Medical Emergencies Management Guidelines

Medical Emergencies Management Guidelines
(AL-QURAN)
Muhammad Umar
MBBS, MCPS, FCPS, FRCP (Glasg), FRCP (london), FACG, AGAF Chairman & Professor of Medicine Rawalpindi Medical College Rawalpindi Chief Gastroenterology & Hepatology Division Holy Family Hospital Rawalpindi
Hamama-tul-Bushra Khaar
BSc, MBBS, FCPS, FRCP (Glasg), FACG Professor of Medicine Rawalpindi Medical College Rawalpindi Consultant Gastroenterology & Hepatology Division Holy Family Hospital Rawalpindi
Medical Emergencies Management Guidelines 2009 Rawalians' Research Forum on GI & Liver Diseases. Library of Rawalians' Research Forum on GI & Liver Diseases - RS/ICT/437 This Medical Emergencies Management Guidelines will serve as educational tool for young physicians of Pakistan. We are thankful to the editors. Although every effort has been made to ascertain the authenticity of the material provided by the contributors and to trace the copyright holders for borrowed material. If any omissions have occurred, the author(s), the editor and the publisher will be pleased to make the necessary arrangements at the first priority.
Designed & Composed by: Jahanzeb Khan Printed & Published in the Islamic Republic of Pakistan on Oct 2009 Rawalians Research Forum Saidpur Road, Satellite Town, Rawalpindi - 46000 Tel: +92 51 4414174 / 4427614 / 9290422 / 9290321-7 Fax: +92 51 9290422 www.rawalianresearch.org Printed by: Pictorial Printers (Pvt) Limited 21-E, I & T Centre Aabpara Islamabad, Pakistan Gastroenterology & Hepatology Division Department of Medicine Holy Family Hospital Rawalpindi Tel: +92 51 4414174 / 4427614 / 9290422 Fax: +92 51 9290422 Email: drumarpk@yahoo.com
About the Authors

Muhammad Umar
MBBS, MCPS, FCPS, FRCP (L), FRCP (Glasg), FACG, AGAF
Graduated in 1981 from Rawalpindi Medical College with distinction and Presidential Gold Medal by President of Pakistan. Started his professional career as Assistant Professor of Medicine after obtaining membership (MCPS) and then fellowship (FCPS) from College of Physicians & Surgeons Pakistan in 1985. He was awarded fellowship from American College of Gastroenterology (FACG) in 2002, Royal College of Physicians London (FRCP), Royal College of Physicians Glasgow (FRCP) in 2006, and American Gastroenterological Association (AGAF) in 2007. He was appointed Assistant Professor, Associate Professor and currently the Professor & Chair of Medicine and Chief of Gastroenterology & Hepatology Division in RMC. He had keen zest for gastroenterology and specifically hepatology, so he started pursuing his career in this field. He established GI & Liver Clinic, GI & Liver Learning Resource Centre, and Liver Research data base at Holy Family Hospital Rawalpindi in 1998. He has contributed to gastroenterology by publishing more than 70 review and original research papers in various national and international journals, two books on hepatology; Evidenced Based Approach to Hepatitis C Management and Hepatitis C in Pakistan. Moreover, he published National Hepatitis Practice Guidelines. He was awarded SJZ Research Award by Pakistan Society of Gastroenterology & GI Endoscopy in 2004. He was the Past President of Pakistan Society of Gastroenterology & GI Endoscopy, President Elect Pakistan Society of Hepatology, and President of Rawalians' Research Forum on GI & Liver Diseases. Medical Director of Holy Family Hospital Rawalpindi (2009), Member of Board of Management of Rawalipindi Medical College and Allied Hospitals He is on Editorial Board of Journal of Rawalipindi Medical College, Associate Editor of Journal of Pakistan Society of Gastroenterology. Editorial Board of Bangladesh Journal of Hepatology, Editorial Board of Libyan Journal of Gastroenterology, and Member of International Cor-Curriculam Committee on GI Endoscopy of OMED, Member Global Guideline Committee of World Gastroenterology Organization (WGO), Clinical Coordinator of National Prevention and Control Program of Hepatitis. He is Chairman ASIAHEP Pakistan. He is author of Standards in Gastrointestinal Endoscopy Training MD Training Program for Gastroenterology and Basic Skills in Gastrointestinal Endoscopy Training Manual and Medical Emergencies Management Guidelines. He is a member of foreign graduate evaluation committee of PMDC.
Hamama-tul-Bushra Khaar
BSc, MBBS, FCPS, FRCP (Glasg), FACG
She graduated from Rawalpindi Medical College Pakistan being Best Graduate in 1981. She obtained fellowship from College of Physicians & Surgeons Pakistan (FCPS) in 1985 and started her career in medicine. She was honored with fellowships from Royal College of Physicians Glasgow (FRCP) and American College of Gastroenterology (FACG) in 2007. She was appointed Assistant Professor, Associate Professor and currently the Professor of Medicine at Rawalpindi Medical College and consultant gastroenterologist at Holy Family Hospital Rawalpindi Pakistan. She had strong interest in gastroenterology and hepatology, so she started pursuing her career in it. She started practicing gastroenterology and developed and Endoscopy Suit at District Headquarters Hospital Rawalpindi in 1995. She has a long list of publications including original and review papers, books, guidelines, and manuals. She has published about 80 research papers, two books on hepatology; Evidenced Based Approach to Hepatitis C Management and Hepatitis C in Pakistan. Moreover, she published National Hepatitis Practice Guidelines and Basic Skills in Gastrointestinal Endoscopy Training Manual, MD Training Program, Standards in Gastrointestinal Endoscopy,. She is Editorial Board of Pakistan Journal of Gastroenterology and Research Director of Rawalians Research Forum since 1998.
Foreword
I bestow all my efforts to Almighty Allah who is the most merciful and compassionate. These guidelines will help the young doctors working in busy and hectic emergency rooms around the globe. These guidelines will also serve as quick reference book for administration of required dose in specially designed and easily understandable format. This module will also help paramedical staffs who are involved directly with patients medication. I have put the SOP (standard operating protocols) for emergency and medical intensive care unit in the 2nd section which is the product of Department of Medicine, Holy Family Hospital to make the facility best of their use. I am thankful to Prof. Muhammad Umar, Prof. Hamama-tul-Bushra, Dr. Saima Usman, and Dr. Zahid Mahmood Minhas for the valuable contribution in finalizing this document. They have helped me in dosage schedule, summarizing and proof reading of this book. I would like to mention Prof. Muhammad Umar who has always been at my back for new ideas and generous academic support. This was his creative mind that encouraged me to write up about the medical emergencies that we face in our hospital. I hope that you will find this document useful.
Dr. Raja Adnan Arif Co-Author
Contributors
Dr. Masood Ahmad
MBBS, FCPS Assistant Professor Medicine Holy Family Hospital
Dr. Zameer Butt

Senior Registar Medicine Holy Family Hospital
Dr. Raja Adnan Arif Dr. Muhammad Khurram

MBBS, FCPS Assistant Professor Medicine Holy Family Hospital MD Research Coordinator Holy Family Hospital
Dr. Zahid Mahmood Minhas Dr. Jahangir Sarwar

MBBS, FCPS Associate Professor Surgery Holy Family Hospital MBBS, MD, DCPS Senior Registrar Medicine Holy Family Hospital
Dr. Abdul Naeem Dr. Saima Usman

MBBS, FCPS Senior Registrar Medicine Holy Family Hospital MBBS Medical Officer Senior Research Officer Holy Family Hospital
Dr. Muhammad Arif

MBBS, FCPS Senior Registrar Medicine Holy Family Hospital
Dr. Muhammad Saleem

MBBS Post Graduate Trainee Holy Family Hospital
Dr. Jawad Zaheer

MBBS, FCPS Assistant Professor Anesthesia Holy Family Hospital
Dr. Marina Khan

MBBS House Physician Holy Family Hospital
Dr. Atifa Shoaib

Associate Professor Pathology Holy Family Hospital
Dr. Qurat-ul-Ain
MBBS House Physician Holy Family Hospital
Dr. Imtiaz Qureshi

MBBS, FCPS Assistant Professor Pathology Holy Family Hospital
Muhammad Bilal
4th Year Medical Student Army Medical College, Rawalpindi
Dr. Gul-e-Atif
MBBS, M.phil Assistant Professor Pathology
Jahanzeb Khan
IT Administrator
Aims and Objectives

