Management of shock in adult trauma

HUAuthorUH
HUChristopher Colwell, MD UH
HUSection EditorUH
HUJohn A Marx, MD UH
HUDeputy EditorUH
HUJonathan Grayzel, MD, FAAEM
UH

Last literature review version 17.3: September 2009 | This topic last updated: September
16, 2009 HU(More)UH
INTRODUCTION Shock refers to inadequate tissue perfusion, which manifests clinically as
hemodynamic disturbances and organ dysfunction. At the cellular level, shock results from
insufficient delivery of required metabolic substrates, principally HUoxygenUH, to sustain aerobic
metabolism.
In the setting of trauma, loss of circulating blood volume from hemorrhage is the most common
cause of shock. Inadequate oxygenation, mechanical vascular obstruction, neurologic
dysfunction, and cardiac dysfunction represent other potential causes or contributing factors [
HU1UH] . Shock is a common and frequently treatable cause of death in injured patients and is
second only to traumatic brain injury as the leading cause of death from trauma [ HU2,3UH] .
This topic review will discuss the evaluation and initial management of shock in the trauma
patient. A general overview of shock, including pathophysiology and differential diagnosis, and
discussions of the management of shock in other clinical circumstances are presented
elsewhere. ( HUSee "Shock in adults: Types, presentation, and diagnostic approach"UH and HUsee
"Pathogenesis of irreversible shock"UH and HUsee "Management of severe sepsis and septic shock
in adults"UH and HUsee "Treatment and prognosis of cardiogenic shock complicating acute
myocardial infarction"UH).
PATHOPHYSIOLOGY AND CLASSIFICATION The pathophysiology of shock primarily
relates to an imbalance in HUoxygenUH supply and demand. Patients in shock suffer from a critical
reduction in the oxygen available to the mitochondria. Adenosine triphosphate (ATP) can still be
synthesized by anaerobic glycolysis, but at only 5 to 10 percent of the normal rate [ HU4UH] .
Anaerobic glycolysis results in the accumulation of pyruvate, which is converted to lactate [ HU5UH] .
( HUSee "Shock in adults: Types, presentation, and diagnostic approach"UH and HUsee "Pathogenesis
of irreversible shock"UH).
The compensatory physiologic responses to acute hemorrhage attempt to maintain adequate
HUoxygenUH delivery to tissues. Stimulation of the sympathetic nervous system results in an
increased heart rate, vasoconstriction, and increased ventricular contractility. As the shock state
progresses, vital organ (eg, brain and heart) perfusion can only be maintained at the expense of
nonvital organs. If the process is not reversed, progressive lactate production leads to
worsening systemic metabolic acidosis, which along with hypoxia ultimately causes the loss of
peripheral vasoconstriction and cardiovascular collapse.
The Advanced Trauma Life Support (ATLS) manual describes four classes of hemorrhage to
emphasize the early signs of the shock state [ HU3UH] . Clinicians should note that significant drops
in blood pressure are generally not manifested until class III hemorrhage develops, and up to 3
percent of a patient's blood volume can be lost before this occurs:
0
Class I hemorrhage involves a blood volume loss of up to 15 percent. The heart rate is
minimally elevated or normal, and there is no change in blood pressure, pulse pressure,
or respiratory rate.
Class II hemorrhage occurs when there is a 15 to 30 percent blood volume loss and is
manifested clinically as tachycardia (heart rate of 100 to 120), tachypnea (respiratory
rate of 20 to 24), and a decreased pulse pressure, although systolic blood pressure
changes minimally if at all. The skin may be cool and clammy, and capillary refill may be
delayed.
Class III hemorrhage involves a 30 to 40 percent blood volume loss, resulting in a
significant drop in blood pressure and changes in mental status. Any hypotension
(systolic blood pressure less than 90 mmHg) or drop in blood pressure greater than 20
to 30 percent of the measurement at presentation is cause for concern. While
diminished anxiety or pain may contribute to such a drop, the clinician must assume it is
due to hemorrhage until proven otherwise. Heart rate ( 120 and thready) and
respiratory rate are markedly elevated, while urine output is diminished. Capillary refill is
delayed.
Class IV hemorrhage involves more than 40 percent blood volume loss leading to
significant depression in blood pressure and mental status. Most patients in class IV
shock are hypotensive (systolic blood pressure less than 90 mmHg). Pulse pressure is
narrowed and tachycardia is marked (>120). Urine output is minimal or absent. The skin
is cold and pale, and capillary refill is delayed.
DIFFERENTIAL DIAGNOSIS Hemorrhage is the most common cause of shock in the trauma
patient. Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from
major external wounds. The thigh can hold up to approximately one liter of blood. Scalp
lacerations can bleed profusely and are often overlooked if significant thoracic or abdominal
injuries are present.
A number of other potential causes of traumatic shock must also be considered, including (
HUshow table 1UH):
Cardiac tamponade
Tension pneumothorax
Pulmonary contusion or hemothorax with resulting dysfunction
Myocardial infarction or contusion (ie, cardiogenic shock)
Spinal cord injury (ie, neurogenic shock)
Effects of pharmacologic or toxicologic agents
Fat or air embolism
In penetrating trauma, diaphragmatic rupture complicated by incarceration of abdominal organs
can lead to septic shock.
PREHOSPITAL MANAGEMENT The prehospital management of patients in traumatic shock
is focused on recognition, rapid transport, and stabilization of the airway, breathing, and
circulation. Prehospital clinicians must be diligent about looking for signs of hypoperfusion,
ideally recognizing traumatic shock before hypotension develops, and providing appropriate
management according to their level of skill. Delayed fluid resuscitation for penetrating trauma
remains controversial. ( HUSee "Prehospital care of the adult trauma patient"UH and HUsee "Delayed
fluid resuscitation/controlled hypotension" belowUH).
EVALUATION AND MANAGEMENT
Recognition Recognition is the first step in managing traumatic shock. Ideally, shock is
recognized before hypotension develops [ HU6UH] . The clinical presentation of traumatic shock
depends on the rate, volume, and duration of bleeding, the patient's baseline physiology, and
the presence of other acute pathologic processes (eg, tension pneumothorax, myocardial
ischemia).
Obvious and immediately detectable manifestations of the shock state include:
Tachycardia
Hypotension
Cool extremities
Weak peripheral pulses
Prolonged capillary refill (>2 seconds)
Narrowing of the pulse pressure (<25 mmHg)
Altered mental status
Large-scale bleeding occurs at five possible locations:
External hemorrhage
Thoracic cavity
Peritoneal cavity
Retroperitoneal space (often from a pelvic fracture)
Muscle or subcutaneous tissue (usually from a long-bone fracture).
When the cause of shock is not obvious, evaluation and treatment occur in tandem. A trauma
ultrasound examination, or Focused Assessment with Sonography for Trauma (FAST), is
performed to look for hemopericardium and intraabdominal bleeding. The three standard initial
trauma x-rays (ie, chest, pelvis, and lateral cervical spine) are obtained. Of these, the portable
chest x-ray is most likely to reveal an injury requiring immediate intervention. Remember that
the presence of one injury in no way excludes the possibility of other, more serious injuries. In
some centers, clinicians may forego plain x-rays if CT scanners are immediately available and
adjacent to the trauma bay.
