Medical

Emergencies
Guidebook
First Edition
2007

Edited by:
Hasan Abu-Aisha
Elwaleed Ali Mohamed Elhassan

Original Copyright © 2007. All Rights Reserved at the Academic Office

of the President of National Ribat University. Khartoum. Sudan
National Library Cataloging - Sudan
616.252 Hasan Abu-Aisha
Medical Emergencies Guidebook /
Hasan Abu Aisha,Elwaleed Ali Mohamed Elhassan
1st edition

ISBN: 978 - 99942 - 862 - 4

1. Medical emergencies. Guidebooks. Handbooks.Manuals

A.Title.
B .Elwaleed Ali Mohamed Elhassan - 1st edition
 Medical
Emergencies
Guidebook

First Edition
2007

Editors:
Hasan Abu-Aisha FRCP (Chief Editor)
Professor of Medicine
Consultant Physician and Nephrologist
National Ribat University Hospital
President, the National Ribat University

Elwaleed Ali Mohamed Elhassan MACP, ABIM

Assistant Professor of Medicine
Faculty of Medicine, University of Khartoum
Director, Ribat Center for Regular Peritoneal Dialysis
Researcher, Academic Office of the President of the National Ribat
University
 Medical Emergencies Guidebook
4

Table of Contents
áeuó≤Ÿo G 6
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Section Editors: 8
Previous Contributors 9
List of Abbreviations Used in This Guidebook 10
Approach to Common Emergency Symptoms 14
Chest Pain 16
Acute Fever 18
Approach to Medical Causes of Acute Abdominal Pain 28
Various General Medical Emergencies 34
Shock 36
Coma 41
Cardiovascular Emergencies 48
Acute Coronary Syndromes 50
Acute Cardiogenic Pulmonary Edema 54
Cardiogenic Shock 55
Endocrine Emergencies 60
Diabetic Ketoacidosis (DKA) 62
Diabetic Lactic Acidosis 66
Hyperosmolar Hyperglycemic State 67
Hypoglycemia 71
Addisonian Crisis 72
Myxedema Coma 73
Thyroid Storm 75
Pituitary Apoplexy 77
Gastro-intestinal Emergencies 78
Acute Diarrhea In Adults 80
Upper Gastro-intestinal Hemorrhage 84
Treatment of Bleeding Esophageal Varices 90
Lower Gastrointestinal Bleeding 100
 5

Hepatic Encephalopathy and Fulminant Hepatic Failure (FHF) 102

Pulmonary Emergencies 112
Management of Acute Asthma Exacerbations in Adults 114
Management of asthma exacerbations in adults 118
Acute Asthma Exacerbations in Adults
Spontaneous Pneumothorax 119
Acute Pulmonary Embolism 123
Renal, Hypertensive and Electrolyte Emergencies 128
Acute Renal Failure 130
Severe Hypertension 135
Hypokalemia 142
Hyperkalemia 145
Hyponatremia 150
Hypernatremia 153
Hypercalcemia 154
Neurologic Emergencies 160
Stroke (Cerebrovascualr Accident) 162
Status Epilepticus 172
Psychiatric Emergencies 180
Psychiatric Emergencies 182
Management of Aggressive Violent Patients 182
The Suicidal Patient 189
The Unresponsive Patient (Stupor) 191
Neuroleptic Malignant Syndrome (NMS) 193
Other Neuroleptic-Induced Problems 195
Appendix 1: National Malaria Protocol 197
Appendix 2: Table of Drugs Used in This Guidebook 198
 Medical Emergencies Guidebook
6

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 7

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 Medical Emergencies Guidebook
8

Section Editors
Cardiac Emergencies
Ahmed Ali Ahmed Suliman
MACP, ABIM
Consultant Physician and Cardiologist
Assistant Professor of Medicine, University of Khartoum

Endocrine Emergencies
Hisham Mohamed Abdel Rahim
FRCP (Edin.)
Consultant Physician and Endcrinologist,
National Ribat University Hospital

Gastrointestinal Emergencies
Amira Abbas Mohamed Fadl
FRCP
Consultat Physician and Gastroenterologist,
National Ribat University Hospital

Pulmonary Emergencies
Ala’Eldin Hassan Ahmed
MD, FRCP, FCCP
Consultant Physician and Pulmonologist
Associate Professor of Medicine, University of Khartoum
Renal, Hypertensive and Electrolyte Emergencies
Neurologic Emergencies
Elwaleed Ali Mohamed Elhassan
MACP, ABIM
Assistant Professor of Medicine
Faculty of Medicine, University of Khartoum

Psychiatric Emergencies
A.E.Abdelghani
MRCPsych (London), DPM(Dublin), DCP(Dublin)
Consultant Psychiatrist,
National Ribat University Hospital
 9

Previous Contributors
Neurology Prof. Dawod Mustafa
Dr. Hasab Elrasoul Siddig Ali
Dr. Mohamed Najeeb
Dr. Ammar Eltahir
Dr. Abashar Hussian

Gastroenterology and Infectious Prof. Salih Yassin

Diseases Prof. Suliman Salih Fudail
Prof. Mohamed Siddig Ali
Prof. Abdul Gadir El Kadro
Dr. Fatima Farah
Dr. Huda Elbagir
Dr. Baha Eldin Gasm Elseed
Dr. Hatim Modawi
Dr. Mohamed Ali Eltahir
Respiratory Diseases Dr. Mohamed Elbagir
Dr. Abdul Lateef Gasem Alla
Psychiatry Prof. Abdul Aal Elidrisi
Cardiology Prof. Siddig Ahmed Ismail
Dr. Nawal Elkordofani
Dr. Mohamed Saeed Akhalifa
Dr. Ahmed Babiker
Dr. Adel Elbushi
Nephrology and Poisoning Dr. Abdul Rahman Ali
Dr. Salma Suliman
Dr. Gahelnabi, M, A
Endocrinology Prof . El-Mahadi Mohamed Ali
Dr. Ali Elzayyat
 Medical Emergencies Guidebook

Appendix : 1
List of Abbreviations Used in This Guidebook
Abbreviation Connotation
ABC Airway, breathing and circulation
ABG Arterial blood gas
ACE Angiotensin converting enzyme
ACE-I Angiotensin converting enzyme inhibitor
ACLS Advanced cardiac life support
ACS Acute coronary syndrome
AF Atrial fibrillations
AG Anion gap
AGN Acute glomerulonephritis
AIN Acute interstitial nephritis
ALT Amino alanine transferase
AML Acute myeloid leukemia
ANA Anti nuclear antibody
ANCA Antictyoplasmic antibody
ARF Acute renal failure
ASO Antistreptolysin antibody
AST Asparatate amino transferase
ATN Acute tubular necrosis
AVM Arteriovenous malformation
AXR Abdominal x ray
BD Twice daily
BP Blood pressure
BPH Benign proststic hypertrophy
BUN Blood urea nitrogen
CAD Coronary artery disease
CAP Community-acquired pneumonia
CBC Complete blood count
CCF Congestive cardiac failure
CCU Cardiac care unit
CHF Congestive heart failure
CK Creatinine kinase
CK MB Creatinine kinase, MB fraction
CML Chronic myeloid leukemia
COPD Chronic obstructive pulmonary disease
CPK Creatine phosphokinse
CSF Cerebrospinal fluid
CT Computerized tomography scan
CVA Cerebrovascular accident
CVP Central venous pressure
CXR Chest-X-ray
D5W Dextrose in water 5%
DBP Diastolic blood pressure
DI Diabetes insipidus
DKA Diabetic ketoacidosis
DM Diabetes mellitus
DSH Deliberate self harm
DVT Deep venous thrombosis
ECG Electrocardiogram
EEG Electroencephalogram
ESR Erythrocyte sedimentation rate
EVL Endoscopic variceal ligation
FHF Fulminant hepatic failure
GCS Glasgow coma scale
GFR Glomerular filtration rate
GI Gastrointestinal
Hb Hemoglobin
HDU High dependency unit
HUS Hemolytic uremic syndrome
IBD Inflammatory bowel disease
ICP Intracranial pressure
 Medical Emergencies Guidebook

ICU Intensive care unit

IM Intramuscular injection
ITU Intensive treatment unit
IV Intravenous injection
JVP Jugular venous pressure
LBBB Left bundle branch block
LDH Lactate dehydrogense
LFT Liver function tests
LMWH Low molecular weight heparin
LP Lumbar puncture
LRTI Lower respiratory tract infection
LV Left ventricle
LVH Left ventricular hypertrophy
MDI Metered dose inhaler
MI Myocardial infarction
MRI Magnetic resonance imaging
NMS Neuroleptic malignant syndrome
NSAID Non-steroidal anti-inflammatory drugs
NST - ACS Non-ST elevation acute coronary syndrome
NSTEMI Non-ST elevation myocardial infarction
O and P Ova and parasites
PAN Polyarteritis nodosa
PCWP Pulmonary capillary wedge pressure
PE Pulmonary embolism
PEFR Peak expiratory flow rate
PO Per orum (orally)
PPI Proton pump inhibitor
PRBC Packed red blood cells
PTH Parathyroid hormone
RBS Random blood sugar
RTA Renal tubular acidosis
rt-PA Recombinant tissue plasminogen activator
RVH Right ventricular hypertrophy
SAH Subarachnoid hemorrhage
SBP Systolic blood pressure
SIADH Syndrome of inappropriate ADH secretion
SIRS Systemic inflammatory response syndrome
SLE Systemic lupus erythematosus
SOB Shortness of breath
STE - ACS ST elevation acute coronary syndrome
STE MI ST elevation myocardial infarction
SVR Systemic vascular resistance
TB Tuberculosis
TDS Thrice daily
TFT Thyroid function tests
TIA Transient ischemic attack
Transjugular intrahepatic porto-sytemic
TIPS
anastomosis
TMP-SMX Trimethoprim-sulfamethoxazole
TTP Thrombotic thrombocytopenic purpura
UA Unstable angina
URTI Upper respiratory tract infection
UTI Urinary tract infection
V/Q scan Ventilation-perfusion scan
VSD Ventricular septal defect
VT Ventricular tachycardia
 Medical Emergencies Guidebook