The aim of these guidelines was to provide a uniform standardize method of management of common medical emergencies in emergency room of Allied Hospitals of Rawalpindi Medical College and other health care facilities in the country. These guidelines are mainly for young residents managing patients as first hand doctors. In this situation, they must be having handy, precise and readily available information for reference to manage serious and difficult emergencies. Another advantage will be an easy access to dosage schedule and methods of adminstration of emergency drugs. Thirdly, book will provide a stepwise management approach of serious patients, which play a pivitol in training program of young trainee in teaching institutions. Finally, it remains my pleasant duty to thank all those who contributed in formulating and publishing these guidelines. I extend my special thanks to Dr. Saima Usman, Dr. Zahid Minhas, Dr. Muhammad Khurram, Dr. Masood Ahmad, Dr. Muhammad Arif, Dr. Muhammad Saleem, and Dr. Abdul Naeem and other contributors for their valuable contribution. My special thanks to Dr. Raja Adnan Arif, who i must confess is the principal author of these guidelines. He also wrote the whole manuscript and made this endeavor happened. I also extend my gratitude to Jahanzeb Khan who designed the book. Finally, I must say that lot of efforts has been done but still there are deficiencies, which need improvement. Comments and feedback will be highly appreciated, so the authors can include those in next edition. Authors also acknowledge all those authors and editors from which this material has been adopted as such to avoid any controversy and confusion in management guidelines. Prof. Muhammad Umar
Medical Director Holy Family Hospital 2009
Contents:
1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. Acute Myocardial Infarction. Acute Left Ventricular Failure. Unstable Angina. Narrow Complex Tachycardia. Broad Complex Tachycardia. Hypertension in Urgency and Emergency. Acute Respiratory Distress Syndrome. Acute Severe Asthma. COPD Acute Exacerbation. Gastrointestinal Bleeding. Variceal Bleeding. Mesenteric Ischemia. Acute Liver Failure Acute Pancreatitis Acute Stroke. Acute Bacterial Meningitis Aseptic Meningitis Status Epilepticus. Acute Renal Failure. Diabetic Ketoacidosis. Hyperosmolar Nonketotic Coma (Honc) Hypokalemia. Hyperkalemia Hypocalcemia Hypoglycemia Adrenal Insufficiency Acute Poisoning & Drug Overdose. Organophosphate Poisoning. Anaphylaxis. Dengue Hemorrhagic Fever. Fever And Neutropenia Tetanus. Bleeding Disorders. Transfusion Therapy Pregnancy & Hypertension. Pregnancy & Diabetes Mellitus. 9 10 11 12 15 17 19 21 23 24 28 29 31 33 35 38 41 42 44 46 47 48 49 51 52 53 55 59 60 61 62 63 64 65 67 69 70 84 89 91 92 93 94 96 98
Appendix: 37. ICU Guidelines 38. SOPs for Emergency Ward Patient Care 39. Surgical Safety Checklist 40. Adult Advanced Life-Support Algorithm 41. Adult Basic Life-Support Algorithm 2005 42. ACLS Pulseless Arrest Algorithm 43. The diagram summary 44. ICU Medications 45. Useful drug's doses for the new house officers 46. References
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1: ACUTE MYOCARDIAL INFARCTION Use protocol: PONA - (Pain killer, Oxygen, Nitrates, Aspirin). o Give oxygen via face mask. o Give analgesic. o Aspirin 300 mg (chew). o Serial EKG. o Call to cardiologist. o Inf. ISOKET (isosorbide dinitrate) 2-10 mg/hr up to 20 mg/hr (Amp. 1 mg/ml = 10 mg in 10 ml) titrate dose according to BP for initial 24 48 hours. o Thrombolise as early as possible. o Beta-blocker if patient is hemodynamically stable (systolic BP > 100), metoprolol (lopresser) 5mg IV every 5 min for three doses only. Avoid in third degree AV block, asthma, heart rates < 60 beats/min and decompensated heart failure. o ACE inhibitors if patient is hemodynamically stable (systolic BP > 100). o Use heparin (followed by warfarin in three months) in patients with anterior wall MI, history of embolism and atrial fibrillation. Indication for thrombolysis o Patients with 2mm ST elevation in two adjacent limb leads. o 1mm ST elevation in two adjacent chest leads. o New onset LBBB. Contraindications for thrombolysis Absolute Contraindications o History of hemorrhagic stroke at any time, non-hemorrhagic stroke within one year. o Marked HTN (systolic 180mmHg and diastolic 110 mmHg). o Active bleeding excluding menses. o Active peptic ulcer disease. o Aortic dissection. Relative Contraindications o Prolonged CPR 10 min. o Recent surgery (less than 2 weeks) or trauma. o Pregnancy. o Active peptic ulcer disease. o SK previously administered between 5 days to 2 years. o INR 02, current use of anticoagulant or known bleeding diasthesis.
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2: ACUTE LEFT VENTRICULAR FAILURE o o o o o o o Prop up, legs dangling over side of bed + oxygen with mask @ 10 15 L/min. Maintain IV lines on both arms. Take BP, pulse, ECG attach cardiac monitor, SPO2. Morphine sulphate 2 5 mg IV over several minute repeat every 10 25 min till effect is seen. Lasix (furosemide) 40 100 mg IV stat can be increased to 200 mg in subsequent doses. Inf. Isoket (isosorbide dinitrate) 2 10 mg/hr up to 20 mg/hr (amp 1mg/ml = 10mg in 10ml) titrate dose according to BP. If BP 100, start nitroglycerine (nitronol) IV 100 200 g/min (10ml = 10mg, dilute in 90ml 5%D/W = 100ml). start at 60 micro drops/min and titrate. Catheterize or provide urinal & monitor intake/output on a chart. Start Inf. Dobutamine @ 2.5 10 /kg/min titrate according to the clinical condition (max 25 /kg/min), dopamine 2 10 g/kg/min and dose can be titrate (max 50 /kg/min).
o o
Above mentioned measures are ordinarily applied simultaneously or nearly so. o Sometimes Aminophylline dose 240 480mg is given. Aminophylline IV [ECG monitoring, 250mg in 500ml of 0.9% saline, load with 5.6mg/kg (2.8 ml/kg) over 20 min followed by infusion 0.9 mg/kg/hr (0.45 ml/kg)]. Features of toxicity are nausea, vomiting and arrhythmias. o Digitalis 1mg infusion (0.75 1mg in atleast 2 hours). o Sometimes rotating tourniquets if above mentioned measure fail. In case of MI, treat accordingly. In case of arrhythmias treat accordingly best approach in this case is DC shock if ventricular tachycardia. In case of LVF with renal failure, high dose diuretics necessary call nephrology Ventilator support if respiratory exhaustion, coma, respiratory arrest.
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3: UNSTABLE ANGINA o o o o o o Give oxygen Analgesia Aspirin 300 mg orally Heparin: IV bolus 60 80 U/kg, infusion 14 U/kg/hr. Serial EKG. IV nitrates: Inf. ISOKET (Isosorbide Dinitrate) 2-10 mg/hr up to 20 mg/hr (Amp. 1 mg/ml = 10 mg in 10 ml) titrate dose according to BP for initial 24 48 hours. Beta blocker Metoprolol 25 mg TID or Atenolol 50 mg OD. For patients already on beta blockers add calcium channel blockers and vice versa. Refer to cardiologist.
o o o
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4: NARROW COMPLEX TACHYCARDIA ECG shown rate of >l00bpm and QRS complex duration of <l20ms (<3 small squares on ECGs done at the standard uk rate of 25mm/s). Differential diagnosis Sinus tachycardia: normal P-wave followed by normal QRS. Atrial tachyarrhythmias: Rhythm arises in atria, AV node in a bystander. o Atrial fibrillation (AF): absent P-wave, irregular QRS complexes. o Atrial flutter: atrial rate 260340bpm. Saw-tooth baseline, due to continuous atrial electrical activity. Ventricular rate often 150bpm (2 : 1 block). o Atrial tachycardia: abnormally shaped P-waves, may outnumber QRS. o Multifocal atrial tachycardia: 3 or more p-wave morphologies, irregular QRS complexes. Junctional tachycardia: Av-node in part of the pathway. P-wave either buried in QRS complex or occurring after QRS complex. o AV nodal re-entry tachycardia. o AV re-entry tachycardia, includes an accessory pathway, eg WPW. Principles of management If the patient in compromised, use DC cardioversion. Otherwise, identify the underlying rhythm and treat accordingly. The chief thing is to decide whether the rhythm is regular or not (likely AF). Vagal maneuvers (carotid sinus massage, Valsalva maneuver) transiently increase AV block, and may unmask an underlying atrial rhythm. If unsuccessful, give adenosine which causes transient AV block. It has a short half-life (10l5s) and works in 2 ways: o By transiently slowing ventricles to show the underlying atrial rhythm, o By cardioverting a junctional tachycardia to sinus rhythm. Give 6mg IV bolus into a large vein, followed by saline flush, while recording a rhythm strip. If unsuccessful, give 12mg, then one further 12mg bolus. Warn about SE: transient chest tightness, dyspnea, headache, flushing. Relative CI: asthma, 2d/3rd.degree AV block or sinoatrial disease (unless pacemaker). Interactions: potentiated by dipyridamole, antagonized by theophylline. Specifics Sinus tachycardia: Identify and treat underlying cause.
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Supraventricular tachycardia: If adenosine fails, use verapamil 2.55 mg IV over 23min. NB: NOT if on a -blocker. If no response, a further 5mg IV over 3min (if age <60yrs). Alternatives: atenolol 5mg IV or sotalol 20120mg IV (over 10min); or amiodarone. If unsuccessful, use DC cardioversion. Atrial flbrillatlan/flutter Manage along standard lines. Atrial tachycardia: Rare: may be due to digoxin toxicity: withdraw digoxin, consider digoxin-specific antibody fragments. Maintain K+ at 45 mmol/L Multifocal atrial tachycardia: Most commonly occurs in COPD. Correct hypoxia and hypercapnia. Consider verapamil if rate remains >ll0bpm. Junctional tachycardia: Where anterograde conduction through the AV node occurs, vagal maneuver are worth trying. Adenosine will usually cardiovert a junctional rhythm to sinus rhythm. If it fails or recurs, blockers (or verapamil not with -blockers, digoxin, or class I agents such as quinidine). If this does not control symptoms, consider radiofrequency ablation. WolffParkinsonWhite (WPW) syndrome Caused by congenital accessory conduction pathway between atria and ventricles. Resting ECG shows short PR interval and widened QRS complex due to slurred upstroke or delta wave. 2 types: WPW type A (+ve wave in V1) WPW type B (-ve wave in V1). Patients present with SVT which may be due to an AVRT, pre-excited AF, or pre-excited atrial flutter. Risk of degeneration to VF and sudden death. Treatment: flecainide, propafenone, sotalol, or amiodarone. Refer to cardiologist for electrophysiology and ablation of the accessory pathway.
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Irregular narrow complex tachycardia Treat as AFby far the most likely diagnosis. Control rate with either beta-blocker or digoxin. If onset < 48h consider cardioversion with either amiodarone, 300mg in over 2060 mm, then 900mg over 24h; or DC shock. Consider anticoagulation with heparin and/or warfarin to reduce the risk of stroke.
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5: BROAD COMPLEX TACHYCARDIA. ECG shows rate of >l00bpm and QRS complexes >l20ms (>3 small squares on ECGs done at the standard UK rate of 25mm/s).
Principles of management If in doubt, treat as ventricular tachycardia (the commonest cause). Identify the underlying rhythm and treat accordingly. Differential Ventricular tachycardia (VT) including torsade de pointes. SVT with aberrant conduction, eg. AF, atrial flutter. Pre-excited tachycardias, eg. AF, atrial flutter, or AV re-entry tachycardia with underlying WPW. (NB: Ventricular ectopics should not cause confusion when occurring singly; but if > 3 together at a rate of >120, this constitutes VT) Identification of the underlying rhythm may be difficult, seek expert help. Diagnosis is based on the history: if IHD/MI the likelihood of a ventricular arrhythmia is >95%, a 12-lead ECG, and the lack of response to IV adenosine. ECG findings in favour of VT: Fusion beats or capture beats. Positive QR5 concordance in chest leads. Marked left axis deviation or rightwards axis. AV dissociation (occurs in 25%) or 2: 1 or 3: 1 AV block. QRS complex >l60ms. Any atypical bundle-branch-block pattern. Management Give high-flow O2 by mask and monitor O2 saturations. Connect patient to a cardiac monitor and have a defibrillator to hand. Correct electrolyte abnormalities. Check for adverse signs. Low cardiac output (clammy, consciousness., BP <90); oliguria; angina; pulmonary edema. Obtain 12-lead ECG, request CXR and obtain IV access. If haemodynamically unstable Synchronized DC shock. Correct any hypokalemia and hypomagnesaemia: 60mmol <CI at 30mmol/h, and 5ml 50% magnesium sulphate over 30min). Follow with amiodarone 300mg IV over 20-60min. For refractory cases procainamide or sotalol may be considered.
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If haemodynamically stable Correct hypokalaemia and hypomagnesaemia: as above. Amiodarone 300mg IV over 2060 min. Alternatively lidocaine 50mg (2.5ml of 2% solution) IV over 2min, repeated every 5min up to 200mg. If this fails, use synchronized DC shock. After correction of VT Establish the cause (via the history and tests above) Maintenance anti-arrhythmic therapy may be required. If VT occurs after MI, give IV amiodarone or lidocaine infusion for 1224h; if 24h after MI, also start oral anti-arrhythmic: sotalol (if good LV function) or amiodarone (if poor LV function). Prevention of recurrent VT: surgical isolation of the arrhythmogenic area or implantation of tiny automatic defibrillators may help. Ventricular fibrillation Use non-synchronized DC shock (there is no R wave to trigger defibrillation). Ventricular extrasystoles (ectopics) are the commonest post-MI arrhythmia but they are also seen in healthy people (often >10/h). Patients with frequent ectopics post-MI have a worse prognosis, but there is no evidence that antidysrhythmic drugs improve outcome, indeed they may increase mortality. Torsade de pointes: A form of VT, with a constantly varying axis, often in the setting of long-QT syndromes. This can be congenital or acquired, eg from drugs (eg some anti-dysrhythmics, tricyclics, antimalarials, and newer antipsychotics). Torsade in the setting of congenital long-QT syndromes can be treated with high doses of -blockers. In acquired Iong-QT syndromes, stop all predisposing drugs, correct hypokalaemia, and give MgS04 (2g IV over 10 min). Alternatives include: overdrive pacing or isoprenaline IVI to increase heart rate.
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6: HYPERTENSION Hypertension Urgency: Asymptomatic severe HTN ie. S220 and D125 that persist after a period of observation with optic disc edema, progressive TOD complications and severe perioperative HTN. Prenatal therapy is not usually required. BP must be reduced with in few hours. Hypertension Emergency: HTN associated with TOD as given below. o HTN encephalopathy (headache, irritability, confusion, altered mental status) o HTN nephropathy (hematuria, protein urea and progressive renal dysfunction) o Intracranial hemorrhage. o Aortic dissection. o Preeclampsia / eclampsia. o Pulmonary edema. o Unstable angina and myocardial infarction. This require reduction of BP within one hour to avoid risk of serious morbidity and death. Parenteral therapy is usually is required. o Inf. Isoket (isosorbide dinitrate) 2 10 mg/hr up to 20 mg/hr (amp 1mg/ml = 10mg in 10ml) titrate dose according to BP. o If BP 100, start nitroglycerine (nitronol) IV 100 200 g/min (10ml = 10mg, dilute in 90ml 5%D/W = 100ml). start at 60 micro drops/min and titrate. o Lasix (furosemide) 40 100 mg IV stat can be increased to 200 mg in subsequent doses. o Captopril 12.5 25 mg orally. o If BP is still high, Labetalol can be considered (20 40 mg given every 10 min to max 300 mg: 2 mg/min infusion). o For patients with refractory HTN and renal failure. Minixidil. Initial goal: Reduce pressure by no more than 25% within minutes to one to two hours and then toward a level of 160/100 with 2 6 hours. Avoid excessive reduction. Malignant Hypertension: Encephalopathy or nephropathy with accompanying papilledema. Treat as HTN emergency. o Give captopril 25mg oral stat monitor BP @ 15min intervals. o If no response (time depends on urgency / emergency), repeat captopril 25mg oral.
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o o o o
If no response, consider S/L adalat drops (4-6 only) avoid in heart failure. It may cause sudden fall in BP, so its use is not highly recommended. If no response, consider Inf. Isoket @ 4-6mg/hr (1 amp = 10 mg, 1 amp in peds chamber, 1mg = 10 drops) and titrate according to BP. If no response, consider tab. Prazosin (minipress) 1mg oral stat and strict bed rest. Get ECG. If patient drowsy or with fits consider HTN encephalopathy start inf. Mannitol 300cc IV stat in 10 min, use treatment as above to lower BP, to stop fits use diazepam. When BP comes to 160/100, patient can be discharged on oral treatment + diet advice + investigations urine R/E, electrolytes, serum Ca, fasting lipids. Stage 2 patient needs more than 1 drug.
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7: ACUTE RESPIRATORY DISTRESS SYNDROME Definition Acute respiratory distress syndrome (ARDS) Clinical = acute onset of severe hypoxemia refractory to O2 and diffuse bilateral pulmonary infiltrates Pathophysioloy = noncardiogenic pulmonary edema Pathological = diffuse alveolar damage American European Consensus Conference (1994): 4 criteria to define ARDS without biopsy Acute onset Bilateral patchy airspace disease PCWP < 18 mmHg or no clinical evidence of LVEDP PaO2 / FiO2 200 [if PaO2 / FiO2 300 acute lung injury (ALI)]
Direct injury Aspiration Pneumonia Near drowning Inhalation injury Pulmonary contusion Etiologies Indirect injury Sepsis Shock Trauma or multiple fractures Hypertransfusion {TRALI} DIC Pancreatitis
Pathopyhsiology intrapulmonary shunt ( ... refractory to FiO2) static compliance (VT / Pplat - PEEP) < 50cc / cmH2O Can develop 2o pulmonary hypertension
Diagnostic studies CXR: bilateral diffuse infiltrates developing within 24 hrs of initial appearance of air-space disease Chest CT: patchy infiltrates interspersed with normal appearing lung, with densities greater in dependant areas of lung Treatment Mechanical ventilation strategies Goals: maintain adequate systemic O2 delivery and minimize ventilator-induced lung injuries (namely: FiO2 0.60, alveolar over distension, tidal opening and collapse of alveoli)
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Strategies Sedation; paralysis if needed (but try to minimize) Improve PaO2 by PEEP and inspiratory time rather than by FiO2 Maintain plateau pressure (Pplat) 35 cm H2O: pressuretargeted ventilation, permissive hypercapnia (keep PaCO2 < 80 and pH > 7.15) Set PEEP > pressure required to prevent end-expiratory alveolar collapse (i.e. set a lower point of maximum curvature on pressure-volume curve or at 10-12 cm H2O and adjust empirically) o Rescue strategies Prone ventilation: 50-75% of patients improve with PaO2 Nitric oxide (inhaled): selective pulmonary vasodilatation in ventilated lung units improved V / Q matching, PA pressures, can PaO2 / FiO2 by 50 mmHg Extracorporeal membrane oxygenation (ECMO) or extracorporeal CO2 removal (ECCO2R) PCWP as low as tolerated Steroids: no benefit in the early phase; ? benefit in late fibroproliferative phase. If no improvement by the day 7 and no evdence of untreated infection (consider bronchscopy, blood, urine and central line tip cultures, sinus and abdominal CT scans), consider methylprednisolone 2 mg / kg / d in divided doses q 6 hrs X 14 days, followed by gradual taper. o
Prognosis Mortality: isolated ARDS = 40%, up to 90% if multiorgan system failure or sepsis.
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8: ACUTE SEVERE ASTHMA: EMERGENCY MANAGEMENT Patients with episodic history of SOB, previously diagnosed asthmatic. Signs of severity o Pulse > 120 b/m. o Respiratory rate 30. o Moderate to severe dyspnea. o Inability to complete one sentence in single breath. o Altered mentation (drowsy, confused patient). o Cyanosis. o Use of accessory muscles of respiration.
Treatment o Oxygen 40 60% (with mask @ 15 L/min oxygen flow) o Nebulize with ventolin soln (salbutamol 2.5 5 mg) q20 min until improvement or toxicity appears Ipratropium 500 g (0.5mg) via nebulizer or Salbutamol 10 15 mg continuously over an hour in severly obstructed adults. Or MDI with spacer device 6 12 puffs of salbutamol for initial therapy if nebulizer is not available. o Inj. Solucortef 250mg IV stat or prednisolone tablet 60 mg PO stat or methylprednisolone 40 60 mg IV q6h. If patient is not improving consider o Aminophylline IV [ECG monitoring, 250mg in 500ml of 0.9% saline, load with 5.6mg/kg (2.8 ml/kg) over 20 min followed by infusion 0.9 mg/kg/hr (0.45 ml/kg)]. Features of toxicity are nausea, vomiting and arrhythmias. Dont give if received oral theophylline or aminophylline in last 24 hours. o 5 mg salbutamol in 500 ml 0.9% saline, infuse at 3 20 g/min (18 ml/hr to 120 ml/hr) start at 5 g/min (30 ml/hr). o In rare case aqueous epinephrine 0.3 ml of 1:1000 solution SC q 20min up to 3 doses. EKG monitoring is necessary. Intubation and ventilation o Worsening hypoxia or hypercapnia, exhaustion or confusion, coma or respiratory arrest. o Chest X-RAY If H/O fever, heart disease, imunosuppressed, previous thoracic surgery, other pulmonary disease, suspicion of Pneumothorax or seizures.
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Admission o Keep low threshold for admission for recent hospitalization, o Failure of aggressive OPD therapy with oral steroids, o Previous life threatening attack (previous respiratory arrest) or intubations. o If PEEP is less than 50% of predicted PaCO242. o Response to initial treatment (60 90 min after three doses of a short acting bronchodialators) is a better predictor of the need for hospitalization than is the severity of an exacerbation.
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9: COPD ACUTE EXACERBATION o o o o o o o o o Dyspneic / cyanosed patients keep them propped up. Likely cause LRTI, other includes Pneumothorax, pulmonary embolism, poor drug compliance, IHD. O2 with nasal cannula / mask @ 3 4 L/min. Nebulize with ventolin solution 5mg repeat after 20 min. if no improvement. Inj. Hydrocortisone (250mg solucortef) IV stat then IV 100mg TDS for 24 hrs. If associated fever, purulent sputum or respiratory failure or pneumonia admit. Attach cardiac monitor, SPO2, take ECG, CXR send baseline labs & sputum R/E. Signs of respiratory failure bounding pulse, flaps, cyanosis, RR >30 with signs of RHF Give initial shots of antibiotics (even if no fever) Inj. Clarithromycin (klaracid) 500mg IV stat or Inj. Cefuroxime (zinacef) 750mg IV or tab erythrocin 500 mg P/O QID or tab augmentin 625 mg TID. Aminophylline IV [ECG monitoring, 250mg in 500ml of 0.9% saline, load with 5.6mg/kg (2.8 ml/kg) over 20 min followed by infusion 0.9 mg/kg/hr (0.45 ml/kg)]. Features of toxicity are nausea, vomiting and arrhythmias. Dont give if received oral theophylline or aminophylline in last 24 hours. Along with steroids, start tab. Terbutaline (Bricanyl) 2.5mg TDS, tab. Theophyline (Theograde) 350mg BD, Atem inhaler 2 puffs TDS, steam/ ventolin inhalation 6 hourly, inhaled steroid (Beclomethasone) 2 puffs QID. If worsening dyspnea despite treatment, SPO2 < 90%, RR >35, or < 14, intubate the patient and consider ventilatory support.
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10: GASTROINTESTINAL BLEEDING Intraluminal blood loss anywhere from the oropharynx to the anus Classification: Upper = above the ligament of Treitz; lower = below the ligament of Treitz Signs: Hematemesis = blood in vomitus (UGIB); hematochezia = bloody stools (LGIB or rapid UGIB); melena = black, tarry stools from digested blood (usually UGIB, but can be anywhere above cecum) Etiologies of upper GI bleed (UGIB) Oropharyngeal bleeding and epistaxis swallowed blood Erosive esophagitis Immunocompetent host: GERD/Barretts esophagus, XRT immunocompromised: CMV, HSV, Candida Varices (l0%) Mallory-Weiss tear (7%; GE junction tear due to retching / vomiting against closed glottis) Gastritis/gastropathy (23%; NSAIDs, H. pylori, alcohol, stress-related mucosal disease) Peptic ulcer disease (PUD) (46%) Vascular malformations Dieulafoys lesion (superficial ectatic artery usually in cardia w/ sudden, massive UGlB) AVMs (isolated or with Osler-Weber-Rendu syndrome) aorto-enteric fistula (aortic graft erodes to 3rd portion duodenum; presents with herald bleed) Neoplastic disease (esophageal or gastric) Other causes: hiatal hernia ulcerations; coagulopathy; amyloidosis; connective tissue disease Etiologies of lower Gl bleed (LGIB) Diverticular disease Angiodysplasia Neoplastic disease Colitis: infection, ischemic, radiation, inflammatory bowel disease (UC >> CD) Hemorrhoids Anal Fissure Clinical manifestations UGIB > LGIB: nausea, vomiting, hematemesis, coffee-ground emesis, epigastric pain, vasovagal reactions, syncope, melena.
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LGIB > UGIB: diarrhea, tenesmus, fresh bleeding P/R or maroon stools Workup History Acute or chronic GIB, number of episodes, most recent episode Hematemesis, vomiting prior to hematemesis, hematochezia, melena, abdominal pain, diarrhea Use of aspirin, NSAIDs, or anticoagulants, or known coagulopathy Alcohol abuse, cirrhosis Prior GI or aortic surgery Physical exam Vital Signs: tachycardia at 10% volume loss; orthostatic hypotension at 20% loss; shock at 30% loss, pallor, telangectasias (alcohol liver disease or Osler-Weber-Rendu syndrome) Signs of chronic liver disease: jaundice, spider angiomata, gynecomastia, testicular atrophy, palmar erythema, caput medusae Abdominal exam: localized tenderness or peritoneal signs Rectal exam: appearance of stools, presence of hemorrhoids or anal fissures Laboratory studies: Hct (may be normal early in acute blood loss before equilibration), platelet count, PT, APTT, BUN/Cr ( ratio in UGIB due to GI resorption of blood or prerenal azotemia), LFTs Nasogastric tube: can diagnose UGIB, remove GI contents (prior to EGD and to prevent aspiration), lavage to see if persistent bleeding (worse prognosis); false negative in setting of UGIB if bleeding is either duodenal or intermittent Diagnostic studies in UGIB: esophagogastroduodenoscopy (EGD) Diagnostic studies in LGIB: (r/o UGIB before attempting to localize presumed LGIB) Bleeding spontaneously stops colonoscopy (identify cause in > 70% and potentially therapeutic) Stable but continued bleeding bleeding scan (99mTc-tagged RBC / albumin): detects bleeding rates 0.1 1.0 ml/min, but accurate localization difficult Unstable arteriography (detects bleeding rates 0.5 1.0 ml/min and potentially therapeutic); intraarterial vasopressin infusion or embolization Exploratory laparotomy
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Treatment The acute treatment of GI bleeding is hemodynamic resuscitation with IV fluid and blood Establish access with 2 large-bore (18 gauge or larger) intravenous lines Volume resuscitation with normal saline or lactated Ringers solution Transfusion therapy (blood bank sample for type & cross; can use Onegative blood if exsanguinating Identify and correct coagulopathies (FFP to normalize PT, platelets to keep count >50,000 / mm3) Nasogastric tube lavage Airway management as needed Consult GI and surgical services as needed
Etiology Varices Options Pharmacologic Octreotide 50g IVB 50g / hr infusion Vasopressin or vasopressin + nitroglycerin (less effective & more complications ? -blockers (non selective) & nitrates when hemodynamically stable Non-pharmacologic Endoscopic sclerotherapy (88% success) or band ligation (> 90% success) Octreotide + endoscopic therapy (> 95% success) Balloon temponade if bleeding is severe Embolization or TIPS if endoscopic therapy fails Pharmacologic Proton pump inhibitors ? Octreotide 50g IVB 50g / hr infusion Non-pharmacologic Endoscopic therapy (injections, thermal contact, laser) Mesenteric arteriography with infusion of vasopressin or embolization Gastric resection if endoscopic and pharmacologic therapy fails Usually stops spontaneously Proton pump inhibitors, H2-antagonists Usually stops spontaneously Endoscopic therapy, arterial vasopressin or embolization, surgery Arterial vasopressin, endoscopic therapy, surgery
PUD
Mallory-Weiss Esophagitis Gastritis Diverticular disease Angiodysplasia
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Poor prognostic sign in UGIB Demographic age > 60, co-morbidities Severity: bright red blood in NGT aspirate, transfusion requirement, hemodynamic instability Etiology: variceal or neoplastic oozing
Appearance of ulcer (from best to worse prognosis): clean base without visible vessel adherent clot active bleeding.
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11: VARICEAL BLEEDING o o o o o IV lines both arms, start IV N/S at rate depending on condition. Send all baseline investigations (serum electrolytes, PT/APTT, Hb, etc) plus blood group and cross match. Arrange for blood / FFPs if PT prolonged, discontinue anticoagulation. Consider giving vitamin K by slow IV infusion. Inj. Sandostatin 50g IV stat, then inf. Sandostatin @ 50g/hr for atleast 48 72 hours ---- OR-----Inj. Novapressin / Terlipressin (1 mg ampule) 2 mg IV stat followed by 1 mg 06 hourly for 72 hours (only caution of old age and IHD). For acid neutralization, inj. Omeprazole 40 mg IV daily infusion. Thiamine 100 mg IV (inj. Benerva) to alcoholics. Pass NGT and start stomach wash with D/W. If bleeding stops, keep on monitoring for pulse and NG bleed one hourly. If bleeding wont stop, pass Sangstakens Tube. Before passing check both balloons with air. Catheterize if in hypotension. Maintain vitals and output monitoring charts preferably in ICU. Urgent endoscopy if possible. Syp. Lactulose 30 cc TID (Detoxicol, Lilac, Duphalac).
o o o o o o o o o
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12: MESENTERIC ISCHEMIA Etiologies of acute small bowel ischemia Arterial embolism (50%): from LA (AF) or LV ( EF) Arterial thrombosis (20%): usually at site of pre-existing atherosclerosis, often at origin of artery Non-occlusive mesenteric ischemia (20%): low cardiac output high doses of -adrenergic agents Venous thrombosis (10%): hypercoagulable states, portal hypertension, malignancy, inflammation (pancreatitis, peritonititis), trauma, surgery Ischemic colitis Non-occlusive, with tow cardiac output superimposed on pre-existing atherosclerosis Clinical manifestations History of signs of chronic mesenteric ischemia: postprandial periumbilical pain, early satiety Acute: sudden onset of abdominal pain out of proportion to abdominal tenderness on exam Subacute: gradual onset of nausea, vomiting, anorexia, bowel habits GIB Physical exam May be unremarkable Mesenteric infarction suggested by abdominal tenderness peritoneal sign distension, absent bowel sounds, exquisite tenderness, + FOBT Diagnostic studies Laboratory evaluation: WBC; amylase, LDH and CPK; metabolic acidosis and lactate (late) Imaging studies o plain radiograph: adynamic ileus o doppler U/S (often difficult because of bowel distention): may show abnormal mesenteric flow o abdominal CT: bowel wall thickening, pneumatosis of bowel wall o angiography: gold standard
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Treatment Volume repletion and optimization of hemodynamics, discontinue adrenergic agents if possible Antibiotics Intra-arterial infusions of thrombolytic agent for acute arterial embolism Anticoagulation for venous thrombosis Intra-arterial infusion of papaverine for non-occlusive mesenteric ischemia Surgery: embolectomy for acute arterial embolism; intestinal resection for mesenteric infarction
Prognosis Mortality 20-70%
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13: ACUTE LIVER FAILURE Definition Acute hepatic disease + coagulapathy + encephalopathy Fulminant = develops within 8 weeks; subfulminant= develops between 8 weeks and 6 months. Etiology Viral (~60%) HAV (0.35% of acute infections), HBV (1%), HCV (<<1%), HDV + HBV (10%), HEV (if pregnant) HSV (immunocompromised hosts), EBV, CMV, adenovirus, paramyxovirus, parvovirus B19. Drug/Toxins (~20%) Acetaminophen Other drugs phentoin, INH, rifampin, sulfonamides,. Tetracycline, amiodarone, prophylthiouracil toxins: fluorinated hydrocarbons, CCI4 Amanita phalloides. Vascular: ischemic hepatitis, Budd-Chiari syndrome, hepatic VOD, malignant infiltration Autoimmune hepatitis Miscellaneous: Wilsons disease, acute fatty liver of pregnancy, HELLP syndrome, Reyes syndrome Idiopathic (~20%) Clinical Manifestations Neurologic o Asterixis o Encephalopathy: stage I = MS: stage II = lethargy, confusion; stage III = stupor; stage IV = coma cerebral edema Cushings reflex (hypertension + bradycardia), pupillary dilatation, decerebrate posturing, apnea. Cardiovascular: hypotension with low SVR Pulmonary: respiratory alkalosis, impaired peripheral O2 uptake, ARDS. Gastrointestinal: GIB, pancreatitis Renal: ATN, hepatorenal syndrome, hyponatremia, hypokalemia, hypophosphatemia Hematology: coagulopathy (due to synthesis of clotting factors DIC) Infection: seen in 90% of patients; SBP in 32% of patients; fever and leukocytosis may be absent Endocrine : hypoglycemia
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Workup Viral serologies Toxicology screen (acetaminophen levels q 1-2 hr until peak determined) Imaging studies (RUQ U/S or abdominal CT, Doppler studies of portal and hepatic veins) Other tests: autoimmune serologies, ceruloplasmin and urine copper Liver biopsy (unless precluded by coagulopathy) Treatment ICU-level care potentially including monitoring and treating ICP, hemodynamic and ventilatory support, reversing coagulopathies, aggressive monitoring for and treatment of infection, D10 drip hypoglycemia, etc. Treatment of specific causes (N-acetylcysteine for acetaminophen, corticosteroids for autoimmune hepatitis, chelation therapy for Wislons disease, etc.) Liver transplantation if poor prognosis (see below) Prognosis Survival 10-50% Predictors of poor outcome (Gastroenterology 97:439, 1989) age > 40; cause other than acetaminophen, HAV and HBV grade III or IV encephalopathy (onset > 7 days after onset of jaundice), PT > 50, bilirubin > 17.5. Liver transplantation 1-year survival rate > 60%
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14: ACUTE PANCREATITIS Etiologies Common: alcohol and gallstones Rare Obstructive (ampullary or pancreatic tumors, pancreas divisum with stenosis of minor papilla) Metabolic (hypertriglyceridemia, hypercalcemia) Drugs (furosemide, thiazides, sulfa, didanosine, protease inhibitors, estrogen, azathioprine) Infection (echovirus, Coxsackie virus, mumps, rubella, EBV, CMV, HIV, HAV, HBV) Trauma (blunt abdominal trauma, post ERCP) Scorpion sting (in Trinidad) Clinical Manifestations Mid epigastric abdominal pain, radiating to the back relieved by sitting forward Nausea and vomiting Fever Physical Exam Abdominal tenderness and guarding, bowel sound (adynamic ileus), palpable abdominal mass If severe: Cullens (Periumbilical) or Grey Turners (flank) signs of retroperitoneal hemorrhage Hypotension or shock Diagnostic Studies Laboratory: amylase and lipase: depending on severing: WBC, Hct, BUN, Ca, glucose LFTs Imaging studies: abdominal CT modality of choice (but may appear normal in up to 28% of mild cases) rapid injection of IV contrast (dynamic CT) to assess integrity of microcirculation & detect necrosis may show calcifications if chronic pancreatitis. CT- guided abscess drainage or fine-needle aspiration of pancreatic necrosis may show calcification if chronic pancreatitis. Endoscopic retrograde cholangiopancreatography (ERCP): generally not indicated except in gallstone pancreatitis with biliary obstruction (see below)
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Treatment Supportive therapy Fluid rescitation (may need up to 10L/day if haemodynamically severe pancreatitis) Analgesia with meperidine Electrolyte repletion Rest the pancreas: NPO; NG suction if protracted nausea and vomiting; ? octreotide in severe cases Antibiotics: Imipenem in patients with necrosis ERCP if gallstone pancreatitis with biliary obstruction Complications Systemic: shock, ARDS, renal failure, GI hemorrhage Metabolic hypocalcemia, hyperglycemia, hypertriglyceridemia Pseudocyst (10-20%) Suggested by persistent pain or persistent elevation of amylase or lipase most resolve spontaneously; if persist. 6 weeks and with pain internal or percutaneous drainage Pancreatic necrosis: treat conservatively for as long as possible; surgery if patient remains unstable Infection(5%); fever and WBC Pancreatic abscess: antibiotics + drainage (CT-guided if possible) Infected pancreatic necrosis (aspiration + bacterial culture): antibiotics + surgical debridment (100%) mortality without extensive debridment) Pancreatic ascites or pleural effusion: indicates disrupted pancreatic duct; consider ERCP with stent placement across duct.
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15: ACUTE STROKE The diagnosis is usually easy when there is a clear history of abrupt onset of symptoms with an expected constellation of neurological signs. The site of the stroke can be diagnosed with good accuracy from clinical findings in a patient with no previous neurological deficit. Clerking should be done in the stroke proforma and need not be repeated in freetext notes, unavailable information can be added later Differential Diagnosis These should be considered when the history is unclear, there are limited risk factors for stroke as in a young patient, or physical findings are not consistent. Space-occupying lesion such as neoplasm, subdural haematoma or abscess if history is protracted. Also consider normal pressure hydrocephalus. Encephalitis/encephalomyelitis if signs of general cerebral irritability associated with fever. Subarachnoid haemorrhage in patient with headache and/or depressed conscious level at presentation. Localising signs less likely with this diagnosis. Trauma - usually obvious. Acute demyelination may be more likely in a younger patient. Cerebral vasculitis may be suspected depending on concomitant findings in rare cases. Initial Management Assess conscious level Assess adequacy of swallow if GCS 15/15 (fill in swallowing proforma) Check for signs of aspiration Patients must have continuous pulse oximetry recording immediately upon admission and for at least 24 hours if immobile. Inspired oxygen should be given if saturations fall below 95%. Low oxygen saturations should alert you to poor postural position, chest infection and aspiration. Check for pressure areas and skin breakdown. Patient will need regular turning and nursed on appropriate mattress if immobilized; i.e. not on A&E trolley! If possible perform 10 point standard abbreviated mental test score. Ensure adequate hydration with intravenous fluids if oral route not possible for sufficient intake.
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Do not insert a urinary catheter immediately if patient is incontinent since continence may be rapidly regained if neurological recovery is rapid. The need for a catheter should subsequently be reviewed daily depending on degree of incontinence, mobility and state of local skin. Speak to patient and family to explain what has happened. At early stage be guarded about prognosis which is variable. Pyrexia following stroke is associated with poor outcome. If temperature rises above 37C give paracetamol 1 gram four times daily by mouth or rectally and signs of infection treated at the earliest opportunity.
Investigations ECG - in particular to screen for atrial fibrillation FBC, U&Es, Creatinine, Albumin, Lipid profile, TSH Glucose a high blood glucose in a diabetic may require pre-meal Actrapid insulin or an intravenous infusion if this is not practical Thrombophilia screen in young patients CXR a department view the following day may be best waited for unless aspiration pneumonia suspected (or other pathology) CT scan of brain - perform as early as possible; 48 hours post stroke maximum acceptable period. This is to exclude hemorrhage, not to locate infarct. Basic Pharmacological Management If CT shows no hemorrhage give stat dose of aspirin 300mg by mouth or rectally if oral route not available, then 75-150mg daily. If hemorrhagic transformation in a primarily ischemic stroke is diagnosed withhold aspirin for 14 days. Anticoagulation with heparin or warfarin should not be undertaken routinely for at least 2 weeks, even if patient is in atrial fibrillation. This is because of increased risk of hemorrhagic stroke. The exception to this rule is the development of above-knee DVT or PE. All patients should have above-knee compression stockings fitted while immobile, unless contra-indicated by peripheral vascular disease, cutaneous ulceration or cellulitis. Thrombolysis is not indicated for ischemic stroke although future trials may identify situations where it could be of benefit. If aspirin is contra-indicated consider use of clopidogrel 75mg daily or dipyridamole MR 200mg twice daily. For recurrent cerebral ischemic events in a patient already on aspirin, dipyridamole MR 200mg twice daily may be added to the aspirin.
