Medical Emergencies Management Guidelines

1Medical Emergencies Management Guidelines


(AL-QURAN)


Medical Emergencies Management Guidelines 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 Rawalian’s 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: [email protected]


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. Muhammad Khurram MBBS, FCPS Assistant Professor Medicine Holy Family Hospital Dr. Jahangir Sarwar MBBS, FCPS Associate Professor Surgery Holy Family Hospital Dr. Saima Usman MBBS, FCPS Senior Registrar Medicine Holy Family Hospital Dr. Muhammad Arif MBBS, FCPS Senior Registrar Medicine Holy Family Hospital Dr. Jawad Zaheer MBBS, FCPS Assistant Professor Anesthesia Holy Family Hospital Dr. Atifa Shoaib Associate Professor Pathology Holy Family Hospital Dr. Imtiaz Qureshi MBBS, FCPS Assistant Professor Pathology Holy Family Hospital Dr. Gul-e-Atif MBBS, M.phil Assistant Professor Pathology

Dr. Zameer Butt Senior Registar Medicine Holy Family Hospital Dr. Raja Adnan Arif MD Research Coordinator Holy Family Hospital Dr. Zahid Mahmood Minhas MBBS, MD, DCPS Senior Registrar Medicine Holy Family Hospital Dr. Abdul Naeem MBBS Medical Officer Senior Research Officer Holy Family Hospital Dr. Muhammad Saleem MBBS Post Graduate Trainee Holy Family Hospital Dr. Marina Khan MBBS House Physician Holy Family Hospital Dr. Qurat-ul-Ain MBBS House Physician Holy Family Hospital Muhammad Bilal 4th Year Medical Student Army Medical College, Rawalpindi 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. Acute Myocardial Infarction. 9 2. Acute Left Ventricular Failure. 10 3. Unstable Angina. 11 4. Narrow Complex Tachycardia. 12 5. Broad Complex Tachycardia. 15 6. Hypertension in Urgency and Emergency. 17 7. Acute Respiratory Distress Syndrome. 19 8. Acute Severe Asthma. 21 9. COPD – Acute Exacerbation. 23 10. Gastrointestinal Bleeding. 24 11. Variceal Bleeding. 28 12. Mesenteric Ischemia. 29 13. Acute Liver Failure 31 14. Acute Pancreatitis 33 15. Acute Stroke. 35 16. Acute Bacterial Meningitis 38 17. Aseptic Meningitis 41 18. Status Epilepticus. 42 19. Acute Renal Failure. 44 20. Diabetic Ketoacidosis. 46 21. Hyperosmolar Nonketotic Coma (Honc) 47 22. Hypokalemia. 48 23. Hyperkalemia 49 24. Hypocalcemia 51 25. Hypoglycemia 52 26. Adrenal Insufficiency 53 27. Acute Poisoning & Drug Overdose. 55 28. Organophosphate Poisoning. 59 29. Anaphylaxis. 60 30. Dengue Hemorrhagic Fever. 61 31. Fever And Neutropenia 62 32. Tetanus. 63 33. Bleeding Disorders. 64 34. Transfusion Therapy 65 35. Pregnancy & Hypertension. 67 36. Pregnancy & Diabetes Mellitus. 69

Appendix:

37. ICU Guidelines 70 38. SOPs for Emergency Ward Patient Care 84 39. Surgical Safety Checklist 89 40. Adult Advanced Life-Support Algorithm 91 41. Adult Basic Life-Support Algorithm 2005 42. ACLS Pulseless Arrest Algorithm 92 43. The diagram summary 93 44. ICU Medications 94 45. Useful drug's doses for the new house officers 96 46. References 98


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.


2: ACUTE LEFT VENTRICULAR FAILURE o Prop up, legs dangling over side of bed + oxygen with mask @ 10 –

15 L/min. o Maintain IV lines on both arms. o Take BP, pulse, ECG –attach cardiac monitor, SPO2. o Morphine sulphate 2 – 5 mg IV over several minute repeat every 10

– 25 min till effect is seen. o Lasix (furosemide) 40 – 100 mg IV stat – can be increased to 200

mg in subsequent doses. 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 μg/min

(10ml = 10mg, dilute in 90ml 5%D/W = 100ml). start at 60 micro drops/min and titrate.

o Catheterize or provide urinal & monitor intake/output on a chart. o Start Inf. Dobutamine @ 2.5 – 10 μ/kg/min – titrate according to the

clinical condition (max 25 μ/kg/min), dopamine 2 – 10 μg/kg/min and dose can be titrate (max 50 μ/kg/min).

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.


3: UNSTABLE ANGINA o Give oxygen o Analgesia o Aspirin 300 mg orally o Heparin: IV bolus 60 – 80 U/kg, infusion 14 U/kg/hr. o Serial EKG. o 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.

o Beta blocker – Metoprolol 25 mg TID or Atenolol 50 mg OD. o For patients already on beta blockers add calcium channel blockers

and vice versa. o Refer to cardiologist.


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 260—340bpm. 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 (10—l5s) 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.