Shock may exist even in the setting of "normal" vital signs, making diagnosis difficult. Young
patients without underlying comorbidities can maintain a blood pressure within the normal range
despite substantial blood loss by compensatory vasoconstriction and increases in heart rate. A
bradycardic response to penetrating intraperitoneal injury, which may be vagally mediated, has
been described [ HU7UH] . Recognizing shock in its early stages is more difficult, but provides
clinicians the opportunity for early reversal of end-organ hypoperfusion. Serial examinations and
serial ultrasound studies can help to identify occult injuries [ HU8UH] .
Alterations in mental status caused by hypoperfusion may be subtle initially and can be difficult
to distinguish from drug or alcohol intoxication or associated head injury. Altered mental status
on presentation or a subsequent decline in mental status, particularly in patients without obvious
evidence of head injury, should raise suspicion for cerebral hypoperfusion. In young, otherwise
healthy patients, subtle alterations such as agitation, confusion, irritability, indifference to
surroundings, or inattention to instructions may be the only sign of early shock. A patient who is
aggravating you or your staff may be showing early signs of shock, not intoxication.
Subtle examination findings may provide evidence of early shock. Pallor or poor capillary refill
may represent peripheral vasoconstriction. Diaphoresis may indicate physiologic stress and
appear before vital sign abnormalities. Mild tachypnea may reflect compensation for metabolic
acidosis. Low urine output may indicate inadequate visceral perfusion. Patients who are unable
to maintain a urine output greater than 0.5 mL/kg/hour and have a high urine specific gravity
may be compensating for hypovolemia.
Elderly patients are more likely to take medications (eg, beta blockers) that affect the
hemodynamic response to injury, and are more likely to have baseline hypertension. It is
important to interpret vital signs with the patient's baseline in mind. The emergency clinician
may need to predict this physiologic baseline based on age and other available information (eg,
medication list). As an example, a systolic blood pressure of 110 mmHg may be dangerously
low in a patient with underlying hypertension.
Nonhemorrhagic causes of traumatic shock may demonstrate typical presentations, but often do
not. As an example, pericardial tamponade is classically described as exhibiting Beck's triad of
hypotension, distended neck veins, and muffled heart sounds, but these are late findings when
present. If significant, on-going hemorrhage exists, tamponade can occur without distended
neck veins. Ultrasound examination is critical. ( HUSee "Management of nonhemorrhagic shock"
belowUH).
A large pneumothorax or hemothorax may be detected clinically by the appearance of
respiratory distress, unilateral diminished breath sounds, or air crepitus on palpation. In the
stable patient with suspected pneumothorax, confirmation by chest radiograph is prudent; in the
unstable patient, immediate treatment with needle decompression or rapid chest tube
placement is necessary, and must not be delayed for radiography. The classic description of a
tension pneumothorax includes ipsilateral absent breath sounds, deviation of the trachea away
from the affected side, and hypotension, from inadequate preload due to compression of the
inferior vena cava. Tracheal deviation and hypotension occur late. Animal studies suggest
hypoxemia may be an earlier sign of tension pneumothorax than hypotension [ HU9UH] .
Neurogenic shock may develop in the patient with a high spinal cord injury. Neurologic deficits
may not be apparent in the unresponsive patient, but are usually obvious otherwise.
Hypotension, which may be mild in these patients, results from the loss of peripheral vascular
resistance. Tachycardia is absent because of the loss of sympathetic tone. Hypotension
associated with neurologic deficits and the absence of peripheral vasoconstriction (these
patients often have warm extremities and good urine output) raises suspicion for neurogenic
shock. Volume status must be closely monitored because excess fluid administration may be
detrimental. Hypotension should not be attributed solely to neurologic injury until hemorrhagic
shock has been ruled out. ( HUSee "Acute traumatic spinal cord injury"UH).
Initial management Management of the patient in traumatic shock is focused on:
Restoring intravascular volume
Maintaining adequate HUoxygenUH delivery
Limiting on-going blood loss
Assessment and treatment are performed simultaneously in the seriously injured patient ( HUshow
algorithm 1UH). The emergency clinician evaluates the airway and hemodynamic status and looks
for hemorrhage while performing the following immediate interventions listed in order of priority:
Establishing a patent and protected airway while protecting the cervical spine
Maximizing oxygenation
Gaining intravenous access and initiating fluid resuscitation
Controlling hemorrhage
Obtaining blood for laboratory and blood bank testing
External hemorrhage is controlled by applying direct pressure. While clamping bleeding vessels
under direct visualization is acceptable when necessary, blind clamping should NOT be
performed.
Scalp lacerations can bleed profusely and are often overlooked if significant thoracic or
abdominal injuries are present. Scalp lacerations can be treated with clips (eg, Raney clips) or
by closing the wound with running (ie, noninterrupted) stitches using heavy suture.
Use of a tourniquet is acceptable to stop hemorrhage in cases of amputation when other
measures have not successfully controlled bleeding. Tourniquets must be released periodically
to avoid prolonged ischemia and possible tissue loss.
Vascular access is obtained as rapidly as possible. Two large-bore (16 gauge or larger)
intravenous (IV) lines placed in the antecubital region is ideal, but not always possible.
Placement of a central venous catheter (size 8 French) is performed when adequate peripheral
access cannot be obtained, and allows measurement of central venous pressure. Central line
placement under ultrasound (US) guidance offers high success rates with fewer complications
than procedures performed without US [ HU10,11UH] . Some experts advocate use of distal
saphenous vein cutdowns due to ease of access and consistency of anatomy [ HU12UH] .
Traumatic shock occurs most often from hemorrhage, generally from an intraabdominal injury in
blunt trauma. Ultrasound (US) is an integral part of the initial evaluation of the trauma patient,
and reliably identifies free intraabdominal fluid in the hands of proficient ultrasonographers [ HU13UH]
. During the initial resuscitation, the Focused Assessment with Sonography for Trauma (FAST)
exam, is performed to assess first for pericardial effusion and then for intraperitoneal bleeding.
Ultrasound has largely replaced diagnostic peritoneal lavage (DPL) in the initial assessment of
the trauma patient, although DPL retains an important role in specific circumstances. If
ultrasound is unavailable or its findings are equivocal or inconsistent with the clinical picture,
DPL or diagnostic peritoneal tap (DPT) provides crucial information. ( HUSee "General approach to
blunt abdominal trauma in adults"UH, section on Diagnostic peritoneal lavage).
Unstable pelvic fractures and associated vascular injuries can cause hemorrhagic shock.
Preliminary stabilization of the pelvis by applying a circumferential pelvic binder or tying a sheet
firmly around the pelvis can reduce bleeding. Such interventions are most important with "open-
book" pelvic fractures (in which the symphysis pubis is disrupted, the pelvis opened, and the
retroperitoneal space enlarged) ( HUshow radiograph 1UH). ( HUSee "Adult pelvic trauma"UH).
Intravenous fluid resuscitation Fluid resuscitation in trauma, including the optimal type and
volume, is the subject of considerable debate. We suggest that initial fluid resuscitation for
trauma patients in hemorrhagic shock consist of two liters of isotonic saline (ie, normal saline,
abbreviated as NS) given as rapidly as possible through short, large gauge (16 or larger)
peripheral IVs. Central venous catheters are used when peripheral IVs are not available.