Approach to Common
Emergency Symptoms

Chest Pain
Edited by: Ahmed Ali Ahmed Suliman

Acute Fever
Edited by: Elwaleed Ali Mohamed Elhassan

Headache
Edited by: Elwaleed Ali Mohamed Elhassan

Acute Abdominal Pain

Edited by: Amira Abbas Mohamed Fadl
 Medical Emergencies Guidebook

Chest Pain
Ahmed Ali Ahmed Suliman

Chest pain is a frequent complaint with a wide differential diagnosis. The

aim of evaluation in an emergency room is to exclude or identify life
threatening conditions and provide emergency treatment.
Any patient presenting with prolonged chest pain >10 min should have a
focused history and examination as well as an ECG. Chest X-ray is ob-
tained if seen necessary.
The emergency room physician should specifically look for the following
serious conditions which may present with chest pain:
Differential diagnosis
1. Acute Coronary syndrome. Please refer to ACS section for more
details.
2. Aortic dissection. Classically there is acute severe persistent stab-
bing chest pain that radiates to the back often in a patient with history
of hypertension or Marfan’s syndrome. Radial pulses may be unequal
and mediastinum may be wide on chest X-ray.
3. Pulmonary embolism. Sudden onset of shortness of breath accom-
panied by central chest tightness or pleuritic type chest pain in a patient
at risk for deep venous thrombosis(postoperative, prolonged bed rest,
prior venous thrombosis, etc.) .Look for evidence of DVT.
4. Pneumothorax. This may be spontaneous or secondary in patients
with lung disease e.g. during acute asthma or in patients with TB. There
is acute shortness of breath with pleuritic pain to the lateral side of the
chest wall with physical signs of pneumothorax- hyper-resonance with
absent breath sounds.
5. Boerrhave’s syndrome. This acute mediastinitis from esophageal
rupture. Central chest pain following prolonged vomiting usually with
circulatory collapse. There may be associated hydropneumothorax.
Confirm with barium swallow. Immediate surgical referral. This is a
rare problem. Beware of the more common scenario of recurrent vomit-
ing with or without chest symptoms in patients with acute myocardial
ischemia.
6. There are other many causes like esophageal reflux, pericarditis, mus
culoskeletal pain etc.
Patients with low risk for coronary artery disease or pulmonary embo-
lism, with atypical chest pain (e.g. ill-defined chest pain to the sides, or
pain exacerbated by movement suggesting muscular pain, sharp short
lived pain..etc.) who have normal examination, ECG and CXR and life
threatening situations excluded, can be given symptomatic treatment
(e.g. NSAID or antacids) and investigated on an outpatient basis.
Chest Pain
 Medical Emergencies Guidebook

*
Acute Fever
Elwaleed Ali Mohamed Elhassan
Definition
Acute fever is defined as fever lasting for 7 days or less.
Common causes of acute fever include:
• Malaria
• Respiratory infections:
o Upper respiratory tract infections (URTI):
tonsillitis, pharyngitis, otitis media, sinusitis.
o Lower respiratory tract infections (LRTI):
pneumonia, bronchitis.
• Abdominal infections:
o Intestinal: enteric fever, dysentery and colitis
o Acute viral hepatitis.
o Liver abscess (amoebic or pyogenic )
o Biliary infections: eg cholecytisis, ascending cholangitis
• Urinary tract infections
• Nervous system infections: meningitis, encephalitis
• Skin: impetigo, erysipelas, cellulitis and abscesses.
• Musculoskeletal system: septic arthritis and acute osteomyelitis.
Diagnostic Approach
Confirm the high temperature. Check the vital signs. Examine thoroughly
for associated signs: neck, throat, skin rash, lymph nodes, chest, liver and
spleen.
The following combinations are helpful diagnostic clues to the subsequent
probable diagnoses:
• Fever, headache, arthralgia and vomiting: malaria.
• Fever, sneezing, cough, runny nose: upper respiratory tract infection.
• Fever, burning micturition, loin or suprapubic pain: UTI.
• Fever, upper abdominal pain and tender mass: hepatitis, liver abscess or
cholecystitis.
• Fever and coma: cerebral malaria, meningoencephalitis or encephalitis.
• Fever, headache and neck stiffness: meningitis or encephalitis.
Pertinent Investigations:
The following investigations may be performed selectively as dictated by
clinical impressions:

* Acknowledgement: many thanks to Prof Gaafar Malik FRCP (Lond), consultant physician and infectious
diseases specialist at the National Ribat University Hospital, for his kind review of this topic
• Total white blood cell count (TWBC): high count with neutrophil pre-
dominance and presence of band cells suggests pyogenic infections
e.g., pneumonia, tonsillitis. pyogenic liver abscess (etc).
• Blood film for malaria (a Giemsa-stained thick and/or thin blood smear
for species identification and quantification of the percentage of para-
sitized red cells).
• Blood cultures: obtain two sets from two separate venipuncture sites.
• N.B: Widal test is of limited clinical utility in acutely ill patients be-
cause positive results may represent previous Salmonella infection.
• Urine analysis: shows pyuria, bacteruria and varying degree of hema-
turia in UTI. Urine culture may reveal particular offending organisms
with specific antibiotic sensitivity.
• Stool analysis: gram stain and culture, microbiology for micro-organ-
isms, pyuria, RBCs and cytotoxin assay for c. difficile.
• Chest x ray: the presence of an infiltrate suggests pneumonia.
• Throat swab, wound swab for gram stain and culture when indicated.
• Lumber puncture in cases of suspected meningitis (once raised intra-
cranial pressure ruled out by lack of papilledema or a negative head CT
scan study).
• Liver enzymes: serum aminotransferases would be very high in acute
viral hepatitis.
• Ultrasound study of the abdomen in cases suspected of hepatic or bili-
ary infections.
Management:
Reduce fever
• Use antipyretics; this also reduces systemic symptoms of headache,
myalgias and arthralgias.
• Paracetamol is generally preferred to nonsteroidal anti-inflammatory
drugs (NSAIDs) because of minimal adverse effects.
• Rapid reduction in body temperature can also be accomplished by cool
or tepid (20 °C) sponges.
• If the patient cannot take oral antipyretics, use parenteral preparations
of NSAIDs or rectal suppositories of various antipyretics.
• Rehydration of the patient either orally or IV will help to reduce the
temperature.
 Medical Emergencies Guidebook

Malaria:
see the protocol for malaria (appendix 1)
Respiratory tract infection:
Viral URTI:
• Offer symptomatic treatment (an antipyretic, antihistamine, antitussive
and a decongestant)
Lower RTI: Community acquired pneumonia (CAP):
• The ability to determine a causative organism in most cases is low.
Thus, therapy for CAP is typically begun on an empiric basis.
• Assess the degree of severity upon historical risk factors, hemodynamic
parameters, physical and laboratory findings. Decide on need for hospi-
talization.
• The “CURB-65” scoring system may be employed for assessing the
severity of CAP and helping decide upon the necessity for admission2
• It is a 6 point score (range 0-5) that gives one point each of the fol-
lowing (See table and chart below). Severe pneumonia is defined as a
CURB-65 score of 3 or more.

Assessment of severity of pneumonia with the CURB-65

scoring system

Item Score
Confusion or new disorientation in person, place, or time) 1
Blood urea nitrogen > 20 mg/dL 1
Respiratory rate 30/min 1
Low Blood pressure (SBP< 90 mm Hg or DBP 60 mm Hg) 1
Age 65 years or more 1
Total

* British Thoracic Society Guidelines for the management of community acquired pneumonia in
adults. Thorax 2001; 56 (supp 14 ):1-64.
 Assessment of severity of pneumonia with the CURB-65 scoring system

Treatment of community acquired pneumonia (CAP) *

Patient Category Suggested Antibiotic Therapy

Outpatients Amoxicillin; OR macrolide (erythromycin,
(not severe) clarithrmycin) if penicillin-allergic

For patients untreated previously in the com-

munity: Amoxicillin OR macrolide: (erythro-
mycin or clarithromycin)
Hospitalized For patients able to take oral medications: Oral
(not severe) amoxicillin PLUS macrolide (erythromycin,
clarithromycin)
For patients requiring intravenous therapy: IV
ampicillin or benzylpenicillin PLUS erythro-
mycin or clarithromycin
Amoxicillin-clavulanate or cefuroxime, ce-
Hospitalized
(severe) fotaxime, ceftriaxone PLUS erythromycin or
clarithromycin
* Re: British Thoracic Society Guidelines (2001)
 Medical Emergencies Guidebook

Urinary Tract Infection (UTI):

• Assess the degree of severity upon historical risk factors, hemodynamic
parameters, physical and laboratory findings. Decide on need for
hospitalization
Acute cystitis:
o Offer a three-day course trimethoprim-sulfamethoxazole (TMP-
SMX), a fluoroquinolone or a week course of nitrofurantoin.
o Pregnancy: obtain a urine culture all pregnant women with
acute cystitis. Use amoxicillin, nitrofurantoin or cephalexin:
each of these drugs is given for three to seven days.

Acute pyelonephritis:
o Outpatients: offer a week course of an oral fluoroquinolone
(e.g.: ciprofloxacin, norfloxacin), trimethoprim or TMP-SMX.
Extend the duration of treatment if the patient fails to respond
adequately.
o Hospitalized patients: use ceftriaxone or gentamicin (3 to 5 mg/
kg for patients with normal renal function) given once daily.
Modify according to urine culture and particular organism
sensitivity.

Acute Fever with Diarrhea:

• Attend to volume repletion (see “Shock” section). Use intravenous
and oral route via Oral Rehydration Salts.
• Specific antibiotic treatment is only indicated in certain situations:
o Bacillary dysentery: offer TMP/SMX or a quinolone
course for 5 days.
o Enteric fever: treat with two week course of amoxicillin
or ciprofloxacin.
o Amebic dysentery and amebic liver abscess: metronidazole
for 5-10 days.
Acute Febrile CNS infections:
Encephalitis:
Use acyclovir for herpes simplex encephalitis.
Meningitis:
• A lumbar puncture (LP) would typically show:
o An elevated pressure (measured by water manometer)
o Pleocytosis (100 to 10,000 WBC/cubic millimeter)
o Elevated protein levels ( >50 mg/dL)
o Decreased CSF glucose levels (< 40 % of simultaneously
measured s. glucose)
o A predominance of neutrophils (80-95%) in the CSF, but a
predominance of lymphocytes can occur
o Gram’s staining of CSF permits the rapid identification of the
causative organism
• If available, and in order to prevent brain herniation, a head CT scan
should be performed before the LP if any of the following features
is present: immunocompromised state, new-onset seizure, signs that
are suspicious for space occupying lesions (papilledema or focal
neurologic signs, not including cranial-nerve palsy), or moderate-to-
severe impairment of consciousness. Such patients should first have
emergent blood cultures and appropriate empirical antibiotic therapy
initiated.
• Droplet precautions should be used for suspected meningococcal
infection patients for 24 hours. Those precautions are not required for
patients with signs of pneumococcal infection (otitis or pneumonia) or
with bacteria other than N. meningitidis identified by Gram’s staining.
Antibiotics:
• Treat adults with community-acquired meningococcal meningitis
empirically with benzylpenicillin.
• Ceftriaxone and cefotaxime are alternatives if meningococcal resistance
is high. Vancomycin is added if the prevalence of penicillin-resistant
pneumococci is high.
• Treat for at least 7 days.
• Persons who have close contact with patients affected with meningococcal
menigitis must receive chemoprophylaxis to eradicate meningococcal
carriage. For this purpose; a short course is used; ciprofloxacin (500
mg PO once) or ceftriaxone (250 mg IM once) *.
* Prevention and Control of Meningococcal Disease: Recommendations of the Advisory Committee on
Immunization Practices (ACIP). Bilukha, et al. Morb Mortal Wkly Rep 2005; 54(RR-7):1
 Medical Emergencies Guidebook

Corticosteroides:
• Intravenous dexamethasone (0.15 mg/kg every six hours) should be
given shortly before or at the time of initiation of antibiotic therapy
in adults with suspected bacterial meningitis who have a Glasgow
coma score of 8 to 11 to reduce the chances of developing permanent
neurological deficits.
• The dexamethasone should be continued for four days if the Gram's
stain reveals organisms consistent with, or the CSF culture grows S.
pneumoniae. On the other hand, dexamethasone should be discontinued
if the Gram's stain and/or culture reveal another pathogen or no
meningitis*.
Table of drugs used in this section:

Drug Main Indication Recommended Dose

Oral, 1000 mg 3-4 times

/day; rectal: 325-650 mg
Paracetamol Pain or fever
every 4-6 hours, do not
exceed 4 g/day.