Supraventricular tachycardia: If adenosine fails, use verapamil 2.5—5 mg IV over 2—3min. NB: NOT if on a β-blocker. If no response, a further 5mg IV over 3min (if age <60yrs). Alternatives: atenolol 5mg IV or sotalol 20—120mg 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 4—5 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, β-blockers (or verapamil— not with β-blockers, digoxin, or class I agents such as quinidine). If this does not control symptoms, consider radiofrequency ablation. Wolff—Parkinson—White (WPW) syndrome Caused by congenital accessory conduction pathway between atria and ventricles. Resting ECG shows short P—R interval and widened QRS complex due to slurred upstroke or ‘delta wave’. 2 types: WPW type A (+ve δ wave in V1) WPW type B (-ve δ 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.


Irregular narrow complex tachycardia Treat as AF—by far the most likely diagnosis. Control rate with either beta-blocker or digoxin. If onset < 48h consider cardioversion with either amiodarone, 300mg in over

20—60 mm, then 900mg over 24h; or DC shock. Consider anticoagulation with heparin and/or warfarin to reduce the risk of

stroke.


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.


If haemodynamically stable • Correct hypokalaemia and hypomagnesaemia: as above. • Amiodarone 300mg IV over 20—60 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 12—24h; 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 β-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.


6: HYPERTENSION Hypertension Urgency:

Asymptomatic severe HTN ie. S≥220 and D≥125 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 μg/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.


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.

o 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.

o If no response, consider tab. Prazosin (minipress) 1mg oral stat and strict bed rest.

o Get ECG. o 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.

o When BP comes to 160/100, patient can be discharged on oral treatment + diet advice + investigations → urine R/E, electrolytes, serum Ca, fasting lipids.

o Stage 2 patient needs more than 1 drug.


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 = non–cardiogenic pulmonary edema • Pathological = diffuse alveolar damage American – European Consensus Conference (1994): 4 criteria to define ARDS without biopsy • Acute onset • Bilateral patchy air–space disease • PCWP < 18 mmHg or no clinical evidence of ↑ LVEDP • PaO2 / FiO2 ≤ 200 [if PaO2 / FiO2 ≤ 300 → acute lung injury (ALI)]

Etiologies

Direct injury Indirect injury Aspiration Pneumonia Near drowning Inhalation injury Pulmonary contusion

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)


o 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: pressure-

targeted 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.

Prognosis Mortality: isolated ARDS = 40%, up to 90% if multiorgan system failure or sepsis.


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 sol’n (salbutamol 2.5 – 5 mg) q20 min until

improvement or toxicity appears ± Ipratropium 500 μg (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. Don’t 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 μg/min (18 ml/hr to 120 ml/hr) start at 5 μg/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.


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 PaCO2≥42. 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.


9: COPD – ACUTE EXACERBATION o Dyspneic / cyanosed patients – keep them propped up. o Likely cause LRTI, other includes Pneumothorax, pulmonary

embolism, poor drug compliance, IHD. o O2 with nasal cannula / mask @ 3 – 4 L/min. o Nebulize with ventolin solution 5mg – repeat after 20 min. if no

improvement. o Inj. Hydrocortisone (250mg – solucortef) IV stat – then IV 100mg

TDS for 24 hrs. o If associated fever, purulent sputum or respiratory failure or

pneumonia – admit. o Attach cardiac monitor, SPO2, take ECG, CXR – send baseline labs

& sputum R/E. o Signs of respiratory failure – bounding pulse, flaps, cyanosis, RR

>30 with signs of RHF o 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.

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. Don’t give if received oral theophylline or aminophylline in last 24 hours.

o Along with steroids, start tab. Terbutaline (Bricanyl) 2.5mg TDS, tab. Theophyline (Theograde) 350mg ½ BD, Atem inhaler 2 puffs TDS, steam/ ventolin inhalation 6 hourly, inhaled steroid (Beclomethasone) 2 puffs QID.

o If worsening dyspnea despite treatment, SPO2 < 90%, RR >35, or < 14, intubate the patient and consider ventilatory support.


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/Barrett’s 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 • Dieulafoy’s 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.


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


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 Ringer’s

solution • Transfusion therapy (blood bank sample for type & cross; can use O-

negative 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 Options Varices Pharmacologic

Octreotide 50μg IVB 50μg / hr infusion Vasopressin or vasopressin + nitroglycerin (less effective & more complications ? β-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

PUD Pharmacologic Proton pump inhibitors ? Octreotide 50μg IVB 50μg / 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

Mallory-Weiss Usually stops spontaneously Esophagitis Gastritis

Proton pump inhibitors, H2-antagonists

Diverticular disease Usually stops spontaneously Endoscopic therapy, arterial vasopressin or embolization, surgery

Angiodysplasia Arterial vasopressin, endoscopic therapy, surgery


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 Appearance of ulcer (from best to worse prognosis): clean base oozing without visible vessel adherent clot active bleeding.