Infusions of large volumes of NS can lead to the development of a nonanion gap
hyperchloremic metabolic acidosis. This does not appear to have significant clinical
consequences. On the other hand, large volume resuscitation using lactated ringers (LR) can
cause a metabolic alkalosis, as lactate metabolism generates bicarbonate. This too does not
appear to have significant clinical consequences. LR and blood must be infused through
separate IV tubing because of the risk of clotting, which may be problematic in the setting of
trauma.
Debate over the best approach to fluid resuscitation in traumatic shock is likely to continue.
Some researchers claim LR is superior to NS in the resuscitation of uncontrolled hemorrhagic
shock, stating that patients who receive large volumes of NS experience increased blood loss
and greater hypercoagulability; other researchers argue just the opposite [ HU14,15UH] . We prefer
NS for the initial resuscitation fluid, but feel it is reasonable to change to LR (L-isomer if
available) after the initial resuscitation (ie, once 3 liters or 50 mL/kg of NS has been infused) in
patients requiring additional IV fluid.
Clear end-points for fluid therapy remain undefined [ HU16UH] . Further resuscitation is based on the
patient's response to initial IV fluids and overall condition. A mean arterial pressure (MAP)
around 65 mmHg or a systolic blood pressure (SBP) around 90 mmHg is a reasonable goal in
penetrating trauma. In blunt trauma patients, particularly those with possible traumatic brain
injury (TBI), a mean arterial pressure above 105 mmHg or a systolic blood pressure above 120
mmHg is reasonable. These goals may need to be adjusted upward in patients with a known
history of uncontrolled hypertension.
The ideal MAP or SBP for the multiple trauma patient remains unclear. Some authors advocate
strictly limiting the amount of IV fluid used for trauma resuscitation in the absence of
hypotension or obvious injury [ HU17UH] . Packed red blood cells are given if the goal blood pressure
is not maintained following the initial IV fluid resuscitation. ( HUSee "Transfusion of red blood cells"
belowUH).
Hypertonic saline has been evaluated extensively, and may provide benefit through osmotic
movement of interstitial fluid into the vascular compartment and modulation of the inflammatory
response to injury [ HU18UH] . While some clinical trials have shown a benefit [ HU19UH] , others have
failed to do so, even in patients who would seem most likely to benefit (eg, patients with

hypotension and severe TBI) [ HU20,21UH] . Further study is needed to clarify the role of hypertonic
saline.
The value of colloids (albumin, HUhetastarchUH, HUdextranUH) for resuscitation of traumatic shock is
unproven. Colloids effectively increase intravascular volume and may maintain plasma oncotic
pressure at more normal levels compared to crystalloids. However, a systematic review of 19
randomized controlled trials comparing resuscitation fluids found that use of colloids did not
improve mortality or morbidity among trauma patients [ HU22-24

UH] . ( HUSee "Treatment of severe
hypovolemia or hypovolemic shock in adults"UH, section on Colloid versus crystalloid).
Research continues into oxygen-carrying resuscitation fluids that can serve as alternatives to
PRBCs. The ideal replacement fluid would transport HUoxygenUH effectively, expand intravascular
volume, exhibit few or no side effects, and demonstrate great durability. Potential replacement
fluids are discussed elsewhere. ( HUSee "Oxygen carriers as alternatives to red cell transfusion"UH).
No human studies exist to support the use of vasopressors in the resuscitation of the adult with
multiple trauma [ HU25UH] .
Delayed fluid resuscitation/controlled hypotension Questions remain whether reversal of
hypovolemia or control of hemorrhage should take priority in trauma resuscitation. Some
researchers describe aggressive fluid administration as ineffective and potentially harmful [
HU26,27UH] , and suggest that limited volume replacement that maintains minimally adequate organ
perfusion may improve outcomes [ HU28UH] . This strategy is often referred to as delayed fluid
resuscitation or controlled hypotension, an approach which targets early fluid resuscitation only
to a systolic blood pressure of 70 mmHg.
Controlled hypotension may be beneficial in patients with hemorrhagic shock due to torso
injuries from gunshot or stab wounds. They may be detrimental to blunt trauma patients with
brain injury, as hypotension reduces cerebral perfusion and increases mortality [ HU29UH] . The
proposed mechanism for improved outcomes with delayed fluid resuscitation is that aggressive
fluid administration might, via augmentation of blood pressure, dilution of clotting factors, and
production of hypothermia, disrupt thrombus formation and enhance bleeding [ HU30,31UH] .
In one widely cited study of 598 patients with penetrating chest injuries treated at a major urban
trauma center, delayed fluid resuscitation until operative intervention to control bleeding was
associated with a statistically significant improvement in patient survival (70 versus 62 percent
in those given immediate fluid repletion) [ HU32UH] . Other results favoring delayed fluid resuscitation
or controlled hypotension have been reported in small clinical trials and a variety of animal
models of hemorrhagic shock [ HU30,33-40UH] .
Adoption of the strategy of delayed fluid resuscitation or controlled hypotension into clinical
practice must be undertaken cautiously [ HU41UH] . In the trial described above, stratification was not
performed to identify which patients might benefit from delayed therapy [ HU32UH] . Furthermore,
primarily young, healthy patients with penetrating trauma were involved, and the mean time
from injury to operation was two hours, results that are not attainable in most circumstances.
We recommend that delayed fluid administration and controlled hypotension should NOT be
implemented unless emergent surgical exploration can be performed [ HU35UH] . Further research is
needed in this area [ HU41,42UH] .
Transfusion of red blood cells When to begin blood transfusion remains an important
unanswered question in trauma research, and often depends on clinical circumstances. As an
example, immediate transfusion of packed red blood cells (PRBC) is needed when
exsanguination is imminent, such as a patient with a thoracic injury whose chest tube placement
releases over two liters of blood. Another patient with a self-inflicted wrist laceration may not
require any blood, despite being hypotensive, because hemorrhage is promptly controlled, the
wound is easily repaired, and comorbidities are absent.
In general, we suggest two units of packed red blood cells (PRBC) be transfused if
hemodynamics fail to improve after the administration of 2 to 3 liters (or greater than 50 mL/kg)
of crystalloid. Further transfusions are given based on the patient's injuries and response to the
initial transfusion.
Typed and cross-matched PRBCs are best, but can require considerable time to prepare. If the
patient's condition warrants, clinicians can transfuse immediately using type O Rh-positive for
males and type O Rh-negative for girls and women of child-bearing age, until type-specific or
typed and cross-matched blood is available.
In most instances, preparation of fully typed and cross-matched blood requires at least 20
minutes, and more likely 30 to 45 minutes. Type-specific blood can usually be obtained within
15 to 20 minutes. In general, type O blood is available immediately, depending on transport time
from the blood bank to the emergency department (ED). Trauma centers often store type 0
blood in refrigerators in the ED.
