion but not allow further disruption of the disrupted aorta.
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Fluid resuscitation should be carried out to reach the target pressure mentioned above. Blood products should be utilized as needed. In hemodynamically stable patients, permissive hypovolemia and aggressive minimization of change in pressure over change in time ( dP/dT), which are widely accepted in the treatment of aortic dissection and aneurysm rupture, should be considered in patients with blunt aortic injuries.
Intraoperative Management
A double lumen endotracheal tube should be inserted if possible to facilitate collapse of the left lung and improve visualization of the disrupted aorta. Hemodynamic monitoring lines should be placed, arterial line in the right radial artery and a right femoral arterial line or pedal artery to monitor distal perfusion. Distal perfusion should be maintained at 50-70 mm Hg. The patient is placed on a Bean Bag to facilitate positioning at a right lateral decubitus position at 45. A left posterolateral thoracotomy is the incision of choice to access the descending aorta. The fourth intercostal space is chosen to enter the chest cavity. Proximal and distal control should be obtained first. The decision to approach and repair this injury either by clamp and sew technique or the utilization of a circulatory assist device is now made. The utilization of a cell saver apparatus is mandatory in these patients. The patient is systemically anticoagulated with 5-10,000 units of heparin intravenously provided there are no contraindications like associated intracranial hemorrhage. A Carmeda (tm) circuit that is heparin bonded can be utilized to preclude the use of any heparin intravenously in cases where bleeding from associated injuries can be fatal. If circulatory assist devices are to be utilized, a left atrial-left femoral artery bypass is utilized with a centrifugal pump. Thermal control devices can be added to the circuit to regulate the patients temperature. If arterio-venous bypass is to be utilized with an oxygenator in patients with poor oxygen saturation due to associated pulmonary injury, systemic anticoagulation with 10-20,000 units of heparin is mandated and cannulation can be done at the inguinal region via femoral artery and femoral vein. Thermal control can be quite helpful in these patients. Passive conduits like the Gott shunt (ascending aorta to distal thoracic aorta) can also be utilized for distal arterial perfusion in lieu of mechanical pumps as already described above. The aortic disruption can be handled by primary repair, end-to-end anastomosis or tube graft interposition. At the completion of the cross clamp period, the patient is weaned off circulatory assistance and the heparin is reversed with protamine sulfate intravenously. The left posterolateral thoracotomy is closed and two 36F chest tubes are left in place to drain the left thoracic cavity. An intrapericardial exploration is also done through the left thoracotomy if a hemopericardium is suspected.
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Nonoperative Management
Nonoperative management of patients with a ruptured aorta is being recognized as a further option in patients with severe concomitant injuries unlikely to tolerate operative repair. Such comorbidities include severe head trauma, major burns, sepsis, and severe multisystem trauma with hemodynamic instability. There is a place for delayed surgical management in this highly selective subset of patients should they survive their other injuries, although their mortality is astronomical. Nonoperative management has also been utilized in some cases of a minor aortic injury. The diagnostic studies may be positive but with only minor changes. Routine and frequent follow-up radiologic studies are a must in these patients.
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Angiographically Placed Stents

Intraluminal stenting has been utilized for patients deemed nonoperable because of severe comorbidities. Although some success has been reported by some authors, further evaluation of this technology is mandated.
Morbidity
Paraplegia is a devastating complication of blunt aortic trauma. The overall incidence is 5-10%. If aortic cross-clamp times greater than 30 minutes are experienced during aortic rupture repair, a greater incidence of postoperative paraplegia is generally encountered. If circulatory assist techniques with distal systemic perfusion are utilized for the repair of the aortic disruption or an aortic cross-clamp time of less than 30 minutes is observed, the incidence of postoperative paraplegia will tend to be in the lower percentage range of 3-5%. Overall, the incidence of paraplegia (with or without special operative techniques or aortic cross-clamp times) in patients that sustained injury to the aorta was 9%. Other possible complications of emergency aortic disruption repair surgery include phrenic nerve injury, recurrent laryngeal nerve injury, lung lacerations, pseudoaneurysms, injury to the pulmonary artery during cross clamping or injury to the thoracic duct resulting in a postoperative chylothorax. Immediate postoperative complications may include ARDS or sepsis, and rarely graft infection.
Mortality
Prehospital mortality in patients with blunt aortic injury is approximately 85% in most studies. In-hospital mortality for untreated patients is 1% per hour for the initial 48 hours. Repair of blunt aortic disruption carries a 31% operative mortality.
References
1. 2. Asensio JA, Hanpeter D, Gomez H et al. Thoracic injuries. In: Shoemaker W, Greenvik A, Ayres SM et al, eds. Textbook of Critical Care. 4th Ed. Philadelphia, PA: W.B. Saunders Co. 1999; 337-348. Kuerer H, Curtiss S, Zisman S et al. Thoracic Aortic Transection: Diagnosis, Management and Survival. Surgical Rounds, August, 1998.
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Fabian T. Prospective Study of Blunt Aortic Injury: Multicenter Trial of the American Association for the Surgery of Trauma. September, 1996. Demetriades D, Gomez H, Hanks S et al. Routine helical CT scan evaluation of the mediastinum in high suspect blunt trauma patients. Arch Surgery 1998; 133(10):1084-1088. Mattox KL, Wall MJ Jr, LeMaire SA. Injury to the thoracic great vessels. In: Trauma, 4th Ed., Mattox KL, Feliciano DV, Moore EE, eds. New York: McGraw Hill and Company 1999; Chapter 27:559-582.
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4. 5.
Penetrating Thoracic Vascular Injuries

Matthew J. Wall, Jr. and Anthony Estrera Incidence
Over 90% of thoracic vascular injuries are due to penetrating trauma, with blunt trauma as the predominant cause of injuries to the descending thoracic aorta. The actual incidence of thoracic vascular injuries in the general population is unknown as a significant number of victims may never reach the hospital setting.
Pathophysiology
Penetrating thoracic vascular injuries can present with external or internal hemorrhage, thrombosis, intimal flaps, or pseudo-aneurysms. External hemorrhage is most common from stab wounds to the base of the neck. Aortic and vena cava injuries can manifest as hemorrhage into the mediastinum or pleural cavity, presenting as either significant hemothorax, mediastinal hematoma, or cardiac tamponade. The presence of a distal pulse does not exclude a proximal injury. Vessels can be completely disrupted with blood flow contained by perivascular tissue. Some injuries may present with complete thrombosis. An intimal flap allows exposure of the subendothelium and possible thrombosis. Moreover, if the intimal flap progresses or enlarges, complete occlusion may result. Thus, the natural history of intimal flaps is unclear though most recommend operation on significant lesions. Alternatively, small intimal flaps, similar to those seen when a cannula is inadvertently placed into an artery, can be observed. Other nonbleeding injuries can develop pseudoaneurysms that can initially be small and very difficult to diagnose. They are more often diagnosed late in the course of patients who were not suspected of having an arterial injury.
- A high clinical suspicion for pseudoaneurysms must be maintained. Evaluation is based on history, physical exam, or on x-ray. One mode of presentation is when the pseudoaneurysm exerts pressure on adjacent structures. - In a patient undergoing arteriography, careful inspection of the study, perhaps with repeat examination in 2-3 weeks, may diagnose pseudoaneurysms earlier, and may allow for technically easier repair.
The large diameter of the great vessels predisposes them to missile embolism. When the missile does not appear on chest x-ray in a patient with a gunshot wound to the chest, one must entertain the possibility of embolization of the bullet, assuming an exit wound has been excluded. The patients body should be surveyed radiographically, and distal pulses checked carefully. Similarly, a
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Matthew J. Wall, Jr., Department of Surgery, Baylor College of Medicine, Houston, Texas, U.S.A. Anthony Estrera, Department of Cardiothoracic Surgery, College of Medicine, Houston, Texas, U.S.A.
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single vascular injury found at operation with a bullet tract which cannot be reconstructed suggests missile embolus.
- The treatment of missile emboli depends on location. Missile emboli located in the arterial system or left side of the heart (i.e., left atrium or ventricle) usually require surgical removal. Missile emboli can lodge in the iliac/femoral vessels or be devastating if they go to the common carotid artery. - Venous missile emboli or right sided cardiac emboli usually lodge in the right ventricle or branches of the pulmonary artery and may be removed if larger than a B-B. - Management focuses immediately on the control of bleeding from the chest injury, and once the patients physiology has stabilized (i.e., resuscitate, correct hypothermia and acidosis), separate incisions can be made to remove the embolized missile.
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It is interesting to note that even significant injuries clot and stop bleeding. It is probably disadvantageous to vigorously resuscitate either with fluids, MAST trousers or pressors to artificially elevate the blood pressure, as this may dislodge a soft clot and increase bleeding. This results in massive swings of the blood pressure.
- A recent randomized controlled trial in patients with penetrating trauma comparing standard fluid resuscitation with no fluid resuscitation until time of skin incision and operative control of the vascular injury demonstrated a significant survival advantage with delayed resuscitation. Thus, cyclic hyper-resuscitation should be avoided.
Presentation
Thoracic vascular injuries commonly occur secondary to penetrating trauma from gunshot wounds, stab wounds and iatrogenic causes. Any penetrating injury that traverses the chest or the base of the neck can produce a thoracic vascular injury. Gunshot wounds are particularly unpredictable; it is unreliable to draw straight lines reconstructing the track of gunshot wounds. The mobility of the shoulder and neck affects the patients position at the instant of wounding and may produce surprising trajectories. Attempts to map trajectories from multiple gun shot wounds are usually fruitless. With this difficulty, our approach is to have a low threshold for evaluating proximate structures and cavities. Stab wounds, despite lower energy, can leave a larger wound track through which the patient can bleed externally. The thoracic outlet is the most superior region of the thorax bordered by the manubrium anteriorly, clavicles and first ribs laterally, and the vertebral column posteriorly. Thoracic outlet injuries are of particular concern when the injury pattern is the gunshot wound traversing the upper mediastinum. The wound may track superiorly such that it avoids the aortic arch, but may injure the brachiocephalic vessels between the neck and the aorta. If these patients are stable in the emergency center, early arteriography is warranted for identification of the injury and appropriate planning for surgical exposure.
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Prehospital and Emergency Center Issues

Patients with potential thoracic vascular injuries should be transported to an appropriate facility that can manage thoracic vascular trauma. Intravenous access should probably be avoided in the upper extremities particularly on the side of injury. Artificial means to elevate the blood pressure such as intravenous fluids, MAST trousers, or pharmacologic pressors prior to vascular control are probably detrimental and should be avoided in the urban setting. The patients should be transported, taking time primarily to establish an airway with an endotracheal tube if needed. In the emergency center patients should be examined and managed according to a plan such as the Advanced Trauma Life Support Protocols. Cervical hematomas dissecting superiorly should lend consideration for early airway maneuvers. Early endotracheal intubation is probably the best course of action. While counterintuitive, prophylactic early tracheostomy in the emergency center might convert a controlled hematoma into uncontrolled exsanguination. After life threatening conditions are addressed the patients injuries are cataloged and the distribution of hematomas, presence of distal pulses as well as neurological function should be carefully documented if possible. Aside from a type and cross match for blood, minimal laboratory tests are necessary. A trauma surgeon should be involved in the care of these patients as early as possible.
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Exposure and Control

Arteriographic evaluation is often not an option for patients with great vessel injuries as they are in extremis and these injuries are diagnosed at operation. When performed in stable patients, due to the large dye column, small pseudo-aneurysms of the aorta are often difficult to see and require views tangential to the expected injury to maximize yield. Alternatively, arteriography is extremely helpful when assessing the brachiocephalic vessels. By delineating the anatomy of the injury, arteriography permits planning the operative strategy. In the operating room, the patient is typically positioned on the operating room table supine and prepped from chin to knees. Single lumen endotracheal intubation is usually adequate.
- Prophylactic antibiotics are given anticipating the need for a vascular graft. - The groins are prepped so that the saphenous vein is available for a graft for vessels less than 4 mm. - The patient in extremis with thoracic outlet injury is approached operatively via left anterolateral thoracotomy for resuscitation with extension to the right side for exposure if needed (Fig. 21.1). - The aorta can be clamped to preserve blood flow to the brain and myocardium. - The extension to the right chest should be directed superiorly to avoid entering a low interspace which limits exposure of the upper right hemithorax. - After proximal control is obtained the incision can be extended by splitting the sternum and adding neck or supraclavicular extensions if needed. - If the injury tract is an anterior mediastinal traverse and the patient is unstable, the median sternotomy with appropriate neck extension may be the empiric
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Patients who require empiric life saving operations as well as patients that require emergency center thoracotomy with thoracic outlet injuries have a dismal prognosis.
Great Vessel Injuries

Penetrating injuries to the thoracic aorta are usually diagnosed at operation through an emergent anterolateral thoracotomy. The ascending aorta is most commonly injured by stab wounds and the descending aorta by gunshot wounds.
- The overall mortality for penetrating injuries to the thoracic aorta is reported to be 50-85%. - Lateral arteriorrhaphy with adjuncts such as partial occluding clamps is the most common mode of repair. More extensive injuries may require graft interposition and the knitted dacron graft is our graft of choice on the soft aorta of the young adult.
Because they are short structures, the intrathoracic vena cavae (inferior and superior) are not commonly injured. Lateral venorrhaphy is the usual method of repair though extensive injuries of the superior vena cava can require graft interposition.
- Injuries to the posterior intrathoracic inferior vena cava are particularly difficult to manage and may require total cardiopulmonary bypass to accomplish repair via a transatrial route.
The azygous vein, while not often considered a great vessel, is associated with a significant mortality if injured. Azygous vein injuries are often found late in the operation and are analogous to vena cava injuries. They are managed with ligation or simple repair.
Thoracic Outlet Injuries

The incisions required to achieve proximal and distal control are multiple (Fig. 21.1). An initial best guess may not turn out to be optimal.
- Injuries to the innominate, right subclavian, right and left carotid arteries are managed through a median sternotomy, with appropriate cervical or supraclavicular extension. - Injury to the left subclavian artery is managed via a high left anterolateral thoracotomy usually via the third intercostal space for proximal control. Distal control is obtained via a supraclavicular incision and the arterial injury is then identified. - Though removal of the clavicle may provide needed exposure, it can be a particularly morbid procedure affecting upper extremity function postoperatively. - Distal subclavian injuries without a medial hematoma can be managed with a supraclavicular incision for proximal control away from the hematoma, combined with a distal infraclavicular incision for distal control and repair.
The brachiocephalic vessels are particularly soft structures and do not tolerate either tension or mobilization. Thus, injuries that can not be primarily repaired will usually require the use of a soft graft such as knitted Dacron.
- Injuries to the innominate artery if small and distal can be managed with primary repair or short segment interposition graft.
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Fig. 21.1. Incisions for proximal vascular control and repair of thoracic outlet injuries. A) Median sternotomy for innominate, right subclavian, right carotid, and proximal left carotid arterial injuries. Cervical or supraclavicular extensions can be added if needed. B) Extension of a left anterolateral thoracotomy forming a book incision. This incision has significant morbidity with little advantage over separate anterolateral thoracotomy with supraclavicular incision. C) Posterolateral thoracotomy for exposure of the descending aorta. D) Anterolateral thoracotomy for resuscitation and exposure of the heart and proximal great vessels. This incision can be carried across the midline for exposure of the hilum of the right lung and the innominate and right subclavian vessels.(E)
Extensive injuries or injuries adjacent to the aortic arch are best managed using the bypass principle as described by Johnston et al (Fig. 21.2).
- The chest is opened through a median sternotomy and the proximal hematoma is avoided. - A 10 mm knitted dacron tube graft is sewn to a convenient spot on the ascending aorta using a partial occluding clamp. - Control is obtained at the distal innominate artery. - The artery is divided and the distal innominate artery is then sewn end to end to the graft reestablishing flow. To complete the procedure a large partial occluding clamp is placed on the arch of the aorta and the origin of the innominate is over sewn.
Injuries to the intrathoracic left common carotid artery are managed similarly to the innominate recognizing that it is a relatively deep structure.
- In the patient in extremis, as a damage control option a carotid shunt may be placed to temporarily reestablish flow and permit resuscitation in the intensive care unit prior to definitive repair.
Attempts should be made to document the neurological status of the arm when dealing with subclavian injuries as significant preoperative associated brachial plexus injury is common. As the brachial plexus surrounds the artery,
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Fig. 21.2. Technique for control and repair of proximal innominate artery injuries. A) Severe intimal disruption associated with minimal external hematoma. B) Aortotomy is performed along the ascending aorta, and a prosthetic graft is sewn end-to-side. A partial occluding clamp is placed at the origin of the innominate artery and a vascular clamp across the distal innominate artery. The artery is divided between the clamps. C) The repair is completed by an end-to-end anastomosis of the graft to the distal innominate artery and by over sewing the origin of the innominate artery.
care must be taken when mobilizing these vessels to avoid a traction injury of the brachial plexus.
- An incision which in the past was advocated for managing these injuries was the left trap door or book exposure (Fig. 21.1) This incision has significant morbidity with very little advantage over the previously mentioned approaches. Book thoracotomy carries a significant incidence of postoperative causalgia that can be extremely difficult to manage.
Brachiocephalic Venous Injuries

Contained venous injuries are usually inferred and managed nonoperatively. Freely bleeding injuries manifest as external hemorrhage, hemothorax or an expanding hematoma and are managed with primary repair, ligation, or graft interposition.
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The jugular or innominate vein, in particular, can be ligated but the superior vena cava should be reconstructed if possible. Arterial-venous fistulas are common and managed with arterial repair and ligation/reconstruction of the vein.
Associated Injuries
Concomitant injuries to the lung are common. In that these patients are cold and coagulopathic, there may be significant hemorrhage from deep within the lung. A useful damage control adjunct is the use of pulmonary tractotomy with selective vascular ligation (Fig. 21.3). The bleeding wound tract is opened with the stapler or between aortic clamps, and bleeding and air leaks are controlled directly. This procedure allows rapid control of deep bleeding and air leaks, thus, shortening operation and avoiding formal lobectomy in a patient with other significant injuries. Associated tracheal injuries can occur and are diagnosed with physical examination or bronchoscopy. Repair can usually be accomplished with absorbable suture. Concomitant esophageal injuries are diagnosed by barium swallow, esophagoscopy or exploration and can typically be repaired primarily. Drains if placed in the neck should probably be brought out the side opposite a vascular repair. A muscle flap can also be interposed to protect a vascular repair.
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Other Issues
When operating on these patients autotransfusion collection systems can be extremely helpful and appropriate blood products should be available. Soft prosthetic grafts are preferred for vessels greater than 4 mm in diameter.
Postoperative Issues
Thoracic epidural catheters are useful in managing postoperative pain allowing more vigorous deep breathing and coughing.
Complications and Postoperative Sequelae

While median sternotomy is relatively well tolerated, thoracotomy can significantly affect thoracic physiology. Difficult weaning from the ventilator should raise suspicion for injury to the phrenic nerve. This can be investigated using fluoroscopy or ultrasound. Examination of motor and sensory function of the upper extremity will lead to early diagnosis of brachial plexus injury.
Rehabilitation
Due to the need for mobility, the shoulder depends on its musculature to maintain stability. The syndrome of capsular adhesions is particularly difficult as patients with even short periods of immobility of the shoulder can have morbidity that can take months to resolve. Rehabilitation services should be instituted as soon as practical after the injury to try to prevent these sequelae. Shoulder stiffness combined with thoracic incisions can be particularly difficult to manage. Rehabilitation services are also useful when partial loss of function of the upper extremity has occurred
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Fig. 21.3. Tractotomy for controlling hemorrhage from the lung parenchyma. The missile tract is opened by dividing the overlying lung between vascular clamps or a stapler. The bleeding vessels in the tract are ligated, and the lung parenchyma pedicles are oversewn.
Medical Legal Issues

Thoracic vascular injuries are some of the most complex and intimidating injuries that the trauma surgeon faces. Patients often present with irreparable vascular and neurologic deficits. It is important to preoperatively assess and record these deficits so that a postoperative deficit is not inadvertently attributed to an intraoperative maneuver. Difficult decisions regarding preservation of structures need to be made in patients that are dying. Many times, rapid dissection is required to obtain vascular control and save the patients life. This can result in neurologic injuries that are predictable. A bad outcome prima facia is not evidence of malpractice.
References
1. 2. 3. 4. 5. Mattox KL, Feliciano DV, Beall AC et al. Five thousand seven hundred sixty cardiovascular injuries in 4459 patients epidemiologic evolution 1958-1988. Ann Surg 1989; 209:698. Bickell WH, Wall MJ, Pepe PE. Immediate versus delayed fluid resuscitation for hypotensive patients with penetrating torso injuries. N Engl J Med 1994; 331:1105. Graham JM, Feliciano DV, Mattox KL et al. Management of subclavian vascular injuries. J Trauma 1980; 20:537. Johnston RH Jr, Wall MJ Jr, Mattox KL. Innominate artery trauma, a thirty year experience. J Vasc Surg 1993; 17:134. Wall MJ, Hirshberg A, Mattox KL: Pulmonary tractotomy with selective vascular ligation. Am J Surg 1994; 168:665.
Diaphragm Injuries
James A. Murray Introduction
In the acute setting diaphragm injuries are generally not life threatening but can be associated with a significant morbidity and mortality due to associated injuries or herniation with cardiopulmonary compromise. In addition, if undetected in the acute setting, delayed presentation of diaphragmatic hernias carries an increased risk of complications.
Sennertus described first postmortem finding of a strangulated diaphragm hernia in 1541. Bowditch made the first antemortem diagnosis of diaphragmatic herniation in 1853. Riolfi performed first surgical repair of diaphragmatic injury in 1886.
Surgical Anatomy
The diaphragm is a thin muscular sheet that defines the border between the thoracic cavity and the abdomen. While its peripheral portion is made of muscle, the central portion is tendinous. The diaphragm is attached to: the xyphoid anteriorly, the lower six ribs and costal cartilage laterally, the lumbar vertebrae posteriorly.
The Innervation of the Diaphragm

Phrenic nervesC3-C5 cervical roots On the diaphragm the phrenic nerve divides into four rami: anterior, anterolateral, posterolateral, posterior. This branching pattern must be appreciated to prevent injury when incising the diaphragm.
Diaphragm excursion
During respiration the diaphragm raises: To the level of the nipples anteriorly (the 5th intercostal space) To the tips of the scapula posteriorly (the 8th intercostal space)
Classification of Diaphragm Injuries

Wounds of the diaphragm are classified by the duration of time between the injury and presentation. Acute phasefrom injury to the time of recovery from the initial insult
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. James A. Murray, Department of Surgery, Division of Trauma and Critical Care, University of Southern California Keck School of Medicine, Los Angeles, California, U.S.A.
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Chronic phasetime after recovery from initial injury during which the patient develops gastrointestinal or respiratory complaints. These symptoms are due to herniation of viscera through the unrepaired defect.
Diaphragmatic Herniation Can Occur in Two Places
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Intrathoracic herniationthis is the most common. The defect is through the muscular portion of the diaphragm and allows communication with the thoracic cavity. Intracardiac herniationvery rare. Defects through the central infracardiac portion of the diaphragm allow communication and herniation into the pericardial sac.
Epidemiology of Diaphragm Injuries Blunt TraumaIncidence

4-6% of patients requiring laparotomy or thoracotomy May be as high as 9.5% in severe accidents Front seat, belted passengers are at higher risk, also passengers with improperly placed lap belts at increased risk
Blunt TraumaMechanism
More common with abdominal trauma than thoracic trauma Due to an increase in abdominal pressure and decrease in abdominal volume Rib fractures may result in lacerations or avulsion of the diaphragm from its attachments
Blunt TraumaLocation
75% of blunt diaphragm ruptures on the left 2025% of blunt ruptures involve the right diaphragm 2% of diaphragm ruptures are bilateral 1% of diaphragm ruptures will be intrapericardial
Blunt TraumaAssociated Injuries

Chest trauma60% Long bone fracture40% Pelvic fractures35% Splenic injury45% Head injury30% Liver28% Right diaphragm injuries have a 100% incidence of associated intra-abdominal injuries. Left diaphragm ruptures have an 80% incidence of associated intra-abdominal injuries.
Penetrating Trauma
The incidence of diaphragm injuries depends upon the location of the injury, the mechanism of injury, the patients clinical status, as well as the method used to detect diaphragm injuries. Thoracoabdominal injuries are at greatest risk for diaphragm injuries (20-50%). Gunshot wounds are more frequently associated with diaphragm injuries than stab wounds (60% versus 30%).
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Symptomatic patients (those with peritonitis or hemodynamic instability) undergoing laparotomy have a greater incidence than asymptomatic patients diagnosed by laparoscopy (60% versus 25%).
Diagnosis
The diagnosis of diaphragmatic injuries can be very difficult especially in the asymptomatic patient.
The clinical presentation of patients with diaphragmatic injuries is quite variable. Patients may: Be asymptomatic Demonstrate nonspecific physical findings Often demonstrate physical findings due to associated injuries, which may determine the need for operative intervention
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In General:
80-90% have significant associated intra-abdominal injuries. 50-90% will present with shock in the emergency department. 25-30% of diaphragmatic injuries will be isolated injuries.
Abdominal Findings
Abdominal distention Scaphoid abdomendue to herniation of abdominal contents into the thoracic cavity Abdominal tendernessmay be mild to diffuse peritonitis
Thoracic/Respiratory Findings
Dyspnea, orthopnea Decreased breath sounds Associated hemopneumothorax Bowel sounds in the thorax Respiratory distress
Cardiac Findings
Tamponade Cardiopulmonary compromise/shock
Radiographic Findings
Preoperative diagnosis of blunt diaphragm rupture can be suspected or diagnosed by the initial chest x-ray.
Plain Radiographs of the Chest

Normal CXR Obscured diaphragm border Irregular contour of the diaphragm Hemopneumothorax Elevated hemidiaphragm (Fig. 22.1) Air bubble, air-fluid level, or mass above the diaphragm Nasogastric tube above the level of the diaphragm
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Fig. 22.1. Elevation of the left hemidiaphragm due to a penetrating injury. Only about 14% of patients with an elevated diaphragm will have a diaphragmatic injury.
A normal chest x-ray does not exclude a diaphragmatic injury. Except for those findings that demonstrate abdominal contents within the thoracic cavity, many of these findings are nonspecific. Contrast studies may be used to diagnose diaphragmatic herniation of hollow viscera: Upper gastrointestinal studies Barium enema
Computerized Tomography
May allow visualization of diaphragmatic hernias (Fig. 22.2) Diaphragm lacerations or perforations not associated with intestinal herniation will not be visualized by CT scans.
Diagnostic Peritoneal Lavage

Diagnostic peritoneal lavage provides a nonoperative, fairly sensitive, yet nonspecific method for detecting diaphragm lacerations. The only finding consistent with a diaphragmatic injury is if lavage fluid is noted in the thoracic cavity or exits through the thoracostomy tube. Small defects in the diaphragm may be associated with little or no bleeding Red blood cell counts for a positive lavage vary from 5,000-100,000 cells/mm3 The sensitivity of DPL improves with lower RBC counts.
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Fig. 22.2. CT scan demonstrates herniation of the stomach within the left chest.
Diaphragmatic injuries may be associated with 05,000 RBC/mm3, and missed by DPL.
Isolated Diaphragmatic Injuries

2530% of patients with diaphragmatic injuries due to penetrating trauma will be completely asymptomaticNo abdominal tenderness and a normal CXR. This group represents the population at highest risk of missed injuries during the acute phase and developing delayed complications. A high index of suspicion must be maintained and aggressive evaluation pursued in this patient population.
DiagnosisChronic Diaphragmatic Hernias

May present years after the initial injury Are associated with a high incidence of complications
Due to the nonspecific nature of the complaints and a remote history of trauma which is often forgotten, or felt to be insignificant, the diagnosis of a chronic diaphragmatic hernia is delayed or not entertained. Many of the clinical and radiographic findings are similar to those for acute herniation.
Abdominal Symptoms
Nonspecific abdominal pain Gastrointestinal obstruction Abdominal sepsis
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Thoracic/Respiratory Symptoms
Chronic cough Respiratory distress Tympany to percussion Bowel sounds in the chest
Radiographic Findings
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Pathognomonic findings include: Air-fluid levels, gastric or colonic markings in the chest (Fig. 22.3) A coiled nasogastric tube above the diaphragm (Fig. 22.4) Any other nonspecific findings such as a pleural effusion, atelectasis, infiltrate may be present Contrast studies and CT scans are best suited to aid in the diagnosis of chronic diaphragmatic herniation (Fig. 22.2).
Surgical Pathology
Blunt rupture of the diaphragm is typically 7-10 cm in length. Herniation is most likely to occur immediately or soon after injury. Penetrating injuries are typically 2-4 cm in length. These may go undetected during the acute phase. These undetected small lacerations are more commonly associated with delayed herniation years after initial injury
Operative Evaluation
Due to the unreliability of physical exam and radiographic findings the only method currently available to definitively diagnosis a diaphragmatic injury in the acute setting is by direct visualization. This can be done with laparotomy, laparoscopy, or thoracoscopy. Asymptomatic patients with penetrating injuries to the thoracoabdominal region should be aggressively evaluated. Some authors have suggested mandatory laparotomy to evaluate high-risk patients suspected of having a diaphragmatic injury. In the asymptomatic patient this policy is associated with a high negative laparotomy rate, greater than 75% There is a significant morbidity and mortality associated with negative laparotomy Minimally invasive surgical techniques allow for a thorough visualization of the diaphragm without prolonged hospitalization and avoid the high complication rate associated with a negative laparotomy. In addition, isolated diaphragmatic injuries can be repaired with these techniques. In the absence of any indication other than the suspicion of a diaphragmatic injury currently we use laparoscopy to evaluate high-risk patients. High-risk patients are defined as patients who are hemodynamically stable without abdominal tenderness with penetrating injuries to either the: left thoracoabdominal region, or (Fig. 22.5) anterior portion of the right lower thorax
Laparoscopic Evaluation of Asymptomatic Patients Following Penetrating Injuries

All patients are admitted for observation and are monitored for evidence of ongoing bleeding or the development of abdominal tenderness. This is for a minimal period of 6 hours (Fig. 22.6).
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Fig. 22.3. Plain CXR showing a chronic diaphragmatic hernia with the stomach noted in the left chest.
Fig. 22.4. Diaphragmatic hernia with the nasogastric tube coiled in the stomach above the level of the left hemidiaphragm.
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Fig. 22.5. Benign appearing stab wound to the left lower chest in stable patient. Had laparoscopy not been performed an injury to the diaphragm would have been missed.
If the patient develops significant abdominal tenderness or demonstrates ongoing bleeding, a laparotomy is performed emergently. Radiographic evaluation of the chest is performed with a delayed CXR, if necessary, prior to performing laparoscopy. If a hemopneumothorax develops, a thoracostomy tube is placed prior to performing laparoscopy. If a diaphragmatic injury is identified during laparoscopy (Fig. 22.7) and the patient was asymptomatic during the observation period, we feel further exploration of the abdomen is not necessary and the defect is closed with either laparoscopic suturing or stapling. If there is suspicion of a hollow viscus injury, further laparoscopic exploration by mobilization of the colon and stomach will be done. If any uncertainty remains, a laparotomy will be performed. Some surgeons prefer thoracoscopy to evaluate the diaphragm. This is an acceptable technique and has both advantages and disadvantages when compared to laparoscopy. (See Chapter on Minimal Invasive Surgery in Trauma) Should the surgeon feel that peritoneal penetration or a diaphragmatic defect is an indication for laparotomy, or that a diaphragm injury should be repaired by open techniques, the six-hour observation period may be shortened or omitted. (For further discussion of the techniques, complications and details please refer to chapter on Minimally Invasive Surgery in Trauma.)
Operative Evaluation of Blunt Injuries

If blunt rupture of the diaphragm is still suspected, operative evaluation should be performed preferably by laparoscopy, yet some surgeons may choose to perform a celiotomy or thoracoscopy.
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Fig. 22.6. Algorithm for evaluation of penetrating thoracoabdominal injuries.
Should only be performed in hemodynamically stable patients Minimally invasive procedures can avoid a negative laparotomy
Conditions which May Mimic a Blunt Diaphragmatic Hernia

Diaphragm eventration (Fig. 22.8) Phrenic nerve paralysis (Fig. 22.9)
Operative ManagementAcute Injuries

Acute injuries are most commonly approached through an abdominal incision due to the need to evaluate for associated injuries. During any laparotomy for trauma a thorough evaluation of each leaflet is mandatory. Once identified an Alliss or Babcock clamp can be placed on the edges of the injury. This allows mobilization of the injury toward the surgeon and stabilizes the diaphragm during the repair. Most acute injuries can be repaired primarily. Nonabsorbable sutures should be used. These should be placed in an interrupted fashion.
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Fig. 22.7. Appearance of diaphragmatic injury seen during laparoscopy.
Either simple, horizontal mattress, or figure-of-eight suturing techniques can be used. A thoracostomy tube is routinely placed to allow re-expansion of the lung and evacuate any residual hemothorax. These same principals apply whether the repair is performed during a laparotomy or laproscopically. Laparoscopic staples have been used in some instances. Experimental evidence in an animal model has shown no difference in the healing of the diaphragm compared to suturing, open or laparoscopic.
Operative RepairChronic Hernia

Either a thoracotomy or laparotomy may be used for repair of a chronic diaphragmatic hernia. Most authors state that a thoracotomy is required to allow lysis of adhesions between the bowel and the chest wall or lung. Abdominal exploration allows evaluation of the herniated viscus following reduction and an opportunity to assess viability and the need for resection. Resection of nonviable bowel is best performed in the abdomen after closure of the defect, preventing contamination of the thoracic cavity. Occasionally enlargement of the defect is required to allow reduction of herniated viscera. Most chronic defects can be closed primarily. If necessary a prosthetic patch can be used to close the defect if tissue loss is present. Laparoscopy and thoracoscopy can be used to diagnosis and repair chronic diaphragmatic hernias. The same principles of open reduction and repair apply when using these techniques.
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Fig. 22.8. Eventration of left hemidiaphragm.
Most Common Herniated Viscera

Omentum Stomach Colon Small bowel, spleen and liver are frequently found in the hernia
Prognosis and Outcome

Early morbidity and mortality of acute injuries to the diaphragm are due to associated injuries. Early diagnosis and treatment of diaphragmatic hernias has a better prognosis than do those that are diagnosed late, in the chronic stages. The morbidity and mortality of chronic diaphragmatic hernias is dependent upon the presence of bowel ischemia, necrosis, and sepsis.

Inadequate evaluation of the diaphragm during laparotomy Lack of clinical suspicion for an occult diaphragmatic injury during the acute phase following injury. Failure to evaluate these stable patients with laparoscopy. Failure to recognize delayed diaphragmatic hernia in patients with a previous history of penetrating thoracoabdominal trauma.
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Fig. 22.9. Phrenic nerve paralysis with the associated elevation of the left hemidiaphragm
References
1. 2. 3. 4. 5. Beal SL, McKennan M. Blunt diaphragm rupture. A morbid injury. Arch Surg 1988; 123:828-832. Demetriades D, Kakoyiannis S, Parehk D et al. Penetrating injuries to the diaphragm. Br J Surg 1988; 75:824-826. Feliciano DV, Cruse PA, Mattox KL et al. Delayed diagnosis of injuries to the diaphragm after penetrating wounds. J Trauma 1988; 28:1135-41. Murray JA, Demetriades D, Cornwell EE et al. Penetrating thoracoabdominal trauma: the incidence and clinical presentation of diaphragm injuries. J Trauma 1997; 43:624-626. Murray JA, Demetriades D, Asensio JA et al. Occult injuries to the diaphragm: Prospective evaluation of laparoscopy in penetrating injuries to the left lower chest. J Am Coll Surg 1998; 187:626-630.
Esophageal Injury
Juan A. Asensio and Esteban Gambaro Historical Perspective
The Edwin Smith Papyrus, written in Egypt between 4-5,000 years ago described amongst its 48 cases, the first reported penetrating wound of the esophagus.
Incidence
It is estimated that at best, busy urban trauma centers admit approximately five penetrating esophageal injuries yearly. Blunt esophageal injury from external trauma is even rarer, with 96 cases reported in the literature since 1900. It is estimated that blunt injuries have an incidence of 0.001%
Mechanism of Injury
Penetrating injuries are the most common causes of esophageal trauma. Blunt injury to the esophagus is quite rare. Other causes of esophageal injuries include spontaneous rupture or Boerhaves syndrome, perforations from benign and malignant disease such as achalasia and esophageal cancer, iatrogenic perforations due to endoscopy and balloon dilatations and perforations secondary to the ingestion of caustic agents. These injuries are caused by nonexternal causes of trauma and will not be covered any further.
Associated Injuries
The esophagus, by virtue of its anatomic proximity to other organs is rarely injured alone. Multiple associated injuries are the rule rather than the exception. There will be approximately two associated injuries per patient coupled with the presence of an esophageal injury. Cervical esophageal injuries are generally associated with injuries to the major blood vessels of the neck, trachea, cervical spine and spinal cord. Associated injuries occurring in conjunction with thoracic esophageal injuries include: major thoracic vascular, cardiac, pulmonary, bony thoracic structures such as ribs, thoracic spine and neurological injuries. Associated injuries occurring concomitantly with intraabdominal esophageal injuries include: gastric, hepatic, and major abdominal vascular injuries.

Cervical esophageal injuries are predominant57%.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A. Esteban Gambaro, University of Southern California, LAC+USC Medical Center, Los Angeles, California, U.S.A.
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The thoracic esophagus is injured in 30% of the cases. Abdominal esophageal injuries occur with a frequency of 17% and are the least common of all esophageal injuries. Combined thoracic and abdominal esophageal injuries occur with a frequency of 2%. In blunt trauma, 82% of injuries occur in the cervical esophagus.
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The diagnosis of esophageal injury requires a high index of suspicion. The esophagus tends to be a relatively silent organ, clinical presentation wise. Most of the clinical findings will usually be attributable to the large number of associated injuries present with esophageal injuries. Physical examination may be characterized by minimal findings. The classical symptoms attributed to esophageal injuries are: pain29%, dysphagia7% and odynophagia3%. They are not uniformly present. An associated pneumothorax or hemothorax is present in 20% of the cases. Subcutaneous emphysema occurs in 19% of the cases. Dysphagia, odynophagia and subcutaneous emphysema are much more prevalent in cervical esophageal injuries than in other anatomic locations of the esophagus. Thoracic esophageal injuries are generally silent. In rare occasions they may be diagnosed when a chest tube is inserted and particulate matter and/or food egress via the chest tube.
Investigations
Cervical esophageal injuries can be diagnosed with an esophagogram which is 80% reliable. Flexible endoscopy is of no use in the diagnosis of cervical esophageal injuries, whereas rigid esophagoscopy is of value, but requires that the patient be placed under general anesthesia. The combination of an esophagogram and rigid esophagoscopy has over 90% reliability in establishing the diagnosis of cervical esophageal injury. Esophagograms are virtually diagnostic for thoracic esophageal injuries. Flexible endoscopy has been reported to be a valuable adjunct in the diagnosis of thoracic esophageal injuries. The diagnosis of intraabdominal esophageal injuries is usually established intraoperatively.
Surgical Management
Neck injuries should be explored through the standard incision at the anterior border of the sternocleidomastoid muscle, extending from the mastoid process to the sternoclavicular junction. Immediate control of life threatening hemorrhage from associated vascular injuries is a must. A thorough and meticulous search to evaluate for the presence of an esophageal injury is then carried out. Thoracic injuries can be explored via the standard posterolateral thoracotomy incision provided that the patients hemodynamic status will allow sufficient time for positioning.
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Fig. 23.1. Esophagram showing a cervical esophageal injury. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
A right posterolateral thoracotomy will identify the vast majority of intrathoracic esophageal injuries, whereas a left posterolateral thoracotomy will identify the lowermost intrathoracic esophageal injuries. Abdominal injuries are approached via a midline incision. A meticulous search in the area of the gastroesophageal junction is a must to identify intraabdominal esophageal injuries. Insufflation of air, sterile saline, and methylene blue dye may identify an esophageal injury not easily seen. All esophageal injuries should be graded utilizing the American Association for the Surgery of TraumaOrgan Injury Scale for esophageal injury (AAST-OIS). Most esophageal injuries can be repaired primarily82%, with a meticulous double layer closure of absorbable and nonabsorbable sutures. Between 3%
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Fig. 23.2. Esophagram showing a mid-thoracic esophageal injury. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
Fig. 23.3. Neck exploration showing a lacerated cervical esophagus. Forceps point to the clearly visible nasogastric tube. An autogenous saphenous vein bypass has been used to repair the associated carotid artery injury. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
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and 4% of all esophageal injuries require resection and diversion or resection and anastomosis. Approximately 11% can be treated by drainage alone. All esophageal injuries should be drained with closed systems. The drains should not be placed in direct juxtaposition to the suture line to avoid esophageal fistula formation. A useful adjunct to the repair of esophageal injuries is the use of muscle or pleural flaps. Abdominal esophageal injuries generally require performing Nissen fundoplication to buttress the repair. In cases of an esophageal suture line dehiscence, generally no attempts at further repair will be successful although occasionally they may be attempted. Treatment will consist of wide drainage and more complex reconstructive procedures including esophagectomy with colonic or gastric interpositions or the use of very complex muscle flaps.
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Mortality
Esophageal injuries carry a significant mortality rate. The mortality rate from penetrating esophageal trauma is 15% and from blunt trauma 10%. Factors that increase mortality in esophageal injuries include delays in diagnosis and definitive surgical repair of greater than 8-16 hours. Mortality rates can triple in patients undergoing surgical procedures after 24 hours.
Morbidity
Esophageal injuries are associated with very high rates of morbidity. Esophageal related complications include: wound infections10%, empyema8%, mediastinitis6%, esophageal fistulas5% and tracheo-esophageal fistulas1%.
References
1. 2. 3. 4. 5. Asensio JA, Berne J, Demetriades D et al. Penetrating esophageal injuries. Time interval of safety for preoperative evaluationhow long is safe: J Trauma 1997; 43:319-324. Asensio JA, Chahwan S, Mackersie R et al. Penetrating esophageal injuries: Multicenter study of the American association for the surgery of trauma: J Trauma (abstract) 1999; 47:207. Cornwell EE, Kennedy F, Ayad IA et al. Transmediastinal gunshot wounds A reconsideration of the role of aortography: Arch Surg 1996; 131:949-953. Weigelt JA. Diagnosis of penetrating cervical esophageal injuries. Am J Surg 1987; 154:619-622. Winter RP, Weigelt JA. Cervical esophageal trauma. Arch Surg 1990; 125:8:49-851.
CHAPTER 24
CT Scan in Chest Trauma

Alison Wilcox and Randall Radin Lung
Posttraumatic lung disease is often underestimated on conventional radiographs of the chest. CT scan is very sensitive in identifying and characterizing lung injury.
Contusion
Usually seen in the setting of blunt trauma, defined as an infiltrate seen almost immediately following trauma.
Laceration or Pneumatocele (Figs. 24.1-24.3)

May be seen in both blunt and penetrating trauma. Defined as an air lucency surrounded by consolidated lung, which represents intraalveolar hemorrhage. Lacerations may extend to the pleural surface and result in pneumothorax.
Aspiration
Blood, from either the mouth or nasopharnyx, or gastric contents, usually in the dependent locations of posterior segments of the upper lobes or superior segments of the lower lobes. If aspiration occurred while the patient was upright, the infiltrate is typically in the basal segments. The type of aspiration is evident by its clinical course as gastric contents tend to produce a flagrant inflammatory response whereas the bland blood aspiration tends to resolve over several days.
Pleura Pneumothorax (Figs. 24.4-24.6)

Easily identifiable on CT. Even small pneumothoraces not identifiable on conventional chest radiographs may be seen, usually anteriorly on the CT.
Hemothorax
CT may identify the high attenuation fluid in the pleural space as blood. If a significant amount of blood is present in the absence of parenchymal findings, a vascular injury, from either great vessels or intercostal vessels, may be present.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Alison Wilcox, Department of Radiology, University of Southern California, Los Angeles, California, U.S.A. Randall Radin, Department of Radiology, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 24.1. Displaced posterior right rib fracture with associated bibasilar lung consolidation, consistent with pulmonary contusion and hemorrhage. A small right pleural fluid collection is also present, probably representing a hemothorax in the setting of trauma.
Fig. 24.2. Figure 24.1 in lung windows demonstrates gas lucencies within the pulmonary hemorrhage, consistent with pulmonary lacerations.
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Fig. 24.3. Posterior left rib fracture and associated pulmonary contusion. Within the consolidation is an air-fluid level, consistent with a pulmonary laceration. A small amount of chest wall emphysema is also present.
Fig. 24.4. A large right pneumothorax (open white arrow) with mediastinum shift to the left, indicating that the pneumothorax is under tension. A subtle posterior right rib fracture is also seen.
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Fig. 24.5. A tension pneumothorax on the left with shift of the mediastinum to the right. There is clear demarcation between collapsed, consolidated lung and gasfilled pleural space. Fig. 24.6. Scout image from figure 24.5 demonstrates the large lucency in the left lower chest, consistent with a pneumothorax in a supine patient. The mediastinal shift is again seen.
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Chest Wall Rib Fractures

CT may occasionally identify rib fractures that are missed on conventional radiographs, usually in a lateral or inferior location. Conventional films remain the mainstay of their discovery
Clavicle and Scapula Fractures (Figs. 24.7, 24.8)

May be identified on CT although usually more commonly seen on conventional radiographs.
Sternal Fractures (Figs. 24.9, 24.10)
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May be the source of significant mediastinal hemorrhage. They are difficult to identify on conventional films even with sternal views. CT, particularly with lung windows, often reveals the sternal fracture, which is usually transverse.
Vertebral Fractures (Fig. 24.11)

CT is the study of choice to evaluate spinal fractures. Often unsuspected fractures are identified on CT with associated prevertebral hemorrhage.
Aorta and Great Vessels

Rupture of the aorta causes approximately 16% of all motor vehicle accident fatalities. Most patients with aortic injury do not survive the initial injury and are not imaged. The well-known signs of great vessel injury on conventional radiographs include apical cap; deviation of trachea, endotracheal tube, or nasogastric tube; indistinct aortic knob or descending aorta, and widening of the superior mediastinum. The last finding is pathologic only when the patient is imaged in the upright, full-inspiratory position. As this is often not possible in critically ill patients, mediastinal widening is often over-interpreted. Although the use of CT to diagnose great vessel injury is still somewhat controversial, many studies have demonstrated the high specificity and sensitivity of its use.
Indirect Signs
Mediastinal Hemorrhage
May be associated with sternal or vertebral fractures. Usually venous in origin, but is worrisome if intimately associated with aorta or great vessels, i.e., obliteration of normal fat planes adjacent to vascular structures.
Direct Signs
Aortic Contour
Focal contour abnormality, usually seen at the level of the left pulmonary artery at the level of the ligamentum arteriosum.
Intimal Flap and/or Associated Thrombus

Linear defect or thrombus within aortic lumen, again usually seen at the level of the ductus.
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Fig. 24.7. Right clavicle fracture
Fig. 24.8. Right scapula fracture with associated surrounding hematoma.
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Fig. 24.9. Four consecutive images from a CT scan demonstrate an anterior mediastinal hematoma with a sternal fracture (white arrow). Although mediastinal hemorrhage may herald great vessel injury, when the hematoma is intimately associated with a fracture, the fracture is the likely source. Since the anterior clear space should contain only fat in the adult patient, any increased attenuation of mediastinal fat should indicate blood.
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Pseudoaneursym (Figs. 24.12, 24.13)

Larger contour abnormality, which is usually focal (to distinguish it from a true aneurysm which is usually diffuse). The intimal disruption may or may not be visible.
Aortic Transection (Fig. 24.14)

Discontinuity of ascending and descending aorta, usually with large associated hematoma and/or pseudoaneursym formation
Aortic Dissection
Intimal flap extending for a distance, may involve either the ascending or descending aorta, though in traumatic dissection the flap usually begins at the ductus. Aortic dissection is more common when preexisting vascular disease is present.
Contrast Extravasation (Fig. 24.15)

Rarely identified as patients are usually too unstable to be evaluated with CT.
Bronchus
Usually unrecognized on initial imaging, with frequent delayed diagnosis. Persistent or increasing subcutaneous emphysema should raise the suspicion of bronchial injury. Persistent pneumothorax results from rupture of the mediastinal pleura or injury to the right mainstem or distal left main bronchus. More proximal bronchial or tracheal injuries result in pneumomediastinum immediately postinjury.
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Fig. 24.10. Another patient with a sternal fracture and small associated mediastinal hematoma. The sternum often fractures in the transverse plane and subsequently may be missed on CT if the image is not through the plane of the fracture. Often the clue to the sternal fracture is the double density indicating a displaced fracture and overlapping bone.
Fallenlung signA conventional radiographic description of peripheral rather than central lung collapse. Though it is rarely identified, it indicates transection of the mainstem bronchus and rupture of the normal hilar attachments. Endotracheal tube with its tip projecting beyond the expected tracheobronchial tree indicates that the tube has traversed a tracheal injury. Similarly, expansion of the tracheal cuff outside the expected confines of the tracheal lumen indicate tracheal injury.
Diaphragm
The incidence of traumatic rupture of the diaphragm is reported as ranging from 1-8%. Although many of these patients have abnormal conventional radiographs, the findings are not specific for diaphragmatic injury. There is often a delay in diagnosis, or the injury may be found at diagnostic laparoscopy or incidentally during laparotomy. Israel et al used thin-section helical CT with coronal and sagittal reformation to detect diaphragmatic injury in the swine. However, thin-section CT of the chest in all trauma patients is not routine. CT is therefore often suboptimal. MRI may be helpful in stable patients or in cases where CT is equivocal. Previously acquired eventrations and asymmetric diaphragm positioning may mimic pathology (Fig. 24.16). Collar-signA sensitive and specific sign of diaphragmatic injury demonstrating, in coronal or sagittal images, the herniation of abdominal fat or con-
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Fig. 24.11. Mediastinal windows of a trauma patient demonstrating prevertebral hematoma and an associated comminuted vertebral fracture. Since the blood is posterior, this should indicate possible spine pathology, even if a fracture is not seen on the thick section chest CT.
Fig. 24.12. Increased attenuation of the mediastinal fat intimately associated with the aortic arch indicates possible aortic injury. In this case there is an obvious medial opacified outpouching of the proximal descending aorta (white arrow), which is diagnostic of a traumatic pseudoaneurysm.
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Fig. 24.13. Confirmatory aortogram demonstrates the contour defect at the level of the ductus (white arrow), diagnostic of a traumatic pseudoaneursym.
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Fig. 24.14. Complete disruption of the normal appearance of the descending aorta. This indicates aortic transection with active extravasation. This patient went directly to the operating room without confirmatory aortogram. Notice also the bilateral pleural fluid collections, consistent with bilateral hemothoraces.
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Fig. 24.15. CT demonstrates active extravasation from a transected aorta. Note the extravasated blood makes delineation of the aorta impossible.
Fig. 24.16. Bowel and omental fat lateral to and superior to the stomach. In addition there is an abnormal contour of what should be the diaphragm posteriorly (white arrow), indicating rupture of the diaphragm with herniation of abdominal contents.
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tents above the diaphragm with a constriction at the level of the diaphragm forming the so-called collar.
Esophagus
Usually seen in penetrating trauma but may occur in blunt chest trauma. Pneumomediastinum is often seen, although the source may not be identified. Extraluminal gas adjacent to the site of injury may lead to the suspicion of injury to the esophagus (Fig. 24.17). Pleural effusion is more common on the left side as a result of esophageal injury. This is often accompanied by left lower lobe atelectasis. V-sign of NaclerioA sign described on conventional radiographs of a small crescent of gas forming a V shape between the descending aorta and the left hemidiaphragm seen with traumatic esophageal rupture (usually secondary to prolonged, violent vomiting).
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Heart
Cardiac contusion is the most common cardiac injury. This is diagnosed with cardiac enzymes and EKG changes. CT scanning is not useful in diagnosis though it may diagnose ancillary findings predominately affecting the pericardium. HemopericardiumHigh attenuation fluid representing blood may fill the pericardium and may cause cardiac tamponade (Fig. 24.18). PneumopericardiumThis is usually associated with pneumomediastinum but may also cause tamponade.
Fig. 24.17. A gunshot wound to the neck, which has fractured the vertebral body. Note the extraluminal gas posterior to the thyroid gland. The trachea appears intact but the esophagus is not well visualized. This patient had rupture of the esophagus confirmed by esophagography.
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Fig. 24.18. High-attenuation fluid surrounding the heart indicates hemopericardium.
Tubes and Lines

CT may correctly identify improper line placement. All tubes and lines should be identified on every CT scan. Nasogastric tubeMay be coiled inappropriately or in the distal esophagus. Inadvertent placement of the NGT in the mainstem bronchus is easily identified (Figs. 24.19-24.21). Endotracheal tubeThe most common inadvertent placement is into the right mainstem bronchus (Figs. 24.22). Subclavian venous lines. May cross the midline into the opposite subclavian vein. May be placed in the left superior intercostal vein, usually from a left subclavian vein approach. May be placed intraarterially (Figs. 24.23 and 24.24). Chest tubesIf not obviously in a pleural location, may be intraparenchymal or within a fissure. May also be placed in the subcutaneous tissues, which may not be recognized on a conventional frontal radiograph (Figs. 25 and 26).
References
1. 2. 3. 4. 5. Wagner RB, Crawford WO, Schimpf PP. Classification of parenchymal injuries of the lung. Radiology 1988; 167:77-82. Mirvis SF, Shanmuganathan K, Miller BH et al. Traumatic aortic injury: Diagnosis with contrast-enhanced thoracic CTFive-year experience at a major trauma center. Radiology 1996; 200:413-422. Murray JG, Caoili E, Gruden JF et al. Acute rupture of the diaphragm due to blunt trauma: Diagnostic sensitivity and specificity of CT. AJR 1996; 166:10351039. Israel RS, McDaniel PA, Primack SL et al. Diagnosis of diaphragmatic trauma with helical CT in a swine model. AJR 1996; 167:637-641. Unger JM, Schuchmann GG, Grossman JE et al. Tears of the trachea and main bronchi caused by blunt trauma: Radiologic findings. AJR 1989; 153:1175-1180.
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Fig. 24.19. Scout image from a CT scan demonstrates a nasogastric tube extending into the left lower lobe bronchus.
Fig. 24.20. CT scan from Figure 24.19 demonstrates the small caliber of the nasogastric tube within the trachea.
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Fig. 24.21. CT scan from figure 24.19 demonstrates the small caliber of the nasogastric tube within the left main bronchus.
Fig. 24.22. Endotracheal tube in the right mainstem bronchus, the most common place for a misplaced endotracheal tube. There is resulting left lung collapse with a left chest tube and left rib fracture. The nasogastric tube is in the esophagus.
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Fig. 24.23. A left central line, which appears to be in the left subclavian artery. (white arrow)
Fig. 24.24. A more caudal image of figure 24.25 demonstrates the venous line coiled in the aorta.
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Fig. 24.25. An intrapulmonary chest tube with surrounding or resulting pulmonary hemorrhage . Chest wall emphysema and a posterior pulmonary laceration are also present.
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Fig. 24.26. An improperly position chest tube within the chest wall, anterior to the scapula. This would probably be missed on the frontal view of the chest.
Emergency Department Thoracotomy

Juan A. Asensio and Kuen-Jang Tsai Introduction
Indications for the use of the Emergency Department thoracotomy that appear in the literature range from vague to quite specific. It has been used in a variety of settings including penetrating and blunt thoracic and/or thoracoabdominal injuries, cardiac and exsanguinating abdominal or extremity vascular injuries.
Historic Perspective
Schiff in 1874 promoted the concept of open cardiac massage. Igelsbrud in 1901 reported the first successful resuscitation of a posttraumatic cardiac arrest patient with open massage. In 1956 Zolls introduced the concept of external defibrillation. In 1960 Kouwenhoven introduced the concept of closed cardiopulmonary resuscitation. Beall in 1961 first proposed that patients experiencing cessation of cardiac action undergo immediate thoracotomy and open cardiac massage, whether in the emergency, operating, recovery room or ward. He also advocated the use of immediate cardiorrhaphy in the emergency room.
Physiology Objectives
Resuscitation of agonal patients with penetrating cardiothoracic injuries. Evacuation of pericardial tamponade. Control of thoracic hemorrhage. Prevention of air embolism. To perform open cardiopulmonary resuscitation which can produce up to 60% of the normal ejection fraction. Repair cardiac injuries. To cross clamp the pulmonary hilum. To cross clamp the descending thoracic aorta.
Effects of Thoracic Aortic Cross ClampingPositive Effects

Preservation and redistribution of remaining blood volume. Improvement of coronary/carotid arterial perfusion. Reduction of sub-diaphragmatic blood loss.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A. Kuen-Jang Tsai, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 25.1. Left anterolateral thoracotomy incision in the 5th intercostal space. Reprinted with permission from Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
Increases the left ventricular stroke work index (LVSWI). Increases in myocardial contractility.
Effects of Thoracic Aortic Cross ClampingNegative Affects

Decreases blood flow to the abdominal viscera to approximately 10%. Decreases renal perfusion to approximately 10%. Decreases blood flow to the spinal cord to approximately 10%. Induces anaerobic metabolism. Induces hypoxia/lactic acidosis. Imposes a tremendous afterload onto the left ventricle (LV).
Effects of Thoracic Aortic Cross ClampingUnknowns

Length of safe cross clamp time. Incidence of reperfusion injury
Indications
Indications for the performance of Emergency Department thoracotomy can be subdivided into three categories: accepted, selective, and rare. Accepted Indications Include:
- Patients sustaining penetrating cardiac injuries that arrive in trauma centers after a short scene/transport time with witnessed and/or objectively measured physiological parameters (pupillary reactivity, spontaneous ventilation even if agonal, presence of a carotid pulse, some measurable blood pressure, extremity movement).
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Fig. 25.2. Depicts the left chest open with a Finochietto retractor. There is a pericardial tamponade compressing the heart. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
Selective Indications:
- Emergency Department thoracotomy should be performed selectively in patients sustaining penetrating noncardiac thoracic injuries due to its very low survival rate. Since it is difficult to ascertain whether injuries are noncardiac thoracic versus cardiac this procedure may be employed to establish a diagnosis. - Emergency Department thoracotomy should be performed selectively in patients sustaining exsanguinating abdominal vascular injuries due to its very low survival rate. Meticulous selection of patients should be exercised. This procedure should be used as an adjunct to definitive repair of the abdominal vascular injury.
Rare Indications:
- Emergency Department thoracotomy should be performed rarely in patients sustaining cardiopulmonary arrest secondary to blunt trauma due to its very low survival rate and poor neurological outcomes. Extreme caution should be exercised in selecting patients for this procedure. It should be strictly limited to those that arrive with vital signs at the trauma center and experience a witnessed cardiopulmonary arrest. Most authors would caution against this indication.
Technique
Emergency Department thoracotomy should be performed simultaneously with the initial assessment, evaluation and resuscitation, using the Advanced Trauma Life Support (ATLS) protocols of the American College of Surgeons (ACS). Immediate endotracheal intubation coupled with immediate venous access and the simultaneous use of rapid infusion techniques complements the resuscitative process.
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Fig. 25.3. Pericardium is grasped between 2 Allis clamps and a sharp incision is made anterior to the phrenic nerve. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
This technique should only be performed by surgeons that have had appropriate training in the performance of this procedure. The left arm is elevated and the entire thorax is prepped rapidly with an antiseptic solution. A left anterolateral thoracotomy commencing at the lateral border of the left sternocostal junction and inferior to the nipple is carried out and extended laterally to the latissimus dorsi. In females, the breast is retracted cephalad.
- The incision is carried rapidly through skin, subcutaneous tissue and the pectoralis major and serratus anterior muscles until the intercostal muscles are reached. - The three layers of these interdigitated muscles are sharply transected with scissors. The pleura is then opened. - Occasionally, the left fourth and fifth costochondral cartilages are transected to provide greater exposure. - A Finochietto retractor is then placed to separate the ribs. At this time the trauma surgeons should evaluate the extent of hemorrhage present within the left hemithoracic cavity. An exsanguinating hemorrhage with almost complete loss of the patients intravascular volume is a reliable indicator of poor outcome.
The left lung is then elevated medially and the descending thoracic aorta is located immediately as it enters the abdomen via the aortic hiatus. The aorta should be palpated to assess the status of the remaining blood volume. The descending thoracic aorta can be temporarily occluded against the bodies of the thoracic vertebrae. Prior to cross clamping the descending thoracic aorta, a combination of sharp and blunt dissection commencing at both the superior and inferior borders of the aorta is performed, so that the aorta may be encircled between the thumb and index fingers.
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Fig. 25.4. The descending Thoracic aorta is then sharply dissected. Note the position of the nasogastric tube, as the esophagus is superior to the aorta. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
- Inexperienced surgeons usually commit the error of clamping the esophagus, which is located superior to the aorta. A nasogastric tube previously placed can serve as a guide in distinguishing the esophagus from the often somewhat empty thoracic aorta. - A Crafoord-DeBakey aortic cross clamp should then be placed to occlude the aorta.
If a cardiac injury is present, the pericardium is then opened longitudinally above the phrenic nerve, pericardial clot and blood are evacuated and the cardiac injury repaired. If a pulmonary hilar hematoma or active hemorrhage are present, cross clamping of the pulmonary hilum with a Crafoord-DeBakey cross clamp may be necessary.
- If a pulmonary parenchymal laceration is detected it should be clamped with Duval clamps.
If associated pathology is then encountered in the contralateral hemithoracic cavity, the sternum is transected sharply and the left anterolateral thoracotomy is then converted to a bilateral anterolateral thoracotomy.
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Fig. 25.5. The descending thoracic aorta is bluntly dissected and a Crafoord-DeBakey cross clamp is applied. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
Ligation of one or two internal mammary arteries may be necessary if the left anterolateral thoracotomy has been extended to the right hemithoracic cavity. Aggressive ongoing resuscitation is needed with warm pressure driven fluid via rapid infusers while this procedure is ongoing.
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Fig. 25.7. Open cardiopulmonary resuscitation after ventricular cardiorrhaphy. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
Fig. 25.8. Internal defibrillation. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
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Fig. 25.9. Cross-clamping of the pulmonary hilum. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
Defibrillation with internal paddles may be needed delivering between 10-50 joules. Epinephrine may also be administrated into either the right or left ventricle or systemically. If air embolism is suspected, the ventricles will need to be aspirated. Occasionally the use of a temporary pacemaker is needed. If the patient is successfully resuscitated, immediate and expedient transportation to the OR is mandated.
Results
The literature abounds with retrospective series describing the use of emergency department thoracotomy. Great difficulties, however, exist in evaluating the results of these series.
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In the review of over 7,335 patients undergoing emergency department thoracotomy there were 551 survivors. The overall survival rate was 8%. The survivor rate for penetrating injuries was 10% and for blunt 1.5%. In two prospective studies dealing with penetrating cardiac injuries the survival rate in patients undergoing Emergency Department thoracotomy was 14-16%. In a prospective two year series reporting 215 patients subjected to Emergency Department thoracotomy, the overall survival rate was 10%. In this series the only survivors experienced penetrating cardiac injuries. None of the patients subjected to Emergency Department thoracotomy for blunt cardiopulmonary arrest, noncardiac thoracic injuries or exsanguinating abdominal vascular injuries survived. In a review of 142 pediatric patients undergoing emergency department thoracotomy, there were 9 survivors for 6% overall survival rate. When stratified by mechanism of injury, pediatric patients undergoing Emergency Department thoracotomy for penetrating injuries had a survival rate of 12% versus a 2% survival rate for blunt cardiopulmonary arrest.
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References
1. Asensio JA, Hanpeter D, Demetriades D et al. The futility of liberal utilization of emergency department thoracotomy. A prospective study. Proceedings of the American Association for the Surgery of Trauma 58th Annual Meeting, Baltimore, Maryland 1998; 20. Asensio JA, Hanpeter D, Gomez H et al. Exsanguination. In: Textbook of Critical Care. 4th Ed. Shoemaker W, Greenvik A, Ayres SM et al, eds. Philadelphia, PA: W.B. Saunders Co, Chapter 4:37-47. Asensio JA, Hanpeter D, Gomez H et al. Thoracic injuries In: Shoemaker W, Greenvik A, Ayres SM et al, eds. Textbook of Critical Care, 4th Ed Philadelphia, PA: W.B. Saunders Co. Chapter 30:337-348. Asensio JA, Murray J, Demetriades D et al. Penetrating cardiac injuries: Prospective one-year preliminary report; An analysis of various predicting outcome. J Amer Coll Surg 1998; 186(1):24-33. Asensio JA, Berne JD, Demetriades D et al. One hundred and five penetrating cardiac injuries. A two-year prospective evaluation. J Trauma 1998; 44(6): 1073-1083.
2. 3. 4. 5.
ABDOMEN
Evaluation of Blunt Abdominal Trauma

Michael Sugrue Historical Background
In Ancient Egyptian times, discussion of abdominal injury has been vaguely reported in the Edward Smith Surgical Papyrus and the Hearst Papyrus 15003000 BC. Progressing through the centuries Hippocrates and Claudeus Galinus made brief references to abdominal evaluation. It is only in the last 30 years that significant advances have been made. The evaluation of blunt injury to the abdomen improved significantly with the introduction of CT scanning and F.A.S.T. Before proceeding however, remember the Key Challenges:
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience Michael Sugrue, Department of Trauma, Liverpool Hospital, Liverpool, Australia
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The Patterns of Blunt Abdominal Injury

Specific injury patterns may be seen with the use of seat belts, handlebar injury, sporting injuries. In general the liver and spleen are most commonly injured in blunt abdominal trauma, Table 26.1. Recognition of the potential for associated injury is crucial in the evaluation of the blunt abdominal trauma patient. For example in the presence of an apparently isolated splenic injury, 10% will have associated injury involving either the diaphragm or small bowel. In the presence of minor splenic injuries however such as a Grade 1 injury, one could anticipate less than 4% having diaphragmatic or bowel injury. Abdominal injury sustained during football or other contact sports may give rise to isolated splenic or renal injuries. Specific injury patterns are seen in bicycle handlebar injuries (Fig. 26.1) with traumatic pancreatic injury and bowel perforation significantly more common. Often handle bar injuries transmit such force as to resemble a penetrating injury. Falls from heights are associated with intra-abdominal injuries in less than 10% of cases with a prevalence of solid organ lacerations, but occasional bowel and bladder ruptures can occur. In the evaluation of patients falling from heights and jumpers, remember retroperitoneal injuries are a significant source of hemorrhage. The classic injury patterns relating to common mechanism are as follows:
Seat belt Side impact Sporting injury Assault with fist Horse kick

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Lap and sash Lap belt only
Jejunal perforation Duodenal or pancreatic injury Hepatic/splenic injury Splenic laceration Pancreatic injury Small bowel perforation
History of Injury
In the evaluation of blunt abdominal trauma (BAT), a detailed accurate history is essential to ensure maximum potential prediction of injuries sustained. In taking the history, use the MIST system:
Mechanism of injury Injury Signs and Treatment
Table 26.1. Typical pattern of intra-abdominal injury in blunt trauma

Organ Injury %
Spleen Liver Renal Small Bowel Diaphragm Bladder Colon Abdominal vessels Other
30 25 20 6 4 4 3 2 6
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Fig. 26.1. Handlebar injury with associated jeunal perforation.
This promotes identification of potential injuries and avoids the pitfalls of a missed injury, which can occur. Interaction between the trauma team and paramedics should be crisp and clear lasting 45-60 seconds. Additional information should be obtained from the patient in the form of AMPLE (Allergies, Medication, Past Illness, Last Meal, Events and Environment related to the injury). This AMPLE approach is advocated by ATLS for good reason. It is particularly important in the assessment of a hemodynamically unstable patient to know what medications they are receiving. Cardiac and other antihypertensive medication may alter a pulse rate or have an effect on blood pressure, making clinical examination difficult.
Clinical Examination
Accurate clinical examination is vital in BAT assessment. It is even more important than with penetrating trauma patients where decision making is often easier. While there are limitations of the abdominal examination in both the conscious and unconscious patient, it provides invaluable information in the early management allowing diagnosis and prioritization. Clinical examination has significant limitations, however, in the following circumstances:
Unconscious patient Intoxicated/drugged patient Uncooperative patient Seat belt mark Pregnant patient Spinal injury
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Clinical examination of the abdomen is unreliable in approximately 50% of blunt abdominal trauma patients. Apart from altered level of consciousness, the variable effect of hemoperitoneum and the variety of potential injury patterns with variable signs from hollow or solid viscus injury make interpretation difficult. The presence of distracting injuries in the multi-injured patient may pose an additional challenge. Strong suspicion of intra-abdominal injury should be considered in the following patients:
- presence of abdominal tenderness and rebound - rigid abdomen - patients with seatbelt marking
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In patients with seat belt marks (Fig. 26.2), determine if there is tenderness or guarding away from the seat belt mark. If there is, suspicion of intra-abdominal injury should be increased significantly. The importance of seat belt marking as a predictor of intra-abdominal injury varies from series to series. Velmahos1 has identified in motor vehicle victims that a seat belt mark is associated with an eight fold increase in intra-abdominal trauma compared to patients without seat belt mark, finding that 23% of patients suffered significant intraabdominal organ injury particularly mesenteric laceration, hepatic, duodenal and jejunal laceration (Fig. 26.3). Bowel sounds are important in blunt abdominal evaluation, with a reduction in bowel sounds commonly seen in patients with peritonism and peritonitis from small bowel injury.
Investigation
Plain X-rays and one shot IVP are of limited importance. A full blood count is useful as an elevated white cell count may help point towards a gastrointestinal perforation and liver function tests will obviously indicate an hepatic contusion. Hematuria is common after blunt renal injury. It is usually microscopic, which in asymptomatic patients does not usually require further evaluation. Macroscopic hematuria always needs investigation, usually indicating a major renal or bladder rupture. Further evaluation of renal pathology is best performed using a CT scan and bladder evaluation using a cystogram.
Tips and Pitfalls

Thirty percent of major renal injuries may exist with a normal urinalysis. There may be little correlation between the severity of renal injury and the presence of hematuria. Only 30% of patients with gross hematuria have serious renal injury. One percent of patients with microscopic hematuria have a significant renal injury. The choice of definitive investigation in BAT rests with diagnostic peritoneal lavage (DPL), FAST, CT scan and laparoscopy. The choice depends on three key factors: 1. Patients stability 2. Prediction of underlying organ injury 3. Experience and facilities of the trauma center
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Fig. 26.2. Seatbelt mark.
Fig. 26.3. Underlying bowel injury.
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Diagnostic Peritoneal Lavage (DPL)

In the presence of hemodynamic instability, a DPL or FAST are ideal in determining the presence of hemoperitoneum and the need for surgery. Remember in up to 50% of patients with suspected intra-abdominal injury who are hypotensive, their hypotension is due to a non-abdominal cause. Therefore rapid assessment of the abdomen is essential. A further key issue in the stable patient is whether one will adopt an operative or nooperative approach. If one is tending to a nonoperative approach, such as in a patient following contact sport injury with potential splenic injury, DPL is contraindicated as a positive result will increase the pressure for operative management, which in a stable patient is inappropriate. DPL has, in the past, been a gold standard for evaluation of hemoperitoneum. It is highly sensitive in detecting the presence of intraperitoneal blood. It has the disadvantage however of not predicting the need for laparotomy per se and will increase nontherapeutic laparotomy rate.
Problems with Diagnostic Peritoneal Lavage:
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Techniqueclosed technique, increased risk of bowel perforation Interpretation of DPL

- While over 50% of surgeons utilize bedside interpretation of DPL effluent, this is fraught with hazards. Ability to read print through IV tubing is an inaccurate art. The effluent should be sent for objective laboratory analysis. - The following constitute a positive DPL: Red cell count > 100,000/mm3 White cell count > 500/mm3 Alkaline phosphatase > 20 IU/L Amylase > 20 IU/L Aspiration of <10cc of frank blood - The use of Gram stains and detection of vegetable matter is not a particularly useful technique. Recently it has been suggested that quantitative white blood cell criteria for detection of intestinal injury, supplemented by an adjusted white cell count/red cell count ratio, will decrease nontherapeutic laparotomy rate associated with DPL. It is suggested that the white cell count to red cell count ratio of 150 or greater, indicates a gastrointestinal tract perforation requiring surgery. - Diagnostic peritoneal lavage has the following disadvantages: Oversensitivegiving rise to nontherapeutic laparotomies Does not provide organ specific diagnosis Misses retroperitoneal hematomas and hollow viscus perforations Invasive Painful in conscious patients. - Sequential DPL (Fig. 26.4) is very useful particularly in multisystem trauma patients undergoing multi-cavity surgery where the DPL catheter can be left in place and repeat diagnostic peritoneal lavage performed. Remember that 25-30 ml of blood in a patient with a normal hemoglobin will result in a red cell count of 100,000/mm3. - Special concerns have been raised in the past in performing DPL in pregnant, pediatric and in patients with pelvic fractures. FAST should be superior in pregnancy. In pediatric trauma, the problem with DPL is its over sensitivity and the tendency to lead to nontherapeutic laparotomies, particularly with solid organ
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Fig. 26.4. DPL catheter left in place.
injuries. In pelvic fractures, care must be exerted as false positive rates of up to 30% have been reported. Recent studies have discounted this. The reported high false positive rate in DPL in the presence of pelvic fractures has been attributed to many factors: Dissection of the retroperitoneal pelvic hematoma Direct placement of the catheter into the retroperitoneal hematoma Extravasation of blood from the retroperitoneal hematoma Time dependent diapedesis of red cells across the peritoneal cavity. cell count, alkaline phosphatase or amylase. It is particularly important to avoid a nontherapeutic laparotomy in patients with pelvic trauma.
Tips
Use an open technique via umbilical cord or linea alba (at the umbilicus), similar to the technique for open insertion of the laparoscopic insertions of umbilical posts. Wide bore DPL catheters and IV tubing will greatly speed up the process.2
CT Scanning
CT scanning of the abdomen in blunt trauma has become increasingly popular. It has the advantages of: Providing organ specific information Determining the presence of hemoperitoneum Providing a base line for further evaluation Providing additional information, such as occult pneumothorax It also has the following disadvantages: Time consuming
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Costly Unsuitable for unstable patients Requires accurate interpretation May be abused to place patient in holding pattern, while thinking of what to do with patient
Tips:
CT scanning requires careful protocols: removing the nasogastric tube in the esophagus, and elevate arms above head to reduce scatter administration of oral contrast (should be done in the resuscitation room) Specially timed studies may be required to look at arterial, venous and portal venous phases. This is particularly important in relation to identifying areas of hypoperfusion, identifying vascular injuries and blushes. Identification of a vascular blush on CT scan indicates the need for surgery or embolization, due to ongoing hemorrhage. It is particularly useful in assessing pancreatic injury (Fig. 26.5). CT scanning has an additional advantage of being able to provide a grade of organ injury for splenic, renal and hepatic injuries. Combination of organ injury grading and blood loss estimation will improve the prediction of requirement for surgery.3 In terms of grading of liver injuries, CT scanning often overemphasizes the grade of liver injury and often underestimates the amount of intraperitoneal bleeding. The identification of a vascular blush on CT scanning in liver, splenic or renal trauma indicates the presence of active bleeding and potential need for embolization or surgery. The use of oral contrast is becoming increasingly more controversial with the recent suggestion that addition of oral contrast does not improve outcome and may increase the risk of aspiration. Oral contrast however, does provide a nicer road map for the radiologist however, it may not increase the detection of gastrointestinal tract perforation. The signs of gastrointestinal tract perforation on CT scans include (Fig. 26.6):
free fluid in the absence of solid organ injury edema of the mesentery extravasation of contrast enhancement thickening and hematoma of the bowel wall free intraperitoneal gas.
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Free intraperitoneal gas in small quantities in the subdiaphragmatic areas can be difficult to interpret and great care must be taken to avoid undertaking a laparotomy on the basis of a small amount of free air.
F.A.S.T. (Focused Assessment with Sonography for Trauma)

Since 1980 there has been increasing use of sonography in BAT. Large series have established its validity in determining hemoperitoneum. FAST does not set out to determine organ specific injury. The particular advantage of FAST is that:
it is simple to perform takes an average 2-4 minutes can be performed at the end of the primary survey and repeated later as needed is noninvasive
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Fig. 26.5. Pancreatic injury clearly seen on CT.
Fig. 26.6. Signs of gastrointestinal tract perforation on CT scan.
FAST itself does not differentiate free fluid from intraperitoneal hemorrhage and care should be exerted in over-reliance on FAST, particularly in patients with potential small bowel perforation. In using FAST, it is important that the operator is credentialled. Random use of FAST will result in erroneous results leading to unfavorable evaluation of BAT patients.
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Credentialing should involve:

- formal training course - specific number of peer reviewed scans including a specific number of positive FASTs4
Tips and Pitfalls

Know your machine. Watch the use of gain as it may interfere with the interpretation of free fluid. The pericardial views are most troublesome. Perform FAST before insertion of urinary catheter. Surgical emphysema makes FAST impossible. Remember to re-evaluate the abdomen if in doubt or clinically indicated.
Laparoscopy in Trauma
Laparoscopy has been undertaken in the evaluation of BAT patients for over 40 years. Its only proven value is in the evaluation of suspected diaphragmatic trauma.
Timing of Investigations
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Prompt evaluation of blunt abdominal trauma will improve not just the management plan but patient outcome. A clear, rapid but thoughtful approach is required.
Tips:
If multiple investigations are to be done, an optimum sequence should be thought out. For example:
FAST (5 min) FAST (5 min)

DPL (20 min) CT (30 min)
DPL (1 hour)
Remember, most conscious patients will need only one evaluation. FAST should be undertaken as an adjunct to the primary survey, usually within 5-10 minutes of patient arrival. In the event of multiple procedures being undertaken, such as chest tube insertion, intubation, urinary catheterization, the team should be appropriately protected and lead-gowned to facilitate the rapid patient assessment.
Unstable Patients
The evaluation of the unstable patient with blunt abdominal trauma is a challenge requiring rapid decision making. The priority should be: A check of airway, breathing and disability to ensure hypotension is not due to non-circulatory cause. The next key question to determineIs there intraperitoneal blood? A temptation to perform a laparotomy as an evaluation in the unstable trauma patient should be carefully evaluated as up to 50% of patients who are hypotensive with suspected intra-abdominal injuries will have a negative or nontherapeutic laparotomy. The options in the unstable patient include diagnostic peritoneal lavage or FAST. Laparoscopy and CT scanning have no role to play in the abdominal assessment of the unstable trauma patient. If in doubt and you have limited resources, a diagnostic laparotomy may be life saving.
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Problem Areas
Abdominal evaluation is problematic in the following circumstances:
Pediatric assessment Pregnancy Unconscious, intoxicated or drug affected patients Associated pelvic trauma Tricks: Distraction of the pediatric patient is the key. Discussion about their school teacher, dog, favorite program on television, or current interests like Pokemon cards, is a guaranteed way of insuring gentle evaluation. Tenderness and guarding in the presence of successful distraction indicates significant abdominal injury and urgent CT scanning should be performed in the stable child. A DPL in a conscious child is very painful.
Pediatric Assessment
Pregnancy
In gravid patients, especially after 24 weeks gestation, abdominal evaluation requires a dual approach, both for the baby and the mother. Challenges occur in relation to radiation dose associated with CT scanning and intervention related to DPL, making FAST an attractive option. Care must be taken in ensuring the operator is credentialled and sonography of the baby must be undertaken by an obstetrician, or a suitably qualified radiologist. - Pitfalls: Ultrasonography is not a particularly sensitive method of detecting abruption of the placenta. As part of abdominal evaluation in pregnancy, CTG monitoring in patients with significant injuries should be undertaken in hospital for a period of at least six hours. In cases of significant risk to the mother or the baby a CT scan is useful, but fully informed patient consent must be obtained in relation to radiation exposure.
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Unconscious, Intoxicated or Drug Affected Patients

In the stable patient after their head has been cleared, the abdomen should be scanned. In the presence of an intracranial hematoma, such as an epidural, the patient should be transferred to the operating room for evacuation and a DPL or FAST in the operating room rather than proceeding with abdominal CT. If the head CT is okay, it is safe to proceed with abdominal CT.
Associated Pelvic Trauma

Pelvic fractures pose a challenge in terms of abdominal evaluation. Most pelvic fracture deaths are related to hemorrhage. The pelvic plain films will usually provide an insight as to the potential for hemorrhage. Associated injuries are common and 10% of patients have bladder injuries, 10% spleen, 7% liver, 7% small bowel, 7% renal and other injuries in 10%. Occasionally there is double jeopardy where two or more body regions require simultaneous treatment. Physical examination is rather limited in patients with pelvic fracture. It has been suggested that DPL is associated with false positive results in patients with pelvic fracture, and that laparotomy is undertaken on the basis of false positive DPL has significantly contributed to increased morbidity and mortality. This is partly true. To avoid this certain precautions must be undertaken: - Early DPL (< 30 minutes after admission) - Avoiding DPL in stable patients with pelvic fracture. - Altering your criteria for positive DPL to include aspiration of 10 ml or more of gross blood.5
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Re-Evaluation of Blunt Abdominal Trauma

While early evaluation and recognition of blunt abdominal injuries is essential, many patients do not often present with classical symptoms, signs or results in investigations allowing an immediate diagnosis. The evaluation of blunt abdominal trauma is a process which must evolve in keeping with the patients condition. Clinical examination including tertiary survey is important. Evaluation of the patient with BAT should follow a system suitable for your institution with the resources available to you. Audit and evaluation of your nontherapeutic laparotomy rate, missed injury rate and complications is essential to ensure improvement and maintenance of high standards. The keys to assessment of blunt abdominal trauma:
1. 2. 3. 4. 5.
listen to the history prompt and timely evaluation in the early resuscitation phase tertiary survey with reassessment perform the right test for the correctly predicted potential injury.
Velmahos GC, Tatevassian R, Demetriades DB. Seat belt mark: A goal for increased vigilance among physicians treating victims of motor vehicle accidents. Am Surg 1999; 65:181-185. Sugrue M, Seger M, Gunning K et al. A modified combination technique for performing diagnostic peritoneal lavage. Aust N.Z. J Surg 1995; 65:54-55. Sugrue M, Knox A, Sarre R et al. Management of splenic trauma: A new CT based splenic injury system. Aust NZ J Surg 1991; 61:349-353. FAST Consensus Conference Committee. Focused Assessment with Sonography for Trauma (F.A.S.T.): Results from an international consensus conference. J Trauma 1999; 46:466-472. Mendez C, Goubler D, Maier RV. Diagnostic accuracy of peritoneal lavage in patients with pelvic fractures. Arch Surgery 1994; 129:477-482.
References
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Evaluation of Penetrating Abdominal Trauma

George C. Velmahos Historical Perspectives
Penetrating abdominal trauma was managed expectantly until the late 19th century. Operative management replaced expectant management in World War I and reduced mortality significantly. Selective management was suggested for the first time in 1960. It was practiced first for stab wounds and later for gunshot wounds with success.
Anatomical Definitions
Injuries to the anterior (true abdomen) or posterior (back) abdomen can cause intra-abdominal organ injuries. The anterior abdomen is defined superiorly by the nipple line, inferiorly by the pubic symphysis and laterally by the mid-axillary lines. The posterior abdomen is defined superiorly by the tips of the scapulae, inferiorly by the gluteal folds and laterally by the mid-axillary lines.
The Objective and the Dilemma

The objective of evaluation of penetrating abdominal trauma is to identify patients in need of operation while at the same time minimizing the risks associated with unnecessary procedures. The dilemma refers to whether the clinical examination is reliable or not, additional diagnostic evaluation is required or not, and routine operation should be the standard of care or not. It is with this objective and dilemma in mind that all the following methods will be reviewed.
Clinical Evaluation
Every patient with a stab wound or gunshot wound to the abdomen should have a detailed clinical evaluation including a rectal examination. A nasogastric and a urinary tube should always be inserted. The clinical examinations should be repeated frequently. The two most common clinical signs strongly suggestive of intra-abdominal organ injury are diffuse abdominal tenderness and hemodynamic instability. Other signs suggestive of intra-abdominal organ injury are localized abdominal tenderness, hematuria, hematemesis or blood in the nasogastric tube, blood in the rectal exam, and diminished or absent lower extremity pulses.
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Fig. 27.1A. The mere presence of a bullet in the abdomen does not indicate the need for surgical exploration. B. This patient had a CT that shows the bullet lying on top of the liver without causing any injury.
Unevaluable patients (intoxicated, intubated, sedated, or with associated head or spinal cord injuries) should be considered to have an intra-abdominal injury until proven otherwise. The bullet trajectory does not accurately predict the probability of intra-abdominal organ injuries.
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Fig. 27.2. Alternative interventional methods to manage a gunshot wound to the abdomen exist. This patient was not operated on but had hepatic angiography with embolization of a bleeding branch of the right hepatic artery.
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Fig. 27.3. Additional studies should be done when indicated. This patient had two transpelvic gunshot wounds, no abdominal tenderness or hemodynamic instability and blood at the urethral meatus. A retrograde urethrogram showed contrast extravasation from the membranous portion of the urethra. Surgical exploration was not necessary.
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Fig. 27.4A. The bullet trajectory is not reliable for predicting significant intra-abdominal injuries and identifying the need for operation. A patient presents with a trajectory that is highly suspicious for intra-peritoneal penetration and significant injuries. The entry wound is in the true abdomen.
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Fig. 27.4B. The exit wound is in the true back.
Is Clinical Evaluation Reliable?