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Dexamethasone 4mg IV three times daily can be used when an infarct shows mass effect with midline shift on CT scan and patient is making poor progress. Antihypertensive treatment should not be initiated until 10 - 14 days have elapsed following the stroke unless malignant hypertension is present. If a patient is already on antihypertensives these should be continued unchanged, although it may be preferable to convert any short-acting preparations to a once daily drug in the same class to avoid large blood pressure fluctuations.
Primary Intracerebral Haemorrhage Management is as above except that anti-platelet and anticoagulant drugs are contra-indicated. Surgical intervention is only warranted acutely in posterior fossa bleeds when advice should be sought from the neurosurgical team at Hurstwood Park. In supratentorial bleeds when coma is deepening, cerebral edema and midline shift are present, IV mannitol 10% l00ml and IV dexamethasone 4mg can be considered, but prognosis will always be very poor at this stage. Subarachnoid Haemorrhage This is now not classified as stroke. It is usually a primary event due to rupture of a berry aneurysm but also can be found after cranial trauma. When the diagnosis is suspected a CT scan should be performed immediately to maximize sensitivity. If the scan is normal the CSF should be examined for red cells and xanthochromia, although the latter may not be evident for 48 hours. Magnetic resonance angiography should not be performed if these investigations are negative. When a positive diagnosis is made administer nimodipine 60mg every 4 hours for 3 weeks by mouth or nasogastric tube. The neurosurgical team at the hospital should be contacted immediately for consideration of angiography and surgery depending on the overall clinical condition. If a previously stable patient has a falling coma score, CT scanning should be repeated to look for rebleed or development of obstructive hydrocephalus that may need shunting.
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16: ACUTE BACTERIAL MENINGITIS Definition Bacterial infection of the subarachnoid space
Microbiology in Adult Meningitis Etiology S. pneumoniae (30-50%) N. meningitides (l035%) Comments Most common cause in adults. Look for distant infection (e.g., Oslers triad = meningitis, pneumonia, endocarditis). Primarily in children and young adults; may be associated with petechial or purpuric rash. Deficiencies in terminal complement components predispose to recurrent meningococcemia, and rarely, meningitis. incidence in children because of H. influenzae type b vaccine. Look for predisposing factors in adults (e.g., CSF leak, recent neurosurgical procedure, trauma, mastoiditis). Seen in elderly, alcoholics, or patients with malignancy, immunosuppression, or iron overload. Outbreaks associated with contaminated milk, cheese, cole slaw, raw vegetables. Despite name, often associated with poly-predominant pleocytosis. Usually nosocomial or post-procedure or in elderly or immunocompromised. Seen with indwelling CSF shunt ( S. epidermidis) or following neurosurgery or head trauma (S. aureus). Suspect parameningeal focus.
H. influenzae (<5%)
L. monocytogenes (5lO%) GNRs (l-lO%) Syaphylococci (5%) Mixed infection
Clinical manifestations Fever (95%) Headache, stiff neck (88%), and photosensitivity MS (80%) including delirium, decreased consciousness, confusion, lethargy; seizures Presentation may be atypical in elderly patients, with primary lethargy and confusion, and no fever Physical Exam Neck stiffness, Kernigs sign (patient supine, with hip flexed at 900, and knee flexed at 900; + if passive extension of knee results in resistance); Brudzinskis sign (patient supine and limbs supine; + if passive neck flexion involuntary hip and / or knee flexion); note, Kernigs and Brudzinskis signs + in only ~ 50% of patients Focal neurologic findings (hemiparesis, aphasia, visual field cuts, cranial nerve palsies)
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Papilledema Rash: macular-papular, petechial, or purpuric Diagnostic studies Lumbar puncture: CSF gram stain has 60-90% senstivity. And culture has 70-85% senstivity. Consider head CT prior to LP if focal neurologic findings, papilledema, or comatose patient opening pressure >45cm carries risk of herniation, ... remove only CSF in manometer and infuse IV mannitol 20% solution (0.25-0.5 g/kg) once 25-30 min
CSF Findings in Meningitis Pressure Condition Appearance (cm) Normal clear 9-18 lymphs 100-10,000 Bacterial cloudy 18-30 polys <500 TB cloudy 18-30 lymphs <300 Fungal cloudy 18-30 lymphs <300 Aseptic clear 9-18 polys lymphs 50-100 50-100 < 45 40-300 < 45 100-200 < 45 1000 100(predom type) 0-5 50-75 15-45 (mg/dl) (mg/dl) WBC/mm Glc TP
Additional CSF studies depending on clinicsl suspicion: acid-fast smear and culture, India ink preparation, cryptococcal antigen (CRAG), fungal culture, PCR (e.g. of HSV); agglutination assays questionable utility Bland cultures
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Clinical scenario Normal adult
Treatment of Meningitis Empiric treatment guidelines Ceftriaxone 2g IV q 12hrs or cefotaxime 1g IV q 4-6 hrs + Vancomycin 1g IV q 12hrs (in case cephalosporinresistant Pneumococcus) + Ampicillin 2 g IV q 4 hrs if suspect Listeria Chloramphenicol + TMP/SMX + vancomycin if -lactam allergic
ImmunoAmpicillin + ceftazidime vancomycin compromised CSF shunts, recent neurosurgery, head Vancomycin + ceftazidime trauma Empiric antibiotics should be started as soon as possible. It concerned about ICP, then obtain BCx start empiric antibiotics obtain head CT LP (if not contraindicated); yield of CSF fluid unlikely to be changed if obtained within ~ 4 hours of initiation of antibiotics. Corticosteroids: no convincing evidence for routine use in adults. However, if ICP, cerebral edema, stupor or coma, consider dexamethasone 1g IV q 6 hrs X 4 d. Prophylaxis: rifampin (600mg PO bid X 2d) or ciprofloxacin (500mg PO X 1) for close contacts of patient with meningococcal meningitis.
Prognosis In-hospital mortality 25% for community-acquired meningitis and 35% for nosocomial meningitis
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17: ASEPTIC MENINGITIS Definition Negative bacterial microbiologic data, CSF pleocytosis without poly predominance Misnomer as aseptic only in sense that less likely to be acute bacterial meningitis, but can be due to both infectious and noninfectious etiologies Etiologies Viral: enteroviruses, HIV, HSV (type 2 more common than I), mumps, lymphocytic choriomeningitis virus, encephalitis viruses (e.g., Eastern, Western, St Louis, California), adenovirus, CMV, EBV Tuberculosis, fungal, spirochetal (Lyme disease, syphilis, leptospirosis), rickettsial, Coxiella, Ehrlichia Partially treated bacterial meningitis Parameningeal focus of infection (e.g., brain abscess, epidural abscess, septic thrombophlebitis of dural venous sinuses, or subdural empyema) Medications: TMP/SMX, NSAIDs, penicillin, isoniazid Systemic illness: SLE, sarcoidosis, Behcets, sjogrens syndrome, rheumatoid arthritis Neoplasms: intracranial carcinomatous meningitis tumors (or cysts), lymphomatous or
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18: STATUS EPILEPTICUS Prodromal Stage In patients with pre-existing epilepsy, status is often preceeded by a prodromal stage. Urgent drug treatment will usually prevent evolution to true status. ONE of the following drug treatments can be used: Diazepam IV 10 - 20mg IV at a maximum rate of 2mg/minute OR Diazepam 10 - 20mg rectally OR Midazolam 10mg IM Early Status - within first 10 minutes Assess cardiorespiratory function, secure airway and resuscitate when necessary. Administer oxygen. Have ventilation facilities available ie. Ambubag. Insert IV lines for fluid and drug administration - do not mix drugs in a single line. Estimate blood glucose using Advantage 2 blood glucose sticks. When in doubt about diagnosis or blood glucose reading is low, give IV thiamine as Pabrinex IV High Potency (1 pair). If hypoglycemic give 50 l00ml glucose 20%. Repeat as necessary. Give lorazepam 4mg IV bolus dose, repeated once after 15 minutes if necessary. In the elderly 2mg may be sufficient. 0-30 minutes Institute regular monitoring (neurological, pulse, BP, ECG). Take blood for: U&Es, glucose, Ca2, LFTs, FBC & clotting, anticonvulsant levels. If seizures continue give ONE of the following anticonvulsant drugs: Phenytoin IV infusion 15mg/kg at a maximum rate of 50mg/min (average adult dose of about 1000mg over at least 20 minutes) with ECG and BP monitoring OR Phenobarbitone IV infusion 10mg/kg at a maximum rate of 100mg/min (average adult dose of about 700mg given over 7 minutes) Establish etiology: If there is a prior history of epilepsy, status is often due to drug withdrawal or reduction. If this is the case, the drug should be reintroduced as quickly as possible. If no previous history of epilepsy, status is likely to be due to an acute brain event. CT and CSF examinations are often necessary.
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30 - 60 minutes If seizures continue consult a neurologist. The patient must be transferred to an intensive care unit. Establish intensive monitoring and give pressor therapy as appropriate. Establish EEG monitoring, as in some patients motor activity may be barely visible. Aim to control cerebral seizure activity, NOT the outward manifestation of seizures. Intracranial pressure monitoring is advisable in a few cases. Refractory status epilepticus (after 60 - 90 minutes) If seizures continue despite the above measures, general anesthesia should be instituted under consultant anesthetist and consultant neurologist supervision. Thiopentone 100 - 250mg IV bolus over 20 seconds then further boluses every 2 - 3 minutes until seizures are controlled. Then give infusion to maintain anesthesia at the level of burst suppression (usually 3 - 5mg/kg/hr) OR Propofol 2mg/kg IV bolus repeated as necessary followed by a continuous infusion of 5 - 10mg/kg/hr initially, and then reducing to 1 - 3 mg/kg/hr to maintain anesthesia at the level of burst suppression. Anesthesia should be continued for 12 hours and then gradually reversed. If seizures recur, anesthesia should be re-instated for 24 hours and then gradually reversed. This cycle should be repeated until seizures are controlled. Common Reasons for Failure of Emergency Drug Treatment Inadequate emergency epileptic drug therapy (especially the administration of too low a dose). Failure to initiate maintenance anti-epileptic drug therapy (seizure will recur as the effect of emergency therapy wears off). Hypoxia, hypotension, cardiorespiratory failure, metabolic disturbance. Failure to treat underlying cause. Failure to identify medical complications (e.g. hyperthermia, DIC, hepatic failure etc.) Mis-diagnosis (pseudo status as common as epileptic status in specialist practice.)
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19: ACUTE RENAL FAILURE (ARF) Definition Acute (over hours or days) deterioration in renal function, characterized by a rise in serum creatinine and urea, often with oliguric or anuria. Causes 1. Hypovolemia. 2. Low cardiac output. 3. Sepsis. 4. Drugs Obstruction. 5. Other eg. hepatorenal syndrome, vasculitis. Investigations 1. U&E, Ca2+, PO43-, CBC, ESR, CRP, INR, LFT, CK, LDH, protein elctrophoresis, hepatitis serology, auto antibodies and blood cultures. 2. Urgent urine microscopy and culture. White cell casts suggest infection, but are seen in interstitial nephritis, and red cell casts an inflammatory glomerular condition. 3. USG of the renal tract. 4. ECG, CXR. Management 1. Treat precipitating cause. Treat acute blood loss with blood transfusion, and sepsis with antibiotics. ARF is often associated with other diseases that need more urgent treatment. For example, someone in respiratory failure and renal failure may need to be managed on ITU, not a renal unit , to ensure optimal management of the respiratory failure. 2. Treat life-threatening hyperkalemia. 3. Treat pulmonary edema, pericarditis and temponade. Urgent dialysis may be needed. If in pulmonary edema and no diuresis, consider removing a unit of blood, before dialysis commences. 4. Treat volume depletion. Resuscitate quickly; than match input to output. Use a large-bore line in a large vein (central vein access can be risky in obvious volume depletion). 5. Treat sepsis. 6. Further care. Has obstruction been excluded? Examine for masses PR and per vaginum; arrange urgent ultrasound; is the bladder palpable? Bilateral nephrostomies relieve obstruction, provide urine for culture, and allow anterograde pyelography to determine the site of obstruction.
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If worsening renal function but dialysis independent, consider renal biopsy. Diet: high in calories (2000-4000kcal/d) with adequate highquality protein, consider nasogastric feeding or parenteral route if too ill.
Prognosis Depends on cause (ATN mortality: surgery or trauma 60%, medical illness 30%, pregnancy 10%). Oliguric ARF is worse than non-oliguric more GI bleeds, sepsis, acidosis, and higher mortality. Urgent dialysis if: K+ persistently high (>6.0mmol/L). Acidosis (pH <7.2). Pulmonary edema and no substantial diuresis. Pericarditis. (In temponade, only dialyze after pressure on the heart is relieved). High catabolic state with rapidly progressive renal failure. Management
Cat heteri ze to asses s hour ly uri ne ou tput, and e stabli sh flui d cha rts Ass ess intravas cular volume, BP, JVP, skin turgor, fluid bal ance sheet, weigh t, CV P, at tach t o card iac monito r Co nside r i nse rting a cent ral venous cannula Inve stigat ions Ide ntify and treat hyperkalemi a Use a ca rdiac monit or If dehydra ted Fluid chall enge: 250500ml of c olloid or sa line o ver 30 min Re assess Repea chall enge i f still dehy drate d. Aim for a CVP of 5 -10cm t Once fluid replet e, con tinue fluids at 2 0ml + pre ous hours urine output per hour vi If volume overl oaded , consider urgent dialy sis A n itrate infusion, fu rosem ide or re na dose d opam ine m ay he lp in t he sh ort l term, especi ally t o mak e spa ce for bloo d tran sfusion etc . but doe n ot alt er out come s Correc t aci dosis with sodium bic bonat e, eg 50ml of 8.4 % IV ar If clinic al suspicion of se psis, take c ultur es, the n tre at vig orously D o not leave poss ible source of se psis (eg. IV line s) in situ if not ne eded Avoid neph rotoxi c drugs, eg. NSA IDs, care w ith g entam icin. Che k D a She et for c at all dr ugs given
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20: DIABETIC KETOACIDOSIS o o o o o o Hyperglycemia > 300 or may be lower, anion gap metabolic acidosis, positive serum ketones. Always suspect when patient is drowsy, hyperventilating, dehydrated even with no history of DM. Maintain IV lines on both arms ideally CVP line. Start IV N/S 1L in 1/2 hr 1L in 1 hr 1L in 2 hrs 1L in 4 hrs 1L in 6 hrs (300-500 ml/hr). Send all investigations Na / K / Cl / HCO3, ketones, RBS, urea, urine R/E, ABGs calculate anion gap (Na [HCO3 + Cl]), ECG. Change in 5% D/W if RBS ~ 250 mg Given inf. KCl (2 amp) if hypokalemia / normal potassium (3.5 4.5 add 20 mmol/L and if less than 3.5 add 40 mmol/L. Give regular insulin 20U IV stat if RBS > 450 followed by 6 U IM hourly (goal is to decrease glucose by 80 mg/hr) when RBS ~ 250, shift to 4 units IM hourly till clinical condition improves, anion gap reverses and ketones become normal. If no response in RBS in 2 hours, double the dose of insulin given. RBS hourly, serum electrolytes / serum ketones 4 hourly. Give broad spectrum antibiotics (Ampicillin, Flagyl, and cefotaxime). Maintain hourly monitoring charts for vitals, insulin, intake / output, electrolytes, clinical condition. Once out of DKA (normal anion gap, normal ketones) start regular Insulin at 2/3 of total dose required to treat DKA and adjust dose according to glucose level.
o o o o o
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21: HYPEROSMOLAR NONKETOTIC COMA (HONC) Definition Extreme hyperglycemia without ketoacidosis + hyperosmolality + MS Precipitants Same as for DKA + dehydration and renal failure. More likely in HONC than in DKA to have severe underlying precipitant. Pathophysiology Occurs in type 2 diabetics Hyperglycemia osmotic diuresis azotemia glucose, etc Clinical Manifestations Dehydration and MS Diagnostic Studies serum glucose (usually > 600 mg/dl) serum osmolality (usually > 350 mOsm/L) No ketoacidosis BUN and Cr; Na may be , , or normal depending on degree of hyperglycemia and degree of dehydration Treatment (always rule-out possible precipitants) Aggressive hydration: either NS or NS depending on degrees of volume and fee H2O depletion Low-dose insulin (e.g. 0.05 U/kg/hr)
dehydration
prerenal
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22: HYPOKALEMIA Workup Rule-out transcellular shifts: alkalemia, insulin, catecholamines, hypokalemic periodic paralysis Determine whether potassium depletion is due to GI (Uk < 15 mEq/L) or renal (Uk >15 mEq/L) losses If renal losses, determine BP and acid-base status GI losses (Uk >25 mEq/d or 15 mEq/L) GI losses plus acidosis: diarrhea laxative abuse, villous adenoma Vomiting and NGT drainage usually manifests as renal losses due to aldosterone and met. alk Renal losses (Uk >30 mEq/d or l5 mEq/L) Hypo-or normotensive o acidosis: DKA, RTA o variable acid-base: Mg depletion (mechanism unclear) o alkalosis: diuretics, vomiting / NGT drainage, Bartters syndrome (loop of Henle dysfunction = effects of furosemide), Gitelmans syndrome (distal convoluted tubule dysfunction = effect of thiazide) Hypertensive o primary hyperaldosteronism (Conns syndrome) o secondary hyperaldosteronism (i.e., high renin states): renal artery stenosis, renin-secreting tumors o pseudohyperaldosteronism: licorice ingestion, Cushings syndrome, Liddles syndrome Clinical manifestation Nausea, vomiting, weakness, muscle cramps ECG: U waves, QT interval, AV block, ventricular ectopics (PVCs, VT, VF) Treatment Potassium depletion ( 1 mEq/L = 200 mEq total body loss): KCL 40 mEq PO q 4-6 hrs for non-urgent cases, KCL 10-20 mEq / hr IV for urgent cases, recheck K frequently Treat underlying cause (if need hydration, avoid dextrose-containing solutions as dextrose insulin intracellular potassium shift) Repeat Mg as necessary
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23: HYPERKALEMIA The danger is ventricular fibrillation. A K+ >6.5mmol/L will usually require urgent treatment, as will those with ECG changes: Tall tented T-waves flat p-waves increased P-R interval. Widening of the QRS complex leading eventually, and dangerously, to a sinusoidal pattern and VF/VT. Workup Rule-out transcellular shifts: acidosis, -blockers, insulin deficiency (untreated IDDM), digoxin intoxication, massive cellular necrosis, hyperkalemic periodic paralysis Determine whether severely decreased GFR or normal GFR If normal GFR, determine why there is effective aldosterone function Decreased GFR Any cause of oligo- or anuric acute renal failure or any cause of endstage renal disease Normal GFR (i.e., hypoaldosteronisms) Hyporeninemic (i.e. type IV RTA usually secondary to diabetic nephropathy, ACEI, NSAIDs) Primary adrenal: Addisons disease, congenital adrenal hyperplasia, heparin Renal tubular disorder: K-sparing diuretics, cyclosporine, SLE, multiple myeloma, amyloid Clinical manifestations Weakness ECC: peaked T waves, PR interval, QRS width, sine wave pattern, EMD Treatment 10ml calcium gluconate (10%) IV over 2min, repeated as necessary if severe ECG changes (may cause skin necrosis if extravasation: avoid injecting into small peripheral cannulae). This provides cardioprotection; it does not change serum potassium levels. Insulin + glucose, eg. 20 U soluble insulin + 50 mL of glucose 50% IV. Insulin moves K+ into cells. Nebulized salbutamol (2.5 mg) also makes potassium enter cells. Polystyrene sulfonate resin (e.g. calcium resonium, 15 gm per 8 hr in water) orally or if vomiting makes the PO route problematic, as a
51
30g enema (followed by colonic irrigation, after 9h, to remove K+ from the colon). Dialysis.
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24: HYPOCALCEMIA
Category Hypoparathyroidism Etiologies Isolated PGA type I (chronic mucocutan. candidiasis + hypoparathyroid + Addisons) s/p thyroidectomy, hypomagnesemia ( secretion and effect) PTH end-organ resistance (... serum PTH) + skeletal abnorm. & retardation (Pseudopseudohypoparathyroidism = syndrome but normal Ca) l,25-(OH)2D3 production + PO4 calcium deposition in soft tissue Pancreatitis, citrate excess (e.g. after multiple blood transfusions)
Pseudohypoparathyroidism Vitamin D deficiency Renal failure Miscellaneous
Clinical manifestations Neuromuscular irritability: perioral parasthesias, cramps, & Chvosteks (tapping facial nerve contraction of facial muscles), + Trousseaus (inflation of BP cuff carpal spasm), laryngospasm. Irritability, depression, psychosis,) ICP, seizures QT Renal osteodystrophy ( vit D& PTH in renal failure): osteomalacia ( mineralization of bone). osteitis fibrosa cystica, and osteoporosis Diagnostic Studies Calcium and albumin, Ca, PTH, vitamin D, l,25-(OH)2D3, BUN, Cr, Mg, PO4, alkaline phosphatase Treatment Symptomatic: intravenous Ca gluconate Asymptomatic: oral Ca and vitamin D supplementation In renal failure, need to give l,25-(OH)2D3 (i.e. calcitriol) In hypoparathyroidism, PTH supplementation not available. ... give l,25(OH)2D3
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25: HYPOGLYCEMIA Etiologies in Diabetics Excessive insulin, oral agents, missed meals, renal failure ( insulin clearance), hypothyroidism Etiologies in Nondiabetics Insulin: exogenous insulin, sulfonylureas, insulinoma, anti-insulin or insulin receptor antibodies. glucose production: hypopituitarism, adrenal insufficiency, glucagon deficiency., hepatic failure, alcoholism Postprandial Clinical Manifestations (glucose < ~ 55 mg/dl) CNS: headache, visual s, MS, weakness Autonomic: diaphoresis, palpitations, tremor Workup 72 hr fast with monitored blood glucoses BUN, Cr, LFTs, TFTs. At time of hypoglycemia: insulin, C peptide ( with insulinoma and sulfonylureas, with exogenous insulin), sulfonylurea levels, and IGF-II Anti-insulin antibodies.
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26: ADRENAL INSUFFICIENCY Etiologies Primary= adrenocortical disease = Addisons disease Autoimmune (most common in industrialized countries) Isolated Polyglandular autoimmune syndromes (PGA) PGA I= Chronic mucocutaneous candidiasis + hypoparathyroidism + Addisons PGA II = Addisons + thyroid disease + IDDM Infection (most common cause worldwide); tuberculosis, CMV, histoplasmosis Hemorrhage, thrombosis, and trauma Metastatic disease (90% of the adrenals must be destroyed to cause insufficiency) deposition disease: hemochromatosis, amyloid, sarcoid. Drugs: ketoconazole, rifampin, anticonvulsants Secondary = pituitary failure of ACTH secretion (aldosterone secretion intact because controlled by renin-angiotensin axis) Any cause of primary or secondary hypopituitarism Glucocorticoid therapy (occurs after 2 wks of suppressive doses; takes 8-12 mos to recover function) Megestrol Clinical Manifestations (N Engl J Med 335:1206, 1996) Primary or secondary: weakness and fatigability (99%), anorexia (99%) orthostatic hypotension (90%), nausea (86%), vomiting (75%), hyponatremia (88%), hypoglycemia, eosinophilia, lymphocytosis, + neutropenia Primary only (extra signs and symptoms due to lack of aldosterone and ACTH): marked orthostatic hypotension (because volume depleted), hyperpigmentation (seen in creases, pressure areas, nipples), hyperkalemia Secondary only: other manifestations of hypopituitarism Diagnostic Studies High dose (250 g) corticotropin stimulation test: normal =pre-or 60 post-cortisol 18 g/dl Abnormal in primary because adrenal gland diseased and unable to give adequate output abnormal in chronic secondary because adrenals atrophied and unable to respond Low dose (1 g) corticotrophin stimulation test: can detect mild secondary adrenal insufficiency
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Other diagnostic tests: insulin-induced hypoglycemia; failure to 11-deoxycortisol after metyrapone Other laboratory abnormalities; hypoglycemia, eosinophilia, lymphocytosis, neutropenia ACTH: in primary, in secondary Imaging CT: small, noncalcified adrenals in autoimmune, enlarged in metastatic disease, hemorrhage, infection or deposition (although they maybe normal appearing) MRI: to detect pituitary abnormalities.
Treatment Acute adrenal insufficiency Hydrocortisone 100 mg IV q 8 hrs Volume resuscitation with normal saline Chronic Hydrocortisone: usually 20-30 mg PO q d (2/3 in am, 1/3 in pm) or prednisone 5-7.5 mg PO qd fludrocortisone (not necessary in secondary adrenal insufficiency): 50-100 g PO q d in am
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27: ACUTE POISONING & DRUG OVERDOSE A. General Guidelines: 1. Maintain adequate airway, breathing and cardiac support. Patients who have ingested a large amount of tricyclic antidepressant may require intubation immediately even if mental status deterioration has not yet occurred. 2. If with mental status abnormalities (i.e. coma, stupor, drowsy), give 50 ml ampule of 50% (1-2 ml/kg) dextrose, followed by Naloxone (Narcan) 2 mg IV, or endotracheally, and administer Thiamine 100 mg IV or IM. Naloxone may be repeated in boluses of 1-2 mg up to 4 mg IV. Obtain an immediate glucose level and administer glucose if the glucose is < 80 mg/dl. Alternatively, glucagon 1 mg IM may be used if IV access is not available. 3. Perform gastric lavage in most adult patients with suspected oral ingestion. The use of ipecac-induced emesis is not recommended anymore. 4. Consider possibility of suicide attempt or intentional poisoning in suspicious overdoses. 5. All female patients with intentional ingestion should ideally have a pregnancy test (check last menstrual period) following informed consent. And if found positive, pregnancy outcome must be followed up. 6. Suicidal precautions should be instituted as needed: Always have a 24-hour responsible watcher. There should be no access to sharp objects such as knives, razors, ropes, or belts inside the room. Always keep windows and balcony locked. Never leave medications bedside. Limit visitors to prevent possible supply of illicit substance. B. Principles of Decontamination: 1. External Decontamination a. Remove clothes. b. Wash skin with soap and water. Note also contamination of hair and fingernails. c. Keep warm; use blankets. Gastric Lavage (Nasogastric tube) a. Contraindications include ingestions of strong acids, alkalis, petroleum distillates (unless volume is large because it may volatilize and cause chemical pneumonitis). b. Airway must be protected with endotracheal tube unless patient is awake, alert and has a gag reflex. Place patient in
2.
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c.
the Trendelenburg and left lateral decubitus position. Position head to one side to minimize aspiration. If patient has respiratory difficulty, consider placing a cuffed endotracheal tube. Begin mechanical ventilation and oxygenation if indicated. Perform gastric lavage unless overdose was parenteral or distant in time. Lavage may be useful if performed within 2 hours of drug ingestion (unless dealing with a delayed release preparation) and longer if anticholinergic drugs (tricyclic antidepressants) or other drugs that delay gastric emptying were ingested.
3.
Activated Charcoal a. Single dose activated charcoal: Always consider giving charcoal after emesis or lavage unless specifically contraindicated, such as if oral antidote will be used or if endoscopy is planned. For example, activated charcoal may be detrimental in Paracetamol ingestion since it binds to Nacetylcysteine. Adult dose of activated charcoal is 50-100 grams (1 gram/kg body weight) in 200 ml of tap water in a thick slurry. Instill slurry by lavage tube or have patient ingest slurry. b. Multiple doses of charcoal: Giving activated charcoal 0.5 gram/kg/body weight q 4-6 hours may be indicated for metamphetamine, phenothiazines, digoxin, theophylline, phenobarbital and organo-chloride pesticides ingestion, because these substances have enterohepatic recirculation kinetics. Note that activated charcoal may cause constipation or fecal impaction. c. Activated charcoal is not effective for alkalis, cyanide, mineral acids, ferrous sulfate and petroleum ingestion. Cathartics (Sodium sulfate) a. Contraindicated in infants, acid and alkali ingestion, patients who will receive an oral antidote, adynamic ileus, severe diarrhea, abdominal trauma, surgery, suspected intestinal obstruction, severe electrolyte loss or dehydration. Magnesium sulfate cathartics are contraindicated in renal failure. Sodium sulfate is contraindicated in hypertension and heart failure. b. Sodium sulfate 15-30 grams (or 250 mg/kg) in 100 ml water given 30 minutes after the activated charcoal. If still without bowel movement within one hour, may repeat procedure.
4.
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5.
Forced Diuresis Warning: Forced diuresis should only be attempted in treatment centers that can monitor hydration and electrolyte status of patients. a. Forced Diuresis: Maintain urinary flow rate of 5-7 ml/kg/hr by infusing normal saline and intermittent boluses of Furosemide 20 mg IV doses. Alternatively, use mannitol 20-100 gm IV, maximum 300 gm. Monitor electrolytes and state of hydration. b. Forced Alkaline Diuresis: May be useful for phenobarbital, mephobarbital, primidone, salicylates, lithium, isoniazid. Adult dose: Sodium bicarbonate 1 -2 amp IV, followed by continuous IV infusion of 1-2 ampules (50-100 mEq) of sodium bicarbonate in 1 liter of 0.25-0.45 and normal saline at 250-500 ml/hr the first 1 -2 hours. Maintain the urine pH of 7.3-9.0. Add additional 0.45% normal saline and intermittent doses of Furosemide 20 mg IV. Increase urine output to 2-3 ml/kg/hour. Miscellaneous Antidotes a. Extrapyramidal reaction to Phenothiazines or Metoclopromide Diphenhydramine 25-50 mg IV or lM q 6 hours X 4 doses; followed by 25-50 mg IV or P0 q 6 hours for 24-72 hours PRN. b. Benzodiazepine overdose (e.g. Diazepam, Midazolam, Lorazepam) Flumazenil 0.5 mg/S ml ampule: 0.2 mg IV q 5-1 5 minutes until the patient wakes up or until 1 mg is reached. Consider gastric emptying, activated charcoal. Administer cathartic and conservative supportive therapy.
6.
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Table. Available Tests and the Specimen Required for Determination. Test RBC cholinesterase Salicylate Methanol Ethanol Paracetamol Sample Required 5 ml heparinized 2 ml serum Plasma Serum Serum/urine 10 ml heparinized blood 50 ml aliquot of 24 hour urine 5 ml serum or 10 ml urine 200 ml aliquot of 24 hour urine sample Serum Urine 10 ml urine 10 ml urine 10 ml urine 15 ml urine 5 ml heparinized blood Special Instructions Freshly collected blood sample; place in ice immediately after collection and during transport to the lab Collect 5 ml blood in a plain tube Collect 5 ml blood with anticoagulant (citrate or oxalate except heparin and EDTA); place in ice Collect 5 ml blood in a plain tube Collect 5 ml blood in a plain tube or 10 ml freshly voided urine Collect 10 ml blood in heparinized tube Collect 24 hr urine (e.g. 8:00 am8:00 am the following day, mix well and submit 50 ml aliquot Collect 10 ml blood in plain tube or 10 ml freshly voided urine Place 10 ml sodium carbonate to the collection bottle, collect a 24 hr urine, mix well and submit 200 ml aliquot Collect 5 ml blood in plain tube Collect freshly voided urine Collect freshly voided urine Collect freshly voided urine Collect freshly voided urine Collect freshly voided urine Collect 5 ml blood in heparinized test tube
Mercury
Isoniazid Coproporphyrin Phenobarbital Amphetamine / Metamphetamine Phenothiazine Paraquat / Diquat Quinidine / Quinine Paranitrophenol Methemoglobin / Sulfhemoglobin
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28: ORGANOPHOSPHATE POISONING (Insecticides / Pesticides) Nursing: NPO; I & O; Insert foley catheter Diagnostics: CBC, Na, K, RBS, BUN, Creatinine, CBG q 12 hours SGOT, SGPT, Amylase, PT, ABG, RBC Cholinesterase, Urinalysis (if urine output is reddish check for Myoglobin), CXR, ECG Therapeutics: 1. Decontamination a. External decontamination: Have the patient rinse gently with alkaline soap or baking soda (10gm in 100 ml water) Change clothes and wash patient with soap using gloves b. Internal decontamination: Insert NGT and do gastric lavage with activated charcoal 100 gm in 200 - 500 ml water 2. Activated charcoal 1 gm/kg PO then sodium sulfate 15-30 grams in water after 30 minutes. Repeat sodium sulfate after one hour if still no bowel movement. 3. Antidote: Atropine Sulfate 0.01-0.05 mg/kg IV q 5 minutes or 1 mg IV usually. Maintain the following parameters: Dry mucosa, HR > 60 bpm (target HR of around 100 bpm), hypoactive bowel sounds, pupils > 4 mm; watch out for Atropine toxicity such as temperature > 39 0C, absence of sweating, psychosis and restlessness. 4. Seizures: Diazepam 5 mg IV q 8 hours. If not control consider Phenytoin IV 5. D50-50 glucose 1 ampoule q 6 hours 6. Mannitol at 1 ml/kg IV in 10 minutes as test dose. If with good urine output, give 2.5-5 ml/kg q 6 hours x 8 doses 7. If with arrhythmia, do not give beta-blockers or Lidocaine; may give calcium-channel antagonists or Phenytoin instead. 8. Avoid the following drugs: Furosemide, beta-blockers, sulfacontaining drugs and aminoglycosides. 9. Correct acidosis with sodium bicarbonate
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29: ANAPHYLAXIS Anaphylaxis is an acute generalized allergic reaction and is most commonly precipitated by the injection of foreign substances, e.g. drugs, vaccines, insect stings. Severe and even fatal reactions can also occur, however, after foods or orally administered drugs. After injections, the reaction may start within seconds or minutes. Onset may be delayed by some hours in the case of oral administration.
Co nsider when compatible his tory of se vere aller gic - type reaction with res piratory d ifficulty an d/or hypo tension e specially if skin ch anges pre sen t.
O xygen Strido r, wheez e, respira tory distre ss or clin ical signs of shock Epinephri ne (adren aline) 1:1 000 0.5m1 (500microrams) IM Re peat in 5 min utes if no clin ical impro vement An tihistami ne (chlorp heniramin e) 10 20mg s low IV
IN A DDITION Fo r a ll severe or recurre nt reactions and patients w ith asthma give hydr ocortison e 100 5 00mg IM or slow IV If clinica l manifes tations of shock do not respon d to drug treatmen t give 1 2 liters IV fluid. R apid infusion may be nec essary.
1. 2.
3. 4.
An inhaled B2 agonist such as salbutamol may be used as an adjunctive measure if bronchospasm is severe and does not respond rapidly to other treatment. If profound shock is judged immediately life-threatening give CPR/ALS if necessary. Consider slow intravenous epinephrine 1 in 10,000. This is hazardous and is recommended only for an experienced practitioner who can obtain IV access without delay. Note the different strength of epinephrine that may be required for IV use. If adults are treated with an Epipen, then 300 micrograms will usually be sufficient. Ensure that the name of the agent is written prominently in the patients notes and on the drug card.
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30: DENGUE HEMORRHAGIC FEVER A. B. C. D. Etiology: Dengue virus Transmission: Through bite of female Aedes aegypti mosquito Symptoms: 2-7 days of fever Complications: Disseminated intravascular coagulation, pleural effusion, hemorrhage, epistaxis, melena, gum bleeding, myocarditis, encephalitis, hypotension, shock, acidosis, death E. Grading: a. Grade I: Fever, (+) torniquet test, decrease platelet, increase hematocrit b. Grade II: Grade I symptoms + spontaneous bleeding; hemorrhages c. Grade Ill: Grade II symptoms + thready pulse, decrease pulse pressure 20 mmHg, or hypotension d. Grade IV: Grade Ill symptoms + profound shock, no blood pressure detected, no pulse. Diet: Avoid dark colored foods (for monitoring of melena) VS: Vital signs q 1-4 hours and watch out for any signs of bleeding; temperature q 4 hr and in between if febrile or with chills Nursing: I & O q shift IVF: D5NM X 8 hours; D5NSS or D5LR for shock Diagnostics: CBC with platelet count, PT, PTT, Torniquet test, Dengue Serology if illness longer than 4 days, Urinalysis, Chest X-ray (check for pneumonia, pleural effusion), Monitor: Platelet count Hematocrit levels q 1 2-24 hours Therapeutics: A. Medical treatment a. Supportive: Hydration, b. Optional medications: H2-blockers if with abdominal pain or gastrointestinal bleeding c. Watch out for complications: i. If there is frank, uncontrollable bleeding, fresh whole blood is indicated. ii. If PT, PTT are prolonged and with thrombocytopenia, fresh frozen plasma transfusion is indicated. iii. If there is disseminated intravascular coagulation, platelet transfusion is indicated. Note: In the absence of bleeding, there is no need to administer platelet transfusion even if platelet count is low. B. Prevention I. Environmental: Get rid of mosquito breeding places II. Vaccine: May be available in the near future
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31: FEVER AND NEUTROPENIA Definition Fever (temp 1O1.30 F or recurrent temps 100.40 F) + neutropenia (polys + bands < 500/mm3) Diagnostic studies Physical exam (mouth, perineum, perirectal areas, catheter sites); rectal exam relatively contraindicated. Physical signs may be subtle as patients are usually unable to generate significant inflammatory responses. Blood cultures (if indwelling catheter, also obtain blood cultures from each port) U/A, UCx, CXR Sputum, stool, peritoneal, or CSF cultures if suggested by localizing signs or symptoms Treatment Initial management of fever and neutropenia
Fever ( 38.30 C) and neutropenia (< 500/mm3) Evaluate Is Vancomycin needed? Indications Severe mucositis Quinalone prophylaxis Colonized with Meth-resistant. S.aureus Pen-Ceph-resitant. S. pneumoniae Obvious catheter-related infection Hypotension Vancomycin + Ceftazidime No indications
Monotherapy
Duotherapy
Ceftazidime or Imipenem
Aminoglycoside + antipseudomonal lactam
Reassess after 3 days
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32: TETANUS A. Etiology: Clostridium tetani, a gram-positive bacteria, produces tetanospasmin causing increased muscle tone and spasms. B. Transmission: Usually a non-immunized person develops a skin injury and comes into contact with infected soil. C. Symptoms: Diagnosis is clinical only. Symptoms initially include jaw stiffness (locked jaw) and dysphagia; then followed by pain or stiffness in the neck, face (sardonic grin), shoulder, back and abdominal muscles. Hands and feet are relatively spared. Onset of symptoms may range from 3-14 days after the injury. D. Complications: Severe cases may develop laryngospasm, apnea, autonomic dysfunction (hypertension, tachycardia, arrhythmia, high fever profuse sweating), aspiration pneumonia, fractures, muscle rupture, rhabdomyolysis, deep venous thrombosis (DVT), pulmonary emboli and decubitus ulcers. Admit to single room. Diet: NPO temporarily VS: Neuro vital signs q 1 hour Nursing: I & O q shift, Seizure precautions Consider nasogastric tube insertion and nutritional support. Avoid stimulation and bright lights; Keep room dark and quiet. Tongue guard; Watch out for respiratory depression; Standby intubation set. IVF: D5NR 1 LX 10 hours Diagnostics: CBC, RBS, Creatinine, K+, Wound G/S & C/S, Urinalysis, Chest X-ray, ECG Therapeutics: 2. Give Anti-toxin: Human Tetanus immunoglobulin Ig (Tetuman Berna,Tetaglobulin) 250 IU/amp, 4 amps IM 3. Give Tetanus toxoid 0.5 ml/amp, 1 amp IM now, then after 1 month, and after 6 months. 4. Start Antibiotics: Penicillin G 3-4 MU units IV q 4 hr (18-24 MU units per day) or Metronidazole 500 mg IV q 6 hr 5. For Muscle Spasms: Diazepam 2.5-5 mg IV q 6 hr or Diazepam drip: 10 mg in 100 ml D5W infuse in 2 hours q 8 hr (maximum of 60 mg per day) 6. Supportive Therapy: a. Respiratory support, protection of the airway, IV hydration b. Prevent DVT, decubitus ulcers and GI bleeding. May give antacids per nasogastric tube c. Pain reliever: ibuprofen 200 mg tab TID per NGT if needed d. Clean wound with hydrogen peroxide and Betadine
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33: BLEEDING DISORDERS Etiologies of bleeding disorders