The safety of the blood supply continues to improve, and although some risk of transmitting
infectious agents persists, such events are rare (the risk for bacteremia is approximately 1 in
100,000 units of platelets and 1 in 500,000 units of PRBCs transfused; the risk of HIV
transmission is estimated to be 1 in 500,000 units of PRBCs; the risk of hepatitis C transmission
is approximately 1 in 100,000 units of PRBCs; the overall risk of any type of viral infection is 1 in
34,000 units of PRBCs) [ HU43UH] . ( HUSee "Transfusion-transmitted bacterial infection"UH and HUsee
"Transfusion transmitted HIV infection and AIDS"UH).
Research continues into oxygen-carrying resuscitation fluids that can serve as alternatives to
PRBCs. The ideal replacement fluid would transport HUoxygenUH effectively, expand intravascular
volume, exhibit few or no side effects, and demonstrate great durability. Potential replacement
fluids are discussed elsewhere. ( HUSee "Oxygen carriers as alternatives to red cell transfusion"UH).
Transfusion of clotting factors and platelets Treatment of hemorrhage with IV crystalloid
and PRBCs increases the risk of coagulopathy from dilution of platelets and clotting factors, and
possibly hypothermia [ HU44UH] . Prevention of coagulopathy with early transfusion of plasma and
platelets is critical in the patient with severe hemorrhage [ HU17UH] . ( HUSee "Massive blood
transfusion"UH).
There remain no clear answers to the questions when and how much to transfuse clotting
factors in trauma patients requiring massive transfusion. If bleeding is severe, clinicians cannot
wait for laboratory values to guide transfusion, and such measurements may be inaccurate in
the setting of massive hemorrhage [ HU45UH] .
For patients with severe, on-going bleeding who have received four units of packed red blood
cells (PRBC), we give one unit of fresh frozen plasma (FFP) for every unit of PRBCs. This
calculation includes the initial four units of PRBCs transfused (ie, four units of FFP are given
once four units of PRBCs are given). For patients with severe hemorrhage, we also give six
units of platelets once six units of PRBCs have been transfused. Hypothermia must be
controlled during transfusions.
Although no prospective, randomized outcome studies exist to determine the best approach to
transfusion [ HU46UH] , a retrospective review has been published using data from a US combat
support hospital during the second Iraq war [ HU47UH] . This review assessed the mortality of 246
severely wounded soldiers that required massive blood transfusion and found that patients
given a higher ratio of plasma to red blood cells (RBC) had significantly higher survival rates.
Patients were divided into three groups based on the plasma to RBC ratio: high ratio 1 to 1.14;
medium ratio 1 to 2.5; and, low ratio 1 to 8. Injury severity scores were identical in all groups,
although the low ratio group had more thoracic wounds and a lower average initial hemoglobin
and blood pressure. Group survival was 65 percent, 34 percent, and 19 percent respectively.
Logistic regression found that the plasma to RBC ratio was independently associated with
survival (OR 8.6; 95% CI 2.1-35.2).
A subsequent retrospective study, also performed in combatants during the second Iraq war,
reported similar findings concerning the importance of using a higher platelet to RBC ratio [ HU48UH]
. Improved survival with more aggressive plasma and platelet transfusion is consistent with
other studies in both military and civilian populations [ HU49-57UH] . The determination of the op
plasma to RBC transfusion ratio awaits further study [ HU58,59
timal
UH] .
In the civilian setting, individual trauma centers have developed effective transfusion protocols [
HU60UH] . Some advocate 2 units of FFP for every 6 units of PRBCs transfused. Other centers
advocate more aggressive approaches [ HU61UH] . At one of the largest United States trauma
centers, six units of FFP and one unit of platelets are given once six units of PRBCs are
transfused [ HU17UH] . Another major urban trauma center transfuses one unit of FFP for each unit of
PRBCs [ HU49UH] .
Some authors advocate using platelet counts and fibrinogen levels to determine when to
transfuse platelets and cryoprecipitate [ HU62UH] . A platelet count of less than 100,000/microL is
treated with ten units of platelets, and a fibrinogen level below 100 mg/dL is generally treated
with ten units of cryoprecipitate (each unit of cryoprecipitate comes from one unit of whole
blood, and raises the fibrinogen level by about 5 mg/dL). Provided massive, on-going
hemorrhage is not present, using laboratory measurements to guide transfusion is a reasonable
approach.
Laboratory tests Hematology and chemistry laboratory tests are of limited use in the acute
management of the trauma patient. Clinicians should consider them adjuncts to diagnosis and
not substitutes for clinical assessment. ( HUSee "General approach to blunt abdominal trauma in
adults"UH, section on Diagnostic testing).
The following laboratory studies are obtained in all patients with traumatic shock:
Type and cross-match several units of packed red blood cells
Baseline hemoglobin or hematocrit
Serum bicarbonate (base deficit) and serum lactate
The emergency clinician should order a blood type and cross-match for any victim of significant
trauma in anticipation of the need for transfusion. The blood bank should be notified directly (ie,
by telephone or in person) of the need for packed red blood cells, and other blood products,
should a trauma victim present with life-threatening hemorrhage.
The hematocrit can be useful as a baseline value, but must be interpreted in light of the clinical
context, including the extent of hemorrhage, time since the injury, premorbid hematocrit, and the
amount of exogenous fluid administration. As an example, the clinician should not be reassured
by a normal hematocrit in the acute trauma victim with hypotension. The hematocrit is most
helpful when measured serially to assess on-going hemorrhage.
Hemorrhagic shock may create a metabolic acidosis with a base deficit (ie, decreased serum
bicarbonate) or increased serum lactate. While such findings suggest shock, clinicians must
interpret them in the context of the patient's clinical appearance. Typically, laboratory values lag
behind clinical improvement after aggressive resuscitation.
Coagulation studies, a platelet count, and serum electrolytes are helpful to determine the need
for blood products and electrolyte replacement, if hemorrhage is on-going. Additional testing
may be needed depending on clinical circumstance.
Management of nonhemorrhagic shock
Pneumothorax - Pneumothorax occurs often in both blunt and penetrating trauma, and
may be delayed ( HUshow radiograph 2UH and HUshow radiograph 3UH). Traumatic
pneumothorax or hemothorax is managed by the placement of a large thoracostomy
tube (36 French or larger) in the lateral chest.
If the clinician suspects a tension pneumothorax and the patient is hypotensive, a needle
thoracostomy can be performed, as a temporizing measure, using a long, large (eg, 12 or 14
gauge) angiocatheter or needle inserted above the rib at the second intercostal space in the
mid-clavicular line or the fifth intercostal space in the mid-axillary line. The ideal length is
unclear, but a 4.5 cm (2 inch) needle is a reasonable first choice. Studies of chest wall thickness
using CT scan suggest this length may be inadequate in some patients, but longer needles
increase the risk of injuring the subclavian vessels or other structures [ HU63,64UH] . Should a 4.5
cm needle fail to decompress a tension pneumothorax and a tube thoracostomy be delaye
clinicians should use a longer needle.
d,
Pericardial tamponade - Pericardial tamponade can occur with penetrating or major
blunt chest trauma. Immediate ultrasonography (US) or echocardiography offers the
best opportunity for rapid, early, and accurate diagnosis. Pericardiocentesis is
performed if pericardial tamponade is suspected and the patient is hypotensive and
worsening despite volume resuscitation. If pericardiocentesis recovers blood and
improves the patient's clinical status, emergent thoracotomy is indicated. If thoracotomy
cannot be performed, pericardiocentesis can be repeated as necessary or a J-shaped
catheter can be inserted into the pericardial space to allow continual drainage of the
hemopericardium.