Susceptible respiratory and

500-1000 mg every 8
Amoxicillin urinary tract infections and
hours
enteric fever

Amoxicillin- Susceptible respiratory tract

1 gram every 8 hours
clavulanate infections

Susceptible respiratory tract Oral: base: 250-500 mg

Erythromycin
infections every 6-12 hours

* Practice Guidelines for the Management of Bacterial Meningitis, The Infectious Diseases Society of
America (IDSA), Allan R Tunkel et al. Clinical Infectious Diseases 2004;39:1267-84
 Susceptible respiratory tract Oral: 250-500 mg every
Clarythromycin
infections 12 hours for 7-14 days

I.M., I.V.: 2-24

million units/day in
divided doses every
Susceptible respiratory
Benzylpenicillin 4 hours depending
infections and meningitis
on sensitivity of the
organism and severity
of the infection

Urinary tract infection 1 gram IV daily

2 g every 12 hours
for 7-14 days (longer
Meningitis courses may be
necessary for selected
Ceftriaxone organisms

I.V.: 2 g once daily;

Pneumonia, community-
> 65 years of age: 1 g
acquired
once daily

I.M., I.V.: 0.75-1.5 g

Susceptible respiratory every 8 hours (up to 1.5
Cefuroxime
infections g every 6 hours in life-
threatening infections)

Trimethoprim- Oral: 1 double strength

Urinary tract infection,
tablet every 12 hours
sulfamethoxazole bacillary dysentery
for 10-14 days
 Medical Emergencies Guidebook

Oral: 50-100 mg/dose

every 6 hours (not to
Nitrofurantoin Urinary tract infection
exceed 400 mg/24
hours)

Mild/moderate:
oral 250 mg every 12
hours for 7-14 days,
I.V.: 200 mg every 12
Ciprofloxacin Urinary tract infection and hours for 7-14 days.
enteric fever Severe/complicated:
oral 500 mg every 12
hours for 7-14 days,
I.V.: 400 mg every 12
hours for 7-14 days
Oral: 500-750 mg
Amebiasis and amebic every 8 hours for 5-10
Metronidazole
liver abscess days

Oral: 400 mg twice

daily for 3-21 days
depending on severity
Norfloxacin Urinary tract infection
of infection or
organism sensitivity;
maximum: 800 mg/day

I.M., I.V.: 1-2 g every

Cefotaxime Urinary tract infection
8 hours

I.V.: 10 mg/kg/dose
Acyclovir HSV encephalitis every 8 hours for 10-15
days
 Oral: 600 mg every 12
hours for 2 days
<1 month: 10 mg/kg/
day in divided doses
Meningococcal meningitis every 12 hours for 2
Rifampicin
prophylaxis days
Infants and Children:
20 mg/kg/day in
divided doses every 12
hours for 2 days
 Medical Emergencies Guidebook

Approach to Medical Causes of Acute

Abdominal Pain
Amira Abbas Mahamed Fadl
Introduction:
Many medical conditions can give rise to abdominal pain, and cause
diagnostic confusion with an acute (surgical) abdomen.
The acute abdominal pain may arise from: (1) stretching, (2) strong violent
contraction,(3) ischemia or infarction of the viscera, or from (4) muscle, (5)
skin, (6) bone, (7) blood vessels and (8) nerves overlying or adjacent to the
abdomen.
In any patient presenting with abdominal pain careful history, examination,
relevant investigations are important, together as well when indicated a trial
of medical therapy is undertaken to avoid an unnecessary laparotomy.
Causes:
The following group of conditions should be considered:
1. Intrathoracic causes:
The lower six thoracic nerves supply both thorax and abdominal wall,
as well as, the heart and pericardium rest on the diaphragm, so thoracic
pathology give rise to abdominal pain-usually upper abdomen (epigastrium,
left or right hypochondrium). Important causes are:
• Myocardial infarction
• Pericarditis.
• Pulmonary embolus.
• Pleurisy and pneumonia.
2. Intra-abdominal and retroperitoneal causes:
1. Congestion of the liver, occurring in congestive cardiac failure and
acute hepatitis.
2. Acute pancreatitis
3. Acute pyelonephritis
4. Bowel ischemia, which may be due to:
a. Sickle cell disease.
b. Henoch-Schonlein purpura
c. Vasculitis as in PAN (polyarteritis nodosa), SLE (systemic lupus
erythematosis.
 d. Atherosclerosis of blood vessels.
5. Constipation. This may cause severe abdominal pain especially in
elderly. Rectal examination and plain abdominal x-ray will confirm
this.
6. Infection:
a. Gastroenteritis, causes colic usually in association of diarrhea and
vomiting.
b. Worms: tape worms can cause quite severe abdominal pain. Ova
and cysts should be looked for in stool analysis.
c. Primary peritonitis: may occur in patients with ascites, as in portal
hypertension or nephrotic syndrome.
d. Typhoid fever.
e. Mesenteric adenitis.
3. Metabolic and endocrine causes:
1. Diabetic keto-acidosis.
2. Hypercalcaemia.
3. Acute intermittent Porphyria.
4. Addison’s disease and crises.
5. Heavy metal poisoning, such as lead toxicity.
4. Neurogenic causes:
• Root pain such as compression from degenerative lesions or malignancy.
The pain is commonly described as a band coming from back to front,
associated with tenderness over involved vertebrae when examining
patient back.
• Tabes dorsalis: the presence of Argyll Robertson pupils (irregular pupils
reactive to accommodation but not to light).
• Herpes zoster: usually pain and parethesia precede the rash before few
days. It is usually unilateral and segmental.
• Psychiatric causes: such as Munchausen’s syndrome: such patients
present with convincing symptoms and signs of various acute conditions
especially involving the abdomen.
Investigations:
Depending on the most likely possibility as obtained from history and
examination, the relevant investigation from the list below are carried out:
1. Plain supine abdominal x-ray.
2. Erect chest x-ray.
 Medical Emergencies Guidebook

3. Blood film.
4. Urine general.
5. Stool general.
6. Ascitic fluid analysis gram stain and culture.
7. Widal test for typhoid.
8. Serum amylase.
9. ECG.
10. Radiological studies such as U/S abdomen, Doppler studies of vessels
or contrast studies.
Management:
Largely depends on the underlying diagnosis.
Approach to Headache in Emergency Department(1)
 Medical Emergencies Guidebook

Approach to Headache inThe Emergency Department(2)

 Medical Emergencies Guidebook

Various
General
Medical
Emergencies

Shock
Edited by: Elwaleed Ali and Mohammad Al-Baqir

Coma
Edited by: Elwaleed Ali Mohamed Elhassan

Approach to Drug Overdose and Poisoning

Edited by: Elwaleed Ali Mohamed Elhassan
 Medical Emergencies Guidebook

Shock
Elwaleed Ali and Mohammad Al-Baqir

Definition:
Shock is a pathological state characterised by significant reduction in
systemic tissue perfusion which results in decreased tissue oxygen delivery.
If not reversed early and adequately it may lead to:
• Cellular hypoxia.
• Disruption of critical biochemical processes, and may eventually
lead to:
o Cell membrane ion pumps dysfunction.
o Intracellular edema.
o Inadequate regulation of intercellular pH.
o Cell death.
For management purposes, shock is divided into two types: hypovolemic
shock and distributive shock.
Hypovolemic Shock
Definition
Hypovolemic shock is caused by decreased circulatory volume manifesting
in tissue hypoperfusion.
Common precipitants are blood loss (internal or external bleeding) or fluid-
loss, e.g. vomiting, diarrhea, burns or sequestration as in pancreatitis.
Management:
• Insert two large-bore cannulae (14 or 16 gauge) into large veins. Central
venous cannulation or cut-down might be utilized if peripheral veins
are inaccessible.
• Infuse one to two liters of isotonic saline or lactated Ringer’s as rapidly
as possible.
• Continue fluid repletion at the initial rapid rate as long as the systemic
blood pressure remains low.
• Monitor clinical signs, including blood pressure, urine output, mental
status, and peripheral perfusion. These are often adequate to guide
resuscitation.
• The development of peripheral edema is often due to acute dilutional
hypoalbuminemia and should not be used as a marker for adequate fluid
 resuscitation or fluid overload.
• Colloids stay longer within the intravascular compartment and are
replaced 1:1 with blood. However, they do not reduce mortality, are not
more effective in preserving pulmonary function and are much more
expensive than crystalloid fluids.
• Consider blood products in hemorrhagic shock. Type-specific or O
negative packed red blood cells (PRBC) are given to maintain the
hematocrit above 30%.
• Whole blood provides extra volume and clotting factors. Transfuse
fresh frozen plasma and platelets when:
o Coagulation studies are abnormal
o Platelet count is < 10,000/µL
o After transfusion of 6 or more units of PRBCs
Distributive Shock
Definition
• Distributive shock refers to shock caused by arterial and venous
dilatation with low systemic vascular resistance.
• It usually arises from sepsis, anaphylaxis or systemic inflammatory
response syndrome (SIRS) produced by severe pancreatitis or burns.
• Sepsis is the most common cause and carries a mortality of 40-80%.
• Typically patients present with fever, chills, hypotension, hyperglycemia
and altered mental status mostly due to gram negative bactremia.
• Effective treatment of septic shock requires resuscitation, supportive
care, monitoring, and targeted antimicrobial therapy and drainage for
infection.
Management:
Resuscitation:
• Assess and support the airway, respiration, and perfusion. Supplement
oxygen to all patients with sepsis, monitor oxygenation with continuous
pulse oximetry. Intubation may be required for airway protection because
of encephalopathy or a depressed level of consciousness complicating
sepsis.
• Administer fluids in well-defined, rapidly infused boluses. Monitor
volume status, (pulse rate, blood pressure, urine output, central venous
pressure or pulmonary capillary wedge pressure if feasible) and look
 Medical Emergencies Guidebook

for features of pulmonary edema before and after each bolus. Repeat
intravenous fluid challenges until hemodynamic parameters are
acceptable or features suggestive of pulmonary edema develop. If the
pulmonary capillary wedge pressure is monitored, do not exceed 18
mmHg.
• Clinical trials have not consistently demonstrated an advantage of
colloid over crystalloid infusion in the treatment of septic shock.
Therefore, crystalloids are preferred.
Vasopressors:
• Vasopressors are useful in patients who remain hypotensive despite
adequate fluid resuscitation or who develop cardiogenic pulmonary
edema.
• In general, agents that augment peripheral vascular resistance, such as
dopamine, norepinephrine, or phenylephrine, are required for initial
stabilization
Source Control:
• Prompt identification and treatment of the culprit site of infection are
essential.
• Potential Gram negative pathogens are generally best covered with two
effective agents from different antibiotic classes, usually a beta-lactam
and an aminoglycoside (eg, a third generation cephalosporin such as
ceftazidime and gentamicin).
• Antibiotics should be appropriately tailored once microbiological data
returns.
• Regardless of the antibiotic regimen selected, patients should be
observed closely for toxicity, evidence of response, and the development
of nosocomial superinfection.
• The duration of therapy depends upon the source of the infection and
the clinical response of the patient.
• Corticosteroids are life-saving in the treatment of shock associated with
acute adrenal insufficiency, but they are of no proven benefit in other
types of shock.
For (Cardiogenic Shock), please refer to Cardiovascular Emergencies
section
Drugs used in this section:

Drug Indication Recommended Dose

Gentamicin Septic shock I.M., I.V.: Severe life-threatening infections:
2-2.5 mg/kg/dose every 8 hours
Note: High-dose, once daily regimens:
Some clinicians suggest 4-7 mg/kg (as
a single daily dose) for all patients with
normal renal function. This dose is at least
as efficacious with similar, if not less,
toxicity than conventional dosing.