Category Thrombocytopenia Defective platelet function Etiologies production: congenital, alcohol / drug induced destruction: autoimmune, drug induced, infections Congenital: membrane or granule abnormalities von Willebrands disease (vWD) Acquired: production of abnormal platelets: myeloproliferative disorders modification of abnormal platelets: uremia, aspirins, NSAIDs Congenital: vWD, hemophilia Acquired: vit. K defic., liver disease, DIC, factor inhibitor, warfarin, heparin
Coagulopathy
Clinical manifestations Mucocutaneous bleeding platelet problems Deep bleeding or hemarthroses coagulopathy Recurrent bleeding or + FHx congenital defect Diagnostic studies Platelet count, PT, PTT; review all medications; review family history for bleeding disorders Peripheral smear to assess for platelet morphology and presence of schistocytes DIC screen: fibrinogen, fibrin degradation products (FDPs), D-dimer (degradation of X-linked fibrin) Mixing study: useful to assess PT or PTT factor deficiency PT/PTT will normalize; factor inhibitor PT/PTT usually stays elevated Coagulation factor levels: useful if mixing study suggests factor deficiency DICall factors consumed, ... factor V, factor VIII Liver disease factors synthesized in liver (all factors except VIII) ... factor V, normal factor VIII Vitamin K deficiency factors II, VII, IX, and X ... normal factor V, normal factor VIII Bleeding time (BT): useful to diagnose a qualitative platelet disorder, but technique imprecise at best Platelet aggregation studies: useful if confirmed defective platelet function.
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34: TRANSFUSION THERAPY