Pericardiocentesis is "classically" performed using the subxiphoid approach [ HU65UH] . However,
some researchers and a large observational study support the use of the paraapical or
parasternal approach under ultrasound guidance [ HU66UH] . Use of the parasternal approach allows
the needle entry site to be closer to the pericardium and eliminates the risk of liver injury. No
controlled trials have compared these approaches in trauma patients. ( HUSee "Cardiac
tamponade"UH).
Emergency thoracotomy - In trauma patients who are profoundly hypotensive despite
aggressive fluid resuscitation, or have lost discernible blood pressure for only a few
minutes, an emergency left lateral thoracotomy to enable decompression of pericardial
tamponade, vascular or pulmonary clamping, and direct suture repair, may be life-
saving. Victims of penetrating trauma, particularly stab wounds to the chest, have vastly
better outcomes in response to emergency department thoracotomy than victims of
blunt trauma [ HU67UH] .
Emergency thoracotomy is most likely to be beneficial in the following settings [ HU67,68UH] :
- Thoracic or trauma surgeon is available within 40 minutes, AND
- Patient has not been pulseless for longer than 20 minutes, AND
- Penetrating trauma is present
If a surgeon is available and the patient has sustained penetrating thoracic trauma leading to
pericardial tamponade, an emergency thoracotomy is indicated. If pericardiocentesis is
incapable of providing adequate drainage and maintaining blood pressure, emergency
thoracotomy is indicated.
After thoracotomy, patients without cardiac activity or blood in the pericardium are pronounced
dead. If present, pericardial tamponade is decompressed, and further treatment given based on
the injuries identified. The descending aorta is cross-clamped if intraabdominal bleeding is
suspected.
Emergency thoracotomy is futile in the following settings:
- No thoracic or trauma surgeon available within 40 minutes
- Blunt trauma without pulse or blood pressure in the field
- Prolonged pulselessness
Pregnancy - Hypotensive pregnant trauma patients are placed in the left lateral
decubitus position or the right side of their backboard is tilted up about 15 degrees in
order to move the gravid uterus off of the inferior vena cava. These maneuvers improve
venous return and may increase the blood pressure.
Monitoring and endpoints for prolonged resuscitation Clear end-points for initial fluid
therapy remain undefined [ HU16UH] . A mean arterial pressure (MAP) around 65 mmHg or a systolic
blood pressure around 90 mmHg is a reasonable goal in penetrating trauma. In blunt trauma
patients, particularly those with possible traumatic brain injury (TBI), a mean arterial pressure
above 105 mmHg or a systolic blood pressure above 120 mmHg is reasonable. Some authors
advocate strictly limiting the amount of IV fluid used for trauma resuscitation in the absence of
hypotension or obvious injury [ HU17UH] . Packed red blood cells are transfused, along with
appropriate replacement of coagulation products, if the goal blood pressure is not maintained
following the initial IV fluid resuscitation. ( HUSee "Transfusion of red blood cells" aboveUH).
Some trauma patients, particularly in community hospitals, must be managed in the emergency
department for prolonged periods when surgical resources or transport is unavailable. It
remains unclear which endpoints are most useful for guiding such prolonged resuscitations.
Those emergency clinicians without access to sophisticated noninvasive technologies rely on
standard physiologic and laboratory measurements to determine whether resuscitation is
adequate. An approach modeled on goal-directed therapy for septic shock, with the important
caveat that greater emphasis be placed on blood transfusion and coagulation factor
replacement, may be helpful [ HU69UH] . ( HUSee "Management of severe sepsis and septic shock in
adults"UH and HUsee "Transfusion of red blood cells" aboveUH).
The following parameters may be used to guide prolonged resuscitation of traumatic shock [
HU69,70UH] :
Blood pressure: maintain MAP above 65 mmHg for penetrating trauma, and above 105
mmHg for blunt trauma
Heart rate: maintain between 60 and 100 beats per minute
HUOxygenUH saturation: maintain above 94 percent
Urine output: maintain above 0.5 mL/kg/hour
Central venous pressure: maintain between 8 and 12 mmHg
Lactate and base deficit: monitor serum lactate and serum bicarbonate every four hours
to ensure end-organ perfusion is adequate or improving with resuscitation
Mixed central venous oxygen saturation: monitor every four hours to ensure end-organ
perfusion is adequate or improving with resuscitation; goal is to maintain above 70
percent
Transfusion of blood products in patients without massive bleeding undergoing prolonged
resuscitation of trauma-related shock may be performed using the following guidelines:
Hemoglobin: transfuse two units PRBCs if hemoglobin falls below 8 g/dL for patients
without risk for acute coronary syndrome (ACS), or below 10 g/dL for patients at risk for
ACS
Platelets: transfuse six units if level falls below 50,000/microL
International normalized ratio (INR): transfuse 2 units of FFP if INR rises above 2
Fibrinogen: transfuse 10 units of cryoglobulin if the fibrinogen level falls below 100
mg/dL
If bleeding is massive and ongoing, laboratory measurements can be inaccurate. Empiric
guidelines for transfusion of blood products in this setting are provided above. ( HUSee
"Transfusion of red blood cells" aboveUH).
Some researchers advocate using the lactate concentration to assess the adequacy of
resuscitation [ HU71-73UH] . Lactate levels may lag behind clinical improvement following aggressive
resuscitation if rapid analyzers are unavailable. Other authors suggest that the magnitude of
metabolic acidosis has prognostic value [ HU74UH] and that the admission base deficit (ie, serum
bicarbonate) may be superior to plasma lactate in predicting injury severity and death [ HU75UH] .
Both endpoints may provide useful feedback about tissue HUoxygenUH debt and the adequacy of
resuscitation [ HU76,77UH] .
Studies have compared noninvasive and invasive (eg, pulmonary artery catheter) monitoring
started in the emergency department for resuscitation of critical trauma patients. Enhanced
noninvasive monitoring appears to be feasible, safe, inexpensive, and equivalent to invasive
monitoring [ HU69,78UH] . Noninvasive monitoring in these studies included such technologies as
thoracic electrical bioimpedance, esophageal doppler monitoring, and orthogonal spectral
imaging, in addition to standard measures, such as MAP, heart rate, pulse oximetry, and carbon
dioxide tension. Many emergency clinicians do not have access to these technologies, and their
role in ED management of trauma awaits further study.
DISPOSITION Definitive management of the patient with traumatic shock often requires
emergency surgery. Emergency clinicians should consult a trauma surgeon as soon as possible
for all victims of significant trauma who may require operative or critical care interventions. If the
patient must be transferred for definitive care, early communication with a trauma center and
preparation for transfer is performed concurrently with assessment and stabilization. The lack of
adequate resources to manage a patient's injuries, including specialty and subspecialty care, is
an indication for transfer to a trauma center.