Phenylephrine Hemodynamic I.M., S.C. : 2-5 mg/dose every 1-2 hours

support as needed (initial dose should not exceed
in shock 5 mg)
I.V. bolus: 0.1-0.5 mg/dose every 10-15
minutes as needed (initial dose should not
exceed 0.5 mg)
I.V. infusion: 10 mg in 250 mL D5W or
NS (1:25,000 dilution) (40 mcg/mL); start
at 100-180 mcg/minute (2-5 mL/minute;
50-90 drops/minute) initially; when blood
pressure is stabilized, maintenance rate: 40-
60 mcg/minute (20-30 drops/minute); rates
up to 360 mcg/minute have been reported;
dosing range: 0.4-9.1 mcg/kg/minute

Continuous I.V. infusion:

Norepinephrine Hemodynamic Adults: Initial: 0.5-1 mcg/minute and titrate
support to desired response; 8-30 mcg/minute is
usual range;
in shock
ACLS dosing range: 0.5-30 mcg/minute
Rate of infusion: 4 mg in 500 mL D5W
o 2 mcg/minute = 15 mL/hour
o 4 mcg/minute = 30 mL/hour
o 6 mcg/minute = 45 mL/hour
o 8 mcg/minute = 60 mL/hour
o 10 mcg/minute = 75 mL/hour
 Medical Emergencies Guidebook

Dopamine Hemodynamic I.V. infusion: 1-5 mcg/kg/minute up to 50

support in mcg/kg/minute, titrate to desired response;
shock infusion may be increased by 1-4 mcg/kg/
minute at 10- to 30-minute intervals until
optimal response is obtained
Note: If dosages >20-30 mcg/kg/
minute are needed, a more direct-acting
vasopressor may be more beneficial (ie,
epinephrine, norepinephrine).
Hemodynamic effects of dopamine are
dose dependent:
o Low-dose: 1-5 mcg/kg/minute,
increased renal blood flow and urine
output
o Intermediate-dose: 5-15 mcg/kg/
minute, increased renal blood flow, heart
rate, cardiac contractility, and cardiac
output
o High-dose: >15 mcg/kg/minute, alpha-
adrenergic effects begin to predominate,
vasoconstriction, increased blood
pressure

Ceftriaxone Septic shock I.M., I.V.: 1-2 g every 12-24 hours

(depending on the type and severity of
infection); maximum: 4 g/day
 Coma
Elwaleed Ali Mohamed Elhassan

Definition:
Coma is a state of unresponsiveness to normal external stimuli.
Causes:
The causes of coma can generally be divided into:
Coma without focal or lateralizing neurological deficits:
1. Metabolic e.g.: hypo and hyperglycemia, uremic
encephalopathy, hepatic failure and thiamine deficiency
2. Endocrine e.g.: hypo and hyperthyroidism and adrenal
insufficiency
3. Electrolyte disturbances: hypo and hypernatremia and
hypercalcemia.
4. Alcohol, ingested drugs and toxins e.g.: opiates,
benzodiazepines, barbiturates and carbon monoxide.
5. Hypo and hyperthermia.
6. Epilepsy.
7. Hypertensive encephalopathy.

Coma with focal or lateralizing neurological signs (due to brainstem

or cerebral dysfunction):
Cerebrovascular accidents
1. Space occupying lesion: (tumor, hematoma or abscess). In
order to produce coma these have to be within the brainstem
or compress it by producing brain shift
Coma with meningeal irritation:
1. Meningitis
2. Encephalitis
3. Subarachnoid hemorrhage.
4. Cerebral malaria
Management:
1. Ascertain a patent airway and adequate respiration. Supplement
with oxygen and intubate if necessary to protect the airway (see
 Medical Emergencies Guidebook

“Shock” section).
2. Quickly assess circulation, record pulse and blood
pressure
3. Place patient on a cardiac monitor if feasible.
4. Insert a peripheral intravenous access and obtain samples for
appropriate investigations:
a. Blood film for malaria.
b. Complete blood count with differential
c. Finger-stick and blood glucose
d. Hepatic, renal profiles and electrolytes
e. Urinalysis
5. Administer IV fluids as needed for hypotension, Give dextrose (50 ml
of 50%) immediately if hypoglycemia is proved or suspected.
6. Control seizures if present (see “Status Epilepticus” section)
7. Reduce high temperature if present with tepid sponging
and antipyretics.
8. Take a quick history from relatives and attendants:
a. Onset of coma?
b. Any observed seizures?
c. Recent complaints: headache, fever, vertigo (etc)
d. Recent medical history: sinusitis, otitis, neurosurgery
(etc)
e. Past medical history: diabetes mellitus, hypertension,
epilepsy, head trauma.
f. Drug or toxins exposure: alcohol, benzodiazepines, opiates...
9. Examine the patient:
a. Assess and record the Glasgow Coma Scale (GCS) for objective
follow-up.
b. Look for signs of trauma in the head (hematoma, CSF or blood
in the nose or ears) or body.
c. Look for stigmata of other illnesses: liver disease, alcoholism,
DM, myxedema.
d. Note the pattern of respiration and smell the breath for fetor
hepaticus, ketosis, uremia)
e. Test for meningeal irritation; do not move the neck unless the
cervical spine is cleared.
f. Examine the heart and lungs for murmurs, rubs, wheezing and
 collapse
g. Examine the abdominal organs, look for ascites, peritonism.
h. Examine the pupils, ocular fundi, brainstem reflexes and
eye movements. Look for local deficits and examine plantar
reflexes.
10. Further investigations may be needed based upon the clues
gathered from above:
a. Obtain a head CT scan for all undiagnosed coma patients and
those with focal neurological signs.
b. Perform a lumbar puncture and CSF analysis in cases
suspected of meningitis or subarachnoid hemorrhage. Avoid
in the presence of papilledema.
c. Transfer the patient to the ICU or a special care room if
feasible
d. Monitor fluid balance with input and output chart. Insert
an indwelling catheter if needed for hemodynamic status
monitoring.
e. Avoid nasogastric tube insertion if airway reflexes are
impaired unless the patient is intubated.
f. Attend to nursing care measures
g. Provide further specific therapeutic interventions once
underlying cause is identified. See “Drug Overdose and
Poisoning” section below, refer to other relevant sections.
 Medical Emergencies Guidebook

Approach to Drug Overdose and Poisoning in

the Emergency Department (1)
Approach to Drug Overdose and Poisoning in
the Emergency Department (2)
 Medical Emergencies Guidebook

Approach to Drug Overdose and Poisoning in

the Emergency Department (3)
 Medical Emergencies Guidebook

Cardiovascular
Emergencies

Editor: Ahmed Ali Ahmed Sulmian

 Medical Emergencies Guidebook

Acute Coronary Syndromes

This is defined as any collection of clinical symptoms, most commonly
including chest pain, that are compatible with acute myocardial ischemia. It
is usually caused by atherosclerotic coronary artery disease (CAD). It has
two major components based on initial ECG *:
ST-elevation Acute Coronary Syndrome (STE-ACS).This is usually
caused by total of occlusion of a coronary artery by a thrombus leading to
total cutoff of blood supply to the myocardium and ST-elevation myocar-
dial infarction (STEMI).
Non-ST-elevation Acute Coronary Syndrome (NSTE-ACS). This is
caused by subtotal (near total) occlusion of a coronary artery by a throm-
bus leading to critical ischemia +/- micro-infarction of the myocardium.
Based on troponin measurements, it is divided into Unstable angina (UA) if
troponins are negative and Non-ST-elevation myocardial infarction if tro-
ponins are elevated. However, management is the same and hence grouped
together. 0912811408
Evaluation of patients with suspected ACS:
Any patient who presents with new onset prolonged chest pain (>10 min)
at rest or with minimal exertion should be evaluated for ACS. Patients
with prior CAD, patients with risk factors like Diabetes Mellitus (DM),
hypertension, smoking, etc., or have chest pain associated with nausea,
vomiting, shortness of breath or chest pain accompanied by pulmonary
edema are more likely to have an acute coronary syndrome.
The following steps should be taken:
1. A cardiac history and examination should be rapidly performed. Ask
about risk factors and history of prior CAD.
2. Attach the patient to a (rhythm) monitor and obtain an immediate ECG.
The ECG will divide patients into 2 categories:
I. STE-ACS . There is persistent new or presumed new ST segment
elevation greater than 0.1 mV(1 mm) in at least 2 contiguous precordial
leads or 2 adjacent limb leads or new or presumed new Left Bundle Branch
Block (LBBB).
II. NSTE-ACS. Threre is persistent or transient ST depression, T

* Adapted from the 2007 Europian Society of Cardiology Guidelines for the Management of Non ST-
segment Elevation Acute Coronary Syndromes (NSTE-ACS); www.escardio.org
waveinversion, flat T waves, pseudo-normalization of T waves or normal
ECG.
3. Draw blood for cardiac enzymes (cardiac troponins T or I are
currently the cardiac markers of reference) random blood sugar,
renal profile and complete blood count.
4. Obtain Chest X-ray if portable X-ray is available or patient can
be moved with a monitor.
Management:
The following common steps should be taken in all patients with an acute
coronary syndrome.
• Admit to CCU. Establish IV access.
• Bed rest with continuous ECG monitoring.
• Supplemental O2 to via nasal cannula at a rate of 4-6L /min to maintain
O2 sat > 90% and at times of chest pain.
• Aspirin 300 mg to crush and swallow then 100-300 mg daily.
• Nitrates. If there is ongoing chest pain give sublingual nitrates- isosorbide
dinitrate or glyceryl trinitrate. Use IV nitrates if pain is continuous or
there is associated high blood pressure or pulmonary edema.
• Analgesia. Morphine IV for pain, anxiety or pulmonary edema.
IV morphine sulphate 4-6 mg every 5 -15 min as needed. Give
metoclopramide 10 mg IV or IM for nausea and vomiting.
• Beta blockers: oral or IV. Give β-blockers to all patients unless there
is a contraindication. For IV, use propranolol or metoprolol. For
hemodynamically stable patients, may use oral atenolol, carvedilol or
bisoprolol. Aim to reduce heart rate to about 60-70/min
• Strict glycemic control in diabetic patients. Regular/soluble insulin
infusion pump is preferred, otherwise SC regular/soluble insulin 6-8
hourly +/- initial IV soluble/regular insulin bolus to keep blood sugar
preferably between 80-160 ( and not beyond 200 mg/dl)
• During the same admission and as soon as possible all patients should
be started on ACEI/ARB, beta-blockers and statins unless there is a
contraindication.
Management specific to ST Elevation myocardial infarction:
• The therapeutic objective in these patients is to achieve rapid, complete
and sustained reperfusion by primary angioplasty or fibrinolytic
(thrombolytic) therapy.
• Primary angioplasty has been shown to be superior to thrombolysis in
 Medical Emergencies Guidebook