11: VARICEAL BLEEDING o IV lines both arms, start IV N/S at rate depending on condition. o Send all baseline investigations (serum electrolytes, PT/APTT, Hb,

etc) plus blood group and cross match. o Arrange for blood / FFPs if PT prolonged, discontinue

anticoagulation. o Consider giving vitamin K by slow IV infusion. o Inj. Sandostatin 50µg IV stat, then inf. Sandostatin @ 50µg/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).

o For acid neutralization, inj. Omeprazole 40 mg IV daily infusion. o Thiamine 100 mg IV (inj. Benerva) to alcoholics. o Pass NGT and start stomach wash with D/W. o If bleeding stops, keep on monitoring for pulse and NG bleed one

hourly. o If bleeding won’t stop, pass Sangstaken’s Tube. Before passing

check both balloons with air. o Catheterize if in hypotension. o Maintain vitals and output monitoring charts preferably in ICU. o Urgent endoscopy if possible. o Syp. Lactulose 30 cc TID (Detoxicol, Lilac, Duphalac).


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 α-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


Treatment • Volume repletion and optimization of hemodynamics, discontinue α-

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%


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: Wilson’s disease, acute fatty liver of

pregnancy, HELLP syndrome, Reye’s 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 → Cushing’s 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


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 Wislon’s 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%


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: Cullen’s (Periumbilical) or Grey Turner’s (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)


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.


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 free-text 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.


• 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 37°C 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.


• 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.


16: ACUTE BACTERIAL MENINGITIS Definition Bacterial infection of the subarachnoid space

Microbiology in Adult Meningitis Etiology Comments

S. pneumoniae (30-50%)

Most common cause in adults. Look for distant infection (e.g., Osler’s triad = meningitis, pneumonia, endocarditis).

N. meningitides (l0-35%)

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.

H. influenzae (<5%)

↓ 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).

L. monocytogenes (5-lO%)

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.

GNRs (l-lO%) Usually nosocomial or post-procedure or in elderly or immunocompromised.

Syaphylococci (5%)

Seen with indwelling CSF shunt ( S. epidermidis) or following neurosurgery or head trauma (S. aureus).

Mixed infection Suspect parameningeal focus. 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, Kernig’s sign (patient supine, with hip flexed at 900, and knee flexed at 900; + if passive extension of knee results in resistance); Brudzinski’s sign (patient supine and limbs supine; + if passive neck flexion involuntary hip and / or knee flexion); note, Kernig’s and Brudzinski’s signs + in only ~ 50% of patients ± Focal neurologic findings (hemiparesis, aphasia, visual field cuts, cranial nerve palsies)


± 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

Condition Appearance Pressure

(cm)

WBC/mm

(predom type)

Glc

(mg/dl)

TP

(mg/dl)

Normal clear 9-18 0-5

lymphs 50-75 15-45

Bacterial cloudy 18-30 100-10,000

polys < 45

100-

1000

TB cloudy 18-30 <500

lymphs < 45 100-200

Fungal cloudy 18-30 <300

lymphs < 45 40-300

Aseptic clear 9-18

<300

polys

lymphs

50-100 50-100

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


Treatment of Meningitis

Clinical scenario Empiric treatment guidelines Normal adult Ceftriaxone 2g IV q 12hrs or cefotaxime 1g IV q 4-6 hrs

+ Vancomycin 1g IV q 12hrs (in case cephalosporin-resistant Pneumococcus) + Ampicillin 2 g IV q 4 hrs if suspect Listeria Chloramphenicol + TMP/SMX + vancomycin if β-lactam allergic

Immuno-compromised Ampicillin + ceftazidime ± vancomycin

CSF shunts, recent neurosurgery, head trauma

Vancomycin + ceftazidime

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


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, Behcet’s, sjogren’s syndrome, rheumatoid arthritis Neoplasms: intracranial tumors (or cysts), lymphomatous or carcinomatous meningitis


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.


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.)


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+, PO4

3-, 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.


• If worsening renal function but dialysis independent, consider renal biopsy.

• Diet: high in calories (2000-4000kcal/d) with adequate high-quality 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

Catheterize to asses s hour ly urine ou tput, and establi sh fluid charts

Ass ess intravas cular volume, BP, JVP, skin turgor, fluid balance sheet, weigh t,

CVP, attach to card iac monito r Co nsider inserting a central venous cannula

Investigations

Identify and treat hyperkalemia Use a cardiac monitor

If dehydrated Fluid challenge: 250–500ml of colloid or saline o ver 30 min

Reassess

Repeat challenge if still dehy drated. Aim for a CVP of 5 -10cm Once fluid replet e, con tinue fluids at 2 0ml + previous hour’s urine output per hour

If volume overloaded , consider urgent dialy sis A n itrate infusion, fu rosemide or “renal dose” d opam ine m ay help in the sh ort

term, especially to mak e space for bloo d tran sfusion etc . but does n ot alter outcome

Correct acidosis with sodium bicarbonate, eg 50ml of 8.4 % IV

If clinical suspicion of sepsis, take cultures, then treat vig orously Do not leave poss ible source of sepsis (eg. IV lines) in situ if not needed

Avoid neph rotoxic drugs, eg. NSAIDs, care with g entam icin. Check Data Sheet for all drugs given


20: DIABETIC KETOACIDOSIS o Hyperglycemia > 300 or may be lower, anion gap metabolic

acidosis, positive serum ketones. o Always suspect when patient is drowsy, hyperventilating,

dehydrated – even with no history of DM. o Maintain IV lines on both arms – ideally CVP line. o 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). o Send all investigations – Na / K / Cl / HCO3, ketones, RBS, urea,

urine R/E, ABGs – calculate anion gap (Na – [HCO3 + Cl]), ECG. o 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.

o 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.

o If no response in RBS in 2 hours, double the dose of insulin given. o RBS hourly, serum electrolytes / serum ketones 4 hourly. o Give broad spectrum antibiotics (Ampicillin, Flagyl, and

cefotaxime). o Maintain ½ hourly monitoring charts for vitals, insulin, intake /

output, electrolytes, clinical condition. o 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.