Product Packed red blood cells (PRBCs ) Platelets Indications and Comments Hb < 7-8g/dl if not critically ill Hb < 10g/dl if active bleeding, cardiac or pulmonary comorbidity, sepsis, or hemoglobinopathy. Tolerate Hb 7-9 g/dl as long as no cardiac disease? Plt < 10,000 Plt <20,000 + bleeding or coagulation disorder Plt <50,000 and major bleeding or pre-procedure Contraindicated in HUS/TTP and the HELLP syndrome Bleeding due to deficiency of coag. factors (e.g.. in DIC, HUS/TTP, liver disease, warfarin toxicity, dilution after massive transfusion of PRBCs) PT and pre-vascular invasive procedure vWD, hemophilia, or fibrinogen <100mg/dl and bleeding or pre-procedure (cryoprecipitate contains vWF, factor III, and fibrinogen) Patients at risk for graft-versus-host disease (e.g. immunodeficiency, s/p transplant, concurrent hematologic malignancy or non-hematologic malignancy and receiving intensive chemotherapy) CMV-seronegative pregnant women, transplant candidates, recipients of transplants, SCID patients, or AIDS patients (regardless of their CMV status). WBCs cause febrile reactions and carry CMV ... consider in patients with documented febrile transfusion reactions, patients who will require multiple transfusions, or patients who need CMV-safe blood when CMV-negative products are not available (although leukodepletion by blood bank soon after collection = CMV-negative). Transfusion Complications Risk (per unit) Infectious 1:100 CMV 1:100 Hepatitis B 1:1000 Hepatitis C <1:250,000 HTLV <1:100,000 HIV 1:5000
Fresh frozen plasma (FFP) Cryoprecipitate Irradiated blood products CMV-negative Leukopoor filtered
Non-infectious Febrile Allergic Delayed hemolytic Acute hemolytic Fatal hemolytic TRALI
Risk (per unit) common 1:63,000 1:103,000 < 1:100,000 1:493,000
Transfusion reactions For all reactions (except minor allergic): stop transfusion; remaining blood product and fresh blood sample to blood bank Febrile: fever and rigors 0-5 hrs after transfusion (due to WBC) o treatment: acetaminophen meperidine; rule-out infection
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Transfusion-related acute lung injury (TRALI): non-cardiogenic pulmonary edema o treatment: ventilatory support, diuresis to any hydrostatic contribution to pulmonary edema Allergic: urticaria, fever, bronchospasm, laryngeal edema, hypotension o treatment: diphenhydramine 25-50mg PO or IV, H2-blocker, methylprednisolone or epinephrine Hemolytic: fever, back pain, renal failure o acute: < 24 hrs after transfusion, due to ABO incompatibility o delayed: 5-7 days after transfusion, due to undetected alloantibodies against minor antigens o treatment: vigorous IVF, maintain UOP with diuretics, mannitol, or dopamine
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35: PREGNANCY & HYPERTENSION