STEMI. This is the better option if such primary angioplasty centers

exist and patients can be transferred to the cath lab within one hour of
presentation to emergency room.
• All patients with STE-ACS should receive thrombolysis as urgently as
possible if they satisfy the following 3 criteria:
1. There is prolonged chest pain more than 10 min and new or
presumed new ST segment elevation greater than 0.1 mV(1 mm)
in at least 2 contiguous precordial leads or 2 adjacent limb leads or
new or presumed new Left Bundle Branch Block (LBBB).
2. Arrival within 12 hours of the start of the pain
3. Absence of absolute contraindications to thrombolysis which
include:
a. Intracranial hemor- b. Known structural c. Any ischemic
rhage at any time vascular lesion in stroke within last 3
the brain eg arterio- months
venous malforma-
tions (AVM)

d. Primary or metastat- e. Suspected aortic f. Active bleeding or

ic cerebral malignant dissection bleeding disorder ex-
tumor cluding menses

g. Significant head or
facial trauma last 3
months

Patients with relative contraindications have higher risk of intracranial

bleeding than other patients. Risk of bleeding from thrombolysis has to
be weighed against risk of death of MI. Two factors favor administering
thrombolysis in patients with a relative contraindication:
a. Presence of high risk markers for death from MI (large anterior
infarct involving most or all precordial leads, hemodynamic
instability, diabetes, pulmonary edema, electrical instability i.e.
sustained or nonsustained VT)
b. Support services in the hospital including ability to adequately
monitor patients, accessibility of blood products like fresh frozen
plasma (or cryoprecipitate or fresh blood), platelet transfusion
 and protamine sulphate to reverse anticoagulation, neurosurgical
support, ability to endoscope rapidly if GI bleed occurs etc..
• For thrombolysis, streptokinase, alteplase, reteplase, tenecteplase can
be used.
• Heparin - whether SC enoxaparin or IV unfractionated heparin - is
indicated in:
a. patients who have received fibrin specific agents like alteplase,
reteplase or tenecteplase.
b. patients who have received non selective thrombolyic agent like
streptokinase or who have not recieved thrombolysis because
of contraindications or delay in arrival who are at high risk for
systemic emboli namely large or anterior MI, atrial fibrillation ,
previous embolic event, or known LV thrombus.
• All patients should be reviewed by a cardiologist or physician with
experience in cardiology for further management. If patients develop
post-MI angina, failure of thrombolysis, or cardiogenic shock seek
immediate transfer to a cardiac facility with cardiac catheterization
facility with aim to urgent revascularisation.
Management specific for Unstable Angina/Non-ST elevation
myocardial infarction(UA/NSTEMI)
On top of the common management steps for ACS these should also receive
the following:
• Anticoagulation with either IV unfractionated heparin or
enoxaparin for 2-7 days after symptoms subside. Fondaparinaux, a
new anticoagulant, has now been adopted by the European Society
of Cardiology (ESC) 2007 guidelines for NSTEMI as first line
anticoagulant therapy for its equal efficacy but superior safety compared
to enoxaparin.
• Clopidogrel (Plavix). Give 300 mg orally as loading dose then 75 mg
orally daily. If the patient is taken to the cath lab load with 600mg.
• Angiotensin converting enzyme inhibitors in diabetic patients, patients
with pulmonary edema, hypertension, or impaired left ventricular
systolic function within 24 hrs of admission.
• GP IIb/IIIa inhibitors for high risk patients specially diabetics and
troponin positive patients who are going for coronary angioplasty.
• Cardiac Catheterization. All patients should be referred for coronary
angiography +/- angioplasty. Patients with refractory chest pain and
 Medical Emergencies Guidebook

ECG changes or elevated cardiac markers despite maximum medical

therapy should be referred for immediate coronary angiography if
feasible. Otherwise, high risk (ECG changes or elevated markers)
patients can be transferred after stabilization.
Acute Cardiogenic Pulmonary Edema
 Cardiogenic Shock
Definition
• Cardiogenic shock is a low output state characterized by elevated
ventricular filling pressures and low cardiac output. This is recognized
clinically by presence of pulmonary edema and persistent systemic
hypotension (SBP<90) for more than 30 min and evidence of vital
organ hypoperfusion (e.g. confusion, cold extremities, oliguria).
• It carries dismal prognosis with very high mortality. It most commonly
occurs in patients who have sustained considerable myocardial damage
after a large myocardial infarction or may occur in patients with
mechanical complications like post MI ventricular septal defect (VSD)
or acute severe valvular regurgitation or in patients with advanced
cardiomyopathies. .
Management
1. Administer supplemental oxygen.
2. Blood pressure support. This is achieved by use of inotropic agents.
The choice of the inotropic agent depends on the BP and clinical state
of the patient:
• If SBP is 60-90 mmHg and NO signs/symptoms of shock-eg
confusion, irritability, cold extremities, oliguria/anuria etcà
Dobutamine is the inotrope of choice at a dose of 2.5-20 mcg/kg/
min IV. Start at a low dose and use increments of 2.5 mcg/kg/min
15-30 min apart to achieve BP ≥ 100 mmHg.
• If dobutamine is not available use dopamine.
• If SBP is 60- 90 mmHg with symptoms or signs of shock à dopamine
at a dose of 5-15 mcg/kg/min. Use increments of 2.5 mcg/kg/min
every 15-30 min to achieve SBP ≥ 100 mmHg. Dobutamine may be
added to dopamine if needed.
• If SBP < 60 mmHg à adrenaline or noreadrenaline at 0.5-30 mcg/
min*.
3. IV Furosemide preferably by infusion to relieve the pulmonary
edema.
4. Intra-aortic balloon pump counterpulsation if available.
5. Correction of underlying cause. If cardiogenic shock occurs in the context

* Adapted from Europian Society of Cardiology 2005 Guidelines on Diagnosis and Treatment of
Acute Heart Failure; www.escardio.org
 Medical Emergencies Guidebook

of acute MI administer reperfusion therapy whether via thrombolysis

or primary angioplasty. In patients with mechanical complications
like ventricular septal defect (VSD) or acute severe mitral or aortic
regurgitation whether following MI, endocarditis, aortic dissection,
immediate cardiac surgery consultation or referral to a center with
cardiac surgery facility.
Drugs used in this section:

Drug Main Indication Recommended Dose

Acute Coronary
Syndrome.
Streptokinase Absolute contraindications 1.5 million units IV
for thrombolytic therapy: over 30-60 min
(1) Intracranial hemorrhage
at any time
(2) known structural
vascular lesion e.g. AVM
10 units IV over 2
(3) Any ischemic stroke
min then 30 min later
Reteplase within last 3 months
another 10 units IV
(4) Primary or metastatic
over 2 min
cerebral malignant tumor
(5) Suspected aortic
dissection (6) Active 15 mg IV bolus, then
bleeding or bleeding 0.75 mg/kg over 30
Alteplase disorder excluding menses min(max 50 mg) then
(7) Significant head or facial 0.5 mg/kg over 60 min
trauma last 3 months. (not to exceed 35 mg)

Acute Coronary Syndrome. Initial dose 300

Contraindications are mg (nonenteric
Aspirin
allergy and active bleeding formulation) followed
including retinal bleeding. by 100 mg/day.
 Acute Coronary Syndrome. 75 mg/d; loading dose
Clopidogrel
(Use if ASA is of 4-8 tablets (300-
(Plavix)
contraindicated) 600mg).

Acute Coronary Syndrome.

Stop if major bleeding oc- 60 U/kg IV bolus (max
curs or if platelet count 5000 U) followed
Unfractionated
drops below 100,000 (con- by 15 U/kg/hr (max
Heparin
sider heparin-induced throm- 1000/hr). Adjust rate to
bocytopenia). Reverse with aPTT 60-80s.
protamine sulphate

Acute Coronary Syndrome.

10 U (1 mg)/kg SC
This is a low molecular
twice daily. An initial
Enoxaparin weight heparin.
bolus 30 mg IV can be
Similar contraindications as
given.
unfractionated heparin.

Fondaparinaux
(a recombinant
Acute Coronary Syndrome.
pentasaccharide 2.5 mg SC daily
terminal unit of
heparin

Acute Coronary Syndrome.

Nitrates are contraindicated
in hypotensive patients.
Caution in patients with
Isosorbide inferior infarct especially 10-40 mg PO BD or
mononitrate when given with B blockers TDS
as severe hypotension
may ensue in patients with
concomitant right ventricular
infarct.
 Medical Emergencies Guidebook

Sublingual: 5mg as
needed. Repeat every 5
min X 3 doses.
Isosorbide
Acute Coronary Syndrome Oral: 10 -20 mg BD or
dinitrate
TDS
IV: Mix with D5w. 1-10
mg/hr

Sublingual: 0.5 mg ev-

Glyceryl ery 5 min as needed x 3
Acute Coronary Syndrome
trinitrate doses.
IV: 10-200µg/min

Acute Coronary Syndrome

Titrate dose to a resting heart
10-80 (usually 20-40
rate 60-70 bpm.
mg) mg orally 2-3
Contraindicated in patients
times daily. For IV use
Propranolol with bradycardia < 60bpm,
give 0.5-1 mg IV fol-
hypotension, severe asthma
lowed 2 hrs later with
or chronic obstructive
the oral dose.
airway disease and
pulmonary edema.
 Medical Emergencies Guidebook

Endocrine
Emergencies
Editor: Hisham Mohamed Abdel Rahim
 Medical Emergencies Guidebook

Diabetic Ketoacidosis (DKA)