DEVELOPING TREATMENTS
Hemostatic agents In some circumstances, external hemorrhage cannot be controlled using
direct pressure and standard dressings. A number of hemostatic products are being developed
to control such bleeding, including HUchitosanUH dressing, QuickClot powder, and fibrin sealant
dressing. Fibrin sealant dressing provided better hemorrhage control in a study using a swine
model of severe extremity hemorrhage [ HU79UH] . Mineral based agents performed best in a
subsequent animal study [ HU80UH] . Although some of these products have been used by military
personnel in combat, controlled studies with human subjects are lacking and it remains unclear
how these products can be used by civilian emergency clinicians. ( HUSee "Fibrin sealant"UH).
Red blood cell substitutes Red blood cell substitutes (eg, hemoglobin-based HUoxygenUH
carriers, perfluorocarbons) continue to be studied in both animal and human trials. Preliminary
research suggests these substitutes, capable of delivering oxygen, may be superior to
conventional methods of resuscitation for hemorrhagic shock. This subject is discussed
separately. ( HUSee "Oxygen carriers as alternatives to red cell transfusion"UH, section on Surgery,
trauma, and hypovolemic shock).
SUMMARY AND RECOMMENDATIONS
Hemorrhagic shock comprises the majority of cases of traumatic shock and is
commonly divided into four classes based on clinical presentation (described in detail
above). Significant drops in blood pressure are generally not manifested until class III
hemorrhage develops, and up to 30 percent of a patient's blood volume can be lost
before this occurs. ( HUSee "Pathophysiology and classification" aboveUH).
Massive hemorrhage can occur in the chest, abdomen, retroperitoneum, and from
major external wounds. The thigh can hold up to approximately one liter of blood. Scalp
lacerations can bleed profusely and are often overlooked. Other potential causes of
traumatic shock may include cardiac tamponade and tension pneumothorax. A detailed
list of potential causes of traumatic shock is provided ( HUshow table 1UH). ( HUSee
"Differential diagnosis" aboveUH).
Obvious and immediately detectable manifestations of the shock state include:
tachycardia, hypotension, cool extremities, weak peripheral pulses, prolonged capillary
refill (>2 seconds), narrowing of the pulse pressure (<25 mmHg), and altered mental
status. ( HUSee "Recognition" aboveUH).
Shock may exist even in the setting of "normal" vital signs. Young otherwise healthy
patients can maintain a blood pressure within the normal range despite substantial
blood loss; subtle alterations such as agitation, confusion, irritability, or inattention may
be their only signs of early shock. Altered mental status from inadequate cerebral
perfusion can be difficult to distinguish from drug or alcohol intoxication or associated
head injury. Altered mental status on presentation or a subsequent decline in mental
status, particularly in patients without obvious evidence of head injury, should raise
suspicion for cerebral hypoperfusion. Other subtle presentations of traumatic shock are
described above. ( HUSee "Recognition" aboveUH).
Initial management of the patient in traumatic shock is focused on restoring
intravascular volume, maintaining adequate HUoxygenUH delivery, and limiting on-going
blood loss. The essential tasks include establishing a patent and protected airway
(while protecting the cervical spine), maximizing oxygenation, gaining intravenous
access and initiating fluid resuscitation, controlling hemorrhage, and obtaining blood for
laboratory and blood bank testing (ie, blood typing and cross-matching). Ultrasound
(US) reliably identifies free intraabdominal fluid in the hands of proficient
ultrasonographers. Management is discussed in detail above and an algorithm is
provided ( HUshow algorithm 1UH). ( HUSee "Initial management" aboveUH).
The best approach to fluid resuscitation remains controversial. We suggest that initial
fluid resuscitation for trauma patients in hemorrhagic shock consist of two liters of
normal saline (NS) ( HUGrade 2CUH). The infusion is given as rapidly as possible through
short, large gauge (16 or larger) peripheral IVs. ( HUSee "Intravenous fluid resuscitation"
aboveUH).
The best approach to blood transfusion in trauma is unknown. We suggest two units of
packed red blood cells (PRBC) be transfused if hemodynamics fail to improve after the
administration of 2 to 3 liters (or greater than 50 mL/kg) of crystalloid ( HUGrade 2CUH).
Further transfusions are given based upon the patient's injuries and response to the
initial transfusion. ( HUSee "Transfusion of red blood cells" aboveUH).
During resuscitation, do not allow an initial favorable response to volume replacement
to distract from possible severe, occult injury. Effective early resuscitation may mask
ongoing significant hemorrhage. Remember that the presence of one injury in no way
excludes the possibility of other, more serious injuries.
Treatment of hemorrhage with IV crystalloid and PRBCs increases the risk of
coagulopathy from dilution of platelets and clotting factors, and possibly hypothermia.
Prevention of coagulopathy is critical, but the best approach is unknown. If bleeding is
severe, clinicians cannot wait for laboratory values to guide transfusion, and such
measurements may be inaccurate. For patients with severe ongoing bleeding who have
received four units of PRBCs, we give one unit of fresh frozen plasma (FFP) for every
unit of PRBCs (ie, four units of FFP are given once four units of PRBCs are given). We
also give six units of platelets once six units of PRBCs have been transfused. ( HUSee
"Transfusion of clotting factors and platelets" aboveUH).
The key to management of nonhemorrhagic causes of shock, primarily tension
pneumothorax and pericardial tamponade, is early recognition based on clinical, x-ray,
and US findings. Emergent thoracotomy may be indicated for pericardial tamponade,
particularly in the setting of penetrating thoracic trauma. ( HUSee "Management of
nonhemorrhagic shock" aboveUH).

Use of UpToDate is subject to the HUSubscription and License AgreementUH.
REFERENCES

1. HUBritt, LD, Weireter, LJ Jr, Riblet, JL, et al. Priorities in the management of profound
shock. Surg Clin North Am 1996; 76:645.UH
2. HUSiegel, JH. The effect of associated injuries, blood loss, and oxygen debt on death and
disability in blunt traumatic brain injury: the need for early physiologic predictors of
severity. J Neurotrauma 1995; 12:579.UH
3. American College of Surgeons. Advanced Trauma Life Support (Student Manual).
American College of Surgeons 1997.
4. HUVukmir, RB, Bircher, N, Safar, P. Sodium bicarbonate in cardiac arrest: a reappraisal.
Am J Emerg Med 1996; 14:192.UH
5. Hindman, BJ. Sodium bicarbonate in the treatment of subtypes of acute lactic acidosis:
physiologic considerations. Anesthesiology 1990; 72:1064.