The sensitivity of clinical examination to identify patients in need of operation exceeds 95% both for stab wounds and gunshot wounds. It is important to repeat the clinical examination frequently and not rely exclusively on the initial assessment. Symptoms that are initially masked will be revealed later.
Additional Diagnostic Tests

A variety of tests have been used to evaluate the abdomen after penetrating injuries, including diagnostic peritoneal lavage, ultrasound, contrast-injection
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Fig. 27.4C. Upon exploration, the entry and exit sites to the peritoneal cavity were close to each other and there was no underlying organ injury.
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in the tract (stabbogram), intravenous pyelogram, contrast cystogram and/or urethrogram, sigmoidoscopy, contrast enema, computed tomography. Diagnostic peritoneal lavage (DPL) has been used with inconsistent results for the following reasons:
- There is no universally accepted red-blood-cell count that characterizes the DPL as positive. For blunt trauma this value is 100,000 RBC/mm3, but for penetrating trauma it is unknown. Values of 100,000, 50,000, 25,000, 10,000, and 1,000 have been used with varying sensitivities ranging from 99-75%. - A positive DPL does not necessarily indicate the need for operation. False positive rates of up to 56% have been reported. - In the presence of diaphragmatic injuries, the negative thoracic pressure may decrease the volume of intra-abdominal blood or blood-stained DPL fluid, and, therefore, create false-negative results.
We do not recommend the use of DPL for penetrating abdominal trauma. Ultrasound performed by the treating physicians in the emergency room has recently become a widely used test. F.A.S.T. (Focused Abdominal Sonography for Trauma) evaluates at least three areas (hepatorenal space, splenorenal space, pelvis) with a possible addition of another two (left and right paracolic gutters) with the single goal of identifying intra-abdominal fluid. Fluid following trauma equals blood. The test is operator-dependent and not specific, i.e., it may identify blood but not its origin or significance. The sensitivity of this test in penetrating abdominal trauma is still unknown. If the limitations of the test are kept in mind, it can be routinely used because it is fast, easy, and noninvasive. It can be repeated frequently. We believe that with increasing experience, ultrasonography will become an important tool in the diagnosis of intra-abdominal trauma.
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Fig. 27.5A. Evisceration is not always an indication for operation, although laparotomy should be considered strongly due to the high incidence (75%) of associated injuries. This patient suffered a stab wound and was explored because there were extensive fascial defects. There was no organ injury.
Fig. 27.5B. This patient had absolutely no symptoms following an abdominal stab wound. The bowel was reduced and the fascia was closed under local anesthesia. The patient had an uneventful recovery.
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The stabbogram consists of injection of contrast into the injury tract to detect possible leakage of contrast into the abdominal cavity. Peritoneal penetration does not necessarily mean intra-abdominal organ injury. The test is only of historic value. Intravenous pyelogram (IVP) and contrast cystogram are useful tests in the evaluation of hematuria following penetrating abdominal trauma when the need for operation is not clearly established. Helical CT scan (with intravenous contrast injection and CT-cystogram) has largely replaced these tests because it provides valuable additional information about organ injuries. IVP may still remain the test of choice for detailed visualization of the ureters when ureteral injury is strongly suspected. One-shot IVP is used under emergency-room conditions in patients who are suspected to have injuries to the urinary tract. It detects or rules out these injuries and reveals the presence of a functional contralateral renal unit, which is important when surgery for removal of the injured renal unit is a possibility. The test is performed by injecting intravenous contrast and taking a plain abdominal radiograph 15 to 20 minutes after injection. The test is associated with a high rate of false-positive and false-negative results. Intraoperative palpation can reveal the presence of a normal-size contralateral kidney if this is deemed necessary. Intraoperative IVP or dye injection (methylene blue or indigo-carmine red) can always be performed according to the circumstances. We do not recommend the use of preoperative one-shot IVP. Rigid sigmoidoscopy is useful in the evaluation of the extraperitoneal rectum. Patients with transpelvic trajectories, gluteal gunshot wounds, and proximity stabbings should be evaluated by sigmoidoscopy. The test is frequently hard to interpret because of the lack of bowel preparation. Blood found should be interpreted as a positive test, regardless of whether the actual injury is visualized or not. Contrast enema is also used to evaluate the extraperitoneal rectum. It is not the test of choice and is usually reserved for cases with equivocal findings on sigmoidoscopy. Helical computed tomography (CT) is emerging as a valuable adjunct in the evaluation of penetrating trauma to the abdomen. It provides precise information on the bullet trajectory as well as on the condition of intra-abdominal organs, particularly retroperitoneal ones. Its indications, although not yet fully explored, potentially are:
- Patients with equivocal clinical signs. - Patients with posterior penetrating wounds possibly involving retroperitoneal organs. - Patients with right-upper-quadrant wounds who are selected for nonoperative management. - Patients who can be discharged directly from the emergency room if an extraperitoneal trajectory is documented.
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Diagnostic Operative Procedures

Diagnostic operative procedures include selective wound exploration and diagnostic laparoscopy and laparotomy. Wound exploration is done to determine if peritoneal penetration has occurred. It is best performed in the operating room but can be done at the bedside with
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adequate local anesthesia. Its sensitivity and specificity are not established. It creates patient discomfort. The presence of peritoneal penetration does not equal intra-abdominal injury. Simple digital exploration can be even more misleading. However, in selected cases it can provide a crude idea of the wound-tract direction. Wound exploration is not indicated in the majority of cases. Diagnostic laparoscopy at this time is useful only for the evaluation of diaphragmatic injuries. About 40% of patients with penetrating trauma of the left thoracoabdominal area have diaphragmatic injuries, and among those, the injury is occult in one-third. Because no other test can reliably rule out diaphragmatic injuries, laparoscopy is an important tool in the evaluation of left penetrating thoracoabdominal trauma. The value of laparoscopy in other types of penetrating abdominal trauma is uncertain. False negative results occur frequently, particularly with retroperitoneal or small bowel injuries. With increasing surgical expertise. laparoscopy may find new roles in the evaluation of this form of trauma. Routine diagnostic laparotomy is still widely used for gunshot wounds though not for stab wounds. Nontherapeutic laparotomy is associated with complications and is not cost-effective as a diagnostic tool.
The Significance of Evisceration from the Wound
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Evisceration of abdominal contents from the wound is associated with significant intra-abdominal organ injury in approximately three-quarters of patients who have no other indication for laparotomy following penetrating abdominal trauma. The type of eviscerating organ (e.g., bowel or omentum) does not predict the need for operation. The high incidence of associated injuries should prompt aggressive management of these patients. Intensive monitoring, additional testing and a low threshold for laparotomy are appropriate.
Routine Exploration or Selective Management: Resolution of the Dilemma

There is agreement that stab wounds should be managed selectively. There is still no consensus on the management of abdominal gunshot wounds. Reasons commonly cited for routine exploration of abdominal gunshot wounds are the following:
Gunshot wounds are associated with a 90% rate of abdominal organ injuries. Clinical examination is unreliable Negative laparotomies are complication-free. Delayed diagnosis of injuries is associated with devastating consequences.
These reasons are proven wrong by recent research:

- The incidence of abdominal organ injury after gunshot wounds to the anterior abdomen is 70%; to the posterior abdomen, it is 30%. About one-third of patients with anterior and two-thirds with posterior abdominal gunshot wounds will have no clinical significant intra-abdominal injury. - Clinical examination is reliable. In large prospective studies, it predicted the need for operation with a sensitivity of 95-100%. If clinical examination is reliable for stab wounds, it must be reliable for gunshot wounds as well.
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- Negative laparotomies are associated with complications in up to 20% of patients, prolonging hospital stay and increasing cost. - Missed injuries are associated with devastating consequences. Close monitoring during the asymptomatic period and operation upon development of symptoms does not increase the risk of complications.
Special Considerations: Gluteal, Thoracoabdominal, and Transpelvic Injuries

Gluteal injuries are associated with high rates of retroperitoneal injuries, particularly of the rectum. The absence of peritoneal irritation and the potential tamponade of bleeding may cause a misleading clinical picture. Close observation and additional studies, when appropriate, are recommended. Rigid sigmoidoscopy should always be done, unless the wound is clearly away from the rectum. Transpelvic gunshot wounds are associated with high rates of significant injuries. Selective management is still appropriate, if a high index of suspicion and low threshold for additional investigation and operation is maintained. Left thoracoabdominal penetrating injuries place the left diaphragm at risk. Laparoscopy is the only reliable tool to diagnose such injuries in asymptomatic patients. Laparoscopy should be performed routinely in such patients when laparotomy is not needed. Right thoracoabdominal injuries may still produce a high rate of occult right diaphragmatic injuries. However, because the liver is buttressing the perforation, herniation of abdominal viscera is rare. Routine laparoscopy is not required for all right thoracoabdominal injuries. Anterior right thoracoabdominal injuries are more likely to be associated with herniation than posterior ones, and may need to be evaluated by laparoscopy in an individual basis.
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Shotgun Wounds
Shotgun wounds behave differently, depending on the distance of the assailant from the patient, the type of gun and the type of pellets. Close-range shotgun wounds (less than 10 feet) usually behave like high velocity bullet wounds. At more than 20 feet they produce damage equal to that produced by low velocity missiles. The range of pellet spread may provide indications of the injury produced. A narrow spread (less than 10 cm) usually indicates a close-range shot that is likely to penetrate the abdominal wall. A spread of over 25 cm is thought to be associated with a low likelihood for deep tissue penetration. Because the variability in injury patterns is great, depending on the type of gun and pellets, the above indicators are unreliable. Clinical examination is the most reliable tool to evaluate for the presence of significant injuries to the abdominals.
Recommendations for Abdominal Penetrating Injuries

Selective management is appropriate for all anterior and posterior abdominal injuries caused by firearms or knives. Patients with diffuse abdominal tenderness or hemodynamic instability, and patients who cannot be evaluated clinically, should be operated on immediately. Patients who are clinically evaluable and have no symptoms should be selected for nonoperative management. Patients with equivocal symptoms should have further diagnostic tests on a caseby-case basis.
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Observation of nonoperatively managed patients should be always performed in monitored areas with house staff available around the clock. Clinical examinations should be repeated on a frequent basis, preferably by the same experienced surgeon. If these prerequisites are not fulfilled, mandatory operation may be a safer solution. If the decision for operation is made, further testing is unnecessary and potentially harmful. The patient should be taken to the operating room without delay. Time is of the essence in the management of trauma patients.
References
1. 2. 3. 4. 5. 6. Demetriades D, Velmahos GC, Cornwell EE et al. Selective nonoperative management of gunshot wounds to the anterior abdomen. Arch Surg 1997; 132:178-183. Velmahos GC, Demetriades D, Foianini E et al. A selective approach to the management of gunshot wounds of the back. Am J Surg 1997; 174:342346. Demetriades D, Rabinowitz B. Indications for operation in abdominal stab wounds. A prospective study of 651 patients. Ann Surg 1987; 205:129131. Renz BM, Feliciano DV. Unnecessary laparotomies for trauma: a prospective study of morbidity. J Trauma 1995; 38:350356. Nagy K, Roberts R, Joseph K et al. Evisceration after abdominal stab wounds: Is laparotomy necessary? J Trauma 1999; 47:622626. Velmahos GC, Safaoui M, Demetriades D. Management of shotgun wounds: Do we need classification systems? Int Surg 1999; 84:99104.
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Hepatic Injuries and Bile Duct Injuries

Thomas V. Berne Anatomical Considerations Anatomy
The liver is divided into its right and left lobes by a plane which passes through the gall bladder and inferior vena cava. The middle hepatic vein often lies in this plane. The portal triad structures divide the liver into eight Couinauds segments (Fig. 28.1).
Anomalies
The most common anomalies are an origin of the right hepatic artery from the superior mesenteric artery (approximately 15%) and a left hepatic artery arising from the left gastric artery (10%).
Grading
The standard for classification of liver injuries is that adopted by the American Association for the Surgery of Trauma (Table 28.1). Although difficult to remember, the first step in learning the classification is noting that lacerations deeper than 3 cm are grade III injuries or greater.
Mechanisms of Injury Blunt

Liver injuries due to automobile crashes, beatings, falls and other external forces cause a variety of hepatic wounds. Rupture of Glissons capsule. Parenchymal fractures, often stellate, radiating outward from the right hepatic dome. There are often irregular fissures extending away from a main fault. These cracks can extend throughout a lobe and into adjacent lobes. The fissures often transect major vascular and biliary structures leading to bleeding and bile leakage into the peritoneal cavity. The liver may be torn from its ligamentous and vascular attachments. Intraparenchymal and subcapsular hematomas may also form.
Penetrating
Stab wounds are generally less devastating than missile injuries (usually gunshot wounds).
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Thomas V. Berne, Department of Surgery, Los Angeles County University of Southern California Medical Center, Los Angeles, California, U.S.A.
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Fig. 28.1. Anatomy of the liver including Couinauds segment.
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The extent of injuries from knives varies with the size of the knife and whether a single thrust was made or a secondary slash was made after insertion. The magnitude of injury from a missile depends on several factors, particularly the velocity of the projectile and its expansion characteristics. Such wounds may cause very small holes up to large burst injuries similar to the stellate blunt injuries.
Diagnosis Findings
There may be no physical findings. Mild to moderate tenderness. More severe tenderness and rigidity may indicate associated hollow viscus rupture, particularly in the right upper quadrant. Abdominal distention. Hypovolemia (hemodynamic instability, falling Hct/Hbs). Fever
Ultrasound
Patients with mechanisms of injury suggesting possible abdominal injuries should have ultrasonic examination of the abdomen carried out immediately. Blood (fluid) is most often seen in Morrisons pouch, around the liver or spleen and in the pelvis. Subcapsular hematomas, intrahepatic hematomas and hepatic fracturing can sometimes be seen.
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Table 28.1. Liver injury scale of the American Society for the Surgery of Trauma
I II
Gradea Hematoma Laceration Injury Description Subcapsular, < 10% surface area Capsular tear, < 1 cm parenchymal depth Subcapsular, 10-50% surface area Intraparenchymal, < 10 cm in diameter 1-3 cm parenchymal depth, < 10 cm in length Subcapsular, > 50% surface area or expanding Ruptured subcapsular or parenchymal hematoma Intraparenchymal hematoma > 10 cm or expanding > 3 cm parenchymal depth Parenchymal disruption involving 25-75% of hepatic lobe or 1-3 Couinauds= segments within a single lobe Parenchymal disruption involving 75% of hepatic lobe or > 3 Couinauds segments within a single lobe Juxtahepatic venous injuries; i.e., retrophepatic vena cava/central major hepatic veins Hepatic avulsion
Hematoma Laceration
III
Hematoma
IV
Laceration Laceration
Laceration
Vascular VI
a
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Vascular
Advance one grade for multiple injuries, up to grade III Reprinted with permission from Moore EE, Cogbill TH, Pachter HL et al. Organ injury scaling of the liver, spleen and kidney. J Trauma 1995; 38:323-324.
The findings of intra-abdominal fluid usually does not identify the liver as the source. May be used regardless of the patients hemodynamic stability.
Computerized Tomography of Abdomen and Pelvis (Abdominal CT Scan)

The abdominal CT scan is presently the most helpful diagnostic study for evaluating possible hepatic injury. CT scans made using spiral technology with intravenous radioopaque dye injection are particularly valuable. Suitable only for hemodynamically stable patients, or in rare patients who are semi-stable (tachycardia and mild hypotension responsive to fluids). Identifies the architecture of hepatic injury and extent of the parenchymal disruption. (Fig. 28.2) Allows for CT injury scoring. Usually identifies the presence of splenic, kidney and bladder injuries. Care should be taken because pancreatic and intestinal injuries can be subtle or show no findings at all.
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Fig. 28.2. High grade (V) liver fracture successfully managed nonoperatively. Reprinted with permission from Moore EE, Cogbill TH, Pachter HL et al. Organ injury scaling of the liver, spleen and kidney. J Trauma 1995; 38:323-324.
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Identifies the presence of intrahepatic Figure 28.3 and subcapsular hematomas (Fig. 28.4). Demonstrates intraperitoneal fluid usually blood. During infusion of radioopaque IV dye the appearance of high density dots (pseudoaneurysms), streaming or lakes may indicate active bleeding. These should be studied angiographically and be embolized (Fig. 28.5). Low attenuation around peripheral sub-segmental portal branches (periportal tracking) indicates severe liver injury (Fig. 28.6). Decreased parenchymal density indicates ischemic injury. May be useful for guiding nonoperative management of abdominal gunshot wounds.
Diagnostic Peritoneal Language

Once a mainstay of the management of blunt abdominal trauma, its value has become limited because many injuries which produce significant intraperitoneal bleeding are now managed nonoperatively if there is no evidence of ongoing hemorrhage or peritonitis and careful observation is possible. Greatest value is in the unstable or semistable patient, who has a serious head injury or pelvic fracture. In such cases if gross blood (10 ml) is obtained upon aspiration, then the patient should go immediately to the OR for exploratory celiotomy. If gross blood is not present the patient should receive a head CT or a pelvic angiogram as they are potentially life saving. If gross blood is not present, but the RBC count is > 100,000/mm3, the patient can still be observed based on other findings.
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Fig. 28.3. Intrahepatic hematomas
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Fig. 28.4. Large subcapsular hematoma
Initial Nonoperative Management Blunt

The majority of hepatic injuries can be managed without operative intervention. Hemodynamically stable patients without peritonitis (exam and/or CT scan) should be initially managed nonoperatively with careful follow-up observation.
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Fig. 28.5. Abdominal CT scan and angiogram following a blunt injury showing an arterial pseudoaneurysm.
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Fig. 28.6. Periportal tracking (arrow) on CT scan.
Hemodynamically unstable patients with evidence of active intraperitoneal hemorrhage or peritonitis should be taken to the operating room for celiotomy. CT evidence of active hepatic bleeding, or in some instances very severe injury (grade IV and above) with slow bleeding (falling Hb/Hct), should have angiographic embolization although still hemodynamically stable, assuming experienced radiologists are available.
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Penetrating
Selective management for abdominal stab wounds has achieved wide acceptance. Some centers now also utilize this approach for missile injuries, but routine exploration of the abdomen is much more widely practiced. When selective management is utilized, initial nonoperative management is indicated when there is hemodynamic stability, stable Hb/Hct values, and no clinical evidence of peritonitis on physical exam and diagnostic studies. Gunshot wound tracts may often be identified by the presence of gas in the tissues seen on CT scan. This may be helpful in planning the management of RUQ injuries. Initial nonoperative management should be limited to clinically evaluable (awake) patients and requires frequent re-evaluation.
Operative Management: Liver

The initial operative incision is almost always through the upper midline. It can be extended downward, off to the right, into the chest as a median sternotomy or as a right thoracoabdominal approach. Nonbleeding lacerations (usually superficial) can be ignored. Bleeding superficial wounds can often be controlled by the application of hemostatic agents and pressure. If actively bleeding injuries are present and direct control is planned it is very helpful to mobilize the ligamentous attachments of the liver (round, falciform and triangular). More serious parenchymal wounds (fissures or missile tracts) with active bleeding require judgment as to how aggressively they should be opened (hepatorrhaphy and tractotomy) in order to directly control hemorrhage with ligatures and hemostatic clips. Bleeding can often be stopped or markedly reduced by occlusion of the portal triad at the foramen of Winslow with a soft vascular clamp (Pringle maneuver). If active bleeding continues, suspect a hepatic vein or inferior vena cava injury or the presence of an anomalous left hepatic artery origin. Liver fractures which are of intermediate depth can be controlled with deep (at or just below the bottom of the fissure) sutures using blunt tipped needles on large (#0 or 1) absorbable suture. These should close the whole depth of the crack, avoid hilar structures and be tied down firmly but not so tightly as to cause extensive necrosis. Pledglets of absorbable hemostatic material allow this tension without cutting. Occasionally it is helpful to fill a hepatic defect by placing vascularized omentum into such fissures before deep suture closure. Extrahepatic arterial ligation can be used to control obvious arterial bleeding but has been largely replaced by selective postoperative angioembolization if that is immediately available. More accurate control of arterial bleeding is possible with this technique. So-called resectional debridement is used for deeper wounds particularly if such a nonanatomical resection removes a large piece of ischemic liver. Intact liver tissue is divided by squeezing between the surgeons fingers (finger fracture) to identify vascular and ductal structures. These structures are individually controlled by ligatures or hemostatic clips as they are encountered. Tracts made by high velocity bullets often present challenging problems. The
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28
use of one or more Foley catheters (Fig. 28.7) will often control such bleeding. It only rarely recurs when the balloons are slowly deflated 3-4 days later. Retrohepatic bleeding is particularly troublesome. A hematoma near the IVC should not be opened unless it is expanding or has already ruptured with bleeding. If it has been decided that operative repair is indicated, rather than packing (see below) the abdominal incision should be extended into the chest as a median sternotomy (usually preferred) or into the right chest (7th or 8th intercostal space) to obtain adequate exposure. Small lacerations of hepatic veins or the IVC can be controlled with vascular suture using finger pressure, sponges on holders or a Satinsky clamp. Usually some kind of vascular isolation of the liver will be necessary for major retrohepatic bleeding. Several forms of vascular isolation of the liver have been advocated. The most easily applied is the multiple vascular occlusion technique of Heaney: clamping of the inferior vena cava in the pericardial sac, the IVC just above the renal veins, the aorta just below the diaphragm (to avoid exsanguination into the lower 1/2 of the body) and a Pringle maneuver. Cold electrolyte solutions and ice saline slush applied to the liver may prolong the tolerable ischemia time, but is unnecessary if the patient is already hypothermic). With bleeding largely controlled, clipping, suture or ligature of injured vascular structures is greatly facilitated. Care should be taken to avoid allowing air to enter open venous wounds to prevent right-sided air embolism. The decision to pack an extensively injured liver should, if possible, be made as soon as it is clear that the patients hepatic wound is not amenable to standard methods of repair. These are most commonly injuries with extensive bilobar fracturing, large subcapsular hematomas and multiple additional extrahepatic injuries. This modality should be chosen as the first method attempted to prevent massive blood loss during predictability unsuccessful attempts at direct control of hemorrhage. Of course, if direct control is initially attempted and the usual indicators for damage control (coagulopathy, profound hypothermia, severe acidosis) occur, the liver should then be packed. Packing can often control an extensive injury, but if bleeding continues after packing, angiographic control immediately after the operation should be arranged. Packing should begin with the placement of gauze laparotomy pads behind the right and left hepatic lobes to prevent backward pressure on the liver from causing IVC occlusion. The raw (injured) areas of liver should be covered with a sheet of hemostatic material or absorbable mesh to lessen bleeding when the pack is removed. The gauze pack should be placed to create pressure which occludes the hepatic injuries as the abdomen is closed. Care should be taken to avoid too tight closure of the abdomen with the development of an abdominal compartment syndrome (see Chapter [Abdominal compartment syndrome]). Rarely, with very extensive liver damage, a total hepatectomy and temporary portocaval shunt followed by hepatic transplantation can be considered. Problems with maintenance during the anhepatic state and the rapid availability of a donor organ make this option of value only where a very active liver transplant program can be quickly accessed. Drains should be of the closed (Jackson-Pratt) type and used only for extensive injuries (grade III or above) unless there is obvious biliary leakage. Injuries to the hepatic artery and portal vein should be repaired using
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Fig. 28.7. Foley catheter used to control bleeding from bullet wound tract
appropriate vascular techniques under circumstances where this is possible. The liver can survive if flow through only one of these structures is preserved. Ligation of the portal vein causes acute portal hypertension with massive bowel edema. Reports indicates that 10-54%, of patients will survive. With portal vein ligation a second look operation should be considered to assess intestinal viability. Arterial ligation is better tolerated but may cause hepatic infarction in some cases.
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Operative Management: Extrahepatic Bile Ducts

The most common injury is to the gallbladder and is usually managed by cholecystectomy although cholecystorraphy with absorbable suture has been recommended by some. Primary repair should be carried out for partial ductal transection or cleanly incised ductal transections without loss of length. More complex injuries with more ductal loss will require choledochojejunostomy to a Roux-en-Y loop. T- tube or small caliber tube stenting of there repairs in widely practiced. Suction drainage (Jackson-Pratt type drains) placed near these repairs is essential.
Early Postoperative Management

The postoperative care of these patients requires considerable vigilance to anticipate, prevent and treat complications. Hemodynamic stability should be achieved as quickly as possible utilizing endpoints of resuscitation with which the individual surgeon is familiar. This may require aggressive blood coagulation factor and fluid infusion (see Chapter 6 [Resuscitation]). An antibiotic, such as a second generation cephalosporin, will usually have been given preoperatively and should not be continued for more than one day
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postoperatively even if there has been of hollow viscus injury. If there is evidence of ongoing bleeding there should be consideration of postoperative angiography. Frequent intraabdominal pressure measurements should be made. Aggressive correction of hypovolemia, coagulation defects, hypothermia and acidosis must begin in the operating room and continue in the ICU.
Late Postoperative Management and Liver Specific Complications Pack Removal

Packs should be removed by 48-72 hours postoperatively, unless there are extenuating circumstances. After that time they become increasingly difficult to dislodge and more likely to become grossly infected (particularly if there has been a hollow viscus injury). Pack removal is facilitated by soaking the gauze with saline (or very dilute H202 in saline: 15 ml of 3% in 1L) to soften them. Ample blood for transfusion should be available in case of renewed hemorrhage. Repacking is usually indicated when this occurs.
Sepsis
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If the clinical picture of sepsis develops an abdominal CT scan is indicated with instructions for percutaneous catheter drainage of fluid (blood, bile or pus) collections unless less than 3 cm or located in an inaccessible area. Most peri- or intrahepatic infected collections can be successfully managed by such drainage and targeted antibiotic treatment. Occasionally operative drainage is required, particularly when the infection is accompanied by a large segment of necrotic liver (sequestrum).
Bile Leaks/Fistulae/Stricture
Drains placed at the time of operation or in the postoperative period can drain large amounts of bile. Most such fistulae require little to be done except render the patient infection free and provide good nutrition. Drains should be left in place. Fat free diets (difficult to maintain adequate calorie intake), H-2 blockers and somatostatin are adjunctive but of unproven benefit. High output for long periods (arbitrarily > 50 ml/day for more than 6 weeks) should prompt further investigation by CT scan, fistulagram and/or ERCP. ERCP with stenting across the ampullary sphincter may be helpful. Almost all such fistulae close, but if after several months closure has not occurred, particularly if there is a proximal stricture, Roux-en-Y jejunal loop placement over the hepatic opening, segmental hepatic resection or other operative procedure may be necessary on rare occasions. Late stricture of extra hepatic bile ducts usually requires reoperation although percutaneous or transampullary balloon dilatation and stenting may be of value.
Hemobilia
The postoperative triad of jaundice, right upper quadrant pain and upper GI bleeding is classical. Unfortunately it occurs only infrequently.
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Fig. 28.8. Angiographic embolization of a bleeding pseudoaneurysm.
Unexplained UGI bleeding must be considered to be hemobilia after any significant liver injury. Psuedoaneurysm causing bleeding can often be seen on contrast CT scan. They are best diagnosed and treated with angiography and arterial embolization (Fig. 28.8).
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Outcomes
The overall mortality rates for liver injury should be in the range of 10%. There is a higher lethality of blunt compared to penetrating. Grade V vascular and Grade VI injuries have > 50% mortality. Mortality reaches 100% if all portal triad structures are transected.
1. 2. 3. 4. Demetriades D, Gomez H, Chahwan S et al. Gunshot wounds to the liver: The role of selective nonoperative management. J. Am Coll Surg 1999; 1888:343-348. Krige JE, Bornman PC, Terblanche J et al. Liver trauma in 446 patients. Surgery 1997; 35:10-15. Pachter HL, Feliciano DV. Complex hepatic injuries. Surg Clinics of No Am 1996; 16:763-782. Schweitzer W, Tanner S, Bear HU et al. Management of traumatic liver injuries. BJS 1993; 80:86-88.
References
CHAPTER 29
Splenic Injuries
John A. Androulakis and Michael N. Stavropoulos Introduction
The spleen is the most commonly injured organ, following blunt abdominal trauma. The injured spleen, ranks second behind the liver as the source of life threatening hemorrhage following blunt trauma.
Reigner, performed the first successful splenectomy, following blunt trauma in 1893. The nonoperative management of splenic trauma, attempted by Bland Sutton in 1912, resulted in a 90% mortality. Routine splenectomy, remained the treatment of choice for injured spleen for most of the 20th century. In 1952 King and Shumacker reported overwhelming sepsis as a possible hazard of the asplenic state in infants. The recognition of the immunologic significance of the spleen, coupled with the renewed attention to its blood supply and the development of CT-scan, has led to a more conservative approach of the management of splenic trauma in recent years.
Anatomy, Structure and Function

Spleen lies in the left upper quadrant of the abdomen at the level of the eighth to eleventh ribs. It is firmly connected to the retroperitoneal space by the splenorenal and splenophrenic ligaments and to mobile adjacent viscera by gastrosplenic and splenocolic ligaments. In children, the capsule is relatively thicker than that of the adults and in splenic parenchyma there is a large amount of functional smooth muscle and elastin. These characteristics result in increased splenic salvage in children with nonoperative management or splenorrhaphy. The splenic artery, before it reaches the spleen, divides into five or more branches which enter the hilum of the organ and ramify throughout its substance into the trabecular arteries. This arterial division creates distinct anatomic segments which allows the surgeon to perform partial resection. The transverse orientation of the segmental arteries through the splenic tissue without
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. John A. Androulakis, Department of Surgery, University of Patras Medical School, Patras, Greece Michael N. Stavropoulos, Department of Surgery, University of Patras Medical School, Patras, Greece
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anastonosis to adjacent vessels accounts for the spontaneous cessation of bleeding after transerve lacerations of the spleen. The spleen represents the largest (25%) reticuloendothelial accumulation in the body. Except for the phagocytosis and synthesis of immunoglobulins which also occur in other organs, a main role of the spleen is synthesis of new antibodies (IgM). This role is extremely important in infancy and explains the special susceptibility to infection after splenectomy in children under two years of age. Spleen also produces monocytes, lymphocytes and plasma cells and is a source of tuftsin and properdin. Tuftsin enhances phagocytosis by neutrophils and properdin is a crucial mediator of complement activation via the alternative pathway. Low IgM, properdin and tuftsin and inability of clearance of intravascular antigens characterize the asplenic state. These deficiencies, result in an increased susceptibility to infectious complication and overwhelming postsplenectomy infection (OPSI) in asplenic patients.
Diagnosis
The diagnosis of splenic trauma should be based on the history of injury and the clinical presentation of the patient. It is confirmed at operation or by means of CT scan or ultrasound.
Mechanism of Injury Blunt Trauma

Compression injury (after left lateral impact or direct blow,) may result in simple splenic fracture or severe stellate fractures. Splenic pulp disruption beneath an intact capsule produces a subcapsular or intraparenchymal hematoma. A left lower fractured rib can tear the spleen. In deceleration injuries, such as in high-speed traffic accidents or falls from heights, the fixed spleen is subject to shear injury as it is torn at sites of supporting ligaments. With severe deceleration, the spleen may be totally avulsed from the retroperitoneum and its hilar vessels (injuries by inertial forces).
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Penetrating Trauma
The type of splenic injury depends on the characteristics of the weapon (type of the gun, length of the knifes blade, etc.) and its trajectory. Gunshot wounds with civilian weapons and stab wounds that penetrate the spleen cause anatomically defined injuries, which are usually less severe than blunt ones.
Underlying Splenic Disease

A diseased or enlarged spleen, produced by hematological disorders, infections or portal hypertension, is more likely to rupture than a normal one, even after a trivial trauma.
The clinical presentation of the patient with splenic trauma varies from severe hypovolemic shock to minimal or no symptoms. The bleeding rate, the age and previous health condition of the patient and prehospital elapsed time are factors influencing the clinical presentation of
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the patient at the time of admission. However, the majority of the patients (75%), show variable signs of hypovolemic shock. The largest group of patients (with an intact sensorium) complains of diffuse abdominal pain more severe in the left upper quadrant and frequently accentuated by deep breathing. Left shoulder pain is a common and clearly useful sign (Kehrs sign), which often can be elicited by placing the patient in the Trendelenburg position.
Clinical Findings on Physical Examination

The lower chest wall, the abdomen and the flank should be inspected for abrasions, contusions, lacerations or penetrating wounds which may be indicative of underlying splenic injury. The patient may be pale with variable tachycardia, hypotension and abdominal distention depending upon the amount of acute blood loss. The palpation of the abdomen, usually reveals diffuse or localized abdominal tenderness and muscle guarding. A palpable mass in the left upper quadrant suggests a large splenic hematoma. Physical examination of the abdomen after blunt trauma is neither sensitive nor specific for splenic injury. The delayed recognition of the splenic injury is one of the most common causes of preventable death, after blunt trauma. The high index of suspicion, the frequent reevaluation of the patient and prompt radiological investigations help to solve this problem.
Investigations
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Chest X-Ray
May be suspicious of splenic injury in up to 50% of patients. Radiological findings suggestive of significant left upper quadrant injury and suspicious of splenic trauma are: Left lower rib posterior fractures (splenic injury occurs in about 20% of cases). Left pleural effusion. Elevated left hemidiaphragm. Left pulmonary contusion. Medial displacement of gastric air bubble. Downward displacement of the left colic flexure.
Diagnostic Peritoneal Lavage (DPL)

It can be utilized in hemodynamically unstable multiply injured patients when there is an immediate need to know if hemoperitoneum exists. It is extremely sensitive but not organ specific.
CT Scan
Contrast enhanced CT scan is the principal and most valuable diagnostic modality, for hemodynamically stable patients. It detects splenic trauma with high degree of accuracy and may also show evidence of active bleeding or false aneurysm (contrast blush) which predict the risk of failure of nonoperative management of blunt splenic trauma (Fig. 29.1A). The accuracy of CT images permits grading of splenic trauma based on the CT scan characteristics of splenic injuries (Figs. 29.2, 29.3). It may miss superficial lacerations. Hemoperitoneum and perisplenic clots, are the most common CT findings indicative of splenic trauma, if lacerations are not identified.
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Fig. 29.1A. Traffic accident: Abdominal CT-scan with intravenous contrast, shows a ruptured spleen with a false aneurysm (arrow)
Ultrasonography (US)
Is a useful primary imaging modality that can be performed in the Emergency Room to reveal free intraperitoneal fluid. US can be used to predict the need for further evaluation or laparotomy as well as for follow-up of injury healing or progress of absorption of a known hematoma.
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Angiography
Angiography is indicated in patients with a blush on CT scan suggesting active bleeding or false aneurysm (Fig. 29.1B).
Delayed Splenic Rupture (DSR)

The presence of a subcapsular splenic hematoma, may result in delayed rupture of the spleen, usually within two weeks of original trauma, but it may occur many weeks later DSR is possibly attributable to the increased osmolality of the contents of a hematoma (due to the disintegration of the red cells) which results in attraction of additional fluid, expansion of the cavity, secondary hemorrhage and finally rupture. DSR produces sudden shock from profuse bleeding and operative or nonoperative management is based on the condition of the patient after initial volume resuscitation. The diagnosis before rupture can be made by the history of a current trauma, abdominal symptoms and signs (abdominal and shoulder pain, palpable tender left upper quadrant mass), an unexplained anemia, and left pleural effusion. It can be confirmed by U/S or CT scan of the abdomen (Figs. 29.3, 29.4).
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Fig. 29.1B. Angiography, confirms the presence of a large splenic aneurysm (arrow).
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Fig. 29.1C. Successful angiographic embolization of the aneurysm. The spleen was successfully managed nonoperatively.
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Fig. 29.2. Abdominal CT scan demonstrating Grade IV splenic trauma.
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Fig. 29.3. Large subcapsular splenic hematoma following blunt trauma. CT scan appearance.
Grading System of Splenic Trauma

The most recent grading system for splenic trauma is the Spleen Injury Scale (1994 revision) promulgated by the Organ Injury Scaling (0IS) Committee of the American Association for the Surgery of Trauma (AAST). This scale is a classification scheme based on the anatomic disruption of the spleen, graded 1-5, representing the least to most severe injury, and corresponding to the International Classification of Diseases, 9th revision (ICD-9) code and Abbreviated Injury Scale (AIS-90) scores. (Table 29.1).
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Fig. 29.4. Large subcapsular splenic hematoma following blunt trauma. U/S appearance.
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The objectives of this scale are to standardize reports, to guide treatment, and to evaluate and compare the results of different therapeutic modalities.
Management Principles
The specific management of the patient with presumed splenic trauma is directed by the hemodynamic condition and clinical findings of the abdominal examination. The hemodynamically unstable patient on admission, who remains unstable after vigorous resuscitation, with suspected splenic injury following blunt or penetrating trauma, should undergo urgent operation regardless of age. A blunt trauma patient, who is hemodynamically stable and has a soft abdomen, is a candidate for nonoperative management. A CT scan with intravenous contrast is essential. If contrast blush is present, angiographic embolization should be attempted (Figs. 29.1A-C).
Nonoperative Management (NOM)

In recent years, the widely accepted NOM of splenic injury in children was extended to adult patients. The patient selection criteria for NOM are: Hemodynamic stability No clinical or radiological (CT scan) evidence of other intraabdominal injuries requiring celiotomy. Limited need for spleen-related transfusion ( 2 units).
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Table 29.1. Spleen injury scale (1994 revision)

Gradea Injury Description AIS-90
I II
Hematoma Laceration Hematoma Laceration
III
Hematoma
Laceration IV V Laceration Laceration Vascular
Subcapsular, < 10% surface area Capsular tear, < 1 cm parenchymal depth Subcapsular, 10-50% surface area; intraparenchymal, < 5 cm in diameter 1-3 cm parenchymal depth which does not involve a trabecular vessel Subcapsular, > 50% surface area or expanding; ruptured subcapsular or parenchymal hematoma Intraparenchymal hematoma > 5 cm or expanding > 3 cm parenchymal depth or involving trabecular vessels Laceration involving segmental or hilar vessels producing major devascularization (> 25% of spleen) Completely shattered spleen Hilar vascular injury which devascularizes spleen
2 2 2
3 4 5 5
Advance one grade for multiple injuries, up to grade III.
Additionally in recent reports, the following subgroups of hemodynamically stable patients are candidates for NOM of their splenic trauma. These are: Patients who are neurologically impaired (head injury, alcohol or drug intoxication). Patients with small isolated penetrating wounds to the spleen. Patients of any age, any AAST grade of splenic injury, any degree of hemoperitoneum and any ISS score.
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Guidelines for Nonoperative Management

Candidates for NOM should be observed in SICU with strict bed rest and prepared for surgery. Serial physical examinations of the abdomen, by an experienced physician. Serial Hct and Hgb. Decompression of the stomach Strict bed rest for 2-3 days but may be individualized according to the hemodynamic and general status of the patient and the degree of splenic injury. Resume diet once the potential for urgent operation and any evidence of associated ileus no longer exists. Serial CT scan evaluations are only performed in patients with severe splenic injuries (grade III or worse). The length of hospital stay (LOS), ranges from 5 to10 days depending on the patients condition and the degree of splenic injury. The restriction of activities varies according to the grade of injury. It has been shown experimentally that an injured spleen managed nonoperatively (healing by secondary intention), has a wound breaking strength equal to that of a
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Fig. 29.5. Ruptured spleen. CT scan appearance and operative specimen.
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normal spleen at 6 weeks postinjury. So, except for the minor grade injuries (I or II) which need minimal if any restriction of activities, in more severe injuries, the patient should be advised to avoid vigorous physical activities for about 6 weeks. In subcapsular hematomas, resumption of physical activities should be considered after resolution of the hematoma. Before the resumption of activities, a CT scan should be done to ensure that the splenic parenchymal architecture has returned to normal and to confirm the absence of a splenic posttraumatic cyst or a pseudoaneurysm formation.
Failure of Nonoperative Management

Any patient who demonstrates hemodynamic instability, signs of peritonitis, or when the total transfusion requirements (because of the splenic injury) exceed two units of blood, is immediately taken to the operating room. The most significant prognostic indicator of failure of nonoperative management in the hemodynamically stable patient is the presence of extravasation of contrast material on contrast CT scan. CT grading of splenic injury does not predict the success of nonoperative management. Success rate of NOM in children is higher than 90%. In adults it is about 70%.
Operative Management (OM)

Principles
The OM of splenic trauma includes splenectomy as well as the various techniques of surgical splenic salvage. The spleen is assessed visually and is palpated. If it appears to be the primary site of life threatening bleeding, splenectomy should be done without hesitation. The decision to perform splenectomy or splenic conservation is based upon the condition of the patient, the severity of the splenic injury, the presence of other associated injuries and the experience of the surgeon.
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Splenic Preservation
Local hemostatic agents and cautery or Argon beam laser. Suturing with or without omental packing. In selected cases a splenic mesh may be useful. Ill-advised attempts to preserve the spleen may result in significant blood loss and postoperative complications.
Splenectomy
In traumatic splenectomies, after rapid mobilization of the spleen, the splenic vessels are clamped and ligated en mass. The clamps should be applied as close as possible to the hilum, in order to diminish the risk of injury to the tail of pancreas, or the gastric fundus.
- Drains of the splenic bed are not routinely used for either splenectomy or splenorrhaphy, except in cases with incomplete hemostasis or associated injuries to the tail of pancreas or other organs.
Autotrasplantation of Splenic Tissue (AST)

AST, has been used to decrease the risk of OPSI in patients with irreparable splenic trauma requiring splenectomy. It has limited clinical application and more studies are needed to confirm the usefulness of this method.
Complications
Postoperative Local Complications
Left lower lobe atelectasis, pneumonia and pleural effusion are the most common complications. Left subphrenic abscess (3-13%) is more frequent in patients with associated hollow viscous injuries. Pancreatitis or pancreatic fistula may occur either as part of the original trauma, or more usually as a consequence of iatrogenic trauma to the tail of the pancreas during operation. Acute gastric distension is more common in children and is prevented by nasogastric suction. Gastric greater carvature necrosis is the result of entrapment of the gastric wall when securing ligatures after division of the gastrosplenic ligament. Postoperative hemorrhage may occur following splenectomy (from inadequate control of the short gastric or hilar vessels) or conservative surgery and may require transfusion or embolization or reoperation. Reoperation for hemorrhage is rare, about 2% for splenectomy and about 3% for splenorrhaphy.
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Systemic Complications
Thrombocytosis (more than 400.000 platelets /mm3) may present between the 2nd and 10th postoperative day, in about 50% of splenectomized patients. This condition is usually resolved within 2 weeks to 3 months.
- It is not clear whether thrombocytosis predisposes to an increased risk of DVT or PE or not. When the platelet count exceeds 1 million/mm3 or if the patient has a previous history of thrombosis, the administration of antiplatelet drugs (i.e., aspirin) is indicated.
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Overwhelming Postsplenectomy Infection (OPSI)

Splenectomy renders patients susceptible to a major long-term risk of infectious complications, mainly due to the deficiency for clearance of intravascular antigens. The most serious of these infections is the rare but highly fatal syndrome of OPSI.
- This syndrome is initially characterized by an abrupt onset of nonspecific flu-like symptoms, (fever, chills, headache, nausea, vomiting, malaise and abdominal pain). - This condition progresses rapidly to respiratory and renal failure, cardiovascular collapse and finally death within hours of onset, if appropriate treatment is not effectively instituted. - Usually the causative organisms are encapsulated, with the Streptococcus pneumoniae responsible for 50-90% of cases followed by Neisseria meningitidis, Haemophilus influenza type B (especially important in children) and group A Streptococci, which cover an additional 25%. - The risk of fatal OPSI is less after splenectomy for trauma than for hematologic disorders. - In general the younger the patient undergoing splenectomy and the more severe the underlying pathological condition, the greater the risk for developing OPSI. - While the 50-70% of serious infections in adults and the 80% of OPSI in children occur within two years postsplenectomy, some degree of risk persists for the duration of life. - The prevention of OPSI is based on the education of the patient, the immunoprophylaxis and chemoprophylaxis. The patients and their families should be informed about the possibility of infections, and a Medi-Alert bracelet should be worn to notify the asplenic state. The patients should be taught to recognize the early signs and symptoms of such infection and to seek early medical care. Pneumococcal vaccination should be performed after recovery and before discharge from the hospital. The protection lasts 5-6 years, after which revaccination is proposed in selected high risk young patients. Influenza vaccination is recommended annually. Children < 2 years should be covered with antibiotics (amoxicillin/ clavulanic acid or sefuroxim). Since only 50% of cases of OPSI are caused by Streptococcus pneumoniae and the vaccine is effective against about 90% of pneumococcal infections, a two-year course of prophylactic antibiotic postsplenectomy is recommended, especially for children and immune-suppressed adults. An alternative is the administration of antibiotics at the first signs of infection as well as prior to any instrumentation or surgical procedure. It should be emphasized that the use of antibiotic prophylaxis and the immunization may reduce but does not eliminate the infectious complications. - The overall mortality rate of OPSI, varies from 50-70%, but the preventive measures and the early diagnosis of OPSI, with the institution of aggressive supportive care and appropriate antibiotic therapy, has greatly improve patient outcome.
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Pitfalls
Delayed diagnosis of splenic hemorrhage following blunt trauma in patients neurologically impaired.
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Undiagnosed splenic hematoma can result in delayed splenic rupture and life threatening hemorrhage. Attempts to salvage the spleen in the presence of multiple associated injuries.
References
1. 2. 3. 4. 5. Brigden ML, Pattulo A L. Prevention and management of overwhelming postsplenectomy infectionAn update. Crit Care Med 1999; 27:836-842 Davis K.A, Fabian TC, Groce MA et al. Improved success in nonoperative management of blunt splenic injuries: Embolization of splenic artery pseudoaneurysm. J Trauma 1998; 44:1008-1015. Lynch AM, Kapila R. Overwhelming postsplenectomy infection. Infect Dis Clin North Am 1996; 4: 693-707. Pachter HL, Guth AA, Hofstetter SR et al. Changing patterns in the management of splenic trauma. The impact of nonoperative management. Ann Surg 1998; 227:708-719. Brasel KJ, Delisle CM, Olson CJ et al. Splenic injury: Trends in evaluation and management. J Trauma 1998; 44:283-286.
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CHAPTER 30
Pancreatic Injuries
Juan A. Asensio and Walter Forno Introduction
Pancreatic injuries are easily missed and quite lethal. They are generally present in association with many other intraabdominal injuries. The pancreas when injured can be an unforgiving organ. Delays in diagnosis can make what is already a difficult surgical tour de force quite challenging with resulting increases in morbidity and mortality. Early diagnosis and repair are the key to improvements in survival.
The first case of pancreatic injury was reported in 1827 by Travers during an autopsy in the records of St. Thomas Hospital in London. Laborderie in 1856 reported a case of penetrating trauma in a young girl that sustained an abdominal laceration with a pocket knife resulting in a prolapse of the pancreas. This was treated with suture transfixion double ligature and removal of the protruding portion resulting in a positive outcome. In 1882 Kulenkampff reported a patient that survived blunt injury to the pancreas with the subsequent development of a pseudocyst. Kocher in 1903 described the surgical approach to the mobilization of the duodenum, the hallmark maneuver used in evaluating both pancreatic and duodenal injuries.
Incidence
The retroperitoneal location of the pancreas plays a strong role in protecting it and thus accounts for its low incidence of injury. Pancreatic injuries occur in approximately 3-4% of all patients sustaining abdominal injuries.
Mechanism of Injury
Penetrating injuries are the most common causes of pancreatic trauma. Penetrating injuries account for 70% of all pancreatic trauma.
Associated Injuries
The pancreas, by virtue of its is anatomic proximity to other organs is rarely injured alone. Multiple associated injuries are the rule rather than the exception. Isolated pancreatic injuries are usually seen in the form of blunt pancreatic transections, generally at the neck of the gland.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A. Walter Forno, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 30.1. CT scan showing transected pancreas at neck directly over the superior mesenteric vessels. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. Philadelphia, PA: W.B. Saunders Co. In Press.
The most frequently injured organs found in association with pancreatic injuries include: the liver19%, stomach16%, spleen11%, colon and duodenum8%. Abdominal vascular injuries occur with a frequency of 14%. Major arterial and venous injuries range from 4.5-5.5%.

The most frequent site of pancreatic injury is the pancreatic head and neck37%. The pancreatic body is injured in 36% of the cases. The least frequently injured portion is the pancreatic tail26%. Multiple sites of injury occur in 3% of the cases.
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Fig. 30.2. ERCP showing a leak from a transected main pancreatic duct secondary to a GSW. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
Diagnosis
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The diagnosis of pancreatic injury requires a high index of suspicion. The diagnosis of pancreatic injury presents a greater challenge after blunt trauma than after penetrating trauma. Clinical presentation can range from a patient presenting in extremis to a picture of perfect hemodynamic stability. Patients presenting a prehospital history of a direct force applied to the midepigastrium, especially those having been struck by steering wheels, patients sustaining head-on collisions or either right or left sided impacts may harbor pancreatic injuries. Because of the pancreass retroperitoneal location, early manifestations of injury may be absent. Physical examination may be characterized by minimal findings. Tenderness of the right upper quadrant, midepigastrium or left upper quadrant as well as rebound tenderness, abdominal rigidity or acute peritoneal signs may be present in a patient harboring a pancreatic injury. Abdominal discomfort and pain may be totally out of proportion to the physical examination findings as peritoneal irritation may occur rather late and may become apparent only when blood or pancreatic enzymes, initially contained within the retroperitoneum, have extravasated into the peritoneal cavity.
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Fig. 30.3. Operative slide showing a pancreatic injury in the head secondary to a GSW. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.
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Investigations
Laboratory tests provide little help in the early diagnosis of pancreatic injuries. The serum amylase should not be used as an indicator for exploratory laparotomy.
- The serum amylase can indicate the presence of pancreatic injury, but may show a wide range of elevations in 10-90% of the patients in whom it is measured. - As many as 40% of patients that sustain pancreatic injury may have a normal initial serum amylase level. - The serum amylase level is a measure of ductal obstruction. The closer the ductal obstruction to the duodenum, the greater the glandular mass secreting behind the obstruction leading to diffusion of amylase into the gland, which is then absorbed by pancreatic venous capillaries, lymphatics or the peritoneal membrane as in the case of ductal transection. Therefore the more proximal obstruction, the greater the rise of the amylase level.
The serum amylase level may have a predictive value in patients admitted for observation and should be monitored at 6-hour intervals. A persistently elevated arising amylase level may of prognostic significance. Plain films of the abdomen are generally of little value in establishing the diagnosis of pancreatic injury. Transverse process fractures of the L1- L2 vertebrae, when present, suggest that the pancreas be investigated for possible injury.
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Ultrasound, although valuable in detecting free intraabdominal fluid and solid organ injury, is not reliable for the diagnosis of pancreatic injuries. CT scan, of the abdomen with intraluminal and intravascular contrast has a high degree of accuracy in detecting injuries to the pancreas. Pancreatic edema, gross enlargement of the gland, direct visualization of a parenchymal fracture or hematoma, fluids separating the splenic vein and pancreatic body and thickened left anterior renal fascia are significant findings.
- CT scan although quite reliable, may occasionally miss pancreatic injuries, especially if done early postinjury. A repeat scan is recommended in suspected pancreatic trauma.
Diagnostic peritoneal lavage may be positive in a high number of patients with pancreatic injuries, however, the positivity is due to associated intraperitoneal injuries and not the duodenal injury itself, as the pancreas is a retroperitoneal organ.
- The presence of significant amounts of amylase in the peritoneal lavage fluid correlates with the presence of intraabdominal injury, but this finding is not specific for pancreatic injury.
The use of ERCP preoperatively will identify the presence of a pancreatic ductal disruption, although its use in the acute diagnosis of pancreatic injuries is not feasible. MRCP (Magnetic Resonance Cholangio-Pancreatogram) is a promising technique, especially in the evaluation of the integrity of the pancreatic duct.
Surgical Management
The pancreas must be thoroughly explored and its anterior and posterior aspects visualized directly. There are three basic exposure maneuvers and two advanced maneuvers to visualize the pancreas in its entirety.
- The three basic maneuvers consist of a Kocher maneuver which will allow visualization of the anterior and posterior portions of the head of the pancreas. The next maneuver to be performed consists of dividing the gastrohepatic ligament to gain access to the lesser sac. This facilitates inspection on the superior border of the pancreas including the head, body and both the splenic artery and vein. The third basic maneuver consists of transection of the gastrocolic ligament and displacement of the stomach cephalad, which permits full inspection of the anterior aspect of the gland along its entire length. - The two more advanced maneuvers to visualize the pancreas consist of the Aird maneuver which involves mobilizing the splenic flexure of the colon and splenic ligaments to rotate the spleen and the pancreas from lateral to a medial. Transection of the retroperitoneal attachments at the inferior border of the pancreas with cephalad rotation of the pancreas will allow for exposure of the posterior aspect of the pancreas.
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Findings that raise the suspicion for the presence of pancreatic injuries include the presence of a central retroperitoneal hematoma, bile staining in the retroperitoneum, edema surrounding the pancreas and lesser sac or any pancreatic hematoma or perforation. The sine qua non of pancreatic injury is the presence of ductal injury. All pancreatic injuries should be graded utilizing the American Association for the Surgery of TraumaOrgan Injury Scale for pancreatic injuries (AAST-OIS).
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The simplest surgical techniques should be selected to manage the lower grade injuries while reserving the more complex techniques for the management of the more severe and advanced grade injuries. Basic surgical principles include debridement of devitalized tissue, conservation of pancreatic tissue to preserve function, and meticulous repair when necessary of pancreatic lacerations with nonabsorbable sutures. The uncinate process is absent in 15% of the patients. Normally a resection to the left of the superior mesenteric vessels extirpates approximately 65% of the gland. Although this is an extensive resection, it is not associated with the development of pancreatic insufficiency. When the uncinate process is absent a resection to the left of the superior mesenteric vessels will result in resection of 80% of the glandular mass and in occasional cases this predisposes to the development of pancreatic insufficiency. Intraoperative pancreatography carries risks and should be used as a last resort. It can be performed through an open duodenotomy and intubation of the ampulla of Vater. An alternative is a needle cholangiogram which occasionally allows for visualization of the pancreatic duct. Intraoperative ERCP has very rarely been utilized to assess ductal integrity. All pancreatic injuries should be drained with closed systems. Approximately 60% of all pancreatic injuries can be treated by external drainage alone. Approximately 70% of pancreatic injuries can be treated by simple pancreatorraphy plus drainage. Injuries that consist of lacerations or violations of the pancreatic capsule, parenchyma and involving minor ducts, but not the major pancreatic ductal system account for 20% of the injuries and can be treated by pancreatorrhaphy and drainage. Injuries that lacerate the pancreatic capsule and parenchyma involving the major ductal system account for 15% of all pancreatic injuries and are generally treated with resection. Injuries that involve the major ductal system but occur to the left of the superior mesenteric vessels should be treated by distal pancreatectomy and splenectomy. This can be rapidly performed utilizing a stapler. We recommend oversewing the staple line with nonabsorbable sutures and the pancreatic duct, if identified, individually ligated. Injuries lacerating the pancreatic capsule, parenchyma and involving the major ductal system if occurring at the neck or to the right superior mesenteric vessels can also be treated with pancreatectomy, although this will be an extended distal pancreatectomy. In cases in which the uncinate process is absent, a consideration for preservation of the distal pancreas with a pancreaticojejunostomy must be entertained. Combined pancreaticoduodenal injuries can be treated either by pyloric exclusion, or in rare cases duodenal diverticularization provided that the duodenum can be repaired primarily. Pancreaticoduodenectomy is formidable procedure and is uncommonly needed in cases of combined pancreaticoduodenal injuries. The indications for pancreaticoduodenectomy (Whipple procedure) are listed below:
- Massive and uncontrollable bleeding from the head of the pancreas, adjacent vascular structures, or both.
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Approximately 28% of all pancreatic injuries are managed by distal pancreatectomy. Only 4% of patients require pancreaticoduodenectomy (Whipple procedure).
Mortality
Mortality rate ranges from 5-54%. Mortality for Whipple resection is about 33%. Most early deaths are caused by exsanguination from associated vascular injuries versus the pancreatic injury itself. Late mortality can generally be attributed to the pancreatic injury and associated complications which include; sepsis, pancreatic fistulas and multiple systems organ failure. Mortality rates can be as high as 90% especially in those patients that undergo delayed surgical intervention.
Morbidity
Approximately 37% of all pancreatic injury cases will experience complications. Pancreatic morbidity is represented primarily by pancreatic fistula formation.
- A pancreatic fistula is defined as drainage of greater than 50 mls that persists longer than two weeks with elevated amylase and lipase levels. - Most pancreatic fistulas are treated with bowel rest, hyperalimentation and the use of a somatostatin analogue. - Posttraumatic pancreatic fistulas occur in approximately 14% of the cases. Fistulas develop in 42% of patients that undergo pancreatorrhaphy and drainage, and in 34% of patients that are treated with simple drainage alone. Fistulas develop in 27% of patients subjected to distal pancreatectomy. - Surgical reintervention is needed for the definitive treatment of pancreatic fistulas in less than 2% of the cases. However, reintervention should be considered for fistulas of greater than two months duration with unrelenting production of high volumes.
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Pancreatic abscess is the second most frequent complication with an incidence of 8%. Posttraumatic pancreatitis has an incidence of 4%. Pseudocysts occur in 3% of all cases while late hemorrhage occurs in 1% of the cases. Pancreatic exocrine and endrocine insufficiency occurs uncommonly.
References
1. 2. Asensio JA, Demetriades D, Hanpeter D et al. Issue editors. Management of Pancreatic Injuries. Current Problems in Surgery. Vol XXXVI, No. 5, p325-420. Wells SA Jr. Ed. St. Louis, MO: Mosby-Yearbook. May 1999. Asensio JA. Operative pancreatograms at 2:00 AM? In: Critical Decision Points in Trauma Care. Proceedings of Postgraduate Course No. 5; American College of Surgeons, p55-57, October, 1992.
Duodenal Injuries
Juan A. Asensio and Walter Forno Introduction
Duodenal injuries are often silent, easily missed and quite lethal. They are generally present in association with many other intraabdominal injuries. Delays in diagnosis and repair can make surgical management a more complex and technically challenging endeavor and increase an already heavy burden of morbidity and mortality. Early diagnosis and repair are the keys to achieving survival and good outcomes.
Larrey reported the first successful outcome from penetrating duodenal injury in 1811. The first successful surgical repair of a duodenal rupture was reported in 1896 by Herczel secondary to blunt trauma.
Incidence
The retroperitoneal location of the duodenum plays a strong role in protecting it and thus accounts for its low incidence of injury. Duodenal injuries occur with the frequency of 3-5% of all patients sustaining abdominal injuries.
Mechanism of Injury
Penetrating injuries account for 78% of all duodenal trauma. Blunt injuries account for 22% of all duodenal trauma. Duodenal injuries can be caused by falls from great heights or by direct impacts. Crush injuries of the duodenum may occur when a direct force is applied against the abdominal wall that is transmitted to the duodenum which is then projected posteriorly against the vertebral column. A good example of crush injuries are steering wheel injuries. Shearing injuries occur when acceleration and deceleration forces are applied to the duodenum. A cause of these are falls from great heights. Duodenal rupture occurs secondary to blunt trauma and is generally confined to the retroperitoneum. These injuries are highly lethal if not detected and repaired promptly.
Associated Injuries
The duodenum, by virtue of its anatomic proximity to other organs, is rarely injured alone. Associated injuries occur with a frequency of 87%.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A. Walter Forno, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 31.1. UGI showing dye extravasation and a duodenal injury at the second portion of the duodenum. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.

The most frequent site of duodenal injury is the second portion33%. The third and fourth portions are injured in 20% of the cases. The least frequently injured portion of the duodenum is the first portion14%. Multiple sites of injury occur in 14% of the cases.
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Fig. 31.2. CT scan showing a double lumen of the duodenum consistent with a duodenal transection. Note edema and fluid surrounding the transected duodenum. Also note the increased space between the duodenum and right kidney. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In press.

The diagnosis of duodenal injury, especially after blunt trauma, requires a high index of suspicion. Clinical presentations can range from a patient presenting in extremis to a picture of perfect hemodynamic stability. Patients presenting with a prehospital history of direct force applied to the mid-epigastrium, especially those having been struck by steering wheels, patients sustaining head-on collisions or right-sided impacts and those sustaining falls from great heights may harbor duodenal injuries. Because of the duodenums retroperitoneal location, early manifestations of injury may be absent. Physical examination may be characterized by minimal findings. Tenderness of the right upper quadrant or mid-epigastrium as well as signs of rebound tenderness, abdominal rigidity or acute peritoneal signs may be present in a patient harboring a duodenal injury. In retroperitoneal rupture of the duodenum, physical findings may be absent until duodenal secretions extravasate into the abdominal cavity.
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Fig. 31.3. Retroperitoneal blow-out of the second portion of the duodenum detected after 48 hours. Note the bile staining within the surrounding tissue and the periduodenal inflammatory process. Reprinted with permission from: Asensio JA, Demetriades D. Textbook of Techniques in Complex Trauma Surgery. W.B. Saunders Co., Philadelphia, PA. In Press.
Investigations
Laboratory tests are often of little help in the early diagnosis of duodenal injuries.
- Serum amylase level is unpredictable. Its elevation is usually moderate.
The serum amylase level may have a predictive value in patients admitted for observation and should be monitored at six hour intervals. A persistently elevated or rising amylase level may be of prognostic significance.
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Plain films of the abdomen are useful only if positive. Positive findings include: air collections outlining the upper pole of the right kidney, retroperitoneal gas, air around the right psoas and in the retrocecal region. These findings are difficult to detect and are often absent or missed. UGI contrast studies can diagnose duodenal leaks secondary to injury or duodenal hematomas. Ultrasound, although valuable in detecting free intraabdominal fluid and solid organ injury, is not reliable for the diagnosis of duodenal injuries. CT scan of the abdomen with intraluminal and intravascular contrast has a high degree of accuracy in detecting injuries to the duodenum. Increase in the space between the duodenum and right kidney is a significant finding, as is extraluminal gas or duodenal wall thickening.
- The CT scan, although quite reliable, may occasionally miss duodenal injuries.
MRI has been described as a diagnostic tool, but remains unproven. Diagnostic peritoneal lavage may be positive in 50-70% of patients harboring duodenal injuries. However, the positivity is due to associated intraperitoneal injuries and not the duodenal injury itself, as the duodenum is a retroperitoneal organ.
Surgical Management
The duodenum must be thoroughly explored with all four portions visualized directly. The duodenum is mobilized by incising the lateral peritoneal attachments and sweeping the second and third portions medially. The ligament of Treitz can also be transected for mobilization of the fourth portion of the duodenum. Findings that should increase the suspicion for the presence of a duodenal injury include: crepitus along the duodenal sweep, bile staining of paraduodenal tissues, documented bile leak or the presence of a right side retroperitoneal or pararenal hematoma. These findings should always be investigated, and never ignored. All duodenal injuries should be graded utilizing the American Association for the Surgery of TraumaOrgan Injury Scale for duodenal injuries (AAST-OIS). The simplest surgical techniques should be selected to manage the lower grade injuries while reserving the more complex techniques for the management of the more severe and advanced grade injuries. Basic surgical principles include debridement of duodenal injuries to viable tissue and meticulous double layer closure for all duodenal injuries. Approximately 75-85% of all duodenal injuries can be repaired primarily utilizing simple surgical techniques. Duodenal injuries should be drained with closed systems; however, these drains should not be placed directly in juxtaposition to the suture line to avoid duodenal fistula formation. Tube duodenostomies should be used rarely. This procedure is controversial. It may be used to decompress the duodenum and protect the suture line. It should be placed retrograde through the proximal portion of the jejunum. The technique of jejunal or serosal patches may be used rarely to protect a suture line. The original duodenal diverticulization procedure should be used rarely and only when precise indications exist, these being an injury through the first portion of the duodenum, pylorus and/or gastric antrum with or without an
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associated pancreatic injury. Reconstruction of these patients requires a vagotomy, gastrojejunostomy and retrograde tube duodenostomy but routine bile duct drainage with a T-tube is not used. Pyloric exclusion is the recommended surgical procedure for patients that incur duodenal injuries encompassing greater than 50% of the circumference of the duodenum with or without associated pancreatic parenchymal injuries, provided that the duodenal injury can be primarily repaired. It does not require a vagotomy. The pylorus is closed with a running nonabsorbable suture and a gastrojejunostomy is performed.
- The pyloric closure will generally open spontaneously in a period of time ranging from four to six weeks and gradually the gastrojejunosotomy will close. Marginal ulceration is quite uncommon.
Pancreaticoduodenectomy is a formidable procedure and is uncommonly needed in cases of combined pancreaticoduodenal injuries.
- The indications for pancreaticoduodenectomy (Whipple procedure) are listed below: - Massive and uncontrollable bleeding from the head of the pancreas, adjacent vascular structures, or both. - Massive and unreconstructable ductal injury in the head of the pancreas. - Combined unreconstructable injuries of the following; duodenum, head of the pancreas and common bile duct. The mortality of patients undergoing Whipple procedures averages 31-36%.
Mortality
Duodenal injuries carry a significant mortality rate. Most early deaths are caused by exsanguination from associated vascular injuries. Deaths solely ascribed to duodenal cause range from 6.5-12.5%. Factors that increase mortality in duodenal injuries include the presence of associated pancreatic and common bile duct injuries. Late mortality can generally be attributed to the duodenal injury and associated complications which include: sepsis, duodenal fistulas and multiple systems organ failure. Mortality rates can be as high as 50% in patients undergoing surgical procedures after 24 hours.
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Morbidity
Duodenal injuries are associated with very high rates of morbidity. Approximately 64% of all duodenal injury cases will experience complications. Duodenal morbidity is represented primarily by duodenal fistula formation resulting from failure of surgical repair secondary to suture line dehiscence and occasionally by duodenal obstruction.
- Posttraumatic duodenal fistulas occur in approximately 7% of all cases and carry a mortality of 14%. - Duodenal fistulas are quite difficult to manage and pose great problems with fluid and electrolyte balance.
Duodenal obstruction occurs between 1 and 2%. Intraabdominal abscesses occur with a frequency of 11-18%. Postoperative pancreatitis occurs in between 2.5 and 15% of the cases.
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References
1. 2. 3. 4. 5. Asensio JA, Buckman RF. Injuries to the duodenum In: Shackelford RT, Zuidema GD, Ritchie WP, eds. Shackelfords Surgery of the Alimentary Tract, 4th Ed. Philadelphia, PA: W.B. Saunders, 1995; Volume II, Chapter 10:110-123. Asensio JA, Stewart BM, Demetriades D. Penetrating Injuries to the Duodenum In: Ivatury RR, Cayten CG, eds. Textbook of Penetrating Trauma Philadelphia, PA: Lea & Febiger 1995; Chapter 49: 610-630. Asensio JA, Stewart BM, Demetriades D. Complex injuries of the Duodenum. In: Maull KI, Rodriguez A, Wiles III, CE, eds. Complications in Trauma and Critical Care. Philadelphia, PA: W.B. Saunders 1995; Chapter 32:364-379. Asensio JA, Gomez HA, Falabella A et al. Duodenal trauma. In: Rodriguez A, Ferrada R, Asensio JA et al, eds. The Pan-American Trauma Society Textbook of Trauma. Cali Colombia: Feriva and Co. 1997; Chapter 26:343-357. Asensio JA, Feliciano DV, Britt LD et al. Issue Editors. Management of Duodenal Injuries. Current Problems in Surgery. Wells SA Jr. ed. St. Louis, MO: MosbyYearbook. Nov. 1993; Vol. XXX, No. 11:1021-1100.
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CHAPTER 32
Colon/Rectal Injuries
Claudia E. Goetter and William F. Fallon Jr. Colorectal Trauma
Colon injury is the second most frequently encountered intraabdominal injury pattern in penetrating trauma. It uncommonly occurs in blunt trauma (2-5% of patients). Injury to the rectum, anus, and sphincter apparatus occurs infrequently. Development of the management of colon and rectal trauma is from the U.S. military experience (WW I through Vietnam) with high velocity gunshot or fragmentation wounds. Extensive tissue destruction and contamination often resulted in septic complications if the colon injuries were repaired. From this developed mandatory colostomy for colon injury and the four basic tenets of management of rectal injury: repair of injury, proximal fecal stream diversion, distal washout of rectal stump, and presacral drainage. More recent civilian experience has challenged many of these dictums for mandatory use.
Pertinent Anatomy
The posterior portions of the ascending and descending colon are retroperitoneal. Injury may occur here without obvious anterior injury. The rectum is 12-15 cm long with the upper portion intraperitoneal and covered by serosa. The middle portion is covered by peritoneum over its anterior surface and is retroperitoneal posteriorly. The distal portion of the rectum is completely below the peritoneum (Fig. 32.1). Because of the lateral bends in the rectum the distance from the anus to the peritoneum is only 3-5 inches. Intraperitoneal injury is possible even with short objects of injury.
Penetrating Trauma
Bowel injury (large or small) is present in 90% of anterior gunshot wounds and 50% of stab wounds. Flank and back injuries are less likely to penetrate the peritoneum. Gunshot wounds (80%) to the lower abdomen, pelvis, buttocks or gluteal region, perineum and upper thighs can have a trajectory through all levels of the rectum, involving the sphincter muscles and penetrating the peritoneum (Fig. 32.2). Stab wounds or impalement (3%), including rectal insertion of objects (6%), are less common and can cause a similar pattern of injury depending upon the length of the implement. Iatrogenic injuries due to obstetric or endoscopic procedures, diagnostic contrast enemas and intraoperative misadventure may occur in patients with previous bowel preparation allowing primary repair without diversion.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. C.E. Goetter, University Hospitals of Cleveland, Cleveland, Ohio, U.S.A. W.F. Fallon Jr., Metro Health Medical Center, Cleveland, Ohio, U.S.A.
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Fig. 32.1. Rectal anatomy showing the three regions of the rectum. Reproduced with permission from Haas et al. Civilian injuries of the rectum and anus. Diseases of the Colon and Rectum. 1979; 22:17.
Blunt Trauma
Blunt colon injuries are usually due to shear injury to the bowel or mesentery from deceleration. Blow-out injuries from compression are less common but can occur. Blunt trauma is an infrequent cause of rectal injury (5-10%). However, the amount of energy associated with this mechanism of injury is so great that the rectal injury is often only one component of multisystem injury and hemorrhagic shock. There is significant risk for infectious sequelae if not identified early or treated aggressively. The cause of this type of injury is usually motor vehicle, motorcycle or pedestrian-vehicular accidents. Pelvic fractures, particularly open pelvic fractures, have potential for rectal injury. This occurs due to penetration of bony fragments through the wall of the rectum and is almost always below the peritoneal reflection. Vascular and urologic injuries are frequently associated. The bladder and urethra must be evaluated in every patient with possible rectal injury. Rectal tears can also occur with less severe injury such as a fall or straddle injury resulting in disruption of the attachments to the pelvis or from shear forces from pelvic structural deformation. These injuries are usually below the peritoneal reflection and may be either partial or full thickness. Often only the presence of extraperitoneal, retroperitoneal air on plain radiography, subcutaneous emphysema on physical examination, the presence of pelvic hematoma or abscess on computerized tomography of the pelvis indicate the presence of an injury.
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Fig. 32.2. GSW trajectory shows the short distance from the perineum to the abdomen and multiple associated injuries. Reproduced with permission from Maull et al. Penetrating wounds of the buttock. S, G & O 1979; 149:856.)
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Devascularization injury with full thickness rectal necrosis is very rare due to the to the rich collateral blood flow through the pelvis. Embolization of the internal iliac vessels and operative pelvic exposure may severely compromise a blood supply that is already limited due to pelvic injury or preexisting vascular disease. Insufflation injury due to air or water under high pressure may result in rectal rupture, retroperitoneal hematoma and intraabdominal perforation. This has been reported with water-skiing and Jet ski activities. Suction injuries with transrectal evisceration in children due to swimming pool drains have been reported as well.
Diagnosis
A high index of suspicion must be maintained to diagnose colon and rectal injuries as these may initially present with only minimal indications of injury. Missed injury in this organ system may be devastating.
Signs and Symptoms

Patient with hemodynamic instability should complete the diagnostic workup and resuscitation in the operating room. Exsanguination is the overwhelming cause of early death with this injury, hence the management of shock takes precedence. DPL may show fecal contamination or a WBC count greater than 200. Symptoms of injury may be minimal in the unresponsive, hypotensive patient and signs of injury may not initially be detected. Rectal examination is performed when feasible.
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Patients with trauma to the torso should be suspected of having a colon injury. Diagnosis is usually made at laparotomy for other reasons. Signs of peritoneal irritation are seen with intraperitoneal injury, but may develop only after a period of observation in small perforations or devascularization injuries. In stable patients, history of straddle injury, pelvic fracture or trajectory of penetrating injuries should suggest the possibility of rectal injury. Symptoms of abdominal pain, pelvic or rectal pain and tenesmus are common. Careful inspection of the anus, perineum and gluteal region may identify lacerations with extension into the anus or rectum. Wounds should not be probed or vigorously explored as this may cause severe bleeding. In impalement injury, the object must be left in place and removed only under controlled circumstances, usually the operating room, to prevent sudden, unexpected exsangination. The history of the events may not be apparent and there may be delay in presentation due to embarrassment or events of abuse. Blunt injuries include minor falls or straddle injury. Penetrating injuries include minor impalement injury, sexual assault, autoerotic or homosexual activity or rectal foreign bodies. These injuries are predominantly intraluminal and are almost always below the peritoneal reflection. There is usually evidence of sepsis with either systemic signs or leukocytosis with delayed presentation.
Clinical Evaluation
A digital rectal examination is performed to evaluate sphincter tone, severe pain on examination, palpable defect or mass, bony fragments in or against the rectal wall and evidence of either gross or occult blood in the stool. The presence of intraluminal blood is highly suggestive of rectal injury regardless of the vector of wounding; its absence does not reliably exclude the presence of rectal injury. Proctosigmoidoscopy is essential with suspicious trajectory or entrance wounds. While not perfect, the combination of digital rectal examination and proctosigmoidoscopy has about 95% diagnostic accuracy and should be performed together with a suspected rectal injury. Further studies add little to this accuracy rate.
Radiographic Evaluation
CT scanning of the abdomen and pelvis with triple contrast can help evaluate the course of a tangential penetrating injury to the back or flank but may be difficult to perform and interpret. Scans with mesenteric hematomas or with free fluid and no solid organ injury are suspicious for hollow viscus injury. CT can help define the extent of pelvic sepsis with delayed presentations of rectal injury and provide the option of percutaneous drainage. There is little utility for radiographic evaluation of rectal injury in the acute setting. Patients with subtle or delayed presentations may have soft tissue air or abscess as their only evidence of injury. Plain radiographs of the pelvis may reveal extraluminal or extraperitoneal air or may be the first indication of a foreign object within the rectum (Fig. 32.3). Anteroposterior and lateral views localize the foreign body. Intrarectal contrast studies must be used cautiously as barium contamination may worsen septic complications in synergy with fecal contamination.
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Fig. 32.3. Retroperitoneal staining indicates possible posterior injury. Reproduced with permission from Burch JM. Injury to the colon and rectum. Trauma, 4th edition. Mattox, Feliciano, Moore ed. Phila, PA: McGraw-Hill 2000:766.
Management Operative Treatment

Preoperative preparation includes vigorous fluid resuscitation, bladder catheterization and broad spectrum antibiotics against bacteroides and other enteric organisms. Operation is performed in modified lithotomy position if rectal injury is suspected. A rigid sigmoidoscope should be available. Patients with exsanguination may require the supine position initially with repositioning once hemorrhage control is achieved. Full abdominal exploration, hemorrhage and contamination control should be completed prior to managing specific intestinal injuries. In an abbreviated damage control laparotomy, the injured colon may be resected with staplers and left closed off until reoperation.
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Nonoperative Treatment
In some circumstances, the choice may be not to operate. Patients who have sustained extraperitoneal iatrogenic injury from diagnostic procedures, minor partial thickness impalement injury and some patients who have free intraperitoneal air but no abdominal symptoms following endoscopic procedures may potentially be nonoperatively managed. Patient selection is critical and they must be followed closely with serial examinations. Gastrointestinal tract rest, intravenous fluid replacement and broad spectrum antibiotic therapy is begun. Delay in abdominal exploration when symptoms develop can be fatal.
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Intraperitoneal Injury
Small colon injuries may be subtle, particularly those at the splenic flexure or in the retroperitoneal portions of the colon. Colon in a trajectory path or associated with bloodstaining of the retroperitoneum must be fully mobilized and carefully inspected (Fig. 32.3). Discrete injury from low velocity penetrating trauma associated with little or no peritoneal soilage can be successfully managed with primary repair alone. Selected injuries without devascularization and significant contamination can be resected and anastomosis performed. Patients with shock, more extensive injury, multiple organ injury, significant intraabdominal contamination by feces in combination with blood or barium, or delay in operation warrant conservative treatment with formation of a diverting colostomy. The most significant factors for infectious complications in civilian rectal injury are delay in the detection of the rectal injury or delay in the performance of the diverting colostomy. Despite the trend to primary repair without colostomy in colon injury, the risk of pelvic sepsis due to the retroperitoneal location of the rectum mandates a colostomy in almost all circumstances. Controversy surrounds the role of distal washout, presacral drainage and type of colostomy. Those who have primary repair without colostomy receive no further surgical treatment. Those with injury treated by colostomy and resection whose injury was above the peritoneal reflection also require no further treatment. Repair with exteriorization is rarely performed today. Repair with proximal diversion is usually reserved for rectal injury. Drainage of the retrorectal space may be indicated if significant retroperitoneal, presacral and pararectal dissection was done to treat injury to the midportion of the rectum. This may be via the perineum near the anococcygeal raphe or transabdominally using closed suction drainage (Fig. 32.4). Distal rectal washout is controversial as there is potential for increasing fecal contamination into the extrarectal tissues in penetrating trauma, though others have noted a decreased incidence of infectious sequelae. It clearly decreases infectious sequelae in rectal injury from blunt trauma, open pelvic fracture and major perineal soft tissue injury. Washout is performed at the termination of the abdominal portion of the procedure via a mushroom catheter through a pursestring suture in the wall of the distal colon. The anal sphincter is dilated and large stool is gently manually removed. Several liters of warm crystalloid are irrigated through the mushroom catheter until clear.
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Subperitoneal Injury
Full thickness injury should be treated in the same manner as the intraperitoneal rectum. A diverting sigmoid loop colostomy is most frequently used because there is often no need for resectional treatment and it is unnecessary to enter the abdomen to accomplish presacral drainage if there is no associated intraperitoneal injury. Distal rectal washout minimizes further fecal contamination. Rectal repair is difficult because exposure is limited. Repair is usually deferred until the risks of fecal contamination and infection are minimal.
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Fig. 32.4. Proximal diversion and presacral drainage as practiced routinely in the past. Reproduced with permission from Baylor College of Medicine.
Severe rectal destruction is uncommon but usually requires a Hartmanns procedure and distal washout is accomplished by local irrigation at the perineum. Repeated local debridement is frequently needed. Rarely, abdominoperineal resection is required.
Perineal and Sphincter Injury
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Damage to the sphincter may be direct or via disruption of nervous or vascular supply. The associated risks are infectious early and incontinence later in the patients course. Rectal mucosal lacerations are repaired with interrupted absorbable sutures in the submucosal layer. The sphincter is repaired with interrupted sutures through the muscle sheaths and repairing the remainder of the injury in layers. This may be difficult and may be deferred for elective repair in patients with multiple or complex injuries. Even without a documented rectal injury, complex pelvic or perineal injuries may require fecal diversion to control septic sequelae. Open pelvic fractures should always have fecal diversion. Foreign bodies can be removed in the emergency department if they can be grasped easily at the anal canal. General anesthesia is necessary for foreign objects that are large, have sharp edges or that have become lodged higher. Gentle technique and ingenuity are required for the atraumatic removal. Blind use of grasping forceps should be avoided. The patient is prepared for laparotomy in the event that the foreign body cannot be removed. Usually the object can be manipulated into range of the proctoscope for grasping and
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removal though rarely the colon will have to be opened and the object extracted. A thorough proctoscopic inspection following foreign body removal is essential to be sure that no objects are retained and that there is no evidence of significant injury to the rectal wall.
Outcome
Early fatalities are due to exsanguination, almost never due to colon or rectum injuries. Late fatalities are due to sepsis and multisystem organ failure (1-5%) which may be due to intestinal injury. Rates of abscess (3-10%) and fistula (1-5%) are lower for primary repair, probably due to primary repair being performed in less severely injured patients.
Mistakes and Pitfalls

Rectal injury can only be diagnosed with a strong index of suspicion. This diagnosis is often overlooked in multiply injured patients. Penetrating trauma may result in retroperitoneal colon injury without evidence of anterior injury. This is also missed by DPL. Mobilize the colon adequately to examine the posterior surface. Bullets which have passed through the colon will contaminate soft tissues. Remove them if possible and beware of them as a septic focus postoperatively. When in doubt, perform a colostomy!
References
1. 2. 3. 4. 5. Fallon WF Jr. The present role of colostomy in the management of trauma. Diseases of the Colon and Rectum 1992; 35:1094. Burch JM, Feliciano DV, Mattox KL. Colostomy and drainage for civilian rectal injuries: Is that all? Annals of Surgery 1989; 209:600. Brunner RG, Shatney CH. Diagnostic and therapeutic aspects of rectal trauma: Blunt versus penetrating. The American Surgeon 1986; 53:215. Ivatury RR, Licata J, Gunduz Y et al. Management options in penetrating rectal injuries. American Surgeon 1991; 57:50. Barone JE, Yee J, Nealon TF Jr. Management of foreign bodies and trauma of the rectum. Surgery, Gynecology and Obstetrics 1983; 156:453.
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CHAPTER 33
Genitourinary Tract Trauma

Eila C. Skinner Kidney Injuries Incidence
Kidneys injured in approximately 10% of all trauma patients Blunt trauma accounts for 90% of renal injuries
Hematuria present in about 95% of cases
- Degree of hematuria does not correlate with severity of injury. - Some severe injuries, such as vascular pedicle injuries, may have no hematuria - Hematuria out of proportion to degree of trauma suggests preexisting renal abnormality (i.e., hydronephrosis)
Injury Severity
Minor injury
- contusion, subcapsular hematoma, superficial laceration - account for 70% of all injuries
Major injury
- deep laceration into collecting system, shattered kidney, pedicle injuries
Associated Injuries
Present in 80-95% of penetrating trauma with renal injuries Present in 40-50% of severe blunt trauma with major renal injuries Nature and extent of associated injuries predicts mortality
Radiologic Evaluation
Adequate visualization of injury is key to safe management. Indication for radiologic studies
- All penetrating trauma with hematuria or close proximity to kidneys - Blunt trauma with gross hematuria or microhematuria and any hypotension
IVP is still valuable screening tool

- Over 90% accurate in identifying injury - Often not able to completely characterize injury
CT scan with IV contrast is more accurate to characterize injury.

- May be used as primary study or to further evaluate abnormal IVP - Should be performed on any stable patient with poorly visualized kidney on IVP - With faster spiral scanners, need to request delayed views to see contrast in collecting system
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Eila C. Skinner, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 33.1. CT scan showing fractured left kidney secondary to blunt trauma. Extravasation of contrast is obvious posterior to the kidney, but the ureter appears intact. This was successfully managed with observation.
- Ideal for determining depth of laceration, degree of extravasation of urine, hematoma, segmental devascularization, and pedicle injuries - Repeat CT should be done prior to discharge in cases of major injuries or extravasation to ensure absence of significant urinoma
Angiography
Best first study for stab wounds with gross hematuria Accurately identifies active bleeding and arterio-venous fistulas Can embolize vessel Often avoids need for open surgery Preserves more renal parenchyma than partial or total nephrectomy
Management
Goal is maximum renal preservation with minimum complications.
Blunt Injuries
Most blunt renal injuries can be managed nonoperatively.
Bed rest until all gross bleeding stops Serial hemograms Follow-up blood pressure check in 2-3 months Repeat imaging in 2-3 months for major injuries
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Indication for renal exploration

- Severe life-threatening bleeding - Major urinary extravasation, especially around renal pelvis (minor extravasation may be observed) May have disruption of uretero-pelvic junction More common in children with blunt trauma - Large devascularized renal segment
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Trauma Management - Expanding or pulsatile retroperitoneal hematoma at urgent laparotomy (without preoperative xrays)
Penetrating injuries more often require exploration

- Stab wounds may be managed nonoperatively with same indications for exploration as blunt trauma
Gunshot wounds have high risk of delayed complications due to blast effect.
- Many centers perform exploration - If not explored, must be carefully monitored with repeat CT scans
Pedicle injuries
- Laceration of main renal veinmay be repaired (or ligated on left if gonadal and adrenal branches are intact for collateral flow) - Laceration or thrombosis of main renal artery may be repaired, but often kidney is not salvageable Thrombosis without bleeding: - Due to high-speed deceleration injury - May be revascularized within first few hours. - If recognized later, can observe. May require delayed nephrectomy due to hypertension.
Expected renal salvage rates

- Blunt traumaover 90% - Penetrating trauma70-85%
Technique of surgical management of injured kidney

- Obtain vascular control of renal artery and vein through retroperitoneum prior to reflecting colon. - Dissect off Gerotas fascia (avoid subcapsular dissection). Useful techniques include: - Upper or lower pole partial nephrectomy - Wedge resection of injured area - Mattress sutures to control bleeding - Restore capsule with peritoneal patch if necessary - Wrap repair with omentum - Drain with suction drains
Complications
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Unnecessary exploration results in higher nephrectomy rate, especially in more severe blunt trauma. Continue bleedingmay be managed by selective embolization. Urinoma
- Need to rule out missed ureteral injury. - Ensure outflow down ureter is openmay require stent. - Drain urinoma percutaneously.
Delayed renal vascular hypertension

- Can result from even minor injuries such as contusion - May require partial or total nephrectomy
Ureteral Injuries Epidemiology

Rarely due to external trauma (most often iatrogenic surgical injury) More likely due to penetrating traumagun shot or stab wounds
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Delay or missed diagnosis is very common
Investigations
IVP with tomography
- 94% sensitive for ureteral injury - Most often see some proximal dilation as well as extravasation
CT scan with excretory phase

- See extravasation around ureter
Retrograde pyelography is definitive study

- Confirms site of injury - May be able to pass stent
Management
Early diagnosis (within 5 days of injury)
- Usually do open repair - Avoid stripping ureter out of Gerotas fasciapreserve vascular supply from gonadal vessels - Debride injured section of ureter (especially important in GSW due to blast effect) - Upper or mid-ureterend-to-end spatulated repair - Lower ureterreimplant ureter into bladder with psoas hitch if needed - Stent and drain repair - Omental wrap if available - If large section of ureter is destroyed and primary repair impossible Ligate ureter and place nephrostomy tube (open or percutaneously), with plan for delayed repair. Nephrectomy is rarely necessary.
Delayed diagnosis (beyond 5 days)

Best managed nonoperatively Stent from below if possible Percutaneous nephrostomy if cannot pass stent Drain urinoma if present Delayed repair or ileal interposition after 3 months if stricture forms
Bladder Injuries Epidemiology

Bladder is mostly extraperitoneal when emptywhen full peritoneal surface expands Injury may be due to blunt or penetrating trauma Often associated with pelvic fracture
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Diagnosis
Over 95% have hematuria, usually gross Any pelvic trauma with hematuria should have cystogram
- Cystogram should include filled (at least 300 cc) and emptied views - CT cystogram appears to be equivalent in accuracy to standard films (only done if CT scan already planned to evaluate trauma)
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Fig. 33.2. Cystogram showing intraperitoneal bladder rupture. This should be repaired and a suprapubic tube placed.
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Type of Injuries
Injuries classified into extraperitoneal or intraperitoneal by cystogram findings (may have both)
- Extraperitoneal more common, often associated with pelvic fracture.
Need to fully evaluate distal ureters in all cases (with IVP, CT or intraoperative exploration)
Management
Intraperitoneal Injury
- All should be explored and repaired - Repair injury from inside of bladder with absorbable suture - Place large bore suprapubic tube and pelvic drain
Extraperitoneal Injuries
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- May be managed with Foley catheter only if extravasation small - Must ensure adequate drainage - Indication for exploration: Large amount of extravasation Possible bony fragments within bladder Difficulties with catheter drainage (i.e., clots) with minor injuries - Technique Enter bladder anteriorly, avoid disturbing pelvic hematoma (especially with pelvic fracture). Repair from within with absorbable suture. Place large-bore suprapubic catheter and pelvic drain.
Urethral Injuries Epidemiology

Most often associated with blunt trauma, especially in association with pelvic fractures or straddle injuries Classified into anterior and posterior injuries
Dried or fresh blood at the urethral meatus on exam is pathognomic of urethral injury Inability to pass urine High floating prostate on rectal examination Extravasation in the scrotum
Investigations
Imaging is by retrograde urethrogram.
- Indicated in all cases of suspected urethral trauma, especially pelvic fracture
Anterior (penile and bulbar urethral) injuries

- Usually caused by straddle fall onto hard object - Occasionally caused by penetrating injuries - Often extravasates blood and urine into scrotum and perineum (butterfly hematoma) - Management Establish urinary drainage, usually with percutaneous suprapubic tube. Exploration is rarely indicated. It should be considered in penetrating injuries and in blunt trauma with large lacerations. - Surgical Technique Deglove penis from corona (circumcising incision) for distal injuries Approach from perineum below scrotum for bulbar injuries. Debride and repair with fine absorbable suture. Leave catheter for 7-10 days. Do antegrade urethrogram prior to removing catheter.
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Posterior (membranous) urethral injuries

- Presentation Over 90% associated with pelvic fracture Usually unable to void Prostate may not be palpable on rectal exam (high-riding prostate) High incidence of associated injuries and severe pelvic bleeding
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Trauma Management In children, disruption may extend through prostatehigher risk of complications - Management Goals of management: - Establish urinary drainage - Minimize long-term complications, including impotence, incontinence, and stricture In most cases, open suprapubic tube bladder drainage with planned for delayed repair is the best approach In selected cases, a guidewire may be passed endoscopically using flexible cystoscopes from above and below, and a catheter passed over the wire into the bladder. Attempts at primary suture repair or open realignment are contraindicated increase risk of bleeding and impotence.
Penile Injuries
Skin Injuries
- May occur from bites or penetrating injuries - Generally can be cleaned, debrided and sutured - Use broad-spectrum antibiotics
Degloving
- Circumferential loss of skin at the base of the penis can result in interruption of distal lymphatics and severe edema. - Usually requires discarding any distal shaft skin and using delayed skin grafts.
Strangulation
- Results when constricting band is left on base of penis-ring, condom catheter, rubber bands, etc. - Need to reduce edema with wrapping - May require anesthesia to remove object
Penile Fracture
Results from sharp angulation of erect penis Often patient reports sudden pain and an audible crack Causes severe bleeding within Bucks fascia Penis becomes acutely grossly edematous and ecchymotic Need to do urethrogram/urethroscopy if hematuria present Requires exploration Deglove penis from corona Locate fracture Debride and repair with fine polypropyline suture with knots inverted May occasionally result in erectile dysfunction
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Amputation
- Often self-inflicted by psychologically ill patient - Amputated part should be placed in sterile bag on (not in) ice - Requires microsurgical repair, including arteries, veins, the corporal bodies, and urethra - Place suprapubic bladder catheter for urinary drainage - Skin is often sloughedmay require skin grafts
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Scrotal Injuries
May be blunt or penetrating injury Need to evaluate for injury to urethra or rectum Scrotal skin injuries
- Lacerations or avulsions may be debrided and sutured, or left open if grossly contaminated. - In complete loss of scrotal skin, testes can be placed in the thigh, or kept covered with moist dressings until delayed mesh skin grafting is performed.
Testicular Injuries
- Patient presents with severe pain and scrotal swelling - If testis is palpable, ruptured testis will feel very irregular - Scrotal ultrasound may be helpful Accuracy only about 75%
Exploration is usually required unless testis is clearly palpably normal.

1. 2. 3.
Trans-scrotal incision Open tunica vaginalis Debride extruded seminiferous tubules Repair tunica with fine absorbable suture If testis is devascularized or severely shattered, perform orchiectomy Drain hemiscrotum with small Penrose drain
Sagalowsky AL, Peters PC. Genitourinary Trauma. In: Walsh PC, Retik AB, Vaughan ED et al, eds. Campbells Urology, 7th Edition. Philadelphia: WB Saunders Company 1998; 3085-3120. Skinner EC, Parisky YR, Skinner DG. Management of complex urologic injuries. Surg Clinics of North Am 1996; 76:861-878. McAninch JW, Carroll PR. Renal exploration after trauma, indications and reconstructive techniques. Urol Clin North Am 1989; 16:203-212.
References
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CHAPTER 34
Abdominal Vascular Injury

Juan A. Asensio and Matias Lejarraga Introduction
Abdominal vascular injuries are amongst the most lethal injuries sustained by trauma patients. Many of these patients present in cardiopulmonary arrest and require drastic life saving measures, such as emergency department thoracotomy, aortic cross clamping and open cardiopulmonary resuscitation. To compound the problem, exposure of retroperitoneal hemorrhaging vessels is quite difficult and requires extensive dissection and mobilization of intraabdominal organs.
Historical Perceptive
Eck, a Russian surgeon, in 1877, was the first to perform a permanent union between two intraabdominal blood vessels when he performed an anastomosis between the portal vein and inferior vena cava. Dorfler, in 1899 recommended fine round needles and sutures to include all layers of the vessel. Clermont, in 1901 successfully performed an end-to-end anastomosis of a divided inferior vena cava with continuous fine silk suture. Voorhees, in 1956 pioneered the use of abdominal aortic prosthetic grafts.
Incidence
In military conflicts abdominal vascular injuries account for about 3% of all vascular injuries. In civilian series injuries to abdominal vessels account for about 30% of all vascular trauma treated in urban trauma centers
Penetrating abdominal injuries are the most common causes of abdominal vascular injuries and account for approximately 90-95% of all abdominal vascular injuries. Approximately 25% of all patients undergoing laparotomies for gunshot wounds of the abdomen sustain abdominal vascular injuries. Approximately 10% of patients undergoing exploratory laparotomy for stab wounds of the abdomen will have abdominal vascular injuries.
Associated Injuries
The abdominal blood vessels, by virtue of their retroperitoneal location and anatomic proximity to other organs are rarely injured alone.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Juan A. Asensio, University of Southern California, Los Angeles, California, U.S.A. Matias Lejarraga, University of Southern California, Los Angeles, California, U.S.A.
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It is estimated that approximately 2-4 associated intraabdominal injuries occur with abdominal vascular injuries.

Abdominal vascular injury associated with blunt trauma most commonly occurs in upper abdominal arteries and veins. Penetrating injuries are unpredictable and may occur within any area of the abdomen often affecting more than one vessel.