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 dehydration prerenal

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 ½ NS depending on degrees of

volume and fee H2O depletion • Low-dose insulin (e.g. 0.05 U/kg/hr)


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, Bartter’s

syndrome (loop of Henle dysfunction = effects of furosemide), Gitelman’s syndrome (distal convoluted tubule dysfunction = effect of thiazide)

• Hypertensive o primary hyperaldosteronism (Conn’s syndrome) o secondary hyperaldosteronism (i.e., high renin states): renal

artery stenosis, renin-secreting tumors o pseudohyperaldosteronism: licorice ingestion, Cushing’s

syndrome, Liddle’s 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


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, β-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 end-stage renal disease Normal GFR (i.e., hypoaldosteronisms) • Hyporeninemic (i.e. type IV RTA usually secondary to diabetic

nephropathy, ACEI, NSAIDs) • Primary adrenal: Addison’s 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 cardio-protection; 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


30g enema (followed by colonic irrigation, after 9h, to remove K+

from the colon). • Dialysis.


24: HYPOCALCEMIA Category Etiologies Hypoparathyroidism Isolated

PGA type I (chronic mucocutan. candidiasis + hypoparathyroid + Addison’s) s/p thyroidectomy, hypomagnesemia (↓ secretion and effect)

Pseudo-hypoparathyroidism

PTH end-organ resistance (...↑ serum PTH) + skeletal abnorm. & retardation (Pseudopseudohypoparathyroidism = syndrome but normal Ca)

Vitamin D deficiency Renal failure ↓ l,25-(OH)2D3 production + ↑ PO4 ↑ calcium

deposition in soft tissue Miscellaneous Pancreatitis, citrate excess (e.g. after multiple

blood transfusions) Clinical manifestations Neuromuscular irritability: perioral parasthesias, cramps, & Chvostek’s (tapping facial nerve contraction of facial muscles), + Trousseau’s (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


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.


26: ADRENAL INSUFFICIENCY Etiologies • Primary= adrenocortical disease = Addison’s disease

Autoimmune (most common in industrialized countries) Isolated Polyglandular autoimmune syndromes (PGA)

PGA I= Chronic mucocutaneous candidiasis + hypoparathyroidism + Addison’s

PGA II = Addison’s + 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 μg) corticotropin stimulation test: normal =pre-or

60’ post-cortisol ≥ 18 μg/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 μg) corticotrophin stimulation test: can detect mild secondary adrenal insufficiency


• 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 μg PO q d in am


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.

2. 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


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.

c. 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 N-acetylcysteine. 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.

4. 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.


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.

6. 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.


Table. Available Tests and the Specimen Required for Determination. Test Sample Required Special Instructions

RBC cholinesterase

5 ml heparinized

Freshly collected blood sample; place in ice immediately after collection and during transport to the lab

Salicylate 2 ml serum Collect 5 ml blood in a plain tube

Methanol Plasma

Collect 5 ml blood with anticoagulant (citrate or oxalate except heparin and EDTA); place in ice

Ethanol Serum Collect 5 ml blood in a plain tube

Paracetamol Serum/urine Collect 5 ml blood in a plain tube or 10 ml freshly voided urine

Mercury

10 ml heparinized blood 50 ml aliquot of 24 hour urine

Collect 10 ml blood in heparinized tube Collect 24 hr urine (e.g. 8:00 am- 8:00 am the following day, mix well and submit 50 ml aliquot

Isoniazid 5 ml serum or 10 ml urine

Collect 10 ml blood in plain tube or 10 ml freshly voided urine

Coproporphyrin 200 ml aliquot of 24 hour urine sample

Place 10 ml sodium carbonate to the collection bottle, collect a 24 hr urine, mix well and submit 200 ml aliquot

Phenobarbital Serum Collect 5 ml blood in plain tube Amphetamine / Metamphetamine Urine Collect freshly voided urine

Phenothiazine 10 ml urine Collect freshly voided urine Paraquat / Diquat 10 ml urine Collect freshly voided urine Quinidine / Quinine 10 ml urine Collect freshly voided urine Para- nitrophenol 15 ml urine Collect freshly voided urine

Methemoglobin / Sulfhemoglobin

5 ml heparinized blood

Collect 5 ml blood in heparinized test tube


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, sulfa-

containing drugs and aminoglycosides. 9. Correct acidosis with sodium bicarbonate


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.

Consider when compatible his tory of severe allergic - type reaction with res piratory d ifficulty and/or hypotension especially if skin changes present.

Oxygen

Stridor, wheez e, respira tory distress or clin ical signs of shock

Epinephrine (adrenaline) 1:1000 0.5m1 (500microrams) IM

Repeat in 5 minutes if no clin ical improvement

Antihistamine (chlorpheniramine) 10 — 20mg s low IV

For a ll severe or recurrent reactions and patients w ith

asthma give hydrocortisone 100 — 500mg IM or slow IV

If clinica l manifes tations of shock do not respond to drug treatment give 1 — 2 liters IV fluid. R apid infusion may be

nec essary.