Hypertensive Disorders of Pregnancy Clinical Finding 1.Time of onset of hypertension 2. Degree of hypertension 3. Proteinuria* 4. Serum urate > 5.5mg/dI 5. Hemoconcentration, thrombocytopenia, liver_dysfunction 6. LVH by ECG Chronic Hypertension < 20 weeks of gestation Mild or severe Absent Rare Absent May be present Gestational Hypertension Usually in third trimester Mild Absent Absent Absent Absent Preeclampsia 20 weeks gestation Mild or severe Usually present Present in almost all cases Present in severe disease Absent of
* Defined as 1 + by dipstick testing on two occasions or 300 mg in a 24hour urine collection. Source: Sibai, SM. (1996). Treatment of hypertension in pregnant women: A review article. N Engli Med. 335, 257-265. Diet: Low salt, high calcium diet VS: q 1 hour with neurochecks Nursing: I&O; Place foley catheter; Check deep tendon reflexes; Urine output, Complete bed rest IVF: D5NM X 12 hours Diagnostics: CBC with platelet count, Blood typing, PT, PTT, SGPT, SGOT, BUN, Creatinine, Uric acid, Urinalysis, 24-hour urine Albumin collection Therapeutics: Mnemonic 4 As (Aldomet, Apresoline, Atenolol, Adalat) A. Gestational Hypertension may be an early manifestation of pre-eclampsia outcome generally is good without drug therapy B. Chronic Hypertension use 4 As (see below) No. 1 -4 C. Pre-eclampsia Target diastolic BP between 80-100 mmHg 1. (Aldomet) Methyldopa 250-500 mg tab TID PO, maximum = 3 gm/day
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2.
3. 4. 5.
(Apresoline) Hydralazine 5 mg slow IVP stat dose q 20 mm up to 4 doses; Apresoline drip D5W 250 cc + 2 amps Apresoline (20 mg/amp) to run initially at 10-15 ugtts/min then to titrate up to 60 ugtts/min or Apresoline 25-50 mg tab TID-QID PO; Maximum of 300 mg/day If patient develops tachycardia, headache or nausea, shift to Nifedipine SL or PO Atenolol (Tenormin) 50 mg tab OD PO (Adalat) Nifedipine 5-10 mg PO or SL q 6-8 hours For patients on NPO, use the following singly or in combination: a. Nifedipine (Adalat) 5-10 mg SL q 6-8 hours Note: Watch out for hypotension with sublingual nifedipine, especially if the patient is also being given Magnesium sulfate. b. Hydralazine (Apresoline) drip: D5W 250 cc + 2 amps Apresoline (20 mg/amp) to run initially at 1 0-1 5 ugtts/min then to titrate up to 60 ugtts/min c. Clonidine (Catapres) drip: D5W 250 cc + 2 amps Catapres (150 mg/amp) to run at 5-30 ugtts/min
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36: PREGNANCY & DIABETES MELLITUS A. Two Types of Diabetes in Pregnancy: 1. Pregestational DM (DM prior to pregnancy) Diagnosis: FBS > 1 26 mg/dl on 2 occasions or RBS > 200 mg/dl or 75 gm 2 hour OGTT> 200 mg/dl 2. Gestational DM a. Screening test (at 24-28 weeks usually or earlier): 50gm 1 hour Oral Glucose Challenge of > 140 mg/dl b. If (+) screening test do Gold Standard for Gestational DM Diagnosis: 100 gm 3 hour Oral Glucose Tolerance Test (OGTT) after an overnight fast of 8-14 hours.
Three-hour 100 gm OGTT National Diabetes Mellitus Data Group Fasting > 105 mg/dl (5.8 mmol/L) 1 hour > 190 mg/dl (10.6 mmol/L) 2 hours > 165 mg/dl (9.2 mmol/L) 3 hours > 145 mg/dl (8.1 mmol/L) If two values are above normal then the patient is (+) for Gestational DM.
B. Complication: Birth defects, abortion, macrosomia, respiratory distress syndrome, stillbirth Treatment: 1. Diabetic diet 2. Insulin treatment: Do not give oral hypoglycemic agents. These are contraindicated during pregnancy. Sample Insulin Regimen: i. Humulin N (intermediate) or Humulin U (Ultralente - long acting) OD in am. ii. Humulin N & R combination (intermediate & short acting) at 6am and 6pm (2/3 of daily dosage to be given at 6 AM and 1/3 of daily dosage at 6 p.m.) Note: Aim for normal blood glucose (FBS 105 and Twohour postprandial blood glucose of 140 mg/dl. 3. Control diabetes at first 6 weeks AOG to prevent birth defects Deliver baby ideally at 36-37 weeks AOG
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INTENSIVE CARE UNIT (ICU) GUIDELINES Admission Criteria to ICU It is based on following factors 1. Severity The condition of the patient is such that disease process has endangered his life. 2. Reversibility The pathological condition is reversible to an extent that it can improve meaningful life span of the patient. Following patients should be admitted in ICU. 1. Patient needing ventilatory support. 2. Patient requiring support for two or more organ systems. 3. Patient with chronic impairment of one or more organ systems who also require support for acute reversible failure of another organ. Following patients should be managed in WARDS and not in ICU. 1. High Blood pressure. 2. Patient with simply CVP monitoring. 3. Patients needing fluid balance. 4. Neurological observations. 5. CRF 6. CLD 7. COPD 8. Renal replacement therapy in stable patients. 9. Pulmonary Tuberculosis 10. Patient needing isolation e.g. Open cases of TB, Meningococal meningitis, Viral Hemorrhagic Fever etc.
General Principles of Monitoring 1. 2. 3. 4. 5. 6. Tailored care approach Repeated clinical examination Repeated vital signs recording Exact Intake/Output Record If there is conflict between clinical assessment and monitor, consider later as wrong Changes and trends are more important than single measurement
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Routine Surveillance Monitoring Vital Signs: 1. They are maintained on an hourly basis in patients on ventilators and in other patients according to the patients conditions. 2. 3. 4. 5. 6. 7. BP Monitoring: Reduction in BP shows failure of normal circulatory compensation. Pulse Pressure: It is difference b/w Systolic and Diastolic BP. It shows early signs of hypovolemia. Monitoring of Heart Rate: It is important in cases of dysarrhythmia. Haematocrit: It increases by dehydration and hypovolemia and decrease in Hemorrhage. Urine Output: It is right approximation of perfusion to this one vital organ. It should be maintained more than 30-40 ml/hr in adults. ECG Monitoring: It is done for cardiac arrhythmias and electrolytes status. Serum Electrolytes.
8.
Chemical assessment of tissue hypoxia 1. 2. 3. 4. 5. 6. Acidosis: PH < 7.2 Base deficit of >5 mEq Bicarbonate < 20 mEq/L Anion gap of > 8 mEq/L Serum Lactate > 2 mEq /L Gastric PH < 7.2 mEq/L
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Preventing complications in ICU Skin and mucosal breakdown 1. Regular turning of sides at least 2 hourly. 2. Passive exercises. 3. Ensure good Oxygen delivery. 4. Maintain adequate temperature. 5. Clean immediately dirty sheets if soaked especially in unconscious and incontinent patients. 6. Skin massage 7. Dusting with talc powder. Pressure Ulcers 1. Increase patients mobility. 2. Pressure reduction beds should be used. 3. Specific Padding. Endotracheal tube 1. Low pressure cuffs 2. Frequent tube repositioning 3. Facial skin protection. 4. Re positioning oral ETT from side to side every 24-48 hours 5. Duoderm under ETT tapes. Tracheostomy Tube 1. Skin breakdown occurs from the secretions that ooze from the Tracheostomy incisions or from ties applied too tightly. 2. Wet and tight tubes should be avoided Feeding Tubes Protective skin barriers like Duoderm should be used. Risk factor for nosocomial infections 1. Immobility. 2. Impaired nutritional status. 3. Extreme of age. 4. Diabetes mellitus. 5. Immunosuppression. 6. Decreased level of consciousness. 7. Use of invasive therapies like NG Tubes, ETT, Tracheostomy, and Vascular access devices. 8. Use of mechanical ventilators. 9. Proximity of the patients.
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Recommended Measures: 1. Meticulous oral care. 2. Avoid stasis of secretions. 3. Turning. 4. Coughing. 5. Deep breathing. 6. Chest Physiotherapy. 7. Selective decontamination of the UI Tract. 8. Repositioning of NO Tubes and suctioning NG Tube before feeding. Musculoskeletal Complications 1. Critically ill patients may develop polyneuropathy due to steroids and neuromuscular blocking agents. 2. 70% of patients with sepsis and MOD have muscular or neuropathic weakness. Recommendation: 1. Regular, passive range of movements. 2. Physiotherapy. 3. Avoid foot drops by splinting. Pulmonary Complications: Causes of Atelectasis 1. Immobility. 2. Unable to breathe deeply. Recommendations: 1. Breathe deeply on regular basis. 2. Chest Physiotherapy. 3. Deep breathing is sufficient for awake patients. 4. For comatose patients 2 hourly repositioning Physiotherapy are required. 5. If mucus plugs present then chest Physiotherapy. 6. For comatose patients IMPPV can be used.
and
chest
Nosocomial Pneumonia: 1. Placing patient at 45 degree recline can avoid aspiration. 2. Patient lying supine aspiration of GIT contents can occur. Unexplained Extubation: 1. Severe cough. 2. When patients mouth the ETT partial or complete extubation can occur. 3. Confusion or anxiety in the patient.
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Recommendations: 1. Suctioning of the tube is explained to the patient. 2. ETT procedure should be explained before placement. 3. Judicious use of sedatives / explanation should be given. 4. Position of ETT should be noted and documented. 5. Patient with cough, secretions should be suctioned regularly. 6. ETT repositioning should be done by 2 staff members, 1st to secure and other to reposition it ITCU Psychosis: Delusions may occur between 3-7 days of ITCU stay. Other Problems: 1. Unfamiliar environment. 2. Lack of control over environment Recommendations: 1. Educate and inform. 2. Minimize number of persons that come into contact with the patients 3. Provide information about the diagnosis, treatment and prognosis. 4. Encourage family participation. 5. Encourage family to bring comfort items form home. 6. Limits staff conversation at the bedside to patient and family. Altered sleep patterns: 1. Obtain vital signs and perform interventions only if necessary. 2. Plan activities to allow sleep at night. 3. Administer sleep medications at night Pain management: 1. Monitor BP during narcotic administration, 2. Give small incremental IV doses of narcotics. 3. Monitor Resp: Rate during narcotic administration. Prevention of Acute Renal Failure 1. 2. 3. 4. 5. 6. 7. Correct hypovolemia. Correct hemodynamics imbalances. Restore cardiac output. Restore intra-arterial pressure. Use judiciously inotropic support & fluid replacement. If required, invasive monitoring should be done. Low dose dopamine at 2 microgram/kg/mm causes selective stimulation of dopaminergic receptors in the kidney.
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Diuretics can be given for oliguria & anuria. Mannitol can be used which decreases cell swelling, causes vasodilatation of intra-arterial vasculature and scavenges free radical. 10. Calcium Antagonists. 11. Theophylline in low doses. Pulmonary Embolism Prophylaxis 1. 2. 3. 4. Heparin (7500 IU BD or 5000 IU TDS). LMW Heparin (according to weight). Compression stockings. IVC filter.
8. 9.
Prophylaxis should be continued even after discharge from hospital. It should especially be given in patients with spinal cord injury / paralysis.
Endotracheal Intubation 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. A size of >7.5mm is used for adults. ETT is checked especially balloon inflated. Ventilation circuit to be attached is checked. Suction catheter and suction machine is checked. A malleable catheter should be available. Tape to tie ETT. A working Laryngoscope is needed. Tube position is assessed by palpating balloon in sternal notch or by X-ray. Both lungs should be auscultated. The tube should be secured and point noted. Regular Pharyngeal and ETT Suctioning done depending on condition. Inadequate insertion of ETT depth can be checked by palpating ETT Cuff over Thyroid cartilage. Use less than 20mmHg pressure for balloon inflation. In prolong ETT intubation, 2-4 hourly deflation of balloon should be considered.
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Techniques of Extubation 1. 2. 3. Patient should be awake, as evidenced by eye opening and purposeful movements. Adequate recovery from muscle relaxant should be established before extubation. Extubation in awake patient is associated with coughing. This increases heart rate, CVP, ICP and IOP. It can cause wound dehiscence. 1.5mg/kg Lignocaine is given l-2 mins before suctioning and extubation. Mouth and Pharynx are suctioned appropriately. 100% of Oxygen is given before extubation. Tube is withdrawn in a single, smooth motion. Facemask is applied with 100% of Oxygen. Extubation should not be done if there is danger of aspiration. Extubation should be avoided if it is considered that reintubation will be difficult.
4. 5. 6. 7. 8. 9.
Tracheostomy Post OP Care 1. 2. 3. 4. 5. 6. 7. 8. Suction should be done as often as required. Tracheostomy tube should be covered with moist gauze piece changed frequently for humidification. Spare tube, introducer; tapes and tracheal dilator should be available at the bedside of the patient. Suction should be done under aseptic conditions. When mucous is tenacious, isotonic saline can be used. If there is an inner tube it should be removed and washed with Sodium Bicarbonate Solution every 4 hourly. Physiotherapy should be done. Regular check for positioning of the Tracheostomy tube.
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Ventilatory support in Asthma Recommended Ventilatory settings TV =68 ml/kg RR= 1012/m PIFR =80-100ml/m as initial ventilatory setting These low levels of minimum ventilation permit a strategy of hypercapnia and respiratory acidosis. If the systemic pH remains above 7.5, this need not be corrected. Low levels of PEEP can be given. (5cm of H2O) Heavy sedation Infusion of meperidine is recommended. Morphine should not be used. Neuromuscular Blockade Vecuronium & Pancuronium are preferred. Accumulative dose may occur in renal failure. Prolonged administration can cause neuropathy. At least one or two twitches rather than total paralysis with no response should be obtained. More than two days of neuromuscular blocking agents should be avoided. The next injection of neuromuscular blocking agent should be given only when needed. Hypotension A transient drop in systolic BP occurs after start of ventilatory support due to sedative effect & PEEP. Pulmonary artery catheterization may be needed if cardiac disease is present. Barotrauma due to hyperinflation can occur which requires strategies to decrease hyperinflation. Monitoring 1. Oximetry 2. Pulsus paradoxus 3. Capnometry 4. Serum electrolytes, serum phosphorus 5. Theophylline levels 6. Chest Radiography a. To rule out barotraumas b. Atelectasis c. Pneumonia d. Pneumothorax e. Check position of ETT
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7.
Weaning a. Most patients improve within 24 48 hrs. b. Mean duration of intubation is 3 5 days. c. Secretions are minimum d. Bronchospasm is managed with nebulized therapy e. No evidence of neuromuscular deficit
General Principles 1. Intubate awake patient in emergency setting 2. Large bore tube should be used 3. Ventilatory settings to avoid hyperinflation COPD General Principles 1. For every 1 liter/min oxygen, there is 8% rise in FiO2. 2. The upper limit of Oxygen delivery is thus 6 liters/min 3. The upper limit of increasing FiO2 is approximately 65% - 75%. 4. This is true for facemask & nasal canullae. Ventilatory setting for COPD 1. Generally used mode is A/C. 2. Tidal Volume is 8 l0ml/kg. 3. Frequency should be minimum at which desired SPO2 is achieved. 4. In-patient with increased HCO3 level, acute increase in minute ventilation can lead to neuromuscular hyper excitability and tetany. Anxiolytics and Analgesics should be used only when required. These may depress ventilatory center and can cause confusion & delerium.
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WEANING Preliminary Assessment This is based on improvement in underlying conditions. 1. 2. 3. 4. 5. 6. 7. 8. Have the causes of underlying respiratory failure been effectively treated or reversed. Is the patient stable, in terms of both inciting illness and any complications? Rule out electrolyte balance. Rule out hypoglycemia. Patient should be alert to protect his airways. Patient should have effective cough. Secretions should not be copious or tenacious. No cardiac dysrhythmia present.
Secondary Assessment 1. Gas Exchange Organ Assessment, 2. Partial oxygen tension PaO2 > 60 %. 3. Or oxygen saturation > 90 % or < fractional concentration of expired gas (FiO2). 4. PaO2 / FiO2 ratio > 200 5. Partial arterial carbon dioxide PaC02 < 45 mm Hg. Ventilating Pump Assessment Rapid shallow breathing index Frequency (f) in breathes per minute divided by tidal volume Vt in liter. During one minute T Tube trial. F / Vt < 105 predicts successful extubation. F / Vt >105 predicts failure.
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Spontaneous breathing trial or PSV of 5 cm H2O for 30-120 min The patient is considered failed trial if any of the following occurs. 1. Respiratory rate >35 breaths 1mm for 5 mm or more. 2. Oxygen saturation < 90%. 3. Sustained change in heart rate > 20 % in either direction. 4. Blood pressure changes to > 180 or < 90 mmHg. 5. Evidence of pt distress. 6. Anxiety or depression. Step Wise Protocol Step I 1. Pt has been on ventilator for less than 2 weeks. (yes / no) 2. No life threatening complications (yes / no). Step 2 1. Is PaO2 / FiO2 > 200 2. Is Oxygen saturation > 90 % or FiO2 < 0.5 3. Is PEEP < 5 cmH2O. 4. Has pt adequate cough during suctioning. 5. The pt is not taking vasopressor (dopamine 5 microgram / min is acceptable) or sedative injection. 6. Ratio of f / Vt <105. Step 3 If all answers are yes, proceed to 2 hours spontaneous breathing trial on CPAP 5cm of H2O maintaining same FiO2. Terminate if any of the following occurs. 1. 2. 3. 4. 5. RR > 35 / min for more than 5 min. Oxygen saturation < 90 %. Heart rate >140 beats per min or sustained 20 % changes in heart rate. Systolic blood pressure >180mm Hg or < 90 mm Hg. Increased anxiety.
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Forgoing life-sustaining therapy in the intensive care 1. To do away with the sufferings of the sick, to lessen the violence of the disease, and to refuse to treat those who are overmastered by the disease, realizing that in such cases medicine is powerless. Nearly dead / Alive on ventilators One who is alive only because be or she is receiving life support in the intensive care unit. With-holding support Never providing the patient with the therapy in question. Withdrawing support Discontinuing already instituted therapy. Foregoing therapy It refers both to the withholding and with drawing of therapy. If ventilatory support is withdrawn vasopressor therapy should be continued. Decision It should be made on individual basis considering disease process, prospects of recovery and after discussing with family.
2.
3.
4.
5.
6.
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Brain Death Definition: An individual who has sustained either 1. Irreversible cessation of circulatory and respiratory functions or 2. Irreversible cessation of all functions of the entire brain including the brainstem is dead (Uniform determination of death act 1991 USA) Determination of Brain death American academy of neurology 1995 summarize the current criteria of brain death as follows: 1. The cause of brain injury must be known. This can be established by history and physical examination, Lab studies such as Blood count, Coagulation studies, Electrolytes, Blood gases, Serum and Urine toxicology and CSF examination. CT / MRI / Angiography is done in some cases to establish the cause of brain death. 2. Metabolic and toxic CNS depression should be excluded 3. Hypothermia should be excluded 4. Normothermia > 32 degree centigrade should be restored before the determination of brain death. 5. There must be no demonstrable brain function. Requirements 1. Consultation of Anesthetist 2. Consultation of Physician 3. Consultation from respective department Criteria of Brain death and method of examination 1. Absence of spontaneous movements, decorticate or decerebrate posturing, Seizures, Shivering, response to verbal stimuli, response to noxious stimuli, administered through cranial nerve pathway. 2. Absent Pupillary reflex to both direct and consensual light reflex. Pupils need not be equal or dilated. The pupillary reflex may be altered by trauma, cataract, high dose dopamine, atropine, bretyllium or MAOI. 3. Absent corneal, occulocephalic, cough and gag reflexes. The corneal reflex may be altered as a result of facial weakness. 4. Absent occulovestibulur reflex, labyrinthine injury or disease, anticholinergic, anticonvulsants, tricyclic antidepressants and sedatives may affect it.
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5. 6.
Failure of heart rate to increase by > 5beats / min after 1-2 mg of Atropine. Absent respiratory effort in the presence of hypercarbia.
Confirmation by 1. EEG 2. Contrast Angiography. 3. Evoke potentials 4. Radioneucleotide cerebral imaging 5. Trans cranial Doppler Conditions that may confound the critical diagnosis of brain death 1. Hypothermia: < 32 degree centigrade 2. Shock / Hypotension 3. Drugs: Anesthetics, Paralytics, Barbiturates, Diazepam, High dose Bretyllium, Amitriptyline, Trichlor Ethylene, Alcohols. 4. Brain stem encephalitis. 5. Gullian bare syndrome. 6. Encephalopathy associated with hepatic failure, renal failure, hyper osmoler coma etc 7. Severe Hypophosphatemia. Apnea test 1. Ventilate for at least 20 mins to produce normal PCO2 (37-40 mmHg) and Hyperoxia with FiO2 1 before discontinuation from ventilator. 2. After discontinuation from the ventilator maintain 100% O2 to ETT at 10 Liters of oxygen / min. 3. Continues Apnea for 5-10 mins until Hypoxia, Hypotension or Ventricular arrhythmias result. 4. Follow PCO2 by ABGs to document a final PCO2 of > 60 mmHg or increase in PCO2 of >20 mmHg or pH < 7.24.
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SOPs FOR EMERGENCY PATIENT CARE All shifts should follow strict timings. NOTES AND EVALUATION House officers and residents are primarily responsible for managing patients in Emergency during their call day. Referred patients should be seen within 10 minutes of referral by CMO. Immediately receive patient, check vitals before digging through old record, lab results, old discharge summary and old charts. SOAP format should be used for patient notes. Proper documentation of symptoms, Management and diagnosis will be done for every patient. Serious patients should be immediately seen and resuscitated. Procedure of referral & consultation will proceed side by side. Monitoring notes should be properly maintained including fluids given and output of patient. ADMISSIONS Duty registrar should decide all admission through ER. After assessment and patients exam complete admission orders including drug prescription immediately. For stat labs inform nursing staff immediately or carry out by your self. Notes on H&P should be completed before shifting to In-Patient. Complete shifting notes before shifting to the ward. Para-medic staff should accompany every admitted patient during shifting to the ward In case of serious patient, house officer should accompany. Before shifting, inform the ward staff on call. If beds are not available in wards, retain patients in ER till arrangement are made; If required discuss with consultant on call or DMS ER. PROCEDURE NOTES Write note for every procedure, which should include Name, Site, Indication, Consent, Sterile prep and anesthesia of procedure. Description of specimen of Fluid and what and where they are sent for with brief clinical notes. Inform patient regarding indications, complications and postprocedure precautions. Get signatures on informed consent. Never forget pending follow up studies like Post-Procedure X-ray.
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DISCHARGES No patient should be discharged without being evaluated by the duty registrar. Keep in mind pending issued and studies. Communicate with all involved parties for smooth discharge. Give clear instructions regarding medicines schedule/side effects/precautions and restrictions on activities/travel/diet in Urdu/local language Make sure by repetition that patient can repeat/recall you instructions. Write discharge diagnosis clearly. Notes should include Chief complaints and H/O Present illness, hospital stay course, your name Hospital no/principal and secondary diagnosis and Procedures. Mention Follow-up plan/condition on discharge/attach Diet chart if required. SIGNOUTS For on-call batch, out going House officer will give written information about their Patients Active issues and it should include Name of patient, ward/bed no. diagnosis, active issue or pending critical labs., consultations and procedures. Also, include certain criteria to act on e.g. Transfuse one unit packed cell if Hct is less than 28. CODE Status must be specified. Highlight worrisome patients, issue of concern and suggestions to deal with them. DEATH/ EXPIRATIONS On being called to pronounce death you must perform certain steps On arrival to bed site observe for respirations, auscultate for heart sound palpate for pulse check pupil and corneal Reflex. Complete death notes on progress sheet and fill death certificate as early as possible. URGENT THROMBOLYSIS In patients with indications for Thrombolysis, every possible effort should be made to achieve urgent Thrombolysis to decrease doorto-needle-time in order to save precious myocardium.
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OCCUPATIONAL RISKS Standard barrier nursing and isolation techniques should be employed in cases of patients with infectious communicable diseases. These measures include: Gloves Masks Careful needle/sharp object handling Prophylaxis in cases of exposure if indicated (e.g. meningococcemia). In case of mishap/exposure, event should be reported to consultant on call, immediately. ACCOUNTABILITY In case of an incident, a committee of ward consultant will review the entire case in detail and will decide about warning/penalty. ETHICAL ISSUES Best interest of the patient should be watched, in case of conflict or confusion, issues should be discussed with consultant on call. CONFIDENTIALITY OF PATIENTS DATA Patients record and data should be kept confidential to watch his/her interests and diagnosis/prognosis should not be discussed with attendants without permission of patient/close attendant. SENIOR CONSULTATION On call consultant/senior registrar should be contacted on phone if required by the registrar on call. If he/she may request to see the patient then on call consultant should try to attend the patient personally within I hour of the request. CONSULTATIONS FROM OTHER DEPARTMENTS/URGENT SCANS Consultants and scans should be decided by the duty registrar and call to the respective department should be written with clear indications/exact questions to be asked and urgency of the consultation.
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PATIENT TRANSFER TO OTHER FACILITIES Once decision is made to transfer the patient to the other hospital for management, contact the concerned doctor/staff there first on telephone and discuss the case in detail and request them to make sure the beds are available for the patient. Note down the contact persons name and designation. Provide detailed notes on the referral slip. Provide ambulance preferably by the hospital through coordination with DMS/CMO, and if patient is serious, a doctor should accompany while transportation. Ambulance should be equipped with resuscitation equipment. RECORD KEEPING ER register shall be filled properly with composite diagnosis or relevant differential for every patient. Duty registrar will sign register at the end of duty, and countersigned by covering consultant for that day before morning meeting. Record of consultations provided to other department should be kept in the registrar. Death notes for patients who expired in ER should be written in the ER registrar immediately after the event. DRUGS & INVESTIGATIONS List of drugs and lab profile available in hospital for ER patients should be available to each shift of ER staff. DUTY TIMINGS House officer = 8 am to 8 pm- second shift 8pm to 8am (nm) Registrar = 8am to 8 am (nm) (batch on call should adjust the timing with mutual understanding) BLS/ACLS TRAINING House officers and registrar should be trained in BLS/ACLS before performing duties in E.R.
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DRESS CODE Dressing should be conservative & modest. No informal clothing (jeans & T-shirts for males), party wears or excessive jewelry (for females) is allowed, during duty hours. Every doctor should wear neat & clean overall, with properly displayed ID card or nameplate.
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Cardiac arrest: Adult Advanced Life-Support Algorithm
Do not interrupt CPR for >10s, except to defibrillate. Resistant VF/VT consider: Amiodarone 300mg IV (peripherally if no central access). A further 150mg may be given, followed by an infusion of 1mg/min for 6h, then 0.5mg/min for 6h. Alteratives to amiodarone are: o Lidocaine 100mg IV; can repeat once; then give 24mg/min IVI. o Procainamide 30mg/min IV to a total dose of 17mg/kg. Seek expert advice from a cardiologist. Asystole with P waves: Start external pacing (percutaneous transthoracic pacing through special paddles). Use endocardial pacing if experienced pacer is available. If unavailable, use atropine 0.6mg/5min IV while awaiting further help. Treat acidosis with good ventilation. Sodium bicarbonate may worsen intracellular acidosis and precipitate arrhythmias, so use only in severe acidosis after prolonged resuscitation (eg 50mL of 8.4% solution by IVI).
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Adult Basic Life-Support Algorithm The algorithm assumes that only one rescuer is present, with no equipment.
Shake and Shout
Head tilt / Chin lift If breathing: Recovery position Look, listen, feel (10 seconds max.)
Each breath over 1 second
Send or go for help as soon as possible according to guidelines