The clinical presentation of patients that have sustained abdominal vascular injuries will depend on whether they present with a contained retroperitoneal hematoma or free bleeding within the abdominal cavity. Obviously those with contained retroperitoneal hematomas will present either hemodynamically stable or with some degree of initial hypotension responsive to intravenous fluids, whereas those with free retroperitoneal and intraabdominal hemorrhage will present profoundly hypotensive. The presence of penetrating abdominal injury associated with massive abdominal dissention and shock usually signals the presence of an uncontained intraabdominal hemorrhage secondary to injury of one of the major abdominal vessels. Abdominal discomfort and pain as well as physical examination findings consistent with peritoneal irritation or signs of peritonitis may be due either to the abdominal vascular injury or to associated abdominal organ injuries frequently associated with intraabdominal vascular injuries. The presence or absence of femoral, popliteal, dorsalis pedis and posterior tibial pulses should be documented in both extremities.
Investigations
Laboratory tests provide little help in the early diagnosis of abdominal vascular injuries. As many patients present with profound hypotension, there are few investigations that can actually be instituted. The use of ultrasound will prove useful in detecting the presence of intraabdominal fluid. A plain radiograph of the abdomen is of diagnostic value particularly in patients sustaining gunshot wounds so that the location and trajectory of the missile can be evaluated. A CT of the abdomen may be obtained in hemodynamically stable patients that have sustained blunt trauma and may be useful in detecting retroperitoneal hematomas or nonvisualizing kidneys secondary to blunt injury to the renal vessels.
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Surgical Management Emergency Department

All trauma patients should be evaluated and resuscitated per ATLS protocols. In patients presenting with a strong suspicion of abdominal vascular injuries, it is not advisable to place intravenous lines in the femoral veins in case there
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are iliac venous or inferior vena caval injuries that may be actively hemorrhaging. Broad spectrum antibiotics are administered prior to surgical intervention. In patients presenting in cardiopulmonary arrest an emergency department thoracotomy will be needed in order to perform open cardiopulmonary massage and to cross clamp the descending thoracic aorta. Time is of the essence and these patients must be rapidly transported to the OR without any further radiographic evaluations or delays.
Intraoperative Management
In the operating room the entire patients torso from neck to mid-thighs is prepared and draped. The area of the mid-thighs is quite important should the necessity arise to obtain an autogenous saphenous vein graft. Abdominal injuries should be explored through a midline incision extending from xyphoid to pubis. Immediate control of life threatening hemorrhage followed by immediate control of sources of gastrointestinal spillage are early goals to achieve. The next step in the management of abdominal injuries consists of thorough exploration of the abdominal cavity. Since the abdominal vasculature resides in the retroperitoneum, a thorough exploration of these structures must be performed utilizing a systematic approach of the anatomic zones of the retroperitoneum. The first and most important goal to achieve in the management of abdominal vascular injuries is hemorrhage control. As in all vascular injuries proximal and distal control of the hemorrhaging blood vessel is ideal. However, in exsanguinating abdominal vascular injuries achieving this rapidly could be quite difficult. In the case in which the patient decompensates during laparotomy, the abdominal aorta can be controlled either digitally at the aortic hiatus, by the use of an abdominal aortic root compressor or by placement of an aortic cross clamp. Once the exsanguinating hemorrhage has been controlled, the trauma surgeon should classify the hemorrhage or hematoma into one of the three zones of the retroperitoneum. There are three zones of the retroperitoneum. Zone I, Zone II, Zone III.
- Zone I begins at the aortic hiatus and ends at the sacral promontory; it is located midline and courses on the top of the spinal column. This zone is divided into Zone I supramesocolic and Zone I inframesocolic. - There are two Zones II. Right and left and are located at the pericolic gutters. - Zone III begins at the sacral promontory and encompasses the pelvis.
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Zone I supramesocolic contains the suprarenal abdominal aorta, the celiac axis and the first two parts of the superior mesenteric artery (superior mesenteric artery: Part 1 from its origin at the aorta to the point where the inferior pancreaticoduodenal artery emerges, part 2 from the inferior pancreaticoduodenal to the origin of the middle colic artery, part 3 from the middle colic artery to the point of origin of the major jejunal branches, ileocolic and right colic, and part 4 the main trunk of these branches). This zone also contains the infrahepatic suprarenal inferior vena cava, the infrarenal inferior vena cava as well as the proximal portion of the superior mesenteric vein. Right and left zones II contain the renal vascular pedicles. Zone III contains both common iliac arteries and veins, as well as their internal and external branches.
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The portal-retrohepatic area is a special area which contains the portal vein, hepatic artery and retrohepatic vena cava. As soon as the trauma surgeon has identified and classified the hemorrhage or hematoma into one of the zones, he must then approach this zone to obtain vascular control and to expose the injured blood vessel to attempt definitive repair. Each zone requires a different and complex maneuver to expose these vessels. Zone I supramesocolic is generally approached utilizing a maneuver that rotates the left-sided viscera medially. This approach requires transection of the avascular line of Toldt of the left colon, along with incising the lienosplenic ligament and rotating the left colon, spleen, tail and body of the pancreas as well as the stomach medially. This exposes the aorta from its entrance into the abdominal cavity via the aortic hiatus and includes exposure of the origin of the celiac axis, superior mesenteric artery and the left renal vascular pedicle. Alternatively the left kidney can be mobilized medially, although this is generally not done.
- An alternative maneuver is to perform an extended Kocher maneuver along with transecting the avascular line of Toldt of the right colon and mobilizing medially the right colon, hepatic flexure, duodenum and head of the pancreas to the level of the superior mesenteric vessels and incising the retroperitoneal tissue to the left of the inferior vena cava. This maneuver exposes the suprarenal abdominal aorta between the celiac axis and the superior mesenteric artery. This has as a disadvantage that the exposure obtained is below the level of any wounds of the supraceliac aorta and the hiatus.
Maneuvers used to expose injuries in Zone I inframesocolic include displacing the transverse colon and mesocolon cephalad, eviscerating the small bowel to the right, locating the ligament of Treitz, transecting it along with the tissue alongside the left of the abdominal aorta until the left renal vein is located. This exposes the infrarenal aorta.
- To expose the infrarenal inferior vena cava the avascular line of Toldt of the right colon is transected along with a Kocher maneuver sweeping the pancreas and duodenum to the left and incising the retroperitoneal tissues that cover the inferior vena cava.
Exposure to right and left Zones II depends as to whether the perirenal hematoma or active bleeding is located laterally or medially. If active bleeding is found medially or there is an expanding hematoma, vascular control of the vessels in the pedicle is preferable.
- On the right, this is achieved by mobilizing the right colon and hepatic flexure as well as performing a Kocher maneuver, exposing the inferior vena cava infrarenally and continuing the dissection cephalad by incising the tissues directly over the suprarenal infrahepatic inferior vena cava. This is done until the right renal vein is encountered. Further dissection superiorly and posteriorly to the right renal vein will locate the right renal artery. - On the left, the left colon and splenic flexure are mobilized. The small bowel is then eviscerated to the right. The ligament of Treitz is located and the transverse colon and mesocolon are displaced cephalad. This should locate the infrarenal abdominal aorta; cephalad dissection will locate the left renal vein as it crosses over the abdominal aorta. The left renal artery will also be found superiorly and posteriorly to the left renal vein.
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Trauma Management - Alternatively, if a perirenal hematoma or bleeding is found laterally with no extension into the hilum of the kidney the lateral aspects of Gerotas fascia can be incised and the kidney elevated and displaced medially to locate the hemorrhage.
Exposure to the vessels in Zone III can be achieved by taking down the avascular line of Toldt of both the right and left colons and displacing them medially. Utilizing a combination of blunt and sharp dissection, the common iliac arteries and veins will then be located. Meticulous attention must be paid to locating the ureter as it crosses the common iliac artery. Dissection is then extended in a caudad direction opening the retroperitoneum over the vessels. The routine principles of vascular surgery also apply to the management of the abdominal vascular injuries. Adequate exposure, proximal and distal control, debridement of the vessel wall, prevention of embolization of clot or plaque, irrigation with heparinized saline, judicious use of Fogarty catheters, meticulous arteriorrhaphy or venorrhaphy with monofilament vascular sutures, avoiding narrowing of the vessel during repair, insertion of an autogenous or prosthetic graft when applicable and intraoperative angiography when feasible, are the mainstays of successful repair. The management of vascular injuries in Zone I, supramesocolic will consist of primary arteriorraphy of the suprarenal abdominal aorta when feasible, and in rare occasions the insertion of a Dacron or PTFE graft.
- Injuries to the celiac axis are usually dealt with by ligation. - Management of injuries to the first two zones of the superior mesenteric artery should be dealt with by primary repair whenever possible. Intense vasoconstriction makes this quite difficult. These injuries can also be ligated as theoretically there are sufficient collaterals to preserve the viability of the small and large bowel. However, profound vasospasm may lead to intense ischemia and bowel necrosis. The first two zones of the superior mesenteric artery can also be repaired either with an autogenous or prosthetic graft. The insertion of a temporary shunt has also been described.
The management of injuries to Zone I inframesocolic employs some of the same techniques as in zone I supramesocolic. In Zones 3 and 4 the superior mesenteric artery should also be repaired, although the main jejunal and colic branches of Zone 4 may be individually ligated.
- The management of inferior mesenteric artery injuries usually consists of ligation. - The management of injuries to the infrahepatic suprarenal inferior vena cava, as well as the infrarenal inferior vena cava, will consist of lateral venorrhaphy whenever feasible. If through and through injuries are found in these vessels both anterior and posterior aspects of the vessel must be repaired. Although the infrahepatic suprarenal inferior vena cava has no venous tributaries it is quite difficult to mobilize. In general, these repairs are accomplished by extending the injury in the anterior wall and repairing the posterior wall from within. This vessel can be mobilized by rotating the right kidney from left to right outside of the renal fossa; however, this maneuver is quite treacherous and not recommended. When there has been massive destruction of the infrahepatic suprarenal inferior vena cava, ligation can be considered; however, survival rates are low. Rarely prosthetic grafts have been utilized in this position. The management of injuries to the infrarenal inferior vena cava consist of lateral venorrhaphy. In the presence of through-and-through injuries, primary repair can be accomplished either by
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extending the venotomy or rotating the vessel. However, this can be quite challenging and involves ligating many of its lumbar veins which are quite fragile. We recommend performing the repair from within the vessel. The infrarenal inferior vena cava can be ligated in cases of massive destruction. Ligation is generally well tolerated. - Injuries to the superior mesenteric vein should be primarily repaired although they can be ligated with serious sequelae to the circulation of the small and large bowel.
Injuries to either right or left Zones II can be quite challenging. Injuries to the renal artery can be either primarily repaired or resected and grafted utilizing either an autogenous or prosthetic graft. Rarely an aortorenal bypass can be performed utilizing a distal site in the anterior wall of the abdominal aorta. Repairs to the renal arteries are quite difficult. Frequently ligation of the renal artery is performed with subsequent nephrectomy. Injuries to the renal veins can also be repaired with primary venorrhaphy or ligation. An injury to the right renal vein that cannot be successfully repaired requires ligation and will demand that a nephrectomy be performed secondary to the lack of venous collaterals. Ligation of the left renal vein is generally well tolerated provided that it is performed proximally and close to the inferior vena cava as there are venous collaterals such as the gonadal and renolumbar veins to handle the venous outflow. Injuries to Zone III can also be quite challenging to manage as they are often associated colonic and genitourinary injuries resulting in contamination. Injuries to the common iliac arteries can be primarily repaired via arteriorrhaphy. Autogenous and prosthetic grafts can also be utilized to repair common iliac arteries. Internal iliac artery injuries are generally dealt with by ligation. Injuries to the external iliac artery can be primarily repaired via arteriorraphy. Iliofemoral bypasses can be performed with autogenous or prosthetic grafts. Although it is quite uncommon to find a saphenous vein of adequate size to perform an iliofemoral repair. When there has been massive destruction of either the common or internal iliac arteries, ligation may be needed. Arterial flow can be restored utilizing a cross over femorofemoral or axillofemoral bypass. These bypasses have the disadvantages of having to involve uninjured vessels and have a high incidence of thrombosis. Injuries to the iliac veins either common, external or internal can be dealt with by ligation, as this is frequently well tolerated, although they can also be dealt with by lateral venorrhaphy. Occasionally access to an injured right external iliac vein may demand transection of the ipsilateral right iliac artery as the vessel lies below the artery. Whenever a trauma surgeon performs an abdominal vascular repair, serious considerations must be given to second look operations to assess for bowel viability. Contamination from gastrointestinal or genitourinary injuries pose great risks for the development of infections in prosthetic grafts inserted to bypass injured vessels. Whenever possible all grafts either autogenous or prosthetic should be reperitonealized. Similarly, for all vascular repairs adjacent to gastrointestinal suture lines, an effort should be made to interpose viable tissue, generally omentum, between the suture lines to prevent vascular-enteric fistulas or anastomotic dehiscence and blow-outs.
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Mortality
Abdominal vascular injuries carry a significant mortality rate. The incidence of exsanguination for penetrating abdominal aortic injuries at both the suprarenal and infrarenal locations is about 55%. The incidence of exsanguination from penetrating injuries to superior mesenteric artery is about 25%. The incidence of exsanguination from both penetrating and blunt trauma to inferior vena cava is about 33%. The incidence of exsanguination for blunt and penetrating injuries to the portal vein is about 30%. The overall mortality rate for abdominal vascular injuries is about 54%. Exsanguination accounts for about 85% of all mortality.
Complications
Abdominal compartment syndrome is very common. Other important complications include thrombosis, dehiscence of suture lines and infection. Vessel occlusion is not uncommon when repairs have been performed in vasoconstricted vessels, such as the renal artery or superior mesenteric artery. The systemic hypovolemia/and intestinal hypervolemia syndrome is common when the portal vein or superior mesenteric vein have been ligated, as there is little venous outflow from the enteric circulation and limited time for the development venous collaterals. Aortoenteric fistulas may develop if no viable tissue is interposed between an aortic and enteric repair, most frequently the stomach. Limb ischemia and compartment syndromes can occur in patients in which there has been a delay in restoration of arterial blood flow. The same complication can occur in patients, that because of poor venous collaterals do not tolerate ligation of the inferior vena cava or iliac veins.
References
1. 2. 3. Asensio JA, Hanpeter D, Gomez H et al. Exsanguination. In: Shoemaker W, Greenvik A, Ayres SM et al, eds. Textbook of Critical Care. 4th Ed, Philadelphia, PA: W.B. Saunders Co. 1999; 4:37-47. Feliciano DV. Abdominal vessels. In: Ivatury R, Cayten CG, eds. The Textbook of Penetrating Trauma. Baltimore, MA: Williams and Wilkins 1996; 56:702-716. Asensio JA, Berne JD, Chahwan S et al. Traumatic injury to the superior mesenteric artery. Amer J Surg 1999; 178(3):235-239. Demetriades D, Theodorou D, Murray J et al. Mortality and prognostic factors in penetrating injuries of the aorta. J Trauma 1996; 40(5):761-763. Asensio Ja, Forno W, Gambaro E et al: Abdominal Vascular Injuries. The Trauma Surgeons Challenge. Annales Chirurgiae et Gynecologiae, 2000; Vol 89:71-78.
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4. 5.
Abdominal Compartment Syndrome

Demetrios Demetriades Definition of Abdominal Compartment Syndrome (ACS)
Increased intraabdominal pressure associated with any of the following tachycardia or hypotension decreased urine output hypoxia or elevated peak inspiratory pressure or unresponsiveness to mechanical ventilation.
Pathophysiology
Normal, resting intraabdominal pressure in the horizontal position is 0 cmH20 Early postlaparotomy pressure is < 10 cmH20 Intraabdominal pressure 20-30 cmH20 may be harmful Intraabdominal pressure > 30 cmH20 is associated with major adverse events from all body systems Cardiovascular effects of ACS Tachycardia Low stroke volume Elevated CVP and PCWP Increased afterload Respiratory effects of ACS Elevated peak inspiratory pressure Decreased Pa02/Fi02 Unresponsiveness to mechanical ventilation Kidney effects Decreased urine output Decreased glucose reabsorption Brain Increased intracranial pressure May have a detrimental effect on head injuries Abdominal viscera Decreased blood flow in celiac artery and superior mesenteric artery Decreased blood flow to intestinal mucosa May increase bacterial and toxin translocation Abdominal wall Decreased blood flow May increase the incidence of wound infection and fascial dehiscence Note: In the presence of resuscitated shock the adverse effects of the ACS may appear at lower intra-abdominal pressures.
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Risk Factors for ACS

Local risk factors Severe abdominal trauma Damage control operations Retroperitoneal hemorrhage Superior mesenteric vessel injury Edematous bowel Portal vein ligation or thrombosis Aortic cross-clamping Tight abdominal closure Systemic risk factors Massive transfusions Prolonged hypotension Fluid overloading Hypothermia
Intraabdominal Pressure Monitoring

Direct measurements Through an intraperitoneal catheter Indirect measurements Nasogastric tube Inferior vena cava catheter Foley catheter in the bladder The bladder pressure technique is the most widely used method for intraabdominal pressure monitoring
Technique of Bladder Pressure Measurement

Place patient in horizontal position. 50-100 mls of normal saline are instilled into the bladder through the Foley catheter. Cross-clamp the tube of the collecting urine bag. Insert a needle into the specimen-collecting port, proximal to the clamp. A CVP set is connected to the needle and the pressure is measured using standard techniques. The pubic symphysis should be used as the zero point (Fig. 35.1).
Alternative Technique for Bladder Pressure Measurement

Place patient in horizontal position. Instill 50-100 mls of normal saline in bladder, through Foley catheter. Create a U-shape loop with the Foley catheter and the urine collection tube with the lowest point of the loop touching the mattress. The distance between the pubic symphysis and the meniscus of the fluid in the tube is the bladder pressure (Fig. 35.2).
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Diagnosis of ACS
The diagnosis is suspected on clinical examination and confirmed by bladder pressure measurements. Clinical findings may include Tachycardia and in severe cases hypotension
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Fig. 35.1. Bladder pressure measurements using a CVP set connected to a Foleys catheter. The pubic symphysis serves as the zero point.
Elevated peak inspiratory pressure, persistent hypoxia, poor compliance. Decreased urine output Tense abdomen Bladder pressure > 25-30 cmH20
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Prevention of ACS
The risk of ACS decreases significantly with appropriate measures. Adequate resuscitation Avoid fluid overloading Avoid hypothermia Keep bowel warm and moist Do not close the abdomen if it cannot be achieved without tension
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Fig. 35.2. Bladder pressure measurements with U-shape loop created with the Foleys catheter. The pressure corresponds with the distance between the pubic symphysis and the meniscus of the fluid in the tube.
Do not close the abdomen in damage control laparotomies In high-risk patients monitor the bladder pressures New therapeutic modalities which may be useful in preventing ACS but still need clinical verification. Mannitol Immunomodulators (anticytokines, oxygen free radical scavengers)
Treatment of ACS
Treatment should be started without any delay in order to avoid organ dysfunction. The improvement usually takes place immediately. Decompressive celiotomy is the only effective treatment. It may performed in the operating room or the ICU. Decompressive laparotomy without appropriate preparation may be associated with severe complications. Hypotension or cardiac asystole may develop in about 10% of cases during opening of the abdomen. This decompensation may be due to sudden hypovolemia due to volume loss in the vasodilated intra-abdominal organs or sudden release of cytokines and products of anaerobic metabolism into the systemic circulation. The complications during decompressive laparotomy may be prevented by preoperative administration of 2 L of 1/2 NS + 50 g Mannitol/L + 50 mEq NaHC03/L. The abdomen is closed temporarily with a prosthetic material such as PTFE, various meshes, or an opened 3-liter dialysis fluid bag (Fig. 35.3). The vacuum pack technique4 is strongly recommended because it facilitates the subsequent definitive abdominal wall closure (Figs. 35.4A,B,C).
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Fig. 35.3. Abdominal wall closure with plastic sheet from a 3-liter dialysis fluid bag.
Technique of Vacuum Pack Abdominal Wall Closure

Place clear plastic sheet from a 3 L IV dialysis bag between bowel and peritoneum (Fig. 35.4A). Place a thick layer of moist gauze dressing over the plastic sheet. Two closed suction drains are placed over the gauze. A second plastic sheet is placed over the gauze and drains and fixed to the skin (about 2 cm from the edge) with stapling (Fig. 35.4B). A large self-adhesive transparent drape (Op-site, Tegaderm) is placed over the whole abdomen. The drains are connected to continuous low suction. The whole dressing becomes firm and stabilized (Fig. 35.4C).
Definitive Abdominal Closure After Decompressive Laparotomy

In some cases improvement of the bowel edema may allow definitive closure with or without a prosthetic mesh and undermining of the skin within a few days of decompressive laparotomy. In many cases definitive closure is possible only many weeks or even months after the initial operation. Skin grafting of the exposed bowel may be necessary as a temporary measure, in order to avoid bowel fistulae and fluid and protein losses from the open abdomen (Fig. 35.5). The definitive closure is attempted usually 6-8 months later, when the wounds have healed and the nutritional status has improved. The fascial defect is closed with a nonabsorbable mesh and the skin is approximated after extensive undermining.
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Delayed diagnosis of ACS because of low index of suspicion Primary closure of the abdomen following a damage control operation. Almost all patients will develop ACS! The abdomen should be closed with a temporary prosthetic material.
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Fig. 35.4A,B,C. Abdominal wall closure with the vacuum pack technique.
Fig. 35.4B. Abdominal wall closure with the vacuum pack technique.
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Closure of the abdomen under tension, after laparotomy for complex trauma! Failure to monitor the bladder pressures after complex abdominal trauma! Decompressive laparotomy to relieve ACS without appropriate preoperative preparation. Risk of severe hypotension or cardiac asystole!
References
1. Eddy V, Nunn C, Morris JA. Abdominal compartment syndrome. Surg Clin N Am 1997; 77:801-812.
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Fig. 35.4C. Abdominal wall closure with the vacuum pack technique.
Fig. 35.5. Temporary abdominal closure with skin grafting on the bowel. The patient will develop a large incisional hernia, which will require repair at a later stage.
2. 3. 4. Ivatury RR, Diebel L, Porter JM et al. Intra-abdominal hypertension and abdominal compartment syndrome. Surg Clin Nort Am 1997; 783-800. Bongard FB, Ryan M, Dubecz S et al. Adverse consequences of increased intraabdominal pressure on bowel tissue oxygen. J Trauma 1995; 39:519-525. Brock WB, Barker DE, Burns RP. Temporary closure of open abdominal wounds: The vacuum pack. Am Surg 1995; 61:30-35.
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CHAPTER 36
Damage Control Operations

Richard J. Mullins and John C. Mayberry Definitive Surgical Therapy Versus Staged Sequential Therapy History
H. Harlan Stone reported in the early 1980s the first damage control operation to manage patients who developed coagulopathy during a laparotomy performed for trauma. Dr. Stone concluded that with this approach the risk of death by exsanguination in this high risk group of patients was reduced from 93 to 35%. Other trauma surgeons expanded the indications for premature termination of a trauma laparotomy. Morris et al calculated that one in ten patients benefited from a staged celiotomy for trauma. They described refinements in decision making regarding packing and unpacking for abdominal bleeding in patient in extremis. Damage control, a term coined by Rotondo et al, is a tactical maneuver and its application has been expanded in the past 20 years as an alternative technique to a surgeons persistence with the conduct of a procedure until either its definitive completion or the patients demise.
Damage Control Strategy

Damage control is a tactic that is intended to preserve a patient who is at risk of being overwhelmed by physiologic dysfunction caused by the patients injuries. Complete repair of injuries is achieved through a series of surgical interventions performed over days. The damage control premise is that a single prolonged operation in seriously injured patients subjects the patient to a physiologic shock of magnitude and duration from which they cannot recover. The goal in damage control is to return to the operating room for definitive repairs of the stable and physiologically improved patients.
Bail-Out or a Preemptive Intervention

Surgeons who accept the hypothesis of damage control should decide, as a premeditated guideline, what will be the scope of damage control application in their practice (Table 36.1). Damage control can be seized upon at the end of a surgical procedure as a rescue intervention in critically unstable patient. Alternatively damage control can be adopted early in a surgical procedure as a precautionary process in a patient judged to be at high risk for physiologic
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Richard J. Mullins, Oregon Health Sciences University, Portland, Oregon, U.S.A. John C. Mayberry, Oregon Health Sciences University, Portland, Oregon, U.S.A.
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Table 36.1. The application of damage control used as either:

Bail-Out Procedure Aborted termination of surgery in a patient at imminent risk of death Preemptive Intervention Calculated early decision to accomplish definitive correction of injuries in a series of procedures
deterioration. Delay of damage control, until it is a bail-out procedure, risks the patients condition will deteriorate into irreversible physiologic dysfunction. On the other hand selecting damage control early may mean an unnecessarily premature termination of surgery in patients who would otherwise have recovered from a single definitive procedure. In this circumstance, damage control subjects the patient to risks and expense of multiple procedures and prolonged surgical therapy. Surgeons should decided what is their preference in the application of damage control and be prepared to make a prompt choice should they encounter a patient who is a candidate for damage control.
Indications for Damage Control

Criteria are available which can guide the surgeon in decision making regarding which patient is a candidate for damage control (Table 36.2).
Shock
Hypotension
The duration of hypotension was recommended as an indication for damage control (Table 36.2).
Volume of Blood Transfused

An easily quantized indication of the magnitude of shock is the number of units of blood required to be transfuse into a patient to accomplish resuscitation from shock. Some authors advocated damage control if more than 15 units of blood are needed. Others have concluded the threshold should be based upon estimated blood loss, with one author advocating a threshold of greater than four liters of blood loss.
Hemodynamic Measures
Measures of central venous or left atrial filling pressure can be used as a guide to hypovolemia. Persistent evidence of hypovolemia despite ongoing resuscitation may be an indication that further dissection and attempts at repair should be deferred until homeostasis has been achieved. However, these measurements may not be readily obtained in the operating room during a emergent surgical procedure in a patient with rapid fluctuations in intravascular volume.
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Table 36.2. Published indications for damage control

Absolute Indications Hypothermia Less Than 35 C Less Than 34 C Less Than 33 C Acidemia pH < 7.10, pH < 7.2 pH < 7.25 Bicarbonate Deficit Exceeds 15 Meq/L Coagulopathy Incessant Microvascular Bleeding None Cloting Blood Prothrombin Time In Excess Of 19 Seconds Fibrinongen Less Than 100 mg/dL Relative Indications Sustained Systolic Blood Pressure < 70 mmHg Blood Loss In Excess Of 4 Liters Transfusion Approaching 15 Units Of Blood Injury Severity Score Over 35
Excessive Risk to Geriatric Patients

Geriatric patients may benefit from implementation of damage control surgery if their hemodynamic status is precarious.
Acidemia
Arterial pH
Arterial blood gas pH in the range 7.10-7.25 has been suggested as an indication for damage control. The surgeon should remain aware that there is an accelerating risk to a patient whose arterial pH is declining rapidly and not depend entirely upon a single pH value to support the decision to implement damage control. The arterial pH can be depressed by elevated partial pressures of the respiratory gas carbon dioxide and thus alveolar hypoventilation, and not hypoperfusion, can be the cause of acidemia.
Bicarbonate Deficit
A bicarbonate deficit which exceeds 10 mEq/L indicates a seriously stressed patient. If bicarbonate deficits exceeds 15 mEq/L the risk of death exceeds 50%. As the intraoperative bicarbonate deficit increases, the patient is a more suitable candidate for damage control.
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Lactate
Some surgeons prefer to depend upon lactate levels to quantitate the magnitude of shock. While elevated serum lactate may be a more sensitive indication of cellular hypoxia, obtaining a lactate level is often delayed compared to the availability within minutes of an arterial blood gas analyses.
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Hypothermia
Core Body Temperature
The body temperature threshold considered critical has varied among authors (Table 36.2). Core body temperature less than 34 C is associated with a reduction in coagulation cascade effectiveness, and patients this cold have a greater risk for bleeding. In patients having an exploratory laparotomy, the exposure of wet viscera to ambient air results in substantial heat loss. These patients benefit from damage control.
Coagulopathy
Micro Damage Control Operations for Bleeding
Bleeding in the critical trauma patient has multiple causes. Hypothermia, depletion of coagulation proteins and platelets, and activation of fibrinolysis can individually, or in concert, cause bleeding. The excess bleeding attributable to hypothermia is a directly reversible coagulation disorder achieved by warming the patient, something that is difficult to do during a laparotomy. Damage control provides an interval to catch up by infusion of fresh frozen plasma, cryoprecipitate and platelets to replenish depleted coagulation factors, and warm up the patient.
Laboratory Test Dependent Diagnosis of Coagulopathy

Coagulation laboratory tests can provide an indication the patient has developed an acute bleeding disorder. However these laboratory tests require a delay, and just as valuable in guiding the decision to default to damage control because of coagulopathy, is the surgeons observations and judgement. Monitoring coagulation tests can provide direct evidence that therapy is accomplishing the intended goal of damage control.
Ancillary Issues Indicating the Benefits of Damage Control

The physiologic criteria for imminent, catastrophic physiologic failure are well established. Other criteria, such as the total number of injuries sustained by the patient, the complexity of these injuries, the time required to accomplish definitive repair, and the experience of the surgeon may be useful in determining the need for damage control. As excellent indication for damage control is a fatigued and overwhelmed surgical team. Damage control has the advantage that critical decisions which do not necessarily need to be made immediately can be deferred. Damage control should supplement the triage decisions made when managing severe multi trauma patients in a mass casualty incident, particularly when the number of surgeons or operating rooms are limited.
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Categories of Injuries Amenable to Damage Control Damage Control During a Laparotomy

Initial Hemostatic Control
The initial step in a laparotomy when hemorrhage is encountered is to pack off the four quadrants of the abdomen, and attempt to achieve by that means control of hemorrhage. The next step is to determine the site, or sites, of bleeding. Control of large arterial vessel hemorrhage is usually accomplished by either vessel ligation or vascular repair. Small arterial or venous vessel bleeding in most circumstances can be temporarily controlled by compression with laparotomy gauze pads. After major hemorrhage has been controlled, the laparotomy pads are systematically removed, and individual bleeding points cauterized, clamped or suture ligated. If the laparotomy pads have achieved a dry field, and the patient has other organs that need repair, the surgeon should decide whether to proceed with damage control. Many trauma surgeons have concluded in retrospect the imprudence of their persistent efforts to achieve complete removal of all tamponade laparotomy pads and found damage control a useful alternative. After the patients physiologic status is improved, the patient is returned to the operating room for removal of the packs (Fig. 36.2).
Management of Hollow Viscous Injuries

For over 20 years, surgeons using damage control have reported the safety and effectiveness of deferral of bowel reconstruction until the second operation. Thus the ends of bowel are ligated or totally occluded by staples or sutures. One advantage of waiting to perform an anastomosis is that the surgeon can be conservative in resections in patients in shock and rely upon a second look within a few hours up to two days, when the patients hemodynamic status has improved, to determine the viability of the bowel. Damage control enables construction of stomas to be deferred, thus avoiding the need to make new abdominal wall wounds in coagulopathic patients. The same techniques can be applied to ureter and bile duct injuries, although in these organs, stents can be inserted into the lumen to achieve temporary drainage.
The Abdominal Compartment Syndrome

The abdominal compartment syndrome is a multiple organ dysfunction syndrome that occurs when pressure within the abdominal cavity exceeds a critical level. Visceral ischemia occurs in patients with the abdominal compartment syndrome. Two hallmarks of the abdominal compartment syndrome are oliguria and impaired pulmonary mechanics. Specific causes of the abdominal compartment syndrome in trauma patients are sudden accumulations of free peritoneal fluid, intra-abdominal and retroperitoneal hematomas, marked visceral edema or distention from intraluminal fluid or air, and the laparotomy pads inserted for compression and hemostasis. Patients with damage control laparotomy are commonly at risk for the abdominal compartment syndrome. If a primary fascial closure is attempted
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Fig. 36.1. The simple technique for measuring abdominal compartment pressure is to determine the height from the pubic symphysis of a column of fluid in the bladder catheters tubing. The threshold pressure consistent with the abdominal compartment syndrome is 30 cm H2O. Reprinted with permission from: Mayberry, J. Critical Care Clinics 2000; 162. 2000 WB Saunders.
Fig. 36.2. Laparotomy gauze pad is being extracted from the undersurface of the liver where the pack had been inserted at the first damage control procedure into a deep liver laceration.
in a high risk patient, the surgeon should monitor if closure causes an unacceptable increase in peak airway pressure during ventilation with tidal volumes under 10 ml/kg. If airway pressures do escalate, prosthesis closure of the abdomen should be accomplished. The bladder pressures can be easily measured by determining the height of a meniscus of fluid in the Foley catheter tubing above the symphysis pubis (Fig. 36.1). If the height of the
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Fig. 36.3. Mesh closure of a patient with a distended abdomen after damage control precludes the development of the abdominal compartment syndrome.
fluid column exceeds 30 cm and the meniscus fluctuates during ventilation, the patient is as substantial risk for visceral ischemia from the abdominal compartment syndrome. Without decompression, the abdominal compartment syndrome will lead to irreversible organ failure.
Mesh Closure of the Laparotomy Wound

An alternative to primary fascia closure is insertion of a prosthetic material to bridge the wound edges. Prosthesis closure of the abdomen must achieve sufficient pressure within the abdomen to assist with tamponade, while not creating a tense abdomen and the abdominal compartment syndrome (Figs. 36.3-36.5). Monitoring the abdominal pressures and other signs of postoperative development of the abdominal compartment syndrome is essential. A compartment syndrome may develop despite the use of prosthesis closure!
Damage Control in Patients with Open Pelvic Fracture

Patients with open wounds and a pelvic fracture are at risk for death by exsanguination. Arterial and venous injuries in the deep pelvis can be a source of unstoppable hemorrhage when there is a wound, commonly a groin crease laceration, which extends to the perineum. Direct access to the bleeding vessels through the wound for suture ligation is often impossible, and furthermore placing these patients with an unstable pelvis in lithotomy position can exacerbate bleeding. A damage control method to achieve hemostasis in patients with an open pelvic fracture is to tightly pack the perineal wounds with gauze, and then with a running suture closure of the skin achieve tamponade. A damage control exploratory laparotomy should be performed if there is evidence of intra-abdominal hemorrhage.
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Fig. 36.4. Opening the mesh for second procedure enables re-exploration without further damage to fascial edges. The polyglycolic acid mesh does not unravel with incision.
Fig. 36.5. It is always beneficial with damage control closure to attempt to interpose omentum between bowel and prosthetic.
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Supplemental hemostatic techniques after damage control procedures in the operating room are angiographic embolization of bleeding arterial pelvic vessels.
Damage Control for Severe Extremity Fracture

The principal of early fixation of long bone fracture has been widely adopted. However while it is possible to immediately repair multiple fractures, there are also circumstances where it is impracticable to subject the patient to sustained limb salvaging surgery. The use of external fixators to immobilize the extremities has been advocated as damage control in these patients. Temporary use of intraluminal vascular shunts may be used to sustain perfusion of an ischemic extremity until acidosis and coagulopathy can be corrected. Patients with severe shock and prolonged procedures on their extremities can develop the abdominal compartment syndrome even thought they did not have a direct abdominal injury.
Tactics and Pitfalls During Follow-Up Surgery in Damage Control

Following a damage control procedure the patient should be returned to the operating room, as soon as the core body temperature, the tissue perfusion, and coagulopathy improve (usually within 12-48 hours). In some cases the optimal time to return the patient to the operating room is after the surgical team has rested and recruited assistance. Continuous bleeding or hematocrit plummeting despite blood transfusion or persistent hypotension after damage control are indications to return to the operating room. In some such circumstances, control of hemorrhage can only be accomplished with ligation of major arterial vessels with the consequence of organ or extremity loss. Worsening acidemia may indicate the patient has infected fluid collection or dead tissue (i.e., bowel) which needs prompt drainage or eradication.
Role of Angiographic Embolization in Damage Control

In selected circumstances, patients with both blunt and penetrating trauma, and persistent hemorrhage in poorly accessible areas can be managed with angiographic techniques. Embolization of arterial bleeding of even 2-3 mm vessels can be immediately hemostatic in patients with coagulopathy.
Returning to the Operating Room

Patients whose wounds were closed with gauze packs should have the packs removed within 48 hours, especially in the presence of hollow viscus perforations. Bacterial overgrowth in these gauze packs may occur and these can become a source of bacteremia as well as setting the stage for local abscess formation. Prolonging the removal of gauze packed against viscera can be a problem because the gauze becomes adherent. Soaking the gauze with saline while gently working the gauze free can avoid tears to fragile organs and vessels.
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Infection Risks
The use of gauze pads to tamponade bleeding has been associated with an increased risk of intra-abdominal infection. The range of intrabdominal abscess has been 10-70%. While data on duration of antibiotic usage in patients without damage control suggests only 24 hours of antibiotic therapy is required in patients who have a bowel injury and prompt surgical correction, it is not known how long antibiotics are indicated in patients who have damage control procedures. The current preference in our practice is a second generation cephalosporin continued until all packs are removed.
Retained Foreign Bodies

In patients who have damage control there is an increased risk that the patient will have a retained foreign body, particularly a gauze pack. When damage control is used, a process should be developed for assuring during follow up procedures all foreign bodies are removed. These procedures would include methods for counting subsequently removed gauze packs and obtaining a completion x-ray.
Enteral Access
Edema and intraluminal distention can make the turgid bowel cumbersome to manipulate. In damage control it is prudent to defer until later operations insertion of intraluminal tubes.
Method for Abdominal Wound Closure

The ideal method of abdominal closure should be effective in prevention of evisceration and massive fluid loss, quickly accomplished, be inexpensive and have a low complication rate. Definitive closure of the abdominal wound is not advisable in the first damage control procedure because of the risk of abdominal compartment syndrome.
References
1. 2. 3. 4. 5. Stone HH, Strom PR, Mullins RJ. Management of the major coagulopathy with onset during laparotomy. Ann Surg 1983; 197:532-5. Morris JA Jr, Eddy VA, Blinman TA et al. The staged laparotomy for trauma. Ann Surg 1993; 217:576-86. Rotondo MF, Schwab CW, McGonigal MD et al. Damage control: An approach for improved survival in exsanguinating penetrating abdominal injury. J Trauma 1993; 35:375-83. Garrison JR, Richardson JD, Hilakos AS et al. Predicting the need to pack early for severe intra-abdominal hemorrhage. J Trauma. 1996; 40: 923-927. Mayberry JC, Mullins RJ, Crass RA et al. Prevention of abdominal compartment syndrome by absorbable mesh prosthesis closure. Arch Surg 1997; 132:957-62.
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CHAPTER 37
CT Scan in Abdominal Trauma

Sravanthi R. Keesara and Nabil A.Yassa Introduction
Trauma to the abdomen accounts for 10% of the traumatic deaths in the United States. Most of these abdominal injuries are from motor vehicle accidents, but penetrating wounds are also common. Blunt trauma injures solid organs more often than hollow organs.
- Solid organs (liver, spleen) may have lacerations and/or subcapsular hematomas. - Hollow organs (bowel, bladder, gallbladder) may rupture from increased pressure.
Deceleration Injuries
- Deceleration causes shearing forces that result in lacerations at points of fixation, such as at the ligamentum teres in the liver or in vessels.
Penetrating Trauma
- Low velocity penetrating trauma (knives, low-velocity bullets) cause damage to organs in their paths, by direct laceration and crushing. - High velocity injuries (high velocity bullets, bombs) may cause damage to tissues away from the missile tract, by transient cavitation or shock waves.
Combination Injuries
According to the mechanism of injury, certain injuries occur together. If one injury is seen, the scan should be scrutinized so as not to miss additional injuries after the first or most prominent injury has been detected. Right package: Right lung contusion/lacerationRight rib fracturesRight pneumothorax/hemothoraxLiverRight kidneyRight adrenalRight hemidiaphragm. Left package: Left lung contusion/lacerationLeft rib fracturesLeft pneumothorax/hemothoraxSpleenStomachLeft kidneyLeft adrenalLeft hemidiaphragm Midline package: Left lobe of liverSternumLower ribsHeart/pericardiumTransverse colonSmall bowelMesenteryPancreasDuodenum AortaIVC Chance type fracture: Lap-type seat belts: Physical exam shows a seat belt burn (hematoma)Spinal injurySmall bowel or mesenteric injuryBladder injury Pelvic fractures: Bladderurethravaginarectum
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Sravanthi Keersara, University of Southern California, Los Angeles, California, U.S.A. Nabil A. Yassa, University of Southern California, Los Angeles, California, U.S.A.
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Investigations
Diagnostic peritoneal lavage (DPL)
- This minilaparotomy (first done in 1965) is a saline lavage of the peritoneum. - DPL provided a go/no go answer for surgical intervention, but it has been found that bleeding often stops on its own or is from a source that may not need surgery. - There is a nontrivial 5% complication rate.
Ultrasound (US)
- Focused US of the abdomen for trauma, an idea that originated in Germany, has been suggested as a replacement for DPL. - US is nearly equivalent to DPL in finding free intraperitoneal fluid, is noninvasive, and can be performed quickly (< 3minutes) and serially over minutes or hours. Advantages of US over CT include the lack of need for patient preparation or movement, ability to be performed even while resuscitating the patient, its rapid acquisition and ability to be done serially. - US can be performed on hemodynamically unstable patients to help determine the need for laparotomy. A quick and thorough search for extra-abdominal bleeding may be performed if US is negative. - Drawbacks of US include the fact that US is very operator-dependent and is difficult to do on some patients due to patient body habitus, inability to roll the patient due to open wounds and that even major retroperitoneal injuries and free air and bowel injuries may be missed.
Computed Tomography (CT) of the Abdomen

- CT has helped decrease the number of explorative, nontherapeutic laparotomies. - The new generation helical and multidetector/multislice CT scanners have a turn-around time for the abdomen that is now under 10 minutes and multiple exams can be performed in a short time on the same patient. In addition to getting an injured patient back to treatment more quickly, shorter scan times decrease motion artifacts. Other advantages include better vascular/parenchymal opacification, reconstructed images with overlapping areas that pick up smaller injuries, and multiplanar reconstructions (in sagittal and coronal planes) that help diagnose injuries of the diaphragm, GB, and spine.
CT Technique
- The abdominal scan should include the inferior part of the chest to pick up associated injuries and extend through the pelvis. - The scans need to be reviewed in soft tissue, lung, narrow and possibly bone windows to pick up lung contusions, pneumothoraces, pneumoperitoneum, bone injury, and subtle abdominal organ injury. - According to the mechanism of injury, certain injuries occur together. If one injury is seen, the scan should be scrutinized so as not to miss additional injuries after the first or most prominent injury has been detected.
IV Contrast
- If no contrast allergy or severe renal insufficiency is present, IV contrast is used. - Nonionic contrast is preferred to decrease the possibility of vomiting as the patient may have a full stomach and/or head injuries. - The Foley catheter should be clamped to allow the bladder to fill with contrast. - Precontrast CT may show acute blood (denser than adjacent soft tissues) better than postcontrast images, but protocols done for trauma do not include
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CT and Bladder Contrast

- Water-soluble contrast is given orally or through a nasogastric tube (NGT). - This was previously controversial due to the possibility of aspiration in an obtunded patient and due to time lost in waiting for contrast to move through the bowel. IV metoclopramide (10-20 mg) given with the oral contrast and suction through the NGT after the study decreases the possibility of aspiration; and since most bowel injuries are in proximal small bowel, little time is lost to wait for contrast transit. - Oral contrast helps to identify bowel leak and to differentiate between unopacified fluid-filled bowel loops and free fluid. - Rectal contrast may be given when colonic injury is suspected. This is especially important in cases with penetrating injury, hematochezia, or pelvic fractures. Thin patients who have little fat may also benefit from rectal contrast. - Bladder contrast may be used for a CT cystogram when bladder injury is suspected.
CT Evaluation of Abdominal and Pelvic Hemorrhage

Very small volumes of abdominal and pelvic hemorrhage can be detected and since this may be the most obvious initial clue for abdominal injury, this should prompt a thorough search for organ injury. Quantification of the hemorrhage on CT to help management was attempted in the past, but this is now considered less useful because some stable patients, even with a large hemoperitoneum, do well without surgery. More important to treatment than the amount of fluid is its location and its appearance on CT and its location. Appearance of Fluid
- CT density is measured in Hounsfield units (HU) and can help determine the type of fluid. - 0-10HU suggests water-density fluid: Urine, bile, chyloperitoneum, pre-existing ascites, DPL fluid. - > 30HU suggests blood. Recent hemorrhage may be homogeneous or inhomogeneous according to age, physical state, and location. - 30-45HU suggests fresh unclotted blood (immediately after hemorrhage) or lysed clotted blood (after several days). - 40-60 and up to 100HU suggests clotted blood (which occurs within hours). - 0-20HU suggests serum (after clotting, the unclotted portion) or old lysed clotted blood (after 2-3 weeks). - 80-300HU suggests active arterial extravasation of blood mixed with IV contrast, which warrants emergency surgery or embolization (Figs. 37.1, 37.2, 37.3). - The sentinel clot sign is a sensitive sign of visceral injury. The densest blood is near the area of extravasation as it clots in an attempt at hemostasis. This sign is especially helpful in a patient with multi-organ injury to find the major source of the hemorrhage.
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Fig. 37.1. Left external iliac artery with active contrast extravasation and retroperitoneal hematoma. (arrow). The image is limited by streaky artifacts from patients upper extremities being adjacent to the pelvis.
Fig. 37.2. Splenic fracture with active extravasation. (arrow)
- Hematocrit effect is the layering of less dense serous fluid on the more dense dependent, sedimented erythrocytes and clot (Fig. 37.4). - Pleural and peritoneal blood is less dense than intramuscular, retroperitoneal, or parenchymal blood.
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Fig. 37.3. Liver laceration with hemoperitoneum and active extravasation. (arrowhead). Spleen (S) is nonperfused indicating infarction.
Fig. 37.4. Hemoperitoneum with hematocrit effect. (arrow)
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Location of Fluid
- Hemoperitoneum initially collects near the source of the injury and then spills over into more dependent portions of the peritoneal cavity. This is another important reason to include the entire pelvis, which may collect the majority of the fluid from any intraperitoneal injury.
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- If CT shows intraperitoneal fluid and no other injuries, this may point to a selflimited injury of a parenchymal organ that does not require any treatment, but because it may indicate a more serious injury like bowel rupture that requires emergency laparotomy, further investigation is needed. HU measurement of the fluid may be performed: If the HU is consistent with blood and there is associated free intraperitoneal air, oral contrast extravasation, thickened or hyperemic bowel, or triangular fluid collections between leaves of mesentery, this suggests bowel injury. A repeat CT with additional oral and rectal contrast may help to confirm. - A repeat CT may be performed after 12-24 hours to search for signs of abdominal injury not present on initial scan.
Shock from hypovolemia and inadequate fluid resuscitation is a common finding in a trauma patient. It can be suggested on CT by the following signs:
- A small constricted aorta. - A collapsed IVC. - Abnormally intense contrast enhancement of the bowel wall and kidneys.
CT Pitfalls in Hemorrhage Evaluation

- The HU of blood can be lower than expected and be mistaken for water-density fluid in the following cases: Pre-existing underlying anemia. Dilutional effects from intraperitoneal fluid such as ascites, urine, or bowel contents. Volume averaging of peritoneal fat or artifacts. - If the HU of the fluid is high, acute vascular extravasation should be considered, but other possibilities include the following: Oral contrast extravasationlook for adjacent injured bowel and the location of the material. The CT with IV contrast can be repeated after a delay. Contrast-enhanced urine extravasationlook for adjacent injured urinary tract. Delayed CT scanning will show arterial blood to be getting less dense and contrastenhanced urine leak to be more dense.
Splenic Trauma
The spleen is the most frequently injured organ in blunt abdominal trauma and accounts for 40% of the abdominal organ injuries. CT Findings
- CT is very sensitive in diagnosing splenic injury and also identifies associated injuries in the chest (rib fractures, lung contusions, diaphragmatic injuries), and the left upper quadrant. - Spectrum of Splenic Injuries - Lacerations, which appear as hypodense irregular branching linear areas, are often associated with hemoperitoneum. Splenic injuries are associated with perisplenic fluid and fluid in the phrenocolic ligament, and the left paracolic gutter (Figs 37.2, 37.5). - Intrasplenic hematomas are broader low density, homogenous or heterogeneous, zones within the splenic parenchyma. - Contusions are less well defined than hematomas. - Subcapsular hematomas are low-attenuation crescentic fluid collections that compress the adjacent contrast-opacified splenic parenchyma. - A shattered spleen consists of small fragments caused by multiple crossing lacerations (Figs. 37.6, 37.7).
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Fig. 37.5. Subtle splenic laceration with small perisplenic hematoma. (arrowhead)
Fig. 37.6. Shattered spleen (S) with perisplenic hematoma. (arrow) (Renal cyst (R) incidentally noted on the right.)
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- Infarction may be caused by a disruption of hilar blood vessels and are nonperfused global or wedge-shaped areas that extend to the surface of the spleen (Fig. 37.3). - Delayed rupture, up to 10 days after the initial injury, does occur. This is associated with subtle low-grade injury and subcapsular hematoma.
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Fig. 37.7. Fractured spleen (SP) (arrowheads), involving the vascular pedicle. Note the distended stomach (ST).
Management of Splenic Injuries

- Several grading systems to help predict management have been published, but because these are based on anatomic criteria rather than the more predictive physiologic criteria (e.g., rate of bleeding) and because CT underestimates injury, these do not accurately predict the need for splenic surgery. - Grading systems are not predictive of a need for surgery, but they do correlate to the rate of healing, which usually takes 4-6 months. - With the conservative non-surgical approach, if there are clinical indications of complications, repeat CT may be needed. - Surgery or embolization is needed if there are large nonperfused portions of spleen, active hemorrhage, or false aneurysms.
CT Pitfalls in Splenic Evaluation

- CT scan obtained too early after contrast injection shows an inhomogeneous pattern of opacification. Repeat CT after equilibrium may be obtained in confusing cases. - The spleen can show an apparent increase in size on follow up scans which is actually the return to normal size after the initial adrenergic contraction in response to volume loss or parenchymal injury. - Splenic clefts may be mistaken for lacerations, but these have a smooth contour, are medially located, and are not associated with a hemoperitoneum. - An elongated left lobe of liver or atelectactic left lung may be confused with splenic injury. - Motion, beam-hardening, or streak artifacts, volume averaging, and unusual windows settings also may cause confusion.
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Hepatic Trauma
Due to its relatively fixed position, large size, and friability, the liver is the second most commonly injured intraabdominal organ in blunt abdominal trauma. Although only half as common as splenic injury, hepatic injury results in greater morbidity. CT Findings
- Lacerations are hypodense irregular linear, or branching regions, which often parallel hepatic and portal venous vasculature. (Fig. 37.8). Parallel lacerations that produce isolated parenchymal fragments produce what has been called the bear claw pattern. - Hemoperitoneum, produced if the lacerations extend beyond thin capsule, may be large due to the dual blood supply and the decreased ability for hemostasis (veins). Liver injuries are associated with fluid in Morisons pouch (hepatorenal space) and the right paracolic gutter. - Multiple lacerations around the confluence of the hepatic veins or IVC may suggest vascular damage. Preoperative notice of possible venous laceration will help prepare surgeons for massive hemorrhage when liver is lifted off the IVC. - Periportal tracking appears as hypodensity along the course of the portal vein. In trauma patients this tracking may have several causes: a) If the tracking is focal and associated with liver laceration or hematoma, dissection of blood or bile along course of portal veins may be the cause. b) More often, the tracking is diffuse and caused by lymphedema and elevated central venous pressure caused by rapid expansion of intravascular fluid in the trauma resuscitation. - Intrahepatic hematomas are mass-like, well-defined hypodense homogeneous or heterogeneous regions in the parenchyma (Figs. 37.9A,B). - Contusions are less well defined than hematomas. - Subcapsular hematomas are hypodense crescentic lenticular fluid collections that cause compression of underlying parenchyma, often associated with rib fractures and penetrating trauma. - Focal devascularization, wedges of isolated hypodense, nonperfused liver, may be produced by multiple lacerations. - Active hemorrhage is a focal, irregular area of hyperdensity, sometimes with adjacent sentinel clot (Fig. 37.3). - Intrahepatic or subcapsular gas may be seen in areas of laceration 2-3 days after trauma and this is probably due to necrosis rather than infection.
Management of Hepatic Injuries

- Several systems for grading hepatic injuries have been suggested, but as with spleen, none correlate with the need for surgery or with subsequent complication. - Delayed complications due to portal triad injury or devitalized liver tissue occur in 20% of liver injuries so a repeat CT before discharge is more important after liver injury than after splenic injury. Any of the following may be found: a) Recurrent bleeding. b) Arterioportal fistula, shown by early, intense contrast enhancement of the portal vein. c) Pseudoaneurysm, round focal areas of intense enhancement adjacent to arteries. d) Biloma, low density round or crescentic areas. Bile in a hematoma delays healing. e) Obstructive jaundice from mass effect of biloma or hematoma
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Fig. 37.8. Liver laceration. (arrow) (StomachS)
CT Pitfalls in Liver Evaluation

- Diffuse periportal tracking can occur in patients with lymphatic obstruction and dilatation of lymphatic channels caused by hepatitis, liver transplant, cardiac failure, cardiac tamponade, and malignant tumors of the liver. This may be differentiated from the focal tracking associated with liver injury. - A prominent cleft in the undersurface of the liver may look like a laceration, but as in the spleen, this will have a smoother contour and not be associated with a hemoperitoneum. - Dilated bile ducts may have the appearance of branching lacerations especially on noncontrast images, but careful analysis can differentiate the two. - An unusually elongated left lobe of the liver that may appear separated from the right lobe may appear to be a laceration. - Streak or beam-hardening artifact from air-fluid levels in the stomach or from ribs, motion artifacts, volume-averaging and unusual window settings can cause confusion.
Gallbladder Trauma
Gallbladder trauma is rare because of its well-protected recess. It may occur when the gallbladder is distended and is often associated with liver or duodenal injuries. Alcohol causes gallbladder distention by increasing bile flow and causing contraction of the spincter of Oddi, making the gallbladder more prone to injury at the same time that the alcohol is making trauma more likely. CT Findings
- Rupture may cause the gallbladder to collapse and spill bile and blood around it. Most commonly, the bile leakage is pericholecystic and contained. This fluid is extraperitoneal so peritoneal lavage may be negative. Intraperitoneal spillage is also possible.
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Fig. 37.9A. Intrahepatic hematoma A. Precontrast images show high density blood. (arrows)
Fig. 37.9B. Postcontrast images show blood to be low density compared to the enhancing adjacent parenchyma. (arrows)
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- Blurring of gallbladder contour, focal wall thickening or discontinuity of the gallbladder wall, and an enhancing mucosal flap in the gallbladder lumen all may be present. - Hyperdense hemorrhage may collect in the lumen, which may distend the gallbladder enough to cause mass effect on the duodenum.
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- Avulsion of the gallbladder may be associated with major blood loss from lacerations of the cystic artery. - Coronal/sagittal reformations on helical CT help to demonstrate the avulsion of the gallbladder out of its fossa.
Management of Suspected Gallbladder Trauma

- Ultrasound and/or hepatobiliary radionucleide imaging may confirm the diagnosis. Follow-up CT scan after 3 weeks may also prove useful.
CT Pitfalls in Gall Bladder Evaluation

- The findings from gallbladder injury are nonspecific (for example, the blood may have come from liver injury), so gallbladder injury is sometimes difficult to diagnose. - GB can reseal after microperforation creating the appearance of a false positive finding. - Hyperdensity in the gallbladder may be mimicked by milk of calcium bile, residual contrast from ERCP, vicarious excretion of IV contrast material, or reflux from oral contrast via a patulous sphincter.
Bile Duct Trauma

Traumatic injury to the biliary system is even less common than that to the gallbladder, but is much more serious as it is associated with a high mortality rate. Injury occurs at areas of relative fixation, for example, at the sites where the hepatic duct exits the liver or where the bile duct enters the head of the pancreas. The diagnosis of bile duct injury is challenging clinically and is rare before surgery. CT Findings
Bile may be contained in an extraperitoneal location. Free uninfected intraperitoneal bile may produce no symptoms. Edema may be seen in the hepatoduodenal ligament area. Associated liver and duodenal injuries are common. Associated injuries of the portal vein or hepatic artery are rare because these are more elastic than the bile ducts.
Pancreatic Trauma
The pancreas is uncommonly injured with blunt trauma. When it does occur, it is usually a result of an anterior midline blow (by a steering wheel, for instance) that causes compression of the pancreas against the vertebral column. It is often associated with injury to the duodenum or liver. Traumatic pancreatic injury is more common in children probably because they have less surrounding fat to buffer a direct blow. CT Findings
- Intrapancreatic contusions and hematomas appear as hypodensities in a focally or diffusely enlarged pancreas. - Lacerations or fractures are linear hypodense areas that are perpendicular to the long axis of the pancreas. These are usually in the neck or head, where the pancreas overlies the spine. Since the elastic pancreatic parenchyma may resume normal contour even with transsection, there may only be the minimal CT findings of peripancreatic subtle edema or fluid (Fig. 37.10). - This fluid may collect in the anterior pararenal space, around the superior mesenteric artery, in the transverse mesocolon and the lesser sac, or between the pancreas and splenic vein. It may result in left anterior pararenal fascial thickening.
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Fig. 37.10. Pancreatic laceration. (arrow)
Management of Suspected Pancreatic Trauma

- A retroperitoneal fluid collection may be the only finding to suggest a pancreatic duct interruption. ERCP or MRI may confirm diagnosis. A follow-up CT after 12-48 hours is more sensitive than the initial CT scan.
CT Pitfalls in Pancreatic Evaluation

- The pancreatic parenchyma may resume normal contour after laceration, so the only finding of injury may be peripancreatic fluid. - The fat plane separating normal pancreas from adjacent unopacified duodenum or jejunum may simulate fracture of the pancreas. Repeat scanning with additional oral contrast may clarify. - Physiologic thinning of the pancreatic neck may also cause confusion. - Volume-averaging, beam-hardening and streak artifacts, motion artifacts, and unusual window settings can cause confusion.
Bowel and Mesenteric Trauma

Several mechanisms can injure the bowel in blunt trauma.
- Direct compression of the bowel between the anterior abdominal wall and the spine causes injury. - Blow-out injury can occur from increased intraluminal pressure. - Tangential shearing forces can tear sites of fixation and cause injury.
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The second and third parts of the duodenum are the most commonly injured parts of the bowel. Duodenal injury, which includes bowel wall hematoma and perforation, is caused by midline compression, so the pancreas should be closely evaluated for associated injuries (Figs. 37.11, 37.12)
- A large hematoma can cause a bowel obstruction. - Fluid, extravasated oral contrast, gas in the retroperitoneal right anterior pararenal space, or an abnormality in adjacent head of the pancreas can suggest a duodenal
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Fig. 37.11. Duodenal hematoma. (arrows)
Fig. 37.12. Small bowel perforation with bowel wall thickening (curved arrow) and a small amount of mesenteric air (long arrow) and fluid. (short arrow)
injury. If the injury is near the ligament of Trietz, the fluid or gas may be seen within the peritoneal space.
The jejenum and ileum are commonly injured at points of fixation such as the ligament of Trietz or the ileocecal valve. The colon, the least common part of bowel to be affected in blunt trauma, is injured by compression. Penetrating trauma of the back and flank is a more likely cause of colonic injury.
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Isolated mesenteric injury is rare but may occur if the mesentery is avulsed from the bowel.
- The CT has a sensitivity of 90% for bowel and mesenteric injuries.
CT Findings of Bowel or Mesenteric Trauma

- Bowel dilatation may be seen (Fig. 37.7). - Bowel wall thickening of greater than that of adjacent bowel loops is seen in both hematomas and rupture. Wall thickening of 3 mm has been mentioned as abnormal, but with incomplete distention, this is difficult to determine (Figs. 37.11, 37.12) Narrow CT window settings may help pick up a subtle intramural hematoma. - Free intraabdominal fluid may be present. This may be low-density bowel contents or high-density acute blood. Free fluid in the absence of solid organ injury should prompt a careful search of bowel and repeat CT with additional oral contrast may be warranted (Fig. 37.12). - Interloop fluid, triangular-shaped collections between the fat-density leaves of the small bowel mesentery, suggests bowel or mesenteric injury. - Misty mesentery, streaky opacities in the mesenteric fat, correlates with smallintestine rupture. This streakiness may indicate edema from direct mesenteric injury or chemical irritation from spilled intestinal contents, or it may be caused by a small amount of fluid or blood. A sentinel clot or active extravasation of contrast-enhanced blood may be spotted next to the injury. - Extraluminal air can be seen in the peritoneum (subdiaphragmatic, anterior to the liver, or between the leaves of the mesentery) (Fig. 37.12), or the retroperitoneum (anterior pararenal space). The free air may be subtle and consist of only a few air bubbles that can be best distinguished from intraluminal air and from fat on broad (i.e., lung) CT window settings. Although some causes of free air are not surgical emergencies (see pitfalls), even a small amount of free air should prompt a careful search for other CT and clinical signs of a serious bowel perforation. - Extravasated oral contrast material, although not common, is the most specific sign. Narrow CT windows may help pick up subtle amounts. - Bowel wall discontinuity is also not common, but obviously very specific. - Bowel wall enhancement with hyperemia may also occur with injury. - Shock bowel can occur with severe hypoperfusion, such as with inadequate fluid resuscitation. The small bowel wall may be diffusely thickened and enhance more than normal. The bowel lumen may be dilated with fluid. The colon is normal however. A slit-like IVC, small reactively constricted aorta, decreased splenic and increased renal enhancement are associated findings. Fluid resuscitation will return the bowel function to normal.
CT Pitfalls in Bowel/Mesenteric Injuries
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- Some patients may have extraluminal air not caused by a significant bowel perforation. Sealed-off intestinal microperforations caused by barotrauma also result in intraperitoneal air, but have no lasting sequela. Dissection of air from chest into the peritoneal cavity can also occur from a pneumothorax,
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subcutaneous air, chest tubes, or mechanical ventilation. Free air from the female genital tract or bladder rupture are also possibilities. - Bowel wall enhancement may be seen in hypoperfused bowel (e.g., shock bowel) as well as in bowel rupture. - CT artifacts as elsewhere in the abdomen can mask or create the appearance of injury.
Renal Trauma
Renal injury is common in blunt abdominal trauma and is often associated with injuries of the adrenal gland (Fig. 37.13) or other organs. The vast majority of these are minor injuries that dont need surgery. Preexisting conditions, such as hypdronephrosis, infection, and poorly protected horseshoe kidneys, make the kidney susceptible to injury even from minor trauma. Clinically, traumatic injury of the urinary tract is rare if there is no hematuria, no hypotension, and no pelvic fractures.
- Hematuria, even microscopic, is more specific than hypotension in predicting renal injury. - Renal pedicle injury, which may have no hematuria, is an important exception.
The most accurate current imaging method to define the extent of renal damage is by CT. Triple-phase CT scanning increases sensitivity of renal injury detection:
- The arterial phase of the CT scan can assess the renal artery. - The nephrographic phase best evaluates renal parenchymal and venous injury. - Delayed CT images obtained after 2-10 minutes help to rule out urine leak.
CT Findings and Management of Renal Injury

- Fluid from renal injury can consist of the following: Hemorrhage. Active arterial extravasation of blood mixed with IV contrast that may be surrounded by less dense blood clot. Extravasated urine mixed with contrast material, which will be contiguous with the urinary collecting system. Arterial bleed is sometimes difficult to separate from urine as they are both very dense initially. The delayed scans after 2-10 minutes will show that the arterial leak gets diluted and less dense after contrast is stopped, but the urinary leak becomes more dense. - Renal injury has been placed into categories that correlate to management. Category I (75-85%) includes renal contusions and small corticomedullary lacerations that do not communicate with the collecting system. Category I injuries need only conservative treatment. - Renal cortical lacerations appear as irregular, linear, hypodense zones, usually extending from the periphery of the renal parenchyma. - Intrarenal contusions may appear as patchy hypodense zones. A striated nephrogram, probably from stasis of urine in the blood-filled tubules, similar to the nephrogram of pyelonephritis, and is another appearance of contusion. - Subcapsular hematomas may be associated and are superficial crescentic areas that compress and distort the normal contour of the opacified renal parenchyma. As with subcapsular hematomas in other organs, the capsule remains intact and contains hemorrhage.
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Fig. 37.13. Left adrenal gland (A) hematoma. Right kidney (R) global infarct.
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Category II (10%) refers to renal lacerations that communicate with the collecting system and to fractured kidneys. Associated hemorrhage and urine can leak into the renal parenchyma and the leaves of the renal fascia as well as into the anterior pararenal space. Treatment is controversial. Even major cortical lacerations are sometimes treated with just a ureteral stent. - Fracture of the kidney (category II) occurs when lacerations connect two cortical surfaces of the kidney through the hilum. The fractures usually parallel intravascular tissue planes so they do not injure the major \vessels (Fig. 37.14) Category III (5%) refers to shattered kidneys and injuries to the renal vascular pedicle. As in category II injuries, fluid can leak into the parenchyma and into the perirenal spaces. a) A shattered kidney occurs when multiple lacerations traverse the kidney and fragment it into several pieces. Unlike simple fractures, a shattered kidney does include injury to the major segmental vessels that usually result in major blood loss. b) Renal pedicle injuries include arterial and venous injuries. - Traumatic renal artery occlusion is caused by deceleration injuries that stretch the proximal renal arteries to produce intimal tears that thrombose and produce arterial occlusion. This may have CT findings of renal or segmental infarction (Figs. 37.13, 37.15, 37.16). - Traumatic renal vein thrombosis may also occur as a result of deceleration injury. The CT scan may show an acutely enlarged kidney, persistent nephrogram on the delayed scans. The actual thrombus in a dilated renal vein is sometimes discernible. Category IV refers to ureteropelvic junction (UPJ) disruption and laceration to the renal pelvis. The CT scan may show: a) Massive amounts of extravasated urine are seen in the medial rather than dorsolateral aspect of the perirenal space; absence of renal parenchymal injury and lack of ureteral opacification are also noted.
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Fig. 37.14. Right kidney fracture with perinephric hematoma and urine extravasation. (arrow)
Fig. 37.15. Segmental infarct of the left kidney. (arrow). Left transverse process fracture is also noted.
b) Absence of renal parenchymal injury and lack of ureteral opacification. c) Retrograde ureteropyelography can confirm the disruption of the UPJ. d) Similar changes may be seen in the rare traumatic ureteral transsection, which is associated with fluid around the psoas muscle as well.
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CT Pitfalls in Renal Trauma Evaluation

- Striated nephrogram may be seen in both infection and contusions.
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Fig. 37.16. Global infarct of the right kidney due to occluded right renal artery. (arrow)
- If no delayed images are obtained, collecting system injuries may be missed. - CT artifacts can cause confusion as elsewhere.
Diaphragm and Lung Bases

The lung bases can be evaluated on the abdominal CT for pneumothoraces, lung contusions, and rib fractures (Fig. 37.17). The left hemidiaphragm is more commonly injured because the liver protects the right.
- Hemidiaphragm hematoma is possible (Fig. 37.18). - Hemidiaphragm rupture is often unrecognized initially, sometimes for years, unless incidentally picked up on an imaging study, at surgery, or if visceral herniation or strangulation occurs (Fig. 37.19).
Vascular Injury IVC

Injury to the IVC after blunt trauma is rare, but its evaluation is important to evaluate fluid replacement.
- Assessment of fluid replacement may be made on the basis of the appearance of the IVC: If it is round and plump, it implies that fluid replacement is adequate. If it is flat and thin, fluid replacement is not sufficient and it implies impending shock. This sign of hypovolemia occurs before clinical manifestations of hypotension or tachycardia. This is especially important in the young where BP and pulse are normal even with massive volume depletion, due to marked vasoconstriction. - Injury to the IVC is more common in penetrating trauma. Irregularity of the caval contour may be seen. Retroperitoneal hemorrhage with the inferior vena cava at its epicenter may also be seen.
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Fig. 37.17. Left rib fractures with associated lung contusion. (arrow)
Fig. 37.18. Hematoma in the right crus of the diaphragm. (C)
Aorta
As with the IVC, a small-constricted aorta suggests hypovolemia and possible impending shock. When aortic trauma is suspected, a single, combined chest-abdomen-pelvis CT scan with one IV contrast bolus is possible with helical CT. Dissection,
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Fig. 37.19. Left diaphragmatic rupture with herniation of the stomach into the hemithorax. Note that the stomach (s) is pressed against the left heart (h) border.
pseudoaneurysm, irregularity of the aortic wall, and periaortic hematoma may be seen (Fig. 37.20).
Traumatic Pseudoaneurysm
Pseudoaneurysms are eccentric saccular collection of contrast adjacent to the injured artery that may contain thrombus. These have an eccentric focus of hyperdensity and surrounding low and heterogeneous density hematoma (Fig. 37.21).
Bladder Trauma
The bladder may be injured by blunt or penetrating trauma. Bladder injury occurs most frequently in association to pelvic fractures (Fig. 37.22). Susceptibility to injury directly correlates to the degree of distention.
- Intramural contusions or hematomas may occur from a direct blow. - Bladder rupture can be of two types. a) Extraperitoneal rupture (80-90%) may occur as a result of direct injury to anterior bladder wall by pelvic fracture fragments or from shearing forces at bladder base. b) Intraperitoneal rupture (15-20%) usually occurs as a result of a direct blow to the bladder dome of a full bladder.
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If the bladder is not filled, its injuries may be missed on CT. The Foley catheter is clamped for at least 5 minutes before the start of scanning. If the bladder is not filled on the original CT, the bladder can be drained, filled with dilute contrast, and reimaged to obtain a CT cystogram. This is very sensitive for bladder injuries, and by comparing to the precystogram study, bladder extravasation can be distinguished from bowel or vascular extravasation.
- If urethral injury is suspected because blood found at the urethral meatus or the Foley catheter cannot be passed easily into the bladder, the urethra is evaluated by a retrograde urethrogram, usually before the CT scan.
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Fig. 37.20. Aortic (a) transsection with extensive extravasation.
Fig. 37.21. Traumatic left groin pseudoaneurysm of left femoral artery with brightly enhancing eccentric focus of contrast and surrounding blood. (arrowheads)
CT Findings of Bladder Trauma

- Intramural hematoma/contusion can appear as focal or diffuse bladder wall thickening with possibly low-density areas. - The two types of bladder rupture may be differentiated on CT, which is of clinical importance because intraperitoneal rupture needs surgery.
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Fig. 37.22. Bilateral pubic rami fractures (curved arrows) with associated obturator internus (o) hematomas.
a) In extraperitoneal rupture extravasated urine and contrast is seen in the perivesicular fat, and it may extend into the perineum, scrotum, thighs, retrorectal presacral space, and into the anterior abdominal wall. The potential space in the anterior abdominal wall between transversalis fascia and parietal peritoneum, extends superiorly in the abdominal wall and can surround the anterior and lateral portions of the peritoneal cavity. Fluid in this space may mimic intraperitoneal rupture at CT. b) In intraperitoneal rupture extravasated urine and contrast material is in the peritoneal cavity surrounding the bladder and bowel loops, in perirenal recesses, in pericolic gutters, and in the Pouch of Douglas (Figs. 37.23A, 37.23B)
CT Pitfalls in Bladder Evaluation

- If the bladder is not filled, injury may be missed. - Patients with urethral injury often cannot have a Foley catheter placed, so bladder filling may be variable and CT cystography cannot be performed. - In extraperitoneal rupture, the extravasated fluid can extend into the potential space in the anterior abdominal wall and mimic intraperitoneal rupture.
References
1. 2. 3. Novelline RA, Rhea JT, Bell T. Helical CT of abdominal trauma. Radiologic Clinics of North America 1999; 37:591-612. Shuman W. CT of blunt abdominal trauma in adults. Radiology 1997 ; 205:297-306. Amorosa TA. Evaluation of the patient with blunt abdominal trauma: An evidence based approach. Emergency Medicine Clinics of North America 1999; 17: 63-75. Lee JKT, Sagel SS, Stanley RJ et al. Computed body tomography with MRI correlation. 1998;1298-1341. Barloon TJ, Weissman AM. Diagnostic imaging in the evaluation of blunt abdominal trauma. American Family Physician 1996; 54:205-209.
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4. 5.
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Fig. 37.23A. Intraperitoneal bladder rupture: KUB shows extravasation of bladder contrast.
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Fig. 37.23B. CT shows contrast in the paracolic gutters. (arrows)
ORTHOPEDIC INJURIES
Extremity Compartment Syndrome

George C. Velmahos and Pantelis Vassiliu Definition and Mechanisms
Compartment syndrome occurs when the pressure increases within the tissue surrounded by a tight fascial envelope beyond a critical level necessary to maintain tissue perfusion. In the vast majority of cases, the increase in pressure is caused by tissue edema or intracompartmental bleeding. Because the body is a compilation of compartments, the syndrome may occur literally anywhere, including the extremities or cranial, thoracic, and abdominal cavities. The extremity compartment syndrome occurs more frequently in the lower rather than upper extremities and calves rather than thighs. The most common causes of extremity compartment syndrome are: fractures, vascular injury, extensive soft tissue contusion, prolonged external pressure, and burns. However, multiple other less frequent causes may lead to increased intracompartmental pressures: snake bite, electrocution, intensive exercise, acute venous obstruction, infiltrated infusion.
Pathophysiology
An initial ischemic insult by any of the above mentioned causes produces cell damage and increases the capillary permeability. Postischemic swelling occurs leading to further compression of the intracompartmental tissue and aggravating the cellular ischemia. During the ischemic phase, the macrophages are primed. Upon reperfusion, the sudden supply of abundant oxygen to the ischemic tissue leads to formation of oxygen free radicals which are responsible for ongoing cellular damage and increased fluid leak in the third space with resulting edema. Although compartment syndrome may not be apparent during the ischemic phase (as in arterial occlusion), it may rapidly form after reperfusion (as in reconstitution of arterial blood flow). The compliance of the fascia progressively decreases as the intracompartmental pressure increases. Experiments have shown that after a pressure of 20 mmHg, relatively small increases in intracompartmental volume (bleeding, tissue swelling) cause exponential increases in pressure. Because at the capillary level the intravascular pressure is 20-30 mmHg, the elevation of extravascular pressure to these levels may lead to occlusion of capillaries and tissue ischemia, even if the blood flow is maintained in the high-pressure system of the main arteries. The different tissues in the compartment have different levels of tolerance to pressure. Nerve tissue is the most sensitive to it, shows signs of dysfunction
Trauma Management, edited by Demetrios Demetriades and Juan Asensio. 2000 Landes Bioscience. George C. Velmahos, Division of Trauma/Critical Care, University of Southern California School of Medicine, Los Angeles, California, U.S.A. Pantelis Vassiliu, Division of Trauma/Critical Care, University of Southern California School of Medicine, Los Angeles, California, U.S.A.
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early, and is most unlikely to return to normal function after relatively short periods of increased pressure.
Anatomy of Extremity Compartments

Lower Extremity:
- Calf (Fig. 38.1): There are four compartments; anterior, lateral, superficial posterior, and deep posterior. The anterior compartment lies between the tibia and the fibula and contains the anterior tibial artery and deep peroneal nerve, which innervates all the muscles of the compartment and supplies sensation to the first web space of the foot. It is the most frequently involved compartment of the four. The lateral compartment lies over the fibula and contains the superficial peroneal nerve but no major vessel. The superficial posterior compartment contains the sural nerve. The deep posterior compartment contains the tibioperoneal arterial trunk and the tibial nerve. - Thigh: There are three compartments; anterior, posterior and lateral. The lateral compartment contains the neurovascular bundle and is the least frequently involved of the three. The sciatic nerve travels through the posterior compartment. - Gluteal: The three muscles of these compartment (gluteus maximus, medius, and minimus) are invested by the fascia lata. The sciatic nerve is in this compartment.
Upper Extremity
- Forearm: There are two compartments; volar and dorsal. The volar compartment contains all the flexors of the hand, as well as the ulnar and radial arteries, and median and ulnar nerves. The dorsal compartment contains the mobile wad, which may be considered as a separate compartment. - Arm: There are three compartments; deltoid, anterior or biceps, and posterior or triceps. The axillary nerve is within the deltoid compartment. The brachial vessels and musculocutaneous, median, and ulnar nerves are in the anterior compartment, whereas the radial nerve is in the posterior.
Hand and foot compartments: Infrequently, there is a need to decompress the hand or foot compartments. There are four hand compartments: central palmar, thenar, hypothenar, and interosseus. Similarly, the foot has four compartments: central, medial, lateral, and interosseous.
Symptoms and Signs

The 6 Ps constitute the hallmark of compartment syndrome: pain, pressure, paresthesia, paralysis, pulseless, and pallor. The two latter are present only in late stages. Even in the presence of a fully developed compartment syndrome, initially there is distal pulse and appropriate color. Pressure stands for the tactile feeling of a tense compartment. Pain is characteristically out of proportion even in the presence of associated extremity injuries. Stretching the muscles included in the involved compartment exacerbates the pain. Paresthesia is an early symptom and needs to be evaluated along the distribution of the involved nerves, whereas paralysis indicates prolonged pressure on the nerve.
Measurement of Pressures
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Intracompartmental pressures are measured directly by the introduction of a needle into the compartment, connected to a pressure transducer. The most frequently used device is the StrykerTM pressure monitor (Stryker Instruments, Kalamazoo, MI).
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Fig. 38.1. Compartments of the calf with the corresponding nerves.
Although there is no absolute normal or abnormal pressure, experimental animal work and human studies support that pressures less than 20mmHg do not usually cause major problems in the majority of cases. Pressures above 30 mmHg are considered clearly abnormal, and pressures in the 20 to 30 mmHg range are in the gray zone. The diagnosis of compartment syndrome should not be based exclusively on the measurement of pressures. A correlation of the patients symptoms with the measured pressures is imperative for correct diagnosis. When the suspicion of compartment syndrome arises, all the compartments of the involved extremity should be measured (Fig. 38.2).
Complications of Compartment Syndrome

Local and systemic complications may arise. Local complications may lead to muscle necrosis and infection (particularly if the skin integrity has been violated). Necrotic muscle is converted slowly to anelastic fibrous tissue with development of Volkmans contractures. Systemic complications are more obvious during the time of reperfusion. Because accumulated toxic substances are released in the general circulation at the time of reperfusion, central organs, including the heart, lungs, or kidneys suffer an acute insult. Death may occur. Myoglobinuria and renal insufficiency may result due to muscle breakdown. Acute respiratory and cardiac failure are also possible. The likelihood of significant systemic insults is proportional to the amount of ischemic muscle. Therefore, reperfusion of compartments which contain large muscles, ischemic for prolonged periods of time, is associated with a higher incidence of systemic cardiorespiratory abnormalities.
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Fig. 38.2. Placement of needle for correct measurement of all calf compartments.
Complications associated with the fasciotomy include infection, venous stasis, inadequate muscle pump function, and disfigurement.
Treatment
The treatment of compartment syndrome is immediate pressure release by opening of the fascial envelope. Usually, two skin incisions are used for compartment syndrome of the calf (Fig. 38.3). A lateral incision midway between the tibia and fibula is used to decompress the anterior and lateral compartments. A medial incision, about 2 finger-breadths medial to the tibia, is used to decompress the superficial and deep posterior compartments. A one-incision four-compartment fasciotomy, although more technically challenging, can be used at this level (Fig. 38.4). All four compartments can be decompressed by a lateral incision, overlying the fibula, by elevating adequate skin flaps. One lateral skin incision is usually adequate for compartment syndrome at the thigh level. The anterior and posterior compartments can be approached by this incision. In the infrequent occasion that the medial compartment is involved, an additional medial incision is necessary. Two skin incisions are used for compartment syndrome at the forearm level. The volar compartment can be decompressed by a medial S-shaped or straight incision, and the dorsal by a straight lateral incision. One medial skin incision across the biceps/triceps groove is adequate to decompress both the anterior and posterior arm compartments. Mannitol has osmotic diuretic and oxygen-free-radical-scavenging actions. As such, it is suggested to be given before reperfusion to protect against systemic insults. It can also be given as prophylaxis against the development of com-
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Fig. 38.3. Two-incision four-compartment fasciotomy at the calf.
partment syndrome. Due to the possibility of diuresis-associated hypotension, it is only recommended for hemodynamically stable patients.
Closure of Fasciotomies
Closure of the fasciotomy site is desirable as soon as possible to decrease infection rates, improve wound care, and shorten hospital stay. A number of methods can be used. Primary skin closure is ideal but not often feasible due to muscle bulging. The shoelace technique (Fig. 38.5) can bring progressively the wound edges together by applying gradual tension through a heavy suture or vessel loop that is threaded through staples placed on the skin edges at the primary operation. The tails of the loops are pulled together on a daily basis, decreasing gradually the distance between the wound edges. The SureClosureTM device (manufacturer, city, state) is an alternative method of progressive primary skin closure. One or multiple devices can be applied under local anesthesia with good results (Figs. 38.6A and 38.6B). Skingrafting is frequently required due to excessive muscle bulging and inability to close the skin primarily by any method.
Prophylactic or Therapeutic Fasciotomies

Because delayed diagnosis of compartment syndrome is related to significant local and systemic complications, many authors recommend prophylactic fasciotomy for patients who have the following criteria:
- Ischemia longer than 6 hours. - Combined arterial and venous injuries of the popliteal artery (particularly if venous ligation is required). - Extensive soft tissue damage.
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Fig. 38.4. One-incision four-compartment fasciotomy at the calf.
On the other hand, other authors prefer to avoid doing a procedure that is associated with short- and long-term morbidity for a disease that is not yet present. They recommend that fasciotomy be done only for established compartment syndrome. We have found that prophylactic fasciotomy increases the risk for local complications and decreases the incidence of primary wound closure, and recommend against it.
Pitfalls in the Diagnosis and Treatment of Compartment Syndrome

The following diagnostic pitfalls must be avoided:
- Failure to suspect the possibility of compartment syndrome development-based on the type and amount of injuryand follow the patient closely. - Failure to recognize the importance of pain out of proportion, and attribution of the severe pain to the existing injuries (remember: a reduced and immobilized fracture should not hurt much after a while). - Failure to correlate the pressures with clinical signs. Normal or near-normal pressures do not exclude the possibility of compartment syndrome (particularly in the presence of hypotension). Monitoring methods have limitations and should not be exclusively relied upon, if the clinical symptomatology suggests otherwise. - Failure to examine under casts or wrapping bandages. This is maybe the most frequent diagnostic pitfall. We recommend that patients who need splints, casts or covering dressings should have windows opened for frequent clinical evaluations.
The following therapeutic pitfalls must be avoided:
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- Inadequate fasciotomies (Fig. 38.7). Subcutaneous fasciotomies are rarely adequate. Proper long skin incisions are necessary in the majority of occasions.
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Fig. 38.5. The shoelace technique. The ends of the vessel loops are pulled progressively every day until the skin edges reapproximate.
Fig. 38.6A. Application of SureClosure on a wide fasciotomy wound.
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Fig. 38.6B. Final result
All involved fascial layers should be opened. The deep posterior compartment is often inadequately decompressed due to its deep anatomical location. - Redevelopment of compartment syndrome after skin closure. Close follow-up is necessary in the hours after primary skin closure, particularly, if closure was done soon after fasciotomy. - Although not proven, mannitol should be given before fasciotomy in patients with stable hemodynamics. We recommend a drip of 1mg/kg mannitol with 40 mEq NaHCO3 in 1000 ml of lactated Ringers solution.
References
1. 2. 3. 4. 5. 6. 7. In: Mubarak SJ, Hargens AR, eds. Compartment Syndromes and Volkmans Contracture. Philadelphia: WB Saunders 1981:1-227. Perry MO. Compartment syndromes and reperfusion injury. Surg Clin N Am 1988; 68:853. Mabee JR, Bostwick TL. Pathophysiology and mechanisms of compartment syndrome. Orthop Rev 1993; 22:175. Velmahos GC, Theodorou D, Demetriades D et al. Complications and nonclosure rates of fasciotomy for trauma and related risk factors. World J Surg 1997; 21:247. Blaisdell FW. Is there a reason for controversy regarding fasciotomy? J Vasc Surg 1989; 9:828. Harris I. Gradual closure of fasciotomy wounds using a vessel loop shoelace. Injury 1993; 24:565. Almekinders LC. Gradual closure of fasciotomy wounds. Orthop Rev 1991; 20:82.
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Penetrating Extremity Injury

Edward Newton Historical Perspective
Much experience with penetrating vascular injuries of the extremities has been gained during military conflicts. The high rate of amputation seen during the American Civil War has progressively declined as diagnostic and surgical techniques improved to allow successful repair of complex vascular injuries. In most countries the incidence of penetrating and blunt vascular injury to the extremities is approximately equal. In the United States, more than 70% are due to gunshot, shotgun or stab wounds.
Incidence
The incidence of penetrating injury to the extremities increased dramatically from 1980-1995 when it began to decline, reflecting the pattern of civilian handgun violence in general. Almost 90% of these injuries occur in males, the majority younger than 40 years old.
Penetrating wounds of the limbs may be isolated or may occur in the context of multiple trauma. In many of these cases injuries to other systems may take precedence in terms of stabilization. Tissues at risk from penetrating trauma include arteries, veins, nerves, bones, joints and soft tissues, and any combination of such injuries is possible and will affect the clinical presentation. In many cases the diagnosis is immediately apparent as massive bleeding from the wound occurs. However, in other cases the vascular or peripheral nerve injury is occult and not immediately apparent on clinical examination. Conscious patients will complain of local pain at the wound site, particularly if a fracture is present. Of particular interest is the presence of signs and symptoms of ischemia in the extremity distal to the wound. Hard clinical findings of vascular injury include:
Absent or diminished distal pulses Unexplained hypotension or anemia Pallor Pulsatile bleeding An expanding or pulsatile hematoma An audible bruit or palpable thrill over the wound
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Edward Newton, Department of Emergency Medicine, University of Southern California, Los Angeles, California, U.S.A.
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Soft clinical findings are less predictive of vascular injury but should prompt further investigation. These include:
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Isolated peripheral nerve deficit Wound in proximity to a neurovascular bundle Diminished pulses compared to the unaffected side Prolonged capillary refill distal to the injury A nonpulsatile hematoma Paresthesia, paralysis
Limitations of Physical Examination

Occult injury to nerve or artery is common after penetrating trauma, particularly if the patient is obtunded, intoxicated or otherwise unable to provide history or cooperate with the neurologic examination. Reliance on a pulse deficit to signify vascular injury is fraught with danger because pulses remain palpable in up to 20% of arterial injuries. Occasionally the pulse may be transmitted through a soft clot or by collateral arterial supply. Certain injuries are subacute on initial presentation. Arteriovenous fistulas (AVF) can occur when there is simultaneous injury to adjacent artery and vein. Although this connection may be present initially, it often matures over several days before it becomes clinically apparent. Pseudoaneurysm formation similarly takes time to fully develop and there may be no abnormal findings on the initial clinical examination. Pulses may be nonpalpable if the patient is in shock, or is severely hypothermic. Certain patients may have congenitally absent pulses in some anatomic locations. Pre-existing vascular disease may similarly obliterate pulses so that comparison to the uninjured limb is essential. A pulse deficit may be due to constrictive dressings or casts rather than a vascular injury and these should be removed if a pulse deficit is discovered. Soft tissue edema associated with trauma progresses over 24-48 hours. Consequently, signs and symptoms of a compartment syndrome may not be apparent initially on physical examination. Frequent re-examination is required in all cases of penetrating limb injury to exclude this complication. Certain compartments are deep and difficult to palpate. Because of the need to discover vascular injuries within the limits of warm ischemic time (approximately six hours) and the limitations of physical examination, in the past many vascular surgeons routinely explored penetrating wounds. With the advent of angiography, these wounds then underwent routine angiography. The high rate of negative studies has prompted the search for less invasive but accurate means of detecting vascular injuries. Angiography performed for proximity wounds results in discovery of an unsuspected vascular injury in 16% of cases.
Investigations
The exact nature of the investigation of penetrating limb injuries depends on the degree of hemodynamic stability that the patient achieves. Unstable patients may require immediate surgical intervention without the benefit of any ancillary investigation. In stable patients injured extremities are examined by plain radiographs in AP and lateral projections to detect foreign bodies, fractures, dislocations, air or
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Fig. 39.1A. Gunshot wounds to both lower extremities. Diminished peripheral pulse and bruit in right leg.
effusion in the joints. The number of intact bullets plus the number of bullet holes should equal an even number. Missing bullets must be located by serial radiographs of adjacent anatomic areas. For example, it is not uncommon for a bullet to penetrate through the upper arm into the chest. Patients demonstrating hard findings of arterial injury can be taken directly to the operating room for exploration. A hand held Doppler unit will often detect peripheral pulses when they are not palpable. However, the Doppler is subject to the same limitations as palpation of the pulse in terms of false negative and false positive examinations. In patients with soft findings of vascular injury an Ankle-Brachial Index or Arterial Pressure Index can be calculated. A standard blood pressure cuff is inflated on the injured and then the uninjured extremity and a ratio of injured to uninjured systolic pressure is calculated. A ratio less than 1.0 is considered abnormal and prompts further investigation by angiography. Lowering the cutoff to 0.90 increases the specificity but decreases the sensitivity of the test and misses too many significant injuries. Angiography is considered the gold standard for detecting arterial injury in an extremity. Because it is invasive with well-defined complications and requires mobilization of specialized resources, arteriography is no longer routinely used for all penetrating extremity trauma even with soft signs of injury. Indications for arteriography include suspicion of arterial injury based on hard findings of injury in a stable patient, a positive ABI, or suspicion of an AV fistula or pseudoaneurysm on physical examination. Newer ultrasonic modalities for detecting vascular injury have emerged recently and have replaced more invasive examinations. Color flow Doppler is relatively portable, noninvasive devices that can detect injuries in both arteries and veins.
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Fig. 39.1B. Angiography shows a popliteal arteriovenous fistula.
Measurement of compartment pressure is indicated if compartment syndrome is suspected based on physical examination or symptoms of ischemia. Commercial devices or a standard manometer can be used to measure compartment pressure. Elevation of pressure beyond 30 mm Hg is abnormal and pressures greater than 45 mm Hg or 15 mm Hg less than diastolic blood pressure require immediate fasciotomy.
Patients with penetrating trauma are managed according to standard field protocols. Patients who manifest hypotension or who have a potentially serious mechanism of injury are transported expeditiously to a trauma center. Intravenous lines can be started in uninjured limbs in route to the hospital and a fluid challenge of 20 cc/kg of crystalloid administered. Active bleeding is compressed by direct digital pressure and the injured limb is splinted.
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Emergency Department Management

Resuscitation is continued according to ATLS principles. If not already established, two large bore peripheral intravenous lines are started in uninjured limbs. Digital pressure is applied to actively bleeding wounds if accessible. Blind clamping of arterial bleeding is discouraged because of the risk of causing damage to adjacent peripheral nerves. Similarly, placement of tourniquets is discouraged because they result in increased compartment pressure and a higher incidence of venous thrombosis. History should be obtained if possible regarding the time and mechanism of injury, handedness, occupation and avocation, presence of symptoms of neurovascular injury, and any conditions that may predispose the patient to wound healing complications such as diabetes, AIDS, asplenia, malignancy or immunosuppression. Management of the patient with an arterial injury must be expedited so that reperfusion can take place within the warm ischemia window of six hours. Delay beyond this time can result in irreversible myonecrosis or ischemic neuropathy. Wounds that produce severe soft tissue damage, open fracture, joint penetration are treated with prophylactic broad spectrum antibiotics such as cefazolin. Tetanus vaccination status should be determined and appropriate boosters administered. Orthopedic consultation is indicated for patients who have sustained fractures or dislocations.
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Operative strategy is dictated by the overall condition of the patient and the specific injuries identified. Coordination of several specialists may be necessary. Patients who are moribund with acidosis, hypothermia and coagulopathy may require a damage control operation with temporary vascular shunting and later definitive repair once resuscitation is completed. Temporary vascular shunts of synthetic material can restore perfusion to an extremity while more critical procedures are completed. The timing of repair is controversial. If time allows, orthopedic repair should precede vascular repair because of fear that manipulation of bone during orthopedic reduction may disrupt a vascular repair. Fracture reduction also restores the anatomic positions and more clearly indicates the length of graft required. Internal fixation of fractures can be performed if wounds are minimally contaminated. Otherwise external fixation is used. When possible, end to end anastamosis of a transected artery is performed if undue tension on the repair can be avoided. If too large a segment of artery is damaged, autologous venous grafts are the preferred material for grafting. Appropriate sized saphenous vein grafts are generally used. Alternatively, synthetic grafts can be used in large caliber arteries (above shoulder and above knee) but these tend to thrombose if used in smaller caliber vessels. Proximal and distal thrombectomy with a Fogarty catheter should be performed before completing the repair to remove any clots that may have formed during the procedure. Infusion of a dilute 1:10 solution of heparin can prevent early thrombosis following the repair without causing systemic anticoagulation and bleeding complications. Adequate wound coverage is essential to prevent infection.
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Fasciotomy is indicated if signs of compartment syndrome occur, if a major artery or vein is ligated, or if the ischemic time exceeded six hours. Repair of major venous injuries is controversial. In the past, venous injuries were simply ligated with relatively little effect on the survival of the patient. However, postoperative edema, deep venous thrombosis and compartment syndrome are more common when the vein is ligated rather than repaired primarily. If the patients condition permits and the vein can be relatively easily repaired, it should be done. Otherwise the vein can be ligated. Increasingly percutaneous endovascular techniques have emerged as alternatives in managing certain vascular injuries. Endovascular placement of a sleeve can successfully exclude a pseudoaneurysm or AV fistula. Also, silastic beads, thrombogenic coils or gel clots can be placed under fluoroscopic guidance to repair these injuries.
Outcomes
Mortality varies tremendously depending on which vessel is involved. High prehospital mortality rates are seen for subclavian artery and vein injuries, iliac or femoral vascular injuries. Operative mortality for subclavian injuries remains approximately 15%. However, the vast majority of patients who survive to reach the hospital will survive in spite of severe vascular injury. Mortality in these patients is primarily related to injury to other systems, although occasional cases of air embolism or postoperative pulmonary embolism may be fatal. The amputation rate for penetrating injury to the extremities is lower than for blunt trauma in which severe mangling of bone, nerve and soft tissues usually determines the need for amputation. Denervated or flail limbs and those with severe soft tissue injury may require amputation in spite of a successful vascular repair. With current vascular repair techniques, the overall amputation rate is approximately 6% for penetrating extremity wounds.
Postoperative Care
Patients must be followed closely following vascular repair. A reperfusion injury has been described for the extremities as well as for the brain and other organs. This phenomenon results in free radical formation, progressive edema and ultimately, compartment syndrome. Early thrombosis of the repair is relatively common and approximately 2.5% of cases require reoperation for thrombosis or leakage of the anastamosis. Pulses should be examined frequently in the postoperative period and flow can be assessed periodically with ultrasound or color flow Doppler. Infection of grafts is relatively common as well and the patient should be assessed two to three days postoperatively for signs of infection such as fever, erythema or purulent drainage. Broad spectrum antibiotics are routinely administered following vascular repair so wounds should be cultured if infection develops because unusual organisms may be selected. Deep venous thrombosis (DVT) is common and may be difficult to distinguish clinically from posttraumatic edema. Doppler studies are accurate in detecting venous thrombosis. If a DVT occurs, it may be necessary to place a Greenfield filter in the IVC as systemic anticoagulation may be contraindicated in multiple trauma patients.
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Late Complications
Inadequate restoration of blood flow to the extremity is associated with intermittent claudication This complication is seen with stenosis at the site of repair or if one of several arteries is ligated e.g., either the ulnar or radial artery in the forearm. Development of a pseudoaneurysm may take many weeks and complications of these injuries are often delayed. Complications occur because of distal arterial embolization or compression neuropathy as the aneurysm grows. AV fistula is often missed on initial presentation. Late symptoms of ischemia, venous engorgement, edema and rarely, high output congestive heart failure can occur. Late infections can occur in the vascular graft or in bone. Symptoms of osteomyelitis include fever, purulent drainage, and pain and they occur in the vicinity of a fracture site. Septic embolization can occur from an infected graft. The average delay in presentation of arterial graft infection was 30 months in one series. Retention of lead bullets within a synovial joint can result in subsequent lead toxicity. Consequently, these foreign bodies should be removed. It has been suggested that repaired arteries manifest accelerated atherosclerosis leading to late arterial insufficiency. Injury to peripheral nerves may render the limb useless. There is a 40-fold increase in suicide among patients with flail upper extremities and depression is common.
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References
1. 2. 3. 4. 5. Weaver FA, Papanicolaou G, Yellin AE. Difficult peripheral vascular injuries. Surg Clin North Amer 1996; 76:843-59. Raskin KB. Acute vascular injuries of the upper extremity. Hand Clin 1993; 9:115-129. Demetriades D, Chahwan S, Gomez H et al. Penetrating injuries to the subclavian and axillary vessels. J Am Coll Surg 1999; 188:290-5. Modrall JG, Weaver FA, Yellin AE. Diagnosis and management of penetrating vascular trauma and the injured extremity. Emerg Med Clin North Amer 1998; 16:129-144. Fry WR, Smith S, Sayers DV et al. The success of Duplex ultrasonographic scanning in the diagnosis of extremity vascular penetrating trauma. Arch Surg 1993; 128:1368-72.
CHAPTER 40
Popliteal Vessel Injuries

Michael S. Walsh and John P. Raj History
Popliteal artery injuries were managed in World War II by ligation of the vessel and this was associated with an amputation rate of 73%. With experience in reconstruction and grafting, the amputation rate was reduced to 32% during the Korean War and 29% in Vietnam.
Incidence
Popliteal artery injuries account for 20% of all battlefield and 5-10% of all civilian arterial injuries. The popliteal artery is injured in 6% of all lower limb injuries. 33% of patients with complete knee dislocations sustain popliteal artery injuries. 16% of patients with posterior knee dislocations will have associated arterial injuries.
Anatomy
The blood supply to the foot and leg (Fig. 40.1) is dependent on the popliteal artery. The collateral circulation around the knee joint is usually not sufficient to supply the needs of the leg and the foot.
Fig. 40.1. The popliteal artery and its branches. Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Michael S. Walsh, Department of Surgery, The Royal London Hospital, Whitechapel, London John P. Raj, Department of Surgery, The Royal London Hospital, Whitechapel, London
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Clinical Features and Investigations Signs and Symptoms