IN A DDITION

1. 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.

2. 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.

3. If adults are treated with an Epipen, then 300 micrograms will usually be sufficient.

4. Ensure that the name of the agent is written prominently in the patient’s notes and on the drug card.


30: DENGUE HEMORRHAGIC FEVER

A. Etiology: Dengue virus B. Transmission: Through bite of female Aedes aegypti mosquito C. Symptoms: 2-7 days of fever D. 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


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

Vancomycin + Ceftazidime

Fever (≥ 38.30 C) and neutropenia (< 500/mm3)

Evaluate

Is Vancomycin needed?

Indications No indications

Severe mucositisQuinalone prophylaxisColonized with

Meth-resistant. S.aureusPen-Ceph-resitant. S. pneumoniae

Obvious catheter-related infectionHypotension

Monotherapy Duotherapy

Ceftazidime or Imipenem

Aminoglycoside + antipseudomonal β-lactam

Reassess after 3 days

Vancomycin + Ceftazidime

Fever (≥ 38.30 C) and neutropenia (< 500/mm3)

Evaluate

Is Vancomycin needed?

Indications No indications

Severe mucositisQuinalone prophylaxisColonized with

Meth-resistant. S.aureusPen-Ceph-resitant. S. pneumoniae

Obvious catheter-related infectionHypotension

Monotherapy Duotherapy

Ceftazidime or Imipenem

Aminoglycoside + antipseudomonal β-lactam

Reassess after 3 days


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


33: BLEEDING DISORDERS

Etiologies of bleeding disorders Category Etiologies

Thrombocytopenia ↓ production: congenital, alcohol / drug induced ↑ destruction: autoimmune, drug induced, infections

Defective platelet function

Congenital: membrane or granule abnormalities von Willebrand’s disease (vWD)

Acquired: production of abnormal platelets: myeloproliferative disorders modification of abnormal platelets: uremia, aspirins, NSAIDs

Coagulopathy Congenital: vWD, hemophilia Acquired: vit. K defic., liver disease, DIC, factor

inhibitor, warfarin, heparin

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 • DIC—all 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.


34: TRANSFUSION THERAPY Product Indications and Comments Packed red blood cells (PRBCs )

Hb < 7-8g/dl if not critically ill Hb < 10g/dl if active bleeding, cardiac or pulmonary co-morbidity, sepsis, or hemoglobinopathy. Tolerate Hb 7-9 g/dl as long as no cardiac disease?

Platelets 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

Fresh frozen plasma (FFP)

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

Cryoprecipitate vWD, hemophilia, or fibrinogen <100mg/dl and bleeding or pre-procedure (cryoprecipitate contains vWF, factor III, and fibrinogen)

Irradiated blood products

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-negative CMV-seronegative pregnant women, transplant candidates, recipients of transplants, SCID patients, or AIDS patients (regardless of their CMV status).

Leukopoor filtered 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

Non-infectious Risk (per unit) Infectious Risk (per unit) Febrile 1:100 CMV common Allergic 1:100 Hepatitis B 1:63,000 Delayed hemolytic 1:1000 Hepatitis C 1:103,000 Acute hemolytic <1:250,000 HTLV < 1:100,000 Fatal hemolytic <1:100,000 HIV 1:493,000 TRALI 1:5000

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


• 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 allo-

antibodies against minor antigens o treatment: vigorous IVF, maintain UOP with diuretics,

mannitol, or dopamine


35: PREGNANCY & HYPERTENSION

Hypertensive Disorders of Pregnancy

Clinical Finding Chronic Hypertension

Gestational Hypertension Preeclampsia

1.Time of onset of hypertension

< 20 weeks of gestation

Usually in third trimester

20 weeks of gestation

2. Degree of hypertension Mild or severe Mild Mild or severe

3. Proteinuria* Absent Absent Usually present 4. Serum urate > 5.5mg/dI Rare Absent Present in almost

all cases 5. Hemo-concentration, thrombocytopenia, liver_dysfunction

Absent Absent Present in severe disease

6. LVH by ECG May be present Absent Absent * Defined as 1 + by dipstick testing on two occasions or 300 mg in a 24-hour 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 A’s (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 A’s (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


2. (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

3. Atenolol (Tenormin) 50 mg tab OD PO 4. (Adalat) Nifedipine 5-10 mg PO or SL q 6-8 hours 5. 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


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 Two-

hour 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


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. Tailored care approach 2. Repeated clinical examination 3. Repeated vital signs recording 4. Exact Intake/Output Record 5. If there is conflict between clinical assessment and monitor, consider

later as wrong 6. Changes and trends are more important than single measurement


Routine Surveillance Monitoring Vital Signs: 1. They are maintained on an hourly basis in patients on ventilators and

in other patients according to the patient’s conditions. 2. BP Monitoring: Reduction in BP shows failure of normal circulatory

compensation. 3. Pulse Pressure: It is difference b/w Systolic and Diastolic BP. It

shows early signs of hypovolemia. 4. Monitoring of Heart Rate: It is important in cases of dysarrhythmia. 5. Haematocrit: It increases by dehydration and hypovolemia and

decrease in Hemorrhage. 6. 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. 7. ECG Monitoring: It is done for cardiac arrhythmias and electrolytes

status. 8. Serum Electrolytes. Chemical assessment of tissue hypoxia 1. Acidosis: PH < 7.2 2. Base deficit of >5 mEq 3. Bicarbonate < 20 mEq/L 4. Anion gap of > 8 mEq/L 5. Serum Lactate > 2 mEq /L 6. Gastric PH < 7.2 mEq/L


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 patient’s 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.