6. HUParks, JK, Elliott, AC, Gentilello, LM, Shafi, S. Systemic hypotension is a late marker of
shock after trauma: a validation study of Advanced Trauma Life Support principles in
a large national sample. Am J Surg 2006; 192:727.UH
7. HUVayer, JS, Henderson, JV, Bellamy, RF, Galper, AR. Absence of a tachycardic
response to shock in penetrating intraperitoneal injury. Ann Emerg Med 1988; 17:227.UH
8. HUBiffl, WL, Harrington, DT, Cioffi, WG. Implementation of a tertiary trauma survey
decreases missed injuries. J Trauma 2003; 54:38.UH
9. HUBarton, ED, Rhee, P, Hutton, KC, Rosen, P. The pathophysiology of tension
pneumothorax in ventilated swine. J Emerg Med 1997; 15:147.UH
10. HUDunning, J, Williamson, J. Ultrasonic guidance and the complications of central line
placement in the emergency department. Emerg Med J 2003; 20:551.UH
11. HUMilling, TJ Jr, Rose, J, Briggs, WM, et al. Randomized, controlled clinical trial of point-
of-care limited ultrasonography assistance of central venous cannulation: the Third
Sonography Outcomes Assessment Program (SOAP-3) Trial. Crit Care Med 2005;
33:1764.UH
12. HUPosner, MC, Moore, EE. Distal greater saphenous vein cutdown--technique of choice
for rapid volume resuscitation. J Emerg Med 1985; 3:395.UH
13. HUMa, OJ, Mateer, JR, Ogata, M, et al. Prospective analysis of a rapid trauma ultrasound
examination performed by emergency physicians. J Trauma 1995; 38:879.UH
14. HUKiraly, LN, Differding, JA, Enomoto, TM, et al. Resuscitation with normal saline (NS) vs.
lactated ringers (LR) modulates hypercoagulability and leads to increased blood loss in
an uncontrolled hemorrhagic shock swine model. J Trauma 2006; 61:57.UH
15. HUTodd, SR, Malinoski, D, Muller, PJ, Schreiber, MA. Lactated Ringer's is superior to
normal saline in the resuscitation of uncontrolled hemorrhagic shock. J Trauma 2007;
62:636.UH
16. Tisherman, SA. Trauma fluid resuscitation in 2010. J Trauma 2003; 54:S231.
17. HUAlam, HB, Rhee, P. New developments in fluid resuscitation. Surg Clin North Am 2007;
87:55.UH
18. HURizoli, SB, Rhind, SG, Shek, PN, et al. The immunomodulatory effects of hypertonic
saline resuscitation in patients sustaining traumatic hemorrhagic shock: a randomized,
controlled, double-blinded trial. Ann Surg 2006; 243:47.UH
19. HUWade, CE, Grady, JJ, Kramer, GC. Efficacy of hypertonic saline dextran fluid
resuscitation for patients with hypotension from penetrating trauma. J Trauma 2003;
54:S144.UH
20. HUCooper, JD, Paul, SM, McDermott, FT, et al. Prehospital hypertonic saline resuscitation
of patients with hypotension and severe traumatic brain injury. JAMA 2004; 291:1350.UH
21. HUBulger, EM, Jurkovich, GJ, Nathens, AB, et al. Hypertonic resuscitation of hypovolemic
shock after blunt trauma: a randomized controlled trial. Arch Surg 2008; 143:139.UH
22. HURoberts, I, Alderson, P, Bunn, F, et al. Colloids versus crystalloids for fluid resuscitation
in critically ill patients. Cochrane Database Syst Rev 2004; :CD000567.UH
23. HURizoli, SB. Crystalloids and colloids in trauma resuscitation: a brief overview of the
current debate. J Trauma 2003; 54:S82.UH
24. HULiberati, A, Moja, L, Moschetti, I, et al. Human albumin solution for resuscitation and
volume expansion in critically ill patients. Intern Emerg Med 2006; 1:243.UH
25. HUSperry, JL, Minei, JP, Frankel, HL, et al. Early use of vasopressors after injury: caution
before constriction. J Trauma 2008; 64:9.UH
26. Veech, RL. Immediate versus delayed fluid resuscitation in patients with trauma. N Engl
J Med 1995; 332:681.
27. Roberts, I, Evans, P, Bunn, F, et al. Is the normalisation of blood pressure in bleeding
trauma patients harmful?. Lancet 2001; 357:385.
28. HUStern, SA, Dronen, SC, Birrer, P, Wang, X. Effect of blood pressure on hemorrhage
volume and survival in a near-fatal hemorrhage model incorporating a vascular injury.
Ann Emerg Med 1993; 22:155.UH
29. HUWinchell, RJ, Simons, RK, Hoyt, DB. Transient systolic hypotension. A serious problem
in the management of head injury. Arch Surg 1996; 131:533.UH
30. HUSolomonov, E, Hirsh, M, Yahiya, A, Krausz, MM. The effect of vigorous fluid
resuscitation in uncontrolled hemorrhagic shock after massive splenic injury. Crit Care
Med 2000; 28:749.UH
31. HUShoemaker, WC, Peitzman, AB, Bellamy, R, et al. Resuscitation from severe
hemorrhage. Crit Care Med 1996; 24:S12.UH
32. HUBickell, WH, Wall, MJ Jr, Pepe, PE, et al. Immediate versus delayed fluid resuscitation
for patients with penetrating torso injuries. N Engl J Med 1994; 331:1105.UH
33. HUDutton, RP, Mackenzie, CF, Scalea, TM. Hypotensive resuscitation during active
hemorrhage: impact on in-hospital mortality. J Trauma 2002; 52:1141.UH
34. HUMapstone, J, Roberts, I, Evans, P. Fluid resuscitation strategies: a systematic review of
animal trials. J Trauma 2003; 55:571.UH
35. Banerjee, A, Jones, R. Whither immediate fluid resuscitation? Lancet 1994; 344:1450.
36. HUCapone, AC, Safar, P, Stezoski, W, et al. Improved outcome with fluid restriction in
treatment of uncontrolled hemorrhagic shock. J Am Coll Surg 1995; 180:49.UH
37. HUKim, SH, Stezoski, SW, Safar, P, et al. Hypothermia and minimal fluid resuscitation
increases survival after uncontrolled hemorrhagic shock in rats. J Trauma 1997;
42:213.UH
38. HUOwens, TM, Watson, WC, Prough, DS, et al. Limiting initial resuscitation of uncontrolled
hemorrhage reduces internal bleeding and subsequent volume requirements. J Trauma
1995; 39:200.UH
39. HUSilbergleit, R, Satz, W, McNamara, RM, et al. Effect of permissive hypotension in
continuous uncontrolled intraabdominal hemorrhage. Acad Emerg Med 1996; 3:922.UH
40. HUMcKinley, BA, Valdivia, A, Moore, FA. Goal-oriented shock resuscitation for major torso
trauma: what are we learning?. Curr Opin Crit Care 2003; 9:292.UH
41. HUKwan, I, Bunn, F, Roberts, I. Timing and volume of fluid administration for patients with
bleeding. Cochrane Database Syst Rev 2003; :CD002245.UH
42. Kwan, I, Bunn, F, Roberts, I, on behalf of the WHO Pre-Hospital Trauma Care S
Committee. Timing and volume of fluid administration for patients with bleeding
following trauma (C
teering
ochrane Review). In: The Cochrane Library, Issue 2, 2001. Oxford:
unologic consequences of blood
Update Software.