Manage the airway You open the airway by tilting the head and lifting the chin but only do this if there is no question of spinal trauma. Use a close fitting mask if available, held in place by thumbs pressing downwards either side of the mouth piece; palms against cheeks. Chest compressions Cardiopulmonary resuscitation (CPR) involves compressive force over the lower sternum with the heel of the hands placed one on top of the other, directing the weight of your body through your vertical, straight, arms. Depth of compression: 4cm. Rate of compressions: 100/min.
Remember that these are guidelines only, and that the exact circumstances of the cardio respiratory arrest will partly determine best practice. The guidelines are also more consensus-based than evidence based, and are likely to be adapted from time to time. For example, as consensus develops about the best recovery position-eg. Semi-lateral position, with under-most arm either straight at the side, in dorsal position, or in the ventral position cradling the head with the upper-most arm crossing it (more stable, but possible risk to arm blood flow).
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ACLS Pulseless Arrest Algorithm
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The diagram in figure summarizes the recommended sequences of CPR, rhythm checks, and delivery of drugs for PEA and asystole based on expert consensus.
Pulseless Arrest: Treatment sequences-Asystole/PEA. Prepare next drug prior to rhythm check. Administer drug during CPR, as soos as possible after the rhythm check confirms no VF/pulseless VT. Continue CPR while drugs are prepared and administered. Ideally, chest compressions should be interrupted only for ventilation (until advanced airway placed) and rhythm check. Search for and treat possible contributing factors.
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ICU MEDICATIONS
Category Target/Class Per kg Dose Average dose
Pressors, Ionotropes and Chronotropes D 0.52 g/kg/min 50-150 g/min Dopamine , D 210 g/kg/min 200-500 g/min , , D >10 g/kg/min 500-1000 g/min Norepinephrine 1 > 1 1- 40 g/min Phenylephrine 1 10-300 g/min Dobutamine 1 > 2 220 g/kg/min 50-1000 g/min Epinephrine 1, 2, 1, 2 2-20 g/min Isoproterenol 1, 2 0.1-10 g/min 0.75 mg/kg over 3 min 40-50mg over 3 min then Amrinone PDE then 5-10 g/kg/min 250-900 g/min 50 g/kg over 10 min 3- 4 mg over 10 min then Milrinone ODE then 0.375 - 0.75 20-50 g/min g/kg/min Cardiac Na channel 1-1.5 mg/kg then 70-100mg then 1- 4 Lidocaine (Class 1B) 1- 4 mg/min mg/min Na channel 17mg/kg over 60 min 1 gm over 60 min then 1- 4 Procainamide (Class IA) then 1- 4 mg/min mg/min Na, K, B, 150mg over 10 min, then Amiodarone CCB (Class III) 1 mg/min x 6 hrs, then 0.5 mg/min x 18 hrs K channel 5-10 mg/kg then 1- 4 350-700 mg then 1- 4 Bretylium (Class III) mg/min mg/min K channel Ibutilide 1 mg over 10 min, may repeat x 1 (Class III) Nitroglycerin NO 10-1000 g/min Nitroprusside NO 0.110 g/kg/min 5-800 g/min direct Epoprostenol 2-20 ng/kg/mm vasodilator Propranolol blocker 0.5-1.0mg q 5min then 1-10 mg/hr 500 g/kg then 20-40 mg over 1 min then Esmolol 1 > 2 blocker 25300 g/kg/min 2-20 mg/min 20 mg over 2 min then 1, 1, and 2 Labetalol blocker 20-80 mg q 10 min or 10-120 mg/hr 2.5-5 mg over 1-2 min repeat 5-10 mg in 15-30 min Verapamil CCB prn 5-20 mg/hr 0.25 mg/kg over 2 min 20 mg over 2min reload 25 Diltiazem CCB reload 0.35 mg/kg x prn mg x1 prn then 5-15 mg/hr then 5-15 mg/hr Purinergic Adenosine receptors in 6 mg rapid push if no response: 12 mg 12-18 mg AVN Enalapril ACE 0.625-2.5 mg over 5 min then 0.625-5 mg q 6 hrs direct Hydralazine 5-20 mg q 20-30 min vasodilator
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Category
Sedation Morphine Fentanyl Thiopental Etomidate Propofol Diazepam Midazolam Ketamine Haloperidol Paralysis Succinylcholine Tubocurare Pancuronium Vecuronium Cisatracurium
Target/Class Per kg
opioid receptors opioid receptors barbiturate anesthetic anesthetic BDZ BDZ anesthetic antipsychotic depolar..paralytic nACh nACh nACh nACh PDE
Dose Average dose
1-unlimited mg/hr 50-100 g then 50-unlimited g/hr 200-400 mg over 2 3-5 mg/kg over 2 min min 0.2-0.5 mg/kg 100-300 mg 1-3 mg/kg then 0.3-5 50-200 mg then 20mg/kg/hr 400 mg/hr 1-5 mg q l-2 hrs then q 6 hrs prn 0.52 mg q 5min prn or 0.5- 4 mg then 1-10 mg/hr 1 2 mg/kg 60-150 mg 2-5 mg q 20-30 min 0.6-1.1 mg/kg 10 mg then 6-20 mg/hr 0.08 mg/kg 0.08 mg/kg then 0.05 0.1 mg/kg/hr 0-10 g /kg/min 5.5mg/kg over 20min then 0.5-1 mg/kg/hr 10 U then 0.1 U/kg/hr 5-10 mg then 1-5 mg/hr 0.1-0.4 U/hr 50 g then 50 g/hr 20 mg/kg at 50 mg/min 1-1.5g over 20-30 min 1-1.5g over 10 min 70-100 mg 2- 4 mg q 30-9O min 5-10 mg over l-3 min then 2-8 mg/hr
Miscellaneous
Aminophylline Insulin Glucagon Vasopressin Octreotide Phenytoin Fosphenytoin Phenobarbital Mannitol 250-500 mg then 1080 mg/hr
V1 receptors somatostatin analog antiepileptic antiepileptic barbiturate
20 mg/kg at 150 mg/min 20 mg/kg at 50-75 1-1.5g over 20 min mg/min 1.5 - 2 g/kg over 30-60 min repeat q 6-12 hrs to keep osm 310-320
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Useful doses for the new house officers