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 and chest

Physiotherapy are required. 5. If mucus plugs present then chest Physiotherapy. 6. For comatose patients IMPPV can be used. 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.


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. Correct hypovolemia. 2. Correct hemodynamics imbalances. 3. Restore cardiac output. 4. Restore intra-arterial pressure. 5. Use judiciously inotropic support & fluid replacement. 6. If required, invasive monitoring should be done. 7. Low dose dopamine at 2 microgram/kg/mm causes selective

stimulation of dopaminergic receptors in the kidney.


8. Diuretics can be given for oliguria & anuria. 9. 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. Heparin (7500 IU BD or 5000 IU TDS). 2. LMW Heparin (according to weight). 3. Compression stockings. 4. IVC filter. Prophylaxis should be continued even after discharge from hospital. It should especially be given in patients with spinal cord injury / paralysis. Endotracheal Intubation 1. A size of >7.5mm is used for adults. 2. ETT is checked especially balloon inflated. 3. Ventilation circuit to be attached is checked. 4. Suction catheter and suction machine is checked. 5. A malleable catheter should be available. 6. Tape to tie ETT. 7. A working Laryngoscope is needed. 8. Tube position is assessed by palpating balloon in sternal notch or by

X-ray. 9. Both lungs should be auscultated. 10. The tube should be secured and point noted. 11. Regular Pharyngeal and ETT Suctioning done depending on

condition. 12. Inadequate insertion of ETT depth can be checked by palpating ETT

Cuff over Thyroid cartilage. 13. Use less than 20mmHg pressure for balloon inflation. 14. In prolong ETT intubation, 2-4 hourly deflation of balloon should be

considered.


Techniques of Extubation 1. Patient should be awake, as evidenced by eye opening and

purposeful movements. 2. Adequate recovery from muscle relaxant should be established

before extubation. 3. 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.

4. Mouth and Pharynx are suctioned appropriately. 5. 100% of Oxygen is given before extubation. 6. Tube is withdrawn in a single, smooth motion. 7. Facemask is applied with 100% of Oxygen. 8. Extubation should not be done if there is danger of aspiration. 9. Extubation should be avoided if it is considered that reintubation will

be difficult. Tracheostomy Post OP Care 1. Suction should be done as often as required. 2. Tracheostomy tube should be covered with moist gauze piece

changed frequently for humidification. 3. Spare tube, introducer; tapes and tracheal dilator should be available

at the bedside of the patient. 4. Suction should be done under aseptic conditions. 5. When mucous is tenacious, isotonic saline can be used. 6. If there is an inner tube it should be removed and washed with

Sodium Bicarbonate Solution every 4 hourly. 7. Physiotherapy should be done. 8. Regular check for positioning of the Tracheostomy tube.


Ventilatory support in Asthma Recommended Ventilatory settings TV =6—8 ml/kg RR= 10—12/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


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.


WEANING Preliminary Assessment This is based on improvement in underlying conditions. 1. Have the causes of underlying respiratory failure been effectively

treated or reversed. 2. Is the patient stable, in terms of both inciting illness and any

complications? 3. Rule out electrolyte balance. 4. Rule out hypoglycemia. 5. Patient should be alert to protect his airways. 6. Patient should have effective cough. 7. Secretions should not be copious or tenacious. 8. 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.


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. RR > 35 / min for more than 5 min. 2. Oxygen saturation < 90 %. 3. Heart rate >140 beats per min or sustained 20 % changes in heart

rate. 4. Systolic blood pressure >180mm Hg or < 90 mm Hg. 5. Increased anxiety.


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.

2. Nearly dead / Alive on ventilators

One who is alive only because be or she is receiving life support in the intensive care unit.

3. With-holding support Never providing the patient with the therapy in question.

4. Withdrawing support Discontinuing already instituted therapy.

5. Foregoing therapy It refers both to the withholding and with drawing of therapy. If ventilatory support is withdrawn vasopressor therapy should

be continued.

6. Decision It should be made on individual basis considering disease process, prospects of recovery and after discussing with family.


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.


5. Failure of heart rate to increase by > 5beats / min after 1-2 mg of Atropine.

6. 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.


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 patient’s 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 post-procedure precautions.

Get signatures on informed consent. Never forget pending follow up studies like Post-Procedure X-ray.


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 Patient’s 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 “door-to-needle-time” in order to save precious myocardium.


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 PATIENT’S DATA

Patient’s 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.


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 person’s 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 counter-signed 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.


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.


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 2-

4mg/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).


Adult Basic Life-Support Algorithm The algorithm assumes that only one rescuer is present, with no equipment.

Send or go for help as soon as possible according to guidelines

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).

If breathing: Recovery position

Each breath over 1 second

Look, listen, feel (10 seconds max.)