43. HUDellinger, EP, Anaya, DA. Infectious and imm
transfusion. Crit Care 2004; 8 Suppl 2:S18.UH
44. HUErber, WN, Perry, DJ. Plasma and plasma products in the treatment of massive
haemorrhage. Best Pract Res Clin Haematol 2006; 19:97.UH
45. HUHo, AM, Karmakar, MK, Dion, PW. Are we giving enough coagulation factors during
major trauma resuscitation?. Am J Surg 2005; 190:479.UH
46. HUZehtabchi, S, Nishijima, DK. Impact of transfusion of fresh-frozen plasma and packed
red blood cells in a 1:1 ratio on survival of emergency department patients with severe
trauma. Acad Emerg Med 2009; 16:371.UH
47. HUBorgman, MA, Spinella, PC, Perkins, JG, et al. The ratio of blood products transfused
affects mortality in patients receiving massive transfusions at a combat support hospital.
J Trauma 2007; 63:805.UH
48. HUPerkins, JG, Andrew, CP, Spinella, PC, et al. An evaluation of the impact of apheresis
platelets used in the setting of massively transfused trauma patients. J Trauma 2009;
66:S77.UH
49. HUGonzalez, EA, Moore, FA, Holcomb, JB, et al. Fresh frozen plasma should be given
earlier to patients requiring massive transfusion. J Trauma 2007; 62:112.UH
50. HUCinat, ME, Wallace, WC, Nastanski, F, et al. Improved survival following massive
transfusion in patients who have undergone trauma. Arch Surg 1999; 134:964.UH
51. HUCosgriff, N, Moore, EE, Sauaia, A, et al. Predicting life-threatening coagulopathy in the
massively transfused trauma patient: hypothermia and acidoses revisited. J Trauma
1997; 42:857.UH
52. HUGunter, OL Jr, Au, BK, Isbell, JM, et al. Optimizing outcomes in damage control
resuscitation: identifying blood product ratios associated with improved survival. J
Trauma 2008; 65:527.UH
53. HUDuchesne, JC, Hunt, JP, Wahl, G, et al. Review of current blood transfusions strategies
in a mature level I trauma center: were we wrong for the last 60 years?. J Trauma 2008;
65:272.UH
54. HUHolcomb, JB, et al. Increased plasma and platelet to red blood cell ratios improves
outcome in 466 massively transfused civilian trauma patients. Ann Surg 2008; 248:447.UH
55. HUMoore, FA, Nelson, T, McKinley, BA, et al. Is there a role for aggressive use of fresh
frozen plasma in massive transfusion of civilian trauma patients?. Am J Surg 2008;
196:948.UH
56. HUTeixeira, PG, Inaba, K, Shulman, I, et al. Impact of plasma transfusion in massively
transfused trauma patients. J Trauma 2009; 66:693.UH
57. HUDente, CJ, Shaz, BH, Nicholas, JM, et al. Improvements in early mortality and
coagulopathy are sustained better in patients with blunt trauma after institution of a
massive transfusion protocol in a civilian level I trauma center. J Trauma 2009;
66:1616.UH
58. HUKashuk, JL, Moore, EE, Johnson, JL, et al. Postinjury life threatening coagulopathy: is
1:1 fresh frozen plasma:packed red blood cells the answer?. J Trauma 2008; 65:261.UH
59. HUSperry, JL, Ochoa, JB, Gunn, SR, et al. An FFP:PRBC transfusion ratio >/=1:1.5 is
associated with a lower risk of mortality after massive transfusion. J Trauma 2008;
65:986.UH
60. HUCotton, BA, Gunter, OL, Isbell, J, et al. Damage control hematology: the impact of a
trauma exsanguination protocol on survival and blood product utilization. J Trauma
2008; 64:1177.UH
61. HUHirshberg, A, Dugas, M, Banez, EI, et al. Minimizing dilutional coagulopathy in
exsanguinating hemorrhage: a computer simulation. J Trauma 2003; 54:454.UH
62. HUFaringer, PD, Mullins, RJ, Johnson, RL, Trunkey, DD. Blood component

supplementation during massive transfusion of AS-1 red cells in trauma patients. J
Trauma 1993; 34:481.UH
63. HUZengerink, I et al. Needle thoracostomy in the treatment of tension pneumothorax in
trauma patients: what size needle? J Trauma 2008; 64:111.UH
64. HUWax, DB, Leibowitz, AB. Radiologic assessment of potential sites for needle
decompression of a tension pneumothorax. Anesth Analg 2007; 105:1385.UH
65. HUVayre, F, Lardoux, H, Pezzano, M, et al. Subxiphoid pericardiocentesis guided by
contrast two-dimensional echocardiography in cardiac tamponade: experience of 110
consecutive patients. Eur J Echocardiogr 2000; 1:66.UH
66. HUTsang, TS, Enriquez-Sarano, M, Freeman, WK, et al. Consecutive 1127 therapeutic
echocardiographically guided pericardiocenteses: clinical profile, practice patterns, and
outcomes spanning 21 years. Mayo Clin Proc 2002; 77:429.UH
67. HUBranney, SW, Moore, EE, Feldhaus, KM, Wolfe, RE. Critical analysis of two decades of
experience with postinjury emergency department thoracotomy in a regional trauma
center. J Trauma 1998; 45:87.UH
68. Baxter, BT, Moore, EE, Moore, JB, et al. Emergency department thoracotomy following
t, HM. Targeted resuscitation strategies after injury. Curr
injury: critical determinants for patient salvage. World J Surg 1988; 12:671.
69. HUBilkovski, RN, Rivers, EP, Hors
Opin Crit Care 2004; 10:529.UH
70. HUGarcia, A. Critical care issues in the early management of severe trauma. Surg Clin
North Am 2006; 86:1359.UH
71. Baue, AE. Physiology of shock and injury. In: Shock and resuscitation, Gelder, ER (Ed),
McGraw-Hill, New York 1993.
72. HUMizock, BA, Falk, JL. Lactic acidosis in critical illness. Crit Care Med 1992; 20:80.UH
73. HUMikulaschek, A, Henry, SM, Donovan, R, Scalea, TM. Serum lactate is not predicted by
anion gap or base excess after trauma resuscitation. J Trauma 1996; 40:218.UH
74. HUBannon, MP, O'Neill, CM, Martin, M, et al. Central venous oxygen saturation, arterial
base deficit, and lactate concentration in trauma patients. Am Surg 1995; 61:738.UH
75. HUDavis, JW, Parks, SN, Kaups, KL, et al. Admission base deficit predicts transfusion
requirements and risk of complications. J Trauma 1996; 41:769.UH
76. HUWilson, M, Davis, DP, Coimbra, R. Diagnosis and monitoring of hemorrhagic shock
during the initial resuscitation of multiple trauma patients: a review. J Emerg Med 2003;
24:413.UH
77. Tisherman, SA, Barie, P, Bokhari, F, et al. Clinical practice guideline: endpoints of
resuscitation. J Trauma 2004; 57:898.
78. HUShoemaker, WC, Wo, CC, Chien, LC, et al. Evaluation of invasive and noninvasive
hemodynamic monitoring in trauma patients. J Trauma 2006; 61:844.UH
7

9. HUAcheson, EM et al. Comparison of hemorrhage control agents applied to lethal
extremity arterial hemorrhages in swine. J Trauma 2005; 59:865.UH
80. HUKheirabadi, BS, Edens, JW, Terrazas, IB, et al. Comparison of new hemostatic
granules/powders with currently deployed hemostatic products in a lethal model of
extremity arterial hemorrhage in swine. J Trauma 2009; 66:316.UH