Essentials of diagnosis:
1. Hyperglycamia i.e. blood glucose > 250 mg/dl.
2. Ketonaemia.
3. Ketonuria > +2 ketonuria
4. Metabolic acidosis: PH < 7.30.
Therefore DKA consists of the biochemical triad of hyperglycemia,
ketonemia and acidemia.
Differential diagnosis:
1. Alcoholic ketoacidosis.
2. Starvation ketosis.
3. Lactic acidosis.
4. Uremic acidosis.
5. Salicylate intoxication.
6. Methanol intoxication.
Clinical Presentation
• Polyuria and polydipsia
• Nausea, vomiting and abdominal pain
• Hypovolemia (decreased skin turgor, dry axillae and oral mucosa, low
jugular venous pressure, and, if severe, hypotension)
• Kussmaul’s respirations (deep rapid breaths) with acetone odor.
• Disturbed mental status progressing to stupor and coma
Precipitating factors:
• It may be the initial presentation of type 1 DM
• Omission of insulin
• Underlying infection and/or sepsis
• Acute coronary syndrome
• Stroke
• Trauma
• Pregnancy
• Surgery
• Drugs (e.g. corticosteroids and high dose thiazides).
Diagnostic studies:
• Random blood sugar, urea, Na+, K+.
• Hemoglobin and white cell count.
• ECG
• Urine general.
• ABG, CXR
• Brain CT if indicated.
• Blood and urine culture.
Treatment:
Is best carried out at ICU if feasible:
1. IV fluids.
2. IV insulin.
3. IV potassium chloride.
4. Bicarbonate therapy
5. Education to prevent recurrence

IV fluids:
Give the following in succession:
• 1 liter of normal saline over 30 minutes.
• 1 liter of normal saline over one hour.
• 1 liter of normal saline over two hours
• Then 500 ml of normal saline every 4 hours for the first 24 hours.
Substitute 5% dextrose in normal saline for normal saline when blood glu-
cose drops below 250 mg/dl.
Observe urine output closely and keep an open eye to avoid volume over-
load in elderly patient and patients with congestive heart failure or renal
failure when central venous monitoring is preferable.

Insulin therapy:
• Administer 10 units of soluble insulin IV immediately, followed by a
continuous IV soluble insulin infusion at a rate of 5 units /hour till the
patient is out of DKA.
• If IV infusion pump is not available soluble insulin can be given as
10 units IV stat and 5-10 units IM every hour till the patient is out of
DKA.
• It is preferable to have serum K+ result before giving IV soluble
 Medical Emergencies Guidebook

insulin. If the patient is hypokalemia avoid IV insulin till hypokalemia

is corrected.
• Monitor blood glucose hourly and ensure the addition of IV dextrose
to the planned IV fluid when blood glucose result drops below 250 mg/
dl.

Potassium replacement:
• If the initial serum potassium is < 3.3 mmol/L, hold insulin and give 40
mmol potassium chloride as an infusion through a central venous line
over one hour until K > 3.3 mmol/L
• If serum K+ > 5.5 mmol/L do not give potassium. However, check
serum K+ after two hours.
• If serum K+ > 3.3 mmol/L < 5.5 mmol/L give 20 to 30 mmol of
potassium chloride in each litre of IV fluid to keep serum K+ at 4 – 5
mmol/L.
• Monitoring serum K+ every 4 to 6 hours.
• Continue with oral potassium for 5 to 7 days to restore total body
potassium level.

Bicarbonate therapy:
• If PH > 7.0 no need for bicarbonate therapy.
• If PH 6.9-7.0 Ë dilute sodium bicarbonate 50 mmol in 200 ml H2O
and infuse at a rate of 200 ml/hour.
• If PH < 6.9 Ë dilute sodium bicarbonate 100 mmol in 400
• Repeat bicarbonate administration every two hours until PH > 7.0.
• NB: monitor serum K+ since it is likely to drop with IV bicarbonate.

Features of resolution of DKA:

• Blood glucose < 200 mg/dl/
• Serum HCO3 > 18 mmol/l
• Venous Ph > 7.3
• If there is an obvious precipitating cause such as sepsis, acute myocardial
infarction the management of the DKA should include measures to
control the precipitation factor e.g. broad spectrum antibiotics for
sepsis.
• If serum glucose does not fall by 50-70 mg/dl in the first hour double
the dose of the IV insulin till serum glucose fall by 50-70 mg/dl/h.
• If intramuscular insulin regimen in used and blood glucose does not fall
by 50-70 mg/dl in first two hours give IV soluble insulin (10) units as a
bolus every hour till blood glucose fall by 50-70 mg/dl/h.
• After resolution of DKA start SC soluble insulin every (4) hours while
monitoring blood glucose OR resume the original daily dose of insulin.
In case of new onset of type 1 DM the total daily insulin requirement
can be estimated as 0.6 units/kg/day. This calculated dose can be divided
to be given every (4) hours.
• Start the subcutaneously soluble insulin regimen before the
discontinuation of intravenous insulin in order to prevent the re-
development of DKA.

Complications of treatment:
• Hypoglycemia
• Hypo and hyperkalemia
• Pulmonary edema
• Cerebral edema
• Renal failure
• ARDS
• Systemic thromboembolism

Notes:
DKA Flow Sheet Setup

Pulse rate Urine Anion Intravenous

Time pH HCO3 Ketones Glucose K Insulin
and BP Output Gap Fluids
 Medical Emergencies Guidebook

Diabetic Lactic Acidosis

Lactic acidosis should be suspected in acidotic, hyperventilating diabetic
patient who has a high anion gap metabolic acidosis not accounted for by
ketones, salicyltes, uremia or methanol.
A lactate level of > 5 mmol/L is arbitrarily considered diagnostic.

Management:
• Take blood for CBC, glucose, urea, electrolytes ABG, serum and urine
ketone , blood lactate and urine general.

Correction of acidosis:
• Acidosis (PH < 7.1) has a negative inotropic effect, and persistent
acidosis will lead to shock and eventual death.
• If pH is below 7 give 2 mmol/kg body weight of sodium bicarbonate
over the first hour and then aliquots of 50 mmol over ½ hour to raise the
plasma bicarbonate to 14 mmol/L over the next 24 hours.
• Ensure that ventilation is satisfactory by giving concentrated oxygen
and observing the blood gas series.
• Hemodialysis and peritoneal dialysis may be used.
• Prognosis is poor.
 Hyperosmolar Hyperglycemic State
Definition
• Hyperosmolar hyperglycemic state is a condition of extreme
hyperglycemia (> 600mg/dL) and hyperosmolality (>310 mOsm/L) in
the absence of acidosis (pH >7.3, HCO3 > 15 meq/L) that is mostly
seen in type 2 diabetes mellitus (DM).
• It occurs in patients with mild or occult DM and most of them are
middle aged to elderly. Underlying renal insufficiency or congestive
heart failure is common and their presence worsens the prognosis.
• Common precipitants for DKA are similar to those of DKA (see
previous section)
Essentials for diagnosis:
• Plasma osmolality > 320 mosmol/kg.
• Arterial pH > 7.30.
• Serum HCO3 > 15 mmol/L
• Level of consciousness: stupor/coma.
Differential diagnosis:
• Diabetic ketoacidosis.
• Hypoglycemic coma.
• Stroke.
• Myocardial infarction.
Precipitating factors:
• Acute infection: pneumonia, urinary tract infection.
• CVA.
• Myocardial infarction.
• Acute pancreatitis.
• Intestinal obstruction.
• Peritoneal dialysis.
• Subdural hematoma.
• Thyrotoxicosis.
• Cushing’s syndrome.
• Acromegaly.
• Drugs : β-Adrenergic blockers, calcium channel blockers,
chloropromazine, diuretics cimetidine, immunosuppressive drugs,
corticosteroid and total parenteral nutrition.
 Medical Emergencies Guidebook

• Previously undiagnosed patients.

Clinical Presentation
• Polyuria and polydipsia
• Hypovolemia (tachycardia, hypotension, dry mucous membranes and
poor skin turgor)
• Lethargy and confusion progressing to convulsions and deep coma.

Diagnostic studies:
• Blood glucose
• Urea and electrolytes
• ABG
• CBC
• Urine general
• ECG
• CXR
• Blood urine & culture
• Brain CT (if stroke is suspected)
Goals of treatment:
• Improve circulatory volume and tissue perfusion.
• Decrease serum glucose and plasma osmolality towards normal levels.
• Correct electrolytes imbalance.
• Identify and treat precipitating factors.
• Education to prevent recurrence.
Treatment:
Preferably carried out at an ICU if feasible:
IV Fluids:
• If patient in cardiogenic shock hemodynamic monitoring is needed.
• If patient is hypovolemic administer 0.9% NaCl (1) litre/hour and/or
plasma expander.
• Evaluate serum sodium :
o If serum sodium is high i e > 150 mmol/L give 0.45 % NaCl at
a rate of 4-14 ml/kg/hour depending on state of hydration.
o If serum sodium is lower or normal give 0.9% NaCl at a rate
of 4-14 ml/kg/hour depending on the state of hydration.
• When serum glucose reaches 300 mg/dl change IV fluid to 5% dextrose
 in 0.45 NaCl at a rate of 500 ml every four hours.
IV insulin:
• Ensure that serum potassium level is satisfactory and follow the safety
guidelines given in the management protocol of DKA.
• Give soluble insulin of 0.15 units / kg/hour as IV bolus and continue
with IV insulin infusion at a rate of 0.1 units/kg/hour.
• Check serum glucose hourly and if serum glucose does not fall by at
least 50mg/dl in the first hour then double insulin dose hourly until
glucose falls at a steady hourly rate of 50-70 mg/dl.
• When serum glucose reaches 300 mg/dl change the replacement IV
fluid to 5% dextrose in 0.45% NaCl and decrease the infusion rate of
intravenous insulin to 0.05-0.1 units/kg/hour to maintain serum glucose
between 250 mg/dl to 300 mg/dl until plasma osmolality is < 315
mosmol/kg and patient is fully alert.
• After recovery from HHS subcutaneous insulin can be resumed on the
same guidelines given in the treatment of DKA.
IV potassium chloride
• Follow the same guidelines given in DKA.
IV heparin:
• Can be given as heparin infusion of 1000 units/hour.
• Observe closely for any bleeding.
• Monitor APTT every (8) hours.
Treatment of underlying condition
Complications of treatment:
• Hypoglycemia.
• Hypo & hyperkalaemia.
• Pulmonary edema.
• Cerebral edema.
• Renal failure.
• Adult respiratory distress syndrome
• Systemic thromboembolism
 Medical Emergencies Guidebook

Notes:

Hyperosmolar Hyperglycemic State

Flow Sheet Setup

Time Pulse rate Urine Glucose K Intravenous Insulin

and BP Output Fluids
 Hypoglycemia
Definition:
Hypoglycemia is the clinical state resulting from low blood glucose, usually
below 60 mg/dL. It must be considered in any confused disorientated,
aggressive or excitable person, especially if they are known to be diabetic
on insulin or taking sulphonylurea.
Common Precipitants:
• In diabetic patients:
o Excessive insulin and oral hypoglycemic agents
(sulphonylureas)
o Missed meals
o Renal insufficiency.
• In non-diabetics:
o High insulin: exogenous insulin, sulphonyurea, insulinoma,
anti-insulin or insulin receptor antibodies
o Low glucose production: hypopituitarism, adrenal insufficiency,
glucagons deficiency, hepatic failure and alcoholism.
o Postprandial.
Clinical Presentation:
These are usually seen with serum glucose of 55 mg/dL or less:
• Central nervous system: irritability, tremulousness, visual
disturbances, confusion, coma or seizures. Autonomic nervous
system: diaphoresis and palpitations.
• Occasionally hypoglycemia may present with focal neurological
signs such as hemiplegia or focal fits.
Management:
• Rapid bedside checking of blood glucose by glucometer rapidly
distinguish between hypo and hyperglycemic coma. However if you
are in doubt give IV 50 ml of 50% dextrose. It will do little harm to a
patient in hyperglycemic coma and will usually restore consciousness
in patients with hypoglycemic coma.
• Never give insulin as a diagnostic test for a diabetic patient who is in
coma. In hypoglycemia it is usually fatal and invariably disastrous
• If the patient can drink, give 25 gram dextrose in orange juice.
• If the patient is comatosed give 25 gram dextrose IV (50 ml of 50%
 Medical Emergencies Guidebook

dextrose) and when the patient is awake a further 25 g to drink.