Clinical signs may be divided into hard signs or soft signs.
- Hard signs signify significant injury to the popliteal vessels and include a cold ischemic extremity, absent or decreased distal pulses, pulsatile bleeding from the popliteal fossa, an expanding or pulsatile hematoma and the presence of a bruit or thrill. - Soft signs include a nonexpanding hematoma, paraesthesias or paresis and proximity of a wound to the neurovascular bundle.
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The presence of peripheral pulses does not always exclude a vascular injury.
Doppler
Doppler ultrasound is a useful adjunct for the assessment of vascular status. An ankle/brachial pressure index of less than 1.0 in the injured limb is a significant predictor of arterial injury. The need to use the Doppler to find a pulse suggests there is a significant vascular injury. An absent Doppler signal at presentation is a bad prognostic sign.
X-Rays
X-rays may give an indication of a vascular injury if there is a large soft tissue swelling or if there are fractures, dislocations or foreign bodies around the knee joint.
Pulse Oximetery
The use of the pulse oximeter to diagnose a vascular injury is limited as patients who are injured may be hypothermic and peripherally vasoconstricted. Often, even the oximetry may be normal even in the presence of significant vascular injury.
Duplex Ultrasonography
This is a useful screening tool in patients who have no signs of vascular injury but have injuries that are in proximity to major vascular structures. Duplex scanning may diagnose arterial and venous injuries. The interpretation of duplex scanning is highly operator dependent.
Angiography
Angiography is the gold standard for the diagnosis of vascular injuries and may be performed in the radiology suite or on-table if the patient is unstable. An angiogram is indicated in patients with soft signs of vascular surgery. Intraoperative angiography should be performed if vascular injuries are suspected proximal or distal to the operative site.
Management
Life threatening injuries are treated first, followed by limb threatening injuries. Patients with lower extremity injuries may fall into four groups:
- Group I: Patients who are clinically unstable with signs and symptoms of vascular injury. They will need rapid stabilization and surgery. If required, an on-table angiogram may be performed.
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Fig. 40.2. Angiogram of a gunshot wound of the popliteal artery.
- Group II: Patients who are clinically stable and have signs and symptoms of vascular injury. They need an angiogram to determine the extent of the injury followed by surgery. - Group III: Patients who are clinically stable with injuries in proximity to vascular structures but have no signs of vascular injury. These patients need a duplex ultrasound. - Group IV: These are patients who are stable with no injuries in proximity to vascular structures and no signs of vascular injuries. These patients should be treated appropriately for their injuries only.
Immediate Surgery
Patients with hard signs such as a cold ischemic extremity, absent or decreased pulses, presence of a bruit or thrill, an expanding or pulsatile hematoma or pulsatile bleeding should be taken to theatre as soon as possible for exploration. If required, an on-table angiogram should be performed. This is especially useful when injuries at multiple levels are suspected.
Damage Control Surgery

This technique should be considered in patients with complex injuries who are likely to develop severe physiological derangement or will need transfer. The immediately life threatening injuries should be treated first and the patient stabilized before proceeding to definitive vascular repair. Damage control consists of inserting a shunt to re-establish leg perfusion until the patient is fit for definitive repair. Shunts should also be inserted if it is anticipated that associated orthopedic repairs will take a prolonged time.
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Surgical Procedure
The incision depends on where the injury is: for above knee injuries, a medial thigh incision is best; for below knee injuries a lower leg incision medially is performed. Obtain proximal and distal control first either with slings or vascular clamps. Inspect and debride damaged tissue. Remove intraluminal thrombus proximally and distally using a Fogarty catheter. On-table angiography should be used liberally in order to identify any thrombus not easily accessible to the first passage of the catheter and to identify other injuries. Flush with heparinized saline. The actual repair depends on the nature of injury.
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Crural Vessels
Injuries to the crural vessels frequently coexist with popliteal vessel injuries. If an injury to the crural vessels is overlooked then the popliteal repair is unlikely to result in limb salvage. If popliteal vessel injuries extend to involve the crural vessels, then the incision can be extended distally on the medial side of the leg. The medial attachments of soleus can be taken down to expose the trifurcation of the popliteal artery. If possible, at least two of the crural vessels should be repaired.
Vascular Repair
Vascular repair of the popliteal vessels is technically demanding and requires careful attention to detail. Simple lateral suture is the method of choice for closing simple transverse lacerations. Use an interrupted 5/0 or 6/0 vascular suture. Vein patch angioplasty is the method of choice for closing lacerations if there is a risk of narrowing the vessel. A suitable piece of vein can be harvested from nearby subcutaneous tissue. Trim the patch to size with gentle curves at each end and to such a width so that, when sutured in place it does not lead to narrowing or undue bulging of the popliteal artery. Use a continuous suture method, making sure that all layers of the vessel wall are taken and placing the sutures close together. In the case of a transection, an end-to-end anastomosis may to be performed. Trim off the damaged artery and cut the ends of the vessel obliquely to reduce the risk of stenosis. Ensure that the vessel ends can be approximated without undue tension. If the vessel ends cannot be approximated without tension, then an interposition graft should be placed. This should normally consist of the long saphenous vein. The vein should be harvested from the groin rather than the ankle since it is stronger and subsequent aneurysmal dilatation is less likely. Bypass procedures should be considered with complex vascular injuries or when contaminated wounds or large amounts of soft tissue loss mean that an extraanatomical bypass is required to ensure graft cover, avoid graft infection and maintain the circulation. Ideally a completion angiogram should be performed to ensure that the anastomosis and the distal run-off are satisfactory.
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Popliteal Vein Injury

Venous injuries should be repaired before repair of the artery. The popliteal vein should be repaired using the same techniques of control and repair outlined above. Veins are not only more friable than arteries but they may also bleed more extensively since they have little medial muscle and spasm is less likely to occur.
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Associated Orthopedic Injuries

The limb should be stabilized orthopedically before proceeding to vascular repair. This ensures that subsequent manipulation of the limb does not compromise the vascular repair. If the orthopedic procedures are likely to be prolonged, temporary shunts to maintain perfusion of the limb should be inserted. Vascular injuries should be ruled out before a tourniquet is applied to an injured limb.
Fasciotomy
Fasciotomies may be required to relieve compartment pressures following reperfusion injury. Patients may lose entire muscle compartments as a result of ischemia following increased compartment pressures. Fasciotomies are indicated prophylactically when the ischemic time is greater than 6 hours, following combined artery and vein injury, when there has been a complex reconstruction or when there is severe soft tissue injury. They are also indicated when the popliteal vein is ligated. A four-compartment fasciotomy to relieve all the compartments in the leg must be done, leaving the wounds open. If a fasciotomy is not performed for any vascular injury, then compartment pressures should be measured. Fasciotomy should be performed if pressures of greater than 30 mm Hg are recorded.
A-V Fistulae
AV fistulae are seen in about 6% of penetrating injuries around the knee. Clinical features include a palpable thrill or a pulsatile mass. Surgical treatment gives excellent results. The interposition of a small muscle pedicle between artery and vein at the time of repair will reduce the incidence of recurrence.
Pseudoaneurysms
May be seen even after seemingly trivial trauma to the popliteal region, they are seen in both blunt and penetrating trauma
Iatrogenic Injuries
They occur as a complication of angioplasty and high tibial osteotomy, arthroscopic surgery, and total knee arthroplasty.
Results
The limb salvage rate after reconstruction following penetrating injuries is about 72%.
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Results are good if there is no delay in operation (< 15 hours after injury), liberal use of four-compartment fasciotomies, and aggressive management of the soft tissue injury. Injuries involving the trifurcation are associated with a very high amputation rate. Vascular injuries after explosions are associated with a worse prognosis. Amputation is required in the presence of irreversible ischemia or extensive tissue damage such as that sustained in severe crush injury. Amputation may also be needed after extensive nerve damage. Delay in resuscitation and definitive treatment may increase the risk for amputation. Involvement of more than two long bone fractures is predictive of amputation. Amputation rates following blunt injury ranges from 36-54% in different series. Patients with no pulse or Doppler signals at presentation are more likely to require amputations. Patients with major soft tissue injury and shock are also more likely to require amputations.
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Not being aware that the popliteal vessels can be injured in any injury involving the knee joint. Not recognizing the clinical features of a vascular injury. Failure to realize that crural vessels may also be involved. Not performing a thrombectomy at the time of an arterial repair. Failure to recognize a compartment syndrome if a fasciotomy is not performed!
References
1. 2. 3. 4. 5. Ordog GJ, Balasubramaniam S, WasserbergerJ et al. Extremity gunshot wounds: Part oneidentification and treatment of patients at high risk of vascular injury. J Trauma 1994; 36(3):358-368. Snyder WH. Popliteal and shank arterial injury. Surg Clin North Amer 1988; 68(4):787-807. Weaver FA, Papanicolau G, Yellin AE. Difficult peripheral vascular injuries. Surg Clin North Amer 1996; 76(4):843-859. Martin LC, McKenny MG, Sosa JL et al. Management of lower extremity arterial trauma. J Trauma 1994; 37(4):591-599. Merrill KD. Knee dislocations with vascular injuries. Orthopedic Clin North Amer 1994; 25(4):707-713.
CHAPTER 41
Hand Trauma
Christopher Shean and Stephen Schnall Introduction
Evaluation of hand trauma requires a systematic approach. Adherence to principles and guidelines allows for optimal treatment.
History
A detailed history must be obtained and include:
Age Occupation Hand dominance Mechanism of injury Time elapsed since injury Presence of systemic diseases Tetanus prophylaxis Allergies Alcohol, tobacco, and substance abuse Previous hand injuries
The importance of thorough history taking cannot be overemphasized. Decision-making in hand surgery is performed only after evaluating the entire patient situation. Treatment plans for similar injuries will vary depending on factors such as age and occupation. Many reconstruction and microsurgical operations are ill-advised in patients that smoke cigarettes or have systemic diseases effecting their blood vessels.
Physical Examination
Observation is paramount; one should always attempt to compare to the uninjured side. There is absolutely no need to poke in the wounds to make a diagnosis. In fact, examination for most tendon and nerve injuries may be performed with the wound covered. Important findings of a hand examination may include:
Swellingmay indicate fracture or ligament injury Discolorationvascular status DeformityFracture or dislocation Break in the normal cascade of the fingers Normally at rest, the fingers of the hand are in gentle flexion with progression to more flexion from index to little finger. With tendon disruption, this normal cascade will be altered (Fig. 41.1). - Location and nature of the wounds clean, contaminated, or infected
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Christopher Shean, LAC + USC Medical Center, Los Agneles, California, U.S.A. Stephen Schnall, LAC + USC Medical Center, Los Agneles, California, U.S.A.
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Fig. 41.1. Hand posture of patient with flexor tendons to long finger lacerated. Note the loss of normal cascade of the fingers witht he long finger held in extension.
Anatomically-Based Hand Examination

- The anatomy of the hand is highly specialized and refined for both intricate movements and strong grip. The fingertips are composed of skin that has great sensitivity. Injuries to structures within the hand can be diagnosed using a sequential exam based on knowledge of hand anatomy. - The framework of an anatomically-based hand examination can be organized into stepwise assessment of specific systems. A summary of this framework is as follows:
Muscles
Muscles that move the hand and fingers can be divided into extrinsic and intrinsic muscles groups, depending on whether the muscles originate in the forearm or the hand. Extrinsic hand muscles originate in the forearm and insert in the hand. This group of muscles can be further subdivided into flexor and extensor muscle groups. Extrinsic flexor muscles originate in the volar forearm and flex the wrist and fingers. Extrinsic extensor muscles originate in the dorsal forearm and extend the wrist and fingers. Intrinsic hand muscles originate and insert in the hand. The intrinsic muscles of the hand include the thenar muscle group, the hypothenar muscle group, the adductor pollicis muscle, the lumbricals and the interosseous muscles.
- Lumbricals and interosseous musclesthese two muscle groups merit special attention due to the complexity of their actions. The lumbrical muscles originate on each flexor digitorum profundus tendon and insert at the radial aspect of the extensor apparatus of the corresponding digit. Because the lumbrical tendon passes volar to the axis of rotation of the metacarpophalangeal (MCP) joints, it serves as a flexor of this joint. However, because the action of the lumbrical muscle
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Nerves
The median nerve delivers motor fibers to the pronator teres, flexor carpi radialis, flexor digitorum sublimis, palmaris longus, flexor digitorum profundus to the index and long fingers, flexor pollicis longus, and the pronator quadratus in the forearm. The anterior interosseous branch of the median nerve carries the motor fibers to the latter three muscles. The median nerve then continues into the hand, passing under the transverse carpal ligament to innervate the thenar muscles and the radial two lumbrical muscles. The recurrent motor branch of the median nerve carries the fibers to the thenar group. The ulnar nerve delivers motor fiber to the flexor carpi ulnaris and flexor digitorum profundus to the ring and small fingers in the forearm. The ulnar nerve then continues into the hand, passing through the ulnar tunnel or Guyons canal to innervate the hypothenar muscle group, the ulnar two lumbricals, each of the interossei muscles, the adductor pollicis, and the deep head of the flexor pollicis brevis. The radial nerve delivers motor fibers to every extrinsic extensor muscle in the forearm. It then continues onto the hand where it carries only sensory fibers and supplies no muscles with motor fibers. The sensory distribution of the median, ulnar, and radial nerves in the hand are displayed in Figure 41.2. It can be seen that median nerve can be reliably evaluated by testing the sensation to the pulp of the index finger; the ulnar nerve by testing the pulp of the small finger; and the radial nerve by testing the dorsum of the first web space. Examining sensation to the hand in a child with an injured hand can sometimes be difficult. In these situations, testing for sensation is more effectively performed by checking for light touch with a piece of tissue rather than with sharp/dull testing by pinprick. An additional method is to submerge the injured hand in water until wrinkling occurs. Since wrinkling of the skin is mediated by the autonomic fibers carried in the sensory nerves, abnormal wrinkling response (i.e., absence of wrinkling) is diagnostic.
Circulation
The hand usually has abundant collateral circulation and redundancy in its vascular supply. The radial and ulnar arteries anastomose with each other via the superficial and deep palmar arches and give rise to the digital arteries. However, there is extensive variation in the distribution of the radial and ulnar arteries. For this reason, the Allens test is helpful in assessing for situations in which one artery has dominance.
- The Allens test is performed by compressing both arteries at the wrist, squeezing the hand to exsanguinate the fingers, then releasing one of the arteries to evaluate
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Fig. 41.2. The sensory distribution of the median, ulnar and radial nerves in the hand.
the filling time to the digits by that artery. Normal refill occurs in less than five seconds. Occasionally, the refill of one of the arteries will be delayed and thus diagnosing a situation in which one artery has dominance. In such situations, injury to one artery can compromise circulation to several digits. - Capillary refill can also be used to evaluate circulation to the hand by compressing the nailbed to cause blanching of its underlying capillary bed. The compression is then released and the time for the bed to refill is assessed. Normal refill occurs in one to two seconds. Delayed refill may indicate a situation in which arterial insufficiency exists. Brisk refill, however, may indicate a situation in which vascular congestion exists.
Hand Exam Maneuvers

Tinels Sign: Tapping over the median nerve at the wrist in a patient with carpal tunnel syndrome may produce tingling paresthesias in the median nerve sensory distribution.
- Tinels testing can also be used to assess regeneration of axons after nerve injury. When the growing ends of a regenerating nerve are tapped, a similar tingling paresthesia can be elicited in that nerves sensory distribution. Thus, recovery after nerve injury or repair can be assessed. However Tinels testing gives no indication of the quality and quantity of eventual nerve recovery
Phalens Test: Wrist flexion increases the pressure on the median nerve. In patients with carpal tunnel syndrome, wrist flexion may produce paresthesias in the fingers rather rapidly. Phalens test is a one-minute wrist flexion test used to help diagnose carpal tunnel syndrome. It is helpful to perform the test on both wrists at same time for comparison. However, since carpal tunnel syndrome commonly affects both wrists in a single patient, a timed Phalens test may prove more helpful. Paresthesias induced by less than 60 seconds of wrist flexion are suggestive of the diagnosis. Extrinsic Muscle Tightness: When the extensor tendons become adherent or
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scarred down over the wrist or forearm, the tendons may limit flexion of the fingers. This situation can be diagnosed by testing PIP joint flexion, with varying degrees of MCP joint flexion. In a patient with extrinsic muscle tightness, PIP joint flexion is present when the MCP joint is held in extension. However, when the MCP joint is held in flexion, PIP joint flexion will be limited. Intrinsic Muscle Tightness: When the intrinsic muscles of the hand become scarred or fibrotic, their excursion and extensibility become limited. This can lead to characteristic findings on hand examination. The intrinsic muscles, as discussed previously, function to flex at the MCP joints and extend at the PIP and DIP joint. When the intrinsics are scarred and shortened, the PIP joints can be passively flexed with the MCP joints held in flexion. However, passive PIP joint flexion is limited with the MCP joints held in extension. Quadriga Syndrome: The tendons of the flexor digitorum profundus originate from a common muscle belly. Therefore any change in the length of one FDP tendon affects the function of the others. Quadriga syndrome occurs when one FDP tendon is shortened with respect to the other tendons. This syndrome may arise in many situations. One example is after avulsion of the FDP tendon from its insertion into the distal phalanx. If during repair of this injury, the tendon requires advancement for secure fixation into the distal phalanx base, then that tendon will be shortened relative to the other tendons. Examination will reveal a flexion deficit of the uninjured digits, which have normal passive range of motion. Tenodesis: The posture of the relaxed hand is determined by the tenodesis effect. The tenodesis effect dictates that a balance of the resting tone of the flexor and extensor muscles produces the posture of the joints in the hand. With the wrist slightly flexed, the relaxed fingers and thumb are normally held in extension. With progressive extension at the wrist, the fingers and thumb will normally assume a more flexed posture. The tenodesis effect is helpful in the uncooperative patient, because injuries to the hand that disrupt the balance between the flexors and extensors, (for example, a flexor tendon laceration) will produce discernible changes in hand and finger posture.
Management
All injured hands should be radiographed to rule out foreign bodies, fractures, and dislocations. Comparison x-rays of the uninjured hand can be helpful. A minimum of three views should be taken: AP, lateral, and oblique. As radiographs are two dimensional representations of three dimensional objects, the presence and location of foreign bodies, fractures or dislocations might be overlooked if an adequate x-ray series is not obtained. Dressings if applied should be bulky and nonconstricting. It is extremely important to try to avoid circumferential bandages that might become constricting with posttraumatic swelling. Appropriate splinting of the injured hand is necessary for patient comfort and to prevent contractures. Generally, the hand is held in the safe position with the metacarpophalangeal joints flexed to approximately 45-60, and the proximal and distal interphalangeal joints extended to neutral.
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Lacerations
The size of a laceration is not related to the amount of damaged structures underlying the skin. Every flexor tendon crossing the wrist may be transected through a skin laceration less than one centimeter in length.
- The practice of probing a laceration in search of injured structures is no longer necessary. One may wonder if lacerations should be explored to clamp bleeding vessels. This practice, also, should be abolished. Nearly all lacerated vessels will coagulate and cease bleeding after the sustained application of direct pressure.
Flexor tendon lacerations occur with penetrating injuries to the volar aspect of the hand and forearm. The posture of the hand and fingers at the time of injury will effect the relationship of the skin laceration to the tendon laceration. That is, if the fingers are flexed at the time of injury, as they would be if a person were grabbing a knife, then the distal flexor tendon stump will be found distal to the skin laceration.
- Flexor tendon injuries have been classified into zones I to V, which have prognostic significance. These zones are as follows: Zone Idistal to the insertion of the flexor digitorum sublimis (FDS) tendon Zone II (no-mans land)from the distal palmar crease to the insertion of the FDS tendon, this is the zone in which the tendons traverse a fibroosseous tunnel Zone IIIthe region from the origin of the lumbrical muscles to the beginning of the fibroosseous tunnel, that is from the distal aspect of the transverse carpal ligament to the distal palmar crease Zone IVthe region of the carpal canal Zone Vproximal to the wrist - Controversies exist related to nearly every aspect of flexor tendon surgery. Research suggests that strength of a tendon repair is related to the size of the suture used and the number of suture strands that cross the repair site. However, with increasing suture size and strands across the repair site, there is increased resistance to tendon gliding. An ideal tendon repair would be strong enough to permit early active motion, without adverse effects on the tendon passage through the fibroosseous tunnel. The importance of postoperative rehabilitation after tendon repairs cannot be overemphasized. Early active motion has beneficial effects on tendon healing. However, there is a significant risk of repair site rupture with many repair types and early active motion. For that reason, most protocols include early passive motion or dynamic splinting. Research toward developing an ideal repair pattern continues.
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Treatment principles for extensor tendon injuries are similar to those for flexor tendon injuries. The importance of postoperative rehabilitation is again paramount. However, the thickness of extensor tendons is less and no fibrosseous tunnel exists on the dorsum of the hand. The unique anatomy of the extensor apparatus and its insertions on the phalanges can be disrupted in locations that lead to specific finger deformities if not addressed early after injury. Examples of these finger deformities include mallet finger and the boutonniere and swan neck deformities.
- Mallet fingers occur after rupture of the terminal extensor tendon insertion into the distal phalanx. This usually occurs after a sudden blow to the tip of the extended finger. Clinically, the distal phalanx droops into flexion and there is loss of active extension at the DIP joint. Radiographs must be obtained because at
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Trauma Management times the tendon avulses from its insertion with fragment of bone. Occasionally, the size of the avulsed fragment and degree of injury to the dorsal joint supporting structures leads to subluxation of the DIP joint. This is one generally agreed upon indication for operative repair. The results of closed treatment of mallet fingers without subluxation at the DIP joint is superior to operative treatment. - Flexion of the PIP joint and DIP joint hyperextension characterize boutonniere deformity. It results from the volar subluxation of the lateral bands usually following unrecognized central slip rupture from the base of the middle phalanx. Early diagnosis of central slip ruptures is important in avoiding this deformity. Clinically, a patient with acute disruption of the central slip will present with a swollen PIP joint and tenderness at the central slip insertion site. If unrecognized, boutonniere deformity can result. Treatment of flexible boutonniere deformities is with prolonged splintage. Established boutonniere deformities with joint contractures require complex reconstructive procedures and intensive postoperative rehabilitation. - PIP joint hyperextension and DIP joint flexion characterize swan neck deformity. It results from the dorsal subluxation of the lateral bands usually following rupture of the FDS tendon insertion or injury to the volar plate of the PIP joint. It can, however, develop after chronic mallet finger deformity.
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Amputation and Replantation

With the advancement of microsurgical techniques and instruments, successful replantation of amputated digits has become almost routine. Many determinants effect the outcome of replant surgery. Mechanism of amputation (i.e., clean laceration vs. avulsion injury), time elapsed since injury, care of amputated part, patient factors such as cigarette smoking and systemic disease, and age of the patient are among the many possible variables which may alter prognosis. Because of this complexity, controversy exists regarding the indications for replantation.
- Generally accepted indications include amputations through the hand and wrist, thumb amputations (Fig. 41.3), multiple-digit amputations, and amputations in children. - Contraindications to replantation include single border digit amputations, avulsion or crush injuries, amputations through zone II, prolonged warm ischemia time (> 12 hours for digits and > 6 hours for more proximal sites), multiple-level amputations, prior impaired hand or digital function, and extreme contamination. In general with each contraindication, functional results after replant are worse than the function obtained if a revision and closure of the amputated part had been performed primarily.
When replantation is indicated, several factors are important to a successful result. Appropriate care of the amputated part is essential. The detached part should be wrapped in saline dressings, cooled in a container placed on ice, and transported to the hospital with the patient. Once at the hospital, radiographs of both the residual limb and the amputated par t should be obtained to assess damage to the bones and joints and to survey for possible retained foreign matter. In general, the sequence of replant surgery follows an order of stabilizing the skeletal structures, repairing lacerated tendons, then performing microsurgical repair or reconstruction of the vessels then nerves.
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Fig. 41.3. Replantation of thumb amputation. A and B) clinical photographs of the amputated thumb, C and D) photographs of the successfuly replanted thumb.
Hand Fractures and Dislocations

In general, most hand fractures and dislocations can be reduced by closed means. It is only when they cannot, that open reduction is indicated. Similarly, most hand fractures and dislocations can be held by external means until stable and healed enough to be left unsupported. It is only when the fractures are unstable by closed means, that percutaneous pin fixation or internal fixation is indicated. A glossary of common hand fractures and dislocations follows: PIP Joint Dislocations: Dorsal dislocations of the PIP joint are the most frequently encountered articular injury in the hand. Most are easily reducible and stable after reduction. These can be managed with early mobilization in a splint that blocks the final 20 of extension. Unstable joints must be protected in a position of flexion to prevent redislocation. Occasionally, the volar plate of the PIP joint can become interposed in the joint and block closed reduction. Phalangeal and Metacarpal Shaft Fractures: As mentioned above, the majority of hand fractures is best treated with closed management. Indications for operative management include:
- failure of closed reduction to maintain length and/or rotational or angular alignment - displaced intraarticular fractures in which joint congruity is lost - unstable fractures with soft-tissue injuries which prevent normal rehabilitation
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MCP Joint Dislocations: These dislocations can be simple or complex. Simple MCP joint dislocations usually present with a history of marked hyperextension at the joint that was easily reduced. If not, simple dislocations are readily reduced in the emergency room and managed with buddy tapping and early motion. Complex dislocations involve a much greater soft tissue injury. The angle of hyperextension is much less and the metacarpal head may be prominent in the palm. The displaced metacarpal head may become trapped volarly between the FDP tendon and the lumbrical muscle. Because of this fact, these dislocations often require open reduction. Boxers Fractures: Fractures of the fifth metacarpal neck resulting from an axial load to the metacarpal head are termed boxers fractures. There are a variety of treatment protocols for this common fracture ranging for immediate mobilization to closed reduction and cast immobilization. Angular deformity up to 70 has been found to have minimal functional sequelae. However, no rotational malalignment is acceptable. It is also important to ensure that the skin over the knuckle is intact. If it is not, the wound is presumed to be the result of contact with a tooth while punching, and requires operative irrigation and debridement to avoid infection. CMC Fracture-Dislocations: Fractures at the CMC joints of the hand typically occur to the fourth and fifth CMC joints as a result of these joints relative mobility. The fifth CMC joint is additionally destabilized after injury by the proximal pull of the ECU tendon. It is important to recognize the dislocation component of this injury to avoid long-term dislocation. These injuries are generally reduced without difficulty, however are unstable after reduction. For this reason, closed reduction and percutaneous pinning of CMC fracturedislocations is advised. Gamekeepers Thumb: A complete tear of the ulnar collateral ligament of the thumb MCP joint is called gamekeepers thumb. It results from a hyperabduction stress to the thumb. It is important to recognize whether or not the rupture of the collateral ligament is complete. Incomplete injuries can be treated nonsurgically. However, with complete tears of the ligament, the adductor pollicis aponeurosis and extensor hood of the thumb can become interposed between the torn ligament and its area of attachment. Complete tears will, thus, not heal without surgery. A complete tear of the ligament is presumed if there is greater than 40 of instability of the MCP joint with a radially directed stress applied to the joint held in 30 of flexion. Bennetts and Rolandos Fractures: An oblique, intraarticular fracture of the base of the thumb metacarpal is called a Bennetts fracture. A comminuted fracture at the base of the thumb is a Rolandos fracture. In both, the first metacarpal dislocates dorsally and proximally due to the action of the abductor pollicis longus. These can be treated by closed means, however often fixation is required to hold the metacarpal reduced while the injury heals. Scaphoid Fractures: The most commonly fractured bone in the wrist is the scaphoid. Clinically, patients with scaphoid fractures present with tenderness in the anatomic snuffbox, just distal to the radial styloid. Often radiographs at the time of injury do not reveal a fracture. In this circumstance, the wrist should be immobilized in a spica cast and repeat radiograph can be taken after 10-14 days. Resorption at the fracture site should permit identification of the fracture if present. Radionuclide scanning can be used to confirm diagnosis of
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scaphoid fracture as early as 24 hours after injury. Scaphoid fractures are managed with 10-12 weeks of spica cast immobilization if nondisplaced. Displaced fractures require open reduction.
Soft Tissue Coverage

Many injuries to the hand are accompanied with soft tissue loss, which can vary from small and insignificant to large requiring reconstructive techniques to obtain coverage. To effectively manage hand trauma, a collection of various coverage procedures should be utilized as indicated. Split and full thickness skin grafts are commonly employed and have distinct advantages and disadvantages. A split thickness graft that includes the epidermis and a portion of the dermis is advantageous because it readily takes. However, it is associated with increased contraction, which can lead to deformity and is less durable. Full thickness skin grafts take less well than split thickness because of its increased thickness. These grafts, however, are more durable and contract less. Full thickness grafts are well suited for coverage about joints, where skin excursion demands are greater.
- A variety of flaps have been described based on the abundant vascular supply of the hand. If circumstances will not permit coverage by a local hand flap, a reversed pedicle flap based on the radial artery in the forearm (Fig. 41.4) is readily available for coverage on the hand. If required, tissue from distant locations such as groin flaps and free tissue transfers may be used to cover soft tissue deficits of the hand. The objective of obtaining adequate soft tissue coverage during reconstructive procedures of the hand cannot be overemphasized.
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References
1. 2. 3. 4. Green DP, Hotchkiss RN. Operative Hand Surgery. 3rd ed. Churchill Livingston. 1993. The Hand, examination and diagnosis / American Society for Surgery of the Hand. 3rd ed. Churchill Livingston. 1990. Hand Surgery Update / American Society for Surgery of the Hand. American Academy of Orthopedic Surgery. 1996. Lister G. The Hand: Diagnosis and Indications. 3rd ed. Churchill Livingston. 1993.
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Fig. 41.4. Radial forearm flap. A) Clinical photograph during the elevation of the forearm flap. B) shows elevated flap and soft tissue defect to be covered on dorsum of hand, C) photograph taken after placement of the flap on dorsum of hand
Long Bone Fractures and the General Surgeon

Jackson Lee
Patients who are involved in blunt force trauma frequently sustain concomitant injuries to the axial skeleton. It is important to understand some of the considerations involved in the diagnosis and management of fractures of the long bones so as to allow for cooperative care of these injures in order to maximize patient outcome. Recent advances in the care of the multiply injured patient have greatly improved the mortality rate. Survival, however, should not be considered the final goal in the care of the injured patient. The goal of any well-organized trauma service should not be focused on just saving lives, but on restoring the injured person back as a functioning member of society. An understanding of the considerations for the management of long bone fractures will greatly facilitate this final goal.
Long Bone Fractures as a Result of Blunt Force Trauma

The presence of long bone fractures in a multiply injured patient is a reflection of the energy expenditure that the patient has been subjected to. The magnitude of this energy expenditure has systemic effects that are still being elucidated. Recently, there has been considerable interest in the effects on the inflammatory system and its role in pulmonary failure and multi-system organ failure. It is important to distinguish whether the patient with long bone fractures has sustained this as an isolated injury or in association with other organ system injury. The amount of energy expenditure that is required to sustain a long bone fracture frequently will lead to occult injures to other organ systems.
Initial Evaluation
The initial evaluation and resuscitative efforts should always be focused on the A,B,Cs. The initial skeletal evaluation should be focused on determining which extremities are injured so those appropriate radiographs can be obtained at the time of secondary survey. A careful documentation of the neurovascular status should be performed at this time. Frequently, this is the only window of opportunity to obtain such important information since in many cases the patient will subsequently be intubated or at the minimal, sedated. Size and quality of open wounds should be well documented and at this time they should be superficially irrigated and dressed with sterile dressings to prevent further contamination. Finally, the injured extremity should be splinted to prevent further injury to soft tissues and neurovascular structures.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Jackson Lee, University of Southern California School of Medicine, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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Once the primary survey has been completed and initial resuscitation has been well underway, the anatomic diagnosis of the long bone fractures should proceed. This is accomplished with plain orthogonal projections of the affected limbs. Radiographs should always be obtained using an AP and a lateral film since films are a two dimensional representation of a three-dimensional object. Acceptable extremity films should always include the joint above and joint below. With these films, the lesion can be adequately characterized. In certain instances where the patient is in extremis and requires immediate life preserving operative intervention, such as an immediate thoracotomy, laparotomy, or craniotomy, radiographic diagnosis may be delayed and subsequently obtained in the surgical suite at the completion of the emergent procedure. It is important to obtain an anatomic diagnosis of the long bone fractures early in the peri-injury period to facilitate appropriate decision making.
Management
The multiply injured patient will benefit from early stabilization of long bone fractures. Depending upon the patients clinical condition however, this initial stabilization may or may not necessarily be the definitive stabilization. The advantages of early stabilization have been well documented. Early stabilization facilitates patient mobilization and simplifies nursing care. By minimizing the need for the patient to be in the forced supine position, pulmonary shunting will be decreased. From the point of view of the injury, there will be a decrease in the bleeding from fracture and soft tissues at the zone of injury, and a decrease in the pain thus decreasing the need for respiratory depressing opiates in the peri-injury period. Systemically, there would be a decrease in the local and systemic inflammatory response. The decision to perform temporary or definitive stabilization should be made jointly with the general surgeon, neurosurgeon and orthopedic surgeon and should be made in real-time and based on the patients physiology. The stabilization of long bone fractures should proceed as soon as the patients clinical condition permits. Frequently, definitive stabilization can proceed after successful emergent exploratory laparotomy or thoracotomy where major sources of bleeding have been controlled, resuscitation has proceeded concomitantly with the surgery, and the patient is not coagulopathic. If the patients condition is not normalized using objective criteria, then the patient should be brought to the ICU with the goal of undergoing a brief period of additional resuscitation before returning to surgery to complete long bone stabilization. It is important to utilize objective criteria to make this determination and refrain from using arbitrary statements such as too much anesthesia or too much surgery as this will lead to a missed opportunity syndrome.
Prioritization
In assessing the orthopedic injuries, certain types of injuries have a much greater impact on patient outcome and are thus addressed first. This prioritization should be made by the most senior and experienced orthopedic surgeon in consultation with the general surgeon, anesthesiologist, and if applicable, the neurosurgeon. This prioritization should be constantly updated in real time and take into account the patients overall status. Multi-trauma patients can decompensate in an unpredictable manner.
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Open Fractures
When a fracture of a long bone is associated with a disruption of the soft tissue envelope, it immediately becomes a nidus of future sepsis in a multiply injured patient. The presence of foreign material along side necrotic soft tissues and bone becomes an excellent culture media for bacterial flora. If this nidus remains unchecked, this can be a source of sepsis. The only effective means to address this situation is aggressive surgical debridement through complete visualization of the entire zone of injury. Following debridement, in order to prevent further soft tissue injury due to continued fracture site motion and to eliminate dead space as a source of infection, skeletal stabilization is performed. Open fractures are graded in their degree of severity by the use of the GustiloAnderson grading system. In this widely used grading system, open fractures are classified by Types I, II, IIIA, IIIB, and IIIC.
- Type I refers to a relatively small wound usually less than 1 cm in size and is believed to be an inside out injury whereby the bone protrudes from inside out to cause a break in the skin. - Type II is a wound of size of greater than 1 cm but less than 10 cm. - Type IIIA is a large extensive wound greater than 10 cm with large flaps but with good bone coverage. In general, these wounds are still closeable without the need for tissue transfers. - Type IIIB is a wound with extensive periosteal stripping and will require local or free tissue transfers for closure. - Type IIIC is any open fracture that has a neurovascular injury that requires repair for limb viability. - Any wounds with farm contamination are immediately graded as a III regardless of the size of the wound. - Although originally the grading of open fractures was dependant on the initial wound size, more recently the concept has evolved to grading intraoperatively after a through examination of the zone of injury.
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The debridement tactic involves systematic identification and removal of all necrotic tissue and bone. Frequently, however, it is not always possible to predict the fate of marginal tissues. In this situation, the tissue in question is allowed to remain and given time to declare themselves, thus necessitating a repeat debridement in 24-48 hours after the initial debridement. For this reason, and also to avoid the creation of an anaerobic environment, open fracture wounds are rarely closed primarily. More recently, when the debridement process leaves large areas of dead space, the space is managed with the use of an antibiotic bead pouch. The bead pouch is created by placing antibiotic beads that are made intraoperatively using polymethylmethacrylate cement and a heat stable antibiotic such as tobramycin powder and sealing the wound closed with a gas-permeable barrier such as OPSITE. The purpose of the beads is to allow the gradual elution of antibiotics into the local area thus maintaining an aseptic environment within the dead space, avoiding the formation of a hematoma that can subsequently become infected. These beads are generally removed at time of repeat debridement to allow for wound closure. Parental antibiotics are also used in open fractures. In general, Type II fractures and higher requires the use of a first generation cephalosporin and an aminoglycoside. Penicillin is added in cases of farm contamination. Antibiotics are given for 48 hours and restarted for an additional 24-48 hours for repeat debridements until the wound is closed.
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The Severe Open Tibial FractureLimb Salvage vs Primary Amputation

One of the most difficult decisions an orthopedic trauma surgeon must make is limb salvage vs primary amputation in the face of a severe open tibia. Generally these are grade IIIB and IIIC injuries. With modern reconstruction techniques such as bone transport, vascular bone transfer and bone grafting, extreme cases of bone loss can be effectively managed. Free tissue transfer has proven to be extremely valuable in managing extensive soft tissue loss. Despite these advances, however, many cases of successful limb salvages are really examples of technology over reason. The true measure of success in these cases should include a measure of the functionality of the reconstructed tibia as well as the person attached to the tibia. It is not uncommon to find in many of these cases, patients that are depressed, unemployed, divorced, and addicted to narcotic medications, and essentially functionally disabled. Primary amputation would have avoided these problems. The problem then becomes how to identify which patients would be candidates for primary amputation. In addition to objective clinical criteria, ideally psychological and social factors should also be factored into the decision. Clearly, a patient that cannot be out of work for a prolonged period of time and does not have a strong social support system cannot tolerate a prolonged lengthy reconstructive process. Even the most experienced orthopedic trauma surgeons cannot agree on a standard course of action. It is well accepted, however, that if amputation is an option, it should be performed on the day of injury as opposed to delaying the decision until a later time. Patients are much more accepting of an amputation when performed primarily than of one performed after an initial debridement. In the first scenario, the patient accepts the amputation as a result of the injury, while in the second scenario, the patient views the delayed amputation as a failure of treatment. Several investigators have attempted to place clinical criteria into scoring systems hoping that they can be used as predictors of success or failure of salvage. Such systems include the mangled extremity syndrome index (MESI), predictive salvage index (PDI), limb salvage index (LSI) and the mangled extremity severity score (MESS). Although the original authors of each of these scoring systems report great success, other investigators have not been able to reproduce their enthusiasm. The predictive value of each of these scoring systems has had variable sensitivity and specificity, and as such, can be used as a guide to decision making, and should not be applied rigidly(1). Vascular factors that tend to indicate failure of salvage attempts include warm ischemia time greater than six hours, blunt infrapopliteal injuries, blunt trifurcation injures, and blunt vascular injury associated with a significant muscular crush injury. The severity of the soft tissue injury can be a factor, particularly if a comorbidity exists that would preclude timely reliable soft tissue reconstruction. Advanced age bodes towards amputation. Overall injury score should be taken into account, since these patients are not good candidates for lengthy repeat surgeries, and cannot tolerate an additional inflammatory load. Prolonged hypotension will tend to extend the zone of injury of the local tissues and thus is a factor for amputation. It is well accepted
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that damage to the posterior tibial nerve, leading to loss of plantar sensation, is a good predictor of amputation. Amputation is highly likely with an ipsilateral foot or ankle injury and concomitant high-grade open tibial injury.
Compartment Syndrome
Extremities that are subjected to high-energy blunt trauma can suffer compartment syndrome. The extremities are composed of fascial spaces, the compartments, which consist of muscles, nerves, arteries and veins. These facial spaces are of fixed volume because of the inexpansiveness of fascial. If the volume of a fixed space is increased, the laws of physics dictate that the pressure of that space will increase. Compartment syndrome occurs when the pressure in a fascial space increases to the point of causing ischemic injury to the structures that traverse that compartment. Injury can precipitate a compartment syndrome through hemorrhage, increased capillary permeability secondary to inflammation, and postischemic swelling secondary to prolonged extrinsic compression. Classically, the five Ps have been described as signs of a compartment syndrome. The five Ps are Pressure, meaning a feeling of tightness on external compression, Pallor, duskiness of the soft tissues, Pain, an increased perception of pain, Pulselessness, and Paresthesia. Of the five Ps, pulselessness, and pallor, and parasthesia are all late signs and as such are not useful clinical indicators. The most reliable sign in an awake and alert patient is pain, and more specifically, pain out of proportion for the injury. In addition, passively stretching the involved compartment will result in significantly increased pain. Clearly, a patient with a tibial fracture will have pain, but this pain is usually controllable with immobilization and analgesic medication. A patient with a compartment syndrome will continue to have uncontrollable pain despite these measures. The index of suspicion should be high in any injury that is secondary to highenergy trauma, since there is likely a significant soft tissue injury. The presence of an open fracture does not preclude compartment syndrome which have been reported in 6-9% of cases. The difficulty in diagnosing a compartment syndrome occurs when the patient is not awake. Since compartment syndrome is related to tissue perfusion pressure the hypotensive patient can experience a compartment syndrome without overt signs. In these cases, compartment pressure measurement is indicated. Several techniques of measuring compartment pressures have been described. These include using an 18-gauge needle attached to a manometer, wick catheters, slit catheters and stic catheters. For continuous measurements, the wick and slit catheters are most accurate. The stic catheter has the advantage of portability but is only reliable when used for momentary measurements. The pressure threshold for fasciotomy has been the subject of much debate. Authors have suggested fasciotomy for pressures anywhere from 30-45 mm Hg. These pressure recommendations have all been based on different measurement methods. Unfortunately, most of these recommendations do not take into account the patients blood pressure, and thus may not be as valuable in a hypotensive poly-trauma patient. The methodology that does take into account the patients condition utilizes a concept referred to as the delta P. Originally described as the difference between mean arterial pressure,
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a recent study demonstrated a high degree of reliability of using the difference between diastolic pressure and measured compartment pressure. In this study, a delta P measurement of diastolic pressure minus the measured compartment pressure of less than 30mm Hg. was deemed significant. When indicated, fasciotomy should be performed emergently. Fasciotomy in an isolated injury is limb saving, but in a multiply injured patient, it must be considered life saving. Complications of an isolated missed compartment syndrome have been classically referred to as Volkmans ischemic contracture, which refers to an extremity where the muscle groups are fibrosed and contracted and are nonfunctional. In a multiply injured patient, missed compartment syndromes can lead to myoglobinuria, renal failure, and sepsis, thus possibly contributing to multiple system organ failure. Fasciotomy is a relatively simple procedure as long as there is an understanding of the anatomy. The forearm has three compartments, a superficial and a deep flexor compartment, and an extensor compartment. Decompression of all three compartments is easily accomplished using a volar Henrys approach. When decompressing the forearm, consideration should also be given to the carpal tunnel as well to avoid compression of the median nerve. The tibia has four compartments, which include the anterior, lateral, superficial and deep posterior. Decompression can be accomplished using the classic twoincision technique where a medial and lateral incision is made and the respective fascia identified and incised. Similarly, using a long single lateral incision, the intermuscular septum between the anterior and lateral compartments is identified, and the respective compartments are released adjacent to the septum, followed by identifying and incising the fascia of the superficial posterior compartment. The deep posterior is identified by retracting the peroneal compartment anteriorly and the superficial compartment posteriorly and following the interosseous membrane. The compartment is released by releasing the compartment off this membrane. It is important to keep in mind the location of the peroneal nerve as it can be injured. In addition, in an injured extremity, the anatomy may be distorted. It is also important to keep incisions wide and to release the fascia to the level of the musculotendinous junction in order to ensure a complete decompression. If the diagnosis has been delayed, it is vital to debride necrotic muscle at this time. The presence of a fracture is an absolute indication for immediate fracture stabilization after decompression. All open tibia fractures should have four compartment fasciotomies performed as part of their irrigation and debridement. In addition to the forearm and tibia, compartment syndromes can occur although less frequently, in the hand, foot, thigh, buttocks, and arm. If clinically present, these too must be addressed.
Fractures with Associated Vascular Injury

Long bone fractures with an associated vascular injury that jeopardizes the viability of the limb are of extremely high priority. Generally the diagnosis is not difficult, with presenting signs such as profuse arterial bleeding, expanding hematoma, absent distal pulses, and pallor of the limb. With impending limb loss, a formal arteriogram is not indicated and can only serve to prolong ischemia time.
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A frequent area of contention occurs regarding the sequencing of these cases, whether the fracture stabilization should occur first versus the vascular repair. Both camps raise valid points. If fracture stabilization occurs after a meticulous vascular repair, then there is the risk of reinjury to the repair when the extremity is brought out to length and alignment. On the other hand, fracture stabilization may be a lengthy procedure and thus will prolong ischemia time if it were to occur prior to vascular repair. Clearly, it makes no sense to perform a vascular repair only to keep the fracture unstabilized, since the repair would be doomed with any subsequent motion, or to ask that the fracture be maintained in an malaligned manner. And conversely, it makes no sense to perform lengthy fracture stabilization and permit the extremity to become ischemic. Rigidity in thinking in these cases is to be condemned. The proper course of action should be arrived at after a thorough review of the fracture complexity, and the period of ischemia. The surgical approach for the fracture stabilization and the vascular repair should also be discussed among the specialist involved to avoid creating narrow soft tissue bridges that would place the extremity in jeopardy. From an orthopedic standpoint, if the fracture stabilization is complex, a temporary bridging external fixator can be applied above and below the injury to achieve control of alignment and length prior to vascular repair. If the vascular repair is complex and the fracture stabilization is relatively simple such as intramedullary nailing or simple plate fixation, a temporary shunt can be placed. When the vascular injury occurs in an open fracture, the area should undergo appropriate irrigation and debridement prior so that vascular repair can occur in a clean soft tissue bed. Cooperation among the specialists will lead to execution of the prime objective, that of a viable and functional patient.
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Fracture of the Femoral Neck in the Young Patient

This injury is of a very high priority because of the disruption of the blood supply to the femoral head and subsequent development of avascular necrosis. Fractures of the femoral neck in the young polytrauma patient differ greatly from the more common femoral neck fractures of geriatric patients. In the latter case, the injury occurs because of osteopenia secondary to advancing age and is a result of relatively low energy. In addition, in the elderly population, if disruption of the blood supply to the femoral neck occurs, prosthetic replacement of the femoral head provides an excellent functional solution in this time limited low demand situation. In the young patient, a fracture of the femoral neck occurs after considerable energy expenditure and most likely results in displacement and disruption of the blood supply. Early diagnosis, reduction and stabilization provide the only means of minimizing the likelihood of avascular necrosis. The diagnosis of a femoral neck fracture is not difficult and is frequently noted on the AP radiograph of the pelvis of the trauma series. Once suspected on the pelvic film, follow up AP and lateral hip films are needed to further define the anatomy of the fracture. Although less common but not rare, and often missed in as much as 30% of the time is the related entity of an ipsilateral femoral neck femoral shaft fracture. In this situation, there is a fracture of the femoral shaft and a concomitant fracture of the femoral neck. The femoral shaft fracture is usually obvious but
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the fracture of the femoral neck is frequently not well visualized. Explanations for why the femoral neck component is often missed include poor quality films, femoral neck obscured by splints, external rotation of the proximal femur due to the shaft fracture, and lack of vigilance. It is not unusual to diagnose the femoral neck fracture by review of the pelvic cuts of the abdominal CT scan. Once diagnosed, timely stabilization of both fractures should be a priority to avoid avascular necrosis (Fig. 42.1A,B).
Floating Knee
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Ipsilateral fractures of the femur and tibia are referred to as floating knee injuries (Fig. 42.2A,B). Clearly a result of high energy blunt force trauma, these injuries frequently result in significant disability in 60-70% of patients. Until the fractures are stabilized, there are risks of popliteal artery injury and irreversible injury to the common peroneal nerve. Patients with this injury seem to experience significant rates of pulmonary dysfunction such as ARDS, fat emboli syndrome and pulmonary emboli. Early stabilization of both lesions is helpful in minimizing disability and complications.
Femoral Fractures
Early stabilization which is defined as within the first 24 hours after injury or when the patient has achieved a normalizing base deficit with a normal lactate level, and is normothermic, normotensive, and not coagulopathic, has been associated with decreasing the length of ICU stay, decreasing pulmonary complications such as ARDS, fat and pulmonary emboli syndrome, decreasing deep venous thrombosis, facilitating nursing care, and decreasing the need for analgesics. The mechanism by which this occurs is not well known and is most likely multifactorial, but early stabilization may contribute to a decreased the systemic inflammatory response to trauma. The majority of femoral shaft fractures are best managed by locked intramedullary nailing. Intramedullary nailing can be performed in a traditional antegrade manner where the nail is inserted through the piriformis fossa, or more recently there has been increased enthusiasm to perform nailing in a retrograde manner where the nail is introduced through the intercondylar region of the femoral condyle. Antegrade nailing in most surgeons hands requires the use of a fracture table and image intensifier. Retrograde nailing can be performed on any radiolucent table with an image intensifier and is ideally suited for the multiply injured patient with concomitant spine or chest injuries, obese patients, and bilateral femoral shaft fractures in that the setup time is minimal. Further studies are currently underway to determine if there are any long term consequences of violating the knee joint. Much has been written recently about the association between intramedullary nailing and the worsening of ARDS in multiply injured patients with a preexisting concomitant pulmonary parenchymal injury. Standard intramedullary nailing involves the process of reaming. Initially, it was thought that the reaming process might contribute to this phenomenon. Reaming is the process by which the intramedullary canal is widened prior to insertion of the nail. It is performed by using an instrument that essentially cores out the intramedullary bone to a defined diameter. Reaming is done to allow for the insertion of
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Fig. 42.1A, B. Multiply injured blunt trauma patient sustaining an ipsilateral femoral neck/ femoral shaft fracture. This was stabilized emergently by performing an open reduction internal fixation of the femoral neck with interfragmentary screws, followed by intramedullary nailing of the femoral shaft using a miss-a-nail technique.
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Fig. 42.1B.
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reaming process causes embolization of marrow contents into the systemic circulation and it is believed by some that this material is harmful to an already injured pulmonary parenchyma. Current animal and clinical studies have not been able to clearly demonstrate reaming as the culprit and have served to provide more questions than answers. Nonetheless, currently, an unreamed technique is an option, however it results in insertion of an implant which may be mechanically inferior but is frequently chosen when faced with this circumstance. Unreamed technique can be utilized in both antegrade and retrograde nailing. Delaying the stabilization of the femur fracture, however, has been shown to be detrimental in this circumstance.
Intra-Articular Fractures
Fractures that involve the articular surface of a joint require special considerations. In these injuries, the cartilage of the joint is disrupted and thus warrants meticulous reconstruction. Examples of such injures include fractures of the tibial plateau (Fig. 42.3), tibial plafond, supracondylar humerus, and supracondylar femur. These injuries are frequently complex and require complex preoperative planning to effect a good outcome. Frequently, additional studies are needed such as CT scans with 3-D reconstruction to further define the anatomy. These injuries therefore are not generally definitively addressed in a multiply injured patient emergently. To promote patient mobilization and to minimize the detrimental effect of fracture site motion and irritation, temporary bridging external fixation is applied initially. Once the appropriate studies are obtained, soft tissue swelling has subsided, and the patients condition is optimal, joint reconstruction can proceed.
Stabilization Options for Long Bone Fractures

External Fixation
External fixation is utilized as a temporary means of achieving skeletal stabilization and is primarily used for the patient in extremis (Fig. 42.4). They can also be used temporarily to span a joint in intra-articular fractures and serve as portable traction. When necessary, they can be applied in an ICU setting under local anesthesia.
Intramedullary Nailing
As previously discussed, intramedullary nailing is the method of choice for most long bone shaft fractures such as the femur and tibia. Nails are inserted through a percutaneous technique and do not require surgical exposure of the fracture site, thus minimizing trauma to the soft tissues and minimizing blood loss. These implants have the capability to be locked at either or both ends thus allowing them to be used regardless of comminution and yet permit reliable control of length and rotation. These devices are load sharing and thus allow earlier weight bearing prior to complete fracture consolidation, and are thus advantageous in the multiply injured patient.
Plate Fixation
Plate fixation is commonly used for stabilization of fractures of the forearm and humerus and is frequently the technique of choice for intra-articular fractures. Traditionally, plate fixation requires extensive exposure of the fracture site. More recently however, percutaneous techniques have become popular.
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Fig. 42.2A, B. Multiply injured blunt trauma patient with a fracture of the left femur and left tibia, a Floating Knee. Patient underwent immediate intramedullary nailing of the femur and tibia.
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Fig. 42.2B.
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Fig. 42.3. A fracture of the tibial plateau, and example of an intra-articular fracture. Notice the disruption of the articular surface of the tibia.
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Fig. 42.4A, B. Multiply injured patient with a femoral shaft fracture and injury to the superficial femoral artery. Patient underwent temporary external fixation of the femur.; A), prior to vascular repair. B) see next page.
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Fig. 42.4B Intramedullary nailing of the femur was performed several days later as definitive treatment for the femoral shaft.
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References
1. 2. 3. 4. 5. Tornetta P III, Olson SA. Amputation versus limb salvage. In: Springfield DS, ed. Instructional Course Lectures 46. Rosemont, IL: American Academy of Orthopedic Surgeons 1997:511-518. Amendola A, Twaddle B. Compartment Syndromes In: Browner B, Levine A, Juipiter J, Trafton P, eds. Skeletal Trauma. 2nd ed. Philadelphia: WB Saunders,1998: 365-389. Pape H-C, AufmKolk M, Paffrath T, et al. Primary intramedullary femur fixation in multiple trauma patients with associated lung contusionA cause of posttraumatic ARDS? J Trauma 1993; 34:540548. Charash WE, Fabian TC, Croce MA. Delayed surgical fixation of femur fractures is a risk factor for pulmonary failure independent of thoracic trauma. J Trauma 1994; 37:667672. Bosse M, Kellem J. Orthopaedic management decisions making in the multipletrauma patient. In: Browner B, Levine A, , Juipiter J, Trafton P, eds. Skeletal Trauma. 2nd ed. Philadelphia: WB Saunders 1998:151-164.
CHAPTER 43
Pelvic Fractures and the General Surgeon

Jackson Lee Anatomy
The pelvis is made up of three bones, the sacrum and two innominate bones. The innominate bone itself is made up of three bones that fuse during growth, the ischium, the ilium, and the pubis. The three bones fuse in the area known as the triradiate cartilage of the acetabulum, which forms the socket portion of the hip joint. The three bones of the pelvis themselves do not have any inherent; they are stabilized by ligamentous structures. Of the named ligamentous structures, the posterior ones are the strongest. Comprised of two groups, the posterior sacroiliac ligaments, long and short, are strong enough to withstand and transmit the force of weight bearing from the lower extremity to the spine and thus provide the major structural integrity to the sacroiliac joint. The less strong anterior sacroiliac ligaments provide additional stability. The ligaments that form the symphysis pubis maintain the integrity of the pubic ring. In addition, there is a set of sacrotuberous ligaments that connects the posterior sacrum to the ischial tuberosity and resists vertical rotation of the innominate bone. The sacrospinous ligament, which connects the sacrum to the ischial spine helps resist external rotation of the ilium. Pelvic stability can be violated by any combination of a break in the integrity of the bony structures or by loss of integrity of the ligamentous structures. When disruptive forces are applied, several factors determine which structure fails. In older patients who are osteopenic, generally, the bony structures fail. Depending on the degree of osteopenia, this may require very trivial forces. Conversely, in young patients with very strong bony structures, there will be a tendency for ligaments to fail. In addition, the rate of force application plays a significant role. A subset of pelvic injuries includes fractures of the acetabulum. Acetabular fractures occur when forces are transmitted along the femoral shaft through the femoral neck and across the femoral head onto the acetabulum. Depending on the relative degree of abduction/adduction, flexion/extension of the hip joint at the time of force application, certain fracture patterns or dislocations can occur.
Pelvic disruptions can occur through several common mechanisms of force application. The first mechanism is an anterior/posterior force application.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Jackson Lee, University of Southern California School of Medicine, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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This can occur when a pedestrian is struck head on by an automobile. The force, which is directed in a posterior direction from anterior, causes an external rotation moment to the ilium or hemipelvis. This causes a disruption of the symphysis pubis and injury to the anterior sacroiliac ligaments. The pelvis books open and hinges on the strong posterior sacroiliac ligament. Variations can occur by applying an external rotation force to both femurs and hips, or by falling from a height and landing on ones back. In these injuries, the posterior sacroiliac ligaments remain intact and competent. Another mechanism (Fig. 43.1), which is in fact the most common is the lateral compression injury. In this mechanism, a lateral directed force is applied on the iliac wing, such as would occur when a car from the side strikes a pedestrian. If the magnitude of the force is low, this will cause a fracture to occur on the anterior aspect of the sacral body with the bone failing in compression and there is a concomitant fracture of the pubic rami. In this situation, the posterior sacroiliac ligaments are spared because they are essentially relaxed by the injury. If the magnitude of the forces is high, a pivoting occurs around the sacral body and thus causes the posterior sacroiliac ligament to be placed under tension and thus failing or a fracture through the iliac wing can occur. Because the sacrotuberous and sacrospinous ligaments are relaxed in this force application, they remain competent and thus there is still some stability vertically and rotationally. The third mechanism that occurs is when the forces are applied to the pelvis in a vertical manner such as would occur from a fall from a height. Essentially, in this mechanism, there are either injuries to the posterior sacroiliac ligaments or fractures of the iliac wings and pubic rami that lead to complete vertical instability.
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Initial Assessment
The recognition of a pelvic fracture may by subtle or obvious. Indications of a pelvic injury may include leg length inequality, scrotal hematoma or swelling, or hematomas around the iliac wings or lower back. If suspected, palpation of the iliac wings will provide useful information about the gross stability of the pelvic ring. More subtle instability can be assessed later on with specific radiographic views and stress views. During the primary survey, however, there is no role for these views. As with all other musculoskeletal injuries, the integument should always be examined, taking note of open wounds and lacerations, suggesting an open injury. Lacerations involving the perineum have great implications regarding the outcome. These patients may require a diverting colostomy to manage bowel contamination. One should also examine for Morel-Lavale lesions. These lesions are closed degloving injuries where the subcutaneous tissue is torn or sheered away from the underlying fascia forming a cavity filled with hematoma and liquefied fat. This lesion is significant in the multiply-injured patient because these lesions can become infected if not recognized and treated in a timely manner, thus presenting a septic load to a patient that may not be able to tolerate one. Open drainage and debridement, followed by dressing changes and packing best manage these lesions. Wound management is by delayed primary closure.
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Fig. 43.1. CT demonstrating a sacroiliac joint dislocation in a patient with an AP compression injury. Despite the widening, the posterior sacroiliac ligaments were intact in this case.
It is always important to keep in mind the likelihood of associated injures when dealing with a patient with a pelvic fracture since the energy transference that occurs does not discriminate among structures. It is very common for these patients to also sustain injuries to abdomen, chest and head. The most common direct causes of mortality are head and thoracic injuries. When evaluating a patient with a pelvic fracture for intraabdominal bleeding, it is important to avoid violation of the retroperitoneal space to allow for tamponade. If a diagnostic peritoneal lavage is contemplated, it should be performed using a supraumbilical approach to prevent a possible entry into the retroperitoneal space through the reflection of the peritoneum that follows the round ligament below the umbilicus. Injuries to the genitourinary track are very common and occur approximately 15% of the time. This can include injures to the renal parenchyma, bladder, and urethra. Signs of genitourinary injury include hematuria, blood at the meatus, and a high riding prostate in a man. The presence of blood at the meatus or a high riding prostate in a man is highly indicative of a urethral injury and is an indication for a retrograde urethrogram prior to Foley insertion in a hemodynamically stable patient. However in the absence of these findings urethral injury cannot be ruled out. In a hemodynamically unstable patient, a single attempt to place a catheter is made by a qualified urologic specialist. In females, catheter placement may be attempted without a urethrogram. Bladder injuries in both men and women correlate with the number of pubic rami fractures. In female patients with pubic rami fractures, it is also important to evaluate for lacerations in the vagina, which communicate with the fracture site, thus necessitating at the minimum a bimanual exam and ideally a speculum examination.
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Injuries to the pelvic ring frequently are associated with injuries to the peripheral nerves. Very commonly, the L5 nerve root is injured when there is a significant lesion posteriorly. The L5 root enters the pelvis under the L5 transverse process and crosses the sacral ala approximately 2 cm medial to the sacroiliac joint and joins the sacral plexus. The sacral roots exit their respective foramen to form the plexus. Fractures involving the sacral body can cause injury to the sacral roots. Frequently patients with pelvic fractures requires early intubation and as such, require early examination and documentation of their neurologic status so as to not to lose this baseline information. Examination should include sensation and motor testing to the lower extremity as well as perianal sensation. The primary survey should include an AP pelvis film. Examination of this film should allow a good estimation of the mechanism of injury, identify fractures and allow inferences of ligamentous injury (Fig. 43.2).
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Initial Management of Bleeding

In the majority of cases, pelvic bleeding is venous or from fracture surfaces. Control of such bleeding can be achieved by avoiding coagulopathy and providing tamponade. Coagulopathy can be secondary to the dilutional effects of resuscitation fluids and blood products as well as hypothermia. Tamponade can be achieved by limiting the ability of the retroperitoneal space to increase in volume. In a patient with an intact pelvis, the potential retroperitoneal space can hold a volume of approximately 2 liters. In the advent of a pelvic injury in which the pubic symphysis is widened by 2 cm more than normal, the potential retroperitoneal space has been estimated to increase to 6 liters. It stands to reason then that controlling the displacement of the pelvic ring can facilitate tamponade. In the field, the MAST suits may be useful especially for long transportations. MAST suits have been shown to stabilize the pelvis. A simple and effective method of controlling pelvic displacement is tying a hospital sheet around the patients iliac wings. In the absence of lower extremity injury, internally rotating both limbs will also serve to decrease pelvic displacement. Both of these methods are essentially equivalent to aplying an external fixator. External fixation is a simple, rapid and effective means of applying early stabilization of the pelvic ring in the emergency department. In addition to controlling potential retroperitoneal volume, it will minimize fracture site motion, thus preventing the dislodgment of newly formed clots and will minimize further injury to the soft tissues. It will also allow a patient to be transported from department to department without fear of further displacement. External fixation has been shown to decrease the mortality rate in unstable pelvic injuries and has decreased transfusion requirements. For external fixation to be maximally effective, it must be applied early before development of a large retroperitoneal hematoma, otherwise the hydraulic forces of the hematoma will not allow reapproximation of the pelvic ring. External fixation is not used as definitive treatment of the pelvic fracture and thus an anatomic reduction is not necessary and valuable time should not be spent adjusting the frame to achieve an accurate reduction. The use of external fixation is not indicated in mechanically stable injuries and is relatively contraindicated in
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Fig. 43.2. Multiply injured patient with a fracture of the left acetabulum and a subtrochanteric femoral shaft fracture.
cases where there is a floating iliac wing or a fracture of the acetabulum since control of the pelvic volume is not possible.
- There are two basic frames that have been described. The traditional frame is an anterior frame utilizing Schantz pins inserted between the inner and outer tables of the anterior iliac wings and attached to a trapezoidal frame. This frame has the advantage of being simple to apply and has a low complication rate. In patients with a significant posterior lesion, it tends to offer less rigid control of the posterior lesion. This was more of an issue when external fixation was the only known means of definitively treating these lesions to union. - For the patient in extremis, a simple construct consisting of one pin in each ilium can be utilized. Despite the advantages of external fixation, it use remains controversial. - More recently, a C clamp frame has been described. This frame can be applied anteriorly to control an anterior lesion or can be applied posteriorly to close a posterior lesion. In applying this frame posteriorly, there is a risk of causing injury or further injury to the superior gluteal artery. In addition, intrapelvic protrusion has been reported. Some authors have suggested that these frames be applied under radiographic control, and thus may be less useful in the emergency department. The efficacy of the C clamp device is currently under study.
Selective angiography can be useful in those patients where bleeding is arterial. Ideally, a process of elimination can identify these patients, where other sources of bleeding have been ruled out. This would include patients who have mechanically stable pelvic injuries, externally stabilized patients and patients who are not candidates for external fixation in which thoracic and abdominal sources have been eliminated. Interestingly, in a recent series of hemodynamically unstable patients with unstabilized pelvic injures in which
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thoracic and abdominal sources of bleeding were ruled out, only 30% had angiographically treatable lesions, thus supporting the belief that hemodynamical instability is a result of venous bleeding. A concern regarding angiography has been raised in patients with acetabular fractures that may require an extended illiofemoral approach for open reduction. In this surgical approach, the gluteal muscles are detached completely from their origins on the ilium and from their insertions on the femur, thus the flaps viability is solely dependent upon the superior gluteal artery and other branches of the internal iliac artery. If the internal iliac artery or superior gluteal artery is embolized, and a sufficient period of time has not occurred to allow for revascularization, the viability of the flap may be jeopardized. In this group of patients, embolization should only be undertaken when a treatable lesion has been identified.
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Fracture Fixation
Definitive fracture fixation is usually not undertaken until signs of active bleeding are absent. This usually does not occur until postinjury day 2 or 3. There is one major exception to this however. An ideal opportunity occurs when a patient has a widened pubic symphysis or a parasymphyseal fracture and undergoes exploratory laporotomy for an abdominal injury. At the completion of the laparotomy, the midline incision is extended to the pubis and plate fixation of the symphysis is undertaken. Performing this fixation imparts significant stability to the pelvic ring, allows immediate removal of the external fixator, and simplifies later supplemental posterior fixation. Definitive fracture fixation requires an accurate diagnosis of the anatomic lesions. Generally the posterior lesion is the most difficult to define. Once the patient is stable to undergo further diagnostic studies, pelvic inlet and outlet views are obtained. The pelvic inlet view is taken with the x-ray tube aimed at a 40 caudad direction and results in a film that allows excellent definition of rotational and AP displacement of the iliac wings. It can also demonstrate subtle displacements of the sacral-iliac joint. The outlet view, taken with the x-ray tube aimed 45 cephalad shows the sacral body in a true AP projection and thus allows definition of sacral fractures and injuries to the sacral foramen. It is also well suited to defining vertical displacement of the iliac wings. A CT scan provides further definition of the injury. In extremely complex situations, 3-D reconstructions may be helpful. When an acetabular fracture is present, Judet views are obtained. These additional views permit the classification of the acetabular fracture and thus allowing one to arrive at a surgical tactic for joint reconstruction. Judet views are essentially 45 internal and external rotation views of the acetabulum and are taken with the pelvis rotated along its longitudinal axis and centering the x-ray beam on the acetabulum. Evaluation of these films is beyond the scope of this review and the reader is referred to classic works for further information. Once the anatomy of the injury is defined, a determination is made on the stability. Stability is defined as the ability of the pelvis to resist normal physiologic forces. Stability may be inferred based on the fracture pattern, physical examination and serial radiographs. Lesions that prove to be unstable are addressed using internal fixation. Fractures of the acetabulum are evaluated based on the stability of the hip joint, the presence of intra-articular fragments and joint congruity (Fig. 43.4).
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The goal of fracture fixation is centered on restoring the posterior anatomy. Fractures of the sacral body and dislocations of the sacroiliac joint are usually fixed using iliosacral screws functioning in a neutral or interfragmentary capacity (Fig. 43.3). These screws are directed into the body of S1, and on rare occasions, into the body of S2. The placements of these screws are guided by image intensification. Iliosacral screws can be placed percutaneously if the fracture is minimally displaced. Displaced fractures will require open reduction, either through a retroperitoneal anterior approach or a posterior approach requiring the patient to be placed prone. Fractures involving the iliac wings are fixed using interfragmentary screws placed between the inner and outer tables and neutralized using plates. The anterior lesions, which include pubic symphysis disruptions and parasymphyseal fractures, are fixed using compression plating. Fractures of the pubic rami may or may not need stabilization depending on the stability of the injury. When the posterior lesion is unilateral, the uninjured side can undergo immediate weightbearing. Weightbearing on the injured side is delayed until the fracture or the ligaments have healed sufficiently.
References
1. 2. Burgess A, Jones A. Fractures of the pelvic ring. In: Rockwood C, Greene D, eds. Fractures in Adults 4th ed. Philadelphia: JB Lippincott, 1996: 1575-1615. Tournetta P III. Pelvis and Acetabulum:Trauma. In: Beaty J, ed. Orthopaedic Knowledge Update 6. Chicago: American Academy of Orthopedic Surgeons 1998: 427-439.
Fig. 43.3. A patient with bilateral sacroiliac joint disruption stabilized with bilateral sacroiliac screws and plate fixation of the symphysis pubis.
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Fig. 43.4A, B. Patient with a transverse fracture of the acetabulum. Plate fixation was performed using a Kocher-Langenbach approach, a posterior approach performed with the patient in the prone position.
3. 4. 5. Kellam J, Browner B. Fractures of the pelvic ring. In: Browner B, Levine A, Jupiter J et al, eds. Skeletal Trauma 2nd ed. Philadelphia: WB Saunders 1998: 1117-1179. Gruen GS, Leit ME, Gruen RJ et al. The acute management of hemodynamically unstable multiple trauma patients with pelvic ring fractures. J Trauma 1994; 36:706-713. Poole GV, Ward EF, Muakkassa FF et al. Pelvic fracture from blunt trauma: Outcome is determined by associated injuries. Ann Surg 1991; 213:532539.
CHAPTER 44
Spinal Injuries
Larry T. Khoo, Wei-Lee Liao and Gordon Engler Cervical and Cervicothoracic Injuries
One of the most mobile and flexible sections of the human spinal column is the region spanning C1 to T2. The cervical spine can be divided into four distinct regions each with their own unique biomechanical, anatomic, and pathological features. These are the 1) occipito-atlanto-axial (O-C1-C2) region, 2) the upper cervical spine (C3-C5), 3) the lower cervical spine (C5-C7), and 4) the cervicothoracic junction (C7-T2).
The Edwin Smith papyrus written 5000 years ago identified cervical spine trauma as devastating injuries and pronounced them as lesions not to be treated. Improvements in legal statutes, restraint systems, emergency transport systems, and general awareness and prevention have decreased the number of complete cervical spinal cord injuries in the last 20 years. The advent of modern neuroimaging techniques and modern spinal instrumentation techniques have improved the ability of physicians to rapidly diagnose, treat, and mobilize patients with cervical injury.
Incidence
There are approximately 5000 to 8000 new cases of traumatic spinal cord injury (SCI) each year in the United States of which 50-60% involve the cervical spine. This high proportion is due to the relative mobility of the region and the inability of passenger restraint systems to constrain the head and neck. The most common causes are vehicular accidents (50%) sports-related (20%), assault-related (20%), and accidental falls or blunt trauma (10%). There is a bimodal distribution of cases with a peak in adolescents and young adults (age 15-30) and a second smaller cluster at age 50-70 due to degenerative disease. The lifetime cost for each patient with quadriplegia averages over $1.5 million.
Classification
Numerous classification schemes have been formulated to categorize the mechanism, bony stability, and degree of neurological injury for cases of cervical injury. They serve to predict the severity of each lesion, the need for early stabilization and surgery, and the ultimate expected outcome of the patient.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Larry T. Khoo, LAC + USC Medical Center, Los Angeles, California, U.S.A. Wei-Lee Liao, LAC + USC Medical Center, Los Angeles, California, U.S.A. Gordon Engler, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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Fig. 44.1. Three-column classification by Dennis. 1) Supraspinous ligament, 2) interspinous ligament, 3) capsular ligament, 4) intertransverse ligament, 5) ligamentum flavum, 6) posterior longitudinal ligament, 7) posterior annulus fibrosus, 8) anterior annulus fibrosus, 9) anterior longitudinal ligament.
- The three-column model of vertebral stability forms the basis for clinical decision-making in spinal trauma (Fig. 44.1)(see also Thoracic and Lumbar Fracture section). This model applies equally well to cervical, thoracic, and lumbar spine injuries. - For cervical injuries, there are more classification schemes than for thoracolumbar injuries due to the unique anatomy of the upper cervical vertebral bodies. Overall, these are similar in their mechanism and morphology to systems used for the thoracic and lumbar spine as well (Table 44.1A, Fig. 44.2). An example of cervical fracture classification is provided in Table 44.1B. Several of the more unique cervical patterns of fracture will be presented later on in the Surgical Indications section.
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Table 44.1A. McAfee classification of vertebral fractures

Injury Type Pathology
Wedge-compression fracture Stable burst fracture Unstable burst fracture Chance fracture Flexion-distraction injury
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Isolated anterior column failure Anteriorand middle-column compression failure, posterior column intact Compressive failure of anterior and middle columns, disruption of posterior column Horizontal vertebral avulsion injury with center of rotation anterior to vertebral body Compressive failure of anterior column, tensile failure of posterior column. The center of rotation is posterior to anterior longitudinal ligament Disruption of spinal canal alignment in transverse plane, shear mechanism common
Fig. 44.2. Schematic of McAfee fractures classification. A) Wedge-compression fracure, B) flexion-distraction fracture (true Chance fracture), C,D) translational fracture, E) flexion-disraction fracture (bony Chance fracture), F) burst fracture (unstable).
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Table 44.1B. Example of cervical fracture classification

Atlanto-occipital dislocation and fracture Occipital condyle fractures Fracture dislocations Atlas C1 ring fractures (Jefferson fractures, any combination of fractures through ring) Combination C1-C2 fractures (atlantoaxial rotatory subluxation with/without other fracture) Hyperextension fracture-dislocations of subatlantal spine Posterior fracture-dislocation of the dens (i.e., odontoid fractures I,II,III) Traumatic spondylolisthesis of the axis (Hangmans fracture and variants) Hyperextension sprain (momentary) dislocation with fracture Hyperextension fracture-dislocation with fractured articular pillar Hyperextension fracture-dislocation with comminution of the vertebral arch Hyperflexion fracture-dislocations of subatlantal spine Anterior fracture-dislocation of the dens (i.e., odontoid fractures I,II,III) Hyperflexion sprain (rare). Posterior ligaments disrupted, but facets not locked. Unilateral or bilateral locked articular facets with or without fracture Teardrop fracture-dislocation
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All patients with head or high-energy trauma, neurological deficit, or complaints of neck pain must be presumed to have a cervical spine injury. A significant number of cervical spine injuries with neurological compromise are immediately fatal due to cardiorespiratory insufficiency from autonomic denervation. Less than one-third of patients with fractures of the cervical spine will have associated neurological deficits. Patients with ligament injuries, however, have a much higher incidence of devastating sequelae (over 65%). The degree of neurological compromise and vertebral instability is usually greater in these cases. Dislocations are the leading cause of cervical injury related death. A systematic examination of every motor and sensory level is needed to accurately assess the level of clinical injury. This can often differ from the radiographic injury level. The American Spinal Injury Association has formulated a standardized system to stratify the degree of patients deficits (Table 44.2A/B). Patients should be classified as either complete (no distal sparing of motor, sensory, or reflex function beyond level of injury) or incomplete (sparing of motor, sensation, peri-anal sensation, and/or rectal tone). This with the degree of bony instability helps dictate whether surgery is indicated (Table 44.6). Stereotyped patterns of cervical spinal cord injury are well described and are useful for descriptive, management, prognostic and archival purposes (Table 44.3). For occipito-atlanto-axial injuries, an onionskin pattern of facial sensory loss due to trigeminal tract injury, lower cranial nerve palsies (especially sixth nerve), carotid and vertebral artery dissections, strokes, and infarctions may all be encountered. Cervical injuries have a high frequency (over 60%) of associated damage to
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Table 44.2A. American spinal cord injury association (ASIA)Grading scale of neurological impairment
Grade Description
A B C D E
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Complete. No sensory or motor function below level of neurologic deficit level. Sacral sparing is absent Incomplete. Sensory but not motor function is preserved below the neurologic deficit level. Incomplete. Motor function is preserved below the neurologic deficit level, and the majority of key muscles below the neurologic deficit level has a muscle grade lower than 3 Incomplete. Motor function is preserved below the neurologic deficit level, and the majority of key muscles below the neurologic deficit level has a muscle grade higher or equal to 3. Sensory and motor function is normal.
Table 44.2B. Asia motor scoring system (100 points)

Right Left Level Muscle Action to test Sensory landmark
0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0 50
0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0-5 0 50
C4,5 C6 C7 C8 T1 L2 L3
Abduct little finger Flexion at the hip Straightening of the knee, Patellar reflex L4 Tibialis anterior Dorsiflexion of the foot L5 Extensor Dorsiflexion of hallucis longus the great toe S1 Gastrocnemius Plantarflexion of the foot, Achilles reflex S2-4 Anal sphincter, Rectal volition, bladder Bulbocavernosus reflex TOTAL POSSIBLE POINTS
Deltoids or Biceps Wrist extensors Triceps Flexor digitorum profundus Hand instrinsics Iliopsoas Quadriceps
Shoulder abduction or elbow flexion Cock up wrist Elbow extension Squeeze hand
Lower shoulder Thumb Middle finger Little finger Armpit Inner thigh Just above patella Medial malleolus Great toe Lateral malleolus Rectal sensation (score only motor)
the great vessels to the neck, thyroid, esophagus, trachea and lungs, mediastinum, ribs, brain stem, oropharynx, skull base, and facial bones. Overall, SCI is associated with other organ injury in 40-60% of cases. Cervical fractures have a 16-20% incidence of noncontiguous distal spine fractures. Neurogenic shock with hypotension (SBP<90) and bradycardia is frequently encountered in patients with cervical spine injury above C5-6. This is a result of sympathetic outflow denervation and resultant unopposed parasympathetic
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Table 44.3. Neurological syndromes of SCI

Syndrome Description Treatment / Prognosis
Bulbar-Cervical
A lesion above C4 that produces almost immediate cardiopulmonary arrest and death if CPR is not started within minutes. Ventilator dependent. Very poor prognosis and long-term survivability. A lesion, occurring almost exclusively in the central portion of cervical spinal cord, that produces sacral sensory sparing and greater weakness in the upper limbs than lower limb. Often preexisting congenital or degenerative stenosis. Hyperpathia to sensory stimuli is common. Lhermittes sign sometimes seen
no acute surgery unless highly unstable wait for hemodynamic and autonomic stability
Central Cord
classic teaching is to postpone surgery allow for cord edema and hematoma to pass delayed surgery to correct stenosis good chance of delayed leg function recovery
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Anterior Cord
A lesion that produces dissociated if compressive element loss of motor function and of seen, early surgical sensitivity to pain and decompression may be temperature, while preserving warranted proprioception. Bilateral worst prognosis with paraplegia. May be result of only 20% motor recovery either anterior spinal artery ischemia or compression from disc or bone. A lesion that produces relatively greater ipsilateral proprioceptive and motor loss and contralateral loss of sensitivity to pain and temperature. Usually from penetrating trauma, epidural hematoma, radiation, large disc herniations, spondylosis Injury to the lumbosacral nerve roots within the neural canal resulting in areflexic bladder, bowel, and lower limbs. Usually poor return of bowel/bladder function best prognosis of incomplete lesions 90% regain ability to ambulate independently rare indications for surgery except sometimes for debridement after penetrating trauma surgery usually beneficial within 24-48 hours delayed root escape or improvement common continued on next page
Brown-Sequard
Cauda Equina
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Trauma Management

Conus Medullaris Injury of the sacral cord (conus) as with cauda equina and lumbar nerve roots within syndrome the neural canal, which usually results in an areflexic bladder, bowel, and lower limbs. Sacral segments may occasionally show preserved reflexes, e.g., bulbocavernosus and micturition reflexes.
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cardiovascular input. Loss of muscle tone distal to the level of injury causes peripheral vascular pooling and relative hypovolemia. This is exacerbated by dehydration in the field and associated blood loss which causes true hypovolemia. Such patients are hypotensive with decreased cardiac output and are characterized by a warm shock type of clinical picture.

For the awake patient, a careful physical and neurological examination can accurately define the level and degree of cervical injury. Due to the often complex trauma involved in cervical spine injury, such a thorough exam is not possible for several reasons:
- Head trauma causing obtundation or neurological deficits masking spinal cord injury. - Obtundation of the patient due to shock, hypoxemia, or toxins. - Critical trauma to other organ systems requiring more urgent management. - Patients can have a syndrome of Spinal Shock which must be differentiated from neurogenic shock. Spinal shock is believed to be the spinal equivalent of concussive injury to the brain. Findings include a loss of distal segmental reflexes and a loss of the bulbocavernosus reflex as a result of this mechanism. Neurological examinations made in the face of such spinal shock must be qualified. The majority of these patients resolve within 5-10 days, but some may take several months. - Exaggerated sympathetic and parasympathetic responses to simple stimuli such as cough, touch, gag, or valsalva maneuver are common after spinal cord injury (SCI) and make management problematic. This syndrome is commonly referred to as dysautonomia. Atropine, pressors, beta-blockers, and even pacemakers are sometimes needed to manage this difficult problem which can last from a few weeks to even a year.
Investigations
For most cases of complex trauma and cervical injury, physical examination and radiographic evaluation form the two pillars of emergent diagnosis. A complete set of emergency room cervical radiographs should include:
1. Standard lateral c-spine visualizing the occiput to at least C6 2. Anteroposterior (AP) view and an open-mouth (OM) view of the odontoid (Fig. 44.3) 3. Lateral swimmers view to examine the cervicothoracic junction (C6-T2) as fractures in this region are often missed by standard c-spine views.
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Fig. 44.3. Odontoid fracture. a) Lateral x-ray with anterolisthesis and fracture of dens tip, b) open-mouth view showing type II fracture line at base of dens, c) axial CT showing fracture at base of dens, d) classification of odontoid body fractures.
A standard lateral view will detect 65-79% of cases. The addition of the AP and OM views will increase the sensitivity to 90-95%. The integrity of the spinal canal is, however, not well demonstrated by any of these views (Figs. 44.3, 44.4).
Computed tomographic (CT) scans are used to delineate the bony anatomy of fractures or deformities seen or suspected on plain radiographs. In many trauma centers, high-speed spiral CT scanning of C1-T1 has become the standard screening tool for cervical injury. CT axial images are the best way to visualize canal compromise by bony fragments. Sagittal reconstructions are helpful to visualize the canal and the overall alignment of C1-T2. Concurrent use of myelography with CT increases the sensitivity for other soft-tissues not well visualized by x-ray (i.e., herniated discs, hematoma). The greatest weakness of plain radiographs and even CT scanning is their insensitivity to ligamentous and soft tissue injury. Subluxations, dislocations, and other deformities have often spontaneously realigned by the time the patient reaches the emergency room.
- Careful inspection of the prevertebral soft-tissue thickness, the atlanto-dens interspace, the basion-dens distance, MacGregors lines, the interspinous process distances and alignment, the alignment of the bodies and facets, and the disk spaces themselves can provide subtle clues of underlying ligamentous
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Fig. 44.4. C4/5 bilateral locked facets. a) lateral x-ray with more than 50% displacement and soft-tissue swelling, b) axial CT showing inferior facets of C4 anterior to superior facets of C5, c) sagittal MRI with deformity and acute herniated disk compressing cord.
injury. Interpretation of all films by a qualified and experienced person is mandatory. Subluxation greater than 3.5 mm at any level on lateral x-ray or angulation greater than 11 of one body relative to the next highly suggests ligamentous laxity. On a lateral C-spine film, a pretracheal soft tissue thickness greater than 6 mm at the base of C2 or 22 mm at the midbody of C6 is highly suggestive of ligamentous injury or underlying fracture. An atlanto-dens interspace greater than 4-5 mm in adults as seen on a lateral x-ray is abnormal. In children, this soft-tissue can be up to 6-9 mm in thickness normally. Rule of Spence states if the sum of the lateral overhang of both C1 lateral masses on C2 is greater than 7 mm as seen on the OM view, the transverse ligament holding the odontoid to the C1 ring is likely torn and requires additional immobilization as a standard collar is inadequate.
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Spinal cord injury without radiographic abnormality (SCIWORA) is seen in a subgroup of those rare children who have spinal cord injury. They are usually 1.5-16 yrs of age. On MRI and surgery, the cord will show contusion, transection, stretch injury, or meningeal rupture. There is a latent period between the time of injury and objective sensorimotor findings of 30 minutes to 4 days in 54% of children. MRI will often demonstrate soft tissue injury in these cases. Flexion-Extension x-rays are controversial in the acute setting and carry a risk of worsening pre-existing injury. They are used to detect occult ligamentous instability especially that of the posterior complex.
- The patient should be cooperative, alert, and neurologically intact. - There should be no fractures or subluxations on the screening films. - The patient should be instructed to slowly flex the head and stop if there is pain. Typically, the patient is lying supine during these films but can be allowed to sit if he is able to. A lateral film is taken at 5-10 increments or at the point where the patient can go no further. This same procedure is repeated in extension. Normally, a small degree of anterior subluxation distributed over all cervical levels is seen in flexion with preservation of the normal contour lines.
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Magnetic-resonance imaging (MRI) is the best means of assessing injury to the ligaments, spinal cord parenchyma, and other paravertebral soft tissues. It is indicated for patients with incomplete or complete deficits, neurological deterioration, fracture level different from level of deficit and suspected cases of ligamentous injury. Recent studies have shown a high rate of missed disk herniations and canal compromise by x-ray and CT (Fig. 44.4c).
- Global use of MRI for patients with cervical injury is limited by prolonged scanning times, lack of adequate equipment and support staff to monitor critical patients in the MRI area, and unavailability of the MRI scanner after hours. Emergent CT myelography via C1-2 puncture to achieve adequate dye concentrations may be used as an alternative in such cases. CT scanning of the spinal canal with the use of high dose intravenous contrast has also been used to visualize hematoma, tumor, and infections in the epidural space.
Education of emergency medical personnel, paramedics, and police officers in proper extrication techniques and immobilization of the cervical spine is crucial to prevent exacerbation of SCI in the field. Proper placement and positioning of a rigid cervical collar and securing the patient to a rigid backboard for transport are essential elements of field management.

In the face of other critical or life-threatening injuries, treatment of cervical spine injuries can take second priority as long as the patients neck is properly immobilized and there is no evidence of evolving deficit. Special areas of concern for cervical injury patients include:
- Hypotension should be treated without any delay in order to avoid secondary cord damage. - Progressive respiratory compromise from cervical injury and thoracic trauma may require emergent intubation. For cases with a high suspicion of SCI and instability, fiberoptic intubation is optimal as it requires little neck movement. If technically unfeasible, standard endotracheal intubation is reasonable with in-line cervical traction to limit movement.
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Trauma Management - Paralytic ileus is common after SCI and should be treated with nasogastric tube placement to prevent vomiting, aspiration, and to decompress the distended abdomen. - An atonic bladder can become severely distended after SCI due to loss of voluntary control. An indwelling catheter should be placed to decompress the bladder and to accurately assess the patients volume status. - Heating and cooling blankets are often needed to treat poikilothermia (loss of thermoregulation) resulting from vasomotor paralysis in SCI patients.
In a series of double-blinded studies (NASCIS I, II, and III), the use of glucocorticoids has not been conclusively shown to have a significant impact on SCI patients. Subgroup analysis of the same data has suggested that complete and incomplete patients who received the drug within 8 hours of injury may have beneficial motor or sensory effects at 6 weeks, 6 months and 1 year.
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- Despite the controversy, many trauma centers in the country have adopted protocols for use of glucocortioids in the management of acutely injured patients. The most common protocol applies to all patients with spinal cord injuries presented within 8 hours of injury. High doses of methylprednisolone sodium succinate (MPSS), are administered as a 30 mg/kg loading dose followed by continuous 5.4 mg/kg/hr dosage for 23 hours. - Relative contraindications to acute steroid administration include penetrating injuries such as stab and gunshot wounds, life-threatening systemic instability, pregnancy, narcotic addiction, very young age, evidence of severe sepsis or infection, and a history of a compromised immune system. - Several other pharmacotherapy agents such as Tirilizad, Lazaroids are currently being investigated. Their clinical benefits remain unclear.
Immobilization with a cervical collar and backboard is indicated for all patients with suspected cervical injury during the acute phase of their evaluation. Extreme care during patient transport, transfers, and movement are essential as well.
- For many patients, a hard cervical collar is inadequate for immobilization beyond the first few hours. Examples include: - Cases of severe ligamentous injury at any level - Severe fractures of the occipito-atlanto-axial areas - Type I, II, III odontoid fractures - Severe flexion distraction injuries - Fractures of the cervicothoracic region
In such cases, additional immobilization can be provided by a variety of possible devices. These devices can be applied in the emergency room by experiences personnel.
- SOMI braceSternal-Occipital-Mandibular-Immobilzation adds additional rigidity over Philadelphia collar to upper cervical spine by addition of cervical posts. Yale orthosis is similar. The SOMI provides moderate resistance against flexion but is inadequate for preventing extension due to weak occiput support. - HALO braceConsists of a form-fitting, lightweight chest vest attached to a CT compatible ring that is anchored to the skull via a set of pins. It is very effective at limiting movement in all planes of the upper cervical spine and can also be used as an adjunct after operative fusion. It is not completely rigid with significant snaking forces especially at the lower cervical spine and cervicothoracic junction. Some complications associated with its use are patient
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intolerance, pneumonia, pin-site infections, and cerebrospinal fluid leakage. They have a 25-50% rate of failure when used alone for bilateral jumped facets and other severe flexion-dislocation injuries. HALO should not be placed acutely in patients with unstabilized thoracic or abdominal injury as access to these areas will be severely limited. - Gardner WellsOne of numerous cranial tongs that are used to not only maintain normal alignment but also to reduce fracture-dislocations and to decompress fragments from the canal via ligamentotaxis. A HALO ring may be used in place of traditional tongs such that it may be attached to a vest at the appropriate time (i.e., after operation).
Surgical Indications
For the majority of cervical spine injury patients early surgery is not warranted due to the attendant risks of polytrauma and multiorgan instability. There are few indications for emergent surgery on spinal injury. These include progressive neurological deficit, incomplete injury, an enlarging hematoma with neurological compression, gross cerebrospinal fluid leak, heavy contamination and soilage due to open or penetrating trauma, and acutely worsened deformity that cannot be reduced by closed means. In patients with complete spinal cord lesions, early surgery does not result in significant return of function over that observed by just rehabilitation alone after one year. The aim of delayed surgery is for stabilization to allow for early mobilization of the patient, psychological benefit, and the initiation of an aggressive rehabilitation program. For most cases, surgery within one week is effective in minimizing pulmonary and infectious complications from SCI. For patients with incomplete spinal cord injury, a careful search for a compressive fragment or other element compromising the spinal canal should be made. For incomplete injury that does not improve with traction or worsens during observation, early surgical decompression and stabilization may facilitate some return of function and prevent further deterioration. An exception is the central cord syndrome which is described in Table 44.3. For such cases, the majority of surgeons will delay intervention for 4-6 weeks to allow resolution of the spinal cord edema and for maximal return of neurological function. A detailed discussion of the techniques of spinal surgery is beyond the scope of this manual. Briefly, spinal surgery is divided primarily into anterior and posterior approaches. The exact choice in approach depends on the pathology and area of instability found in each case. Anterior techniques include cervical discectomy, corpectomy, with strut grafting, and cervical plating. Posterior approaches include the use of interspinous, interlaminar, interfacet wiring with bony grafting. Modern advances in instrumentation have also made the use of lateral mass screws and plates as well as pedicle screws and rod systems possible in the cervical spine. Complex deformity correction is difficult intraoperatively and should be essentially completed by closed reduction means. Due to the weaker nature of cervical constructs, HALO or other rigid cervical orthoses is needed postoperatively to supplement the fusion for several weeks.
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Specific C-Spine Injuries

Atlanto-occipital (AO) Dislocation
- 1% of cervical spine injuries
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Trauma Management - Extreme range of presentation: intact or with bulbar-cervical dissociation and arrest. May also have lower cranial deficits and worsening with cranial traction (see below). - Stability depends on ligaments of occipito-atlanto-axial complex of which the alar ligaments and tectorial membrane are the most important for AO stability. - Cervical traction should not be used to reduce this dislocation. Can use 2-4 lbs for immobilization purposes. It is controversial whether AO injuries should be operatively fused or simply immobilized with a HALO brace for 4-8 months.
Atlas (C1) Fractures

- Account for 3-13% of cervical fractures. Patients will have an isolated fracture of C1 (56%), combination C1-2 fractures (44%), head injuries (21%), and noncontiguous subaxial cervical spine fractures (9%). - Sir Geoffrey Jefferson fractureclassically described as fracture through thinnest portion of C1 arch in four places causing a blowout appearance with centrifugal displacement of the ring. This fracture is unstable as a result. - There are many variants of C1 ring fractures ranging from isolated linear breaks which are stable to the above. Careful x-ray and CT visualization is needed to diagnose them. See Investigations below Rules of Spence. - Most are neurologically intact due to the large canal diameter at C1. - Isolated C1 (Atlas) Fractures Based on the rules of Spence, nondisplaced fractures (37%) can be treated in a SOMI or standard cervical collar. Fractures with a total displacement of < 7mm (47%) can be managed in a rigid collar, SOMI, or HALO vest. Those with > 7 mm total displacement (16% of cases) should be managed with prolonged HALO immobilization. Few cases require surgical intervention. Nonunion after bracing is rare.
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Hangmans Fractures
- Also known as traumatic spondylolisthesis of the axis resulting from hyperextension and axial loading. This results in a bilateral fracture through the pars interarticularis which connects the C2 body to the posterior laminar ring. - There is usually accompanying angulation and subluxation of C2 on C3. - Type 1-Less than 3 mm subluxation. Stable. Rare deficit. Can be immobilized - Type 2-C2/3 disk and posterior longitudinal ligament disrupted with greater than 4 mm subluxation and angulation over 11. Rarely have a deficit, but may have early instability requiring surgery. - Type 2aLess displaced but more angulation (> 1.5) than type 2. These are result mainly from a severe flexion injury and require surgery. Cervical tong traction often worsens the angulation. - Type 3C2/3 facet capsules are disrupted with fracture through isthmus as well. Both the anterior and posterior longitudinal ligaments are torn. Facets often locked. Mainly from severe flexion. These are rare injuries usually with neurological deficit and can be fatal. As a group, 95% are neurologically intact with most minor deficits recovering in 1 month. Persistent pain and occipital neuralgia is not uncommon. Nonsurgical reduction of stable Type 1 and 2 fractures produces adequate reduction in 97-100% of cases. A simple collar or SOMI for 8-14 weeks is adequate in over 95% of patients. Unstable type 2, 2a, and 3 fractures, should undergo early immobilization with either gentle traction with minimal weight or a HALO vest. If reduction
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is achieved with gentle traction, a trial of HALO vest immobilization for 8-12 weeks in type II fractures. Inability to reduce type II injury, failure of external immobilization, disk herniation, progressive deficit, and type III fractures should undergo surgical fixation.
Odontoid Fractures (Fig. 44.3)

- Account for 10-15% of cervical spine fractures and usually require significant force in the young (i.e., MVA, fall from height, etc). In patients over age 70, simple falls with head injury can produce fractures in an osteoporotic C2 body. - There is a high incidence of immediate fatalities estimated at 25-40% in the field. Common symptoms are high posterior cervical pain, paraspinal spasm, the need of the patient to support the head with the hands when rising from the supine to the upright position, upper extremity paresthesias, and hyperreflexia. - They are subclassified on the basis of the vertical location of the fracture (Fig. 44.3d). Type 1-fracture through tip of dens, may be unstable Type 2-fracture through base of dens, most common There is a 30% nonunion rate for cases > 4 mm displacement. For cases with > 6 mm displacement, up to 70% nonunion reported. Surgical treatment is recommended for patients over 7 years old who have > 6 mm displacement, instability in a HALO, and nonunion. Type 3-fracture through the body of C2 involving the marrow, over 90% of these cases will heal with HALO immobilization and analgesics.
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Subluxation and Locked Facets

- Minor flexion injuries may cause subluxation or unilateral locked facets if there is a rotary component. Severe flexion injuries can result in bilateral locket facets. Facets that are not completely locked are termed perched facets (Fig. 44.4). - Patients with unilateral locked facets are usually neurologically intact. - Bilateral locked facets are usually associated with a greater amount of injury to the facet capsules and long spinal ligaments. As such they have a much higher proportion of neurological injury. - Attempts at early reduction with traction and manipulation under radiographic guidance are indicated. Caution to exclude a herniated disk seen in 10-30% of these cases should be exercised. Up to 70% of these patients may fail subsequent HALO immobilization and require surgery. Patients with bilateral locked facets should undergo surgical ORIF.
Thoracolumbar Spine Fractures

The region of the human spine from T1 to L5 can be divided into three distinct segments based on their anatomical differences and predisposition to injury.
- The thoracic segment, from T1 to T9, has a lower incidence of fracture owing to the relative stability afforded by the rib cage. Because a greater amount of force is required to overcome this stability, fractures in this area typically herald serious injury to the thoracic cavity and content. - The region between T10 and L2, commonly known as the thoracolumbar spine, is where the majority of spine injuries occur. The lack of support from the rib cage and its relatively more rigid construct make the thoracolumbar spine more vulnerable to external forces by acting as a stress riser at this region.
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Trauma Management - The region from L3 to S1 forms the lower lumbar spine. Due to its greater mobility, this segment of the spine experiences a different fracture pattern when compared to the rest of the spine.
Incidence
Approximately 40,000 potentially unstable injuries to the thoracic and lumbar spine occurred each year in the U.S, an incidence of 1 per 20,000 per year; 50-70% occurred between T10 and L2. Most common mechanisms of injury include motor vehicle accidents (40%), violence (36%), sports (15.2%), and falls (7.5%) with patients are predominantly male and under 30 years of age.
Classification
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Like the cervical spine, many classification schemes have been proposed to describe spinal fractures. Three-column theory: The spinal column is divided in three distinct parts. The anterior column includes the anterior longitudinal ligament, the anterior annulus, and the anterior half of the vertebral body. The middle column consists of the posterior longitudinal ligament, the posterior annulus, and the posterior half of the vertebral. The posterior column encompasses the neural arch, facet joints, and capsules, ligamentum flavum, and remaining ligamentous complex (Fig. 44.1).
- Failure of at least two columns leads to instability and is indicative of surgical management.
The McAfee classification identifies six fracture types based on their morphological features on CT scans (Table 44.1, Fig. 44.2).
The clinical work-up and management of patients with thoracic and lumbar (TL) injury is very similar to that already described for cervical SCI. Roll patient to allow inspection and palpation of spinal column, checking for localized tenderness, gaps between spinous processes, swelling, and deformities. Even in cases of established thoracic or lumbar fracture, patients should not be kept on a backboard for very long. Usually strict flat bedrest is adequate during the acute management of the patient. Once the patient has been stabilized, a TLSO (Thoracic-Lumbar-Sacral Orthoses), 3-point extension, Jewett, LSO, or other rigid brace can be placed to allow for some mobilization of the patient. The degree of neuronal compromise is assessed by performing a careful neurological examination, including a complete evaluation of patients motor and sensory functions. The ASIA impairment scale helps define the extent of neural injury (Table 44.2A, 44.2B). Several subtypes of incomplete neural injury have been described and should be identified (Table 44.3). An alternative way to categorize a fracture and determine treatment is to consider the degree of injury (Table 44.4). For thoracic and lumbar injuries, 70% will have no neurological deficit at presentation.
- The majority of patients with only compression fractures have no deficit
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Table 44.4. Stratification of instability for treatment

Injury Degree Pathology First Severe compression fractures (> 40%) or seat belt injury Treatment External immobilization
Second Third
Burst fractures with or without neurologic injury Severe burst fractures with 3-column involvement or fracture-dislocations
Open reduction and stabilization Realignment and/or decompression and stabilization
- Patients with mild bony flexion-distraction injuries and seat-belt type injuries are usually intact.
Patient may experience spinal shock, producing neurologic impairment away from suspected site of spinal injury that usually resolves within a few days. Neurogenic shock from isolated thoracic and lumbar injury without cervical involvement is rarer but can occur. Autonomic hyperreflexia can occur in 30-50% of patients with lesions above T7 (see C. Rehabilitation and Chronic Management). It is essential to elicit bulbocavernosus reflex and check for anal tone as part of the neurologic examination. Preservation of perianal pinprick sensation, voluntary rectal tone, and great toe flexion are considered signs of sacral sparing and reflect some structural continuity of the spinal tract. Attempts to preserve and improve the neural functions should be done in a timely fashion.
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Investigation
Radiographic assessment of the injury forms the cornerstone of diagnosis and management of spinal injuries. The common modalities include plain x-rays, computed tomography, and magnetic resonance imaging. As opposed to the cervical spine, there is no standardized set of thoracic and lumbar radiographs. When the patient is awake and able to relay where he has spinal tenderness, AP and lateral views of the spine should be obtained in that region. These films must include recognizable vertebral landmarks (i.e., cervicothoracic junction, lumbosacral junction, eleventh/twelfth rib) such that one can accurately count and localize the level of fracture and injury. For a comatose or noncooperative patient, it is generally prudent to obtain a full set (AP/ lateral thoracic, lumbar, sacral) of films to rule out injury (Fig. 44.5). If one fracture is detected, a complete spinal series is indicated to rule out noncontiguous fractures even if the patient is not symptomatic at other levels. Such concurrent fractures occur in 10-30% of cases. No well-defined rules for detecting ligamentous instability exist for the thoracic and lumbar spine as they do for the cervical spine. A careful inspection of the distances between the spinous processes on the AP view and for any other evidence of subtle deformity can help detect ligamentous injury. Patients with severe fractures of the thoracic spine should have a full radiographic evaluation of the bony rib cage and sternum as there is a high incidence of associated fracture. For lumbosacral fractures, a full radiographic evaluation of the pelvis and proximal femurs is indicated as well.
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Fig. 44.5. Thoracolumbar (T12) fracture. a) lateral x-ray of a T12-thoracolumbar burst fracture, b) sagittal MRI shows conus compression by bone and hematoma, c) axial CTs show sagittal split, laminar fracture, and bone fragments in canal.
CT is the diagnostic test of choice to delineate the bony anatomy. For thoracic fractures between T2-T8, the scapula and upper extremities make lateral radiographs virtually impossible. CT scanning with sagittal reconstruction in this area is the only good way to visualize the alignment and bony relationships here. Intrathecal contrast and/or myelograms should be considered to evaluate soft tissue masses within the canal. For severe thoracic and lumbar fractures, concurrent CT scanning of the thoracic and abdominal cavities is prudent as well. MRI is helpful in assessing the integrity of the spinal ligaments, which are crucial in determining the stability of the spinal elements. MRI is indicated if patient has
- progressive neurologic deterioration, - incongruous neurologic and skeletal injuries, - unexplained neurologic deficit.
Preoperative digital spinal angiography can be performed to identify and avoid surgical interruption of the radiculomedullary artery of Adamkiewicz. This artery occurs at T5-8 in 15%, T9-12 in 75%, and L1 or L2 in 15% of patients. Severe fractures of the thoracic and lumbar spine are sometimes (<10%) associated with vascular injury to the great vessels. Standard angiography or, recently, high-speed CT angiography should be used in any suspicious cases.
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Prehospital management of the patient with thoracic and lumbar injury is very similar to that described for cervical patients. Particular attention to maintain the patient on a backboard during transport and to keep him as flat as possible is essential. Braces for the thoracolumbar area are not usually applied in the field as access is needed to the chest, abdomen, and pelvis during acute trauma management.