Head tilt / Chin lift

Shake and Shout

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.


ACLS Pulseless Arrest Algorithm


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.


ICU MEDICATIONS

Dose Category Target/Class Per kg Average dose

Pressors, Ionotropes and Chronotropes

Dopamine D β, D α, β, D

0.5—2 μg/kg/min 2—10 μg/kg/min >10 μg/kg/min

50-150 μg/min 200-500 μg/min 500-1000 μg/min

Norepinephrine α1 > β1 1- 40 μg/min Phenylephrine α1 10-300 μg/min Dobutamine β1 > β2 2—20 μg/kg/min 50-1000 μg/min Epinephrine α1, α2, β1, β2 2-20 μg/min Isoproterenol β1, β2 0.1-10 μg/min

Amrinone PDE 0.75 mg/kg over 3 min then 5-10 μg/kg/min

40-50mg over 3 min then 250-900 μg/min

Milrinone ODE 50 μg/kg over 10 min then 0.375 - 0.75 μg/kg/min

3- 4 mg over 10 min then 20-50 μg/min

Cardiac

Lidocaine Na channel (Class 1B)

1-1.5 mg/kg then 1- 4 mg/min

70-100mg then 1- 4 mg/min

Procainamide Na channel (Class IA)

17mg/kg over 60 min then 1- 4 mg/min

1 gm over 60 min then 1- 4 mg/min

Amiodarone Na, K, βB, CCB (Class III)

150mg over 10 min, then 1 mg/min x 6 hrs, then 0.5 mg/min x 18 hrs

Bretylium K channel (Class III)

5-10 mg/kg then 1- 4 mg/min

350-700 mg then 1- 4 mg/min

Ibutilide K channel (Class III) 1 mg over 10 min, may repeat x 1

Nitroglycerin NO 10-1000 μg/min Nitroprusside NO 0.1—10 μg/kg/min 5-800 μg/min

Epoprostenol direct vasodilator 2-20 ng/kg/mm

Propranolol β blocker 0.5-1.0mg q 5min then 1-10 mg/hr

Esmolol β1 > β2 blocker 500 μg/kg then 25—300 μg/kg/min

20-40 mg over 1 min then 2-20 mg/min

Labetalol α1, β1, and β2 blocker

20 mg over 2 min then 20-80 mg q 10 min or 10-120 mg/hr

Verapamil CCB 2.5-5 mg over 1-2 min repeat 5-10 mg in 15-30 min prn 5-20 mg/hr

Diltiazem CCB 0.25 mg/kg over 2 min reload 0.35 mg/kg x prn then 5-15 mg/hr

20 mg over 2min reload 25 mg x1 prn then 5-15 mg/hr

Adenosine Purinergic

receptors in AVN

6 mg rapid push if no response: 12 mg 12-18 mg

Enalapril ACE 0.625-2.5 mg over 5 min then 0.625-5 mg q 6 hrs

Hydralazine direct vasodilator 5-20 mg q 20-30 min


Dose Category Target/Class Per kg Average dose

Sedation Morphine μ opioid receptors 1-unlimited mg/hr Fentanyl μ opioid receptors 50-100 μg then 50-unlimited μg/hr

Thiopental barbiturate 3-5 mg/kg over 2 min 200-400 mg over 2 min

Etomidate anesthetic 0.2-0.5 mg/kg 100-300 mg

Propofol anesthetic 1-3 mg/kg then 0.3-5 mg/kg/hr

50-200 mg then 20-400 mg/hr

Diazepam BDZ 1-5 mg q l-2 hrs then q 6 hrs prn

Midazolam BDZ 0.5—2 mg q 5min prn or 0.5- 4 mg then 1-10 mg/hr

Ketamine anesthetic 1 – 2 mg/kg 60-150 mg

Haloperidol antipsychotic 2-5 mg q 20-30 min

Paralysis Succinylcholine depolar..paralytic 0.6-1.1 mg/kg 70-100 mg Tubocurare nACh 10 mg then 6-20 mg/hr Pancuronium nACh 0.08 mg/kg 2- 4 mg q 30-9O min

Vecuronium nACh 0.08 mg/kg then 0.05 - 0.1 mg/kg/hr

5-10 mg over l-3 min then 2-8 mg/hr

Cisatracurium nACh 0-10 μg /kg/min Miscellaneous

Aminophylline PDE 5.5mg/kg over 20min then 0.5-1 mg/kg/hr

250-500 mg then 10-80 mg/hr

Insulin 10 U then 0.1 U/kg/hr Glucagon 5-10 mg then 1-5 mg/hr Vasopressin V1 receptors 0.1-0.4 U/hr

Octreotide somatostatin analog 50 μg then 50 μg/hr

Phenytoin antiepileptic 20 mg/kg at 50 mg/min 1-1.5g over 20-30 min

Fosphenytoin antiepileptic 20 mg/kg at 150 mg/min 1-1.5g over 10 min

Phenobarbital barbiturate 20 mg/kg at 50-75 mg/min 1-1.5g over 20 min

Mannitol 1.5 - 2 g/kg over 30-60 min repeat q 6-12 hrs to keep osm 310-320


Useful doses for the new house officers Drugs Dose and frequency Notes

Analgesics

Aspirin 300-900mg/4-6 h PO, max. 4g/24h

Diclofenac 50 Mg/8h PO/PR Ibuprofen 400mg / 6h PO, max. 2.4

g/24 h

SE of NSAIDS: gastritis; bronchospasm; hypersensitivity. CI: GI ulcer/bleeding; NSAID-induced asthma; coagulopathy. Avoid aspirin in children (risks Reye’s syndrome)