• Glucagon 1 mg IM can be given in patient whose hypoglycemia is
proving difficult to control with glucose infusions. Glucagons raises
blood glucose to within the normal range in 5-10 min, although its
action is short lived.
• Recovery is usually complete in 10-15 min, but may occassionally take
up to 1 hour despite adequate blood glucose levels.
• In case of delayed recovery from hypoglycemia coma consider the
administration of IV dexamethasone.
• If hypoglycemia attack is precipitated by sulphonylurea or longacting
insulin it is advisable to admit and observe the patient for 48 hours in
order to avoid the danger of recurrent hypoglycemia episodes over the
next 24 – 48 hours
• Moreover, after the initial correction of hypoglycemia start your patient
in 10% or 20% dextrose drip over 24-48 hours to maintain blood glucose
between 90-180 mg%.

Addisonian Crisis
Addisonian crisis may be:
• primary due to destruction and/or atrophy of the adrenal gland, or
• secondary due to failure of the hypothalamic-pituitary-adrenal axis.
• The usual cause of secondary hypoadrenalism is the previous
administration of exogenors steroids.
Diagnosis:
• It should be considered in any hypotensive patient, who may also be
vomiting, especially if they have received steroids within the past
year.
• It may be precipitated by infection, myocardial infarction, stroke,
trauma, surgery, parturition or any metabolic stress.
• It may complicate septicemia caused by pyogenic organisms (such
as the meningococcus) and is said to be due to hemorrhage into the
adrenals.
Management:
• Take blood for baseline CBC, ABG ,electrolytes, urea, blood glucose
and plasma cortisol, urine general andCXR.
• If you suspect Addison’s disease, you should perform a short synacthen
 test before giving any steroid replacement, so that you can retrospectively
confirm your diagnosis.
• Take a resting sample for cortisol analysis, then give 250 microgram of
tetracosatrin IV and take cortisol samples ½ and 1 hour later.
• However if tetracosatrin is not available do not delay management
since that may cost the patients life.
• Abdominal X-ray may show adrenal calcification.
Steroid replacement
• Give 100 mg of hydrocortisone IV followed by 50 mg IV every 8
hours.
• Estimate blood glucose and if less than 2-3 mmol/L (40 mg/dl) give 25
grams of glucose orally or IV.
• Start IV fluid preferably with CVP line and give at least one litre of
normal saline in the first hour, and then as necessary to keep the CVP
within the normal range.
• If there is clinical evidence of sepsis start an IV broad spectrum
antibiotics.
• Potassium supplement may be needed after initial resuscitation with
normal saline/glucose and IV glucocorticoids.

Myxedema Coma
• This represents the most severe extreme of hypothyroidism. The
presence of stroke, chloropromazine overdose and cold weather
increases the susceptibility to this type of coma.
• Before coma supervenes the patient may have been mentally dulled or
psychotic.
• Usually the patient has the classic appearance and signs of myxedema.
Hypotension and bradycardia are invariably present.
Management
• Measure blood glucose, CBC, urea, electrolytes, cortisol, T4 and T3.
• Hydrocortisone 100 mg IV stat and then 50 mg IV every 8 hours.
• Give thyroxine 300 to 500 micrograms IV bolus and then 100 mg IV
daily thereafter. The dose can be halved if you are confident that your
patient is suffering from ischemic heart disease.
• Continue with oral thyroxine as 100-200 micrograms OD thereafter.
• Monitor ventilation by blood gas assessment, supportive ventilation is
 Medical Emergencies Guidebook

needed in most cases.

• For hypothermia use lots of blankets
• For hypoglycemia give 50ml of 50% dextrose as frequently as
necessary.
• For hypotension it is advisable to monitor the central venous pressure
and to use inotropes to maintain the tissue perfusion and support the
cardiac function.
• Provide glucose to avoid hypoglycemia.
• Treat the precipitating cause.
 Thyroid Storm
Definition:
This is an extreme form of thyrotoxicosis manifested by marked delirium,
severe tachycardia, vomiting, diarrhea, dehydration and in many cases,
high fever. The mortality is high.
Common precipitants are stressful illness, thyroid surgery, radioactive
iodine administration induction of anaesthesia, systemic illness (particularly
infection or sepsis) or premature discontinuation of antithyroid treatment in
patients with hyperthyroidism..

Clinical Manifestations:
• Cardiovascular symptoms include tachycardia to rates that can exceed
140 beats/min, along with congestive heart failure in many patients.
• Hyperpyrexia, agitation, delirium, psychosis, stupor, or coma are
common and are considered by many to be essential to the diagnosis.
• Severe nausea, vomiting, or diarrhea, and hepatic failure with jaundice
can also occur.
Management:
• Admit the patient in an intensive care unit if feasible. Provide full
hemodynamic and respiratory support.
• Take blood for CBC, glucose, urea, electrolytes ,cortisol, T4 and T3
levels.
• Correct hyperpyrexia aggressively with a cooling fan, tepid sponging,
paracetamol and chlorpromazine 100 mg stat followed by 50 mg six
hourly. Avoid aspirin, which can increase serum free (T4) and (T3)
concentrations by interfering with protein binding.
• Give propranolol by intravenous route, if available, in a dose of 0.5-2 mg
every 4 hours. Concurrently, give propranolol orally or via nasogastric
tube at a dose of 60 to 80 mg every four hours.
• Administer carbimazole (Neomercazole) 80 to 120 mg initially & then
20 mg six hourly or propylthiouracil 800 to 1200 mg initially and then
200 mg every six hours via nasogastric tube or rectally as necessary
• Propylthiouracil is the drug of preference because it also inhibits
peripheral conversion of T4 to T3.
• It is best to give the carbimazole or propylthiouracil 1 hour before
giving the potassium iodide , as this will ensure that the blockade of
 Medical Emergencies Guidebook

organification of iodine is established before the potassium iodide is

given.
• Potassium iodide (orally or IV) may also be administered to block
the release of thyroid hormone but this should not be used as the sole
treatment preoperatively.
• The administration of potassium iodide without prior treatment with a
thionamide may exacerbate hyperthyroidism.
• Potassium iodide can be given as 200 mg IV over one hour and then
100 mg qds.
• High dose B-blockers should also be instiuted. Propanolol 2 to 5 mg
IV every 4 hours or 320 to 480 mg daily by mouth in divided doses to
control heart rate.
• Occasional patients have a severe associated myopathy that may lead
to hypoxemia. This may give rise to ventilatory failure. So monitor
the arterial blood gas and be prepared to institute intermittent positive
pressure ventilatory support.
• Treat the underlying cause.
 Pituitary Apoplexy
Pituitary apoplexy occurs when sudden hemorrhage and/or nercosis cause
sudden expansion of a pituitary tumor.
Diagnosis:
• Patient will present with a sudden onset of headache, visual impairment
or loss, and ophthalmoplegia.
• The patient becomes stuporous and may lapse into coma. Neck stiffness
may be present.
• CT scan or preferably MRI of the head may show pituitary hemorrhage
and supraseller mass effect.
• Lumbar puncture is contraindicated because this presentation is
consistent with temporal lobe herniation.
Management:
• Request urgent neurosurgical consultation, since the relief of pressure
by a transnasal decompression is the procedure of choice.
• Gives dexamethasone 6 mg IV every six hours.
• Support circulation & ventilation.
 Medical Emergencies Guidebook

Gastro-intestinal
Emergencies

Editor: Amira Abbas Mohamed Fadl

 Medical Emergencies Guidebook

Acute Diarrhea In Adults

Definition:
• Acute Diarrhea: is the passage of a greater number of loose form stools,
than the normal, lasting less than 14 days.
• Diarrhea can be viewed as increase in the quantity of water and
electrolytes in stools, leading to a frequent production of unformed
stools. It is the impaired balance between resorption and secretion
in the intestinal wall which leads to the increased wateriness of the
feces.
Pathogenesis:
• Non-invasive micro-organisms lead to diarrhea through a variety of
interactions with the intestinal mucosa. Enterotoxic E.coli and Vibrio
cholerae do not spread beyond intestinal lumen producing diarrhea
through the production of enterotoxins which in turn induce fluid
secretion. Some micro-organism, such as Giardia lambelia, damage
the resorption surface of the microvilli, which in turn can lead to a
disaccharidase deficiency.
• Invasive micro-organisms penetrate the intestinal epithelium resulting
in an inflammatory disorder. The most well known example is that of
Shigella infection. Campylobacter and Salmonella too can invade the
intestinal mucosa.
Causes
Non-
Bacterial Viral Parasitic infectious
• Sheiglla • Rotavirus • Gardia • Acute
• Compylobacter • Norwalk virus • Entamoeba diverticulitis
jujeni • Cryptosoridium • Inflammatory
• Salmonella species bowel disease
• E.Coli
• Colisridium difficili
• Vibrio species
The transport vehicle of the common classic pathogens

Vehicle Classic Pathogen

Vibrio cholera, Norwalk virus, Giardia
Water
and Cryptosporidium
Salmonella, Campylobacter and Shigella
Poultry
species
Beef E.Coli
Sea food Vibrio and Salmonella species.
Cheese Listeria species
Eggs Salmonella species
Staphylococci, Salmonella and
Cream
Clostridia.
Pies Salmonella, Campylobacter
Person to person
Shigella, Cryptosporidium, Clostridium
(including sexual contact)

Clinical Assessment:
Important Questions to Answer
1. Small bowel diarrhea or large bowel diarrhea?
2. Presence of fever?
3. Presence of blood?
4. Symptoms of nausea and vomiting?
5. Symptoms of abdominal pain?
6. Is there dehydration?
Note:
Large volume diarrhea suggests small bowel origin. Usually it is unduly
offensive and
contains large amount of fats.
Small volume diarrhea with tenismus suggests large bowel origin.
 Medical Emergencies Guidebook

Assessment of Dehydration:
-Tachycardia -Dry tongue
-Postural drop of the blood pressure -Loss of skin elasticity
Possible risk factors for infectious diarrhea:
1. Recent travel especially to endemic areas.
2. Unusual food or eating habits.
3. HIV infection risks as in Homosexuals and IV drug abusers.
4. Recent use of antimicrobials, especially in the elderly and
immunocoprommised.
Investigations:
1. CBC
2. Stool general
3. Stool culture
4. Toxins in stool: such as Colistridium deficile
5. Blood urea and electrolytes.
Management:
Three important elements to consider:
1. Replacement of established losses.
2. Replacement of ongoing losses.
3. Replacement of normal daily requirement.