It is essential to identify and address any life-threatening injury before attending to the patients spinal cord injury. However, proper precautions should be taken to prevent further neurological injury. Concomitant injuries occur in 47-60% of patients of spinal injury. These injuries may confuse or mask the clinical presentation of spinal injury. A complete trauma work up is necessary to delineate these injuries. Persistent localized tenderness despite normal radiographs is associated with occult fracture in more than 30% of patients. Hemodynamic stability is often compromised in patients with spinal cord injury. Hypotension is a common presentation secondary to either neurogenic shock, or hypovolemic shock. Neurogenic shock is characterized by a loss of vascular tone followed by an increase in vascular capacitance. It is typically associated with cord trauma above T6 resulting in sympathetic denervation. It is rarely seen in thoracolumbar injury. It is treated with volume replacement followed by vasopressors if shock persists. Lumbosacral spinal injuries are often accompanied by pelvic trauma. A complete pelvic, renal, gynecologic, urologic investigation should be performed.
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Surgical Indications
The stability of the injury, determined by structural integrity and neurological status, dictates the management of the patient (Table 44.5). For stable fractures, a conservative management combining adequate immobilization and appropriate physical therapy will suffice. The only exception is when canal compromise and neural deficit are documented and deterioration occurs. In case of unstable fracture, prompt surgical stabilization and decompression has been shown to produce early mobilization and fewer late complications resulting from prolonged bed-rest. When the canal is compromised, surgical decompression of the spinal cord may lead to a better long-term prognosis and improved recovery. Though controversial, early surgical management in these patients has led to early mobilization and resulted in less long-term complications
Management in the Operating Room When to Operate

The primary accepted indication for emergent surgical treatment in a patient with a thoracolumbar fracture is progressive neurologic deterioration. For patients with multi-system injury, early surgery (24-48 Hrs) can result in increased blood loss and is associated with a higher incidence of complications.
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Table 44.5. Surgical management guidelines for SCI

Spine Structure Neurologic Treatment
Stable Stable Stable Unstable Unstable
Normal Complete Incomplete Complete Incomplete
Nonsurgical Nonsurgical Decompression and stabilization, anterior or posterior Posterior stabilization Decompression and arthrodesis, anterior with plates, posterior or 360
What Approach to Take
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Patient with a distractive injury of the posterior elements that occurred with flexion-distraction injuries, Chance-type injuries, and fracture-dislocations are best treated with posterior instrumentation. Patients with unstable burst injuries and incomplete paraplegia associated with high-grade spinal canal stenosis from anterior bony or soft-tissue compression may benefit in the long term from immediate anterior decompression. Patients with unstable burst fractures and lesser degrees of canal stenosis can be treated by posterior instrumentation. Indications for anterior decompression and grafting include anterior neural compression and increasing neurologic deficit, incomplete recovery, persistent pain, deformity, or pseudoarthrosis. Late indications for surgery again include nonunion, persistent instability, pain, and pseudoarthrosis as well. Intraoperative somatosensory-evoked potential (SSEP) monitoring is indicated in patients who are neurologically intact or who have incomplete paraplegia.
Outcome of SCI Patients Rehabilitation

Studies have indicated that early initiation of rehabilitation results in earlier discharge and improved mobility. Rehabilitation should be a multi-disciplinary effort, including contribution from physicians, nurses, physical and occupational therapy, social workers, and psychologist. The primary goal is to restore physical strength, improve daily living skills, and achieve emotional stability. Studies have demonstrated that patients admitted to the system within 24 hour of injury are less impaired at discharge than those with same impairment who are admitted later. The long-term survivability in spinal cord injury depends on the age of patient at injury and the extent of the injury (Table 44.6). Because of their often sedentary lifestyle, difficulty in adjustment, and use of urinary catheterization, health providers of patients with spinal cord injury must be aware of some potentially fatal long-term complications (Table 44.7). Prolonged ventilator dependence, chronic atelectasis and recurrent pneumonia, deepvein thrombosis, spasticity, Charcot-type progressive deformity, syringomyelia, shoulder-hand syndrome are all problems facing the chronic SCI patient. Autonomic hyperreflexia (AH) is a particularly dangerous aspect of chronic SCI management. It is characterized by an exaggerated autonomic response
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Table 44.6. Survivability of SCI subgroups based on age

Age at injury Paraplegic Incomplete 33.2% 18.0% 6.5% Paraplegic Complete 32.1% 17.0% 5.9% Quadriplegic Incomplete 27.4% 13.8% 4.2% Quadriplegic Complete 20.1% 9.3% 1.9%
20 40 60
Table 44.7. Leading causes of death in SCI

Cardiac disease Diseases of the respiratory system Accidents, poisoning, violence Circulatory disease Infection Genitourinary Neoplasm 20.9% 20.5% 9.7% 8.8% 8.8% 4.0% 3.9%
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(usually sympathetic) to normal or mildly noxious stimuli. These include bladder distension or irritation (76%), colonic distension or impaction (19%), skin ulcers or infection (4%), DVT, and other cutaneous or visceral stimuli.
- It occurs in 30% of quadriplegic and high paraplegic patients from 4-16 weeks after injury and usually does not occur in lesions below T6. - It is manifested by paroxysmal HTN (90%), anxiety, diaphoresis, piloerection, pounding headache, mydriasis, blurred vision, flushing (25%), tachycardia (38%), bradycardia (10%), fasciculations, increased spasticity, priapism, and Horners syndrome. Hyperhydrosis and facial flushing with pallor and vasoconstriction elsewhere differentiate AH from pheochromocytoma. - Treatment includes elevating the HOB, eliminating the offending stimulus (check bowel, bladder, skin, binding clothes, etc), seizure prevention in hypertensive crisis, antihypertensive medications (nifedipine, hydralazine, nipride), and relief of spasm with diazepam which is also an anxiolytic. - Recurrent AH can be treated by phenoxybenzamine (alpha-blockade), betablockers, Pyridium to prevent UTI, good bowel/bladder/and skin regimen, and appropriate anesthesia during any manipulation or procedures.
References
1. 2. 3. 4. 5. Aebi M. Surgical treatment of cervical spine fractures by AO spine techniques. In: Bridwell KH, DeWald RL, eds. The Textbook of Spinal Surgery. Philadelphia: Lippincott 1991; 1081-1105. Chapman JR, Anderson PA. Thoracolumbar spine fractures with neurological deficit. Orthop Clin 1994; 25(4):595-611. Fessler RG, Masson RL. Management of thoracic fractures. In: Menezes AH, Sonntag VKH, eds. Principles of Spinal Surgery New York: McGraw-Hill 1996; 899-918. Harris JH, Mirvis SE. The radiology of acute cervical spine trauma, 3rd ed. Baltimore: William & Wilkins 1996. Rizzolo SJ, Cotler JM. Unstable cervical spinal injuries: Specific treatment approaches. J Am Acad Ortho Surg 1993; 1:57-66.
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6. 7.
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Waters RL, Adkins RH, Hu SS et al. Penetrating injuries of the spinal cord: Stab and gunshot injuries. In: Frymoyer JW, ed.The Adult Spine: Principles and Practices, 2nd ed. Philadelphia: Lippincott-Raven 1997; 919-930. Wilberger JE, Sarkarati M, Benzel EC et al. Medical management of adult and pediatric spinal cord injury. In: Benzel EC, ed. Spine Surgery: Techniques, Complication Avoidance, and Management. New York: Churchill Livingstone 1999; 1303-1320.
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MISCELLANEOUS TOPICS
CHAPTER 45
Pediatric Trauma
M. Margaret Knudson Epidemiology of Pediatric Trauma
Injuries remain the number one cause of death and disability among children and adolescents. Most deaths that occur in children occur in the prehospital setting; thus injury prevention programs are the most effective method of preventing death following injury. Data on the mechanism of injury in pediatric trauma collected by the National Pediatric Trauma Registry (NPTR) is shown in Figure 45.1. Note that most of these children were not using appropriate protective devices when the injuries occurred. Other data from the NPTR has shown that: blunt injuries are the most prevalent in all age groups falls are the major mechanism of injury in children < 10 yrs old pedestrian injuries carry the highest mortality in children < 10 yrs old in adolescents, motor vehicle trauma is the major mechanism in adolescents, GSW are the most lethal (10% mortality) overall mortality in children reaching a hospital is low, 3% those that die in the hospital do so within 24-96 hours
Prehospital Care
As with adult trauma patients, injured children should be transported quickly to a center equipped to care for them. This might be a general trauma center or a pediatric hospital that also serves as a trauma center. All prehospital vehicles that transport the injured must carry equipment for various sizes of children. Appropriate prehospital measures for injured children include: application of oxygen intubation of children in shock, or with airway compromise intubation of children with major head trauma (i.e., GCS < 8) measurement of oxygen saturation with pulse oximetry measurement of blood pressure with proper-sized cuff application of measures to prevent heat loss establishment of IV access only if transport time >20 minutes maintaining cervical spine precautions
Resuscitation Airway
Intubation of a child should proceed promptly if the child has airway compromise, a major head injury (GCS<8), or is hypoxic and or in shock.. The technique of rapid sequence intubation is outlined in Algorithm 1. Important considerations in pediatric airway include:
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. M. Margaret Knudson, University of California, San Francisco, California, U.S.A.
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Fig. 45.1. Mechanism of injury in pediatric trauma. Data from the 1999 Report of the National Pediatric Trauma Registry.
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errors in airway management have resulted in prehospital deaths infants are obligate nose breathers; thus the nares should be cleared the sniff position (advanced midface) holds the airway in neutral the sniff position can be obtained by placing a small towel behind the occiput, while maintaining spine precautions simple clearing of the airway should be attempted first for children less than 12 years, nasotracheal intubation in contraindicated the appropriate sized endotracheal tube can be estimated from the diameter of the childs small finger (Table 45.1) the pediatric larynx is anterior and cephalad compared to an adult the pediatric trachea is short (5 cm at birth) and soft cuffed endotracheal tubes are generally not used once the tube is secured, listen in the axilla for breath sounds confirm placement of the endotracheal tube with a chest x-ray emergency room tracheostomy is contraindicated in a child the preferred surgical airway is a temporary needle cricothyroidotomy
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Venous Access and Fluid Resuscitation

Once the airway has been secured, resuscitative efforts should be directed at establishing intravenous access. A protocol should be established (and followed) so that valuable time is not wasted by numerous attempts at establishing lines. Development of hypotension following hemorrhage is a relatively late sign of shock in children and demands prompt attention (Table 45.2). make two attempts at peripheral access preferred peripheral access sites include the back of the hands, antecubital fossa, and saphenous vein at the ankle
Table 45.1. Appropriate tube sizes for children

Age Endotracheal Tube Thoracostomy Tube
Premature infant Toddler 6 year old Adolescent
2.5 mm 3.0 mm 5.5 mm 7.0 mm
12F 20F 24F 32 F
Adapted from Lubitz DS, Siedel JS, Chameides L et al. A rapid method for estimating weight and resuscitation drug dosages from length in the pediatric age group. Ann Emerg Med 1998;17:567.
Table 45.2. Normal vital signs by age

Pulse Systolic blood pressure Respiratory Rate
Infant (< 1y) Preschool (<5y) Adolescent (>10y)
160 140 120
80 90 100
40 30 20
Adapted from: ATLS, 1997, American College of Surgeons, Pediatric Trauma, Chapter 10.
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if two attempts are unsuccessful move on to alternative methods preferred alternative method in a child < 6 years is intraosseous access established at the proximal tibia (uninjured extremity) or distal femur preferred alternative method in a child > 6 years is a percutaneous femoral line placed by an experienced physician once venous access has been established, follow the resuscitation protocol outlined in Algorithm 2 note that all fluids should be warmed crystalloid boluses can be given three times if the child remains unstable after three boluses, blood should be administered while preparing for surgical control of bleeding
Head Trauma
Head injuries are the major cause of death among injured children and those that survive have a high rate of permanent disability. Mass lesions are relatively less common in children than in adults but intracranial hypertension is more common (see Fig. 45.2). The management of major brain injuries in children includes: avoidance of secondary brain insults (hypotension/hypoxia) liberal use of CT scans rapid control of scalp lacerations as children can lose significant amounts of blood from these areas early intubation for children with GCS 8 use of the pediatric version of the GCS (Table 45.3) liberal use of ICP catheters to monitor cerebral perfusion pressures use of measures to control seizures and fever early attention to nutritional needs maintaining a euvolemic state maintaining CO2 in the normal range (35 mm Hg)
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Spinal Cord Injury

The relatively large size of the head and weak cervical musculature make the upper cervical spine more susceptible to injury in the young child. In older children, the lower cervical spine is injured most frequently. Radiological evaluation of the pediatric spine can be challenging for the following reasons: normal skeletal growth centers can be mistaken for fractures the growth center of a spinous process may resemble a fracture basilar odontoid synchrondosis appears at the base of the dens in children < 5 years of age apical odontoid epiphyses appear as separations (5-11 years old) pseudosubluxation occurs as an anterior displacement of C2/C3 movement at this joint of up to 3 mm may be normal increased distance between the dens and the anterior arch of C1 occurs in 20% of young children spinal cord injury may occur without radiologic abnormalities (SCIWORA) in as many as 50% of children SCIWORA should be treated with a steroid bolus and the injury confirmed with MRI scanning
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Fig. 45.2. CT scan of the head in an infant. Note the major skull fracture and severe swelling with right to left shift and obliteration of the right lateral ventricle.
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Table 45.3. Adaptation of the GCS for children: Verbal score

Response Score
Appropriate words, smiles, follows Cries but consolable Inconsolable, persistently irritable Restless, agitated No response
5 4 3 2 1
Adapted from: ATLS 1997, American College of Surgeons, Chapter 10: Pediatric Trauma.
Chest Trauma
Major chest injuries are the second leading cause of death in pediatric trauma. Rib fractures occur less commonly than in adult patients, but when they do occur are indicators of major chest injury. Cardiovascular injuries can also occur following major chest trauma. Evaluation and treatment of chest injuries in children includes: a high index of suspicion for pulmonary contusion which is usually not evident on the initial chest x-ray but may present later as hypoxia performance of a surface echocardiogram in children with evidence of major chest injury and/or cardiac arrhythmias insertion of the appropriate-sized chest tube for pneumo- or hemothorax (see Table 45.1) evaluation of the aorta by spiral CT scanning and/or thoracic four-vessel angiography in children with a major mechanism of injury (high speed MVA, fall or pedestrian struck), a widened mediastinum on chest x-ray or mediastinal hematoma seen on spiral CT performance of bronchoscopy in children with a large amount of subcutaneous emphysema, major air leak or persistent pneumothorax after insertion of a chest tube, in search of major bronchial disruption.
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Abdominal Injuries
Evaluation: Abdominal injuries are common in the pediatric population and represent an area where prompt recognition and treatment can significantly impact morbidity and potentially mortality. Because of the difficulty in examining the pediatric abdomen, patients who meet the following criteria should be considered for objective evaluation of the abdomen: major mechanism of injury abdominal pain/tenderness abdominal wall/flank abrasions or bruises history of hypotension uncorrected base deficit unexplained drop in Hct level presence of pelvic fracture presence of rib fractures presence of hematuria associated major head/spinal injury precluding accurate exams
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Most children will be stable and are best evaluated by CT scanning of the abdomen and pelvis, usually performed with both IV and GI contrast agents. Unstable children benefit from a bedside ultrasound examination (FAST exam or focused sonographic assessment for trauma) which examines the pericardial space, right and left perirenal spaces, and the pelvis for the presence of blood (fluid) (Fig. 45.3). Bedside, portable ultrasound exams performed by the surgeon have replaced diagnostic peritoneal lavage in the evaluation of the pediatric abdomen in most trauma centers. Table 45.4 lists the advantages and limitations of abdominal CT versus ultrasound in the evaluation of blunt abdominal trauma.
Solid Organ Injuries

The liver and the spleen are the most frequently injured organs in the abdomen and more than 90% of these injuries will respond to observational treatment in the pediatric population (Fig. 45.4). The protocol for successful management of solid organ injuries in the pediatric population includes: establishing the severity of injury by CT scanning admission of all children to the ICU for at least 24-48 hours serial Hct/Hb levels until stable serial abdominal exams by an experienced surgeon resumption of ambulation when Hct is stable and hematuria resolved resumption of diet when ileus resolves discharge from the hospital when eating/ambulating follow-up scan prior to discharge for all splenic/renal injuries follow-up scan prior to discharge for selected liver injuries prompt operative intervention for persistent or delayed hemorrhage, hemodynamic instability, signs or symptoms of missed intestinal injuries or renal necrosis/major extravasation (Fig. 45.5) follow-up imaging for all injuries prior to resuming contact sports
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Fig. 45.3. Ultrasound exam of the right upper quadrant demonstrating free fluid (blood) between the liver and kidney.
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Table 45.4. Ultrasound versus abdominal CT scanning

CT Scanning Ultrasound
Hemodynamic stability Location Ease of repeatability Organ specificity Sensitivity for fluid Evaluation of retroperitoneum Sensitivity for intestinal injuries Experience required
required X-ray department moderately easy high high detailed limited for interpretation
not necessary bedside very easy low depends upon amount limited limited for performance and interpretation
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Fig. 45.4. CT scan of the abdomen in a child, demonstrating a splenic injury with extravasation of intravenous contrast suggesting active bleeding.
Intestinal injuries: Approximately 5% of all children who sustain blunt abdominal trauma will have a hollow viscus injury. These injuries may initially be subtle, but morbidity increases with operative delay. Unfortunately, neither CT nor ultrasound is sensitive to the presence of a hollow viscus injury, and because most solid organ injuries are treated nonoperatively, the treating physician must be aware of the signs/symptoms/associated findings in children with intestinal injuries, which include: the presence of a lap-belt mark on the abdominal wall the presence of a lumbar Chance fracture (Fig. 45.6) the presence of fluid on the abdominal CT scan without an associated solid organ injury bowel wall thickening, free air, or contrast extravasation seen on abdominal CT scanning
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Fig. 45.5. CT scan of the abdomen in a child showing right renal injury with active extravasation.
uncorrected base deficit rising WBC postinjury delayed development of nausea/vomiting/abdominal tenderness/or distention following blunt abdominal trauma Pancreatic/duodenal injuries: A direct blow to the epigastrium from the handlebars of a bicycle, a kick, or impact during contact sports can injure the duodenal and/or the pancreas. Most duodenal injuries in children are not full-thickness and result in a submural hematoma that responds to nasogastric suction and watchful waiting. Most pancreatic injuries can also be treated without operation, unless there is evidence of major ductal disruption (Fig. 45.7)
Fractures
Pelvic fractures are unusual in pediatric trauma but their presence suggests associated intra-abdominal and/or genitourinary tract injuries. The following features are characteristic of extremity fractures in children: growth plate involvement can result in a shortened extremity incomplete fractures may involve only one cortex (Greenstick) bending can occur without fracture lines (buckle fracture) fractures may be absent on initial films and seen only on subsequent imaging vascular injuries accompany supracondylar fractures at the elbow or knee proportionally more blood is lost from fractures in children when compared to adults failure to recognize/promptly treat fractures can result in permanent disabilities decreased use of the extremity may be a subtle sign of fracture in a small child who cannot complain of pain a search for extremity fractures should be part of the tertiary survey following trauma
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Fig. 45.6. MRI scan demonstrating thoracic spine fracture resulting from a lap belt. This child was paraplegic.
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Child Abuse
Approximately 5/10,000 children suffer from abuse or neglect and many children die each year following intentional injuries inflicted by their parents or caregivers. Signs and symptoms of abuse include: a history of repeated emergency visits for minor injuries a discrepancy between the story provided by different caregivers doctor or ER shopping by caregivers in order to avoid suspicion bites and burns (including cigarette) in unusual places lower extremity burns that spare the feet (emersion) evidence of multiple fractures of different ages, especially in children less than 3 years old multiple subdural hemorrhages without skull fracture retinal hemorrhages perioral or genital injuries
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Fig. 45.7. Pancreatic injury following child abuse. Note the near total separation of the head/body of the pancreas at the level of the spine.
Recognition or suspicion of child abuse requires that the physician report the case to the child protective services agencies immediately. In addition to fulfilling the law, this reporting may save the child from mortal injuries in the future.
Psychological Factors
Despite recovery from the physical trauma, many children fail to recover from the emotional trauma and these disabilities may persist for life. Parents too may require treatment for the emotional trauma that affects them during their childs hospitalization and recovery from major injuries, and tend to underplay the psychological symptoms of their children. True PTDS symptoms are present in at least 50% of children who are hospitalized following trauma. The symptoms of psychological stress that are common in children following a major injury include: sleep disturbances behavior changes include rage attacks decreased academic performance intrusive thoughts separation anxiety mood disturbances phobias accident related play Interventions directed at recognizing and treating these psychological problems in injured children could have a significant impact on their ability to fully recover from their trauma
Performance Indicators
Because death following trauma is relatively uncommon among injured children when compared to adults, the quality of a pediatric trauma system must focus on
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morbidity, not mortality. Review of the system and commitment to continuous improvement must be the goal of all who provide care to injured children. Table 45.5 lists topics for performance reviews in pediatric trauma.
Injury Prevention
Injury prevention has the potential to significantly impact death and disability following pediatric trauma. Currently available injury prevention measures could prevent most unintentional injuries in children. Active prevention measures, which require some action by the parent/child (i.e., seatbelts or carseats), are less effective than passive measures (i.e., airbags). Examples of injury prevention programs that have been show to be effective in the pediatric population include: bicycle helmet use decreases head injuries by 85% smoke detectors and fire-retardant clothing reduce the incidence of burns traffic calming measures reduces pedestrian injuries safe storage of firearms reduces unintentional shooting deaths by 23% car seat use prevents ejection/injuries in infants community based violence prevention programs have resulted in a 50% reduction of assault and gun injuries in some communities Sadly, most parents and physicians are poorly educated in the area of injury prevention. Attention to this important topic in the next century has the greatest potential to impact the lives of children and adolescents.
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Table 45.5. Examples of pediatric trauma performance measures

Appropriateness of resuscitation volumes Problems with vascular access Problems with intubation/extubation Problems with hypo/hypercapnea Missed injuries Failure to provide rehabilitation services Failure to provide psychological support for family and child Adapted from: Resources for Optimal Care of the Injured Patient. 1999 Committee on Trauma, American College of Surgeons.
References
1. 2. 3. 4. 5. 6. Tepas JJ. Resuscitation of the injured child. In: Trunkey DD, Lewis FR eds. Current Therapy of Trauma, 4th edition. St. Louis: Mosby Inc. 1999;. 81-88. American College of Surgeons Committee on Trauma: Pediatric Trauma. In: Advanced Trauma Life Support for Doctors, American College of Surgeons Press, Chicago 1977; 353-375. Fallat ME, Casale AJ. Practice patterns of pediatric surgeons caring for stable patients with traumatic solid organ injury. J Trauma 1997; 43:820-24. Kurkschubashe AG, Fenday DG, Tracy TF et al. Blunt intestinal injury in children; diagnostic and therapeutic considerations. Arch Surg 1997; 132:652-58. Wesson DE, Scorpio RJ, Spence LJ et al. The physical, psychological, and socioeconomic costs of pediatric trauma. J Trauma 1992; 33:252-57. Rivara FP, Grossman DC, Cummings P. Injury prevention (Part 1). NEJM 1997; 337:542-48 and NEJM (Part 2) 1997; 337:613-18.
CHAPTER 46
Geriatric Trauma
The geriatric population is the fastest growing group of the general population, and geriatric trauma accounts for a significant portion of admissions to trauma centers. Due to different physiology, different types of injuries and different outcomes, geriatric trauma patients often require a much more aggressive evaluation and management than younger patients.
Epidemiology
Falls are the most common mechanism of injury in the geriatric population. Ground falls are very common due to many factors: impaired proprioception, muscle weakness, dementia, syncopic episodes. Motor vehicle accidents (MVA) are the second most common mechanism of injury in this age group. Longer reaction times, preexisting medical problems and impaired vision and hearing are important contributing factors.
- In Los Angeles there are about 10 trauma deaths due to MVA per 100,000 population older than 60 years. This is much higher than younger age groups.
Auto-pedestrian accidents are the third most common cause of injury in the geriatric population.
- In Los Angeles there are about 9 deaths due to pedestrian accidents per 100,000 population older than 60 years. This is more than twice the rate observed in younger individuals.
Suicides are very common in older age groups.

- In Los Angeles there are about 23 deaths due to suicide with penetrating trauma per 100,000 males older than 65 years. In females of the same age group, this figure is 1 per 100,000.
Age-Related Physiology and Effect on Trauma

- Dementia may complicate clinical evaluation. - Brain atrophy and fragile bridging veins predispose to subdural hematomas. - Epidural hematomas are not common due to firmer adherence of the dura on the skull in elderly individuals. - Anticoagulant medications predispose to intracranial hemorrhages even after minor injury. - The incidence of intracranial hemorrhage in individuals older than 60 years, after minor head injury is about 16% as compared to only about 6% in younger victims.
Spine
- Higher incidence of spinal fractures due to osteoporosis - Higher incidence of upper cervical spine injuries, especially odontoid fractures - Narrowed spinal canal predisposes to cord injury
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- Higher incidence of central cord syndrome following overextension injury to the cervical spine.
Cardiovascular System (CVS)

- Decreased cardiac output, inability of the heart to respond to endogenous or exogenous signals to increase the output. - Associated ischemic myocardial disease or conduction abnormalities - Hypertension - Medication such as beta-blockers, calcium channel blockers, diuretics may affect the clinical presentation, the resuscitation efforts, and the outcome.
Respiratory System
- Decreased pulmonary compliance, vital capacity, pO2. - Due to reduced physiological reserves, respiratory failure may appear much earlier and after fairly moderate trauma.
Kidneys
Decreased creatinine clearance and concentration ability Diminished tolerance to hypotension and nephrotoxic drugs.
Initial Evaluation and Management

Due to the limited physiological reserves, any delays in diagnosis and treatment can be fatal. Early, aggressive evaluation and monitoring are essential, even for fairly moderate-severity trauma. During the Primary Survey of the ATLS remember the following age-related conditions:
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Airway/C-Spine
Dentures Upper cervical spine fractures (especially odontoid) are not uncommon and may not give severe clinical signs.
Breathing
Flail chest may not be very obvious on clinical examination due to rib cage rigidity. Respiratory decompensation may occur rapidly due to reduced respiratory reserves and severe chest pain. Early intubation and respiratory support is recommended in borderline cases, before transportation for complex or prolonged radiological investigations.
Circulation
The initial blood pressure and pulse rate may be misleadingly normal and cardiovascular collapse may occur quickly and unexpectedly. Many geriatric patients are on cardiac medications which may interfere with the cardiac response to trauma. Diuretics may be associated with significant intravascular depletion. A normal blood pressure or mild hypotension in a hypertensive patient may signify hypotension. The heart often fails to increase the cardiac output in order to meet increased oxygen demands. Early blood transfusions to maintain the hemoglobin at slightly higher levels than in younger individuals, may be helpful. The hypotension is more likely to be cardiogenic in origin than in younger patients. Always consider the possibility of myocardial infarction.
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Disability
Preexisting dementia may interfere with GCS reliability. Subdural hemorrhages are common and may not be clinically obvious on admission. Liberal CT scanning is recommended.
Exposure/Environment
Geriatric patients lose temperature very easily and hypothermia occurs much faster than in younger populations. Take appropriate steps to prevent this serious complication.
Specific Anatomic Injuries in Geriatric Patients

Head/Spinal Trauma
High incidence of subdural hematomas, low incidence of epidural hematomas. Central cord syndromes without skeletal injury. Survival and neurological outcome are worse than younger populations. Higher incidence of upper C-spine injuries. Liberal CT scanning.
Chest trauma
- Multiple rib fractures are associated with a high incidence of respiratory failure and death. Adequate pain control, preferably by epidural anesthesia, is highly desirable. Early mechanical ventilation may be necessary. - Higher incidence of aortic rupture. Liberal CT scanning of the mediastinum even in moderate injuries.
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Abdominal Trauma
- More difficult to evaluate clinically due to blunting of peritoneal signs. Liberal use of abdominal CT scanning. - Nonoperative management of solid organ injuries (liver, spleen) is less successful than in younger populations.
Skeletal Trauma
- Long bone fractures even with fairly minor trauma, such as ground falls. - Long bone fractures are associated with significant morbidity and mortality and they should be treated as severe injuries. Admission to the ICU, Swan-Ganz placement, and early operative management are critical for a good outcome.
General Management
Aggressive early evaluation, monitoring, and management. Stable looking patients may deteriorate and die very fast! Moderate severity injuries (i.e., multiple rib fractures, long bone fractures, pelvic fractures) require ICU admission. Swan-Ganz catheter placement is strongly recommended in order to optimize fluid administration. The geriatric patient can easily go from hypovolemia to overloading and cardiac failure. Close monitoring and a liberal policy of endotracheal intubation for geriatric patients transported from the emergency room to the radiology suite for multiple investigations.

Underestimate the risks of relatively moderate trauma in geriatric trauma. Sudden, unexpected, and catastrophic deterioration may occur. Underestimate the significance of otherwise minor rib fractures. Pneumonia and respiratory failure are very common. Adequate analgesia and liberal use of epidural anesthesia are very important.
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Underestimate the importance of minor head injuries. There is a high incidence of intracranial pathologies. Liberal policy of head CT scan should be a standard practice. Send a geriatric trauma patient even with fairly minor injuries, from the emergency room to the radiology suite for multiple investigations without close continuous monitoring. Sudden deterioration may occur in a suboptimal environment. Consider a liberal policy of endotracheal intubation and respiratory support during prolonged radiological investigations.
References
1. 2. 3. 4. 5. Demarest GB, Osler TM, Clevenger FW. Injuries in the elderly: Evaluation and initial response. Geriatrics 1990; 45:36-42. DeMaria EJ. Evaluation and treatment of the elderly trauma victim. Clin Geriatr Med 1993; 9:461-471. Knudson M, Lieberman J., Morris J et al. Mortality factors in geriatric blunt trauma patients. Arch Surg 1994; 129:448-453. Martin RE, Teberian G. Multiple trauma and the elderly patient. Emerg Med Clin North Am 1990; 8:411-420. Santora TA, Schinco MA, Trooskin SZ. Management of trauma in the elderly patient. Surg Clin North Am 1994; 74:163-186.
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CHAPTER 47
Trauma in Pregnancy
John Fildes and Timothy Browder Introduction
Trauma is the leading cause of death from ages 1 through 44. It reaches its peak during the ages of 15 through 35 when as many as 80% of deaths are caused by injury. This is also the peak age for pregnancy. Research shows that trauma is the leading cause of death during pregnancy. The incidence of intentional injuries such as assaults, domestic violence and homicide are increased during pregnancy. The guiding principal in the treatment of a pregnant trauma patient is to treat the mother first. The best way to help the baby is to help the mother. The treatment priorities for the pregnant patient are the same as for the nonpregnant patient. In this chapter the nuances of physical examination and clinical evaluation will be presented with special attention towards the physiologic changes of pregnancy.
Primary Survey
Approach the injured pregnant patient in a systematic fashion. Examine and address the airway, breathing, circulation, and disability. Also expose the patient to identify all injuries. It is an error to concentrate on the pregnancy and its potential problems before insuring that the maternal life threats have been identified and managed. Airway: Be sure that the airway is patent and unencumbered. Make liberal use of oxygen. The fetal oxygen hemoglobin dissociation curve is positioned to the left of the maternal curve. Small changes in the maternal oxygenation can result in significant changes in the fetal oxygenation. High flow oxygen through a non-rebreather mask is adequate for spontaneously breathing patients.
- In the event that endotracheal intubation is required the rapid sequence technique is preferred. Urgent intubation is a common practice in obstetrical anesthesia for fetal distress. These experiences here have demonstrated that rapid sequence intubation can be safely performed. The best agents include those that are short acting, rapidly metabolized and possess a long history of safety in pregnancy. Morphine, midazolam and succinylcholine are commonly used in this setting. Cricoid pressure must be maintained during intubation. - Aspiration is a common complication in obstetric intubations. This is caused by relaxed lower esophageal sphincter pressure, decreased gastric emptying and increased gastric acidity. Ventilator settings must keep the oxygen saturation near 100%.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. John Fildes, University of Nevada School of Medicine, Las Vegas, Nevada, U.S.A. Timothy Browder, University of Nevada School of Medicine, Las Vegas, Nevada, U.S.A.
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Breathing: Auscultation must be performed at the axilla and apex of both lungs. The diaphragm is pushed higher as pregnancy advances. This is particularly true in a supine position. Breath sounds may not be present in the lower chest as they are in a nonpregnant patient. Care should be taken during insertion of a chest tube so that the diaphragm is not injured.
- The physiological changes in advanced pregnancy include increased tidal volume and minute ventilation but not tachypnea. This should be interpreted as a sign of respiratory distress. Functional residual capacity is decreased which alters pulmonary reserve. Oxygen desaturation can be very rapid.
Circulation
- Maternal hemodynamics must be aggressively supported. Begin by establishing two large bore IV sites above the diaphragm. Patients should be resuscitated with isotonic crystalloid solution and blood as appropriate. - Maternal circulatory volume is increased by as much as 30-40%. During hemorrhagic shock, the maternal blood volume is supported by uterine vasoconstriction. This shunts blood to the mother and may result in fetal distress. Therefore, tachycardia and hypotension are late signs of maternal hemorrhage. It is wise to aggressively resuscitate these patients until their circulatory status is more precisely assessed. - The supine hypotensive syndrome can occur in women in the second half of pregnancy. The uterus is large enough to compress the inferior vena cava and bifurcation of the iliac veins. This reduces the return of preload to the heart. Rotating the patients right side upward 15 to 20 degrees and manually displacing the uterus to the left can reverse the supine hypotensive syndrome. Patients who are in spinal immobilization can be left on the backboard with the cervical collar in place and the entire apparatus can be elevated on the right side.
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Disability: A quick neurological survey includes the Glasgow coma scale, pupillary reactivity and the presence or absence of movement in all four extremities. Injuries to the brain can be lateralized by the pupillary examination. The Glasgow coma scale determines the mental status. The level of injury to the spinal cord is determined by the combination of motor and sensory findings seen on physical exam. Spinal cord injuries at any level will obscure important physical findings in the abdominal and obstetrical exam. Exposure: The patients must be completely exposed so that all injuries can be identified. Care must be taken to prevent hypothermia through the use of warming lights, blankets and warmed IV solutions.
Secondary Survey
This is the first system by system physical exam performed on the patient. It is also the first time that the fetus is assessed. Labs and x-rays are ordered at this time. The patient usually receives medications as required. Each of these issues requires special consideration in the pregnant trauma patient. Remember the guiding principal is: treat the mother first. Missed injuries in the mother will have a negative impact on fetal well being. So be sure to order all necessary labs, diagnostic studies and medications. Perform a complete examination of the neurologic, cardiac and pulmonary systems. Abdominal Exam: The abdomen should be inspected, auscultated, palpated and percussed. Signs of shock and peritonitis mandate laparotomy just as they
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would in a nonpregnant patient. The abdominal exam is the first time when the uterus is examined. Check the fundal height carefully. In the supine position, the fundus reaches the umbilicus between 20 and 24 weeks (Fig. 47.1). This is a critical piece of information for clinical decision making.
- If fetal distress is present then resuscitation is intensified. Maternal injuries must be rapidly identified and surgically addressed. If the pregnancy is 24 weeks or more then simultaneous emergency caesarian section must be performed. If the pregnancy is less than 24 weeks then intensifying resuscitation and addressing maternal injuries treats fetal distress. Caesarian section is not recommended on such an immature fetus because survival is poor.
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Pelvis and Vaginal Examination: Evidence of pelvic fracture or instability must be identified. The pelvic ligaments soften as the pregnancy progresses. Pelvic relaxation can result in a widening of the pubis that mimics diastasis. Identify point tenderness in this area as a marker for acute injury. The pelvic outlet tracts must be examined. A complete rectal exam must be performed. A vaginal examination is performed using sterile gloves. The presence of blood or amniotic fluid in the vagina, cervical tenderness and uterine contractions are serious findings that must be communicated to the consulting obstetrical team immediately. Laboratories: CBC, blood chemistry, PT/PTT, and blood type are commonly ordered for trauma patients. The CBC may show a reduced hemoglobin and hematocrit. This anemia of pregnancy is seen in the second and third trimesters. It is caused by a disproportional expansion of the plasma volume compared to the red blood cells. Hemoglobin less than 11 g/dL is abnormal. The PT/PTT should be normal.
- The blood type should be checked for Rh status. Trauma can cause disruption of the placenta with admixture of maternal and fetal blood. Rh-negative mothers can receive fetomaternal transfusion from an Rh-positive fetus. In ninety percent of cases this Rh antigenemia can be neutralized by the administration of 300 international units of Rh-immune globulin within 24 hours of injury. The Kleihauer-Betke test can be used to calculate the volume of fetal blood present in the maternal circulation. Additional doses of Rh-immune globulin can be given if required. Three hundred international units of Rh-immune globulin will neutralize 30 ml of fetal blood.
X-rays: All necessary x-rays should be obtained. The greatest risks of fetal radiation exposure is during the first trimester. A missed maternal injury is more likely to have a negative effect on the fetus than the judicious use of diagnostic x-rays. Radiographs of the C spine, chest, and extremities can be performed with a lead apron across the abdomen. The absorbed radiation dose is negligible. Care should be taken not to exceed five rads of radiation exposure at anytime. This is most important when x-rays of the lumbar spine, pelvis, and hips are being performed. Abdominal trauma should be initially evaluated by ultrasound. If CT scan is required the spacing of cuts passing through the uterus should be increased to 1 cm. Medications: Medication safety is a common issue in the treatment of patients who are pregnant. The most common medications administered to trauma patients are analgesics, antibiotics and tetanus toxoid. Analgesics like morphine and meperidine have been used for many years and possess a good safety profile. If necessary they can be reversed with naloxone. Second and third generation cephalosporins are safe and effective against the most common organisms
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Fig. 47.1. In the supine position, the fundus reaches the umbilicus between 20 and 24 weeks.
encountered in a trauma situation. Tetanus toxoid and tetanus immune globulin are safe and should also be administered when required.

Prepare the OR as you would for a major trauma case. There should be adequate IV access, fluid and blood warmers and ample blood products. The abdomen should be entered through a midline incision. This will allow the uterus to be moved from side to side and all quadrants to be exposed. If a cesarean section needs to be performed, a transverse uterine incision can be made using the exposure provided by the midline abdominal incision. If the
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pregnancy is less than 24 weeks gestational age, uterine injuries should be directly repaired and expectant management exercised. There is no need to evacuate the uterus when fetal death is present. Spontaneous delivery will usually occur within 24 to 48 hours. Hysterectomy is indicated only when there is irreparable injury to the pelvic and uterine vascular structures. If the pregnancy has advanced beyond 24 weeks, obstetrical and neonatal support should be immediately available. The development of fetal distress may require caesarian section and resuscitation of the infant. Occasionally the fetus is injured too. A second surgical team should be assembled to manage the newborns injuries.

The management of a traumatized pregnant patient requires strong trauma team leadership. Well meaning support staff and consultants will try to divert attention towards the fetus. It is imperative that the mothers care be prioritized in order to support the fetus. Remember the guiding principal is: treat the mother first.
References
1. 2. Fildes J, Reed L, Jones N et al. Trauma: The leading cause of maternal death. J Trauma 1992; 32:643-645. Esposito TJ, Gens DR, Smith LG et al. Trauma during pregnancy: A review of 79 cases. Arch Surg 1991; 126:1073-1078. Henderson SO, Mallon WK. Trauma in pregnancy. Emerg Med Clin North Am 1998; 16:209-228. Kissinger DP, Rozycki GS, Morris JA Jr et al. Trauma in pregnancy: Predicting pregnancy outcome. Arch Surg 1991; 126:1079-1086. Perlman MD, Tintinalli JE. Evaluation and treatment of the gravida and fetus following trauma during pregnancy. Obstet Gynecol Clin North Am 1991; 18:371-371.
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3. 4. 5.
Interventional Radiology in the Care of the Trauma Patient

Trevor D. Nelson and M. Victoria Marx Diagnostic Arteriography (Figs. 48.1, 48.2)
In the setting of trauma, arteriography is useful to identify or exclude arterial injury, arterial occlusion, and/or an arterial source of hemorrhage. The diagnostic arteriogram may be followed by a percutaneous interventional procedure such as embolization or stenting.
Indications
Blunt trauma to the chest with imaging findings or clinical history suggestive of aortic or great vessel injury. Pelvic fractures with clinical or radiological suspicion of significant bleeding. Selected cases with penetrating trauma for evaluation of proximity vessels (i.e., neck) or active bleeding for areas which are difficult to access surgically. Long bone fracture with expanding hematoma, vascular compromise, or proximity to a critical vessel. For example, popliteal artery injury has a high association with posterior fracture-dislocation of the knee. Selected hemodynamically stable patients with solid organ injuries, with clinical or CT evidence of active bleeding or aneurysms.
Contraindications
Hemodynamic instability is a strong contraindication for angiography. Bleeding from pelvic fractures or other surgical inaccessible areas are the only exemptions. Allergy to iodinated contrast
- A history of contrast reaction requires appropriate prophylaxis prior to arteriography. - Optimal premedication consists of 50 mg oral prednisone 13, 7 and 1 hour prior to arteriography, followed by 50 mg IV diphenhydramine. In cases where prior reaction has been severe, IV administration of an H2 blocker, such as cimetidine, is also recommended. - A reasonable premedication protocol in an emergency situation, where a 13 hour delay is not in the best interests of the patient, is intravenous administration of 100 mg hydrocortisone, 50 mg diphenhydramine, and 300 mg cimetidine at the start of the procedure.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Trevor D. Nelson, Department of Radiology, LAC + USC Medical Center, Los Angeles, California, U.S.A. M. Victoria Marx, Department of Radiology, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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Fig. 48.1A. Aortic rupture secondary to deceleration injury. Portable chest xray demonstrates widening of the upper mediastinum (arrows) with loss of aortic knob definition. Life support appliances, snaps, and a zipper overlie the image. The presence of these extraneous items is distracting but serves to suggest that the patient is quite ill.
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Fig. 48.1B. Aortogram demonstrates a traumatic pseudoaneurysm (arrows) projecting off the left posterolateral aspect of the aorta about 3 cm) beyond the origin of the left subclavian artery. The pseudoaneurysm indicates that there has been a rupture of the aorta at that point.
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Fig. 48.2. Brachial pseudoaneurysm and arteriovenous fistula secondary to knife wound. A. This brachial arteriogram (image centered at the elbow) demonstrates a large pseudoaneurysm projecting off the ulner-interosseous trunk just past the origin of the radial artery. The faint streak of contrast in the soft tissues of the elbow represents early filling of the basilic vein, better demonstrated in the next image. Fig. 48.2. B. The pseudoaneurysm is well filled with contrast. Contrast also fills the basilic vein (arrow), indicating the presence of an arteriovenous fistula arising from the area of injury. Because this injury involves supply to the hand, percutaneous treatment was bypassed in favor of open surgical repair.
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Renal Insufficiency
- Iodinated contrast is nephrotoxic especially in hypotensive patients. - In select cases, use of an alternative contrast agent, such as carbon dioxide or gadolinium may be appropriate. These agents are not used routinely because image quality is inferior to that provided with standard contrast.
Coagulopathy
- Coagulation factors and platelet count should be corrected prior to arteriography in order to minimize the risk of procedure-related hemorrhage. - Prothrombin time (PT) should be less than 1.5 times control. - Partial thromboplastin time should be less than 150% of normal. - Platelet count should be greater than 50,000/ml.
Pregnancy
- Ionizing radiation should be avoided during pregnancy if possible. If, however, arteriography is necessary for the medical care of a pregnant woman, it should
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Complications
Complications of arteriography can relate to the iodinated contrast, the arterial puncture, or the internal catheter manipulation. Contrast Reaction
- Although the majority of allergic-type contrast reactions are minor and selflimited, death can occur in about 1/20,000 reactions. See table below for details regarding contrast reactions.
Incidence related to type of contrast Reaction Severity Example Ionic Nonionic
Mild Moderate Severe
Nausea / vomiting Localized urticaria Bronchospasm Diffuse urticaria Cardiovascular collapse Laryngeal edema
5% 0.5% 0.05%
1% 0.1% 0.01%
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- Major risk factors for development of a contrast reaction are a history of prior reaction, and/or reactive airway disease. - Patients with a history of a prior contrast reaction require steroid premedication prior to each contrast exposure (see above for specifics). - The use of nonionic contrast for arteriography is standard in most angiography suites. If it is not in standard use, nonionic contrast should be used in all patients at high risk for, or with a history of, contrast reaction. - Prehydration (unless contraindicated) will reduce the severity of reactionassociated hypotension. - Standard intraprocedural monitoring includes pulse oximetry, EKG monitoring, and frequent recording of blood pressure. All angiographic suites must have supplies for, and personnel experienced in, management of contrast reactions. - Patients should be instructed to notify staff if chest tightness, throat tightness, or nasal congestion occur during the procedure. Early intervention will decrease severity of a reaction.
Contrast-Induced Nephropathy
- Contrast-induced creatinine elevation is usually mild and temporary. In rare instances, however, short-term or permanent hemodialysis may be necessary for treatment. - Maintenance of adequate hydration during and after arteriography can decrease the nephrotoxic effect of contrast.
Puncture Site Complications

- At the end of a diagnostic arteriogram, the arterial catheter is removed and the arteriotomy is compressed, either manually or mechanically, for 10-15 minutes. Patients must then remain supine with the affected leg straight for 4-6 hours (2 hours for a femoral vein puncture used for pulmonary arteriography).
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- Puncture site complications include bleeding, hematoma, pseudoaneurysm, and arterio-venous fistula. In rare cases, infection can also occur. - At the femoral artery location, the incidence of significant puncture site complications (those requiring operative intervention or transfusion) is less than 1% for diagnostic arteriography. Incidence is higher (3-5%) when arteriography is followed by a percutaneous interventional procedure such as embolization or vessel recanalization. This increase in risk relates to increased catheter diameter, increased procedure time, and increased need for intraprocedural anticoagulation. - Several puncture site closure devices have become commercially available recently. These devices are inserted through the percutaneous puncture tract at the end of the arterial procedure to plug the tract and/or to close the arterial defect. Use of these devices is proliferating rapidly. Their role in the management of trauma patients has not yet been determined. - Risk factors for the development of puncture site complications include hypertension, coagulopathy, underlying atherosclerotic disease, inadequate postprocedure compression of the puncture site, and inability of the patient to cooperate with instructions to remain immobile. - Pseudoaneurysm at the puncture site can be treated by ultrasound-guided compression of the pseudoaneurysm, with or without direct thrombin injection. - An arterio-venous fistula manifests as a palpable thrill at the puncture site. The diagnosis can be confirmed with ultrasound. Many small AVFs close spontaneously. Those that persist may be managed with percutaneous embolization or surgical ligation.
Complications of Intra-arterial Catheter Manipulation Intravascular injury can occur as a result of catheter and guide-wire manipulations. Types of injury include rupture, dissection, intramural hematoma, thrombosis, and nontherapeutic embolization of thrombus. Scrupulous technique, a large selection of catheterization equipment, and high quality imaging are required to avoid these injuries. In a dedicated angiographic laboratory, incidence of catheterrelated complications is less than 1% for diagnostic arteriography and is about 5% for more complex interventional procedures. Most catheter-related complications are recognized during the angiographic procedure and can be managed immediately by percutaneous means. Complications Specific to Pulmonary Arteriography
- Acute right heart failure - Cardiac arrhythmiaincluding right bundle branch block, ventricular tachycardia, ventricular fibrillation, and asystole.
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Periprocedural Care Issues

Postprocedure care should include:
- Bed rest keeping the leg with the puncture site straight. - If an upper extremity arterial access site was used, the affected arm should be kept at rest for 24 hours. - Frequent vital signs, puncture site checks and peripheral pulse examinations for the first 24 hours. A typical protocol is to assess the patient at 15 minute intervals for one hour, 30 minute intervals for 1 hour, 1 hour intervals for 2 hours, and 4 hour intervals for 20 hours. Outpatients can be discharged at 4 hours and followed with a phone call at 24 hours. - Maintenance of hydration.
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Therapeutic Embolization (Figs. 48.3-48.5) Definition and Embolic Materials

Therapeutic embolization refers to the intentional occlusion of blood vessels using percutaneous transcatheter techniques under fluoroscopic guidance. A variety of embolic materials are available; choice of embolic agent varies with indication and operator preference. In the trauma patient, the most commonly used embolic agents are oxidized cellulose sponge (Gelfoam), polyvinyl alcohol sponge (PVA, Ivalon), and metallic coils. Their characteristics are noted below. Gelfoam Gelfoam is supplied in small sterile sheets. For intra-arterial application, the material is cut into tiny (about 1 mm) cubes. The interventional radiologist suspends the cubes in contrast and injects them into the arterial tree under fluoroscopic guidance. The cubes move with arterial flow until they lodge in a branch roughly equivalent to their diameter. The level of embolization can be controlled in a rough manner by increasing or decreasing the size of the cubes.
- Gelfoam is a temporary embolic agent. The material will become phagocytized, and the vessel will recanalize in about 5-10 days. Gelfoam is frequently used to treat diffuse posttraumatic hemorrhage, such as is seen with pelvic fractures, where the goal is to stop hemorrhage quickly without creating long term vascular compromise.
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Polyvinyl Alcohol Sponge Polyvinyl alcohol sponge is the material out of which kitchen sponges are made. Medical grade PVA is supplied in 1cc vials of sized particles that range in diameter from 50-1200 microns. For injection, the interventionalist suspends the particles in contrast and injects them into the arterial tree through an angiographic catheter under fluoroscopic control. Larger sizes are used typically to control hemorrhage, to act as a carrier for delivery of intra-arterial chemotherapy, and to occlude arteriovenous malformations. The smaller sizes are typically reserved for indications where tissue necrosis is a desired endpoint such as tumor embolization. The larger the particle, the more central the level of arterial occlusion.
- PVA is inert and results in permanent, or at least long-term, vessel occlusion. Recanalization can occur after weeks to months. In the setting of diffuse traumatic hemorrhage, PVA is less frequently used than Gelfoam, but may be indicated if initial Gelfoam embolization fails, or if hemorrhage recurs following initially successful Gelfoam embolization.
Metallic Coils Metallic coils are ideal for focal occlusion of a vessel at a point source of hemorrhage or injury. Coils are designed to occlude vessels that range in size from 1-15 mm in diameter. An embolization coil is made of a short segment of guidewire material that is covered with strands of Dacron fiber. The fibers are biocompatable and thrombogenic. For insertion, the coil is straightened out
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Fig. 48.3A. Mesenteric branch vessel hemorrhage due to gunshot woundsource of hemorrhage not found at exploratory laparotomy. Postoperatively, the patient had persistent hemorrhage from a left upper quadrant drain. A. Superior mesenteric arteriography demonstrates extravasation of contrast from a small mesenteric branch (arrows) in the left upper quadrant. Note its proximity to the large surgical drain in the pancreatic bed.
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48.3B. Digital subtraction subselective arteriogram done in preparation for embolization of bleeding vessel. The tip of the catheter (long white arrow) is just proximal to the site of hemorrhage. A large collection of extravasated contrast pools against the surgical drain (black arrow indicates drain). The short white arrow indicates the artery distal to the site of hemorrhage. This vessel was occluded with a series of microcoils introduced via the angiographic catheter.
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Fig. 48.4. Hemorrhage related to pelvic fracture. Embolization with Gelfoam particles. A. Early phase film during pelvic arteriogram. Note that the right-sided pelvic vessels are smaller and less well filled than those on the patients left. This finding is the result of compression by a large right sided pelvic hematoma.
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Fig. 48.4B. Later phase film during pelvic arteriogram. Multiple sites of punctate hemorrhage (black arrows) are identified in the right internal iliac arterial tree.
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Fig. 48.4C. Selective right internal iliac arteriogram done in preparation for embolization. Black arrowheads indicate the location of the angiographic catheter tip. The long black arrow demonstrates an exact site of hemorrhage from a branch of the obturator artery along the pelvic sidewall. The white arrows indicate puddles of extravasated contrast. The bleeding vessels were occluded with Gelfoam particles to provide temporary occlusion.
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Fig. 48.5. Hemorrhage related to femur fracture. Embolization of the deep femoral artery with metallic coils. A. Following internal fixation of a right femur fracture, this patient developed a rapidly expanding thigh hematoma. Deep femoral arteriography (white arrowheads indicate location of catheter tip) demonstrates extravasation of contrast (white arrows) from a muscular branch vessel in close proximity to the site of fracture.
48.5B. In preparation for embolization, the catheter has been advanced into the bleeding branch (arrowheads indicate location of catheter tip). White arrows indicate pooling of extravasated contrast from the lacerated vessel.
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48.5C. Final arteriogram following occlusion of the bleeding vessel with multiple metallic coils. Arrows indicate coils. Arrowheads indicate catheter tip. Note absence of extravasated contrast.
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to allow its passage through an angiographic catheter. The device regains its predetermined coil shape as it emerges from the tip of the catheter. In order to use coils, the interventionalist must advance the catheter to the exact site of intended coil deposition. The coil is deployed under fluoroscopic guidance. The diameter of the coil should be slightly greater than that of the vessel so that radial forces will keep it in stable position.
- Metallic coils are made of either stainless steel or titanium. They are visible on plain radiographs. They will not cause electronic metal detectors to alarm because they are so small.
Other A variety of other materials are used for therapeutic vascular occlusion. They include detachable balloons, new particulate materials, liquid sclerosants (e.g., absolute alcohol), and glue. None of these agents are widely used to treat trauma patients.
Indications
Hemorrhagewhen surgical intervention has failed, or in situations where surgical intervention is associated with an unacceptably high risk of failure, morbidity and/or mortality. In most instances, hemorrhage requiring percutaneous embolization is the result of bony fracture, nonpenetrating trauma with solid organ fracture, or penetrating trauma due to gunshot wound or knife wound. Examples include:
Intraperitoneal hemorrhage resulting from hepatic or splenic injury. Retroperitoneal hemorrhage from renal or muscular injury. Pelvic hemorrhage related to pelvic fracture. Muscular hemorrhage of the upper or lower extremities related to penetrating trauma or fracture.
Interventional Radiology in the Care of the Trauma Patient - Facial hemorrhage related to fracture.
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Vascular injuryTraumatic arterio-venous fistula, pseudoaneurysm, or dissection may benefit from embolization. Prophylactic EmbolizationProphylactic embolization of both internal iliac arteries may be used to control an expanding retroperitoneal hematoma associated with pelvic fracture even if no clear bleeding site can be found.
Contraindications
All contraindications to arteriography apply also to therapeutic embolization. Inability to safely deliver embolic agent to the desired location is a contraindication to therapeutic embolization. The most common reason for this is technical inability to thread the angiographic catheter into a peripheral enough, and/or stable enough, position. With modern microcatheters and guidewires, this problem is relatively rare.
Complications
All complications of arteriography apply also to therapeutic embolization. Target organ ischemia can occur if the site of arterial occlusion is peripheral to all collateral arterial supply. This problem is unusual in trauma patients because the embolic materials used in this setting occlude vessels at the small artery level; most organs have rich collateral networks beyond this level.
- Organ ischemia is most likely when liquid sclerosing agents or extremely small embolic particles (< 150 micron diameter) are used. Organ ischemia is rare following embolization with Gelfoam cubes or PVA particles greater than 250 micron in diameter. - Risk factors for development of organ ischemia are embolization of the small bowel or colon, diabetes, atherosclerotic disease and previous radiation therapy to the region. - Focal organ ischemia is expected following renal embolization. This is welltolerated in patients with normal baseline renal function. - Focal organ ischemia may lead to infection and abscess formation. This is of particular concern following splenic embolization.
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Nontarget Embolization Nontarget embolization occurs when embolic material is deposited in an unintended location. Nontarget embolization may or may not result in organ ischemia. Nontarget embolization is most frequently the result of technical error.
- Nontarget embolization to the lungs occurs when embolic material passes through an arterio-venous fistula.
Postembolization Syndrome Postembolization syndrome consists of fever, nausea, and pain referable to the site of embolization. Leukocytosis may also occur. The syndrome is the result of organ ischemia. It typically resolves in 24-48 hours. It is seen infrequently in trauma patients; it is much more common following embolization of hepatic or renal tumors where tumor necrosis is the intention of the procedure.
- Note that on cross-sectional imaging, gas bubbles are commonly present in the embolization bed. They are the result of tissue necrosis and do not correlate with the presence of infection.
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Preprocedure preparation should include:
- An intravenous prophylactic dose of broad-spectrum antibiotic.

- All postprocedure care measures listed for diagnostic arteriography. - Serial hematocrit determination. Falling hematocrit may signal a need for repeat embolization, a need to search for a new site of hemorrhage, or a need for surgical intervention. - Monitoring for (and possible management of ) postembolization syndrome and/ or infection. See complications above for details of postembolization syndrome.
Stents and Stent-Grafts (Fig 48.6) Definition

An intravascular stent is a tubular metallic mesh scaffold that is designed to buttress open a diseased blood vessel. It is most commonly used to treat symptomatic arterial stenoses related to atherosclerotic occlusive disease. Stents come in a variety of diameters and lengths; they can be inserted percutaneously. They have been in widespread use since about 1990.
- A stent-graft is a metallic vascular stent that is covered or lined with biocompatible fabric such as polytetrafluoroethylene. The fabric acts as a physical barrier between the intraluminal and extraluminal space. - Although not yet FDA approved for treatment of traumatic vascular injury, the use of stent-grafts for management of arterial trauma is rapidly gaining acceptance in the clinical community.
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Evolving Indications
Traumatic DissectionParticularly in locations with difficult surgical access such as the intrathoracic carotid artery or the vertebral artery. PseudoaneurysmA stent-graft will exclude the pseudoaneurysm from arterial flow and result in thrombosis. Arterial RuptureA stent-graft will seal the rupture. Arteriovenous FistulaA stent-graft will occlude the fistulous communication between artery and vein
Evolving Contraindications
All contraindications to arteriography apply also to stent and stent-graft placement. Vessel size that is too small to accommodate an implanted device. Minimum arterial diameter for stent and/or stent-graft placement is currently 6 mm. Vessel size that is too large for available devices. Stents and stent-grafts can be custom-made but there is rarely the luxury to wait for this step in the acutely injured patient. Technical factors related to arterial anatomy. Vessel tortuosity and proximity of the lesion to critical branch vessels may make stent placement impossible or extremely high risk. Ongoing bacteremia which could seed on the device and result in endarteritis.
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Fig. 48.6. Subclavian artery pseudoaneurysm resulting from iatrogenic injury. Treated with covered stent placement. A. A subclavian arteriogram was performed to evaluate a pulsatile mass at the base of the right neck following a failed attempt at dialysis catheter placement. This early arteriogram film demonstrates narrowing of the subclavian artery (SC) and faint filling of a large vascular space (black arrows). BC = brachiocephalic artery; C = carotid artery; V = vertebral artery.
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48.6B. Late phase film from the same arteriogram demonstrates the large pseudoaneurysm more clearly (black arrows).
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Fig. 48.6C. A Palmaz stent covered with a short segment of 4 mm diameter PTFE graft material was deployed across the arterial defect. On this final arteriogram, arrows indicate the ends of the stent-graft. Note that the vertebral, carotid, and subclavian arteries remain patent. The pseudoaneurysm no longer fills with contrast. Black arrow indicates a small embolization coil deployed in the proximal thyrocervical trunk. This was placed to prevent backfilling of the pseudoaneurysm which arose in close proximity to that branch vessel.
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Fig. 48.6D. Follow-up arteriogram done 4 months after stentgraft placement demonstrates durability of the result. Black arrows indicate ends of the stent-graft. SC = subclavian artery; C = Carotid artery; white arrow = embolization coil; RT = right.
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Fig. 48.7. Pulmonary angiogram and inferior vena cavagram performed in preparation for vena cava filter placement. A. Left pulmonary arteriogram demonstrates a large acute embolus (upper margin outlined by white arrows) in the descending pulmonary trunk. A smaller more distal embolus is also noted (black arrows).
Complications
All complications of arteriography apply to stent and stent-graft placement. Device misdeployment Device migration Device infection Device thrombosis Device leakThis complication is specific to stent-grafts where exclusion of extravascular pathology is a desired endpoint.
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- An intravenous prophylactic dose of broad-spectrum antibiotic. - Imaging studies to allow complete and accurate characterization of the arterial lesion and the artery size. In addition to arteriography, computed tomography and intravascular ultrasound may be necessary for treatment planning.

- All postprocedure care measures listed for diagnostic arteriography. - Immediate follow up physical examination and imaging to assess vessel patency and to confirm that underlying lesion has been adequately treated. - Delayed follow up assessment to ensure that treatment is durable.
Vena Cava Filter Placement (Figs. 48.7, 48.8) Definition and Overview of Devices
Vena cava filters are percutaneously implanted devices that are used to prevent pulmonary embolism in select patients. Eighty-five to 95% of pulmonary
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Fig. 48.7B. Contrast cavography demonstrates that the inferior vena cava is patent without filling defect or evidence of anatomic anomaly. Caval diameter just below the renal veins is 21.2 millimeters, which is appropriate for any design of filter placement.
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emboli arise in the iliofemoral veins; therefore, most vena cava filters are placed in the inferior vena cava (IVC). Hence the common designation IVC filter. The filters can be used, however, in the superior vena cava to trap thrombi originating in the upper extremities. The devices are made from a variety of metals including stainless steel, titanium, and nitinol (a nickel-titanium alloy). They are deployed in the vena cava under fluoroscopic guidance and assume their functional shapes upon release from their deployment systems. Four filters are FDA-approved for use in the United States. All are permanent and all are associated with roughly equivalent efficacy and complication rates. All may be inserted from the jugular or femoral approach. Temporary filters, designed for patients at temporary risk for pulmonary embolism, are under investigation. The four vena cava filters available in the United States are:
- Greenfield filter (Boston Scientific Inc., Natick, MA). This is the oldest filter design, introduced into clinical use in about 1975. The design resembles the skeleton of a badminton birdie or an umbrella. There are actually three variations of the Greenfield filter available currently: the original 24 Fr design, a 12 Fr titanium version and a 12 Fr stainless steel version. - LGM filter (also known as the Venatech filter) (Braun/Vena-Tech, Evanston, IL). This filter is similar in design to the Greenfield filter but its ribs are flat rather than round and its introducer system is slightly smaller. In addition, it incorporates vertical struts peripherally to prevent tilting. - Birds Nest filter (Cook Inc., Bloomington, IN). This filter consists of two V-shaped struts that anchor the device to the caval wall. In between the struts is a nest of tiny metal wires. This filter design allows placement in vessels up to 4 cm in diameter; the other designs are limited to vessels less than 2.8 cm in diameter.
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Fig. 48.8. Radiographic appearance of four types of vena cava filter available in the United States. All are in position in the IVC below that level of renal veins. A. Stainless steel over-the-wire Greenfield filter. Arrows indicate location of filter feet. Density where the filter legs join is termed the filter nose.
48.8B. LGM Venatech filter. Arrowhead indicated filter nose. White arrows indicate location of filter base. Black arrow indicates the upper end of one of the lateral struts which serve to minimize tilting of the filter within caval lumen.
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- The Simon-Nitinol filter (C.R. Bard, Inc., Covington, GA). This filter consists of two sequential filtering cones. It has a very flexible 7 Fr introducer system, which may be inserted from a peripheral upper extremity vein.
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48.8C. Birds nest filter. Only the V-shaped struts are visible on most radiographs. The upper strut lies with its feet (black arrows) pointed towards the patients head and its apex (black asterisk) pointed towards the patients feet. The lower strut lies in the opposite orientation with feet (white arrows) pointed caudally and the apex (white asterisk) pointed cranially. Anchoring barbs are located on each filter foot. In between the struts lies a nest of fine stainless steel wire that is not discernible on this image.
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48.8D. Simon-nitinol filter. This filter has two levels of filtration: An upper mushroom (black arrow) and a lower cone that is similar in design to the Greenfield filter. The base of the lower cone is indicated with the white arrow. White arrowhead indicates the filter apex.
Technical Points
Contrast cavography is required prior to filter deployment to exclude variant renal vein or caval anatomy and to identify intraluminal thrombus. The presence of either may impact the filter deployment site. Pulmonary arteriography may be performed immediately prior to, and through the same venous access site, as filter placement.
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Indications
Deep venous thrombosis and/or documented pulmonary embolus plus any of the following:
- Contraindication to anticoagulation - Failure of anticoagulation as manifested by progression of a DVT or recurrent PE while on adequate anticoagulation. - Complications of anticoagulation such as stroke, gastrointestinal hemorrhage, spontaneous retroperitoneal hematoma, adrenal hemorrhage, heparin-induced thrombocytopenia, and coumadin-related fat necrosis.
Prophylaxis against pulmonary embolism in patients at high risk for development of lower extremity deep venous thrombosis. This indication is highly relevant to the trauma patient population because pulmonary embolism is one of the most common causes of unexpected death in this group of hospitalized patients. Predisposing factors include:
Multiple, severe, long bone fracture Complex, pelvic fracture Spinal cord injury Severe, closed head injury Any other combination of injuries likely to result in prolonged immobilization
Contraindications
All relative contraindications to arteriography apply to vena cava filter placement.
- Note: vena cava filter placement can usually be accomplished safely in coagulopathic patients using small profile devices from the internal jugular or upper extremity approach.
Absence of venous access to the desired filter deployment site due to chronic or acute venous occlusion. Insufficient length of patent cava for deployment. In the inferior vena cava, this can occur with acute or chronic IVC occlusion that extends up to the hepatic veins.
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Complications
All complications of arteriography apply to vena cava filter placement. Recurrent pulmonary embolism despite a properly functioning filter. This occurs in 2-5% of patients with IVC filters. Chronic lower extremity swelling occurs in 5% of patients with IVC filters. Filter misdeployment. This occurs as a result of technical error. Filter migration. When IVC filters migrate, it is usually towards the iliac vein confluence away from the heart. Migration into the heart, however, has been reported. Percutaneous retrieval of migrated filters is possible. Filter fracture. This occurs rarely as a result of chronic mechanical stress. Penetration of filter legs through the caval wall into aorta or bowel has been reported as a rare complication of some filter types. Pneumothorax occurs in less than 1% of procedures done from a jugular vein access site when venous puncture is performed using real-time ultrasound guidance.
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- All preparation measures noted for diagnostic arteriography.

- All postprocedure care measures listed for diagnostic arteriography. - The head of the bed should be elevated at least 30 during the initial bed rest period if the jugular vein approach was used for filter placement. - Supplying the patient with a wallet card identification card for the filter that has been implanted. - Clear indication in the medical record of the presence and location of a caval filter.
Imaging-Guided Vascular Access and Associated Venous Interventions (Fig 48.9)

During the initial management of an acutely injured patient in the emergency department environment, imaging guidance for vascular access is rarely necessary. However, during prolonged hospitalization, central venous access sites can thrombose and/or become progressively difficult to catheterize. When this happens, use of imaging guidance in the interventional radiology suite can increase the likelihood of success and decrease the complication risk of vascular access catheter placement.
Catheter Types and Indications

Note that a wide variety of catheter material, sizes and designs are available. Detailed discussion of each is beyond the scope of this text. General classes of venous access catheters are noted below. All are designed to lie with their tips in the central vena cava. Standard Central Venous Catheter (CVC)
- Access sites: internal jugular, external jugular, or subclavian vein.
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Peripherally Inserted Central Catheter (PICC)

- Access sites: antecubital, basilic, cephalic, or brachial vein. - Indications: intermediate term (1-20 weeks) venous access. - Role of peripheral access: to decrease risk of infection.
Tunneled Central Venous Catheter (i.e., Hickman and Broviac catheters)

- Access sites: internal jugular, external jugular, or subclavian vein. - Indications: long-term venous access where clinical care requires frequent infusion encounters for delivery of medication, hydration, and/or hyperalimentation. - Role of the tunnel: to stabilize the catheter via a tissue ingrowth cuff and to decrease risk of infection requiring catheter removal.
Contraindications
Coagulopathysee angiography section for guidelines regarding management of coagulopathy. Ongoing bloodstream infection. Placement of a permanent central venous catheter should be postponed until the patient has been on antibiotics for a minimum of 48 hours and blood cultures are negative for bacterial growth. Central venous occlusionsee below for associated procedures. Known allergy to central venous catheter material. Central venous catheters are made of either silicone or polyurethane. If a patient has a sensitivity to one of the materials, care must be taken to use the alternate type of catheter.
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Fig. 48.9. Foreign body retrieval: PICC catheter fragment in pulmonary arterial tree. A. Portable chest x-ray demonstrates a long catheter fragment in the pulmonary vascular tree. One end of the fragment lies in a peripheral right pulmonary arterial branch (indicated by two white arrows). The other end of the fragment lies in the descending left pulmonary artery (indicated by single white arrow).
Note: iodinated contrast is rarely required for central venous catheter placement. Therefore, neither allergy to contrast, nor renal insufficiency, is a contraindication to image-guided venous access catheter placement.
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Associated Venous Procedures

Foreign body retrieval: Guidewire and/or catheter fragments can be retrieved from central venous circulation, heart or pulmonary arterial tree using fluoroscopic guidance and angiographic snares. Fibrin sheath stripping: Central venous catheters frequently become coated with a thin layer of fibrin that may prevent aspiration through the catheter and limit infusion. It is possible to prolong the life of these catheters by using an intravascular snare to strip the fibrin off the catheter. This procedure requires fluoroscopic guidance but no contrast. The fibrin sheath embolizes to the lungs. This is well-tolerated in most people occasionally a patient will experience focal self-limited chest pain. Most patients have no symptoms related to the procedure. The procedure should be avoided in patients with limited pulmonary reserve or pulmonary hypertension. Thrombolytic therapy: Acute central venous thrombosis can be treated with catheter directed lytic therapy if clinical symptoms warrant aggressive intervention. The major risk of this therapy is hemorrhage. Central venous angioplasty: Central venous stenosis can result in debilitating symptoms such as chronic lower extremity swelling and SCV syndrome. Central venous stenosis can also result in poorly functioning dialysis grafts and
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Fig. 48.9B. Midportion of the retained catheter fragment has been snared (white arrow). The catheter is in the process of being retracted into the inferior vena cava. Black arrows indicate the ends of the catheter fragment.
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Fig. 48.9C. The catheter is being pulled down the inferior vena cava (arrow). It was removed via a femoral vein sheath without complication.
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limit usable venous access sites. Balloon angioplasty can result in temporary or permanent improvement in central venous luminal area. Central venous stent placement: Permanent stent placement is indicated for symptomatic central venous stenoses that do not respond to balloon angioplasty or recur following balloon angioplasty. Risks are the same as those for arterial stent placement.
Nonvascular Drainage Tube Placement (Figs. 48.10, 48.11) Definition

Drainage tubes may be placed percutaneously, using imaging guidance into fluid collections, the renal collecting system, and the biliary tree. Gastric and transgastric jejunal feeding tubes can be placed in a similar fashion. Although there are a wide variety of tubes available, they share several common characteristics: all are made of flexible polyurethane-like material that allows for a thin-walled design; all are designed to track over an angiographic guidewire; all are designed with internal fixation devices, such as pigtails, to help guard against dislodgement; and all have multiple sideholes to facilitate drainage or infusion. Diameters range from 614 French. Imaging guidance modalities for insertion include fluoroscopy, CT, ultrasound used alone or in combination.
Indications
Indications noted below are specific to trauma patients. Other indications for percutaneous tube placement exist but are not pertinent to this population. Fluid Collections: The most common indication for drainage tube placement in trauma patients is intra-abdominal or pelvic abscess occurring as a delayed complication of injury. Other fluid collections, such as lymphocele, urinoma, biloma, empyema, and infected pancreatic pseudocyst are also amenable to percutaneous drainage. Renal Collecting System: Percutaneous nephrostomy is indicated to control traumatic upper urinary tract leak or to drain upper urinary obstruction. Gastrointestinal Tract: Long term enteric nutritional support is required by many severely injured patients. Percutaneous fluoroscopically-guided gastrostomy or gastrojejunostomy tube placement is one of several ways to secure long-term stable access to the gastrointestinal tract for feeding. This method may be preferred for patients who have contraindications to general anesthesia, per-oral endoscopy, or abdominal surgery. Percutaneous gastrostomy may also be performed to decompress gastric or small bowel obstruction.
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Contraindications
Lack of a safe percutaneous access route to the target site. Coagulopathy. Allergy to iodinated contrast Ascites, peritoneal dialysis, ventriculo-peritoneal shunt. Although not absolute contraindications to percutaneous tube placement, the presence of ascites, or an intraperitoneal medical device, increases the risk of immediate and delayed complications in instances where the tube traverses the peritoneal cavity.
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Fig. 48.10. Biliary leak following motor vehicle accident. Existence of bile leak was noted at exploratory laparotomy but site of ductal injury could not be identified. Therefore, two subhepatic Jackson-Pratt drains were placed. Postoperatively, a percutaneous transhepatic biliary drainage tube was placed. A. Scout film from biliary drainage tube injection. Black arrows indicate the percutaneous transhepatic drainage tube. JP drains lie adjacent to it. White arrowhead indicates a Dobhoff tube.
Fig. 48.10B. Cholangiogram. The biliary drainage tube is now filled with contrast (black arrow). Contrast fills intrahepatic ducts (left ducts are indicated with black arrowheads). Contrast extravasates from the central left duct (white arrow); some of it drains into the JP drain. The leak healed over a 4 week period.
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Fig. 48.11. Ureteral laceration with urinoma. A. CT scan demonstrates a large fluid collection along the right psoas muscle. A needle has been placed in the collection (arrow) in preparation for drainage tube placement. Fluid had high creatinine level.
Complications
Immediate complications
- Hemorrhage - Sepsis - Nontarget organ injury
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Delayed Complications
- Tube blockage, fracture, or dislodgment. Tubes that will be in place for a prolonged period of time should be changed electively at regular intervals to minimize the risk of tube-related complications. Reasonable tube change intervals are: Biliary drainage tube Nephrostomy tube Gastrostomy tube Gastrojejunostomy tube Fluid collection tube 6-8 weeks 12-14 weeks 9-12 months 12-16 weeks 4-6 weeks
- Cellulitis: Cellulitis, or more severe infections, at the tube insertion site can be prevented by optimizing skin care. Treatment of an insertion site infection may require local, oral, or intravenous antibiotic care depending on severity. Surgical drainage and/or tube removal may also be required in severe cases.
- Granulation tissue. Granulation tissue at a site of tube insertion can be minimized by stabilizing the position of the external portion of the tube. It is treated with silver nitrate cauterization. - Tract erosion. The diameter of a percutaneous tract can enlarge beyond that of
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Fig. 48.11B. Antegrade pyelogram following right percutaneous nephrostomy demonstrates ureteral transection with urine leak (black arrow). A percutaneous nephrostomy tube has been inserted into the kidney via a lower pole calyx. White arrow = localizing needle in the renal pelvis used to inject contrast to guide tube placement. Arrowhead = urinoma drainage tube. Although the drainage tubes controlled the leak temporarily, this ureteral injury required operative repair.
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the tube going through it. The risk of this problem is minimized by ensuring that the tube remains in stable position, and functions properly. If tract erosion occurs, placement of a larger diameter tube may be required to prevent pericatheter leakage of bodily fluid. In severe cases, tube removal may be necessary to allow healing of the tract.
References
1. 2. 3. 4. 5. 6. Kandarpa K, Aruny JE, eds. Handbook of Interventional Radiologic Procedures. Boston: Little, Brown & Co., 1996. Ben-Menachem Y. Angiographic control of hemorrhage in trauma. In: Coldwell D, ed. Radiologic Interventions: Embolotherapy. Baltimore: Williams & Wilkins, 1997; 6-60. McArthur CS, Marin ML. Stent-Grafts for Vascular Trauma. In: Dolmatch BL, Blum U, eds. Stent-grafts. Current Clinical Practice. New York: Thieme, 2000. Savader S, Ronsivalle JA. Permanent inferior vena cava filters. In: Savader S, Trerotola SO, eds. Venous Interventional Radiology with Clinical Perspectives. New York: Theime, 1996. McDermott VG, Schuster MG, Smith TP. Antibiotic prophylaxis in vascular and interventional radiology. Am J Roentgen 1997; 169:31-38. King BF Jr. Intravascular contrast media and premedication. In: Bush WH, Kreck KN, King BF Jr, Bettman MA, eds. Radiology Life Support. London: Arnold, 1999.
Minimally Invasive Surgery in Trauma

James A. Murray Introduction
Minimally invasive surgery is a useful diagnostic and therapeutic tool in a small group of selected patients with blunt or penetrating trauma.
Laparoscopy in Trauma History

Heselson in 1963 described laparoscopic evaluation of penetrating abdominal trauma and its use in avoiding negative laparotomies.
Indications
Penetrating left thoracoabdominal trauma for suspected diaphragmatic injuries, in a hemodynamically stable patient with no signs of peritonitis.
- The incidence of diaphragmatic injury in gunshot injuries to the left thoracoabdominal area and no peritoneal signs is about 13%. In stab wound it is about 26%. - Laparoscopic repair of a diaphragmatic injury may be performed with staples or sutures.
Penetrating injuries to the anterior right thoracoabdominal area

- Although the liver protects against herniation in posterior and lateral right diaphragmatic injuries, anterior injuries are not adequately protected and herniation may occur.
Tangential gunshot wounds to the abdomen in the absence of signs of peritonitis in order to evaluate peritoneal evaluation. This is not a generally accepted indication because peritoneal violations is not necessarily associated with significant intra-abdominal injury requiring surgical repair. Blunt torso trauma in a hemodynamically stable patient with a persistently elevated diaphragm, in order to rule out diaphragmatic rupture. Laparoscopy has also been used to detect intraperitoneal bleeding and solid organ injuries. These indications have not gained popularity and have limited or no practical use. In ICU critically ill patients with suspected acalculous cholecystitis. For diagnosis and repair of delayed diaphragmatic hernias.
Limitations
Laparoscopy has major limitations in detecting hollow viscus perforations, pancreatic and other retroperitoneal injuries.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. James A. Murray, Division of Trauma and Critical Care, Keck School of Medicine of the University of Southern California, Los Angeles, California, U.S.A.
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In the presence of associated severe head trauma, abdominal insufflation may increase the intracranial pressure. Laparoscopy in this condition is relatively contraindicated.
Technical Aspects of Laparoscopy

Laparoscopy has been performed at the bedside in the emergency room under local anesthetic with intravenous sedation. It has not gained significant popularity because it is usually painful and the small scopes used do not provide adequate visualization of the diaphragm. Most centers perform laparoscopy in the operating room because it has the following advantages.
Able to perform both diagnostic and therapeutic procedures Able to rapidly convert to laparotomy Additional ports may be placed for retraction and better visualization Larger scopes may be used for better visualization Better positioning of the patient allows maximal visualization
Patient Positioning
- After placement of the trocars the bed can be rotated with the affected side up to allow better inspection of the area of concern. - Reverse Trendelenburg position allows for better inspection of the diaphragm. - The site of the injury should be prepped into the field, By pushing on the injury site the surgeon can identify the corresponding intra-abdominal region. - The ipsilateral thorax should be prepped in the event a thoracostomy tube is required.
Port Placement
- A supraumbilical port (1-5 cm above the umbilicus) or occasionally one in the upper quadrant allows better visualization of the upper abdomen and the diaphragm especially for lateral and posterior thoracoabdominal wounds.
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Pneumoperitoneum
- The pneumoperitoneum can be induced with either a Veress technique or open technique depending on the surgeons preference. - The patient should be closely monitored during insufflation of the abdomen. If a defect in the diaphragm is present a tension pneumothorax may rapidly develop. The surgeon and anesthesiologist should be communicating closely during this time. Signs of a tension pneumothorax include: Hypotension, tachycardia, hypoxemia, elevation of peak airway pressures, reduction of tidal volumes, if pressure control ventilation is being used. - The development of a tension pneumothorax requires immediate release of the pneumoperitoneum and decompression of the thoracic cavity with a thoracostomy tube. - Once the thoracostomy tube is in place, insufflation may be reattempted. Occlusion of the defect in the diaphragm will be necessary in order to achieve sufficient pneumoperitoneum and can be achieved by initially using slightly lower insufflation pressures to allow placement of a second port. A Babcock forceps can be used to grasp the defect and occlude it. If a pneumoperitoneum cannot be maintained, conversion to a gasless technique is possible if the appropriate retractors are available, but a laparotomy may be necessary.
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Laparoscope
- A 0 laparoscope provides adequate visualization for most diagnostic procedures, especially for anterior injuries. - For posterior and lateral wounds or therapeutic procedures a 30 angled scope provides better visualization, especially in the recesses above and behind the spleen and liver.
Thoracoscopy in Trauma
History
- Branco in 1946 used thoracoscopy to evaluate penetrating thoracic injuries.
Patient selection
- The patient must be hemodynamically stable. - Due to the need for double-lumen intubation, the patient must be able to tolerate single-lung ventilation. - In patients with an obliterated pleural space, thoracoscopy is contraindicated.
Indications
In selected cases with suspected diaphragmatic injury
- Posterior diaphragmatic injuries are better visualized by thoracoscopy than laparoscopy - Laparoscopy is preferable during the acute phase because it offers the advantage of evaluation of the intra-abdominal cavity. - Diaphragmatic repair may be performed with staples or sutures
In cases with suspected delayed diaphragmatic hernias

- Reduction of the hernia and repair of the defect may be performed thoracoscopically.
Assessment and possibly control of ongoing slow intrathoracic bleeding

- The patient should be hemodynamically stable. - A pericardial window may be performed. - Bleeding from the thoracic wall or the lung may be controlled with electrocautery or hemoclips.
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Evacuation of a retained hemothorax

- The evacuation ideally, should be performed within 3-5 days after the injury, before clot organization takes place.
Decortication for posttraumatic empyema or lung entrapment due to fibrothorax.
Thoracoscopy versus Laparoscopy

Many advantages and disadvantages are present when comparing thoracoscopy and laparoscopy for evaluating patients with occult diaphragmatic injuries. Advantages of thoracoscopy over laparoscopy:
Avoids the potential complication of a tension pneumothorax. The posterior aspect of the diaphragm may be better visualized. Residual blood may be evacuated from the thorax. Repair of the diaphragm may be technically easier.
Disadvantages of thoracoscopy over laparoscopy

- Requires double lumen intubation to allow the lung to be collapsed. - Due to the concern about an intra-abdominal injury, if a diaphragmatic injury is present the abdomen must be evaluated with either laparoscopy or laparotomy.
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Technical Aspects
Due to the rigidity of the thorax insufflation is not required. Both thoracoscopic and standard open instruments can be used for thoracoscopy. In order to obtain maximal visualization of the thoracic cavity the ipsilateral lung needs to be deflated. This usually requires a double lumen endotracheal tube for intubation. Patient Positioning
- Generally the patient is positioned in the full lateral decubitus position. Preparations should be made in the event a posterolateral thoracotomy is necessary
Port Placement
- If a chest tube is present this site can be used for the initial port and allows evaluation of the thoracic cavity prior to placing subsequent ports. - In the absence of a chest tube the first port can be placed in the sixth or seventh intercostal space in the midaxillary line. - Once the thoracic cavity is inspected additional ports can be placed higher in the chest, typically in the third or fourth intercostal spaces in the anterior and posterior axillary lines. - If possible some of the ports can be placed to allow incorporation into a thoracotomy incision. - By rotating the camera between each port, full inspection of the thoracic cavity is possible.
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- A 0 scope can be used but a 30 angled scope provides better visualization of the costophrenic recesses. - After evacuation of residual clots the thoracic cavity can be fully inspected. By moving the camera and instruments between each port, all areas of the thoracic cavity can be inspected and accessed for therapeutic procedures. If difficulty is encountered or an area is not fully accessible, additional ports should be placed. This should allow evacuation of all retained clots, control of hemorrhage, repair of diaphragmatic injuries and inspection of the pericardium and pericardiotomy. - Chest tubes can be positioned under direct thoracoscopic visualization. - Upon completion of the procedure the lung should be inspected to insure it inflates properly.

Laparoscopy may miss hollow viscus perforations. During abdominal insufflation in the presence of a diaphragmatic injury there is a risk of tension pneumothorax. Close monitoring of the blood pressure, heart rate, Sa02 , and airway pressures are critical.
References
1. 2. Fabian TC, Croce MA, Stewart RM et al. A prospective analysis of diagnostic laparoscopy in trauma. Ann Surg 1993; 217:557-565. Murray JA, Demetriades D, Asensio JA et al. Occult injuries to the diaphragm: A prospective evaluation of laparoscopy in penetrating injuries to the left lower chest. J Am Coll Surg 1998; 187:626-630.