Drugs Analgesics Aspirin Diclofenac Ibuprofen Paracetamol Codeine phosphate Dihydrocodeine tartrate Meptazinol Oxycodone Pethidine Tramadol Morphine Antiemetics Cyclizine Metaclopramide Ondansetron Antihistamines Chlorphenamine Cetirizine Levocetirizine Fexofenadine Loratadine Desloratidine 10-20mg IM/IV, max. 40mg/24h or 4mg/6h PO 5-10mg/24h PO 5mg/24h PO 120-180mg.24h PO 10mg/24h PO 5mg/24h PO SE of antihistamines: drowsiness; urinary retention;dry mouth; blurred vision;GI disturbance;arrhythmias. Drowsiness is less commoner with newer drugs, eg cetirizine, fexofenadine. 50mg/8h PO/IM/IV 10mg/8h PO/IM/IV 8mg/8h PO, 4mg IM/IV May cause extrapyramidal especially in young adults. SE, 300-900mg/4-6 h PO, max. 4g/24h 50 Mg/8h PO/PR 400mg / 6h PO, max. 2.4 g/24 h 0.5-1g/4-6h PO, max 4g/24h 30-60mg/4h PO/IM max. 24mg/24h 30mg/4-6h PO, or 50mg/46h IM/SC 200mg/3-6h PO, or 50100mg/2-4h IM/IV 5mg/6h PO 50-100mg/4h PO/IM/SC 50-100mg/4h PO/IM/IV 5-10mg/4h PO/IM/SC SE of NSAIDS: gastritis; bronchospasm; hypersensitivity. CI: GI ulcer/bleeding; NSAID-induced asthma; coagulopathy. Avoid aspirin in children (risks Reyes syndrome) Avoid if hepatic impairment Patients with chronic pain (eg malignancy) may require higher doses. SE of opioids: nausea and vomiting; constipation; drowsiness; hypotension, respiratory depression, dependence. CI: acute respiratory depression, acute alcoholism. Use carefully in head injury, as may hinder neurological assessment. Dose and frequency Notes
Gastric acid reducing drugs Cemetidine Ranitidine Omeprazole Esomeprazole Lansoprazole Pantoprazole Heparin Unfractional heparin Enoxaparin DVT prophylaxis: 5000u.12h SC DVT prophylaxis: 2040mg/24h SC. DVT/PE treatment: 1.5mg/kg/24h SE of heparins: bleeding; thrombocytopenia; hypersensitivity; hyperkalemia; osteoprosis after prolonged use. CI: coagulopathy; peptic ulcer; recent cerebral bleed; 400mg/6-12h PO 150mg/12h PO 20-40mg/24h PO 20-40mg/24h PO 15-30mg/24h PO 20-40mg/24h PO SE of H2-blokers: GI disturbance; LFT. SE of PPIs: GI disturbance; hypersensitivity. Acid-reducing drugs may mask symptoms of gastric cancer; use with care in middle-aged patients.
Medical Emergencies Management Guidelines SC until warfarinized. Unstable angina: 1mg/kg/12h SC for 2-8 days DVT prophylaxis: 3500u/24h SC (eg starting 2h pre-op). DVT/PE treatment: 175u/kg/24h SC till warfarinized. DVT prophylaxis: 25005000u/24h SC. DVT/PE treatment: 200u/kg/d SC (18000u/24h max.) Unstable angina: 120u/kg/12h SC (up to 10,000u/12h max.) for 5-8 days.
98 recent trauma or surgery; active bleeding.
Tinzaparin
Daltaparin
Hypnotics Temazepam Zopiclone 10-20mg PO at night 3.75-7.5mg PO at night SE: drowsiness; dependence. Zopicolone also causes bitter taste and GI disturbances. CI: respiratory depression; myasthenia.
Tranquillizers Haloperidol 2-5mg IM/IV initially, then every 4-8h till response. Max. 18mg in total. SE: extrapyramidal effects, sedation, hypotension, anti-muscarinic effects, neuroleptic malignant syndrome.
Others Naloxone In opiate overdose : 0.82mg IV repeated every 23min to a max. of 10mg if respiratory functions does not improve. To reverse opiate-induced respiratory depression: 100-200g IV every 2 min. To reverse benzodiazepines: 200g IV over 15s, then 100g every 60s if required, up to 1mg maximum. SE: tachycardia; fibrillation. Can precipitate opiate withdrawal.
Flumazenil
SE: convulsions (esp. in epileptics); nausea and vomiting; flushing. Avoid if patient has a life-threating illness controlled by benzodiazepines (eg status epilepticus).
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REFERENCES 1.
Rosen's Emergency Medicine: Concepts and Clinical Practice, 3-Volume by John A. Marx James Adams Peter Rosen Robert S. Hockberger Ron M. Walls Emergency Medicine: A Comprehensive Study Guide 6th edition by Judith E Tintinalli Marriott's Practical Electrocardiography by Galen S. Wagne Clinical Procedures in Emergency Medicine by James R. Roberts Emergency Medicine: Just the Facts, Second Edition by O. John Ma Goldfrank's Toxicologic Emergencies by Lewis Goldfrank Atlas of Emergency Medicine by Kevin Knoo Emergency Medicine: A Comprehensive Study Guide by Judith E. Tintinalli, Kelen, Gabor D. Kelen, American College of Emergency Physicians Staff, American College of Emergency Physicians Emergency Medicine Manual by O. John Ma, Judith E. Tintinalli, Gabor D. Kelen, Judith Tintinalli, J. Stephan Stapczynski Clinical Procedures in Emergency Medicine by James R. Roberts, Jerris R. Hedges, Arjun S. Chanmugam Emergency Medicine : Just the Facts by O. John Ma, Judith E. Tintinalli, Gabor D. Kelen, J. Stephan Stapczynski, David M. Cline Emergency Medicine Secrets by Vincent J. Markovchick ( Editor) , Peter T. Pons ( Editor) Poisoning and Drug Overdose by Ilene B. Anderson ( Editor) , Neal L. Benowitz ( Editor) , Paul D. Blanc ( Editor) Common Medical Diagnoses: An Algorithmic Approach by Patrice M. Healey, Edwin J. Jacobson Advanced Medical Life Support by Twink M. Dalton, Daniel Limmer, Joseph J. Mistovich, Howard Werman, Dan Limmer
2. 3. 4. 5. 6. 7. 8.
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16. 17. 18. 19.
International Trauma Life Support by John R. Campbell Little Black Book Of Emergency Medicine by Diaz Emergency Medicine: An Approach to Clinical Problem-Solving by Glenn C. Hamilton, Arthur B. Sanders, Alexander T. Trott, Gary Strange Handbook of Cardiac Emergencies by Ian McConachie ( Manufactured by) , David Hesketh Roberts ( Editor)

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