Paracetamol 0.5-1g/4-6h PO, max 4g/24h

Avoid if hepatic impairment

Codeine phosphate 30-60mg/4h PO/IM max. 24mg/24h

Dihydrocodeine tartrate

30mg/4-6h PO, or 50mg/4-6h IM/SC

Meptazinol 200mg/3-6h PO, or 50-100mg/2-4h IM/IV

Oxycodone 5mg/6h PO Pethidine 50-100mg/4h PO/IM/SC Tramadol 50-100mg/4h PO/IM/IV Morphine 5-10mg/4h PO/IM/SC

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.

Antiemetics

Cyclizine 50mg/8h PO/IM/IV Metaclopramide 10mg/8h PO/IM/IV May cause extrapyramidal SE,

especially in young adults. Ondansetron 8mg/8h PO, 4mg IM/IV

Antihistamines

Chlorphenamine 10-20mg IM/IV, max. 40mg/24h or 4mg/6h PO

Cetirizine 5-10mg/24h PO Levocetirizine 5mg/24h PO Fexofenadine 120-180mg.24h PO Loratadine 10mg/24h PO Desloratidine 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.

Gastric acid reducing drugs

Cemetidine 400mg/6-12h PO Ranitidine 150mg/12h PO

SE of H2-blokers: GI disturbance; ↑ LFT.

Omeprazole 20-40mg/24h PO Esomeprazole 20-40mg/24h PO Lansoprazole 15-30mg/24h PO Pantoprazole 20-40mg/24h PO

SE of PPIs: GI disturbance; hypersensitivity. Acid-reducing drugs may mask symptoms of gastric cancer; use with care in middle-aged patients.

Heparin

Unfractional heparin DVT prophylaxis: 5000u.12h SC

Enoxaparin DVT prophylaxis: 20-40mg/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;


SC until warfarinized. Unstable angina: 1mg/kg/12h SC for 2-8 days

Tinzaparin DVT prophylaxis: 3500u/24h SC (eg starting 2h pre-op). DVT/PE treatment: 175u/kg/24h SC till warfarinized.

Daltaparin DVT prophylaxis: 2500-5000u/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.

recent trauma or surgery; active bleeding.

Hypnotics

Temazepam 10-20mg PO at night Zopiclone 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 : 0.8-2mg IV repeated every 2-3min to a max. of 10mg if respiratory functions does not improve. To reverse opiate-induced respiratory depression: 100-200µg IV every 2 min.

SE: tachycardia; fibrillation. Can precipitate opiate withdrawal.

Flumazenil To reverse benzodiazepines: 200µg IV over 15s, then 100µg every 60s if required, up to 1mg maximum.

SE: convulsions (esp. in epileptics); nausea and vomiting; flushing. Avoid if patient has a life-threating illness controlled by benzodiazepines (eg status epilepticus).


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

2. Emergency Medicine: A Comprehensive Study Guide 6th edition by Judith E Tintinalli

3. Marriott's Practical Electrocardiography by Galen S. Wagne

4. Clinical Procedures in Emergency Medicine by James R. Roberts

5. Emergency Medicine: Just the Facts, Second Edition by O. John Ma

6. Goldfrank's Toxicologic Emergencies by Lewis Goldfrank

7. Atlas of Emergency Medicine by Kevin Knoo

8. 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

9. Emergency Medicine Manual by O. John Ma, Judith E. Tintinalli, Gabor D. Kelen, Judith Tintinalli, J. Stephan Stapczynski

10. Clinical Procedures in Emergency Medicine by James R. Roberts, Jerris R. Hedges, Arjun S. Chanmugam

11. Emergency Medicine : Just the Facts by O. John Ma, Judith E. Tintinalli, Gabor D. Kelen, J. Stephan Stapczynski, David M. Cline

12. Emergency Medicine Secrets by Vincent J. Markovchick ( Editor) , Peter T. Pons ( Editor)

13. Poisoning and Drug Overdose by Ilene B. Anderson ( Editor) , Neal L. Benowitz ( Editor) , Paul D. Blanc ( Editor)

14. Common Medical Diagnoses: An Algorithmic Approach by Patrice M. Healey, Edwin J. Jacobson

15. Advanced Medical Life Support by Twink M. Dalton, Daniel Limmer, Joseph J. Mistovich, Howard Werman, Dan Limmer


16. International Trauma Life Support

by John R. Campbell

17. Little Black Book Of Emergency Medicine by Diaz

18. Emergency Medicine: An Approach to Clinical Problem-Solving by Glenn C. Hamilton, Arthur B. Sanders, Alexander T. Trott, Gary Strange

19. Handbook of Cardiac Emergencies by Ian McConachie ( Manufactured by) , David Hesketh Roberts ( Editor)

Medical Emergencies Management Guidelines

Documents

Transcript of Medical Emergencies Management Guidelines