3. 4. 5.
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Zanzut LF, Ivatury RR, Smith RS et al. Diagnostic and therapeutic laparoscopy for penetrating abdominal traumaa multicenter experience. J Trauma 1997; 42:825-829. Oschner MG, Rozycki GS, Lucente F et al. Prospective evaluation of thoracoscopy for diagnosing diaphragmatic injury in thoracoabdominal trauma: A preliminary report. J Trauma 1993; 34:704-9. Uribe RA, Pachon CE, Frame SB et al. A prospective evaluation of thoracoscopy for the diagnosis of penetrating thoracoabdominal trauma. J Trauma 1994; 37:650-654.
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CHAPTER 50
Ballistics of Gunshot Injuries

Kenneth G. Swan and K.G. Swan, Jr. Introduction
Despite the recent decrease in crime and murder rates, physicians and surgeons today still face a steady influx of patients who have been wounded by guns, many with increasing caliber1 and rate of fire, the bullets from which are more tissue destructive and potentially traveling at greater velocities. Those treating such patients should be knowledgeable about wound ballistics and the ballistic properties of modern weapons.
Explosive mixture of saltpeter, charcoal and sulfur described by Roger Bacon, 1242 Introduction of firearms in Europe in the 14th century.2 First recording of a gunshot wound by the German surgeon, Pfolspeundt, 1460 Invention of the rifle in the 15th century Alleged poisonous nature of gunshot wounds (GSW), 15th and 16th centuries Recognition that injured tissues were crushed rather than poisoned, mid 16th century Replacement of black by smokeless powder and smooth by rifled barrels, 19th century Revolver patented by Samual Colt, 1835 Machine gun introduced by Richard Gattling, 1860s Hollow nosed bullets designed and distributed from British arsenal in Dum Dum, India, 19th century Cavitation recognized as a principle in wound ballistics by Woodruff 18983 Hague Conference 1899 outlawed Dum Dum bullets, mandated copper jacketing of lead bullets in war High velocity refined and implemented (M-16 rifle, 3240 feet per second), 20th century.
Incidence
Gunshot wounds (GSW) are the eighth leading cause of death in the United States today,4 killing approximately 35,000 Americans and wounding almost ten times that number with an estimated cost to US taxpayers of four billion dollars per year.5 Although motor vehicle crashes are the leading cause of trauma deaths in the US today (44,000 per year),4 these have declined significantly in recent years whereas those from guns have not. If current trends continue, guns are predicted to be the leading cause of trauma death by the year 2003.5
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Kenneth G. Swan, Department of Surgery, UMDNJ/New Jersey Medical School, Newark, New Jersey, U.S.A. K.G. Swan, Jr., Department of Surgery, UMDNJ/New Jersey Medical School, Newark, New Jersey, U.S.A.
Ballistics of Gunshot Wounds
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Definition of Terms
Ballistics The science of the motion of a projectile through the barrel of a firearm (internal ballistics), during its subsequent flight through space (external ballistics) and during its final complicated motion after striking the target (terminal ballistics) Wound Ballistics Terminal ballistics when the target is in animal tissue Caliber Diameter of bullet/missile or barrel/bore of weapon, expressed in hundredths (two digits) or thousandths (three digits) of an inch or in millimeters Round or Cartridge (Fig. 50.1A) Casing, powder, primer and bullet Bullet (Fig. 50.1B) Missile contained in cartridge Shell Cartridge casing Muzzle Distal end of the barrel; Breech: proximal end of the barrel Muzzle Velocity Velocity of missile as it exits the muzzle of a gun Range Distance covered by fired missile (effective, maximal effective, maximal) Kinetic Energy Mass times velocity squared divided by two Dissipation of Kinetic Energy, Kinetic energy transfer equals KE impactKE exit Secondary Missiles Objects to which kinetic energy of missile is imparted in GSW Cavitation Separately covered subsequently Powder Burn Tattooing of target by incinerated powder (Fig. 50.2) Yaw (Fig. 50.3A) Deviation of base of missile (versus point) from its long axis of flight Tumbling Forward rotation of missile on its long axis of flight (Fig. 50.3B) Entrance Wound Wound of presumed entrance of missile in target Exit Wound Wound where missile presumably exited target Small Arms Pistols or rifles carried by one person Semiautomatic Weapons Weapons which chamber a round automatically. Trigger must be pulled for each round fired Automatic Weapons Weapons which fire continuously with one trigger pull Chamber Breech end of the barrel, where trigger mechanism and firing pin are located
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Fig. 50.1. A) Shotgun cartridge cutout to reveal contents: powder, wadding and pellets. B) Handgun cartridge cutout to reveal powder and bullet further cut to reveal copper jacket and lead core.
Handgun Small arm fired with one hand (pistol or revolver) (Table 50.1) Rifle Shoulder held small arm, barrel of which is grooved helically to impart spin to the bullet (Table 50.2)
Kinetic Energy (KE) and Its Dissipation or Transfer (KE)

KE = missile mass (M) x missile velocity (V) squared / 2 M = bullet weight in grains

Fig. 50.2. M-16 rifle wound of left side of soldiers chest showing entrance (powder burns) and exit wounds.
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V = bullet velocity in feet per second KE = M(VENVEX)2 / 2 EN = entrance EX = exit Wound damage correlates dissipation or transfer of kinetic energy. As exit velocity approaches zero, maximal dissipation of kinetic energy or its transfer is accomplished and maximal tissue damage for that missile occurs. Many design features alter bullet velocity within the target.
- Copper jacketing of bullets (often called full metal jacketed or military rounds) minimizes the deformation of the softer lead within the target (Fig. 50.4). - Soft pointed bullets (Fig. 50.4A) (those without a complete copper jacket) deform on impact and dissipate kinetic energy as velocity is reduced within the target. - Hollow pointed (Fig. 50.4B) (Dum Dum) bullets tend to flatten on impact and impart maximal kinetic energy transfer. - Black talon rounds (Fig. 50.5A, B) combine the properties of soft pointed
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B
Fig. 50.3. A) Yaw is the lateral movement of a projectiles base along the long axis of its flight. B) Tumbling is the forward rotation of a missile along its long axis of flight.
Table 50.1. Ballistic properties of handguns and their bullets

Caliber* Bullet Weight (Grains) 50 71 158 250 Muzzle Velocity (Ft/S) 820 910 870 860 Kinetic Energy (Ft-Lbs) 75 130 267 413
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25 32 38 45
*Size in hundredths of an inch 1grain = 60 mg. At the muzzle
Table 50.2. Ballistic properties of rifles and their bullets

Caliber* Model Bullet Weight (Grains) 40 55 122 147 Muzzle Velocity (Ft/S) 1255 3240 2300 2750 Kinetic Energy (Ft/Lbs) 141 1289 1470 2520
22 223 30 308
Long Rifle M-16 AK-47 M-14
*In hundredths (two digits) or thousandths (three digits) of an inch At the muzzle
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Fig. 50.4A. 380 caliber handgun rounds left to right copper jacketed, noncopper jacketed and hollow pointed.
and hollow pointed bullets as well as configure a partial copper jacket into symmetrical barbs with unique wounding potential.
Secondary Missiles
A primary missile (bullet) may impart kinetic energy to dense tissues such as bone or teeth and endow them with wounding potential. (Fig. 50.6) Secondary missiles also can derive from inanimate objects such as coins or dog tags found on the target. Secondary missiles of teeth must be considered when gunshot wounds to the face occur. These are infective and must be identified radiographically, particularly if lodged in the brain where brain abscess may ensue.
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Cavitation
Low velocity missiles tend to push tissue aside producing a path of injury approximating the transverse diameter of the missile (Fig. 50.6). As velocity increases kinetic energy of the missile is transmitted laterally to form within milliseconds a water vapor filled cavity at sub-atmospheric pressure. The cavity continues to enlarge even after passage of the missile causing damage well beyond the actual path of the missile (Fig. 50.6). Negative pressure within the cavity can suck air borne material such as dust and microorganisms into the wound. Cavitation is inversely proportional to the tensile strength of the target, i.e. greatest in liver, least in bone, intermediate in skeletal muscle.
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Fig. 50.4B. 223 caliber M-16 rifle rounds left to right copper jacketed and soft pointed.
Fragmentation
Low velocity missiles (<103 feet/sec) tend to retain their configuration within the target (Fig. 50.6). Very high velocity missiles* (~3 x 103 ft/sec) tend to yaw, tumble and fragment within the target (Fig. 50.6). Such fragments take erratic courses within the target and dissipation or transfer of kinetic energy is maximized as is tissue destruction.6
* Definition of high versus low velocity is imprecise. In general, handguns are considered low velocity (<103 feet per second) and rifles and shotguns high velocity (>103 feet per second). The importance of these definitions lies in a missiles greater tendency to cause cavitation and to fragment as it approaches velocities of 3 x 103 feet per second.7
Multifactorial Aspect of Wound Ballistics

No single result can be predicted with complete certainty.8 Kinetic energy dissipation, transfer, cavitation, fragmentation are all complexly inter-related.
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Fig. 50.5A. Black talon 9 mm round, side view with recovered bullet showing flattening of nose and barbs from copper jacket.
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Fig. 50.5B. Same as 5A except seen nose first
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Fig. 50.6. Schematic representation of bullet/missile traveling through target. A) Low velocity, no cavitation, entrance and exit small; B) High velocity, cavitation, entrance and exit small; C) High velocity, thinner target, larger exit; D) High velocity, large cavity, small entrance, exit may not occur; E) Higher velocity, asymmetric cavitation as bullet begins to deform, tumble and fragment; F) Deformation of bullet and creation of secondary missiles upon penetrating bone.
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Target mass and composition are added variables. Secondary missiles are neither uniform nor predictable. Wound ballistics is thus, an imprecise science in contrast with internal and external ballistics, both of which are relatively precise in mathematic expression.
Shotgun Wounds
Shotguns have smooth as opposed to rifled barrels or bores. The shotgun cartridge contains many pellets or a single slug (Table 50.3). The mass of the missile/missiles is approximately 10x that of a rifle or a handgun bullet. Muzzle velocity ~1500 feet per second Dissipation of kinetic energy in air is rapid, hence wound damage is much more dependant upon range. At close range ( 5 meters) the shotgun, regardless of pellet size, can produce a devastating wound.
Surgical Excision of Bullets: Indications

Plumbism, saturnism Embolization, migration Occasionally, a source of infection Associated foreign body (e.g., clothing) Erosion into neighboring structures Forensic concerns Stigma Phobia Longterm risk of cancer in extremity sinus tracts
Rubber and Plastic Bullets

Used in riot control to reduce wounding caused by lead Have caused skull fractures (close range), even death from brain injury Injuries from rubber bullets 4x that from plastic bullets (Northern Ireland experience)
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Pneumatic Weapons
Muzzle velocities in excess of 100 feet per second are possible. BB and pellet guns fire missiles.177 inches in diameter (18 caliber). Fatalities from brain and myocardial damage have been reported. Eye injury and loss of eyesight are relatively more common injuries. Uncommonly seen today Lead oxide within bullet tip British used fulminate of mercury, 1862 Detonation on impact Relatively high failure rate, potential danger to health care workers
Explosive Bullets
Lead Intoxication
Plumbism, Saturnism Rare but long recognized complication of retained lead bullets or their fragments
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Table 50.3. Ballistic properties of shotguns and their loads; standard shotgun cartridges
Gauge Diameter (in) Caliber Pellet or slug weight (oz) Grains #9 Pellets, 8 caliber Kinetic Energy (ft. lbs.)
410 20 12
0.410 0.615 0.729
410 615 729
0.562 0.875 1.000
070 420 480
328 512 588
385 800 2100
Location in synovial lined spaces, joints, meningeal spaces especially problematic Insidious nature, long interval between wounding and symptoms Encephalopathy, colic, anemia, proteinuria, death Diagnosis is based on elevated blood or urine levels of lead Chelation is possible, surgical removal may be necessary
Microbial Contamination of Bullet

Bullets have been thought to be heat sterilized by internal ballistics. Experimental evidence and anecdotal data indicate this is not necessarily true. Bullets should not be ruled out as possible sources of infection. Missiles which traverse the colon and lodge in muscle are especially infective.9 Missiles which deform on impact (e.g. black talon) can drag clothing into wound and cause cloth foreign body, which is highly infective. Wadding within shotgun cartridges can be driven into wounds where it is both radiolucent and infective
Bullet Embolism
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Bullets or missile fragments may enter vascular structures. Venous emboli may travel to the right heart and the lung. Venous emboli in lower extremities may fall by gravity to distal locations or lodge in valves. Arterial emboli may cause acute arterial insufficiency, necrosis and gangrene if not identified. Shotgun wounds to the chest and neck may result in pellet embolism to the brain and indicate skull radiography. Buckshot colic is caused when a shotgun pellet embolizes or erodes into a ureter
Shooting Incident
Documentation of the wounding event should be part of the medical history. Weapon: either handgun (low velocity), rifle or shotgun (high velocity). Caliber: either of weapon or its bullet Range: distance between shooter and victim Such information is usually known by the victim, witnesses or law enforcement officials.
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Medical Legal Concerns

Treating physicians and others often are careless with forensic evidence. Cut around and not through bullet holes in clothing of the victim. Save garments with bullet holes or powder burns. Submit bullets or fragments received from the victim to the Surgical Pathology Dept. Sign the base of the bullet and record the signature in the medical record. Describe number, location and size of apparent entrance and exit wounds. Indicate, if possible, entrance versus exit wounds.
References
1. 2. 3. 4. 5. 6. 7. 8. 9. Caruso RP, Jara D, Swan KG. Gunshot wounds: bullet caliber is increasing. J Trauma 1999; 46:462-465. Billroth CAT. Historical studies of the nature and treatment of gunshot wounds from the fifteenth century to the present time. Translated by CP Rhoads. Yale J Biol Med 1931-1932; 4:16-36, 119-148, 225-257. Woodruff CE. The causes of the explosive effect of modern small caliber bullets. NY Medical Journal 1898; 67:593-601. Hoyert DL, Kochanek KD, Murphy SL. National Vital Statistics Reports from the Centers for Disease Control and Prevention. National Center for Health Statistics. National Vital Statistics System 1999; 47:19. Violence in America: Public Health CrisisThe Role of Firearms. The Violence Prevention Task Force of the Eastern Association for the Surgery of Trauma. J Trauma 1995; 38:163-168. Swan KG, Swan RC. Gunshot wounds: Pathophysiology and Management, 2nd Edition. Yearbook Medical Publishers, Chicago, Illinois, 1989. Swan KG, Swan RC. Principles of ballistics applicable to the treatment of gunshot wounds. Surg Clin North Amer 1991; 71:221-239. Fackler ML. Letter to the Editor. J Trauma 1997; 43:386-387. Tzeng S, Swan KG, Rush BF. Bullets: A source of infection? American Surgeon 1982; 48:239-240.
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CHAPTER 51
Blast Injuries
Avraham I. Rivkind and Tal Luria Target Population and Environmental Characteristics
Civil casualties caused by terrorist acts are an ever-growing global problem. The contrivances, either homemade or military devices, are designed to spread death and destruction to the utmost, and to that end they rely mostly on explosives that propel metallic fragments. From the point of view of the bombmaker, blast is a desirable side effect, and in many instances it is even the primary goal. The chain of violence targeted at the innocent citizen has brought blast injuries from he battlefield to our front door.
Patterns of Injury
Explosions produce compound injuries of types that many hospitals have barely experienced. This chapter deals specifically with blast injuries, which are differentiated into four patterns of mechanism of injury, as follows: Primary mechanism injurycaused by the resultant force of the blast wave itself and by its effect on air expansion; hence, perforation of the ear drum, different types of lung and intestinal injuries. Secondary mechanism injurycaused by the wreckage, i.e., fragments of casing, metal, glass, masonry, etc. being propelled at high speed by the force of the explosion. Tertiary mechanism injurycaused by the rapid passive movement of the body by the blast wave, inflicting damages ranging from bruising to loss of limbs, severed at the site by the blast wave. Flash burns consequent on the heat generated by the explosion.
Environmental Effects
Blasts Occurring
- In wide open-air spaces: upon detonation of an explosive charge in a completely open space, the resulting blast wave strength decreases exponentially with its distance from the epicenter of the explosion, leaving most of the damage to be done by secondary and tertiary mechanisms of injury. - In closed spaces: in contrast to open-space blast injuries, the causative factor here is mainly the primary mechanism of injury, albeit closely followed by secondary and tertiary mechanisms of injury. The limiting walls reflect the shock wave, thus increasing the generating pressure and lengthening its duration. The same is applicable to flash burns. - In confined spaces: this is a new category, which was defined by us after bomb explosions in partly roofed street markets and malls. The injuries share some of
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Avraham Rivkind, Hadassah Medical Center, Jerusalem, Israel Tal Luria, Hadassah Medical Center, Jerusalem, Israel
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the characteristics of the aftermath of blasts in an open space (shrapnel wounds and severed limbs) and in closed space (ear injuries and flash burns).
- Under water: characteristically belong in the realm of explosions initiated by the military. They cause severe primary blast injuries, with little or no damage due to other mechanisms of injury. It should be borne in mind that each environment targeted for explosion carries its own particular characteristics, which run from the size of the explosive device itself and the materials used to the density of the crowd, proximity of the bystanders to the epicenter of the explosion, the type of blast-energized debris, the clothing worn by those exposed to the blast, to the ambient temperature and humidity. All these factors affect the preponderance of specific wounds.
Specific Mechanisms of Injury Primary Blast Injuries

This type of injury affects vital parts of the body, as follows: EarThe tympanic membrane is a very delicate structure that is liable to suffer injuries from rather low blast forces. Clinical signs are tinnitus, deafness, bleeding and/or perforation. LungBecause of the expanding nature of the alveoli, quite high pressures are needed to cause blast injury to the lungs. Most lung injuries will therefore be seen in conjunction with multiple shrapnel wounds, limb(s) severed by the blast itself, moderate to severe burns and fractures, with clinical appearance of tachypnea and dyspnea that must be verified by chest X-ray and objective evidence of hypoxia. CardiovascularThe immediate response to the blast wave consists of a singular form of cardiogenic shock, resulting from myocardial depression without compensatory vasoconstriction. Severe hypotension, profound bradycardia and low cardiac output, as opposed to normal systemic vascular resistance and stroke volume, constitute this unique physiologic state. Transient papillary muscle ischemia may become part of the clinical picture. IntestineThe gastrointestinal tract, being rather expandable and flexible, sustains primary blast injuries only when exposed to relatively high blast pressures, such as are encountered in underwater explosions. Intestinal involvement may appear hours to days after the primary injury, with signs of peritonitis and/or ileus which are undiscoverable in the interim period. Nervous SystemVagal parasympathetic excitation causing bradycardia, reduced cardiac index together with shallow breathing sometimes ensuing in apnea. Numerous changes in the brain, involving chiefly the microglia, may occur. As a consequence of nerve injury, patients suffer from headache and pain along the limbs. AmputationWhere the blast wave causes internal fracture of bone, the immediately following blast wind will complete the process of severing the limb. Such amputations are usually seen in the shaft of long bones.
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Secondary Blast Injuries

This specific damage is inflicted by fragments originating in the explosive device itself, or such as are caused by debris from the nearby environment, propelled by the blast wind and hitting the victim in various topographical areas of the body. Especially endangered are exposed parts, i.e., head, neck
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and extremities, although the wind force may cause fragments to penetrate into the torso (Fig. 51.1). Shrapnel may cause perforation of vascular structures and other viscera. Multiple shrapnel wounds should be suspicious of additional internal injuries.
Tertiary Blast Injuries

This type of injury is due to the blast wave displacing the whole body, or part of it, at high velocity which is terminated by impact with a solid surface (walls, vehicles, etc.) or with a very large fragment of debris. The outcome of this violent thrust are bruises and bone fractures from head to foot, laceration of internal organs (most commonly muscles and spleen), brain or lung contusion, and even the end phase of amputation (by the blast itself).
Flash Burn Blast Injuries

The heat generated by the explosive device, as well as the blazing objects at the site that caught fire in the wake of the explosion, present the danger of burn casualties. The bulk of burns occur in conjunction with other injuries, such as wounds caused by blast-propelled debris and/or blast lung. The exposed body parts (head, neck and extremities) are most prone to be involved in flash burn damage; nonetheless, secondary burns may be caused by ignition of the victims clothing.
Investigation
Patients who have been exposed to air blast might, at first sight, appear unharmed, but in reality they may have serious internal injuries (Table 51.1). Hence, all appropriate diagnostic tools should be utilized to detect injuries in susceptible organs (e.g., ears, lungs, the great vessels, intestines, spleen, liver, vascular bed of the intestines) that can not be assessed by the naked eye or simple physical examination. Treatment should be managed according to the ATLS protocol.
Primary Investigation
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Blood samples for blood gases are a sine qua non in order to assess the patients lung function. Chest X-ray must be performed so as to provide:
- Verification of pneumo/hemothorax - Evidence of the classic butterfly appearance of a lung that sustained blast injury (Figs. 51.2A, 51.2B); in our experience, the incidence of blast lung injury varies from 4.5% in open-space bomb explosion victims to 13.2% in closed-space detonation casualties - A starting point in the approach to the lung condition - A first means to assess eventual widening of the mediastinum, a condition that may be indicative of vascular injury, and if confirmed should prompt the use of angiographic procedures (Figs. 51.3, 51.4).
ECG is necessary in all blast injury victims, irrespective of age, to assess eventual involvement of the heart.
Secondary Investigation
Ear examination, to search for micro- and macro drum perforation and hemotympanum
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Fig. 51.1. Abdominal X-ray demonstrating a nail in the abdominal cavity.
Table 51.1. Probability of lung injury in patients suffering from compound insults*
Shrapnel to head and abdomen Burns (10%) + abrasion to face + abdominal injury Burns (10%) + skull fracture (s) Rib cage fracture
Open space 33% Confined space Closed space N/A 100%
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36% 83% N/A
22% 100% N/A
100% 87% 100%
*The data relate to damage caused by explosive devices composed of 10-15 kg TNT, nails and pellets. N/A, data not available.
Diagnostic peritoneal lavage (DPL) serves to assess peritoneal contents for blood and internal organ injury; an indwelling catheter should be left in place for re-examination after 48 hours of hospitalization and treatment in the intensive care unit. Focused abdominal sonography for trauma (FAST) should be applied to explore the peritoneum for free fluid, laceration of the liver, spleen, kidney and intestines.
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Fig. 51.2A. Chest x-ray on admission showing widened mediastinum. Note first signs of butterfly pattern.
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Fig. 51.2B. Classic appearance of butterfly pattern.
Management Prehospital
The site of an explosion causing blast wounds is considered a hot zone in the sense that a second explosive device may go off at any moment in the immediate
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Fig. 51.3. CT scan of the thorax showing disruption of the aorta caused by a flying nail. Fig. 51.4. Angiography demonstrating laceration of the innominate artery.
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vicinity. Therefore, the goal should be to spend as little time as possible at the site where a premeditated explosion has occurred or in a location where multiple explosions might be expected, taking of course into account the condition of the wounded. In any event, the advocated policy is scoop and run, while following the ATLS guidelines regarding airway breathing and circulation. Intravenous lines, using peripheral large bore catheters, may be established on the way to the hospital.
In-Hospital
Special attention should be paid to the possible presence of some unique manifestations, as outlined below:
Tension Pneumoperitoneum
Air in the peritoneal cavity may be caused by hollow viscus injury, or it may be a manifestation of barotrauma to the lung caused by either the blast itself or by ventilation (see below). Pneumoperitoneum has a devastating effect on hemodynamic and respiratory physiology, which is expressed, inter alia, in reduced venous return, reduced compliance (by about 40%) and reduced FRC. This specific injury should receive immediate attention by means of bedside laparotomy followed by closure of the abdomen with artificial materials, such as saline bags (a.k.a., the Bogota Bag), to prevent accumulation of pressure. in the abdominal cavity.
Ventilation
Respiratory management in patients suffering from blast injury is a mandatory and urgent part of the treatment spectrum. The blast lung injury (BLI) score is an effective tool to assess lung involvement, as shown in Table 51.2, and plan treatment accordingly. A prime aim is to provide sufficient amounts of oxygen to the tissues in order to prevent deterioration of the already compromised patient. Table 51.3 lists the modalities to be used according to the BLI score. Prophylactic chest tube insertion in case of moderate to severe BLI score should be considered because of the enhanced risk of tension pneumothorax; the latter, in turn, is due to the high pressure used to attain adequate oxygenation coupled with the massive damage already sustained by the lung parenchyma. In considering the option of bilateral chest tube insertion, the general condition of the patient plays a primary role. Acute respiratory distress syndrome (ARDS) may result from alveolar disruption, intrapulmonary hemorrhage, smoke inhalation, aspiration, shock, fluid loading, and secondary infection.
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Delayed Intestinal Perforation

Intestinal perforation may occur directly upon either primary or secondary blast injury. Intestinal perforation may manifest itself as long as 48 hours after the initial blast injury. The late sequelae are due to a peculiar cause and effect: damaged mucosa allows the introduction of mucus into the bowel wall under pressure. The mucus dissects the intestinal layers that results, after a latent period, in multiple minute perforations.
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Table 51.2. Blast lung injury (BLI) severity score

PaO2/FIO2 Chest radiograph Broncho-pleural fistula
Severe BLI < 60 Massive bilateral lung infiltrates Yes Moderate BLI 60 200 Bi- or unilateral lung infiltrates Yes/no Mild BLI > 200 Localized lung infiltrates No
Table 51.3. Treatment according to BLI score

BLI Mild Moderate Severe PEEP < 5 cm H2O > 5 cm H2O >10 cm H2O Assisted ventilation No PPV PPV PCV, one-lung, N2O, HFJV, ECMO
PEEP, positive end expiratory pressure PPV, positive pressure ventilation PCV, pressure controlled ventilation HFJV, high frequency jet ventilation ECMO, extra corporeal mechanical oxygenation
Major blast trauma increases the probability of covert intestinal perforation. Close observation during the first 48 hours is essential to detect concealed or developing perforation. Diagnostic means are physical examination, DPL, abdominal sonography. Surgical intervention is obligatory upon the first signs of perforation of the intestines.
Fungal Infection
Explosions in confined spaces, especially street markets, may be opportune spaces for victims to contract fungal disease. Risk factors for the development of candidemia include smoke inhalation, extensive burns, open wounds and multiple blood products. We have encountered development of candidemia in 58% of those admitted to the ICU after being injured by an explosive device that had been placed in a partly covered street market. Early respiratory colonization (1-4 days after injury) of Aspergillus or Rhizopus sp. was noted by us in 19% of the hospitalized blast injury patients.
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Posthospital Care
Chronic pain, a side effect seen in many patients surviving blast trauma may be due to damage caused to microglia in the CNS inducing local neuronal insult peripheral nerves articular joints, either by local trauma or ischemia due to emboli Decreased lung function, recurrent pneumonia, and hyperactive airways. Peritoneal adhesions causing intestinal obstruction and/or abdominal cramps as a consequence of undiscovered micro-perforations in patients managed conservatively. Posttraumatic stress disorder is a common reaction in survivors of blast injuries, which may be compounded by incidents of terrorism.
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References
1. 2. 3. 4. 5. Cooper GJ, Maynard RL, Cross NL et al. Casualties from terrorist bombings. J Trauma 1983; 23:955-967. Katz E, Ofek B, Adler J et al. Primary blast injury after a bomb explosion in a civilian bus. Ann Surg 1988; 209:484-488. Irwin RJ, Lerner MR, Bealer JF et al. Cardiopulmonary physiology of primary blast injury. J Trauma Injury Infect Crit Care 1997; 43:650-655. Hull JB, Cooper GJ. Pattern and mechanism of traumatic amputation by explosive blast. J Trauma Injury Infect Crit Care 1996; 40:S198-S205, Pizov R, Oppenhein-Eden A, Matot I et al. Blast lung injury from an explosion on a civilian bus. Chest 1999; 115:165-172.
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Forensics for Trauma Care Givers

Thomas T. Noguchi Medicolegal Issues
Not all trauma cases will end up in court, but trauma caregivers should be aware that in every step of your patient care, there is a medicolegal aspect to be considered. It would be too late to worry about the medicolegal issues when you receive a subpoena to appear in court. It is important to be aware of the pitfalls dealing with medicolegal issues and be ready and prepared. Questions may be asked long after the patient has left the emergency room. Good documentation is critical.
Lawyers Interest
What Who Where When Why How What was the weapon? Who did it? Where did it happened? When did it happened? Why did it happened? How did it happened?
Case 1: Issue: Knife Wound: What Was the Weapon?

A friendly fight escalated to knife fighting. A passerby found an unconscious man in a pool of blood. The patient was taken to the Medical Center. In the middle of the pool of blood, there was a pocketknife. Was this knife the weapon? Wound in the chest appeared larger than a wound caused by a pocketknife. A larger kitchen knife was found in a nearby trashcan. Had the size of the stab wound not been stated, the pocketknife may have been erroneously stated as the weapon, which caused the wound.
Case 2: Issue: Who Did It?

A group of gang members confronting another gang, began a turf fight. A man in the front of a group received a through-and-through gunshot wound to the chest. Many members of his gang behind him were shooting. In the emergency room, the physician noted the gunshot wound in the chest, but documented no detailed description. During the cross examination, a lawyer challenged the physician that the two wounds caused by the throughand-through gunshot were similar, the gunshot wound in the right shoulder may be the entrance wound, suggesting that a member of his own gang standing behind him may have accidentally shot him. The lawyer created a reasonable doubt as to who shot him.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Thomas T. Noguchi, Emergency & Medical Surgery, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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The photograph reveals a ring of abrasion caused by a bullet as it enters the tissue. This phenomenon can also be observed on the clothing. During the cross-examination attorney will check the certainty and credibility of witnesss statement. If it is not written, it is impossible to remember in detail, and under questioning, your testimony can become unclear or uncertain (Fig. 52.1).
Citation: Entrance wound: There is a rim of abrasion caused by the bullet as it enters the tissue. A few grains of unburned powder and blackened edges caused by burned powder are seen.
Case 3: Issue: When Did It Happen?

The child was found unconscious and brought into the emergency room. The story given to the physician was that the child had fallen from the crib. In order to check the statement, the age of the bruises became important. Were they fresh or were there signs of healing? The baby sitter was suspected to have caused the bruises. In order to establish credibility, independent medical opinion based on the appearance of the injuries may be sought (Fig. 52.2).
Citation: Four bruises on the left leg: child suspected of being a victim of abuse. Issue was raised whether or not these marks could have been caused by a hand.
Case 4: Issue: Where Did It Happen?

Issue became very heated when the family of an unconscious man initiated litigation against the arresting police officer. The man under influence of alcohol was disturbing the peace on the street. The police officer responded to the scene and the man resisted arrest and a struggle ensued, resulting in his fall. The allegation was that he was beaten by the police officer. Close examination of the wound on the back of his head revealed a grid like pattern of the lid of a manhole. The matter was settled.
Case 5: Why Did It Happen?

The defense attorney gave self-defense as reason. It would be important to know whether or not the assailant had lunged toward the defendant and fearing for his life, the defendant had shot him. The defense attorney needs to vigorously claim the gunshot wound in the chest was the entrance wound.
EvidenceCare of Wound
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The wound is also evidence to the lawyer and judge. Any object removed from clothing and the body should be described, saved and photographed.
Wound Characteristics Change with Time

Describe the wound accurately as you first see it at the initial examination, since its appearance and character will change with time and treatment. Descriptions of the wound many days after the fact will be of very little value. Record the following: Size Shape Color Consistency Architecture Architecture includes the anatomic landmark and changes of structure near the wound.
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Fig. 52.1. Entrance wound. There is a rim of abrasion caused by a bullet as it enters the tissue. A few grains of unburned powder and blackened edges caused by burned powder.
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Fig. 52.2. Four bruises in the left leg suspected victim of child abuse. Issue was raised that if marks were caused by a hand squeezed.
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Contemporary and factual information will have much bearing on the final legal decision making.
Adversary System
Adversary technique is very different and foreign to us, but it is important to know why this is done. The legal profession is dedicated to the search for truth by taking an adversary position and carefully examining the evidence. The opposing attorney will conduct a cross-examination of your knowledge to make sure the evidence as introduced, is pertinent and relevant to the case. For every medical decision we make at the Medical Center for the care of the trauma patient, medicolegal issues can be raised. Often the lawyer questions each issue by saying how do you know for sure?
Accuracy and Credibility

Although we are often under pressure to move on to another case, it is very important to document basic information on each case as it is being handled: date and time, right and left designation, treatment given, sequence of event, etc. If there were a series of small errors in documentation, despite your diligent work, the jury can only interpret that the treating physician was NOT careful. Your descriptions would be more accurate in detail, if it is documented right away.
Chain of Custody of Evidence

An unbroken chain of custody of evidence must be recorded. Record should include who received the evidence first and gave it to whom, and in sequence all persons who handled the evidence until the evidence is introduced in court. An object found in or on the body, such as bullet, should be saved, placed into the standard container as written in the procedure manual for the institution. Know what happens after an object is placed in container. Who was present at the time of transfer. Do not give evidence to anyone who may claim to be the representative of the investigative agency. Your evidence is the only one in the world. Do not lose track of it. Know where it is at all times. The following information should be documented in the patient record and the specimen container: Name of patient ID/case number Description of the object, size, shape, color, consistency Location where taken Day and time taken Removed by whom Whoever takes custody of the evidence needs to sign for it with written date and time of transfer, location, the name of person from whom received and the name of receiver. Whoever received the evidence will be responsible for the custody until he/ she releases it to another person. This record of the chain of custody must be kept, because it may be asked to be presented in court as proof of the authenticity of the evidence. If there is no proof of continuous and unbroken chain, any information or test data obtained from the evidence may not be admissible. This means that the evidence does not exist as far as the court is concerned.
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Contact Wound
The contact entrance wound may not show an abundance of gunshot residue on the skin surface. Most of the gunshot residue will have been driven into the wound with small amounts of burned and unburned powders on the edge of the gunshot wound and on the clothing. Sometimes, we observe a muzzle impression mark.
Close Range WoundThree Inches

Gunshot residues on the white cloth (experimental shot) consist of burned and unburned gunpowder, which often contains a primer compound, and occasionally minute fragments of shavings from the bullet and casing. Granular fine dots are unburned powder, generally disk-shaped and the fine soot is burned power. Because of absorption by the clothing, these fine particles may not be found on the skin. Occasionally, a shaved bullet is found on the clothing fabric. For this reason, clothing should be also properly saved (Fig. 52.3).
Citation: Gunshot residue deposited from the muzzle of Smith and Wesson (S & W) .38 Special revolver. The cloth-covered board was placed three inches away. The barrel was placed perpendicular to the board.
Distance Gunshot Wound

Although gunshot residue may be found at a distance of two feet from the muzzle, it is difficult to recognize in shots beyond 12 inches. However, lack of recognizable gunshot residue does not mean that the wound is due to a distant shot, because the residue may have been absorbed by the layers of clothing.
Atypical Gunshot Wounds

Groove like GSW: A groove-like gunshot wound may be observed, which may often be mistaken for laceration (Fig. 52.4).
Citation: There is an entrance wound on the right. The exit wound extends as a groove like wound
Stellate entrance woundCharacteristic blasting tear. It is often mistaken for an exit wound because it is large and irregular. When a muzzle is firmly pressed on the scalp, basting gas enters into the subgeleal tissue, causing a tearing effect. Whenever the tissue is above a hard substance, such as the skull, explosive blast gas undermines into the subcutaneous tissue and bursts open the skin (Fig. 52.5). The entrance wound with marked tear in the right temporal area. There is a portion of rim of abrasion (indicated by arrow). Tearing effect on clothing: Contact shot made on a sheet of cloth placed over a wood board shows the marked tearing of the fabric (Fig. 52.6).
Citation: Tearing effect of blasting gas. Gunshot residue is underneath the fabric.
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Gunshot residues may be absorbed by an object, such as the sleeve, during a struggle, so the round gunshot residue could appear as half moon shaped. The assailants sleeve may also contain a portion of gunshot residue. Ovoid pattern may be seen when the shot hits at an angle. Intermediate target: the bullet strikes an intermediate target, such as a glass plate causing shattering and enlarging the scattering pattern. Exit wound may sometimes have the appearance of an entrance wound, when the exit wound is shored or in contact with a hard surface such as when the victim is lying on the floor.
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Fig. 52.3. Gunshot residue deposited from the muzzle of Smith and Wessen (S&W) 38 Special revolver. The cloth-covered board was placed three inches away. The barrel was placed perpendicular to the board.
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Fig. 52.4. There is an entrance wound in the right and the exit wound which extends as a groove like wound.
Error Rate
Determining the entry and exit wounds in clinical setting may be difficult. It should be kept in mind that not all gunshot wounds will be typical. There are factors preventing the forming of a textbook like pattern. Compared with the data
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Fig. 52.5. The entrance wound with marked tear in the right temporal area. There is a portion of rim of abrasion.
from forensic autopsy reports, the error rate of predicting the entrance and exit wounds under clinical conditions increases to approximately 50% in multiple gunshot wounds. For this reason, it is important to describe the gunshot wound as accurately as possible.
How the Distance of Shooting Is Determined

The crime laboratory generally conducts test shootings and compares the gunshot residue pattern on the wound and clothing. Unless such test shots are made, it is difficult to precisely determined the muzzle distance.
Bullets
Preservation of the striation is essential. Metal forceps with a protective rubber tip should be used to extract the bullet. The bullet is often found beneath the skin and sometimes found it between the layers of the clothing.
Citation: Striation marksStriation marks on the sides of bullets come from the rifling of the gun barrel. From the left: a .38 Special lead bullet, a .38 semijacketed bullet and a deformed 9mm fully-jacketedbullet (ball) fired from a semi-automatic pistol.
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EvidenceOther Wounds
Stab Wound
Size and type of the stabbing weapon
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Fig. 52.6. Striation marks Striation marks on the sides of bullets come from the rifling of the gun barrel. From the left, .38 Special lead bullet, .38 semi-jacketed bullet and deformed 9mm fully jacket bullet (ball) fired from the semi-automatic pistol.
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Fig. 52.7. Tearing effect by blasting gas See gunshot residue is deposited underneath of the fabric.
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Length and thickness and characteristics such as serrations Defense wound
Blunt Wound
Direction and the amount of force Identifiable pattern such as bumper mark
Issue of Degree of Intoxication

The patients state of mind can be important in litigation. The standard toxicological test on blood and urine should be routinely ordered. Often the degree of intoxication or affected physical and mental state under influence of drug becomes an important deciding fact. Specimens drawn a day late will not represent the state of intoxication at the time of the event.
Clothing
Clothing is very important evidence. Blood stains and blood-spattering patterns can be recognized. To the naked eyes, fine evidence may not be visible, but with the use of photographs and chemical tests, such pattern can be recognized. Gunshot residues would be important for determination of the range of fire and position of the gun. Lost buttons or tears in the clothing can be important factors in solving issues. How to preserve it: Clothing should be hung to dry without causing contamination of bloodstains. Properly dried clothing is essential for DNA and other serological testing. The assailant may have deposited biological fluid on the clothing of the victim. Occasionally, bite marks may be found and saliva may be collected.
Testimony in Court Preparation Before Going to Court

Subpoena
When you receive a subpoena, you should respond and prepare for the case. Subpoena is a legal document for you to appear in the court at a specific time and place or produce specified document for the attorney to examine prior to the legal proceeding. Consult your attorney and do not ignore the notice. You may be cited for contempt of court if you ignore it. If you are not able to appear in the court at the specified time, notify the attorney who is issuing it so another date can be set. Once the court date is set, it is difficult to change the date. The subpoena may instruct you to be on call or on one-hour call.
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Understand Why Lawyer Asks Certain Questions

Unlike us concentrating on treating the patient to save a life, the lawyer represents the interests of his client and is dedicated to resolving the legal conflict, working vigorously to win the case. Using the adversary system, the lawyer seeks the truth to help his client. We are often offended when the lawyer asks questions and challenges our opinion. The lawyer has a job to cross-examine you to make sure the evidence is properly introduced and admitted.
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Without written detailed description, such as acute symptoms, swelling, redness, fresh blood, or findings of older healing injuries such as with marginal zone of discoloration, scar, etc. it will be difficult or impossible to remember all the details which may be asked in court.
Burden of Proof
Burden of proof is laid to the party initiating the litigation. In criminal and civil cases, the requirement for proof is different. In criminal cases, the district attorney must present the proof of guilt of the defendant beyond a reasonable doubt. In civil cases, the acceptable proof would be based on the preponderance of evidence that it is more likely to be true than not.
Hypothetical Question
Attorneys may ask for an opinion after asking a hypothetical question. This question may be long and contains some of the facts, and you will be asked if you have an opinion. If the answer requires yes or no, state so. Then you will be given opportunity to explain. If the question is not answerable, the judge may allow your explanation.
Deposition
In preparation for trial in a civil case, a deposition is often taken. Your testimony is taken in a court of law with an attorney for both parties present and is recorded by a certified court reporter. Nowadays, video taping is also often done. It is a part of the discovery procedure and may result in a settlement without going to trial. Trauma caregivers should not consider this procedure to be less important than court proceeding. In some states, deposition is also taken in criminal cases.
Day of Testimony
Be well prepared and be confident. Wear a business suit or dress conservatively. Keep your facts straight on date, time, sequence of events. Remember the lawyer is well prepared to cross-examine you. Take all documents that were requested. No additional material should be with you. Listen to the lawyers question and answer it briefly. Do not be argumentative. Do not volunteer answers. The lawyer has specific questions and answers in mind. The lawyer deals with one piece of evidence at a time. When you take the stand, the jury sees you for the first time. The jurys job is to determine your reliability and whether you are a credible witness or not. Watch your tone of voice, body language and facial expression. Look and maintain eye contact with the jury. Do not look down while you are speaking. This may be interpreted by the jury that you are uncertain. In using charts or X-ray films, first point to the relevant item, then look at the jury and talk to the jury. Do not talk to the black board or the display. Remember that you are not an advocate. Simply and briefly, directly answer the questions asked with no elaboration. Witness should not be biased or partial. Your credibility is important. This is a serious business and trauma caregivers should be well prepared. We should be sincere, factual witnesses and not take sides.
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Endocrine Problems in Trauma

Elizabeth O. Beale Introduction
Endocrine diseases are important in trauma patients because: Clinical features are often similar. Some endocrine diseases, particularly diabetes mellitus and hypothyroidism, are common and are associated with important medical disorders and longterm medication. Trauma frequently exacerbates a pre-existing endocrine disorder. In extreme cases, fatal exacerbation can occur. Trauma may cause development of a new endocrine disorder.
Diabetes mellitus (DM) and Hyperglycemia

DM is defined as a fasting plasma glucose > 126 mg/dL or two random plasma glucoses > 200 mg/dL.
Causes of DM
80% NIDDM; 10% IDDM; 10% specific causes e.g., exocrine pancreas disorder.
Incidence of DM in Exocrine Pancreas Disorders

Distal pancreatectomy: 20-40% 40-80% pancreas resection: 40% 80-90% pancreas resection: > 60% 100% pancreas resection: 100% Acute pancreatitis: 2-18%.
Causes of Hyperglycemia in the Trauma Patient

Stress (this increases insulin counterregulatory hormones: cortisol, epinephrine, glucagon); infection (overt or occult); overfeeding (parenteral or oral); medications (glucocorticoids, sympathomimetic agents, cyclosporine); insufficient insulin or oral hypoglycemic agents ( missed therapy, increased needs); volume depletion.
Clinical
No history of diabetes does not exclude the diagnosis. Acute Medical Problems: hyperglycemia, hypernatremia, hyperkalemia or hypokalemia, diabetic ketoacidosis (DKA), nonketotic hyperglycemia (NKH), myocardial infarction, gastroparesis, abdominal pain, infection. Associated Chronic Medical Problems: cardiovascular disease, peripheral vascular disease, hypertension, renal impairment, peripheral and autonomic neuropathy, impaired vision due to retinopathy or cataracts, obesity, foot ulcer. Trauma and its management can convert a stable chronic medical problem into an acute unstable condition. In particular excess fluid during resuscitation can precipitate fluid overload and nephrotoxic drugs can cause overt renal failure.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Elizabeth O. Beale, LAC + USC Medical Center, Los Angeles, California, U.S.A.
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Diabetic Foot Ulcers and Trauma

Diabetic foot ulcer is the cause of two-thirds of nontraumatic limb amputation in the USA. Nontraumatic is a misnomer as the majority of ulcers start with minor foot trauma. Signs of an acute inflammation may be absent due to impaired circulation. The mainstays of treatment are extensive debridement, good local wound care, relief of pressure and close monitoring. Osteomyelitis is likely to be present in an ulcer in which bone is visible, the ulcer depth is > 3 mm or if the patient has an ESR > 40 mm/hr with no other apparent cause. X-rays, CT and MRI can help diagnose osteomyelitis.
Posttraumatic Osteomyelitis
Trauma is a major cause of osteomyelitis in diabetics. Infection may be introduced at the time of the accident (especially MVA) or during management (especially by orthopedic devices) and is usually polymicrobial. The usual site of osteomyelitis following major trauma is the tibia or femur. Treatment involves careful debridement, obliteration of dead space, good wound drainage, wound protection and specific antibiotics.
Management of Uncomplicated Diabetes Mellitus and Hyperglycemia

A reasonable goal in the acutely ill patient is a plasma glucose between 100-200 mg/dL. Therapy depends on the degree of trauma and hyperglycemia:
- Minor trauma and normoglycemia: continue usual treatment and monitor glucose regularly. - Minor trauma and mild hyperglycemia: SQ regular insulin (Table 53.1). - Moderate to severe trauma or moderate to severe hyperglycemia: IV regular insulin (Table 53.2).
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Measure glucose hourly until levels are 100-200 mg/dL for 4 hours, then 2-4 hourly. Monitor potassium and phosphorous in patients on IV insulin as they may fall rapidly. Increase the infusion rate by 50% increments for each glucose range > 200 mg/dL if glucose is not in the goal range by 3-4 hours. Insulin requirements increase with severe infection or illness, glucocorticoids, vasopressor infusions, excessive calories and in patients significantly > 70 kg. Decrease the infusion rate if the glucose falls > 80 mg/dL/hour and in patients much < 70 kg.
Guidelines for Semi-Elective Surgery in Patients with Diabetes Mellitus

Preoperatively: Schedule diabetic patients for morning surgery. Do not give the usual oral hypoglycemic therapy or regular (short-acting) insulin on the morning of surgery. Do give one-half of the patients usual morning dose of long-acting insulin SQ. Start dextrose containing IV. Measure the preoperative glucose: < 200 mg/dL: no preoperative insulin is necessary; 200 mg/d: add Human Regular insulin to the dextrose IV fluids (5 units regular insulin/L 5% dextrose) and follow the insulin algorithms above. Use
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Table 53.1. SQ regular insulin algorithm

Blood Glucose (mg/dl) Regular SQ Insulin (units/4-6 hourly)
200-250 251-300 301-350 > 350
2 4 6 8
Table 53.2. IV regular insulin infusion algorithm

Blood Glucose (mg/dL) Regular Insulin Intravenous Infusion Rate (units/hr)
< 100-0 101-120 121-150 151-20 201-250 251-300 301-350 351-400 > 400
0 1 1.5 2 2.5 3 4 6 8
Standard IV infusion: 250 Units Human Regular Insulin in 250mLs of 1/2 NS: i.e., 1 Unit/mL
the SQ algorithm insulin if the patient is usually controlled on oral agents and the IVI algorithm if the patient is usually controlled on insulin. < 100 mg/dL:-give 1/2 ampule 50% dextrose. Recheck glucose in 1/2 hour. Repeat if glucose remains <100 mg/dL. During anesthesia and in the postanesthesia recovery room: Glucose should be measured hourly and IV insulin infusion used to control glucose. Postoperatively: Measure the immediate postoperative glucose and manage as for preoperatively.
Emergency Surgery in Patients with Diabetes Mellitus

Immediately check glucose, urea and electrolytes, ABG and pH, urine and plasma ketones. If there is DKA or HNK delay surgery (if possible) for 3-4 hours until these are controlled. In patients without severe metabolic problems, treat as for semi-elective surgery. An apparent acute surgical abdomen may be due to DKA: if the patient is < 25 years the problem is more likely to be metabolic, if > 25 years it is more likely to be a true acute surgical problem. When there is doubt as to the cause of the abdominal pain, and if clinically feasible, conservative medical management should be undertaken to correct the metabolic problems. The pain will usually resolve in 3-4 hours if metabolic in origin.
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Management of Hyperglycemia on Parenteral Nutrition (PN)

If the glucose is persistently > 200 mg/dL: STEP 1: Add 0.1 units of regular insulin/g dextrose to the PN solution (e.g., 20 units/L of 20% dextrose). STEP 2: Increase the PN insulin by 0.05 units of regular insulin/g of dextrose/ day up to 0.2 units of insulin/g dextrose (e.g. 40 units/L of 20% dextrose). STEP 3: Add supplemental SQ insulin. STEP 4: Start a separate insulin infusion.
Diabetes mellitus Emergencies Diabetic Ketoacidosis (DKA)

This is a potentially fatal complication of DM that may be precipitated by trauma.
Causes Of DKA in the Trauma Patient

Missed therapy, excess stress hormones, infection.
Clinical
Polyuria, polydipsia, weakness, visual disturbance, altered mental state, nausea, vomiting, abdominal pain, Kussmauls respiration, ketotic fetor, hypothermia.
Investigations
Hyperglycemia: in 15% of patients serum glucose is < 300 mg/dL.Serum bicarbonate: < 15 mEq/L. There is typically an increased anion gap metabolic acidosis. Hyponatremia: this is frequently pseudohyponatremia due to the high glucose levels. Ketonemia: significant at a serum dilution of 1:2. Ketones may be falsely negative. Potassium: high or low (with total body depletion).Tall peaked T-waves on EKG with hyperkalemia. Phosphate: high or low (with total body depletion). Hyperamylasemia, lipasemia: these do not necessarily indicate pancreatitis.
Principles of Management
The acronym D.I.A.B.E.T.E.S helps with remembering the important points in management.
NB: The following are typical doses and may need to be adjusted for the individual patient. D: Dehydration. Give 2-3 liters of normal saline (NS) in the first 2-3 hours. Then adjust fluids according to volume status and serum sodium level. I: Insulin Usually 5-10 U/hr. Give 0.1 U/kg bolus then 0.1 U/kg/hr IVI . Always use Human Regular insulin. Aim to decrease the serum glucose by about 75 mg/hr. Continue insulin until a few hours after the anion gap has returned to normal and is stable. A/B: Acid Base. Bicarbonate has not been shown to improve outcome, but many physicians will give it if the pH is < 6.9. E: Electrolytes. KCl 40 mEq/hr IVI. Avoid if EKG shows tall, peaked T-waves. Phosphate if <1.0 mg/dL. Phosphate can cause calcium to fall so magnesium may be given to stimulate PTH action and maintain normocalcemia. T: Triggers. Ascertain and treat the cause of DKA especially infection and myocardial infarction.
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E: Evaluate progress. Use a flow chart. Monitor vital signs, fluid balance, insulin, electrolytes. S: Sugar. Hypoglycemia can occur rapidly with irreversible brain damage. Measure hourly glucose until glucose is in the normal range, then 2 hourly. Change to a dextrose solution when glucose is < 250 mg/dL but continue insulin until the anion gap is normal.
Nonketotic Hyperglycemia (NKH) Causes of NKH in a Trauma Patient

Trauma, infection, gastrointestinal bleeding, pancreatitis, myocardial infarction thiazides, glucocorticoids, phenytoin.
Clinical
Typically occurs in patients > 60 years who are socially isolated and bedridden. Two-thirds of patients have no history of DM. Profound dehydration. 50% of patients are initially misdiagnosed as having a primary neurologic defect. 25% have coffee ground naso-gastric aspirate. 60% have underlying infection. Many have underlying renal and cardiac dysfunction.
Investigations
Glucose: > 600 mg/dL: usually in the 1000 mg/dL range; WCC: 15,000-20,000; hemoconcentration; osmolarity > 340 mosm/L; hyponatremia; hyperkalemia or hypokalemia; small increase in anion gap but no ketoacidosis.
Management
Fluids: the initial replacement fluid is usually NS but 1/2 NS can be given if Na > 145 mEq/L. Rehydrate cautiously due to possible underlying cardiac and renal failure. Replace the first 1/2 of fluids over 12 hours and the second 1/2 in next 12 hours. Insulin: In NKH glucose will fall with fluids alone. Insulin may cause glucose and fluid to shift into cells causing shock. Therefore insulin should be given only once the patient has been fluid resuscitated and if glucose remains high. Insulin is usually required in lower doses than that used for DKA. Monitor serum glucose carefully to avoid hypoglycemia. Search for and treat underlying cause.
Hypoglycemia
This may rapidly cause brain damage. Clinical features may easily be mistaken for those due to trauma.
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Causes of Hypoglycemia in the Trauma Patient

Sudden withdrawal of nutritional support, especially parenteral nutrition. Withdrawal or decreased doses of corticosteroids or sympathomimetic agents. Renal dysfunction, severe hepatitis, sepsis, diabetic gastroparesis. Primary or secondary adrenal insufficiency, hypothalmic or brain stem injury. Insulin or oral hypoglycemic agents. Excessive loss or use of glucose. Alcohol. Propranolol. Salicylates. Antihistamines.
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Clinical Features
Tachycardia, restlessness, sweating, altered mental state including coma.
Investigations
Stat glucose level on any patient with altered mental state. When glucose < 60 mg/dl adrenaline rises; < 50 mg/dl: cognitive dysfunction.
Management
Treat for presumed hypoglycemia if unable to check glucose levels immediately. If alert and not NPO: give 15 grams glucose orally. This is equivalent to 2 cubes of sugar or 1/2 cup (4 oz) fruit juice. If not able to take orally and IV access available: give 25-50 grams 50% dextrose water IV. If not alert and no IV: Give 1 mg glucagon IM or SQ. Check glucose every 15 minutes and repeat treatment until glucose is greater than 80 mg/dL.
Thyroid Nonthyroidal Illness Syndrome (NTIS) or Euthyroid Sick Syndrome or Low T3 Syndrome
This refers to thyroid function test abnormalities in an euthyroid patient and is found in up to 75% of hospitalized patients. It may be difficult to differentiate from hypothyroidism and less commonly from hyperthyroidism.
Causes of NTIS in a Trauma Patient

Any moderate to severe acute or chronic illness. Medications: dopamine, dobutamine, glucocorticoids, frusemide, anticonvulsants, NSAIDs
Clinical Features
Clinically euthyroid, but features of the acute illness may make this difficult to determine.
Investigations
Avoid doing thyroid function tests unless there is a strong clinical suspicion of thyroid pathology. There is no certain way to differentiate hypothyroidism from NTIS but hypothyroidism is suggested by a history of thyroid disease or surgery, clinical features of hypothyroidism and certain lab features:
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Lab Test TotalT3 TotalT4 T3RU TSH freeT4
NTIS N or N or N
Hypothyroidism N or or
Hyperthyroidism N or
Management
Usually no treatment is necessary. T3 and T4 therapy have been recommended in cases with a very low T4 (< 4 g/dL). The condition usually resolves with resolution of the primary illness.
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Hyperthyroidism
Symptoms and signs of sympathetic stimulation are similar to those occurring with trauma. Rarely, trauma may precipitate thyrotoxic storm in a patient with pre-existing thyrotoxicosis. More commonly trauma and therapy for trauma (dopamine, glucocorticoids) suppress TSH leading to a biochemical picture similar to hyperthyroidism in the absence of clinical thyrotoxicosis.
Causes of Hyperthyroidism in the Trauma Patient

Thyroiditis may rarely occur secondary to vigorous palpation of the neck, manipulation of the thyroid gland during neck surgery or seat belt trauma.
Pre-Existing Causes for Hyperthyroidism

Graves disease, toxic multinodular goiter (MNG), solitary toxic nodule, postpartum thyroiditis (5-10% of postpartum women), subacute thyroiditis, overmedication with exogenous thyroid hormone.
Clinical
Thyroiditis causes transient neck pain and tenderness. The thyroid is diffusely enlarged in Graves disease, irregularly enlarged with MNG. Tachycardia, palpitations, anxiety, tremor, acropachy, pretibial myxedema, proptosis, ophthalmoplegia, weight loss, fatigue, associated conditions e.g., DM, cardiac failure.
Investigations
Thyroid hormones: increased serum T4 and T3, decreased serum TSH. Thyroid scan (this is seldom indicated in the acutely ill trauma patient): thyroiditis shows decreased uptake, Graves disease: diffuse increased uptake, toxic MNG: heterogeneous uptake, solitary nodule: localized uptake.
Management
There are three treatment options but only medical therapy is indicated in the acutely ill trauma patient. Medical: methimazole: initial dose: 15-60 mg/day; maintenance: 5-15 mg/ day or propylthiouracil: initial dose: 50 mg 8 hourly; maintenance:100 mg 8 hourly. Monitor for agranulocytosis (every 2-4 weeks), liver toxicity, skin rashes. Beta-blockers can be used to reduce sympathetic stimulation: use with caution with cardiac decompensation. For rapid reduction in thyroid hormone levels, ipodate or iodine solutions may be used. Radioactive iodine and surgery: these are definitive ablative therapies for patients with hyperthyroidism well-controlled on oral medication.
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Hypothyroidism
2-3% of the US population are hypothyroid. 10-20% of women > 50 years have subclinical hypothyroidism (high TSH only). 6% of postpartum women have transient hypothyroidism.
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Causes of Hypothyroidism in the Trauma Patient

Inadvertent stopping of thyroid replacement therapy; secondary to hypothalamic or pituitary injury or surgery; ischemic necrosis of the pituitary with severe shock. Injury to the thyroid is more likely to cause acute thyrotoxicosis than hypothyroidism.
Pre-Existing Causes for Hypothyroidism

Hashimotos disease, prior radioiodine or surgery, hypopituitarism.
Clinical
Signs and symptoms may develop insidiously after withdrawal of treatment or hypothalamic-pituitary. Fatigue, cold intolerance, hypertension, bradycardia, cardiomegaly, congestive cardiac failure, carpal tunnel syndrome, delayed relaxation of tendon reflexes, periorbital swelling, enlarged, normal or small thyroid, reduced respiratory drive, failure to wean from ventilator, constipation, megacolon, confusion, psychosis, subnormal temperature response with infections. Hypotension and heart failure have been reported during surgery with severe hypothyroidism.
Investigations
High TSH, low serum T4 and T3. Similar changes may occur with NTIS. Normochromic, normocytic anemia, or iron deficiency anemia with heavy menses. Hyponatremia (due to SIADH), hypercholesterolemia, raised CPK. There may be associated adrenal insufficiency (with low serum cortisol). EKG: bradycardia, low voltage.
Management
In the acutely ill patient, treat for hypothyroidism if there is a strong clinical suspicion of the condition. The usual treatment in young individuals is levothyroxine (LT4) 1.6 g/kg/day. Elderly patients and those with known or suspected heart disease are started on a lower dose of LT4 (25 g/day) which is increased only every 2-3 months until the TSH is normal. Patients who are NPO for a few days can go without therapy due to the long half-life of T4. 70-80% of the daily oral T4 dose can be given IV to patients unable to take orally long-term. Emergency surgery in patients with known uncontrolled hypothyroidism: if there is no known ischemic heart disease give LT4 and monitor postoperatively for complications. In patients with known ischemic heart disease proceed without LT4 to limit oxygen demand. Mortality and major complication rates in patients with mild to moderate hypothyroidism undergoing emergency surgery are similar to rates in euthyroid patients.
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Thyroid Emergencies Thyroid Storm

This rare but frequently fatal condition may be precipitated by trauma. Signs of sympathetic excess may be attributed to trauma.
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Causes of Thyroid Storm in the Trauma Patient

This may occur in a patient with pre-existing, poorly controlled hyperthyroidism and trauma (to the neck or elsewhere), surgery (thyroid or nonthyroid), infection.
Clinical Features
The features are of severe thyrotoxicosis, usually with a fever > 102F.
Lab Tests
Low TSH. Raised T4,T3, glucose, urea, calcium, liver enzymes. Raised WCC and anemia.
Management
Do not wait for laboratory confirmation. Treat on clinical suspicion. PTU 300-400 mg or methimazole 10-40 mg po or by NG tube immediately and 6-8 hourly or if NPO, give rectal methimazole 30-40 mg 6-8 hourly. 1 hour after antithyroid drugs give 1-2 gm sodium iodide IV and give every 24 hours or 5 drops saturated solution of potassium iodide po every 6 hours. Dexamethasone 2 mg IV every 6 hrs. Propranolol 40-80 mg po or 1-2 mg IV every 6-8 hrs: use cautiously with cardiac failure. Oxygen, IV fluids + phenobarbital, glucose, B vitamins. Antipyretics and external cooling if temp >105F.
Myxedema Coma
A rare condition with a 100% mortality if untreated that may be precipitated by trauma. The altered mental state, hypothermia and bradycardia may be attributed to head injury.
Causes of Myxedema Coma in a Trauma Patient

Myxedema coma usually occurs in an elderly patient with pre-existing hypothyroidism and a precipitating event such as trauma, prolonged cold exposure, infection, surgery, myocardial infarction, respiratory failure, GIT bleeding or CNS depressant drugs.
Clinical Features
The features are of severe hypothyroidism with hypothermia, bradycardia, stupor, decreased hypoxic and hypercapnic ventilatory drive, pericardial, pleural and peritoneal effusions. There is relative insensitivity to catecholamines before starting LT4 therapy and hypersensitivity after. There may be a goiter or a thyroidectomy scar.
Investigations
Raised TSH. Low T4 and T3. Anemia, hyponatremia, hypoglycemia, raised cholesterol, increased CPK. CO2 retention, hypoxemia. EKG: sinus bradycardia, AV block, low voltage, T-wave flattening, increased QT interval.
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Management
Do not wait for laboratory confirmation. Treat on clinical suspicion: LT4 0.5 mg IV followed by 0.025-0.05 mg each day until patient can take orally. Then LT4 po 0.05-0.1 mg daily. Hydrocortisone 75 mg IV every 6 hours until adrenal insufficiency is excluded. CVS, respiratory support. Slow external rewarming for moderate hypothermia, central if severe.
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Thyroid Nodules
Thyroid nodules are present in 6% of the population and are usually detected incidentally. About 10% are malignant and are typically painless with normal thyroid function tests. The patient should be referred for further work-up especially if there is hoarseness, rapid growth of the nodule, obstruction or evidence of local invasion.
Goiter
A goiter may cause airway obstruction in the trauma patient. The goiter may be retrosternal and undetectable on neck palpation. When endotracheal intubation is necessary, awake fiberoptic intubation is recommended. Obstruction may occur postextubation in a patient with no obstruction prior to intubation. A flow-volume loop can help detect upper airway obstruction: extrathoracic obstruction primarily decreases inspiratory airflow and intrathoracic obstruction, expiratory airflow.
Adrenal Insufficiency (AI)

This generally refers to an insufficiency of endogenous glucocorticoids. Mineralocorticoid insufficiency may also occur with primary adrenal insufficiency and with severe medical illness. AI is fatal if untreated and responds only to glucocorticoids, but diagnosis is difficult. It is much commoner than previously recognized in critically ill patients.
Incidence
Trauma patients: blunt abdominal trauma: 0.1%; evidence of adrenal injury on CT scan following blunt abdominal trauma:5%; SICU trauma patients: 0.7%. ICU patients: overall: 1%; patients > 55 years with a stay of > 2 weeks in the ICU: 10%.
Causes of AI in the Trauma Patient

AI is rarely caused directly by trauma as this requires > 90% of the adrenal cortex to be destroyed but may develop secondary to disease processes.
Causes of AI in the Critically Ill Patient

Infections: bacterial esp. TB, meningococcemia; viral especially HIV; fungal. Adrenal hemorrhage and infarction due to massive retroperitoneal bleeding, thrombocytopenia, anticoagulant therapy. Abrupt withdrawal of chronic high dose glucocorticoid therapy or megestrol acetate therapy. Transient ACTH deficiency postabdominal surgery in elderly patients. Cytokine induced inhibition of ACTH. Panhypopituitarism due to tumors, infections, infiltrates, head trauma, aneurysm. Increased metabolism of cortisol: phenytoin, phenobarbital, rifampicin. Changes in cortisol synthesis: ketoconazole, etomidate.
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Causes of AI in the General Population

Autoimmune adrenalitis (including Addisons disease), metastases, Sheehans syndrome, pituitary apoplexy, isolated ACTH deficiency, withdrawal from glucocorticoid therapy.
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Clinical
Clinical signs are notoriously nonspecific and signs and symptoms may be altered by the trauma or therapy. Adrenal hemorrhage causes acute onset of flank pain and hypotension. Orthostatic hypotension, shock, nausea, vomiting, gastro-intestinal pain, constipation, psychosis hyperpigmentation, vitiligo, loss of axillary and pubic hair, fever, weakness, fatigue, anorexia, arthralgia, myalgia, weight loss.
Investigations
Baseline and stimulated serum cortisol: these are often unhelpful in the trauma patient as results usually take 2-3 days to obtain and there is no serum cortisol level at which the diagnosis of adrenal insufficiency can definitely be excluded. There is a growing consensus that in ICU the baseline serum cortisol should be > 15 g/dL and the stimulated serum cortisol 30-60 minutes after 250 g ACTH IV >18-20 g/dL. The concept of relative adrenal insufficiency is replacing that of absolute AI. There is no exact definition but it should be suspected in a patient with hypotension poorly responsive to vasopressors, a response to ACTH stimulation < 7-10 g /dL, and improvement with physiological replacement doses of glucocorticoids (100 mg hydrocortisone 8 hourly). Eosinophilia, lymphocytosis, mild normocytic, normochromic anemia, hyponatremia, hyperkalemia, hypoglycemia, hypercalcemia. ACTH is not helpful in the acute situation but if over 100 pg/mL suggests primary adrenal insufficiency. Adrenal CT scan: enlarged adrenals occur with active TB, fungal infection, metastases, HIV infection and lymphoma; atrophy with chronic autoimmune adrenalitis. Pituitary and hypothalamus scanning: MRI may detect soft tissue lesions of the pituitary and hypothalamus; CT scanning may show bony invasion or calcification.
Management
Maintenance therapy: for patients with known adrenal insufficiency and a nonstressed clinical state: hydrocortisone 15-20 mg in morning, 5-10 mg in early afternoon. Prednisone (2.5-7.5 mg nightly) or dexamethasone (0.250.75 mg nightly) may be used in place of hydrocortisone. Glucocorticoids can be given IV if patient is NPO or vomiting. Fludrocortisone 0.05 mg-0.2 mg daily for primary AI. Stress therapy for patients with known or suspected adrenal insufficiency and a stressful clinical state (e.g. trauma, infection, diagnostic or surgical procedures): for mild to moderate stress give 2-3 times the usual maintenance dose. For severe infections or surgery give 100mg hydrocortisone intravenously 8hourly. Taper stress doses over 1-2 days after stress has resolved. Adrenal crisis: start treatment on clinical suspicion. Do not wait for cortisol results. Give hydrocortisone 100 mg IV 8 hrly.If biochemical testing is not complete give dexamethasone 4 mg daily in place of hydrocortisone as this does not cross-react with the measurement of serum cortisol. Usually several liters of 0.9% dextrose saline are needed. Look for the cause.
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Adrenal Incidentalomas
Adrenal incidentomas are detected incidentally on 1-5% of abdominal CT scans. There may be features of hormone excess (Cushings syndrome, pheochromocytoma) or a malignant primary. Serum potassium is often abnormal with cortisol-producing adenomas. Investigations include a malignancy work-up and cortisol and catecholamine measurements. The lesion is usually electively resected if biochemically active or > 6 cm.
Hypercalcemia
Hypercalcemia is often detected on routine screening and needs further work-up. Severe cases can be life-threatening. Signs and symptoms may mimic those due to trauma.
Causes of Hypercalcemia in the Trauma Patient

1) Immobilization hypercalcemia may occur after spinal cord injury, burns, or hip fracture. This is mostly seen in adolescent males and is probably due to hypersensitivity to parathyroid hormone. 2) During the recovery phase of acute renal failure. 3) Parenteral nutrition. 4) Pseudohypercalcemia with venous stasis during blood draw and with severe dehydration.
Causes of Hypercalcemia in the General Population

Malignancy 45%. Hyperparathyroidism 45%. Other: 10%.
Clinical
Irritability and confusion, weakness, fatigue, anorexia, photophobia, volume depletion, cardiac depression, bradyarrhythmias, heart block, cardiac arrest, constipation, polyuria, nephrolithisiasis
Investigations
If hypercalcemia is detected, the level should be checked twice to confirm the diagnosis. If necessary, correct serum calcium for either hyperproteinemia or hypoproteinemia. EKG: short QT, prolonged PR interval, T wave changes. Abdominal X-ray: nephrolithiasis
Management
This depends on the level of hypercalcemia and the clinical condition. Mild, chronic hypercalcemia (11-12 mg/dL): oral phosphate can be given if the serum phosphate is < 4 mg/dL pending definitive treatment. Granulomata are treated with glucocorticoids. More severe and symptomatic hypercalcemia: rapid volume expansion with NS 2-4 L/d until normovolemic. Furosemide 80-100 mg IV every 1-2 h may be given to a well-hydrated patient to aid sodium and calcium diuresis. Monitor for fluid overload and replace electrolytes as needed. Block bone resorption with pamidronate 90 mg infusion over 24 hours until levels normalize then 30-60 mg every few weeks for long-term control. Calciton in-4-8 U/kg every 12 hours SQ or IM for rapid short-term control. Life-threatening (e.g., 18-20 mg/dL or severe clinical features): hemodialysis, IV EDTA. General: mobilize patient as soon as possible; restrict calcium intake; avoid hypercalcemic drugs: thiazides, vitamin A and D; look for cause: serum PTH level; malignancy work-up.
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Diabetes Insipidus (DI)

DI is caused by decreased antidiuretic hormone (ADH, vasopressin) or resistance to its action. Untreated DI can cause fatal dehydration or permanent brain damage due to hypernatremia. Overtreatment can cause fatal overhydration and hyponatremia. DI must be differentiated from other causes of polyuria in the trauma patient
Cause of DI in Trauma Patients

This is usually central DI. 1) Head injury. DI usually occurs with severe closed head injury but has been reported with very minor head injury. The usual cause is an MVA that shears the pituitary stalk or causes hemorrhage and ischemia in the posterior pituitary or hypothalamus. 2) Cerebral hypoxemia e.g. following asphyxia, cardiac arrest or shock. 3) Cerebral edema and herniation. 4) Postneurosurgery.
Other Causes of DI
1) Central DI (insufficient ADH) due to tumor, strokes, infections, neurosurgery. 2) Nephrogenic DI (resistance to ADH) due to acute or chronic renal failure, hypercalcemia, hypokalemia, sickle cell disease, drug related (lithium, demeclocycline, loop diuretics).
Clinical
Onset of DI ranges from hours to days postinsult. The patient is often unconscious due to head injury. 70% have skull fracture. 40% have cranial nerve damage. Polyuria often > 250 mL/hour. Polydipsia: if conscious. Triphasic DI has been described in trauma and neurosurgical patients: i.e., DI, followed by inappropriate antidiuresis, then recurrent DI. Most posttraumatic DI after mild head injury resolves in 3-5 days but resolution has been reported up to 10 years after the accident, and it may be permanent.
Investigations
Polyuria typically > 3 L/day. Intake depends on level of consciousness and whether thirst mechanism is intact. Serum sodium > 145 mEq/L. Posm> 295 mOsm/kg. Urine SG < 1.010. Uosm < 300 mOsm/kg.
Management
1) Exclude other causes of polyuria: overhydration, solute diuresis especially mannitol, myoglobin following Rhabdomyolysis, urea during recovery phase from acute renal failure, glucose. 2) Give water to restore and maintain hydration: conscious patients with mild DI can drink ad lib if their thirst mechanism is intact. Otherwise give IV dextrose water (low solute fluids). 3) Central DI is treated with DDAVP. The usual starting dose is 1 mg and maximum dose is 1-4 mg 12 hourly. To avoid dangerous overhydration monitor urine output and serum electrolytes hourly. DDAVP should only be readministered when dilute polyuria restarts. 4) Give stress doses of hydrocortisone until associated adrenal insufficiency has been excluded. 5) Nephrogenic DI is treated with 12.5-25 mg hydrochlorothiazide daily or bid.
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Growth Hormone (GH)

GH is not indicated as anabolic therapy in critically ill patients due to increased mortality. GH has been shown to decrease dependence on parenteral nutrition
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by 40% in the short bowel syndrome when used in conjunction with glutamine and a modified diet.
References
1. 2. 3. 4. 5. Gavin LA. Perioperative management of the diabetic patient. Endocrinology and Metabolism Clinics of North America 1992; 21:2 457-475. De Groot L. Dangerous Dogmas in Medicine: The nonthyroidal illness syndrome. JCEM 1999; Volume 84 (1):151-164. Robinson GA. Verbalis JG. Diabetes insipidus. In: Bardin CW, ed. Current Therapy in Endocrinology and Metabolism. 6th ed. St Louis Missouri: Mosby-Year Book Inc. 1997:1-7. Wilmore D, Lacey J, Soultanakis R et al. Factors predicting a successful outcome after pharmacologic bowel compensation. Annals of Surgery 1997; 226(3) 288293. The Endocrine Response to Acute Illness. Jenkins RC, Ross RJM, eds. Frontiers of Hormone Research. Volume 24 Karger Switzerland 1999.
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MOF Failure: MOF Syndrome

H. Gill Cryer Definition
The multiple organ dysfunction syndrome is characterized by widespread systemic organ dysfunction of variable severity after injury, infection, or other major physiologic insult. It is now recognized that the syndrome is a dynamic continuous process that usually begins with a systemic hyperinflammatory process which may progress or resolve but is followed by a hypoimmune response which may resolve or progress over a variable length of time. It is likely that all organ systems are involved in the process to some degree but the clinical presentation varies considerably between individual patients. The most common organ to develop obvious clinical failure is the lung followed by the liver, kidney, gut, and cardiovascular system. Multiple organ dysfunction syndrome has now become the number one cause of late death in trauma and surgical patients.
1969 Francis Moore and colleagues clearly described the syndrome physiologically and pathologically in their treatise entitled Posttraumatic pulmonary insufficiency. 1975 Eiseman and colleagues coined the term Multiple Organ Failure and stressed the importance of avoiding surgical technical complications in preventing the syndrome. 1980 Fry and colleagues demonstrated the importance of uncontrolled infection and proposed it as the principle etiology of the syndrome. 1985 Goris and colleagues demonstrated that at least 50% of patients with multiple organ failure syndrome did not have an obvious source of infection and proposed that a dysregulated hyperinflammatory state led to generalized autodestructive inflammation in the majority of patients with this syndrome.
Diagnosis of Multiple Organ Failure

Clinical diagnostic criteria for multiple organ system failure are not yet standardized. Currently the syndrome is defined and quantitated based on variable severity of organ dysfunction markers in the lung, kidney, gut, liver and sometimes the hematologic and neurologic systems. Several authors have developed multiple organ dysfunction scores in an attempt to define this process, which can be used in a number of different ways. It probably makes best sense to follow the score across time beginning on the first day of injury.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. H. Gill Cryer, UCLA Medical Center, Los Angeles, California, U.S.A.
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Table 54.1. Multiple organ failure score

Pulmonary dysfunction* Renal dysfunction Hepatic dysfunction Cardiac dysfunction Grade 1 ARDS score > 5 Creatinine > 1.8 mg/dl or dialysis Bilirubin > 2.0 mg/dl DO2I 600 with inotropes Grade 2 ARDS score > 9 Creatinine > 2.5 mg/dl Bilirubin > 4.0 mg/dl DO2I 450-600 with or without inotropes Grade ARDS score > 13 Creatinine > 5.0 mg/dl Bilirubin > 8.0 mg/dl DO2I < 450 with or without inotropes
ARDS: Adult Respiratory Distress Syndrome *ARDS score = A+B+C+D+E A. Pulmonary findings by plain chest radiography 0 = normal 1 = diffuse, mild interstitial marking/opacities 2 = diffuse, marked interstitial/mild air-space opacities 3 = diffuse, moderate air-space consolidation 4 = diffuse, severe air-space consolidation B. Hypoxemia (PaO2/FiO2 0 = > 250 1 = 175-250 2 = 125-174 3 = 80-124 4 = < 80 C. Minute Ventilation (l/min) 0 = < 11 1 = 11-13 2 = 14-16 3 = 17-20 4 = > 20 D. Positive End Expiratory Pressure (cmH2O) 0=<6 1 = 6-9 2 = 10-13 3 = 14-17 4 = > 17 E. Static Compliance (ml/cmH2O) 0 = > 50 1 = 40-50 2 = 30-39 3 = 20-29 4 = < 20
Incidence
Five to seven percent of emergency surgical procedures. 15% of patients with injury severity score 15 50% of patients with injury severity score 25 and 6 unit blood transfusion over 24 hours.
Predisposing Factors
Shock (25%) Massive blood transfusion ( 6 units) 30% Massive crystalloid resuscitation ( 6 liters) 30% Infection (25%) Chest injury (10%) Multiple long bone fracture (10%) Retained necrotic or inflamed tissue (10%)
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Pathogenesis
Remarkably the pathogenesis of the multiple organ failure syndrome remains incompletely understood, but it is most likely related to some combination of a dysregulated hyperinflammatory response, maldistribution of microcirculatory blood flow, ischemia reperfusion injury, and dysregulation of immune function.
MOF Failure: MOF Syndrome
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The initiating event is thought to be hyperactivity of the inflammatory response characterized by generalized mediator activation, hypercoagulability, complement activation, activation of immune cells including mast cells, PMNs, monocytes, and macrophages in a generalized fashion which attacks the endothelial lining of micro blood vessels in various organs causing increased permeability and a generalized inflammatory response in the affected tissues. In addition, a complicating factor seems to be plugging of the microcirculation as a result of deposition of fibrin, leukocyte plugging and generalized swelling of endothelial cells as a result of the inflammatory response. As the inflammatory response progresses and the microvascular blood supply decreases in various organs, organ dysfunction ensues gradually over time as the process affects more and more of the organs tissue. Eventually the dysregulated hyperinflammatory response is replaced with a counter hypo inflammatory response after a variable period of time. A hypo immune response ensues with elaboration of counter inflammatory mediators such as interleukin-10, interleukin-13, and PGE2. As a result a change in T-helper cell phenotype occurs from predominantly Th1 to Th2 lymphocyte populations. These and other factors lead to a decreased ability of fixed macrophages and circulating PMNs to counter bacterial and viral invasion. If this process continues unabated a chronic infectious state results with gradual deterioration of the patient until death. The patient may succumb as a result of overt organ dysfunction or as a subsequent complication of overwhelming infection.
The multiple organ dysfunction syndrome is now known to be a dynamic process which occurs with variable clinical sequalae both in terms of severity and changes over time. There appear to be two distinct groups of patients, one, which develops the syndrome quite early usually after a major injury or episode of hemorrhagic hypotension, and a second group which develops the syndrome later often as a result of a surgical complication or the late development of infection. In actuality these two presentations are probably different clinical manifestations of the same underlying process. It now appears that the syndrome can be either mild or severe in its initial presentation and may progress in a variety of ways.
Therapeutic Maneuvers and Treatment Prevention

Our ability to treat the full blown multiple organ failure syndrome is limited, and therefore, the most successful strategy is to identify the patient at risk for developing multiple organ failure before they have developed it or while it is in its initial mild phase. It is imperative to limit the number of operative complications. Debride necrotic tissue, stop contamination, and prevent hematoma formation. Important decisions include definitive operation versus damage control procedure to prevent coagulopathy, hypothermia, massive blood loss and abdominal compartment syndrome.
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Optimal resuscitation by maximizing oxygen delivery and consumption with appropriate blood product usage and the use of controlled reperfusion techniques to minimize ischemia reperfusion injury. Adequate oxygenation but avoidance of pulmonary injury with high airway pressures and high FiO2. Ventilator settings should minimize airway pressure and FiO2 by the use of moderate levels of PEEP, inverse ratio ventilation and permissive hypercapnia. Nutritional support should be started early using enteral immune enhancing diets in-patients at high risk. TPN supplementation with avoidance of high carbohydrate and lipid infusion. Infection should be treated aggressively often times with empiric antibiotics and antifungals. Immune enhancementat the present limited to immune enhancement diets; however, the near future may bring means to modulate the immune system in a more organized fashion.
Organ Specific Support

These areas are treated in greater depth in other chapters of this manual. Cardiovascular: maximize DO2 and VO2 with cardiotonics, keep hemoglobin between 10-12, and perhaps use colloids after initial crystalloid resuscitation. Pulmonary: moderate levels of PEEP minimizing peak airway pressures and FiO2, permissive hypercapnic and frequent position changes. Renal: avoid nephrotoxic drugs, maintain organ perfusion, maintain tubular flow with manitol and loop diuretics, maintain nonoliguric state and perform dialysis early when oliguria develops. GI, liver: feed enterally early using feeding tubes past the ligament of Treitz while decompressing the stomach. GI bleeding prophylaxis with H2 blockers or sucralfate; consider monitoring gastric mucosal blood flow with tonometry. Immune system: immune enhancing diets, new concepts, and antioxidants.
References
1. 2. 3. 4. 5. Cryer H Gill. Ischemia reperfusion as a cause of multiple organ failure. Baue, Faist, Fry. Multiple organ failure. In press. Eiseman B, Bert R, Norton L. Multiple organ failure. Surg Gyn 1997; 144:323-326. Sauia A, Moore FA, Moore EE. Multiple organ failure can be predicted as early as 12 hours after injury. J Trauma 1998; 45:291-303. Cryer HG, Leong K, McArthur DL et al. Multiple organ failure: by the time you predict it its already there. J Trauma 1990; 46:597-606. Barquist E, Kirton O, Windsor J et al. The impact of antioxidant and splanchnic directed therapy on persistent uncorrected gastric mucosal pH in the critically injured trauma patient. J Trauma 1998; 44:355-359.
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Surgical Nutrition
Edward E. Cornwell Introduction
The ancient Greeks and Egyptians are credited with the first use of a nonoral route of nutrition, administering wine, milk, or broth by the use of rectal syringes. In the late 1700s John Hunter instilled nutrients into the stomach by way of a catheter and syringe. One of the earliest descriptions of the parenteral route was by Sir Christopher Wren who infused wine into the veins of dogs in 1656. In more modern times Dudrick and associates adopted a method of infusing concentrated dextrose solution into the jugular veins of dogs, and in 1952 Aubaniac described the method for percutaneous placement of a subclavian venous line. Since the early 1970s, when hyperalimentation was used for patients with gastrointestinal fistulas, nutritional support by way of enteral and parenteral nutrition has become a multidisciplinary endeavor involving physicians, nurses, dieticians, and pharmacists. The concept of nutritional support for critically ill and injured surgical patients is one of the major medical advances of the last quarter of the 20th century.
The Goal of Nutritional Support

The goal of nutritional support in the management of trauma patients is to:
- prevent nutrient deficiencies that may be brought on by the increased metabolic demands associated with critical injury; - provide appropriate doses of nutrients consistent with existing metabolic demands; - avoid complications related to the technique of provision of nutritional support; - improve patient outcome as it relates to septic complications, wound healing, and regaining of daily functions.
Who Should Receive Nutritional Support?

There is no evidence supporting routine nutritional support of surgical patients with normal baseline status who are not critically ill. Nutritional support is reserved for patients who are malnourished on admission or have diseases (severe trauma, burns, severe surgical infections) that place them at high risk for the development of malnutrition.
- Malnutrition is defined as impairment of normal anabolic processes caused by insufficient energy or protein. - Malnutrition in surgical patients may result from; a) decreased caloric or protein intake (e.g., secondary to GI obstruction, anorexia); b) nutrient losses
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What Components Should Be Provided?

Recommended nutrient provisions were formulated by the 1997 Consensus Statement on Applied Nutrition in ICU patients by the American College of Chest Physicians. Caloric requirements are typically expressed in terms of total energy expenditure (TEE). TEE is determined by three components:
- Basal Energy Expenditure (BEE) is the caloric expenditure of a person at rest whos fasted more than 10 hours. - Diet Induced Thermogensis (DIT) is the energy expenditure for food consumption (eating, digestion, absorption, hydrolysis) and is typically 5-10% of TEE. - Activity Energy Expenditure (AEE) represents energy secondary to physical activity (the work of breathing, etc) and may account for 15-40% of TEE. - Most patients will be adequately fed with 25-30 total kilocalories/kg body weight/day. - Protein sources should account for 15-20% of the total calories administered per day (estimated at 1.2-1.5 g/kg/day). - Carbohydrate sources should be responsible for 30-70% of the total calories administered, up to 2-5 g of glucose/kg/day. - Fat sources should account for 15-30% of the total calories administered per day. - The caloric and protein requirements need to be increased in certain clinical settings such as patients with systemic inflammatory response syndrome (SIRS) or with major head trauma. - Multivitamins and trace elements such as copper, manganese, selenium, and chromium are also supplied.
Which Route?
There is ample laboratory and clinical evidence to suggest that nutrition should be provided enterally whenever possible. The advantages of enteral support relative to total parental nutrition (TPN) are:
- lower cost - promotion of intestinal function and bile flow by stimulating secretion of intestinal hormones such as gastrin and cholecystokinin - prevention of intestinal mucosal atrophy - maintenance of mucosal integrity - inhibition of bacterial overgrowth - avoidance of central venous catheter related complications (pneumothorax, catheter infection) - lower incidence of noncatheter related septic complications.
When to Feed
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The advantages of enteral nutrition are largely lost if initiated once sepsis/ hypermetabolism has already occurred. While not precisely known, it would appear that obtaining approximately 50% of nutritional requirements within the first 48 hours after injury is a reasonable goal.
- Enteral feeding stimulates increased gut oxygen demand, and case reports have described intestinal infarction associated with the initiation of early jejunal feeds in hypermetabolic patients requiring vasopressors. Therefore jejunal feeds should be initiated only after hemodynamic stability has been achieved.
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Formulas for Nutritional Support

A large number of stock formula preparations for both parenteral and enteral feeds are available for use by patients in hospitals. These formulas vary from hospital to hospital, and most patients receive adequate support with one of the stock formulas. With both parental and enteral preparations, the occasional patients requiring custom mixing of amino acids, dextrose, and fats may be achieved if supplementation of individual nutrients is desired.
Immune-Enhancing Diets
With appreciation of the gut as a major immune organ, special attention needs to be given to immune-enhancing diets. Certain nutrients which exert pharmacologic effect and modulate healing and immune function are considered essential components of immune-enhancing diets. These include:
- Arginine, a semi-essential amino acid which is involved in collagen synthesis and increases the response of peripheral T lymphocytes to mitogens. - Glutamine is an amino acid that is mobilized from peripheral tissue such as skeletal muscle during the early catabolic response to major trauma. The use of glutamine deficient diets has been associated with intestinal mucosal atrophy during stress states in several animal models. - Omega-3-fatty acids are present in fish oils, canola oil, etc. They are thought to enhance the immune response by decreasing the synthesis of prostaglandins that are inhibitory to the function of immune cells. - Synthetic ribonucleic acids (RNA) have been postulated to support proliferation of intestinal crypt cells and lymphocytes.
Early studies showing clinical benefits of the immune-enhancing diets were criticized because the group receiving experimental diets frequently benefited by receiving a greater amount of caloric and nitrogenous (protein) support, thus making it difficult to determine whether the benefits were attributable to immune enhancement or the increase in nitrogen and calories.
- On the basis of the existing studies, and in consideration of the increased expense associated with immune enhancing diets, recommendation cannot be made for the routine administration to all trauma patients. - The weight of the literature would support providing this to the most severely injured patients, such as those identified by injury severity scores (ISS) > 21.
Complications
Complications of enteral nutrition occur in about 10-15% of patients and include:
- Diarrhea
There are multiple potential causes of diarrhea related to enteral feeding including:
low fiber solutions administration of hypertonic formulas use of formulas with high fat content - Aspiration
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Treatment to prevent aspiration includes:

Monitoring gastric residual volume (every 4-6 hours) Cessation of feedings when residual volumes exceed 100-150 cc. The head of the bed should be elevated to at least 30% at all times.
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Complications of parenteral nutrition may be mechanical, infectious, or metabolic.

- Mechanical complications include complications of central venous catheterization including pneumothorax, catheter misdirection, arterial puncture, or air embolism. Venous thrombosis may occur as a delayed complication that manifests as ipsolateral arm and neck swelling. - Catheter-related sepsis occurs in 2-8% of adults receiving central TPN. Skin flora is the most important source that colonizes the catheter tunnel. - Metabolic complications include hyperglycemia, hyperlipidemia and associated reticuloendothelial cell dysfunction, and hepatic complications (elevation of transminases, cholestasis, and fatty infiltration). - Electrolyte and acid base abnormalities may also complicate TPN administration. Refeeding of the malnourished patient promotes intracellular shifts of magnesium, potassium, and phosphate. Hypophosphatemia is a common resulting abnormality that may cause hemolysis, Rhabdomyolysis, and increased hemoglobin oxygen affinity due to decreased production of 2,3-diphosphoglycerate. Metabolic acidosis has been described to occur related to acid moieties present in TPN solution.
References
1. 2. 3. 4. 5. Brown RO, Hunt H, Mowatt-Larssen CA et al. Comparison of specialized and standard enteral formulas in trauma patients. Pharmacology 1994; 14:314-320. Cerra FB, Lehmann S, Konstantinides N et al. Improvement in immune function in ICU patients by enteral nutrition supplemented with arginine, RNA, and menhaden oil is independent of nitrogen balance. Nutrition 1991; 7:193-199. Kudsk KA, Minard G, Croce MA et al. A randomized trial of isonitrogenous enteral diets after severe trauma. An immune-enhancing diet reduced septic complications. Ann Surg 1996; 224:531-543. Mendez C, Jurkovich GJ, Garcia I et al. Effects of an immune-enhancing diet in critically ill injured patients. J Trauma 1997; 42:993-942. Moore FA, Moore EE, Kudsk KA et al. Clinical benefits of an immune-enhancing diet for early postinjury enteral feeding. J Trauma 1994; 34:607-615.
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Acute Burn Injury

Jeffrey R. Antimarino and Warren L. Garner Epidemiology
There are more than 2 million people burned In the United States each year. Approximately 10% of these burns will require hospitalization. Children between the ages of 1-5 make up 50% of the burned population. The most common cause in this age group is scald injury. Structural fires account for only 5% of all burn admissions but are responsible for almost half of the burn-related deaths.
Classification
Burn injuries are classified by size and depth.
- First-degree burns are superficial injuries to the epidermal layer of the skin. The skin is red, dry and painful. Sunburns are classic examples of first-degree burns. - Second-degree burns involve the epidermal and the upper portion of the dermis. These burns are also described as partial thickness. Clinically, it may be difficult to distinguish between superficial and deep second degree burns. The skin is typically red, edematous and has a wet and glistening appearance. Blisters are common. The skin blanches on palpation. Superficial dermal involvement may take 7-10 days to re-epithelialize; however, deep dermal involvement may take as long as three weeks to heal. An antimicrobial dressing such as Silvadene should be used until complete re-epithelialization takes place. - Third degree burns involve the entire thickness of the skin. This is also termed full thickness injury. The skin is pale, dry and does not blanch on palpation. The skin is typically insensate and may have a leathery texture. - Fourth degree burns involve underlying tissues such as fat, muscle and bone.
The size of the burn is classically described as percentage of the total body surface (TBSA). There are many ways to determine the TBSA. The easiest way to estimate the percent burn is to use the Rule of Nines (Fig. 56.1). In this method the body is divided into regions and each region is quantified as a multiple of nine. Each arm and the head are 9%; the legs are 18% and the torso is 36%. These numbers are slightly different for infants since their head occupies a greater surface area percentage than an adult head. The most accurate method is to use predetermined charts of body percentage, Lund-Browder charts (Fig. 56.2). Another method is to use the patients hand to estimate percent involvement, as the human palm is roughly 1% of the total body surface area. Only second and third degree burns are included in the estimation of burn size.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Jeffrey R. Antimarino, LAC + USC Burn Center, Los Angeles, California, U.S.A. Warren L. Garner, LAC + USC Burn Center, Los Angeles, California, U.S.A.
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Fig. 56.1. Wallaces Rule of Nines for estimation of burn size.
Admission Criteria
The American Burn Association has published generalized guidelines for admission to a burn center (Table 56.1).
Pathophysiology and Tissue Response

The mechanism of tissue damage is two-fold following a burn injury. First, the initial thermal injury causes three zones of injury. The Zone of Coagulation is an area of irreversible cell death and protein coagulation. The immediate surrounding area is called the Zone of Stasis. This is an area of decreased perfusion and is at risk for further cell death. The most peripherally affected area of injury is called the Zone of Hyperemia. This area will usually go on to heal spontaneously. Second, the thermal injury causes the release of several local inflammatory mediators such as prostaglandins, bradykinins, histamine and cytokines. These vasoactive mediators cause significant alterations in the capillary endothelium and basement membrane, which results in tissue edema and ischemia. It is this local reaction that can cause further tissue loss in the Zone of Stasis.
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Fig. 56.2. Estimation of burn size - Lund and Browder Chart.
Table 56.1. Guidelines for referral to a burn center

Second and third degree burns > 10% TBSA in patients less than 10 years of age and greater than 50 years of age. 2. Second and third degree burns > 20% in all other age groups. 3. Second and third degree burns with serious threat of functional or aesthetic impairment involving the face, hands, feet, perineum and major joints. 4. Third degree burns > 5% in any age group. 5. Inhalation injury with any burn. 6. Electrical burns, including lightning. 7. Circumferential burns. 8. Burn injury in patients with significant premorbid medical conditions that could complicate management, prolong recovery or affect mortality. 9. Any burn patient with concomitant trauma in which the burn poses the greatest risk of morbidity or mortality. If the trauma injury poses the greatest risk, then the patient should be treated in a trauma center until stabilized. 10. Hospitals without qualified personnel or equipment for the care of children should transfer burned children to a burn center with these capabilities. 1.
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Burn injury not only affects local tissues but can also initiate a systemic response. Burns larger than 15-20% TBSA cause a significant release of vasoactive mediators into the systemic circulation. These mediators cause endothelial cells in distant capillary beds to change shape, resulting in capillary leak syndrome. This results in hypovolemia due to large shifts of fluid and proteins out of the vasculature and into the tissues. Large burns also activate the complement and coagulation cascades resulting in thrombosis of the microvasculature. The accumulation of oxygen free radicals in burned tissue also increases tissue damage and increases edema. Other organ dysfunction is common after larger TBSA burn injuries. Myocardial suppression is seen in burns greater than 40% TBSA, possibly due to the release of the inflammatory cytokine TNF. Patients with large burns have been found to have suppression of most immune functions including decreased neutrophil chemotaxis, phagocytosis and killing; decreased cell-mediated and humoral-mediated immune responses as well as impairment of other cell types including macrophages and natural killer cells. Hemolysis is also common in large burns. Red blood cell destruction can be as high as 40% of the circulating volume.
Fluid Resuscitation
Volume status is a concern for any person sustaining a second or third degree burn; however, only burns involving greater than 20% TBSA need formal fluid resuscitation. Burn injuries less than 20% TBSA can be treated with liberalized oral intake and intravenous fluids to maintain urine output 0.5 cc/ kg/hr for an adult and 1 cc/kg/hr for a child. There have been several formulas derived to resuscitate patients with large burns; however, the Parkland formula has become the standard method.
- According to the Parkland formula, in the first 24 hours a patient should receive 4 cc/kg/%TBSA burned of Ringers lactate. Only the body percentage of second and third degree burns is used for this calculation. Half of the calculated fluid should be given in the first eight hours from the time of the burn. The other half is given over the subsequent 16 hours. - Example: a 70 kg man sustains a 50% second and third degree burn. Using the Parkland formula he would require 14 liters of lactated ringers in the first 24 hours (4 cc x 70 kg x 50). During the second 24 hours following a burn about half of the fluid given during the first 24 hours is needed. - It must be emphasized that the Parkland formula or any other formula is only a guide. The goal of any resuscitation attempt is to maintain adequate end organ perfusion. Generally, urine output is an accurate measurement of volume status and tissue perfusion. The formula should be adjusted to maintain adequate urine output as described above. The formula should also be adjusted depending on the patients underlying medical condition such as cardiac or pulmonary disease.
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The use of 5% albumin in the resuscitation protocol is controversial. It is certainly detrimental if used within the first 24 hours since this will result in extravasation of proteins into the surrounding tissues, which leads to increased pulmonary and tissue edema. In patients with very large injuries and resuscitations (greater than 60% TBSA), there may be a benefit from albumin administration (0.5 cc/kg/%TBSA burned 5% albumin). There is little clinical evidence that the use of hypertonic solutions or dextran decreases the amount
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of fluid needed for adequate resuscitation and some evidence that these solutions increase end organ dysfunction. The use of Swan-Ganz catheters is beneficial in those patients who do not respond as expected or where the urine output may not be an accurate reflection of volume status. Patients with serious inhalation injury, burn-induced cardiac dysfunction or pre-existing congestive heart failure, renal or hepatic insufficiency are good indications for the use of a Swan-Ganz catheter.
Acute Management
All burn patients should be evaluated as a trauma victim. The first priority is to establish an adequate airway, ventilation and systemic circulation. A primary survey should be performed to identify and treat any immediate life threatening injuries. A secondary survey, head-to-toe examination, should then be performed. Approximately 15% of burned patients have concomitant injuries. Patients that have sustained large burns become hemoconcentrated; therefore, a burn patient with a low hematocrit on arrival to the emergency room should be examined for other sources of blood loss. During the secondary survey all burn wounds should be gently washed and any loose or dead skin should be debrided. Access lines should be placed soon after arrival, if possible, in unburned sites. Any line placed prior to the skin being thoroughly cleansed should be replaced within 48 hours to lessen the risk of infection. Patients with large burns including the extremities will need an arterial line, as the tissue edema that develops due to the burn may interfere with the blood pressure cuff s ability to measure an accurate blood pressure. A nasogastric or Dobhoff tube for alimental feeding should also be placed soon after admission. It is extremely important to begin nutritional support within the first 6 hours after admission for three reasons.
- First, burn victims develop a large catabolic process secondary to the systemic inflammatory response. The basal metabolic rate may rise to 3-5 times normal rates. The Curreri formula (25 kcal/kg + 40 kcal/TBSA) can estimate the patients caloric requirements. The protein requirement also rises. An average person requires approximately 1gm of protein/kg/day. Patients with large burns require two to four times that amount. - The second reason for beginning tube feeds is to prevent translocation of intestinal bacteria. It is not uncommon for a large burn to cause an ileus. If a patient is not tolerating tube feeding, the use of Reglan and/or Erythromycin may be helpful. - The third reason for beginning tube feeds is to prevent stress ulceration. Patients with large burns have been shown to have a high incidence of developing gastric ulcers, specifically called Curlings ulcers. Early tube feeding decreases the risk of developing these ulcers.
Escharotomy
Circumferential full thickness burns can impair blood flow to underlying tissue as well as distal parts of extremities. As the tissues swell due to the release of local and systemic vasoactive cytokines, the skin in a full thickness burn is unable to expand. The skin therefore, can act as a tourniquet. The burn eschar needs to be incised in order to allow expansion of the tissues and to maintain tissue perfusion. Full thickness burns are insensate; therefore
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escharotomies may be performed at the bedside using a scalpel or electrocautery with minimal sedation. Escharotomies are performed along the medial and lateral aspects of the upper and lower extremities. If the hands are involved then incisions along the dorsum of the hand, along the radial border of the thumb and small finger and along the ulnar border of the index, long and ring fingers If the chest is involved, incisions are made vertically along the mid-axillary lines, and horizontally following the costal margin and the clavicles. It is unnecessary to incise vertically over the sternum. Incisions need only be carried through the eschar until reaching the subcutaneous fat layer. It is important to incise along the entire length of the eschar. If perfusion is not restored, compartment pressures should be measured and fasciotomies performed if necessary.
Wound Management
After initial inspection of all burned areas, all necrotic or loose skin should be debrided, blisters should be ruptured and all areas should be gently cleaned with mild soap and water. The wound should be treated with a daily antimicrobial dressing. The treatment of intact blisters is somewhat controversial, although the senior author believes that removal of most blisters and initiation of antimicrobial dressings results in simplified and effective care. Systemic antibiotics are not effective in preventing wound infection and should be started only if there are signs of cellulitis. There are several topical antibiotic dressings that can be used. The most commonly used agent is silver sulfadiazine (Silvadine). Silvadine has many advantages. It has a wide spectrum of coverage, has few complications, is painless and easily removed. Polysporin and Bacitracin are common agents. They are inexpensive and painless; however have a narrow spectrum of coverage. Bactroban is a relatively newer agent. It has a broader spectrum than polysporin and bacitracin but is expensive. Mafenide (Sulfamylon) is the only agent that effectively penetrates the burn eschar. It is the agent of choice for treating significant burns to the ears to prevent chondritis. Mafenide can cause metabolic acidosis. The newest agent is Acticoat. This is a gauze-like dressing made of silver. Acticoat is moistened with sterile water and then placed directly over a wound or skin graft. The water releases the silver ions, which have excellent antimicrobial properties. The advantage to Acticoat is that the dressing need only be changed every three to four days.
Inhalation Injury
Inhalation injury has an enormous impact on the survivability of a burn. The evaluation and management of this pathology are described in a separate chapter.
Indications for Surgery
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Surgery is indicated for all full thickness burns to the face, hands and involved joints. Surgery is also indicated for full thickness burns larger than 1-2 cm2 on the trunk or extremities and partial thickness burns that have not healed within three weeks from the time of injury. The goal of surgery is to remove all nonviable tissue and close all open wounds. In the vast majority of patients this can be accomplished with one procedure
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that should be performed within a week of injury. This decreases septic complications, speeds wound healing and increases the rate of functional recovery. In the case of a large burn with limited donor sites, the surgery must be carefully planned to meet these criteria. Excisions must be prioritized. In patients with massive injuries the first priority should be to excise those areas that can most significantly decrease the necrotic load: torso and extremities. The face has the lowest priority since it is a small area and due to the rich blood supply becomes infected less often. The choice to stage excisions or debride all necrotic tissue and use other products along with autografts to close the wound in one sitting depends upon the individual surgeons preference.
Skin Grafts and Skin Alternatives

There are several options for closure of the wound bed after debridement of all nonviable tissue. Partial thickness wounds will re-epithelialize spontaneously and do not require an additional procedure for wound closure. Full thickness wounds require skin grafting or some alternative. The most useful and common method of skin grafting is to use autologous split thickness skin. Harvesting at 0.008-0.015 inch, depending on the patients age and the donor site, creates a donor wound which heals spontaneously in 10-14 days. Unmeshed split thickness grafts, also called sheet grafts, are the best coverage when long-term flexibility and appearance are the primary consideration. They should always be used to cover areas of the face and hands and should be strongly considered when grafting any burn in a child. The downside is that in large burns, donor sites are limited; therefore, it is difficult to graft an entire large wound with sheet graft. Meshed grafts also offer advantages. The need for a large donor site is decreased. Meshed grafts have a lower incidence of loss due to seroma and hematoma. The disadvantages of meshed grafts are that they never lose a cobblestone appearance and have a higher rate of contraction. There are many alternatives to autografting. Allograft, cadaveric skin, is the traditional method to temporarily close a wound bed after excision. Allograft encourages vascular ingrowth so the wound bed is better prepared for subsequent autografting. The disadvantages of allografts are its limited supply, variable condition of the skin since donors may be elderly and the small risk of viral transmission. Research advances have led to the development of both synthetic and bioengineered alternatives to allografts. The first of these products, Biobrane, is a sheet of nylon mesh impregnated with collagen that is bonded to a silicone rubber membrane. Biobrane can be used to cover partial or full thickness wounds to help prevents fluid loss and to prevent bacterial invasion. Trancyte is a product that combines Biobrane with a protein matrix derived from neonatal fibroblasts. This protein matrix is proposed to contain wound-healing factors. Trancyte can be used to cover partial or full thickness wounds. Trancyte promotes rapid epithelialization of partial thickness wounds. It is more resistant to infection than other products. Integra is a permanent dermal replacement product. Integra consists of a bilaminar membrane of bovine Type I collagen crosslinked with chondroiton-6-sulfate and a silicone elastomer epidermal equivalent. Integra is used in full thickness wounds. It causes vascular ingrowth into the dermal component. This process takes 2-3 weeks. At that time the silicone layer can be removed and
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an ultra thin, .006 inch, split thickness skin graft can be used to cover the Integra.
Nonthermal Burns Chemical Burns

Chemical burns constitute a small percentage of admissions to a burn center. These injuries can occur at home by mishandling common cleaning agents or at work by industrial exposure. Unlike flame injuries, chemical injuries can continue to cause damage as they are absorbed by the tissues. The degree of injury from a chemical burn depends upon the agent, the concentration of the agent and the duration of exposure. The most important part of therapy is irrigation of the exposed area with copious amounts of water. The water will dilute the chemical agent. As a rule, acids tend to be less damaging than alkaline agents. The acidic agents are neutralized quickly; however, alkaline agents hydrolyze fats and proteins as they are absorbed. These reactions form ions that induce further chemical reactions, which continue to penetrate into tissues. Alkaline burns are more common than acidic burns because these agents make up common household cleaning agents including bleach, sodium hydroxide (Drano) and lime.
Electrical Burns
Electrical injuries make up less than 5% of burn center admissions. These injuries can be initially deceiving because the apparent skin involvement is small compared to the amount of destruction that may have occurred. Electrical injuries are divided into high and low voltage. Low voltage injuries are usually seen with household currents. These injuries are usually small thermal injuries without the sequelae seen in high voltage injuries. High voltage injuries (>1000 volts) have skin involvement at contact sites and larger destruction of deeper tissues. These currents can cause cardiac arrest, dysrhythmias and Rhabdomyolysis. All patients sustaining a high voltage injury should have an EKG and electrolytes sent on admission to the emergency room. A Foley catheter should be placed immediately to check for Rhabdomyolysis. The extremities should be examined for compartment syndromes. Most sequelae of high voltage injuries occur within the first 24 hours after the time of injury. If the original EKG is negative and the patient has no history of cardiac disease then cardiac monitoring is unnecessary. It should also be noted that these patients should be carefully examined for fractures as high voltage injuries have a significant incidence of falls.
Patient Outcomes
Patient outcomes have improved drastically over the past two decades. In 1971, 50% of patients admitted with a burn 40% TBSA died. In 1990, the same patient would routinely survive. Increases in survival are due almost exclusively to improvements in resuscitation, the treatment of inhalation injury and improvements in critical care practices. There is data that shows that many burn survivors can readjust after the injuries and regain a lifestyle that is satisfactory to them. A study in 1989 showed that the most significant variables influencing return to work after injury are degree of
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burn, burns to the hands, type of work and age of the patient. On average, a person sustaining a 5% TBSA burn will return to work within one month, a person with a 10% TBSA burn will return within six months and patients with 20% TBSA burns return within 1-1.5 years. Patients less than 45 years of age are also more likely to return to work. Burn patients require a large support system after surviving their injuries to help integrate back into their lifestyles. These people must have not only a strong social circle but must also be willing to participate in interdisciplinary groups such as counseling, occupational and physical therapy.
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CHAPTER 57
Inhalation Injury
John F. Fraser and Michael Muller Introduction
Inhalation injury may be defined as an airway or pulmonary parenchymal injury due to the components of smoke: heat, particulate matter, irritants, and asphyxiants. In the presence of burns, inhalation injury is a greater contributor to overall mortality and morbidity than either percentage body surface area burn or age, with the majority of victims dying at the scene, due to hypoxia and asphyxiation. Inhalation injury is present in between 20 and 30% of all burn victims. Whilst the mortality associated with cutaneous burns has fallen dramatically, this improvement has not been reflected in inhalation injury. The difficulty in diagnosis and quantification of the injury, and the delay in symptom presentation account for some of these problems. There is significant morbidity and mortality both immediately and throughout recovery.
History
Recorded as early as the first century AD, by Pliny, describing the killing of prisoners by exposure to greenwood fires. Major recognition received after the Coconut Grove Night Club disaster Nov 28th 1942 in the United States in which 491 people were killed.
At Risk
Unable to escape fire due to
- Extremes of age - Immobility due to other trauma - Reduction of level of consciousness: alcohol, drugs, effects of smoke.
Lack of functional smoke detector Chronic pulmonary disorders: asthma, COPDmorbidity of smoke inhalation increased.
Assessment of Smoke Inhalation Patient

History
Was the fire in an enclosed space. Duration of exposure. What type of material burned, e.g., paints, chemicals. Level of consciousness on scene.
Note: Burns and smoke inhalation victims should be treated as a trauma patient, with trauma protocol being followed as routine. This includes cervical immobilization until injury is excluded.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. John F. Fraser, University of Queensland, Royal Brisbane Hospital, Herston, Australia Michael Muller, University of Queensland, Royal Brisbane Hospital, Herston, Australia
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Inspection
- Stridor: indicates severe laryngeal edema and the possibility of imminent airway obstruction - Voice hoarsenessan excellent warning sign - Tachypnea - Use of accessory muscles - Persistent cough - Soot in oropharynx - Singed nasal hair
Examination
Confusion/disorientationindicating hypoxia and/or presence of asphyxiants Wheeze Soot-stained sputum Central facial burn Burn involving central face: 60% incidence of inhalation injury. Burn involving no facial burn or only peripheral facial burn has 20% incidence of inhalation injury. - Increasing size of cutaneous burn indicates an increased likelihood of smoke inhalation
Investigations Arterial Blood Gasesmandatory

- Oxygen saturation(SaO2)however, SaO2 is inaccurate in the presence of significant carboxyhemoglobin (COHb) or methemoglobinemia. - CarboxyhemoglobinThere is a significant variation in carboxyhemoglobin concentrations in the community. Breakdown in hemoglobin results in minor concentrations, and a city lifestyle is associated with significant concentrations.
Chest x-rayFrequently normal initially but essential nonetheless as baseline assessment and to exclude trauma. BronchoscopyThe gold standard for diagnosis of inhalation injury. Xenon 133 lung scanA useful adjunctive test when bronchoscopy equivocal. Smoke inhalation/burn injury are frequently associated with other trauma and appropriate examination should be undertaken.
Pathophysiology
Inhalation injury induced by smoke can be separated into: Thermal Injury
- Air of 300C at the oropharynx is cooled to 50C on arrival at the trachea. The vocal cords also reflexively adduct at 150C. Direct thermal injury below the cords, is therefore uncommon. Steam, however, is an important exception as it has a latent heat capacity that is 4,000-fold that of dry air and can thus inflict a severe thermal injury to the lower airway. This results in depilation of the cilia and cast formation from sloughing of the necrotic tracheal and bronchial mucosa. Small airway plugging and air-trapping with subsequent bronchopneumonia and atelectasis then occurs.
Irritants and Toxins

- Smoke is a heterogeneous substance whose composition depends on the material combusted and the environment in which the combustion occurred. There are two separate phases of toxins: particulate and gaseous.
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ManagementEarly
Humidified OxygenMany smoke inhalation victims will require this alone, but, as symptoms can be slow to develop, they should continue to be monitored closely. Supplemental oxygen is the mainstay of treatment of carbon monoxide poisoning and humidification helps to loosen secretions and therefore aid expectoration. IntubationApproximately 50% of all patients with smoke inhalation require endotracheal intubation and most of these will have co-existent burns. Intubation is indicated by the need to support ventilation and to protect the airway of the unconscious patient. It is the specific case of thermal injury to the upper airway that requires special attention. The upper airway, and in particular the larynx, is an excellent absorber of heat. This protects the lower airway from significant thermal damage, with the exception of steam inhalation. The absorption of heat is the main contributor to upper airway and laryngeal swelling, which can precipitate acute airway obstruction. If there are signs suggestive of significant upper airway injury (voice changes, stridor, and air hunger), a definitive airway should be secured immediately. The conscious patient is able to protect his/her own airway effectively, and removal of these valuable protective reflexes by sedation or excessive analgesia should be avoided if at all possible. Direct vision of the laryngeal inlet in the spontaneously breathing patient is the safest option. Either direct laryngoscopy, or fiberoptic bronchoscopy with local anesthesia or inhalational induction may be used. The airway is maintained, as the patient self ventilates, and the risk of losing the airway is diminished. In burns, suxamethonium causes refractory hyperkalemia after 24-48 h in burns but can be used in the acute setting. Nondepolarizing agents should be used with great caution as there is a risk of the airway being lost. The largest compatible endotracheal tube should be used to facilitate suctioning and/or bronchoscopy. Swelling of the face generally worsens during the resuscitation and acute phase, and the endotracheal tube should be left uncut to avoid losing the end of the endotracheal tube into the oropharynx as the
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face swells. The tube should be well secured, though ties should be loose enough to allow for the facial swelling, and re-evaluated regularly. The cuff of the endotracheal tube should be filled with enough air to avoid a leak, and should be reassessed regularly. The swelling that occurs at the damaged laryngeal inlet/upper trachea may increase the pressure on already compromised tracheal mucosa and result in tissue necrosis. Regardless of the method chosen, the most experienced person available should be in charge of the intubation. OxygenationIf significant CO poisoning is suspected/proved, the patient should be ventilated on 100% oxygen for at least 48-72 hrs to facilitate maximal dissociation of carboxyhemoglobin from hemoglobin. There are risks of prolonged high oxygen concentration, such as compromise of the already impaired mucociliary mechanism and absorption atelectasis but they are outweighed by the risk of long term sequelae from carboxyhemoglobin poisoning. Hyperbaric treatment is effective in rapidly reducing the carbon monoxide levels and speeding the dissociation of carbon monoxide from cytochrome c oxidase but has not been shown to improve outcome in randomized controlled trials and is associated with risks, both to patients and staff. It is used in some centers. VentilationThe recently introduced high frequency, flow interrupted ventilator, which results in pulsatile flow, has become popular and may reduce mortality and the incidence of barotrauma and ventilator associated pneumonia. There may be a reduction in barotrauma associated with open lung ventilation strategy (tidal volume 6-8 ml/kg) and optimum positive end expiratory pressure. This modality, or pressure limited ventilation, should be instituted early to limit the effects of air trapping and barotrauma. Fluid resuscitationThe presence of inhalation injury necessitates an increased fluid requirement over and above that calculated for the cutaneous burn. However, it is difficult to quantify inhalation injury and hence the exact volume needed. At least a 30% increase fluid requirement is required. Frequently even more is required. Paradoxically, there is an increased risk of pulmonary edema in smoke inhalation, if fluid resuscitation is insufficient. As with all burns, fluid resuscitation is calculated by a chosen formula (e.g., Parkland formula), but this should only be used as a framework. If the clinical indicators of resuscitation indicate hypovolemia, e.g., hypotension, tachycardia, reduced urine output or developing lactic acidosis, further fluid should be administered or causes for failure of fluid resuscitation should be considered. DrugsSteroids have been shown to increase mortality in a randomized trial in inhalation injury. Antibiotics should only be used for clinically suspected or proven infections. Prophylactic antibiotics merely select out resistant organisms, which frequently become problematic. Beta agonists should be used for persistent wheeze, though frequently they are ineffective, as the wheeze is related to particulate matter and chemical irritants. Oxygen should be humidified, and this can be supplemented with nebulised saline prephysiotherapy/bronchoscopy. There is also data showing that nebulised heparin and N-acetylcysteine reduces morbidity and mortality in inhalation injury. ECMO-extracorporeal membrane oxygenation has been shown to be of some benefit in those with smoke inhalation alone. Results in those with concomitant burn injury have been thoroughly disappointing.
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Carbon Monoxide Poisoning

Carbon monoxide (carboxyhemoglobin) is formed from combustion of carbon at low oxygen tension. carboxyhemoglobin causes tissue hypoxia in a number of ways: Carboxyhemoglobin binds to hemoglobin with 250 times the affinity of oxygen to hemoglobin. Thus the oxygen carrying capacity of the blood is severely reduced even with small concentrations of carboxyhemoglobin. An environmental carboxyhemoglobin concentration of 0.1% produces approximately equal concentrations of O2HB and COHB. Carboxyhemoglobin induces a leftward shift in oxygen dissociation curve, facilitating oxygen uplift at the lungs, but making delivery of oxygen at the tissues more difficult. Carboxyhemoglobin binds not only to Fe in hemoglobin, but also to myoglobin and the cytochrome system. Thus, even when all the carboxyhemoglobin has been converted to oxyhemoglobin, the tissue is still unable to utilize the oxygen. Significant carboxyhemoglobin poisoning causes myocardial dysfunction, further reducing oxygen delivery to tissue
Treatment
Remove from environment Provide maximal supplemental oxygenThe half life of carboxyhemoglobin is reduced significantly with supplemental oxygen and more so with hyperbaric oxygen (Table 57.2) As carboxyhemoglobin concentrations increase as more smoke is inhaled, the carboxyhemoglobin concentration can be used as an approximation of degree of smoke inhalation. The elimination of carboxyhemoglobin is predictable( if inspired oxygen is known), hence a nomogram can be used to extrapolate carboxyhemoglobin levels to the time of injury, and this level may be used as a predictor of outcome (Fig. 57.1). Supportive therapy
Cyanide
Thermal decomposition of all nitrogen contained in both natural and synthetic polymers may result in the production of the histotoxic poison, cyanide. Cyanide has a high affinity for ferric iron resulting in the inhibition of a number of metabolic processes, most importantly oxidative phosphorylation. Cyanide combines specifically with cytochrome AA 3, reducing electron transport, inhibits mitochondrial oxygen utilization and hence cellular respiration. This results in anaerobic metabolism with the production of lactic acidosis. The toxicity of cyanide is synergistic with concomitant poisoning with carboxyhemoglobin. Exhaled breath detectors and
Table 57.1. Variations in carboxyhemoglobin concentrations

Environment Carboxyhemoglobin concentration
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Endogenous production City dweller Heavy smoker
0.3-0.8% 1-5% 5-10%
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Table 57.2. Carboxyhemoglobin half life and ambient oxygen tensions

Breathing medium Half life (minutes)
Room air (21% oxygen) 100% normobaric oxygen 100% oxygen-3 atm
320 90 23
Fig. 57.1. Nomogram for estimation of initial level of carboxyhemoglobin; Reprinted with permission from: Clarke et al, Lancet 1981; 1332-1335.
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gas chromatography methods can both reliably detect cyanide, but are not used routinely. There is no rapid laboratory assay for blood cyanide. A high level of clinical suspicion is justified if a smoke inhalation is diagnosed combined with an rising lactate, which cannot be explained by hypovolemia or concomitant carboxyhemoglobin poisoning. A high mixed venous oxygen may also be present, indicating the failure of the cells to uptake oxygen.
Treatment
Supportive
100% oxygen and endotracheal intubation if indicated, with appropriate level of monitoring. Intravenous fluid and consider NaHCO3 for presumed/proven metabolic acidosis.
Specific Antidotes
All the specific antidotes carry some risk, and this should be considered when administering them on a presumptive diagnosis alone. Administration of sodium or amyl nitrates, inducing oxidation of hemoglobin to methemoglobin, which provides an alternative substrate for the cyanide. Thus the cytochrome oxidase is restored, at the expense of reducing the oxygen transport capacity, which itself can result in hypoxia. Hyperbaric oxygen has been used in combined carboxyhemoglobin/cyanide poisoning, but also in isolated cyanide treated with sodium nitrate, where the dissolved plasma oxygen compensates for the reduced oxygen carrying capacity of the methemoglobinaemia. Agents, such as cobalt EDTA or hydroxycobalamin, chelate the cyanide, and the resultant compounds are eliminated by renal excretion. Cardiovascular instability and anaphylaxis can occur with cobalt EDTA. Hydroxycobalamin is safer, though doses of between 70 and 150 mg/kg are required. The mitochondrial enzyme rhodanase catalyses cyanide, complexing it with sulfur to produce the less toxic thiocyanate molecule. The rate-limiting step is the endogenous sulfur supply. Administration of sodium thiosulphate provides a sulfur bank and results in the formation of the relatively innocuous thiocyanate. However, the reaction is slow and produces a problematic osmotic diuresis. It is the safer of the nonchelating agents.
Conclusions
Inhalation injury is a major contributor to mortality in burn victims. The injury is a composite of hypoxia, thermal damage, particulate inhalation and chemical asphyxiation. Whilst most deaths occur in the prehospital setting, there is a large scope for treatment optimization in the emergency rooms and ICU. The mainstay of treatment is supportive, together with appropriate investigation and monitoring. However, novel therapies, including high frequency ventilatory strategies and nebulization of heparin and NAC are beginning to improve the outcome. The optimum method to reduce morbidity and mortality from this challenging condition, however, is prevention. This requires education and utilization of relatively cheap and accessible smoke detectors.
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Reference
1. 2. 3. 4. 5. Kinsella J, Rae CP. Smoke Inhalation and airway injury. Ballieres Clinical Anaesthesiology Balliere Tindall 1997; 385-406. Desai MH, Mlcak R, Richardson J et al. Reduction in mortality in paediatric patients with inhalation injury with aerosolized Heparin/ Acetylcystine therapy. J Burn Care and Rehab 1998;19 (3); 210-212. Thompson PB, Herndon DN, Traber DL et al. Effect of mortality of inhalation injury. J Trauma 1986; 26:163-165. Cioffi WG, deLemos RA, Coalson JJ, et al. Decreased pulmonary damage inn primates with inhalation injury treated with high-frequency ventilation. Ann Surg 1991; 218:328-335. Prien T, Traber DL. Toxic smoke compounds and inhalation injurya review. Burns 1988; 14(6):451-460.
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CHAPTER 58
Management of the Potential Organ Donor Patient

Bradley J. Roth
The worldwide shortage of viable organs for transplantation makes identification and optimal management of potential donors essential. The key to successful management of the potential organ donor consists of three steps: 1. Recognizing and continued aggressive hemodynamic monitoring of those patients that may have suffered a fatal head injury. 2. Understanding the legal and medical steps required to declare brain death. 3. Understanding the rapid hemodynamic changes which occur with brain death and quickly correcting the multiple physiologic abnormalities.
The Physiological Consequences of Traumatic Brain Death Secondary to Trauma

In the setting of fatal head injury and brain death, several physiologic changes result in significant instability: 1. Increased catecholamine release and an autonomic storm prior to herniation makes the neurotrauma patient less likely to manifest hypovolemic shock with hypotension as early as other trauma patients. 2. Most neurotrauma patients will have a total body (intravascular and extravascular) fluid deficit secondary to mannitol and other diuretics. 3. Up to 85% of patients with severe intracranial injuries will develop diabetes insipidus (DI) resulting in further fluid loss. 4. Thromboplastin release secondary to severe head injury results in a significant incidence of disseminated intravascular coagulopathy (DIC). 5. A scalp laceration, which may be associated with head trauma, can be a source of significant hemorrhage. 6. During the autonomic storm that is associated with herniation, many patients develop neurogenic pulmonary edema, resulting in hypoxia and left ventricular dysfunction. 7. Once herniation is completed and mid-brain death occurs, autonomic vasomotor activity is lost and severe distributive shock occurs. 8. In addition to the above effects, brain herniation also causes an intercellular metabolic dysfunction related to the processing of triiodothyronine (T3). If all of the above are not corrected rapidly the patient will progress into irreversible cellular dysfunction, hypoxia, shock, and cardiac arrest. Patients who suffer brain death from a non-traumatic etiology generally do not develop the rapid hemodynamic changes seen in neurotrauma patients.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Bradley J. Roth, Defense Medical Readiness Training Institute, Joint Trauma Training CenterBen Taub General Hospital, Houston, Texas
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Clinical Evaluation for Brain Death

Definition: Death due to neurologic failure (brain death) is defined as an irreversible state in which there is no neurologic function of the brain and brain stem. Two licensed physicians should independently perform the following neurologic examination. The examining physicians should document their findings in the patient record. The criteria for documenting brain death may vary depending on hospital policy or state regulation. Also, the requirements for children may differ from those for adults.
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Criteria
All of the following must be true: normothermia (core temperature > 95 F) absence of pharmacologic effect (negative toxicology)
Barbiturate level < 5. Other levels (if present) must be individually evaluated to determine if they are contributory to decreased neurologic function. Trace levels do not absolutely rule out the ability to determine brain death. Check with your individual lab.
electrolytes (ranges for normal neurological function)

Sodium 125 - 160, potassium 3 - 7, magnesium 1 - 4, phosphorus 1 - 8, glucose 50 - 400
absence of neurologic function of the brain or brain stem.

- negative corneal reflex - absent papillary reflex - absent oculocephalic reflex (negative dolls eyes) - absence of response to cold caloric stimulation (direct instillation of 60 cc iced solution into each ear canal fails to cause ocular motion) - no spontaneous respirations after an apnea test. (See apnea test below)
Spinal reflexes may be present, but do not change the status of the patient if brain stem function is absent.
Apnea Test
Patient should have ventilator adjusted resulting in normal pH and PaCO2, with 97-100% saturation. Preoxygenate for 5-10 minutes with 100% FiO2. Disconnect patient from ventilator and place a catheter down the length of the endotracheal tube. The catheter should be connected to 100% O2 at 12-15 liters/minute. (This continuous supply of oxygen ensures the patient is oxygenated but will not ventilate the patient adequately.) Continue to monitor the pulse oximeter during the test. If the SaO2% declines below 90% an ABG should be obtained and the patient placed back on the ventilator.) Observe the patient for approximately 10 minutes for respiratory effort. The test is stopped when the ABG PaCO2 > 60 mm Hg and rises 20 mm Hg above baseline. The test should be terminated early and the patient placed back on the ventilator if spontaneous respiration is noted, the oxygen saturation is < 90%, and/ or the patient becomes hemodynamically unstable. The apnea test is a clinical determination of brain death. Alternative methods such as nuclear flow studies may be used in cases where the clinical evaluation is
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impractical; however, the clinical determination alone is sufficient to determine death based upon neurologic function. If the patient is too hemodynamically unstable to perform an apnea test, a nuclear flow study should be able to determine brain viability. Serial EEGs may take too long and result in loss of the potential donor secondary to cardiac failure.
Management Protocol for the Potential Organ Donor

This protocol was developed to manage trauma patients in an ICU setting or on a ward when an ICU bed is not immediately available. When the following protocol is adhered to closely a 90% success rate has been achieved (patient able to qualify for donation). The management protocol should be followed as a bridge from trauma service/ICU care until the regional organ procurement agency has received consent to manage the care of the patient or a decision to withhold care is made. The T-4 Protocol that follows is part of the resuscitation protocol. Never discuss organ donation with the family, but rather call the local regional organ procurement agency. The likelihood that a family member will donate organs is significantly increased when specialists from an organ procurement agency, rather than the primary care team, speak to the family. Prior to starting the protocol all patients should be evaluated by a neurosurgeon. The neurosurgeons opinion should be that the patients injury is 1) nonsurvivable, 2) would not benefit by neurosurgical intervention, 3) but the patient requires continued resuscitation by the Trauma or Critical Care Services. The following are common problems usually encountered during resuscitation: DIC: If a patient has clinical signs of DIC, transfuse immediately with 4-6 units of FFP. Delaying transfusion while waiting for lab results with uncontrolled hemorrhage is not indicated. Maintain Hct > 30 with PRBC. DI: If patient is normotensive, serum sodium > 148 and urine output (UOP) > 500cc/hr, give 1-2 micrograms of DDAVP IVP (q 2-8 hours as needed) and replace UOP cc for cc with 1/2 NS or D5W every hour for UOP > 200 (example: for UOP of 1000 cc replace with 800 cc of 1/2 NS). In some patients a DDAVP drip maybe helpful. A common error is to assume that a high UOP is from DI, when it is in fact from earlier doses of furosemide and/or mannitol. Tachycardia and hypertension: This commonly occurs prior to complete herniation and should not be treated unless instructed by the neurosurgery critical care team. Use only short acting agents. Neurogenic pulmonary edema: Increase ventilator support as needed. With severe problems of oxygenation alternative modes of ventilation may have to be considered (inverse I:E ratio high frequency or percussinator ventilation). Hypokalemia and/or hyperglycemia: Use sliding scales as needed. Hypothyroid: Many patients have a T-3/T-4 abnormality and require additional thyroxin. Start patients on thyroxin protocol (attached: T-4 Donor Protocol) once declared brain dead or as soon as they fail to have spontaneous respirations via an apnea test. Aspiration: Following trauma that results in a decreased mental status, patients often aspirate. These patients should have their airway cleared with bronchoscopy as soon as possible. Cardiac arrest: Follow ACLS guidelines.

Patient Evaluated in ER
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A S A P
1. Labs obtained: ABG/serum lactate/ CBC/PT/PTT/lytes 2. Transfuse to maintain Hct > 30 3. Bolus 1 liter NS 4. Control active bleeding 5. Maintain MAP > 70 with fluid bolus/ dopamine 6. Place large trauma central line 7. Transfer to ICU as quickly as possible 8. Protect against hypothermia
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Patient MAP > 70 YES
NO
Continue to fluid resuscitate as needed, and correct lab abnormalities Caution: Patients may go from hypertension to hypotension rapidly! (End points of resuscitation should include normalization of base deficit/lactate, CVP and/or PAOP between 8-15, and minimal use of pressors) Rules of 100s: SBP > 100 mm Hg, UOP > 100, PaO2 > 100. Maintenance fluid: Early NS or LR; then adjust as indicated.
1. Continue to fluid resuscitate with 5% albumin and NS (Continue with this protocol until MAP > 70) 2. Double the dose of dopamine q5 minutes to maintain MAP > 70 3. Once dopamine is at 20 g/kg/min, if MAP < 70, start epinephrine drip. 4. Double epinephrine drip q5 minutes and bolus over 20 minutes with 100 cc of 25% albumin in 1 liter NS. 5. Is CVP > 12 and/or PAOP (wedge) > 16? NO: Continue to bolus with above NS/albumin solution. YES: Does the patient have clinical symptoms and laboratory values suggestive of DI (diabetes insipidus)? -UOP > 600 cc/hour and serum sodium > 150? NO: Consider starting norepinephrine or neosynephrine if CI > 4 YES: Start vasopressin at 1-8 units/hour and replace UOP over 200cc with 1/2 NS cc for cc every hour (Norepinephrine, neosynephrine, and vasopressin should not be used if SVRI > 1100)
T-4 Donor Protocol

This is one example of a thyroxin/tri-iodothyronine supplementation Your local organ procurement agency may follow a different protocol. Pretreatment:
- Hydrate donor to a minimum central venous pressure >7 - Transfuse with PRBC to obtain and maintain hemoglobin >10 and/or hematocrit >30 - Correct electrolyte abnormalities
Prerequisite:
Donor is requiring a combined vasopressor need greater than 15 mcg per minute
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T-4 Protocol:
Administer IV boluses of the following in rapid succession: 1 amp of 50% dextrose IVP 2 grams of methylprednisolone IVPB 20 units regular insulin IVP 20 mcg Thyroxin (T-4) IVP Start a drip of 200 mcg T-4 in 500cc Normal Saline (.4 mcg/cc). Administer at 25 cc (10 mcg) per hour initially. Reduce levels of other pressors as much as possible and then adjust T-4 as necessary to maintain desired pressure. - Donors > 100 lbs give above dose - Donors 50-75 lbs give 13 cc/hr = 5.2 mcg/hr - Donors 75-100 lbs give 19 cc/hr = 7.6 mcg/hr After 30 to 60 minutes the donor will usually become tachycardic with an increase in temperature and blood pressure. Monitor K+ (serum potassium) levels carefully. Serum potassium levels usually decrease and require aggressive replacement.
Note: The opinions or assertions contained herein are the private views of the author and are not to be construed as official or as reflecting the views of the Department of the Army or the Department of Defense.
References
1. 2. 3. 4. 5. 6. 7. 8. Jonas M, Oduro A. Management of the Multi-Organ Donor, In: The Multi-organ Donor, Selection and Management, Ed: Higgins RS, Sanchez JA, Lorber MI, Baldwin JC. Blackwell Science, Inc. Malden , MA. 123-139, 1997. Novitzky D, Cooper DK, Reichart B, et. al. Hemodynamic and metabolic responses to hormonal therapy in brain dead potential organ donors. Transplantation 1987;43:852-854. Novitzky D, Cooper DK, Chaffin JS, et al. Improved cardiac allograft function following triiodothyronine therapy to both donor and recipient. Transplantation 1990;49:311-316. Bittner HB, Kendall SH, Chen EP, Van Trigt P. Endocrine changes and metabolic responses in a validated canine brain death model. J Crit Care 1995;10:56-63. Mertes PM, Abassi KE, Jaboin Y, et al. Changes in hemodynamic and metabolic parameters following induced brain death in the pig. Transplantation 1994; 58:414-418. Chen HI. Hemodynamic mechanisms of neurogenic pulmonary edema. Biol Signals 1995;4:186-192. Novitzky D, Cooper DK, Morrell D, Isaacs S. Changes from aerobic to anaerobic metabolism after brain death, and reversal following triiodothyronine therapy. Transplantation 1988;45:32-36. Wijdicks EM. Determining brain death in adults. Neurology 1995;45:1003-1011.
Hypothermia in Trauma Patients

Thomas V. Berne Etiology in Trauma Patients Environmental
Injury occurring outdoors in a cool or cold ambient temperature, particularly if immersion occurs or there is exposure to wind Additional loss of heat occurs in the hospital particularly when a patient is undressed and uncovered in a cool room
Administration of Cold Fluid or Blood

Crystalloids are often kept at room temperature (22o C.) and infused rapidly for the treatment of hypovolemia Blood stored at 4 o C is rapidly infused for the treatment of major hemorrhage Ventilation with cool dry gas
Physiology
Definitions and mortality in trauma cases Hypothermia is considered to be present if core body temperature falls below 35C. If core body temperature falls below 34oC., it has reached a serious level with mortality in trauma patients reported from 16-60% If core body temperature falls below 32oC., it has reached a critical level, with mortality rates between 85-100%
Responses
37-35C: hyperdynamic, shivering and vasoconstriction 35-33C: confusion, severe shivering 33-30 C: bradycardia, falling cardiac output, cardiac irritability, hypoventilation, hypotension, cold diuresis, muscle rigidity Below 30C: loss of consciousness and reflexes, flaccidity, hypotension, acidosis, widening of QRS complexes, prolonged PR and QT intervals, T-wave inversion, Osborne J waves (a hump immediately following the QRS complex) appears below 28C. Atrial fibrillation, ventricular fibrillation, fatal arrhythmias and then asystole at temperatures around 22C Oxyhemoglobin dissociation curve shifts to the left, PO2 and PCO2 falls 4%-5% per each degree of temperature reduction. ABGs are difficult to interpret because they are corrected to 37C in the lab Coagulopathy develops progressively as temperature falls because both platelets
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Thomas V. Berne, Department of Surgery, Los Angeles County University of Southern California Medical Center, Los Angeles, California, U.S.A.
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and clotting factors do not function normally. Again, tests run at 37C maybe misleading.
Prevention and Treatment
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Emergency Department/Radiology Department

Maintain ambient temperature above 80F. After removing trauma victims clothing to do complete examination, then cover with blankets (preferably warm). Use reflective garments, particularly to cover the scalp. Warm all IV fluids (keep Ringers-Lactate stored in an incubator at 37C). Institute these measures as soon as possible if a serious injury has occurred; hypothermia is much easier to prevent than treat.
Operating Room
Continue measures mentioned above. Cover appropriate parts of the body with a warm airflow blanket (e.g., Bair HuggerTM). Have heating blanket under the patient. Lavage operative cavity with warm saline (40C, kept in incubator in O.R. suite). Copious irrigation allowing contact to high blood flow viscera (i.e., bowel, liver, lungs). Apply directly to a cold asystolic heart. Humidification and warming of inhaled anesthetic gas
Intensive Care Unit

Same as E.R./Radiology and O.R. Active core rewarming should be considered for critical hypothermia Most efficient method for trauma patients is extracorporeal arteriovenous or venovenous rewarming, using the heat exchanger from the rapid blood infusion set Hemodialysis utilizing a heat exchanger is equally efficacious More rapid rewarming is possible with cardiopulmonary bypass, but requires heparinization and cannulation is more difficult (operative) Peritoneal dialysis and pleural irrigation are also used but much slower than extracorporeal methods Infusion of crystalloids (Ringers Lactate or Saline) at 40C. can be helpful as patients are often hypovolemic
Value of Hypothermia
Because metabolic rates drop in hypothermic organs, its is postulated there may be some benefit to individual organs such as the brain, heart, kidneys, etc. It is difficult to utilize this potential benefit clinically without incurring the deleterious effects previously discussed. Potentially, total circulatory arrest could be employed along with profound hypothermia to allow for the repair of otherwise lethal injuries in a bloodless field. Although possible in laboratory animals, it will be difficult to translate to the uncontrolled environment in which we encounter such seriously injured trauma (e.g., battlefield patients). When repairing renal or hepatic vascular injuries, surface cooling or even intra-arterial cooling (if organ preservation solution is available) can be used to extend the safe ischemic period. Mild hypothermia may be useful in the Intensive Care Unit management of head injuries.
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References
1. 2. 3. 4. 5. Gentilello LM, Cobean RA, Offner PJ et al. Continuous arteriorenous rewarming: Reversal of hypothermia in critically ill patients. J Trauma 1992; 32:316-327. Jurkovich, GJ Greiser, WB Luterman A et al. Hypothermia in trauma victims: An ominous predict of survival. J Trauma 1987; 1019-1024. Kim SH, Stezoski SW, Safar P et al. Hypothermia, but not 100% oxygen breathing, prolongs survival time during lethal uncontrolled hemorrhagic shock in rats. J Trauma 1998; 44:485-491. Valeri CR, Casiday G, Khuri S et al. Hypothermia-induced reversible platelet dysfunction. Ann Surg 1987; 205:175. Peng RY, Bongard FS. Hypothermia in trauma patients. J Am Coll Surg 1999; 685-694.
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CHAPTER 60
Trauma Scores
D. Bowley and Ken Boffard Introduction
Estimates of the severity of injury or illness are fundamental to the practice of medicine. The earliest known medical text, the Smith Papyrus, classified injuries into three grades, treatable, contentious and untreatable. The Glasgow Coma Scale (GCS), devised in 1974, was one of the first numerical scoring systems (Table 60.1). The GCS has been incorporated into many later scoring systems, underscoring the importance of head injury as a triage and prognostic indicator. Modern trauma scoring methodology uses a combination of an assessment of the severity of anatomical injury with a quantification of the degree of physiological derangement to arrive at scores that correlate with clinical outcomes. Trauma scoring systems are designed to facilitate prehospital triage, identify trauma patients suitable for quality assurance audit, allow accurate comparison of different trauma populations and organize and improve trauma systems.
Physiological Scoring Systems

Introduced by Champion et al, the Revised Trauma score (RTS) evaluates blood pressure, Glasgow Coma Scale and respiratory rate to provide a scored physiological assessment of the patient. The difference between RTS on arrival and best RTS after resuscitation will give a reasonably clear picture of prognosis. By convention the RTS on admission is the one documented. The RTS (nontriage) is designed for retrospective outcome analysis. Weighted coefficients are used, which are derived from trauma patient populations and provide more accurate outcome prediction that raw RTS (Table 60.2). Since a severe head injury carries a poorer prognosis than a severe respiratory injury, the weighting is therefore heavier. The RTS therefore varies from 0 (worst) to 7.8408 (best). The RTS is the most widely used physiological scoring system in the trauma literature. The Pediatric Trauma Score (PTS) (Table 60.3) has been designed to facilitate triage of children. The PTS is the sum of six scores, and values range from 6 to +12, with a PTS of <8 being recommended as a trigger to send to a trauma center. The PTS has been shown to accurately predict risk for severe injury or mortality, but is not significantly more accurate than the RTS and is a deal more difficult to measure.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. D. Bowley, Johannesburg Hospital, Johannesburg, South Africa Ken Boffard, Johannesburg Hospital, Johannesburg, South Africa
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TAble 60.1. The Glasgow coma scale

Parameter Eye opening Response Nil To pain To speech Spontaneously Nil Extensor Flexor Withdrawal Localizing Obeys command Nil Groans Words Confused Orientated Score 1 2 3 4 1 2 3 4 5 6 1 2 3 4 5
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Motor response
Verbal response
Table 60.2. Revised trauma score (RTS). The values for the three parameters are summed to give the raw RTS. Weighted values are summed for the RTS.
Clinical Parameter Category Score x weight
Respiratory rate (Breaths per minute)
10-29 > 29 5-9 1-4 0 > 89 76-89 50-75 1-49 0 13-15 9-12 6-8 4-5 3
4 3 2 1 0 4 3 2 1 0 4 3 2 1 0
0.2908
Systolic blood pressure
0.7326
Glasgow Coma Scale
0.9368
Anatomical Scoring Systems

The Abbreviated Injury Scale (AIS) was developed in 1971. The AIS grades each injury by severity from 1 (least severe) to 5 (survival uncertain), within six body regions (head/neck, face, chest, abdominal/pelvic contents, extremities and skin/general. The AIS has been periodically upgraded and AIS-90 is currently being revised.
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Table 60.3. Pediatric trauma score (PTS). The values for the six parameters are summed to give the overall PTS.
Clinical Parameter Category Score
Size (kg)
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> 20 10-20 < 10 Normal Maintainable Unmaintainable > 90 50-90 < 50 Awake Obtunded / LOC Coma / decerebrate None Minor Major/penetrating None Closed fracture Open/multiple fractures
2 1 -1 2 1 -1 2 1 -1 2 1 -1 2 1 -1 2 1 -1
Systolic blood pressure (mmHg) Central Nervous System
Open wound
Skeletal
Table 60.4. ISS body regions

Number Region
1 2 3 4 5 6
Head & Neck Face Thorax Abdomen Extremities External
In 1974, Baker et al created the Injury Severity Score (ISS) to relate AIS scores to patient outcomes. ISS body regions are listed in Table 60.4. The ISS is calculated by summing the square of the highest AIS scores in the three most severely injured regions. ISS scores range from 1-75 (since the highest AIS score for any region is 5). By convention an AIS score of 6 for any region (defined as a nonsurvivable injury) becomes an ISS of 75. The ISS only considers the single, most serious injury in each region, ignoring the contribution of injury to other organs within the same region. Diverse injuries may have identical ISS but markedly different survival probabilities (ISS of 25 may be obtained with isolated severe head injury or by a combination of lesser injuries across different regions). Also, ISS does not have the power to discriminate between the impact of similarly scored injuries to different
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organs and therefore cannot identify, for example, the different impact of cerebral injury over injury to other organ systems. In response to these limitations, in 1997, the ISS was modified to become the New Injury Severity Score (NISS) as the simple sum of the squares of the three highest AIS scores regardless of body region. NISS is able to predict survival outcomes better than ISS. The Anatomic Profile (AP) was introduced in 1990 to overcome some of the limitations of the ISS. AIS scoring is used, but four body regions were chosen (head/brain/spinal cord, thorax/neck, all other serious injury and all nonserious injury). The AP score is the square root of the sum of the squares of all the AIS scores in a region, thus enabling the impact of multiple injuries within that region to be recognized. Component values for the four regions are summed to constitute the AP score. A modified Anatomic Profile (mAP) has recently been introduced which is a four number characterization of injury, the four component scores are the maximum AIS score and the square root of the sum of the squares of all AIS values for serious injury (AIS 3) in specified body regions (Table 60.5). This leads to Anatomic Profile Score, the weighted sum of the four mAP components. The coefficients are derived from logistic regression analysis of admissions to four Level 1 trauma centers (the controlled sites) in the Major Trauma Outcome Study. A limitation of the use of AIS-derived scores is their cost. International Classification of Disease (ICD) taxonomy is a standard used by most hospitals and other health care providers to classify clinical diagnoses. Computerized mapping of ICD-9CM rubrics into AIS body regions and severity values has been used to compute ISS, AP and NISS scores. Despite limitations, ICD-AIS conversion has been useful in population-based evaluation when AIS scoring from medical records is not possible. Severity scoring systems have also been directly derived from ICD coded discharge diagnoses. Most recently the ICD-9 Severity Score (ICISS) has been proposed, which is derived by multiplying survival risk ratios associated with individual ICD diagnoses. Neural networking has been employed to further improve ICISS accuracy. ICISS has been shown to be better than ISS and to outperform TRISS in identifying outcomes and resource utilization. However, modified-AP scores, AP and NISS appear to outperform ICISS in predicting hospital mortality. There is some confusion as to which anatomic scoring system should be used. However currently, NISS should probably be the system of choice for AIS-based scoring. Organ Injury Scaling (OIS) is a scale of anatomic injury within an organ system or body structure. The goal of OIS is to provide a common language between trauma surgeons and facilitate research and continuing quality improvement. It is not designed to correlate with patient outcomes. The OIS tables can be found on the American Association for the Surgery of Trauma (AAST) web site. Additional information and guidance can be found at the Eastern Association for the Surgery of Trauma website. Moore and colleagues facilitated identification of the patient at high risk of postoperative complications when they developed the Penetrating Abdominal Trauma Index (PATI) scoring system. In a group of 114 patients with gunshot wounds to the abdomen they showed that a PATI score > 25 dramatically increased the risk of postoperative complications (46% of patients with a PATI
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Table 60.5. Component definitions of the modified anatomic profile

Component Body region AIS severity
mA
Head/brain Spinal cord
3-6 3-6 3-6 3-6 3-6
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mB
Thorax Front of neck
mC
All other
mA, mB, mC scores are derived by taking the square root of the sum of the squares for all injuries defined by each component
score of > 25 developed serious postoperative complications compared to 7% of patients with a PATI of < 25). Further studies have validated the PATI scoring system.
Outcome Analysis Systems

For head-injured patients it was found that the level of coma on admission or within 24 hours expressed by the Glasgow coma scale correlated with outcome. The Glasgow outcome scale was an attempt to quantify outcome parameters (Table 60.6) for head-injured patients. The grading of depth of coma and neurological signs was found to relate strongly to outcome, but the accuracy of individual signs limits their use in predicting outcomes for individuals (Table 60.7). In 1982 the American College of Surgeons Committee on Trauma began the ongoing Major Trauma Outcome Study (MTOS), a retrospective, multi-center study of trauma epidemiology and outcomes. MTOS uses Trauma Score and Injury Severity Score Analysis (TRISS) methodology to estimate the probability of survival, or P(s), for a given trauma patient. P(s) is derived according to the formula: P(s) = 1/(1 + e-b), where e is a constant (approximately 2.718282) and b = b0 + b1(RTS) + b2(ISS) +b3(age factor). The b coefficients are derived by regression analysis from the MTOS database (Table 60.8). The P(s) values range from zero (survival not expected) to 1.000 for a patient with a 100% expectation of survival. Each patients values can be plotted on a graph with ISS and RTS axes (Fig. 60.1) The sloping line represents patients with a probability of survival of 50%, these PRE charts (from PREliminary) are provided for those with blunt or penetrating injury and for those above or below 55 years of age. Survivors whose coordinates are above the P(s)50 isobar and nonsurvivors below the P(s)50 isobar are considered atypical (statistically unexpected) and such cases are suitable for focused audit. In addition to analyzing individual patient outcomes, TRISS allows comparison of a study population with the huge MTOS database. The Z-statistic identifies if study group outcomes are significantly different from expected outcomes as predicted from MTOS. Z is the ratio: (A-E)/S, where A = actual number of survivors, E = expected number of survivors and S = scale factor that accounts
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Table 60.6. Glasgow outcome scale

i. ii. iii. iv. v. Death (D) Persistent vegetative state (PVS) Severe disability (SD) Moderate disability (MD) Good recovery (GR)
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Table 60.7. Outcome related to signs in the first 24 hours of coma after injury. Outcome scale as described by Glasgow group.
Dead or vegetative, % Moderate disability or good recovery, %
Pupils: reacting nonreacting Eye movements intact absent / bad Motor response Normal Abnormal 39 91 33 90 36 74 50 4 56 5 54 16
Fig. 60.1. PRE Chart. L = survivors, D = nonsurvivors.
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Table 60.8. Coefficients from major trauma outcome study database.

Blunt bo = -1.2470 b1 = 0.9544 b2 = -0.0768 b3 = -1.9052 Penetrating -0.6029 1.1430 -0.1516 -2.6676
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Table 60.9. Coefficients derived from MTOS data for the ASCOT probability of survival, P(s).
Type of injury k-Coefficients Blunt Penetrating
k1 k2 (RTS GCS value) k3 (RTS SBP value) k4 (RTS RR value) k5 (AP head region value) k6 (AP thoracic region value) k7 (AP other serious injury value) k8 (age factor)
-1.157 0.7705 0.6583 0.281 -0.3002 -0.1961 -0.2086 -0.6355
-1.135 1.0626 0.3638 0.3332 -0.3702 -0.2053 -0.3188 -0.8365
for statistical variation. Z may be positive or negative, depending on whether the survival rate is greater or less than predicted by TRISS. Absolute values of Z > 1.96 or < -0.96 are statistically significant (P < 0.05). The so-called M-statistic is an injury severity match allowing comparison of the range of injury severity in the sample population with that of the main database (i.e., the baseline group). The closer M is to 1, the better the match, the greater the disparity, the more biased Z will be. This bias can be misleading, for example, an institution with a large number of patients with lowseverity injuries can falsely appear to provide a better standard of care than another institution that treats a higher number of more severely injured patients. The W-statistic calculates the actual numbers of survivors greater (or fewer) than predicted by MTOS, per 100 trauma patients treated. The Relative Outcome Score (ROS) can be used to compare W-values against a perfect outcome of 100% survival. The ROS may then be used to monitor improvements in trauma care delivery over time. TRISS has been used in numerous studies. Its value as a predictor of survival/ death has been shown to be from 75-90% as good as a perfect index, depending on the patient data set used. However, TRISS methodology does have major limitations, it is costly and labor intensive and also maybe inaccurate in some subgroups of patients, especially in severe trauma. A Severity Characterization of Trauma (ASCOT), introduced by Champion
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et al in 1990, is a scoring system that uses the Anatomic Profile to characterize injury in place of ISS. Different coefficients are used for blunt and penetrating injury and the ASCOT score is derived from the formula: P(s) = 1/(1 + e-k). The ASCOT model coefficients are shown in figure 10. ASCOT has been shown to outperform TRISS, particularly for penetrating injury.
Summary
Trauma scoring systems and allied methods of analyzing outcomes after trauma are steadily evolving and have become increasingly sophisticated over recent years. Trauma scoring systems are designed to facilitate prehospital triage, identify trauma patients whose outcomes are statistically unexpected for quality assurance analysis, allow accurate comparison of different trauma populations and organize and improve trauma systems. They are vital for the scientific study of the epidemiology and the treatment of trauma and may even be used to define resource allocation and reimbursement in the future. Trauma scoring systems that measure outcome solely in terms of death or survival are at best blunt instruments. Despite the existence of several scales (Quality of Well-being Scale, Sickness Impact Profile etc.) further efforts are needed to develop outcome measures that are able to evaluate the multiplicity of outcomes across the full range of diverse trauma populations. Despite the profusion of acronyms, scoring systems are a vital component of trauma care-delivery systems. The effectiveness of well-organized, centralized, multidisciplinary trauma centers in reducing the mortality and morbidity of injured patients is well documented. Further improvement and expansion of trauma care can only occur if developments are subjected to scientifically rigorous evaluation. Thus, trauma scoring systems play a central role in the provision of trauma care today and for the future.
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References
1. 2. 3. 4. 5. 6. 7. 8. American Association for the Surgery of Trauma web site. www.aast.org Boyd CR, Tolson MA, Opes WS. Evaluating trauma care: The TRISS method. J Trauma 1987; 27:370-377. Champion HR, Sacco WJ, Copes WS et al. A revision of the trauma score. J Trauma 1989; 29(5):623-629. Champion HR, Copes WS, Sacco WJ et al. Improved predictions from a severity characterization of trauma (ASCOT) over Trauma and Injury Severity Score (TRISS): Results of an independent evaluation. J Trauma 1996; 40(1):42-48. Eastern Association for the Surgery of Trauma website. www.east.org Moore EE, Dunn EL, Moore JB et al. Penetrating Abdominal Trauma Index. J Trauma 1981; 21(5):439-444. Osler T, Baker SP, Long W. A modification of the Injury Severity Score that both improves accuracy and simplifies scoring. J Trauma 1997; 43(6):922-926. Tepas JJ 3rd, Ramenofsky ML, Mollitt DL et al. The Pediatric Trauma Score as a predictor of injury severity: an objective assessment. J Trauma 1988; 28(4):425-429.
CHAPTER 61
Crush Syndrome
Gail T. Tominaga Crush Injuries Mechanism
Crush injuries are caused by continuous prolonged pressure on the body. The major factor in producing crush injury is the length of time the pressure is applied. The shortest duration reported in the literature is one hour. Patients who survive to reach medical attention have crush injuries to the extremities and not the torso. The prolonged pressure required to cause this syndrome usually causes immediate death if applied to the torso. Crush injuries occur in disaster situations, such as earthquakes, bombings, train accidents and mine accidents. Prolonged extrication of victims is the rule rather than the exception.
Following extrication, the patient usually suffers no pain and has no physical complaints. Main complaints are emotional. Immediately following extrication, a severe neurologic deficiency, mainly flaccid paralysis of the injured limb, may be present. Sensory loss to pain and touch is seen in a patchy pattern. Limb edema is initially not present. Gross edema takes time to develop and can progress to marked edema. Distal pulses are present even in the presence of gross edema. Investigation for additional injuries is warranted if pulses are not demonstrated. After extrication, the patient becomes severely hypovolemic, which may develop into severe hypovolemic shock and death. The skin and subcutaneous layers are not injured, but the underlying muscles are severely damaged. The involved muscles bleed profusely when cut which may be misleading. Associated injuries may be present due to the mechanism of injury, i.e., entire body trapped under a collapsed building.
Pathophysiology
Continuous pressure causes muscle damage resulting in loss of the muscle cells ability to control fluids. This causes an influx of fluid into the muscles resulting in edema and elevation in compartment pressure.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Gail T. Tominaga, John A. Burns School of Medicine, The Queens Medical Center, Honolulu, Hawaii, U.S.A
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Differential Diagnosis
Crush injury is differentiated from arterial occlusion by the lack of damage to the skin and the presence of pulses. Direct pressure injuries (i.e., being run-over by a tire of an automobile) can be differentiated by the presence of skin and subcutaneous tissue injury with undamaged muscle. Elevation of pressure in compartment syndrome causes occlusion of venous drainage from the compartments, which further elevates the pressure eventually causing muscle injury. In crush injuries, the muscle injury causes edema, which then leads to elevation of compartment pressures. The flaccid paralysis from crush injury is not related to the distribution of nerves in the affected limb. Their symptoms may mimic spinal cord injury. Normal anal sphincter tone may help exclude the presence of an acute spinal cord injury.
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Treatment
Treatment is aimed at prevention of the crush syndrome. Treatment of closed crush injuries is conservative. They should not be routinely explored since the intact skin acts as a barrier against infection. The use of fasciotomies is controversial. Routine use should not be advocated. Fasciotomies will not reverse muscle necrosis in the absence of compartment syndrome. If compartment pressures are elevated (greater than 40 mm Hg), fasciotomies should be performed. At the time of fasciotomy, extensive resection of all dead muscle should be performed at the first operation. Dead muscle can not be identified by lack of bleeding. Identification of dead muscle is by its reaction to direct physical or electrical stimulation. Open crush injuries have a greater potential for bacterial contamination and should be widely debrided.
Outcome
There is little data on functional outcome of limbs suffering from crush injury. Both open and closed crush injuries have a risk of developing local myonecrosis and compartment syndrome. Following the acute phase, there is a recuperation of the sensory loss accompanied by a transient period of paresthesia with severe pain. Sensation can recover but may take up to one year. Infection and recurrent bleeding often complicate fasciotomies. Outcome may be better in limbs not treated by fasciotomy.
Crush Syndrome
Crush syndrome refers to the systemic manifestations of muscle necrosis including myoglobinuric renal failure, shock, and the cardiac sequelae of acidosis and hyperkalemia. It is also referred to as traumatic Rhabdomyolysis. It is a life and limb threatening condition.
Crush Syndrome was first applied to the ischemia-induced syndrome of myonecrosis, myoglobinuria, and renal failure seen during the London Blitz in World War II.
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The severity of the clinical manifestations is proportional to the amount of injured muscle. There is frequently a delay in diagnosis following admission. This results from:
- failure to suspect the diagnosis - preoccupation with other overwhelming injuries or medical problems - presence of a comatose patient or a patient with altered sensorium who cannot complain of pain or who has an unreliable examination
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Extrication of survivors and decompression of injured limbs may paradoxically accelerate the development of shock and hemoconcentration. Crush syndrome manifests with the systemic signs and symptoms resulting from the products of devitalized tissue entering the circulation. These include:
- Hyperkalemia, which may occur within the first hour and can increase to dangerous levels leading to arrhythmias and death. - Dangerous degrees of hyperphosphatemia, hypocalcemia, hyperuricemia, and metabolic acidosis which may present just hours after extrication. - Hemoconcentration and thrombocytopenia, which may suggest the onset of diffuse intravascular coagulation.
The first urine specimen may appear dark due to myoglobin in the urine. This can be mistaken for hematuria.
Pathophysiology
The membranes of the injured muscles lose their integrity and become permeable. Water enters the cell freely resulting in severe muscle edema. Massive uptake of extracellular fluid (ECF) by the swelling of crushed muscle can occur. Within hours, the entire 14L of ECF can be sequestered in the crushed injured muscles resulting in hypovolemic shock and death. Penetration of calcium into the muscle after crush injury activates autolytic enzymes and interferes with mitochondrial integrity leading to muscle cell anoxia and acidosis. Efflux of potassium into the extracellular fluid can cause cardiac arrest within 2 hours of extrication. Myoglobin, phosphate, creatine phosphokinase, and purines efflux from the damaged muscle cell into the ECF. The synergistic combination of hyperkalemia and hypocalcemia cause cardiovascular suppression, which sensitizes the kidney to the nephrotoxic metabolites leaking from the crushed muscle. Myoglobin also chelates renal vasodilatory nitric oxide which intensifies renal vasoconstriction contributing to acute renal failure. There is increased production of muscular nitric oxide accompanied by muscular vasodilation and hyperperfusion of the injured limb leading to aggravation of hemodynamic shock.
Diagnosis/Clinical Investigations
The diagnosis should be suspected in any patient with a history of prolonged immobilization and blunt trauma/crush. Hyperkalemia, hypocalcemia, hyperphosphotemia, and metabolic acidosis appear before azotemia and within hours of extrication.
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Myoglobinemia, elevated creatine phosphokinase and urine microscopy demonstrate heme pigment without red blood cells in the urine sediment when Rhabdomyolysis is present. Hemoglobinuria may or may not be present. The diagnosis should be suspected in any patient requiring massive fluid resuscitation following soft tissue trauma.
Immediate medical management should be directed at the hypovolemic shock. Intravascular fluid volume should be rapidly replaced with crystalloid and should begin as soon as one of the trapped limbs is freed during extrication. Once the patient is fully extricated, blood pressure and urine output should be closely monitored.
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Management and Treatment

Early, aggressive fluid resuscitation with isotonic saline is imperative. Whole blood should not be used since these patients are already hemoconcentrated. Maintenance of a high urine output, of at least 100-200 mL/hr, will help prevent renal failure. Massive fluid resuscitation (10-20 L/day) is often required. After adequate volume replacement and documentation of urine flow, mannitol alkaline diuresis should be instituted. Mannitol should not be given to anuric patients. Once urine flow is documented, mannitol diuresis should be instituted. A 20% solution of mannitol at a rate of 1-2 g/kg body weight should be administered over 4 hours. Mannitol doses should be titrated to urine output but doses above 200 g/day should be avoided. Intravenous mannitol doses greater than 200 g/day can cause acute renal failure that is reversible by hemodialysis. The urine should be tested frequently for the presence of myoglobin. Maintaining an alkaline urine (pH > 6.5) by infusing sodium bicarbonate IV (1-2 mEq/kg/hr) to increase the urine solubility of myoglobin and hemoglobin may reduce the likelihood of precipitation and occlusion of renal tubules by these pigments. Myoglobin is not a direct toxin. In the presence of aciduria, myoglobin is converted to ferrihemate which is toxic to renal cells. If bicarbonate administration produces metabolic alkalosis (pH > 7.45), acetazolamide (500 mg IV) should be administered until urinary myoglobin disappears. Acetazolamide will correct metabolic alkalosis and increase urinary pH. Massive volume replacement and mannitol diuresis may not be tolerated well by geriatric patients or patients with limited cardiac function. Closer hemodynamic monitoring with a pulmonary artery catheter, gentler resuscitation, and diuresis with furosemide may be needed. Electrolyte abnormalities should be corrected except for hypocalcemia. Supplemental calcium should not be administered unless there is a danger of hyperkalemic arrhythmia.
Complications
If intravenous volume replacement is inadequate or is delayed for more than six hours, acute renal failure will develop.
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Outcome
There is high mortality in patients with crush syndrome who are not adequately fluid resuscitated. Deaths within the first hours of injury are due to shock and hyperkalemia. Late deaths (7-12 days) are caused by myoglobinuric acute renal failure or multiple organ failure. Patients who survive the crush syndrome and acute renal failure usually recover completely. Patients with associated truncal injuries (i.e., abdominal injuries) have a higher mortality rate when compared to those without truncal involvement.
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In crush injuries, the lack of complaints by the conscious patient may be misleading. In the comatose patient, the presence of other injuries and lack of adequate history may delay diagnosis of crush injuries. There must be a high index of suspicion for early diagnosis and treatment. Nonviable tissue may be present below deceptively normal appearing skin and dermis and must be debrided prior to closure of any open crush injury. Patients sustaining crush injuries can be deceptively stable only to deteriorate within hours of extrication. Inadequate debridement of open wounds can occur since the injured muscle in crush injuries bleeds when cut. The muscle must be stimulated electrically or manually to determine viability. The amount of crystalloid fluid resuscitation is often underestimated due to the underestimation of underlying muscle damage.
References
1. 2. 3. 4. 5. Oda J, Tanaka H, Yoshioka T et al. Analysis of 372 patients with Crush syndrome caused by the Hanshin-Awaji earthquake. J Trauma 1997; 42(3):470-476. Better OS. Rescue and salvage of casualties suffering from the crush syndrome after mass disasters. Military Medicine 1999; 164:366-369. Reis ND, Michaelson M. Crush injury to lower limb: treatment of the local injury. J Bone Joint Surg Am 1986; 68A:414-416. Abassi ZA, Hoffman A, Better OS. Acute renal failure complicating muscle crush injury. Seminars in Nephrology 1998; 18(5):558-565. Rubenstein I, Abassi Z, Milman F. Involvement of nitric oxide system in experimental muscle crush injury. J Clin Invest 1998; 101:1325-1333.
Anesthesia of the Traumatized Patient

Michael J Sullivan and Earl Moore-Jefferies Introduction
Death of patients secondary to trauma occurs in a tri-modal distribution. The first peak of mortality starts from the time of injury up to one hour after the injury. More than fifty percent of trauma deaths occur in this phase. Even with the provision of immediate medical care, death occurs. The injury sustained is so severe that internal compensatory mechanisms coupled with medical intervention are overwhelmed. The second peak occurs from one hour up to four hours after injury. Physiologic reserve and medical intervention sustain life until compensatory mechanisms are exhausted and mortality ensues. The third peak of mortality is seen one to five weeks after initial insult. A secondary insult occurs such as sepsis or organ dysfunction becomes organ failure. This chapter presents a framework for the anesthetic management of traumatized patients. Aggressive and appropriate anesthetic care can reduce the incidence of intraoperative mortality and postoperative complications.
Airway
Airway management in the trauma patient is always first! Provide supplemental oxygen while assessing the patient. Surgical establishment of the airway is an option that should be entertained early. It is best not to wait until every method of tracheal intubation is tried and unsuccessful before surgical intervention is considered. Assessment of the airway is done prior to direct laryngoscopy in the hope that a preintubation exam will prognosticate the ease or difficulty in viewing the glottis during direct laryngoscopy. As the view of the glottis is the central point of airway management, the Cormack-Lehane scoring system grades the view of the glottis during laryngoscopy from one to four. A grade 1 score represents full visualization of the glottis, grade 2 is a partial view, grade 3 is epiglottis only, and grade 4 indicates that no laryngeal structures are seen. A short neck is associated with difficulty in visualizing the glottis. A receding mandible, defined as the inability to place three fingerbreadths between the mandibular symphysis and the hyoid bone, limits the space available to displace the tongue. Prominent upper incisors and/or a small mouth limit the viewing size available when a laryngoscope and endotracheal tube are placed in the oropharynx. Limited jaw opening can prevent placement of the laryngoscope in the mouth. Limited range of motion of the cervical vertebra prevents alignment of the neck to facilitate viewing the glottis.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Michael J. Sullivan, LAC + USC Keck School of Medicine, Los Angeles, California, U.S.A. Earl Moore-Jefferies, LAC + USC Keck School of Medicine, Los Angeles, California, U.S.A.
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Traumatic facial and laryngeal injury can add to the aforementioned problems. Any disease process that manifests as swelling or edema of the lips, tongue, pharyngeal tissues and epiglottis may create a difficult airway. Failed intubation attempts traumatize the oropharyngeal tissue, increasing secretions, and produce swelling. Fractures of the mandible usually do not increase the difficulty for intubation. The mandible can be displaced to facilitate viewing of the glottis. Any displacement of the jaw should be accomplished after induction of anesthesia, as it is painful.
The Pediatric Airway

There are several differences in head and neck anatomy that make visualization of the glottis technically more difficult.
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- A small child may have a prominent occiput bringing the mouth to a position too far anterior to the larynx. A shoulder roll compensates for the increased occiput size of the pediatric head. Readily available materials may be used: a towel, hospital gown or intravenous fluid bag. - The infant has a relatively large tongue in relationship to the size of the oropharynx. This increases the risk of a lax tongue causing obstruction and thereby requires more technical expertise. - The larynx is higher in the neck creating a more acute angle between the oropharynx and the larynx. To compensate for this anatomical difference, straight blades are more useful than the curved blades. Gentle external pressure on the thyroid cartilage displaces the larynx posterior aiding in visualization. - The epiglottis is short, stubby, and soft, obstructing the view of the vocal cords. The narrowest part of the infant larynx is below the level of the vocal cords. The endotracheal tube may pass through the vocal cords only to meet resistance. If this occurs, change the tube size to one size smaller. - Uncuffed endotracheal tubes are preferred for children less than 10 years of age. A leak should be present around the tube at peak airway pressures greater than 20 mmHg.
Many aids are available for definitive airway management: estimation of the infants weight; calculation of medication of doses; endotracheal tube size; and the distance the tube should be inserted. The following are guidelines.
- The weight can be estimated for a child from one to ten years old by: [Patients age x 2] + 9 = weight in kilograms. Using this formula the weight is estimated to be 11 kilograms. A one year old generally weighs about 10 kilograms. - Endotracheal tube size is calculated by [age + 16] / 4 = endotracheal tube size. Endotracheal tube sizes that are one size larger (5.5) and one size smaller (4.5) have to be immediately available. The distance of endotracheal tube insertion is roughly three times the tube size; a size 5.0 endotracheal tube would be inserted to a distance of 15 mm measured from the lips.
Basic Airway Management

Initial interventions include basic airway maneuvers. A variety of objects can mechanically cause partial or complete airway obstruction; the tongue, vomitus, blood, dentures, swollen or distorted tissues, and foreign bodies are common causes. Clearing of these objects with suction re-establishes the airway. Positioning of a patient on their side facilitates external drainage of secretions, vomitus, or blood instead of pooling in the oropharynx in a supine patient.
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Reflex clenching of the jaw and cervical spine precautions may hinder the ability to place the patient on his side and clear the airway. Available and working suction is absolutely essential. Several types of suction catheters are available. Suctioning techniques are to remove any foreign objects in the oropharynx while minimizing the trauma to the delicate tissues of the oropharynx. Lax pharyngeal musculature and tongue occlusion can be managed with one of three maneuvers. For all techniques the patient is assumed to be in the supine position.
- The first is the neck lift-head tilt. Suspected cervical spine injury is a contraindication to this technique. One hand is placed on the back of the neck and the other is placed on the forehead, an upward movement of the hand on the neck with a downward motion of the hand on the forehead opens the mouth and relieves the airway obstruction. - The chin lift maneuver can be used with possible cervical spine injury. The thumb is placed just below the border of the lower lip and several fingers of the same hand are placed on the volar surface beneath the patients chin. As the mandible is gently lifted by the fingers, the mouth is opened by downward traction on the lower lip. - In the jaw thrust maneuver, usually the index and middle finger are placed on the section of the mandible that is superior to the angle of the mandible and inferior to the ear. Forward displacement of the mandible is done and opening the mouth is achieved with downward displacement of the lower lip by the thumbs (Table 62.1). - Bag-mask assisted ventilation or complete bag-mask ventilation can be used in conjunction with the chin lift or jaw thrust maneuver. A tight mask seal can be accomplished with minimal pressure.
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Two adjunctive artificial airways that improve assisted ventilation are the oropharyngeal and nasal pharyngeal airway devises. The oropharygeal airway is shaped like a question mark. ? The nasal pharyngeal airway is a soft tube that is flared at one end. The nonflared end is inserted into the nare and the entire length of the tube is advanced until the flared end rests at the nasal opening. Surgical gel lubrication facilitates this placement. The tube should always be inserted so the direction of advancement is parallel to the hard and soft palate. Occasionally resistance is met when about one-third of the tube has been inserted. Maintain constant forward pressure but do not force the tube past the obstruction, after several seconds the tube will then advance into the proper position.
Intubation Techniques Direct Laryngoscopy

Two basic blades are used, the curved Macintosh blade or the straight Miller blade. They come in sizes one through four, the larger the numerical designation, the larger the blade. Usually size three or four blades are used for adult patients. Endotracheal tube size is also given a numerical description, ranging from size 3-8 in half size increments, the number is the internal diameter in millimeters of the tube The larger the tube number the larger the tube size. Averaged sized
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Table 62.1. Basic airway management

Suction the oropharynx of secretions Give supplemental oxygen Relieve pharyngeal tissue obstruction Neck lift-head tilt-contraindicated in suspected cervical injury Chin lift Jaw thrust Placement of oral airway or nasal trumpet Bag mask assisted ventilation
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adult women need a 7.0-7.5 mm tube and averaged sized adult males need a 7.5-8.0 mm sized tube. Proper positioning is having the bed at a good height and the patient in the sniff position, neck flexion and head extension (provided there is no suspicion of C-spine trauma). The following steps are for the novice laryngoscopist and can be modified or deleted as proficiency improves. The clinical scenario is of an ideal patient for intubation.
- An induction agent is given and the laryngoscopist is standing at the head of the bed. The patient enters the anesthetized state and becomes apneic. - Bag-mask ventilation with chin lift now easily supports ventilation. - The muscle relaxant is given and after the appropriate time interval, the patients muscles are lax. - The following is for the Macintosh blade: Step one is opening the mouth as wide as possible using the finger and thumb of the right hand pushing on the premolars. Second, position the tip of laryngoscope blade at the tip of the tongue. Insert the blade in the right side of the mouth sliding the blade over the right side of the tongue. As the blade pushes the tongue to the left and out of the field of vision, rotate the handle so that it points to the umbilicus instead of the nipple. Continue to insert the blade until the handle gently touches the lower lip. The blade will come to rest in the proper position in the vallecula anterior to the epiglottis. The handle should now be parallel to the floor, pointing to the patients umbilicus and inserted into the mouth the length of the blade. The right hand can be removed from the teeth. Keeping the handle parallel to the floor and midline, dislocate the jaw by pushing the handle away from oneself and shortening the distance between the end of the handle and the umbilicus The next motion is to lift the handle up while keeping it parallel to the floor. If visualization of the vocal cords is still not optimal continue to lift the laryngoscope in the vertical direction. The head may be lifted up off the occipital towels. The head will not slip and fall off of the blade and the vocal cords will come into view. The endotracheal tube can now be placed in the trachea.
Rapid Sequence Induction

This is a specific technique combining pharmacologic agents and direct laryngoscopy in the trauma patient to prevent aspiration of gastric contents. Trauma patients are considered to have full stomachs.
- Preoxygenation is essential. It increases the time a patient can tolerate apnea while the laryngoscopist attempts to secure the airway. Causes of failure to preoxygenate are insufficient time of preoxygenation and failure to breath 100%
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oxygen through a sealed system. Several methods of preoxygenation are advocated. The traditional method is 100% oxygenation over 3-5 minutes. If shortening the time for preoxygenation is required to prevent further morbidity, four deep breaths over 30 seconds is the standard method. Patients have been shown to desaturate faster with this method. An eight deep breath in 60 seconds technique may be superior to the 4 breaths or 3-5 minute method. - Cricoid pressure is applied as an induction agent is given. The cricoid cartilage is a circular and rigid ring. An assistant exerts pressure on the cricoid cartilage causing it to occlude the esophagus. Cricoid pressure is maintained until the cuff of the endotracheal tube is inflated and the endotracheal tube is verified to be in the trachea. The lungs may be ventilated with cricoid pressure applied if the need arises. Occlusion of the esophagus with cricoid pressure occurs even with the presence of a nasogastric tube (Table 62.2).
Induction with an intravenous agent is given according to the patients cardiovascular status. In a hypotensive patient, sodium thiopental and propofol can be safely used, although etomidate or ketamine may support blood pressure better. Succinycholine, a rapid acting muscle relaxant, is immediately given after an induction agent. Give the full dose of muscle relaxant. If succinycholine is contraindicated, a high dose of a short acting nondepolarizing neuromuscular blocking drug can be used. Once the patient is induced, placement of an endotracheal tube is performed (Table 62.3).
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The Laryngeal Mask Airway

The Laryngeal Mask Airway (LMA) is an airway management device intended as an alternative to face mask use. It is inserted without instrumenting the oropharynx, nor with the requirement of visualizing the vocal cords. It can provide a clear airway and be inserted with minimal stimulation if the pharyngeal reflexes are sufficiently depressed. The person performing the LMA insertion is positioned at the head of the patient. The patients head is positioned with the neck flexed and the head extended. Anesthetic induction is performed to blunt protective airway reflexes. A black line runs the length of the airway tube along the greater curve portion for orientation. This black line is orientated toward the upper lip. Place the tip of the mask against the hard palate. Advance the LMA along the hard palate toward the soft palate directing the force of the index finger into the hard palate and the movement of the hand into the mouth. Continue to advance the LMA until resistance is felt. Using the other hand grasp the proximal end of the breathing tube section to stabilize the LMA and remove the insertion hand out to the patients mouth. This will prevent displacement of the LMA. Inflate the cuff with just enough pressure to obtain a seal. The LMA may appear to back out of the patients mouth with cuff inflation; this is the tube settling into position in the hypopharynx.
Operating Room Preparation

Preoperative preparation of the operating room is essential. Presetting the ventilator for a standard 70 kg patient, a tidal volume 700 ccs at a rate 10 breaths per minute, with an I:E ratio of 1:2 will temporarily ventilate a small female to a large male safely. Many acutely injured patients are hypovolemic. Equipment and supplies to rapidly place large bore peripheral intravenous lines, (14 gauge or 16 gauge
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Trauma Management
Table 62.2. Rapid sequence induction

Preparation
Operating room prepared:
Airway equipment prepared:
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Monitors:
Assistant: Position:
Procedure Preoxygenation:
Medications for induction, paralysis, sedation, analgesia Resuscitation fluids available with infusion devices Ventilation machine/anesthetic machine checked Suction Bag mask ventilation Oropharyngeal/nasopharyngeal airways Laryngoscope handle and blades Endotracheal tubes Electrocardiographic Pulse oximetry Automatic noninvasive blood pressure cuff Dedicated person to assist laryngoscopist during tracheal intubation Patient positioned with neck flexed and head extented Four deep breaths over 30 seconds, eight deep breaths over 60 seconds, or three to five minutes of normal respirations, all at an FiO2 of 1.0 ( 100% oxygen ) Applied by assistant at induction of anesthesia Intravenous medication to anesthetize the patient Facilitate endotracheal intubtion
Cricoid pressure: Induction: Muscle paralysis:
Table 62.3. Induction medications

Drug Intravenous Dose mg/kg Onset min Clinical Action (min)
Thiopental Etomidate Ketamine Propofol Muscle Relaxants Depolarizing Succinycholine Nondepolarizing Rocuronium Atracurium Vecuronium Mivacurium
3-5 mg/kg 0.3-0.4 mg/kg 1-2 mg/kg 2 mg/kg 1-2 mg/kg 0.6-1mg/kg 0.5 mg/kg 0.08-1.0mg/kg 0.2
<1 <1 <1 <1 <1 1-3 2-3 2-3 1-2
5-10 3-5 5-20 8 2-5 10-30 20-40 30-40 15-20
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angiocatheter) and central lines are mandatory. Have rapid fluid warmers to attach to these catheters. After successful venous cannulation comes arterial catheterization. Arterial catheters, pressure tubing and pressure transducers should be ready. A second pressure transducer for central venous pressure monitoring is recommended. If technical ability allows, time permits, and it is clinically indicated, a pulmonary artery catheter is valuable. Understand that a Swan Ganz catheter is not a therapeutic measure and that the optimal use of a pulmonary artery catheter is before organ failure begins. Warm the operating room and/or the patient. Hypothermia increases the risk of infection, bleeding complications, cardiac dysfunction, adverse therapeutic drug effects, increases protein catabolism, increases postoperative recovery time, and increases mortality. Mortality in trauma is related to temperature. Up to 100% mortality is seen with core body temperature less than 32Celsius. Alert the blood bank if they are not automatically notified that blood products may be necessary.
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Intraoperative Monitoring
Clinical, monitored, and laboratory variables are useful markers of the success of resuscitation of the traumatized patient. Vital signs by paramedics at the scene of injury or vital signs recorded in the emergency department are a starting point. In the operating room, noninvasive monitors are rapidly applied: electrocardiographic leads are placed, pulse oximetry, a blood pressure cuff, and a skin temperature probe. Foley catheterization of the bladder will allow quantification of urine output. Cannulation of an artery will provide instantaneous awareness of blood pressure along with the ability to sample blood for arterial blood gases. Central venous catheters provide the ability to measure central venous pressure, place a pulmonary artery catheter, and administer resuscitative fluids. No anatomical disruption should be present between the access site and the right atrium or the fluids will leak out the injury site and not perfuse the vasculature. This may occur with abdominal injury and femoral vein access. Other monitors are an esophageal temperature probe, which is also an esophageal stethoscope, a naso- or orogastric tube, and a precordial stethoscope.
Markers of Resuscition Vital Signs

Altered vital signs are nonspecific but sensitive for shock. Pain, anxiety, temperature, therapeutic medications, and illicit drugs can influence them. Some patients have physiologic reserves that allow them to maintain vital signs in the normal range until terminal cardiovascular collapse. Vital signs still are the most commonly used parameters in assessing adequacy of resuscitation. In certain patients the normalization of vital signs is all that is needed. A decrease in heart rate, an increase in blood pressure, a decrease in the FiO2 needed to maintain an adequate PaO2 , an increase in urinary output, and longer time intervals between therapeutic interventions signals a movement toward normal homeostasis. Clinically this can be described as pulse less than 100 bpm, pulse pressure greater than 30 mmHg, urine output greater than 0.5-1.0 ml/kg, absence of metabolic acidosis, and minimal effects of positive pressure ventilation.
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Base Deficit
Easily calculated from arterial blood gas analysis, base deficit is the sum of all metabolic acids including lactate caused by hypoperfusion and ischemia. Base deficit can be an accurate predictor of mortality in multiple trauma patients. The magnitude of the initial base deficit has been a reliable early indicator of the severity of the volume deficit. The amount of fluid required for resuscitation was greater in patients with the more severe base deficit than in patients with a less severe base deficit. Base deficit is easy to use and obtain from a arterial blood gas. Its limitations are that the use of bicarbonate during resuscitation and any pre-existing medical conditions that result in chronic elevations or reductions in bicarbonate levels falsely skew the results.
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Arterial Blood Gas

Arterial blood gas analysis reveals information on the global acid base status, efficiency of oxygenation and ventilation, and hemoglobin and hematocrit. Normalization of each of these parameters suggests that resuscitation is reversing the shock state. A decreasing pH in the trauma patient is generally due to metabolic acidosis secondary to hypoperfusion or a respiratory acidosis secondary to underventilation. Fluid replacement and increasing the minute respiration will correct this. Improvement of oxygenation is manifested by an adequate pa02 with a decreasing FiO2 level.
Serum Lactate
Lactate levels are a marker for anaerobic metabolism. The amount of lactate produced is believed to correlate with the total oxygen debt, the magnitude of hypoperfusion, and the severity of shock. High serum lactate levels have been associated with high mortality among critically ill patients. However lactate as a marker has its limitations. Some patients experience a resolution of their lactic acidosis but it is not always accompanied by improvement in systolic blood pressure or survival. Lactate is cleared by the liver, therefore liver injury or hepatic disease can decrease lactate clearance leading to high levels not associated with ongoing tissue hypoxia. Tissues that are not perfused during true ischemia do not contribute to lactate levels that are measured in the laboratory. Lactate offers no information on regional distribution of tissue hypoxia and blood flow.
Oxygen Transport Parameters

The critical molecule that is transported by the cardiovascular system is oxygen. It has been found that the total oxygen debt and the rate of accumulation of the debt are both critical determinants of survival. Arterial-venous oxygen content difference along with cardiac output can be measured with a pulmonary artery catheter and an arterial line.
Gastrointestinal Tonometry
Stomach mucosa is used to assess tissue perfusion. A tonometer is a nasogastric tube that has a fluid filled balloon distally. It measures the partial pressure of carbon dioxide in the gastrointestinal mucosa by allowing the equilibration of the partial pressure of carbon dioxide in the fluid filled balloon with that of gastric mucosa. Assuming that excess production of CO2 occurs during hypoxia, an increasing value of CO2 should reflect tissue hypoperfusion. Because
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the gut is highly susceptible to hypoperfusion, changes in pH may be an early indicator of concurrent global hypoperfusion and impending shock.
Choice of Marker
All of the clinical and laboratory markers of hypovolemic shock and adequacy of resuscitation have utility and limitations as tools to help us manage and treat patients. In the very dynamic situation of resuscitating a patient, no one marker can achieve the goal of telling us our patients are in this much shock and needs this much resuscitation in this much time or these organs are going to die and take the entire organism with it. The best we can do is use a combination of markers and look for patterns that support our observations that the patient is getting better or is not getting better.
Resuscitation Fluid Therapy

There is much passion involved in any discussion about appropriate fluid replacement. Successful resuscitations have been accomplished with every intravenous fluid available. Ultimately it is up to the clinician to decide the most advantageous use of each fluid. Crystalloid solutions are water with cations and anions, with or without glucose, in various concentrations and osmolarities to mimic the water and salt milieu of the human body. They are the least expensive of the various solutions, are not allergenic, immunogenic, or toxic. They equilibrate across all solute compartments quickly and have an intravascular half-life of about 15 minutes. Three times the amount of crystalloid is given for the amount of blood lost. These are usually the first fluids administered for resuscitation in acute hypovolemia shock. They rapidly restore volume, urinary output, and keep blood viscosity low. Colloids that are used in clinical practice contain a large macromolecular moiety in iso-osmotic saline. The common moieties are; albumin, polypeptide gelatin, dextran, or hydroxyethylstarch. The colloid moiety had a higher water binding capacity than does the Na cation in crystalloid solutions and can retain a large fraction of infused fluid in the vascular space. The increase in the plasma volume persists for longer periods with the infusion of colloids. The blood loss volume is replaced in a one to one ratio with colloid solutions. They can have allergenic, coagulopathic or immunogenic reactions. The synthetic colloids and processed albumin and protein fractions have minimal if any risk of infection. Volume loss can be corrected with either crystalloid or colloids. Only blood and blood products can correct defects in either oxygen carrying capacity or coagulation. Current practice is a one-to-one ratio of replacement for each volume of blood lost. The benefit of transfusion is the restoration of intravascular volume and oxygen carrying capacity. The risks of transfusion ranges from an allergic reaction to a fatal hemolytic transfusion reaction. Infectious risks range from hepatitis B to HTLV I and II (Table 62.4). Massive Transfusion
- Complications unique to massive transfusions are coagulopathy, hypothermia and metabolic derangements. Massive transfusion is the replacement of more than one blood volume within several hours. - Coagulopathy can occur when replacement fluids (crystalloids, colloids or PRBCs) dilute platelets or protein factors below a level at which they can
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Table 62.4. Risks per unit of blood that are negative in laboratory testing
Minor allergic reactions Bacterial infection ( platelets) Viral hepatitis Hemolytic transfusion reaction HTLV I/II infection HIV infection Acute lung injury Anaphylactic shock Fatal hemolytic reaction Graft vs host disease Immunosupression 1:100 1:2,500 1:5,000 1:6,000 1:200,000 1:420,000 1:500,000 1:500,000 1:600,000 rare unknown
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HTLV = human T-cell leukemia-lymphoma virus; HIV = human immunodeficiency virus source: Klein H. G. Allogeneic transfusion risks in the surgical patient. Am J Surg. 170(suppl 6A):21-26, 1995
function. Clinically this is recognized by microvascular bleeding, oozing, or no clot formation at wound, surgical or invasive catheter puncture sites. There is no single laboratory coagulation test that will give complete information on homeostatic function during massive transfusion. PT, PTT and thrombin time have not reliably predicted perioperative bleeding. Dilutional coagulopathy is more commonly due to a thrombocytopenia than a coagulation factor deficit. - Platelet transfusion is recommended with platelet counts less than 50 x 109/liter and clinical evidence of bleeding. If there is any evidence of prior platelet dysfunction, platelets are given with intermediate platelet counts of 50-100 x 109/ liter. Other authors believe that intraoperative bleeding occurs at platelet counts below 100 x 109/liter which occurs at about 10 units of transfused blood. Both schools believe that platelets should generally be given before giving FFP. - For normal hemostasis to occur about 20% of factor V and 30% of factor VIII need to be present. Percentages below this level usually do not occur until greater than one blood volume has been replaced. In the clinical setting when PT and PTT can not be obtained in a timely fashion, with evidence of bleeding and with replacement of one blood volume FFP can be given. The risks of a transfusion reaction are equal for FFP and red blood cells. Generally two units will correct most coagulopathies. - Metabolic problems associated with massive transfusions are citrate toxicity, hypocalcemia, hyperkalemia, hypothermia, and acidosis. Citrate toxicity is secondary to the administration of large quantities of citrated blood components. This can acutely lower the serum calcium level. The liver quickly metabolizes citrate, however in states of shock, liver function is impaired and citrate may not be cleared as rapidly. Citrate induces hypocalcemia causing hypotension, narrowing of the pulse pressure, increased cardiac filling pressures, gross muscle tremors and prolonged QT interval on electrocardiogram. All of these signs, except prolonged QT interval, are seen in shock regardless of calcium level and therefore not specific for hypocalcemia in the situation it is most likely to be encounteredmassive transfusions. Exogenous calcium is given when the measured ionized calcium level is low or falling in the face of ongoing blood transfusions.
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Hyperkalemia is seen with massive transfusions that require blood replacement in a short amount of time. The older the unit of red cells the higher the potassium level in the stored blood. Potassium leaves viable erythrocytes and increases the concentration in plasma of stored blood. After 21 days of storage plasma potassium concentrations approach 25-30 mEq/liter. Massive transfusions that occur over 8 hours may never need treatment for hyperkalemia because the potassium can redistribute to the intracellular space. Current rapid infusion technology allows blood infusion of 100 ml/min per machine. If two rapid transfusion devises are being used simultaneously acute hyperkalemia can occur. The best intraoperative clinically useful marker for acute hyperkalemia is the electrocardiogram. Peaking of the T waves signifies a potassium level that is clinically significant. Laboratory values of potassium may not be significantly high but the associated hypocalcemia narrows the range of safety for potassium levels. Treatment of hyperkalemia ranges from surgical control of hemorrhage, administering calcium, hyperventilation, administration of bicarbonate, insulin and glucose, and rarely the administration of epinephrine. - Hypothermia occurs in massive transfusions for multiple reasons, environmental exposure prior to arrival, low ambient operating room temperatures, large exposed wound surfaces, anesthetic drugs, and infusion of fluids below body temperature. Warming blood prior to infusion is essential to combat intraoperative hypothermia. - Infusing stored blood is infusing an acid load. The pH of stored blood is 6.66.9 due to the slow accumulation of carbon dioxide and lactic acid from erythrocyte metabolism and the citric acid in the anticoagulant. With normal tissue perfusion this acid load is rapidly metabolized and lactate and citrate are converted to bicarbonate in the liver. This alkalization is variable depending upon the functional status of the liver and is rarely a problem in massive transfusions.
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Options in Emergent Transfusions

The universal donor blood Type O Rh-negative red blood cells can be given immediately without laboratory verification of compatibility. If two units or less of this type of blood is administered, the patients own blood type still can be given subsequently. With larger transfused amounts of universal donor blood administered, transfusing the patient with their own type and crossed matched blood can lead to transfusion reactions. The second option is type specific red blood cells. Typing looks at the ABO and Rh blood antigens. ABO and Rh compatible blood can be selected from the stock and issued within 5-10 minutes. Delays in receiving type specific blood are usually due to transportation of specimens and red blood cells between the laboratory and the patient. Type specific blood is safe and has a very low potential for a transfusion reaction. Groups at higher risk are previously transfused patients and multiparious woman. They may harbor undetected antibodies. A third option is Type O Rh-positive red blood cells when blood is needed immediately. Men and women past child-bearing age or who have undergone a hysterectomy can receive Rh-positive blood. This increases the pool of universal donor blood available for transfusion. This blood should be considered when the above two options are not available. Type and crossed matched blood takes at least 45 minutes to check compatibility. Both ABO and all other red cell antigens can be tested.
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In acute hypovolemic shock situations intraoperative blood cell salvage can be utilized to decrease the amount of blood bank blood units transfused. With massive blood loss both blood salvaged and typed blood may need to be given.
Anesthesia and Analgesia

Patients may present in such extremis that none to minimal anesthetic medications are needed. In this situation usually a medication that will blunt intraoperative recall, such as a benzodiazipine is given. As resuscitation improves hemodynamics other medications to blunt pain are given, such as opoids. The most common are alfenta, fentanyl, sufenta, and morphine (Table 62.5). The placement of an endotracheal tube allows control of the sided effect of respiratory depression. In special circumstances, regional anesthesia can be used alone or in combination with a general anesthetic. An example is the operative repair of a traumatic knee injury where neuro-axis anesthesia is combined with a general anesthetic. The measurement of pain and the amount of analgesic medication needed to alleviate this pain in an anesthetized, traumatized patient is a best guess. Acute pain, like acute trauma, activates the same sympatho-adrenal response systems. Increased heart rate, increased blood pressure, increased respiratory rate, and increased anxiety are present. Other medications can be used in conjunction with opoids for pain control. Benzodiazipines will act in conjunction with opoids in achieving sedation and analgesia (Table 62.6). Ketamine, intravenous nonsteroidals, and even rectal acetomenaphin has analgesic properties.
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Conclusion
Anesthesia of the traumatized patient involves having an operating room prepared with the necessary airway, venous access, and monitoring equipment. Management of the airway, fluid resuscitation, and analgesia are paramount to improve successful outcome after an acute injury that requires operative repair.
Table 62.5. Intravenous opoid analgesia

Drug Intravenous Dose mg/kg Per dose titration mg
Demerol Morphine Fentanyl Sufentanyl Alfentanyl
0.1-1.0 mg/kg 0.1 mg/kg 0.004-0.02 mg/kg (4-20 g/kg ) 0.005-0.010 mg/kg (5-10 g/kg) 0.008-0.020 mg/kg (8-20 g/kg)
25 mg increments 2-4 mg 0.025 mg (25 g/kg) 0.005 mg (5 g) 0.05 mg (50 g/kg)
Table 62.6. Amnestics

Drug Intravenous dose Titrate 1-2 mg 0.5-1 mg 0.2-0.4 mg Onset (min) Clinical Action (min)
Diazepam Midazolam Lorazepam
2-3 <1 2-3
15-60 20-30 30-240
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References
1. 2. 3. 4. 5. Mallampati SR, Gatt SP, Gugino LD et al. A clinical sign to predict difficult tracheal intubation: a prospective study. Can Anaesth Soc J 1985; 32:429-434. Eckenhoff JE. Some anatomic considerations of the infant larynx influencing endotrachel anesthesia. Anesthesiology 1951; 12:401. Brain AIJ. The laryngeal maska new concept in airway management. Br J Anaesth 1983; 55:801-804. Jurkovich G, Greiser W, Luterman A et al. Hypothermia in trauma victims: an ominous predictor of survival. J Trauma 1987; 27:1019-1024. Davis JW, Shackford SR et al. Base deficit as a guide to volume resuscitation. J Trauma 1990; 28:1464-1467.
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CHAPTER 63
Transfusion Therapy
Gay Wehrli and Ira A. Shulman Background for Transfusion Definitions
Group: refers to a persons blood group, including A, B, O, or AB. Type: refers to a persons blood type, either positive or negative, for the presence or absence of the Rh(D)-antigen respectively. Expected Antibody: an antibody, which occurs naturally, unstimulated
- Group O people have anti-A, anti-B, and anti-AB - Group A people have anti-B - Group B people have anti-A
Unexpected Antibody: an antibody, formed due to alloimmunization (exposure to a foreign antigen). Alloimmunization may occur during pregnancy or transfusion. Screen for Antibodies: the test used to look for unexpected antibodies in the patients serum, tests for 18 specific antibodies required by the FDA, and hundreds of other antibodies, not required by the FDA. Panel: if the screen for antibodies is positive it is followed with an antibody identification work up, called a panel to ensure the antibody identification. Crossmatch: the patients serum is tested with the donor red blood cells (RBCs) to detect incompatibility and to prevent transfusion reactions due to antibodies present in the recipients serum. Group Specific: refers to a blood product, which is the same ABO group as the intended recipient. Type Specific: refers to a blood product, which is the same Rh(D)-antigen type as the intended recipient. Antigen negative: refers to a blood product known to lack a specific antigen, the absence of a specific antigen may be indicated on the products label. Uncrossmatched Release: refers to a blood product, which is dispensed for use prior to completing pretransfusion compatibility testing. Requires a clinicians approval prior to transfusion, indicating knowledge of incomplete testing. Leukocyte Reduced: indicates white blood cells (WBCs) have been removed from a blood product to a count of < 5x106. Typically used to prevent nonhemolytic febrile transfusion reactions. Also used to decrease the risk of cytomegalovirus (CMV) transmission when patients are at risk for CMV. Irradiated: indicates the blood product has been irradiated to inhibit WBC replication. Typically used to prevent graft versus host disease in an immunosuppressed patient at risk for graft versus host disease.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Gay Wehrli, University of Alabama at Birmingham, Birmingham, Alabama, U.S.A. Ira A. Shulman, Department of Pathology, University of Southern California, Los Angeles, California, U.S.A., E-mail: ishulman@usc.edu
Transfusion Therapy
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Massive transfusion: when the patients blood volume is replaced or exceeded within a 24-hour period.
Blood Bank and Transfusion Medicine Service

Pretransfusion compatibility testing is done to prevent ABO incompatible transfusions, which can be fatal, although, access to blood components must not be delayed in a life or death situation.
Timing for Testing (after receiving a patients properly labeled blood sample)
ABO Group and Rh type determination: 10-15 minutes ABO Group, Rh type determination, and screen for antibodies: 30-60 minutes If an unexpected RBC antibody is identified in the screen for antibodies, an antibody panel: 90 minutes
- The turn around time to identify the antibody may be extended from hours to days depending on the specificity of the antibody.
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Timing for Preparation and Availability of Blood Products (after receiving a patients blood sample)
Uncrossmatched, group specific blood: 15-20 minutes Crossmatch compatible blood: 35-45 minutes Frozen plasma: 20-30 minutes Cryoprecipitate: 5-10 minutes Frozen RBCs (typically used when a patient has an unusual antibody requiring a rare donor RBC unit): 60-90 minutes to prepare for transfusion, but hours to days to obtain from blood center.
Standard Operating Procedures (SOPs)

SOPs are created by the blood banking and transfusion medicine service in conjunction with other departments, which will use the SOP to provide steps taken to rapidly provide blood components during an emergency situation. Personnel responsible for following these SOPs, including laboratory technologists, nurses and physicians, require adequate training and competency in the procedures. The SOPs should address patients suddenly needing blood during an existing hospitalization as well as patients brought to the hospital needing acute, emergent treatment. Following SOP guidelines minimizes the risk of patient misidentification, specimen mislabeling, administering the wrong unit of blood, undue delay providing blood for transfusion, and/or an ABO incompatible transfusion.
Emergency Transfusion
Complete pretransfusion patient testing may be waived in a dire emergency where uncrossmatched RBC units are dispensed immediately for the unstable patient. The RBC unit is labeled to indicate: Emergency Blood Release. Blood issued without complete compatibility testing. (Or some similar wording.) The Food and Drug Administration (FDA) mandates that physicians requesting an emergency, uncrossmatched transfusion, document the blood was needed before compatibility testing could be completed.
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Requiring written documentation by the requesting physician prior to an emergency transfusion may be inappropriate, because this could lead to delays in blood availability.
Administration of Blood Products Pretransfusion Clerical Checks

Check the physicians order to transfuse. Check for a completed and signed informed consent to transfuse (in the emergent situation this may not be feasible to obtain). Properly identify the patient. Properly identify the blood product to be transfused. Confirm that the identity of the patient and blood product match each other.
Emergency Alias Names
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A system should exist to assign temporary identification for an unidentified patient, such as an alias name and medical record number. The Los Angeles County + University of Southern California Medical Center has created a successful mechanism to achieve this goal. The Department of Medical Records generates an extensive list of male and female aliases.
- Each alias consists of a unique medical record number (MRUN) and an alias name: The MRUN consists of seven digits (using the numbers 0 through 9). MRUNs are never recycled. The last name is an alphanumeric number from one to ninety-nine. These last names are cycled (i.e., after one through ninety-nine are used, the list goes back to one). The surname is a generic male or female name. Twenty male and twenty female names are used. Each of the twenty names begins with a different letter and is used in alphabetical order. These names are also cycled. The combination of ninety-nine last names and twenty surnames provides 1,980 male alias names and 1,980 female alias names.
The list of male and female alias MRUNs with assigned names is given to the Emergency Department administration.
- The administration creates packets for each alias. The packets are labeled on the outside with the alias MRUN and assigned name using red ink for female aliases and black ink for male aliases. - The packets consist of the patient identification (I.D.) plate, which includes the MRUN, gender (M for male or F for female), alphanumeric last name, and surname. All documentation for the patient will be imprinted with this I.D. plate. - Additionally each packet contains a patient chart including all of the following, which are prelabeled using the I.D. plate: Two patient identification arm bands Paper tie-on, identification tag Physical exam sheet General consent form Four labels for blood tubes
Transfusion Therapy Radiology request and record sheet Blood bank request sheet
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The patient should continue to use the alias name until the patient has been stabilized and a correct identity has been determined. When both of these have occurred, the name change should be made through the Department of Medical Records. The patients MRUN should not change unless the patient has a historical MRUN, which should be referenced.
- Permanent records should be maintained of all patient aliases (MRUN and name) used with corresponding true identities if known.
Intravenous (IV) Line and Timing of Transfusion

Transfusion of any blood product should begin within 30 minutes from the time it was dispensed from the Blood Bank, unless the blood is stored in an authorized and properly monitored refrigerator (or cooler), in compliance with federal, state and local regulations and hospital policy. The transfusion may occur as fast as the patient tolerates the volume. Transfusion of any blood product should not exceed 4 hours. 18 gauge catheters are most commonly used.
- Smaller catheters will slow the flow rate. - Smaller catheters may damage the RBCs.
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Solutions Used with Transfusion

0.9% Sodium Chloride, USP (NaCl) may be used with the transfusion of blood products. Plasma or albumin is an acceptable alternative to use with the transfusion of blood products. Do not add 5% dextrose solutions to the blood container because this may cause osmotic hemolysis of RBCs. Do not add Lactate Ringers solution to the blood container because this may cause RBC clotting. Do not add medication through the IV line to be used for transfusion.
Blood Filters
Standard (170 micron) filters are used for all blood products to prevent transfusion of clotted blood and other debris. Leukocyte reduction filters are used to decrease the WBC content of red blood cell and platelet products (see definition for leukocyte reduced).
Blood Warmers
Blood warmers are used to increase the temperature of the unit of blood at the time of transfusion.
- The cold temperatures may reduce the temperature of the sinoatrial (SA) node placing the patient at risk of ventricular arrhythmias.
Blood may be warmed to 42C. Indications for use of blood warmers:

Massive transfusion, > 100 cc/minute for 30 minutes. Adults being transfused at a rate > 50 cc/kg/hour. Children being transfused at a rate > 15 cc/kg/hour. When administering blood rapidly through a central line.
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Patient Monitoring During Transfusions

The patient needs to be monitored immediately before, during, and up to several hours following the transfusion. Documentation of the transfusion must include:
- Date and time when transfusion begins and ends. - Vital signs including blood pressure (BP), temperature (T), respiratory rate (RR), heart rate (HR) before, during (every 15-30 minutes), and after the transfusion. - Premedication and/or medication during or following the transfusion, which is related to the transfusion. - Product type and amount of product transfused. - Signs and symptoms, which occur before, during, or following the transfusion. - Transfusion reactions (see Acute Transfusion Reaction section).
Emergency Transfusion of Blood Components
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Whole Blood
Volume: 450-500 cc Components: RBCs, plasma, WBCs, platelets
- The platelets become nonviable after one day of product storage at 4C. The WBCs disintegrate over the storage period of the product, so that by the end of storage, 50% of the WBCs remain.
Indication: to increase the oxygen carrying capacity of a patient with acute hypovolemia. Expected effect: hematocrit increases 3% (hemoglobin increases 1 g/dL).
- However, since whole blood is only given to bleeding patients, the increment is rarely achieved.
Group and type requirements:

- First choice: crossmatch compatible whole blood. - Second choice: group specific, uncrossmatched whole blood. Whole blood contains a significant amount of plasma with the naturally occurring antibodies. Using uncrossmatched, group specific whole blood carries the greatest risk of any uncrossmatched transfusion. - The risk lies in clerical error, where a patient receives the wrong unit of whole blood leading to a hemolytic transfusion reaction due to the transfusion of incompatible red cells or to the transfusion of naturally occurring, but incompatible antibodies.
Packed Red Blood Cells (PRBCS)

Volume: 300 cc Components: RBCs, small amount of plasma, WBCs
- The platelets become nonviable after one day of product storage at 4C. The WBCs disintegrate over the storage period of the product, so that by the end of storage, 50% of the WBCs remain.
Indication: to increase the oxygen carrying capacity of a patient. Expected effect: hematocrit increases 3% (hemoglobin increases 1 g/dL).
- However, when given to bleeding patients, the increment is rarely achieved.
Group and type requirements:

- First choice: crossmatch compatible pRBCs. - Second choice: group specific, uncrossmatched pRBCs.
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- Third choice: O negative, uncrossmatched pRBCs. These become the first choice in the emergent situation until group specific, uncrossmatched or crossmatch compatible pRBCs are available. Group O, Rh-negative pRBCs carries a low (but not a zero) risk of hemolytic transfusion reaction. There is essentially no risk of the group O Rh-negative transfused pRBCs being hemolyzed by a recipients anti-A, anti-B, or anti-AB since group O RBCs lack A and B antigens. The nominal amount of anti-A, anti-B, and anti-AB contained in the plasma of group O pRBC will typically be diluted out once transfused. Therefore there is essentially no risk that the recipients own red cells will be hemolyzed by the expected antibodies found in the pRBC unit. The hemolysis risk of transfusing uncrossmatched O Rh-negative pRBCs lies in unexpected alloantibodies (e.g., Rh, Kell, Kidd, or Duffy), that are not detected in the patient until the screen, and/or panel for unexpected antibodies is completed. Using group O Rh-negative pRBCs in the emergent situation is preferable to Rh-positive. If there is a shortage of O Rh-negative units, females with childbearing potential should be given preference for these units. Patients with anti-D will also require Rh-negative units. A male patient or female patient with no childbearing potential may receive Rh-positive units. If no Rh-negative units are available, Rh-positive units may be used, however, consideration should be given to administering IV anti-D to prevent alloimmunization in the Rh-negative patient. - IV anti-D will coat D-antigen positive RBCs thus preventing the recipients immune system from responding to the presence of transfused D-antigen positive red cells and thus preventing alloimmunization. Should group O pRBC units be used in the emergent situation, crossmatching must be performed as soon as possible, to detect unanticipated incompatibility.
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Fresh Frozen Plasma (FFP), Solvent-Detergent Treated Plasma (SD-Plasma), and Donor Retested Plasma (DR-Plasma)
Volume: FFP DR-Plasma SD-Plasma Components: plasma-containing plasma) and complement. Indications:
- To replace clotting factors in a patient undergoing massive transfusion. - Bleeding patients with a clotting factor deficiency, when factor concentrates are not available. - Patients taking Coumadin who are bleeding.
180 cc - 300 cc 180 cc - 300 cc 200 cc coagulation factors (1 IU of factor/mL of
- There are reduced amounts of factors V, VIII, VIII:C because these are labile.
Expected effect: increase factor levels by 20% if administered at a dose and rate indicated below Group and type requirements (crossmatching is not required):
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Trauma Management - Group specific plasma. Group A patients may receive group A or AB plasma. Group B patients may receive group B or AB plasma. Group AB patients may receive group AB plasma. Group O patients may receive group A, B, AB or O plasma. - Rh type does not have to be considered.
Dose: 10-20 mL/kg body weight (a standard dose would be 4-6 units in an adult).
Cryoprecipitate
Volume: 15cc Components: plasma containing fibrinogen (> 150 mg), fibronectin, and factor VIII:C (> 80 IU), factor XIII, and vonWillebrands factor (Factor VIII:vWF) Uses:
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- To replace fibrinogen. - Second line treatment for vonWillebrands disease or Hemophilia A (factor concentrates are the first line treatment).
Expected effect: fibrinogen increases 5 mg/unit (an average adult dose is 10 units, which would increase the fibrinogen level by 50 mg).
- However, when given to a patient with a consumptive coagulopathy such as disseminated intravascular coagulation (DIC), this increment is rarely achieved.
Group and type requirements (crossmatching is not required):

- Group specific plasma is preferred. Group A patients may receive group A or AB plasma. Group B patients may receive group B or AB plasma. Group AB patients may receive group AB plasma. Group O patients may receive group A, B, AB or O plasma. - Rh type does not have to be considered.
Dose: 1-2 units/10 kg body weight (a standard dose would be 10 units in an adult).
Platelet Concentrate and Platelets, Pheresis

Volume: Components:
- Platelet concentrate contains plasma, > 5.5 x 1010 platelets, white blood cells, and < 0.5 cc RBCs - Platelet pheresis contains plasma, > 3 x 1011 platelets, white blood cells, and < 2 cc RBCs.
Platelet concentrate 40 - 70 cc Platelets, pheresis 100 - 500 cc
Use: for bleeding patients with low platelet counts or for bleeding patients with normal platelet counts but abnormal functioning platelets. Expected effect:
- Platelet concentrate increases the platelet count by 5-10 x 103/uL - Platelet pheresis increases the platelet count by 30-60 x 103/uL
Group and type requirements (crossmatching is not required):

- Group specific platelets are preferred. Group A patients may receive group A or AB platelets; use group O or B as last resort. Group B patients may receive group B or AB platelets; use group O or A as last resort.
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Group AB patients may receive group AB platelets; use group O, A, or B as last resort. Group O patients may receive group A, B, AB or O platelets. - Rh type specific platelets are preferred.
Dose:
- Platelet concentrate: 1 unit/10 kg body weight (average adult dose is 5-7 units). - Platelet pheresis: 1 unit/50 kg body weight
Acute Transfusion Reactions Steps to Take in the Event of a Transfusion Reaction

Step 1: Discontinue the transfusion. Step 2: Continue IV fluids (0.9% NaCl). Step 3: Check and document vital signs and the amount of blood product transfused. Step 4: Perform a clerical check (ensure the patient identity and blood product identity match). Step 5: Notify the physician caring for the patient. Step 6: Notify the Blood Bank. Step 7: Collect and correctly label a red top tube and purple top tube of blood. Step 8: Send the samples collected in step 7 and the remainder of the blood product (or empty blood product) with the tubing (but without the needle) to the Blood Bank.
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Mild Allergic Reaction

Signs and Symptoms: localized hives and/or pruritis. Actions to Take:
- Follow steps 1-5. - Administer the following as clinically indicated: Antihistamine (e.g., diphenhydramine 25-50mg PO/IM/IV q6h). - The transfusion may be continued if the signs and symptoms improve within 30 minutes.
Moderate to Severe Allergic Reaction

Signs and Symptoms: hives, shortness of breath, wheezing, hypotension, and/ or anaphylaxis. Actions to Take:
- Follow steps 1-8. - Administer the following as clinically indicated: Antihistamine (e.g., diphenhydramine 25-50 mg PO/IM/IV q6h). Epinephrine (e.g., 0.3-0.5 mg {0.3-0.5 ml of 1:1000 solution} SQ q20 min). Vasopressor (e.g., dopamine 400 mg in 250 ml D5W at 2-20 ug/kg/min). Corticosteroids (e.g., methylprednisolone 125 mg IV q6h).
Febrile Reaction
Signs and Symptoms: increase of temperature 1.8F with or without chills. Actions to Take:
- Follow steps 1-8. - Administer the following as clinically indicated: Antipyretic (e.g., acetaminophen 325-650 mg PO/PR q4h).
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Volume Overload Reaction

Signs and Symptoms: shortness of breath, pulmonary edema, and/or hypertension. Actions to Take:
- Follow steps 1, 3, 4 and 5. - Administer the following as clinically indicated: Diuretic (e.g., furosemide 1mg/kg body weight or 20-80 mg IV).
Septic Reaction
Signs and Symptoms: chills, fever, hypotension, and/or nausea and vomiting. Actions to Take:
- Follow steps 1-8. - Administer the following as clinically indicated: Antibiotic (review gram stain and culture results of blood product to determine which antibiotic to administer).
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Acute Hemolysis
Signs and Symptoms: shortness of breath, anxiety, pain at infusion site, chest and flank pain, shock, renal failure, and/or bleeding. Actions to Take:
- Follow steps 1-8. - Administer the following as clinically indicated: Vasopressor (e.g., dopamine 400 mg in 250 ml D5W at 2-5 g/kg/min). Diuretic (e.g., furosemide 1mg/kg body weight or 20-80 mg IV). - Maintain airway. - Maintain renal blood flow and diuresis (see above for diuretic). - Monitor coagulation and watch for DIC. Request the following labs: - CBC (Complete Blood Count) - PT (Prothrombin Time) - PTT (Partial Thromboplastin Time) - Fibrinogen Level - D-Dimer Test for Fibrin Derivatives (Cross-Linked Fibrin Derivatives) or - FDP (Fibrin Degradation Products)
Transfusion Related Acute Lung Injury (TRALI)

Signs and Symptoms: chills, fever, shortness of breath, respiratory failure, and/ or noncardiogenic pulmonary edema. Actions to Take:
- Follow steps 1-8. - Administer oxygen. - Intubate (mechanical ventilation) if necessary.
Risk of Transfusion Transmitted Viruses Transfusion Risks Per Unit of Blood

The risk of transfusion transmitted human immunodeficiency virus (HIV) is 1/200,000-2,000,000 units. The risk of transfusion transmitted hepatitis B virus (HBV) is 1/30,000250,000 units.
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The risk of transfusion transmitted hepatitis C virus (HCV) is 1/30,000150,000 units. These risks will continue to decline with the advent of new testing to detect the viruses.
References
1. 2. 3. 4. 5. 6. Goodnough LT, Brecher ME, Kanter MH et al. Medical progress: Transfusion medicine (First of Two Parts)Blood transfusion. N Eng J Med 1999; 340:438-447. In: Harmening DH, ed. Modern blood banking and transfusion practices. 4th ed. Philadelphia: F.A. Davis Company 1999. In: Menitove JE, ed. Standards for blood banks and transfusion services. 19th ed. Bethesda: American Association of Blood Banks, 1999. In: Rossi EC, Simon TL, Moss GS et al, eds. Principles of transfusion medicine. 2nd ed. Baltimore: Williams and Wilkins, 1996. In:Triulzi DJ, ed. Blood transfusion therapy. 6th ed. Bethesda: American Association of Blood Banks, 1999. Vengelen-Tyler V, ed. Technical manual. 13th ed. Bethesda: American Association of Blood Banks, 1999.
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CHAPTER 64
Venous Thromboembolism After Injury

George C. Velmahos Definition
Venous thromboembolism (VT) consists of two clinical entities that have the same pathophysiology, deep venous thrombosis (DVT) and pulmonary embolism (PE).
Incidence
The incidence of DVT varies widely among studies according to type and severity of trauma, age, method of prophylaxis, and intensity of surveillance. Overall, the incidence is approximately 12% of trauma patients who require admission to the hospital. The incidence of PE is 1.5%. Between one-fifth and one-third of patients who develop PE after trauma die from it.
Location of Thrombi
Any vein in the human body may clot. Our knowledge of the most common sites of thrombosis is limited by the accessibility of these sites for diagnostic evaluation and our aggressiveness in suspecting and evaluating DVT. The majority of thrombi are formed in the lower extremities, although the upper extremities may account up to 20% of DVT found after trauma. The majority of lower-extremity thrombi are located proximally (above the knee) rather than distally. This may be related to easier accessibility of femoral veins compared to below-the-knee veins for instrumentation and evaluation. The precise incidence of pelvic vein thrombosis is not known. PE can originate from any vein but is suspected to occur more frequently after dislodgment of clot from proximal lower extremity veins. Autopsy studies have shown that upper extremity or neck veins can be sources of PE.
Clinical symptoms and signs are extremely unreliable and carry a sensitivity and specificity of 30% for detecting DVT. The sensitivity and specificity of clinical symptomatology for PE is even lower. The most common symptoms are pain, tenderness on palpation and swelling. Homans sign is positive when pain is elicited at the calf upon forced dorsiflexion of the toes. It is also both insensitive and nonspecific. The condition that describes the marked swelling and cyanosis following complete iliofemoral venous thrombosis is phlegmasia cerulea dolens. It is associated with generalized obstruction of the extremity venous system, including the deep and superficial components. The obstruction to venous outflow may compromise the arterial blood inflow and lead to venous gangrene.
Trauma Management, edited by Demetrios Demetriades and Juan Asensio. 2000 Landes Bioscience. George C. Velmahos, Division of Trauma/Critical Care, University of Southern California School of Medicine, Los Angeles, California, U.S.A.
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The symptoms and signs of PE, like those of DVT, are unreliable. Dyspnea and tachypnea are the most commons signs. Tachycardia, pleuritic pain, hemoptysis and fever are additional elements of the clinical presentation. Many patients will have DVT or PE with no symptoms or will be unable to verbalize them.
Diagnosis of DVT
Contrast venography is considered the gold standard for diagnosis of DVT. Intraluminal defects or acute termination of the opaque contrast column are considered pathognomonic findings. However, the test has the following limitations:
- It requires transport to the radiology department and therefore is unsuitable for many critically ill patients. - It is associated with local complications such as pain, thrombosis and chemical cellulitis, and systemic complications such as anaphylactic reactions, renal and cardiac dysfunction. - It is associated with a low but real false-positive and false-negative rate (approximately 5%). - It may not offer adequate visualization of the inferior vena cava and pelvic veins.
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Impedance plethysmography is a noninvasive method that measures changes in blood volume in the leg. The sensitivity and specificity of the test is debated. Its main disadvantage is that it cannot provide information on the precise location and extent of the thrombus. False positives and false negatives may be produced by multiple technical (skin movement, incorrect position of the tourniquet) or pathophysiologic causes (muscle tension, increased central venous pressure, venoconstriction, arterial insufficiency). Its use is limited. Duplex ultrasonography is currently the most frequently used test (Fig. 64.1A, 64.1B). Normal blood flow in the veins is spontaneous and phasic with respirations, can be augmented by elevating the lower extremity or by manual compression, and can be interrupted by performing the Valsalva maneuver. In the absence of the above characteristics, venous blood flow is abnormal and a thrombosis is diagnosed. The advantages of the test are:
- It is noninvasive and associated with almost no complications. - It can be performed at the bedside and repeated frequently (Fig. 64.2).
The disadvantages of the test are:

- It is operator-dependent. - It offers poor visualization of the veins below the knee and above the inguinal ligament. - Although its sensitivity and specificity range from 80-100% in nontrauma patients, these values have never been studied in the trauma population.
D-dimers are products of degradation of the clot. In the presence of VT (DVT or PE), the blood levels of D-dimers are high. Although the experience with this test in trauma patients is still limited, studies show that if the levels are normal, VT can be safely excluded. If the levels are abnormal, further evaluation is necessary because of a significant number of falsely positive tests.
Diagnosis of PE
The gold standard for PE diagnosis is pulmonary angiography (Fig. 64.3). The sensitivity and specificity of the test is over 95%, but it is invasive and associated with contrast-, transport-, catheter-, and access-site-related complications.
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Fig. 64.1A. Partial jugular vein thrombosis around central line. Observe the freefloating tail of the clot.
Fig. 64.B. The same patient showing the partial thrombosis in a different view.
Ventilation and perfusion (V/Q) scan is a test that has much lower accuracy but is not associated with major complications. A V/Q mismatch suggests the presence of PE. The interpretation of a V/Q scan offers a high, intermediate, low or no probability for PE. High or low probability V/Q scans are associated with a rate of 15% of false-positive or false-negative results respectively. PE exists in 70% of intermediate-probability scans.
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Fig. 64.2. Almost complete subclavian vein thrombosis. Central lines are usually the cause. It is frequently missed because the upper extremities are not evaluated as regularly as the lower extremities for deep venous thrombosis. Although the exact significance of upper extremity venous thrombosis is unknown, there is documentation in the literature of pulmonary embolism originating from upper extremity and neck veins.
Fig. 64.3. Angiography is very sensitive in detecting small pulmonary emboli. One such embolus is detected at the distal end of a secondary branch of the pulmonary artery.
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CT angiography is a recently developed technique that outlines the pulmonary vascular tree by thin cuts of the pulmonary fields during simultaneous contrast injection. Helical CT technology is required with special software for reconstruction of the images. The accuracy of CT angiography in diagnosing PE is reported to be higher than 90% but there have been no studies in trauma patients (Fig. 64.4A, 64.4B). The estimation of the late pulmonary dead space fraction (Fdlate) is a new method that has been successfully tested for the bedside diagnosis of PE in a limited number of patients. It requires a special respiratory monitor to obtain the CO2 expirogram. Duplex venous scanning is completely unreliable for the diagnosis of PE. False negatives are over 50%. A peripheral venous clot may be absent in the presence of PE for various reasons. The origin of the clot may be a vein not subjected to scanning, a clot may exist but is not identified by Duplex, or the clot may have traveled to the lungs. At this time, a V/Q scan is the screening test of choice. In most centers, a pulmonary angiogram is reserved only for equivocal cases. However, the inaccuracy of the former test and invasiveness of the latter make the diagnosis of PE difficult. If CT angiography proves to be a reliable tool, it may become the test of choice.
Fig. 64.4A. CT angiography is emerging as a new, more convenient and less invasive tool for the evaluation of possible pulmonary embolism. Its reliability in critically injured patients has not yet been established, particularly in the presence of significant intrathoracic pathology. This patient had a CT angiogram that was reported as negative for pulmonary embolism.
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Fig. 64.4B. Pulmonary arteriography, done immediately after the CT angiogram, showed the presence of multiple emboli. One of these emboli is shown in this view.
Rationale for VT Prophylaxis

Trauma patients are at increased risk for VT. The posttraumatic activation of the inflammatory cascade affects coagulation mechanisms and distorts the balance between clot formation and lysis. PE is a potentially lethal disease. Most of the patients who die from PE do so within 30 minutes of the event, before therapy becomes effective. DVT is highly morbid, with 30-50% of patients suffering the long-term sequelae of postphlebitic syndrome.
Patients at High Risk for VT

All trauma patients are at risk for VT. The following criteria have been found to increase the already high risk:
- Spinal cord injury - Spinal fractures
652 Head injuries Long bone fractures Age more than 55 Major abdominal and particularly pelvic operations Venous injury
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Methods of Prophylaxis
The methods of prophylaxis can be grouped as pharmacological and mechanical. The most frequently used pharmacological methods are: low-dose heparin (LDH), low-molecular-weight heparin (LMWH) and Coumadin. The most frequently used mechanical methods are: calf-length or thigh-length sequential compression devices (SCD), arteriovenous foot pumps (AFP), and vena caval filters (VCF). LDH is the drug that has been used for the longest time. - It may be given in four forms:
5,000 units subcutaneously 12-hourly 5,000 units subcutaneously 8-hourly weight-adjusted dose subcutaneously weight-adjusted dose intravenously (1-2 units/kg/hour)
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There is little evidence that any dosing scheme is better than another.
- It has been shown to decrease VT rates significantly among nontrauma, especially elective general surgery and orthopedic, patients. - It is inexpensive and therefore, cost-effectiveness can be established easily. - It is associated with complications such as bleeding (3%), thrombocytopenia (1%), and allergic reactions.
LWMH has a mean molecular weight of 4,000 to 5,000 daltons (compared with 12,000-16,000 daltons of unfractionated heparin).
It binds only to Xa and not to antithrombin III, as unfractionated heparin does. It has better bioavailability and a longer half-life than unfractionated heparin. It is more expensive than LDH. It is given subcutaneously once or twice daily in a fixed or weight-adjusted dose.
Coumadin is used for prophylaxis mostly in elective surgery. Its use in the acute posttraumatic phase is limited because:
- it is associated with bleeding, - coumadins anticoagulant effect cannot be easily reversed, - the enteral absorption may be unpredictable in patients with posttraumatic hemodynamic alterations.
SCD and AVF prevent VT by a mechanical (intermittent compression of the veins by simulation of the muscle pump) and a fibrinolytic effect (release of tissue plasminogen activator). They are associated with no complications. However, they cannot be applied in patients with extremity injuries or operations. Patients low compliance due to perceived local discomfort or system malfunction may account for failure rates up to 50% of adequate VT prophylaxis. VCF offers mechanical interruption of the flow of clots travelling from peripheral veins to the pulmonary circulation. There are multiple designs but the Greenfield filter is the most popular. VCF prevent only PE, not DVT. Associated complications occur in 7% of patients and consist of malplacement, migration, vessel perforation, IVC thrombosis and access-site-related problems such as bleeding and thrombosis. The long-term results in trauma patients are not known.
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Comparison of Safety and Efficacy of Prophylactic Methods

A complete meta-analysis of all up-to-date literature evidence revealedcontrary to common beliefsthat there is no difference in safety and efficacy between the different methods of VT prophylaxis. Because the available data is limited and of poor quality, such differences may exist and could be proven with better trial design and larger sample sizes. The most promising drug seems to be LMWH. In two prospective randomized controlled trials, it outperformed LDH in preventing DVT. Its cost-effectiveness is still unknown. There is no evidence suggesting superior safety of any of the pharmacological methods. Combination methods have not been proven to be better than single methods.
Pitfalls in Prophylaxis
The belief that VT is a disease that does not occur early after trauma. About 6% of all PEs occur within the first 24 hours, and 12% within the first 48 hours. Prophylaxis should be started as early as possible. Prescription of SCD without strict monitoring. Frequently the device is not functioning or simply not worn. The protective effect of SCD dissipates within minutes after it is removed. Nurses and patients should be trained accordingly. Exclusion of the possibility of VT because the patient is receiving adequate prophylaxis. Among critically injured patients, 13% develop VT despite thromboprophylaxis. Patients at high risk should be screened routinely by Duplex scan. Reliance on clinical symptomatology to diagnose VT. The majority of patients will have atypical or no symptoms. A low level of suspicion should be maintained. Patients at high risk should be screened routinely (once or twice weekly).
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Selection of Patients who Need Prophylaxis

Patients with any of the above-mentioned high-risk criteria should be considered for prophylaxis. Patients with ongoing bleeding, serious posttraumatic coagulopathies, or significant intracranial hemorrhage should not receive pharmacological prophylaxis until the bleeding is controlled, the coagulopathy corrected, or 3-5 days have passed from the head injury. Such patients should be considered for early placement of VCF by balancing the risks and benefits. Additional patients to be considered for VCF are those with multiple long-bone and/or pelvic fractures or with lifelong VT risk due to permanent neurologic deficits that will not allow proper mobilization (spinal-cord or severe brain injuries). Patients with minor to moderate trauma receive the best prophylaxis if they are encouraged to walk. The practice of keeping potentially ambulatory patients in bed in order to wear SCDs should be condemned.
Treatment of VT
The standard treatment of VT is intravenous unfractionated heparin titrated to prolong the APTT to 1.5-2 times normal for the first 5-7 days. In patients who can tolerate oral intake, coumadin is started almost simultaneously and
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continued for 3-6 months after the heparin is discontinued on the fifth to seventh day. Trauma patients with VT are likely to be severely injured, cannot be fed orally, and must have intravenous heparin for longer periods of time. New evidence suggests that LMWH is equally or more effective and safe than LDH at a dose of 1 mg/kg or an equivalent of 200-250 anti-Xa IU/kg subcutaneously 12-hourly. It is proposed that coagulation parameter monitoring is not necessary. A VCF can be inserted if there are contraindications to full anticoagulation, or if recurrence is noted despite therapeutic levels of anticoagulation. Thrombolysis by r-tPA (recombinant tissue plasminogen activator) or urokinase is associated with high rates of bleeding. Trauma or surgery within 10 days are contraindications to thrombolysis. Resolution of clot should be expected in 70% of the cases. No proven benefit is found between bolus versus continuous doses or systemic versus local infusion of thrombolytic agents. Embolectomy by surgical removal of clot from the pulmonary artery is reserved for patients who manifest severe hemodynamic instability with no improvement by other therapies. It is an operation with very high mortality and is practiced very rarely in trauma patients.
Pitfalls in Therapy
Inadequate coagulation parameter monitoring during heparin anticoagulation. An APTT level of less than 1.5 normal is associated with high rates of recurrence. A level of more than 2.5 normal is associated with high rates of bleeding. Failure to initiate therapy for PE before definitive diagnosis is made, if suspicion is high and contraindications to therapy do not exist. Most patients who will die from PE will do so within the first hour. If the patient survives the initial event, the focus should be shifted towards preventing a recurrence by starting early therapy. Definitive diagnosis may be time-consuming. Treatment should be started while diagnosis is pursued and then discontinued if the tests are negative for PE. Exclusive reliance in IVC filters to treat PE of unknown origin. Although the majority of PEs will originate in the lower extremities, some clots will be dislodged from the upper torso or upper extremities.
References
1. 2. 3. Velmahos GC, Kern J, Chan L et al. Prevention of venous thromboembolism after injury: An evidence-based report. Part I. J Trauma, in press. Velmahos GC, Kern J, Chan L et al. Prevention of venous thromboembolism after injury. An evidence-based report. Part II. J Trauma, in press. Velmahos GC, Nigro J, Tatevossian R et al. Inability of an aggressive policy of thromboprophylaxis to prevent deep venous thrombosis in critically injured patients: Are current methods of DVT prophylaxis insufficient? J Am Coll Surg 1998; 187:529-533. Geerts WH, Jay RM, Code KI et al. A comparison of low-dose heparin with lowmolecular-weight heparin as prophylaxis against venous thromboembolism after major trauma. N Engl J Med 1996; 335:701707. Venous thromboembolism: An evidence-based atlas. Hull RD, Raskob GE, Pineo GF, eds. New York: Futura Publishing Company, Inc., 1996.
4. 5.
Trauma Program Manager

Kathleen E. Alo and Pamela M.Griffith
The role of the Trauma program manager (TPM) is multi-facetted and encompasses a wide variety of distinct functions. In the past the role has been titled Trauma Nurse Coordinator. An overview of the TPM role is highlighted. However, due to the specific needs of our readers, the greatest focus of this chapter is on the trauma Performance improvement functions of this role. For success, it is suggested that a TPM be flexible, self-motivated, self-directed, assertive, goal-directed, diplomatic, tenacious, an analytical thinker, able to communicate well, work independently, and have strong interpersonal skills.1,2,3 The 1999 American College of Surgeons resource document describes the TPM as Fundamental to the development, implementation and evaluation of the trauma program. 4 Non-heading terms in this Chapter, which are bolded, are defined in the final section, Performance improvement Glossary.
Overview of Operational Functions of TPM

There are 10 distinct functions performed or overseen by the TPM. These functions are implemented differently within each Trauma Centerspecifically tailored to the needs of that institution.
1. Clinical Activities Monitoring trauma care across continuum of care, policy and procedure development, clinical practice guidelines, clinical care resource evaluation, case management. 2. Program Administration Managing operational, administrative, financial aspects of the program. Supervising, hiring and firing trauma program staff. Evaluating and setting trauma care prices, assisting with hospital and/or physician billing. 3. Trauma Registry Supervising or performing trauma patient data collection, coding and scoring. Designing and validating database, designing and analyzing trauma reports for performance improvement, research, resource planning, epidemiology and injury prevention. 4. Consultant/Liaison Stabilizing complex network of caregivers as a liaison with numerous surgical and nonsurgical departments, as well as, extra-facility agencies, trauma system administrators, and prehospital care organizations and providers.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. Kathleen E. Alo, Los Angeles County / USC Medical Center, Los Angeles, California, U.S.A. Pamela M. Griffith, Childrens Hospital Los Angeles, Los Angeles, California, U.S.A.
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Trauma Management 5. Trauma System Evaluation / Design Trauma system designing, planning, implementation and evaluation at the local, regional and national levels. Facilitating appropriate regulations and legislation regarding trauma care and systems. 6. Education Providing trauma care education for trauma center staff, as well as inter-facility and regional professional staff. Conducting individual case reviews, community education, and participating in offering and/or instructing in ATLS, PALS, and other provider training. 7. Research Facilitate trauma research topic selection, protocol design, analysis and documentation and distribution of findings. Providing data and data analysis for basic and clinical trauma related research. 8. Injury Prevention Directing and conducting community health education and injury prevention programs. These may occur at many different locations including local schools, retirement areas, hospital foundations, and community, religious or social groups. 9. Survey Coordination Plan and coordinate hospitals overall preparedness to demonstrate compliance with all trauma care standards. Assure completion of presurvey packet. Gather all supporting documentation to achieve and maintain trauma center designation. 10. Performance improvement Monitors patient care and system issues. Develops quality indicators, conduct audits, evaluates trends and events while maintaining confidentiality, outlining and following through on appropriate corrective actions. Works to improve clinical outcomes.
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Process of Trauma Performance Improvement

Trauma Performance improvement (PI) programs should provide a structured approach to continually improving trauma care. A primary objective is to reduce inappropriate variation and undesired outcomes in care.4 The complete process must be well documented (Fig. 65.1). The following components are important in every trauma PI effort:
1. Identification of Trauma Patients In an optimal system, all injured patients would be included in your trauma performance improvement program. If this is not practical, at least all of the most severely injured patients should be included. 2. Identification of Issues Concurrent ReviewReview of patient care while it being delivered Retrospective ReviewReview of patient care after discharge TrendingReview of care issue in multiple patients over time 3. Trauma PI Indicators - A trauma PI indicator or audit filter is one method intended to identify cases for which a review of the clinical care is needed. The review may examine the care in a peer review setting or as a system root cause analysis evaluation. - Indicators should stimulate curiosity and creativity in developing meaningful discussions and opportunities to improve care. Variety is important, as the PI program must address issues across the continuum of care.
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Fig. 65.1. Trauma performance improvement process.
Adult and Pediatric Focus A comprehensive program includes specific indicators for both the adult and pediatric population. In addition, the pediatric population should be summarized and analyzed separately in order to address needs specific needs of this specialized population. Primary Outcomes A thorough mortality review is necessary on all patients who expire from injury in the Trauma Center. Functional Outcome Measures A variety of scoring systems that quantifies the patients ability to independently perform activities of daily living and reintegrate into society. For example, Functional Independence Measures Score (FIMS). Sample Indicators The following table reflects a wide range of potential indicators. The list is
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Table 65.1. Sample trauma quality indicators/audit filters

All Trauma Deaths Major Complications All Trauma Transfers Delay in Diagnosis Error in Diagnosis Error in Technique Scene Time > 20 Minutes Absence of Paramedic Report on Medical Record for EMS Patients No Trauma Team Activation for Qualifying Patient Not Met by Trauma Surgeon on ED Arrival GCS < 14 without CT Head within 2 hours of ED Arrival GCS < 8 Leaving the ED without a Mechanical Airway GSW Abdomen Who is Managed Non-operatively Abdominal Injuries and Sys BP<90, Undergoing Ex Lap > 1 After Arrival Ex Lap > 4(-6) after ED Arrival EDH or SDH Receiving Crainiotomy > (2-)4 hours After Arrival (Excludes ICP monitoring) Open Long Bone Fxs with > (6-)8 hours Between Arrival and Debridement (Exc Low Velocity GSWs) Abdominal, Thoracic Vascular, or Cranial Surgery > 24 hours After Arrival Admitted to a Non-Surgical Service (Exclude Isolated Ortho/Neuro). ICU Stay 2 times Average Trauma ICU LOS Uplanned Return to the OR with in 48 hours of Initial Procedure Re-intubation within (24-)48 hours of Extubation Deep vein thrombosis, Pulmonary embolism, Decubitus Non-admitted Trauma Pt Returns within 72 hours and is Admitted ED Arrival to Disposition Time > 2 hours Non-Compliance with Hospital Criteria for Trauma Center Designation Transferred from Another Facility After > 6 hours Absence of Sequential ED Neurologic Eval on pts with Skull Fx, Intercranial, or Spinal cord injury Absence of Hourly Documentation on Trauma Patients Until Disposition Adults with Non-fixated Femoral Diaphyseal Fractures Adults Receiving Platelets of FFP Within 24 hours of Arrival (after receiving 8 units of blood) Blunt Head Injury with Field GCS =14 with Abnormal Head CT & Craniotomy Pediatric Blunt Trauma Undergoing Abdominal Surgery Lower Extremity Injuries Who Develop Compartment syndrome Chest Injuries Developing Empyema
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4.
5.
6.
7.
not complete but is meant to be a guide illustrating the variety of possible filters (Table 65.1). Reviews - Multi-Disciplinary Peer ReviewDetailed review of individual patients care across the trauma care continuum among peers. - System Root-Cause AnalysisDetailed review of the problem, including all steps and related processes potentially affecting the issue. Conclusions Consensus evaluation as to whether an opportunity for improvement exists. A causative factor should be determined, to assist in planning appropriate corrective actions, whenever possible. These factors are generally knowledge, system or performance / behavioral deficits. Corrective Actions An action is only necessary if an opportunity for improvement exists. Must correspond with identified causative factor. May include, education, counseling, change in protocol, resource enhancement, refer to another area for further review and disciplinary action. Follow-up and Loop Closure Assure the corrective action has been completed and has accomplished the desired effect. If desired effect did not occur, additional actions may be required, until improvement is achieved.
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Principles of Performance Improvement

Program must address the injured patients ongoing needs and required services across the continuum of care Multi-Disciplinary Approach
- Relationship between Disciplines Should include General Surgery, Neurologic Surgery, Orthopedic Surgery, Emergency Medicine, Prehospital Care, Anesthesia, Critical Care, Pediatrics, Radiology, Nursing, Respiratory Care, Laboratory and Blood Bank, Infection Control, Physical Therapy, Hospital, Administration, Pathology and any other involved service. - Relationship with Individuals Objective, nonsectarian interaction regardless of domain and patients physical location
Process and Outcome Measures should be utilized in trauma PI plan.

- Process measures evaluate appropriateness, availability, efficiency, timeliness and continuity of care - Outcome measures evaluate the quality, value, safety, respect, caring, effectiveness and efficacy of care ExamplesTable 65.2. - Focus on various Dimensions of Performance
Causes of variance in process and outcome should be evaluated and documented clearly on each case reviewed
- Three potential causes of variance include (one or more): Knowledge Deficit - A major causative factor - Corrective actions should be educationally based and NOT PUNITIVE System Deficit
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Table 65.2. Process vs. outcome measures

Process Outcomes
Timeliness of Radiological Films Availability of Call-panel Errors in Judgement Errors or Missed Diagnosis Readmission to Hospital Unplanned Returns to the OR Errors in Technique
Morbidity Mortality Length of Stay (LOS) Cost Splenic Salvage Functional Outcome Measures Patient Satisfaction
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- A major causative factor - Corrective actions usually require task forces, or PI teams - May require root-cause analysis - Hospital Administration may need to be involved Performance or Behavioral Deficit - An infrequent causative factor - Corrective actions should be handled individually - Documentation should be considered in the credentialing, privileging, and competency evaluation process Mortality reviews should also evaluate and come to a conclusion regarding preventibility - Include only one of the three potential conclusions: Nonpreventable Potentially Preventable Preventable - Every death deemed preventable or potentially preventable should have corrective action(s) aimed at averting mortality in similar cases
Responsibility and Accountability for PI

- Ultimate responsibility rests with the hospitals governing body Integration with hospital organizational structure is essential - Specific Authority must be designated through the Trauma Director - Day-to-day operational responsibility rests with the TPM
Performance improvement Setting

- Trauma Center Hospital-specific PI issues Filters, peer reviews, focused reviews, trending, outcomes i.e., Timeliness to the OR - State or Regional Trauma System Review of issues across a multi-center trauma system Trending, filters, analysis of system-wide issues i.e., Evaluation of field triage criteria - Benchmarking Compare local or regional measures with those from other similar Trauma Centers, and systems.
Utilization of the Trauma Registry

The Trauma Registry is the core of a trauma program. It is the objective reflection of care given to injured patients. Analysis of trauma data is the
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basis of clinical decision-making, hospital policy, and the foundation for research, prevention, and legislative advocacy. The hospitals trauma registry should be incorporated into larger databases regionally and nationally, in order to capitalize on its full potential. Uses of the trauma registry include:
- Epidemiology of Injury Identification of Injury-related Public Health Issues Influences Development of Injury Prevention Program - Performance improvement Trauma Care Assessment Trauma System Evaluation Institutional Benchmarking - Program Resource Needs Assessment - Research Basic and Clinical Outcomes Related
Performance Improvement Glossary

Appropriateness Availability Continuity Continuum of Care Cost of injury Dimensions of Performance The degree to which the care and services provided are relevant to an individuals clinical needs, given the current state of knowledge.5 The degree to which appropriate care is available to meet an individuals needs. 5 The degree to which the care of individuals is coordinated among practitioners, among organizations, and over time. 5 The phases of injury intervention, from a traumatic incident through each phase of care concluding with rehabilitation and reintegration into society. Injury and trauma care results in unintended costs to the individual, the healthcare system, and society at large (Table 65.3). Nine definable, measurable, and improvable attributes of organization performance related to doing the right things right 5 (appropriateness, availability and efficacy) and doing things well (timeliness, effectiveness, continuity, safety, efficiency, and respect and caring). The degree to which care is provided in the correct manner, given the current state of knowledge, to achieve the desired or projected outcome(s) for the individual. 5 The degree to which the care of the individual has been shown to accomplish the desired or projected outcomes. 5 The relationship between the outcomes (results of care) and the resources used to deliver care. 5 A measure used to determine, over time, an organizations performance of functions, processes, and outcomes. 5 The rate, proportion or incidence of disease in an area, locality, nation, or region. For instance, complications rate. The proportion of deaths to an area, locality, nation, or region. For instance, deaths rate.
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Effectiveness Efficacy Efficiency Filter/Indicator Morbidity Mortality
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Table 65.3. Cost of injury

Individual costs Societal costs Health system costs
Co-Payments Self &/or Under-Insured Loss of Life Quality of Life Functional Outcome
Health Insurance Costs Mortality Rate Morbidity Rate Years of Productive Life Loss
Unreimbursed Hospital / MD Costs Cost Shifting Healthcare Resource Availability
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Performance To measure, evaluate and improve functions, processes and Improvement (PI) outcomes of health care delivery. Similar terms include quality assurance, quality management, quality improvement, total quality management, organization wide performance improvement. 5 Quality of Care The degree to which health services for individuals and populations increase the likelihood of desired health outcomes and are consistent with current professional knowledge. 5 Quality of Life A individuals belief in the ability to utilize the characteristics and attributes both physical and nonphysical that constitute the basic value of a persons own life. Respect and Caring The degree to which those providing services do so with sensitivity for the individuals needs, expectations, and individual differences, and the degree to which the individual or a designee is involved in his or her own care decisions. 5 Safety The degree to which the risk of an intervention (for example, use of a drug or a procedure) and risk in the care environment are reduced for a patient and other persons, including health care practitioners. 5 Timeliness The degree to which care is provided to the individual at the most beneficial or necessary time. 5 Value The quality of a service or object, which is thought of as being more or less desirable, useful, estimable, important etc. Often considered as the degree of worth.
References
1. 2. 3. 4. 5. Beachley M, Snow S; Trimble P. Developing trauma care systems: the trauma nurse coordinator. J Nsg Admin 1988; Vol 18(7,8):34-42. Blansfield JS. The career spectrum in emergency nursing: trauma nurse coordinator. J Emerg Nsg 1996; Vol. 22(6):486-488. Flint CB. The role of the trauma coordinator: A position paper. J Trauma 1988; Vol. 28(12):1673-1675. American College of Surgeons. Resources for Optimal Care of the Injured patient. Chicago, IL: ACS 1998; 5:23-25, 16:69-76. Joint Commission: Hospital Accreditation Standards. Oakbrook Terrace, IL: Joint Commission on Accreditation of Healthcare Organizations 1999:281-307.
Fat Embolism
George Androulakis and Demetrios Demetriades Definition
Fat embolism is a recognized serious complication characterized by pulmonary or central nervous system dysfunction or both. It results from fat microemboli to the skin, lungs, brain and other tissues usually after long bone or pelvic fractures or orthopedic procedures that require intramedullary manipulation.
First described by Zenker in 1861, while its clinical manifestations have been recognized for more than 100 years. Since 1861 more than 2.000 reports and articles have been published on the process of fat embolization.
Incidence
There is evidence that marrow fat embolization occurs in almost all patients who sustain a long bone or pelvic fracture and it refers to the presence of fat globules in the lung parenchyma and peripheral circulation. Still, only a minority, 1-5% of these patients develop clinical symptoms related to the so called fat embolism syndrome. Thus petechial rash, thrombocytopenia, pulmonary distress and mental disturbances with an onset of 12-48h after a fracture.
Pathophysiology
There are two main theories on the pathogenesis of the fat embolism syndrome: the mechanical theory and the biochemical theory. a) Mechanical Theory When a bone fractures, the disruption of fat cells and venous sinusoids allow fat to enter the venous circulation. Spongiosa bone particles and larger fat globules block the smallest branches of the pulmonary vasculature, while small fat droplets, push through the lung capillaries and enter the systemic circulation and embolize other organs. Major systemic embolization has also been ascribed to the migration of these globules to the pulmonary veins through pulmonary precapillary shunts. b) Biochemical Theory
The current biochemical theory is based on the fact that fatty acids, whether freely circulating or formed within the pulmonary system, cause endothelial damage and are directly toxic to pneumocytes. Capillary leakage, perivascular bleeding, platelet adhesion and clot formation are considered to be the main factors responsible for tissue damage and organ dysfunction.
Trauma Management, edited by Demetrios Demetriades and Juan A. Asensio. 2000 Landes Bioscience. George Androulakis, University of Athens, Athens, Greece Demetrios Demetriades, University of Southern California, Los Angeles, California, U.S.A.
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Fig. 66.1. MRI of brain fat embolism. Note the high-intensity areas on the T2-weighted images.
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The origin of the free fatty acids may be twofold. In the first case, free fatty acids are mobilized from the fracture site by the lysis of triglycerides. When formed in excess, they are only partly bound to albumin. These fatty acids are then carried along with the venous circulation, and enter the pulmonary capillary bed where they have a direct toxic effect on the endothelial cells and pneumocytes. - In the second case, the high levels of circulating free fatty acids, observed after major injuries, are assumed to be associated with the increased release of catecholamines, the latter induce lipolysis which lead to high levels of free fatty acids.
Clinical Manifestations
Many patients with fat embolism remain asymptomatic. Signs and symptoms may include: Respiratory symptoms, characterized by tachypnoea, dyspnea and sometimes cyanosis, accompanied by a decrease in pO2. Pulmonary signs are present in about 75% of fat embolism patients; a minority (10%) develop respiratory insufficiency that requires mechanical ventilation. Cerebral manifestations, unrelated to head injury. These occur in more than 80% of cases. The patients may show a wide range of clinical symptoms, such as confusion, drowsiness, lethargy, convulsions and coma. Occasionally cerebral manifestations may be the only symptoms of FES. Petechial rash on the mucous membranes and skin on the anterior part of the thorax and neck. This is observed in more than 50% of fat embolism patients. The clinical signs usually do not appear until at least 6-12h have elapsed following the accident. Major signs appear in 60% of the patients within 24h and in 85% of the patients within 48 h. Earlier clinical manifestation is possible, but rare. Onset after 72h has also been described in exceptional cases. Occasionally, the clinical
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symptoms of a late-developing fat embolism syndrome imitate those of massive thromboembolism of the pulmonary artery. Several minor symptoms may accompany the main clinical picture of this syndrome. The most important ones are: early fever, an unexplained anemia and thrombocytopenia from day 1 onwards, retinal changes, jaundice, renal function tachycardia.
Respiratory System
The pulmonary manifestations start with hypoxia-induced tachypnea and subsequent hyperventilation. Moderate to severe cyanosis may be present. If respiratory insufficiency is combined with progressive anemia, cyanosis may be absent. Chest radiographs show multiple bilateral diffuse infiltrates called the snow storm appearance, especially in the upper and middle parts of the lungs. Pulmonary function usually recovers completely within 1 week.

An initial symptom-free interval of about 24h is common. The first clinical symptoms may include delirious restlessness, somnolence or confusion. As the pathophysiological process progresses, stupor and even complete loss of consciousness (coma) may develop. Severe cerebral involvement has been described in patients with little or no pulmonary involvement. In the majority of cases, there is complete cerebral recovery. In patients with multiple skeletal injuries who are also suffering from craniocerebral injuries, the origin of the neurological signs and symptoms is often difficult to establish. An initial symptom-free interval may help to make a differential diagnosis. b) Petechial Rash
Petechiae are present in about 50-60% of cases, and they often appear after an interval of 24-28h. They are most frequently found in both axillae, on the anterior side of the chest and neck, around the navel, the conjunctivae and the mucous membranes of the mouth. The anatomical substrates of the petechiae are similar to those observed in the brain, lungs, eyes and other organs involved in the pathological process. Microscopic examination may reveal small droplets of fat that are obstructing capillaries and are surrounded by small perivascular hemorrhages.
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Diagnosis
The diagnosis of fat embolism is usually an exclusion diagnosis. The diagnostic criteria are based on the classic Gurd criteria. Gurds criteria, are divided into major and minor criteria: Major Criteria
- Hypoxemia with no other clear cause - CNS depression - Axillary or subconjunctival petechiae
Minor Criteria
Tachycardia (more than 110 beats/min) Pyrexia (temperature more than 38.5C) Retinal changes on fundoscopic exam (fat or petechiae) Unexplained anemia
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At least one of the major criteria and three minor criteria or two major and two minor criteria are required for the diagnosis of FES.
Radiological Diagnosis
a) Chest RadiographsThe chest radiograph findings of FES tend to lag at least 12-24 hours behind the clinical, blood gas, and platelet changes. The clinical and arterial blood gas (ABG) changes usually become clinically obvious at least 12-24 hours before any radiologic abnormalities appear. When radiographic changes become apparent, they resemble those of other types of acute respiratory distress syndrome (ARDS) and include early congestion and diffuse infiltrates. If the radiologic changes occur before clinical respiratory changes, one should suspect pulmonary contusion. b) Computed Tomography Scan and Magnetic Resonance Imaging of the Head Before it is assumed that the neurologic changes occurring after major trauma are the result of FES, a computed tomography (CT) scan of the head is needed to rule out space-occupying lesions. In FES the brain CT usually shows no abnormality. Differentiating the changes of FES from diffuse axonal injury may be very difficult. A magnetic resonance imaging (MRI) scan is usually diagnostic and shows scattered spotty high-intensity areas on T2 weighted images or low-intensity areas on T1 weighted images involving the cerebral white matter, corpus callosum and basal ganglia.
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Therapy Prophylaxis:
Modified surgical techniques, such as unreamed rodding, have been described to reduce the bone marrow release into the circulation significantly and therefore minimize the risk for developing FES, although other studies challenged this recommendation. The early adequate administration of analgesia to limit the sympathomimetic response to injury in order to avoid increased liberation of free fatty acids by accelerated lipolysis may be useful, although not proven. Heparin alcohol, bile salts, or steroids have all been used without any proven benefit. Outcome The reported overall mortality ranged from 10-20% in the 1970s to 5-10% today. Mortality is related to the severity of FES and to associated injuries.
Conclusions
FES remains a diagnosis of exclusion based on clinical criteria. Clinical apparent FES is unusual. Early intramedullary fixation, especially with the unreamed technique, does not increase the incidence of FES. The management of FES remains primarily supportive, with only a small number of patients requiring advanced, aggressive critical care.
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References
1. 2. 3. 4. 5. Wilson RF, Georgiadis GM. Fat embolism syndrome. In: Wilson RF, Walt AJ, eds. Management of trauma: pitfalls and practice. 2nd ed. Philadelphia: Williams & Wilkins, 1996:703-725. Gurd AR. Fat embolism: an aid to diagnosis. J Bone Joint Surg Br 1970; 52:732-744. Ten Duis H.J. The fat embolism syndrome. Injury 1997; 28:77-85. Bulger EM, Smith GD, Maier RV et al. Arch Surg 1997;132:435-439. Hofmann S, Huemer G, Salzer M. Pathophysiology and management of the fat embolism syndrome. Anaesthesia 1998; 53:35-37.
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CHAPTER 67
Alcohol, Illicit Drugs and Trauma

Howard Belzberg Principles of Management
Every trauma patient presents with the possibility that acute or chronic drug or alcohol use will complicate his or her hospital course. Alcohol and drugs are among the most common underlying causes of both accidental and intentional injury. The consequences of pretrauma drug and alcohol use are extremely variable. Some investigators have found that, for a given severity of injury, patients with positive alcohol levels seem to have a lower mortality. Others have found no influence, or a higher mortality. Some investigators have found that greater resuscitation volumes were required in patients with alcohol in their systems at the time of trauma, or that catecholamine response in trauma patients was blunted by alcohol. The underlying disease processes associated with chronic abuse may not be the same as the acute impact of drugs or alcohol. The following elements associated with drug or alcohol use must be considered in the development of the therapeutic and monitoring plan:
acute intoxication chronic intoxication tolerance habituation addiction/withdrawal/abstinence syndromes comorbidities associated with a particular drug or alcohol
Alcohol
Alcohol is by far the most commonly abused substance. As many as 52% of a recent series of severe trauma victims were positive for alcohol on admission to the hospital. Respiratory Problems
- Altered mental status, especially episodes of stupor and coma, put alcohol-intoxicated patients at high risk of aspiration.
Cardiovascular Problems
- Cardiomyopathy is present in as many as one-third of chronic alcohol abusers. In many of these cases, the cardiac compromise may be subclinical, with symptoms developing when the patient is stressed by trauma or surgery. - Arrhythmias are a common manifestation of alcohol-related cardiac compromise. Atrial fibrillation, atrial flutter and premature ventricular contractions (PVCs) are frequently observed.
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- Acute alcohol ingestion leads to reduced vascular reactivity and potential hypotension. - General anesthesia may exacerbate this hypotension, or paradoxically cause hypertension due to increased metabolism of anesthetic agents due to enzyme induction.
Liver Problems
- Cirrhosis is a serious consequence of alcohol abuse and may affect the outcome after trauma.
Coagulation Problems
- Both coagulation and fibrinolysis are altered by alcohol consumption. Platelets are reduced due to suppression of megakaryocyte maturation. Platelet aggregation in response to various stimuli including collagen and adrenaline is inhibited by alcohol consumption. - The clinical manifestation of these abnormalities is a prolonged bleeding time.
Renal Function Problems

- Alcohol reduces the secretion of antidiuretic hormone, which induces a significant diuresis, primarily of free water. - There is also an increase in excretion of magnesium and phosphate, which often leads to metabolic complications.
Acid-Base and Electrolytic Problems

- A variety of acidosis problems are associated with acute and chronic alcohol ingestion. - Most common is lactic acidosis. - Alcoholic keto-acidosis may be induced due to accumulation of metabolites such as beta-hydroxybutyrate. - Magnesium deficiency is common in the alcoholic patient, often requiring major replacement. While magnesium levels are widely available, the intracellular nature of this ion leads to difficulty in evaluating the total body magnesium. Thus, low serum levels of magnesium (< 2 mg) are likely to be associated with hypomagnesemia, while apparently normal levels do not necessarily ensure adequate magnesium stores. - Phosphorus deficiency is common among alcoholics, ranging from 2.5-30.4%. It becomes an emergency at levels below 1.1 mg/dl, potentially inducing Rhabdomyolysis, hemolysis or respiratory muscle failure. Phosphorus deficiency can be caused by the malnutrition and endocrine abnormalities associated with alcohol abuse.
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Nutritional Problems
- Thiamine deficiency and B6 deficiency are common in alcohol abusers, and are associated with both poor nutritional intake and absorption abnormalities.
Withdrawal or Abstinence Syndromes

- The abstinence syndrome is characterized by progression through tremulousness to hallucinosis to delirium tremens. - Alcohol withdrawal is the most complex of the abstinence syndromes. The spectrum of symptoms ranges from intoxication, coma, blackouts, rum fits or withdrawal seizures, tremulousness and hallucinations to delirium tremens. - The full-blown delirium-tremens syndrome is characterized by confusion, hallucinations, agitation, sleeplessness and profound hyperactivity of the autonomic nervous system manifested by tachycardia, diaphoresis, fever and occasional vascular collapse.
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Principles of Treatment for the Chronic Alcohol User

Therapy for alcohol intoxication, complications and withdrawal symptoms must be individualized. Symptoms and physiologic complications must be identified and treated aggressively. Specific electrolyte and acid-base disturbances should be corrected.
- Dehydration should be anticipated and treated with infusion of normal saline. - Initially, glucose solutions should be avoided due to the risk of inducing neurologic deterioration due to Wernicke-Korsakoff syndrome. - The saline solution should have multiple vitamins, especially B vitamins, and thiamine (50 mg per liter) added once hypovolemia has been controlled. - Magnesium deficiency should be treated with 2 grams of magnesium per liter of intravenous fluids. A total of 8 grams should be administered to ensure adequate stores. - Replacement of phosphorus can usually be achieved with oral supplementation. Extremely low levels of phosphorus may be treated with intravenous phosphorus salts at a dose of 1 mmole per kilogram of body weight, administered over 24 hours. Care should be taken to avoid hypocalcemia associated with the administration of phosphorus, and potassium replacement should be performed. - The ketoacidosis associated with acute alcohol intoxication is best treated with volume expansion and low-dose glucose administration after vitamin therapy. - The administration of glucose may increase the utilization of phosphorus, causing a reduction below initial levels. Therefore, close monitoring and replacement of phosphorus should be performed.
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Treatment of Cardiac Rhythm/Contractility

Support for inadequate cardiac contractility should be provided aggressively. Vitamin replacement may reverse some of the underlying pathology. Digitalization should be considered early if contractility is impaired. Aggressive hemodynamic monitoring and support with inotropes should be provided as needed. However, in most cases, there is an excess of catecholamines circulating due to increased sympathetic tone. - Tachyarrythmias are most commonly due to sympathetic stimulation; treatment is with beta-blockers (propranolol) or false neurotransmitters (clonidine).
Treatment of Abstinence Syndrome

- Treatment of abstinence syndrome is not standardized. - Mild symptoms are effectively treated with mild sedation using benzodiazepam or chlorpromazine. - More severe symptoms require higher doses and combination therapy, including haloperidol, benzodiazepam, with or without clonidine. Therapy using these agents must be titrated to effect, occasionally requiring dosages sufficient to require ventilatory support. - Alternatively, the use of an alcohol infusion will reverse the neurologic and hemodynamic effects of the withdrawal syndrome. A 10% solution of ETOH should be titrated to achieve a trace level of alcohol in the blood.
Treatment of Neurologic Problems

- Thiamin, B vitamins, electrolyte replacement with magnesium, phosphorus and potassium, and sedation are the major therapies for the neurologic complications.
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- Alcohol withdrawal seizures occur as the alcohol level is decreasing in a given patient. Treatment for these seizures is symptomatic, with benzodiazepam or barbiturates. - Long-term therapy of alcohol withdrawal seizures is not indicated.
Cocaine
Cocaine is one of the most commonly abused substances in trauma victims. In a recent review, evidence of cocaine use was found in 26.7% of all New York City residents sustaining fatal injuries. One-third of deaths after cocaine use were the direct result of the drugs effects, but two-thirds of the deaths resulted from traumatic injuries from homicides, suicides, traffic accidents and falls. Neurologic Effects
- Dopaminergic and neuroadrenergic pathways in the central nervous system probably mediate the effects of cocaine. - Euphoria is followed rapidly by despair. Repeated doses often lead to return of the euphoric state and are at the core of the binge-type abuse pattern. Ultimately, the increased use of cocaine may lead to a state of excited delirium associated with hyperthermia, agitation and often vascular collapse and death. - There is a high incidence of hemorrhagic and ischemic strokes, as well as ruptured aneurysms.
Cardiovascular Effects
- Initial effects are vagotonic, inducing a transient bradycardia. In some chronic abusers of cocaine, there is a persistent suppression of the tachycardic response to stress. In most cases, the vagolytic episode is rapidly replaced by a sympathetic stimulation induced by reduced reuptake of catecholamines. This is often complicated by severe hypertension, tachycardia and chest pain.
Respiratory Effects
- Respiratory arrest is an occasional complication of cocaine abuse. - The underlying pathology may be bronchiolitis obliterans with organizing pneumonia, interstitial pneumonitis, or pneumothorax with or without pneumomediastinum.
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Hematological Effects
- Disseminated intravascular coagulation occurs in severe cases of cocaine overdosage.
Abstinence Syndrome
- Although there is a high level of desire to continue cocaine use in an effort to regain the euphoria and avoid the depression associated with cessation of cocaine use, there is not a clear withdrawal syndrome as in opiates or alcohol abuse.
Treatment of Cocaine Use

Treatment of neurologic problems
- Agitation is the most common presenting problem. It is best treated with benzodiazepines. - Seizures are typically solitary and require only protective therapy. Status epilepticus should be treated with intravenous benzodiazepines followed with phenytoin.
672
Trauma Management
Table 67.1. General approach to acute drug and alcohol toxicity

1. 2. 3. 4. 5. 6. 7. When In Protect Airway Ventilatory Support Support Circulation with Volume Control Hypotension with Dopamine Control Agitation with Benzodiazepines Control Hypertension with Calcium Channel Blockers Encourage Urine Flow with Mannitol and Bicarb Doubt Try Naloxone
There are many agents recommended to reduce the desire for cocaine use and the emotional and psychological effects of chronic cocaine use. In particular, antidepressants and dopamimetic agents may reduce the dysphoria and depression associated with discontinuing cocaine use. Treatment of Cardiovascular Function
- There are several unique features of treating the hypertensive, arrhythmic and ischemic cardiac complications associated with cocaine. - Beta-blockers, although they may be effective, should be avoided because of the possibility of rebound hypertension due to unopposed alpha effect. - Nitrates, either sublingual or intravenous, are effective in lowering the blood pressure, reducing cardiac ischemia and limiting the size of infarctions. - If nitrates fail, phentolamine or calcium channel blockers are preferred, especially if chest pain is persistent. - Aspirin and thrombolytics may be used for coronary occlusion; however, the risk of intra-cranial bleed must be excluded prior to such therapy. - Arrythmias are best controlled with calcium channel blockers.
67
Treatment of Hyperthermia
- Acute cocaine intoxication may induce hyperthermic crisis. Treatment should be initiated immediately with surface-cooling measures. - Calcium channel blockers are also effective in the treatment of cocaine-induced hyperthermia.
Opiates
The opiates include a large number of substances, some of which are used for clinical purposes, and some of which are purely illicit. Specific agents include opium, morphine, codeine, fentanyl, heroin (also known as smack, scag, junk and other names) and methadone. There are many combinations and various other preparations available legally and illegally. The physiologic damage associated with opiates, unlike alcohol, is limited, with relatively few systemic complications. However, there are severe physiologic consequences to the cessation of opiate use once tolerance and addiction have been established. Acute opiate intoxication is the most life-threatening complication with this category of drugs. Direct depression of respiratory centers may lead to cardiopulmonary arrest. The specific antidote for opiate intoxication is naloxone. Naloxone treatment must be titrated to ensure three effects:
- Dosage Most patients will respond to .8-1.2 mg; however, larger or repeated doses may be required.
673
- Duration Some of the opiate preparations may have a protracted half-life, and a single injection of naloxone may not provide reversal of adequate duration. Typically, naloxone will have a duration of action of 1-2 hours while many of the opiate preparations may have a duration of action of 3-6 hours. In these cases, a continuous intravenous infusion may be required. - Withdrawal Acute withdrawal symptoms may be precipitated by the use of naloxone. Care must be taken to provide adequate symptomatic therapy for withdrawal syndrome.
The physiologic damage associated with opiates, unlike alcohol, is limited, with relatively few chronic systemic complications. The most significant medical issues in chronic opiate abuse are secondary complications including:
Malnutrition Infections and sexually transmitted diseases (hepatitis B and C, AIDS) Bacterial endocarditis, skin and soft tissue infections, tuberculosis Complications of injection and impurities (thrombophlebitis, pulmonary fibrosis, talcosis, pulmonary vascular abnormalities, bullous disease, especially of the upper lung fields)
There are severe physiological consequences to the cessation of opiate use once tolerance and addiction have been established.
- The abrupt discontinuation of opiates precipitates a withdrawal syndrome, which is typically no more severe than a serious bout of influenza. - The symptoms of nausea, vomiting and anxiety can be treated with combinations of benzodiazepam and clonidine. - In severe cases or in the presence of unstable medical conditions, methadone may be used to replace the opiate, with a reduced euphoria component.
67
References
1. 2. 3. 4. 5. OConnor PG, Samet JH, Stein MD. Management of hospitalized intravenous drug users: Role of the internist. Am J Med 1994; 96(6):551-558. Spies CD, Dubisz N, Neumann T et al. Therapy of alcohol withdrawal syndrome in intensive care unit patients following trauma: Results of a prospective, randomized trial. Crit Care Med 1996; 24(3):414-422. Spies CD, Rommelspacher H. Alcohol withdrawal in the surgical patient: Prevention and treatment. Anesthesia & Analgesia 1999; 88(4):946-954. Cornwell EE III, Belzberg H, Velmahos G et al. The prevalence and effect of alcohol and drug abuse on cohort-matched critically injured patients. Am Surgeon 1998; 64:461-465. Li G, Keyl P, Smith GS et al. Alcohol and injury severity: Reappraisal of the continuing controversy. J Trauma 1997; 42(3):562-569.
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Trauma Management
INDEX A
Abdominal compartment 310, 362, 363, 368, 369, 374, 376-379 Abdominal compartment syndrome (ACS) 310, 362, 363, 368, 369, 374, 376-379, 579, 662 Abdominal trauma 30, 38, 209 Acidemia 71, 372, 373, 378 Adrenal insufficiency 567, 570-573, 575 Advanced Trauma Life Support (ATLS) 16, 28, 70, 82, 201, 225, 231, 273, 283, 357, 417, 483, 484, 491, 493, 546, 550, 656 Alcohol 22, 51, 76, 125, 210, 321, 389, 426, 506, 510, 554, 567, 594, 666, 668, 669, 670, 671, 672, 673 Alcohol abuse 669, 671 Ankle injury 51, 127, 141, 415, 421, 423 Anticonvulsants 88, 568 Aorta 27, 70, 192, 197, 199, 205, 221-227, 229-233, 235, 258, 260, 262, 263, 265, 268, 271, 274, 275, 277, 310, 358-362, 380, 385, 394, 399, 485, 502, 519, 548 Audit filters 659
C
Caliber 84, 266, 269, 311, 417, 533, 536, 537, 539, 541-543 Carotid artery 128, 135-140, 199, 222, 230, 233, 253, 512, 514 Catheterization 73, 123, 290, 344, 476, 505, 584, 629 Celiac axis 358-360 Chest trauma 7, 194, 199, 200, 210-212, 217, 220, 238, 254, 265, 485, 494 Chest tube 18, 27, 192, 195, 196, 198, 199, 213, 217, 218, 220, 250, 269, 270, 290, 485, 497, 530, 550 Chest wall injury 212 Child abuse 489-491, 554 Cirrhosis 669 Clavicle 21, 127, 135, 141, 143, 144, 148-150, 172, 173, 177-182, 190, 232, 258 Clindamycin 57 Coagulopathy 22, 64, 75, 310, 370, 373, 378, 379, 417, 453, 503, 505, 520, 523, 579, 602, 607, 631, 632, 642, 653 Colon injury 340, 347 Colostomy 340, 345, 347 Compartment syndrome 24, 310, 362, 363, 368, 369, 374, 376-379, 405-410, 412, 414, 416, 418, 425, 441, 442, 579, 619, 659 Consciousness 5, 21, 25, 54, 85-90, 96, 122, 123, 193, 284, 575, 594, 607, 665 Cost of injury 661, 662 Cytomegalovirus (CMV) 636
Index
B
Basilar skull fracture 22, 93, 97-99 Bile duct trauma 391 Bladder injury 380, 382, 400 Bladder pressures 366, 368, 375 Bladder trauma 400, 401 Blast effect 350, 351 Blast injuries 544-546, 551 Blast lung injury 546, 550, 552 Brachial plexus injury 171, 178, 179, 183, 184 Brain death 87, 88, 602, 603, 606
D
Damage control operations 364, 370, 373 Deep vein thrombosis (DVT) 323, 418, 477, 519, 646, 647, 651-654, 659
Index Diabetes insipidus 575, 576, 602, 604 Diabetes mellitus 563-566 Diagnostic peritoneal lavage (DPL) 26, 27, 29, 240, 241, 284, 286, 287, 290-292, 296, 297, 316, 330, 337, 342, 347, 381, 382, 547, 551 Diaphragm injury 244 Disseminated intravascular coordination (DIC) 602, 604, 642, 644 Duodenal injury 330, 333-335, 337, 338, 392
675
H
Hematuria 284, 293, 299, 348, 349, 351, 354, 395, 452, 485, 486, 620 Hemothorax 21, 25, 69, 74, 127, 141, 191, 195, 196, 199, 212, 213, 214, 217-220, 229, 234, 246, 250, 254, 380, 485, 529, 546 Heparin 138, 226, 417, 519, 597, 600, 601, 652-654, 666 Hepatic artery 294, 303, 309, 310, 359, 391 Hepatic trauma 388 Hepatitis 389 Hypercalcemia 573-575 Hyphema 98 Hypocalcemia 620, 621, 632, 633, 670 Hypokalemia 567, 575, 604 Hypomagnesemia 669 Hypotension 19, 43-47, 49, 51, 58-62, 69, 70, 76-78, 80-82, 88, 135, 141, 152, 196, 200, 212, 286, 290, 305, 316, 357, 363, 364, 366, 368, 371, 378, 395, 398, 409, 410, 413, 416, 440, 462, 467, 475, 482, 483, 485, 493, 497, 504, 528, 545, 570, 573, 579, 597, 602, 604, 607, 632, 643, 644, 669, 673 Hypothermia 22, 75, 310, 312, 364, 365, 373, 417, 453, 494, 497, 566, 571, 579, 604, 607-609, 629, 631-633, 635 Hypovolemia 11, 72, 81, 89, 200, 226, 304, 312, 362, 366, 371, 385, 398, 399, 464, 494, 588, 597, 600, 607, 631, 640, 670
E
Elbow dislocation 51 Empyema 191, 192, 198, 199, 217, 220, 253, 529, 659 Endotracheal intubation 5, 6, 13, 18, 41, 52, 65, 68, 73, 78, 131, 160, 169, 212, 231, 273, 467, 494-496, 572, 596, 600 Enteral nutrition 582-584 Epidural hematoma 85, 87, 93 Esophageal injury 249-251, 253, 265 Explosions 425, 544, 545, 550, 551 Extremity fracture 378
F
Fasciotomy 408-412, 416, 418, 424, 425, 441, 442, 619 Fat embolism 663-665, 667 Femur fracture 8, 446, 509 Flail chest 19, 22, 51, 187, 188, 189, 190, 194, 212, 223, 493 Foreign bodies 17, 128, 343, 346, 347, 379, 414, 419, 421, 430, 624
G
Gallbladder trauma 389, 391 Gelfoam 23, 506, 508, 511 Glasgow Coma Score (GCS) 6, 8, 9, 18, 21, 26, 87-90, 122, 127, 480, 483-494, 610, 617, 659 Growth hormone 40, 575
I
Iliac vessels 342 Intercostal nerve block 51, 187 Intraabdominal pressure 312, 363, 364 Intracranial hematoma 87, 291 Intracranial hypertension 90, 483
Index
676 Intracranial pressure (ICP) 8, 40, 41, 43, 46-48, 52, 54-63, 86, 88-90, 92, 126, 363, 483, 528, 659 Intracranial pressure monitoring 89
Trauma Management
O
Organ donation 604 Osteoporosis 492 Oxygen saturation 71, 73, 76, 81, 213, 226, 480, 496, 595, 603
L
Laparoscopy 239, 242, 244, 245, 246, 247, 248, 261, 284, 290, 299, 300, 301, 527-531 Laparotomy 27, 29, 31, 36, 201, 238, 239, 242, 244-247, 261, 286-288, 290-292, 299-302, 310, 317, 343, 344, 346, 350, 356, 358, 366-368, 370, 373, 374, 376, 379, 381, 385 Le Fort fractures 100 Liver injury 288, 305, 306, 313, 388, 389, 391, 630 Loop closure 659 Lung injury 188, 191, 197, 212, 214, 217, 219, 220, 254, 546, 550, 552, 633, 644
Index
Pancreatitis 323, 332, 338, 563, 566, 567 Pelvic fracture 8, 12, 23, 24, 27, 222, 291, 306, 343, 345, 351-353, 376, 400, 451-453, 457, 485, 498, 508, 510, 511, 519 Pelvic injury 342 Performance improvement 655, 656, 659, 660-662 Pericardial tamponade 20, 69, 72, 73, 81, 218, 271, 272 Pericardial window 529 Peroneal compartment 442 Peroneal nerve 406 M Pneumothorax 7, 19, 20, 22, 27, 40, 52, 72-74, 80, 127, 128, 177, 186, Mandibular fracture 100, 109 191, 195-197, 212, 213, 215, 217, Median nerve 51, 176 218, 220, 250, 254, 256, 257, 260, Mesenteric injury 380, 394 287, 380, 394, 485, 519, 528-530, Mesenteric vessels 326, 331, 359 550, 582, 584, 671 Mesh closure 376, 377 Popliteal artery 409, 420, 423, 444, Methylprednisolone 468, 606, 643 501 Mortality review 657 Portal vein 310, 311, 356, 359, 362, Multiple organ dysfunction syndrome 364, 388, 391 374, 577, 579 Pregnancy 25, 29, 286, 291, 468, Myoglobinuria 49, 73, 407, 442, 619 496-498, 500, 503, 636 Presacral drainage 340, 345, 347 N Pringle maneuver 309, 310 Pulmonary artery pressure 75, 78 Nerve block 51, 187 Pulmonary contusion 19, 25, 191, Nerve grafting 171, 179, 180 194, 212-214, 217, 218, 220, 254, Nerve injury 21, 130, 160, 171, 172, 257, 316, 485, 666 174, 177, 180, 227, 413, 426, 429, Pulmonary embolism 418, 515, 516, 545 519, 646, 648, 651, 659 Nerve repair 179, 180, 182 Pulmonary injury 173, 182, 191, 193, Nerve transfer 179, 180, 183, 184 199, 220, 226, 580 Neurogenic shock 20, 27, 76, 462, 464, 473, 475 Q Nutrition 111, 312, 566, 567, 574, 575, 581, 582-584 Quality improvement 613, 662
Index
677 Splenic trauma 292, 318, 385 Splinting 13, 51, 107, 112, 182, 430, 431 Sternal fracture 190, 258, 260 Stress ulceration 589 Subarachnoid hemorrhage 72, 90, 92 Subdural hematoma 84, 91 Systemic inflammatory response syndrome (SIRS) 582
R
Rectal injury 23, 340, 341, 343, 344, 345, 346, 347 Renal trauma 288, 395, 397 Resuscitation 3, 4, 5, 8, 11, 13, 14, 17, 20, 25, 28, 41, 51, 62, 66, 69, 72-76, 80, 82, 158, 195, 205, 210, 218, 220, 224, 226, 230-233, 236, 271, 273, 276, 288, 292, 311, 317, 320, 342, 344, 356, 365, 371, 385, 388, 394, 417, 425, 438, 453, 480, 482, 483, 491, 493, 498, 500, 563, 578, 580, 588, 589, 592, 596, 597, 604, 610, 621, 622, 629-631, 634, 635, 668 Retina 96 Retrograde urethrogram 295, 353, 400, 452 Retroperitoneal hematoma 287, 330, 342, 350, 357, 382, 453, 511, 519 Rhabdomyolysis 40, 73, 575, 584, 592, 619, 621, 669 Rib fracture (s) 174, 186, 257, 269, 485, 494
T
Tachycardia 2, 11, 19, 20, 40, 55, 57, 59, 60, 69, 74, 76, 78, 80-82, 89, 196, 200, 212, 305, 316, 363, 364, 398, 477, 497, 505, 528, 568, 569, 597, 604, 647, 665, 669, 671 Tension pneumothorax 7, 19, 20, 22, 72, 74, 80, 195, 196, 212, 213, 215, 220, 256, 528-530, 550 Terrorist acts 544 Tetanus 102, 417, 426, 498, 499 Thoracostomy 7, 14, 19, 20, 25, 141, 195, 198, 206, 212, 213, 217, 220, 240, 244, 246, 483, 528, 530 Thoracotomy 27, 143, 191, 192, 196-199, 204-207, 210, 212, 214, 217-220, 226, 231, 232, 234, 235, 238, 246, 250, 251, 271-276, 278, 279, 356, 358, 438, 530 Thrombocytopenia 82, 519, 572, 620, 632, 652, 663, 665, 666 Thyroid emergencies 570 Total parenteral nutrition (TPN) 580, 582, 584 Traction injuries 172 Traction injury 234 Transfusion 75, 77, 78, 312, 320, 322, 323, 373, 378, 453, 498, 505, 578, 604, 631, 632, 633, 636-641, 643-645 Trauma nurse coordinator 655, 662 Trauma program manager 655 Tube thoracostomy 19, 20, 195, 198, 212, 217, 220
S
Saphenous vein cutdown 19 Scoop and run 201, 550 Sepsis 16, 56, 69, 71, 77, 92, 227, 241, 247, 312, 314, 332, 338, 343, 345, 347, 468, 525, 567, 582, 584, 623 Shock 4, 7, 8, 9, 11-13, 18-20, 24, 26, 27, 39, 58, 69-73, 75-82, 92, 127, 195, 196, 200, 209, 212, 218, 239, 315-317, 341, 342, 345, 357, 363, 370-372, 374, 378, 380, 385, 394, 395, 398, 399, 414, 425, 462, 464, 473, 475, 480, 482, 497, 544, 545, 550, 567, 570, 573, 575, 578, 602, 609, 618-622, 629-634, 644 Skull fracture 22, 85, 93, 97, 98, 99, 485, 489, 546, 575 Small bowel injury 284 Spinal cord injury 20, 21, 23, 40, 69, 76, 458, 461, 463, 464, 467, 469, 475, 476, 478, 483, 519, 574, 619, 651, 659
Index
678
Trauma Management Vein injury 424 Vena cava filters 515, 516, 526 Vena cava injury 309 Ventilation 4, 5, 7, 9, 11, 13, 18, 19, 23, 41, 52, 54, 55, 62-65, 70, 77, 78, 79, 191, 205, 272, 363, 375, 376, 395 Vertebral artery 92, 128, 152, 154-156
U
Ureteral injury 526 Urethral injury 353, 400, 402, 452
V
Vaccination status 417 Vascular injury 22, 24, 73, 74, 101, 133, 135, 141, 143, 152, 173, 177, 179, 182, 183, 199, 230, 254, 273, 321, 356, 357, 398, 405, 413-415, 418, 421, 422, 424, 425, 440, 442, 443, 474, 511, 512, 546
Index

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v a d e m e c u m

Demetrios Demetriades, M.D., Ph.D., F.A.C.S.

Juan A. Asensio, M.D., F.A.C.S.

GEORGETOWN, TEXAS U.S.A.

Emergency Room Care

3. Ultrasound in Trauma ................................................................ 29

4. Analgesia and Sedation in Trauma .............................................. 39

5. Emergency Airway Management in the Trauma Patient ............. 54

6. Shock and Resuscitation ............................................................. 69

8. Maxillofacial Trauma .................................................................. 94

10. Penetrating Injuries of the Neck ............................................... 127

11. Carotid Artery Injuries ............................................................. 135

12. Subclavian and Axillary Vascular Injuries .................................. 141

13. Vertebral Artery Injuries .......................................................... 152

14. Laryngotracheal Injuries ........................................................... 157

15. Traumatic Brachial Plexus Injuries ............................................ 171

17. Penetrating Chest Injuries: Evaluation and Management .......... 195

18. Cardiac Injuries ........................................................................ 200

19. Lung Injuries ............................................................................ 212

20. Blunt Aortic Trauma ................................................................ 221

21. Penetrating Thoracic Vascular Injuries ...................................... 229

22. Diaphragm Injuries .................................................................. 237

23. Esophageal Injury ..................................................................... 249

24. CT Scan in Chest Trauma ........................................................ 254

25. Emergency Department Thoracotomy ..................................... 271

27. Evaluation of Penetrating Abdominal Trauma .......................... 293

28. Hepatic Injuries and Bile Duct Injuries .................................... 303

29. Splenic Injuries ......................................................................... 314

30. Pancreatic Injuries .................................................................... 326

31. Duodenal Injuries ..................................................................... 333

32. Colon/Rectal Injuries ................................................................ 340

33. Genitourinary Tract Trauma ..................................................... 348

34. Abdominal Vascular Injury ....................................................... 356

35. Abdominal Compartment Syndrome ........................................ 363

36. Damage Control Operations .................................................... 370

37. CT Scan in Abdominal Trauma ................................................ 380

39. Penetrating Extremity Injury .................................................... 413

40. Popliteal Vessel Injuries ............................................................. 420

41. Hand Trauma ........................................................................... 426

43. Pelvic Fractures and the General Surgeon ................................. 450

44. Spinal Injuries .......................................................................... 458

46. Geriatric Trauma ...................................................................... 492

47. Trauma in Pregnancy ................................................................ 496

49. Minimally Invasive Surgery in Trauma ..................................... 527

50. Ballistics of Gunshot Injuries .................................................... 532

51. Blast Injuries ............................................................................. 544

52. Forensics for Trauma Care Givers ............................................. 553

53. Endocrine Problems in Trauma ................................................. 563

54. MOF Failure: MOF Syndrome ................................................. 577

55. Surgical Nutrition ..................................................................... 581

56. Acute Burn Injury ..................................................................... 585

57. Inhalation Injury ...................................................................... 594

58. Management of the Potential Organ Donor Patient ....................................... 602

59. Hypothermia in Trauma Patients ............................................. 607

60. Trauma Scores .......................................................................... 610

61. Crush Syndrome ....................................................................... 618

62. Anesthesia of the Traumatized Patient ...................................... 623

63. Transfusion Therapy ................................................................. 636

64. Venous Thromboembolism After Injury ................................... 646

65. Trauma Program Manager ........................................................ 655

66. Fat Embolism ........................................................................... 663

67. Alcohol, Illicit Drugs and Trauma ............................................ 668

Index ........................................................................................ 674