Rehydration:- using Oral Rehydration Solution (ORS) (even when there

is vomiting)
• IV fluids for severe dehydrated cases.
• Diet: Fasting is often not necessary, instead allow small meals.
• Avoid milk and caffeine
• Antdiarrheal medications: such as Loperamide are used for symptomatic
treatment. Avoid in Infectious diarrhea.
• Antimicrobial: Not to be prescribed routinely. Most cases are self-
limiting.
• Consider using antimicrobials in (see table below):
o Persistent bacterial and parasitic causes.
o Patients with artificial prostheses.
o Immunocompromised patients.
o Elderly patients.
Recommended Antimicrobial therapy

Organism Appropriate therapy (oral; adult dose)

Shigella Ciprofloxacin500mg bd-3/7
Ciprofloxacin500mgbd-10/7; or Amoxicillin 750
Salmonella mg 6hrly; 14/7 or Co-trimoxazole 960 mg BD;
14/7
Erythromycin 250 mg 6hrly; 5/7; or Clarithromycin
Campylobacter
250 mg 6hrly; 5/7
Doxycycline200mg day1, then 100mg daily;
Yersinia 4/7; or Co-trimoxazole 960 mg BD; 5/7; or
Ciprofloxacin 500 mg BD; 5/7
Tinidazole 2g once daily; 3/7 ; or in dysentery:
Amoebic
Metronidazole 750mg 8hrly; 5/7
Ciprofloxacin 1g once only ; or Vibramycin
Vibrio sp.
300mg once only
Giardia sp. Tinidazole 2g once only
Albendazole 400 mg OD; 3/7 ; or ivermectine
Strongyloides
150-200 ug/kg once only
Paromycine500-1000 mg TDS; 14/7; or
Cryptosporidium
Azithromycin 500 mg OD; 3/7
Metronidazole 500 mg TDS; 10/7; or Vancomycin
Clostridium difficle
125 mg 6hrly; 10/7
Cyclospora Co-trimexazole 960 mg TDS; 14/7
Trichuris Mebendazole 100mg BD; 3/7
 Medical Emergencies Guidebook

Upper Gastro-intestinal Hemorrhage

Introduction:
Acute upper gastrointestinal bleeding is the commonest emergency managed
by gastroentrologists. It has an incidence ranging between 50 to 150 per 100
000 of the population each year worldwide. In spite of the vast development
in technical equipments such as endoscopes and improvements in medical
and surgical expertise, the mortality remained unchanged over the last few
decades, which is about 10% in non-variceal bleeding and up to 30% in
variceal bleeding. Mortality is reported to be lower in specialized units and
this probably because of adherence to guidelines and protocols.
Definitions :
• Hematemisis is vomiting fresh red blood.
• Coffee ground vomiting is vomiting of altered black blood.
• Melena is the passage of black tarry stools.
• Hematochezia is passage of fresh blood coming from an upper GIT
source.

Etiology:
Varices
Peptic ulcer
Gastrointestinal erosions
Esophagitis
Mallory Weiss tear
Upper gastrointestinal malignancy
Vascular malformation
Undentified

Admission arrangements:
Patients with upper gastrointestinal bleeding should be admitted ideally to
a specialized gastrointestinal unit, which are usually jointly managed by
medical and surgical staff. When local circumstances do not permit this
then they should be admitted to an acute general medical ward where the
staff have experience in managing such patients. Severely ill patients are
best admitted to a high dependency unit or intensive care unit.
Blood tests taken urgently at initial presentation
• Hemoglobin, platelet count, and white blood cell count
• Hematocrit
• Urea, creatinine and electrolytes
• Blood grouping and cross matching
• Prothrombin time
Assessment of bleeding severity:
It is essential to categorise patients at the time of admission into high or
low risk of death. Rockall et al defined independent risk factors (see table
below) which were subsequently shown to accurately predict death. These
includes:
1. Increasing age: Death is rare in patients under 40 years of age but
higher in patients aged 60 years and above, reaching 30% in patients
aged more than 90years.
2. Comorbidity: The number and severity of comorbid illnesses are closely
related to mortality in patients admitted with GIT bleeding. Patients
who have advanced liver or renal disease and those with disseminated
cancer fare worst. It is crucial that complicating diseases affecting the
heart, respiratory system and central nervous system are recognized and
appropriately managed
3. Shock: Defined as a pulse rate of more than 100 beats/min and systolic
blood pressure of less than 100mmHg.
4. Endoscopic findings: Normal upper GIT endoscopy, Mallory Weiss
tear or the finding of an ulcer with a clean base are associated with a low
risk of rebleeding and death. In contrast, active bleeding from a peptic
ulcer in a shocked patient carried an 80% risk of continuing bleeding or
of death. A non-bleebing visible vessel is associated with a 50% risk of
rebleeding in hospital.
 Medical Emergencies Guidebook

Rockall scoring system for risk of rebleeding and death after

admission to hospital for acute gastrointestinal bleeding

Score
Variable
0 1 2 3
Age (y) < 60 60 -70 > 80
No shock Tachycardia Tachycardia
(systolic pulse > 100 pulse >120
Shock BP>100, Hypotension Hypotension
pulse<100) Systolic BP < Systolic BP <80
100
Nil major Cardiac failure, Renal
Comorbidity ischemic heart failure,
disease, Others disseminated
malignancy
Mallory Weiss All other Malignancy
tear, diagnoses upper
Diagnosis No lesion, and GI tract
No
SRH
None or dark Blood in upper
spot GI tract,
Major SRH adherent
clot, visible or
spurting vessel

Each variable is scored and the total score calculated by simple addition . SRH: stigmata of recent hemorrhage.

For practicality it is important to classify patients with upper GIT

bleeding on admission into:
1. Mild to Moderate bleed
2. Severe bleed.
This classification is especially relevant in the absence of immediate
endoscopy service.
1-Mild to moderate bleed:
• Age less than 60 years.
• Pulse and blood pressure normal.
• Insignificant comorbidity.
• Hemoglobin concentration >10gm/dl.
2- Severe bleed:
• Age >60 years.
• Pulse > 100 beats/min .
• Systolic BP <100 mmHg.
• Hemoglobin < 10gm/dl.
• Significant associated medical diseases.
Management:
Resusitation:
The first and prime goal is to maintain oxygenation and to restore blood
volume.
Intravenous access :
Two large bore cannulae should be placed. In patients with significant
cardiac disease or patients with severe bleed a central venous line (CVP
LINE) is ideal for monitoring and replacement of fluids and blood. (A
clinical guide to management of hypovolemic shock is shown in the table
below.)
A urinary catheter to monitor hourly urine output.
Patients with severe bleed are fasted until hemodynamically stable.
Upper GIT Endoscopy within the first 24 hours of admission as it is:
• Diagnostic.
• Prognostic.
• Therapeutic.

Drug therapy three classes of drugs may be considered:

Acid suppressing drugs:
1. An acidic environment makes a blood clot less stable. A pH > 6 is
necessary for platelets aggregation while a clot lysis occurs when the
pH falls < 6.
2. Intravenous Proton pump inhibitors are superior to H2 blockers.
Somatostatin: High dose intravenous somatostatin has been shown to
suppresses acid secreation and reduces splanchnic blood flow, so it works
as an alternative haemostatic agent.
Antifibrinolytic drugs: Tranexmic acid therapy reduces the need
for surgical intervention and tends to reduce mortality in ulcer bleeding
patients.
 Medical Emergencies Guidebook

Surgery:
The surgical team should be consulted early in the assessment of patients
with :(1) severe bleed (2) uncontrolled hemorrhage by endoscopic
intervention (3) rebleed after an initial endoscopic control.
Follow up:
• Patients who bled from ulcers should receive ulcer healing drugs plus
Helicobacter pylori eradication if tested positive for it.
• Trials showed that eradication of H. pylori reduces the risk of recurrence
of ulcers and rebleeding.
• Ulcers associated with non-steroidals drugs (NSAIDs) should be given
proton pump inhibitors (PPI) for healing. If the need for NSAIDs
continued to be needed it should be covered by a PPI.
• Patients who bled from gastric ulcers should have a repeat endoscopy
after 6 weeks to assess healing and exclude malignancy.
Algorithm for The Management of
Acute Gastrointestinal Hemorrhage

No SRH
 Medical Emergencies Guidebook

Treatment of Bleeding Esophageal Varices

Definitions:
Esophageal varices are portosystemic collaterals, i.e. vascular channels that
link the portal venous and the systemic venous circulation. They form with
portal hypertension prefentially in the submucosa of the lower esophagus
(less often in gastric fundus, but varices may form in any location along the
GIT.
Pathogenesis:
Two important factors exist in the pathophysiology of portal hypertension,
vascular resistance, and blood flow. Applying Ohm’s law P = F x R, where
P= pressure gradient through the portal venous system, F= volume of blood
flowing through the portal venous system, R=resistance to flow. Changes in
either F or R affect the pressure.
A pressure difference between portal and systemic circulation (hepatic
venous pressure gradient, HVPG) of 12mm Hg is needed to form varices.
Higher pressure increases risk of bleeding.
Mortality /Morbidity:
Variceal hemorrhage is the most common complication associated with
portal hypertension. Almost 90% of patients with cirrhosis develop varices
and approximately 30% of varices bleed. The first episode of variceal
hemorrhage is estimated to carry a mortality rate of 30-50%, in spite all the
developments in medicine.
Common Causes of Portal Hypertension:
Prehepatic causes
• Portal vein thrombosis
• Splenic vein thrombosis
Intrahepatic (predominantly presinusoidal) causes:
• Schistosomiasis
• Primary biliary cirrhosis (early stage)
Intrahepatic: predominantly sinusoidal / post sinusoidal
• Hepatic Cirrhosis
• Primary biliary cirrhosis (advanced stage)
• Congenital hepatic fibrosis
Post hepatic:
• Inferior vena caval obstruction
• Budd-Chiari syndrome
Differential diagnosis:
Includes all causes of upper GIT bleeding. (see Upper G.I.T bleeding
section)
It’s worth noting that peptic ulcer disease is common in cirrhotics. Thus,
diagnosis of upper GI bleeding requires endoscopy
Treatment approaches:
Three different clinical situations have to be distinguished:
1. Treatment of acute variceal hemorrhag.
2. Prevention of a first variceal bleed (primary prophylaxis)
3. Prevention of re-bleeding after an initial bleeding episode
(secondary prophylaxis)
Treatment of acute variceal hemorrhage
Resuscitation
• This is the prime step of management. It includes securing airway,
giving oxygen, stabilization of circulation. (ABC measures)
• Blood should be replaced at a modest target of Hematocrit of 25-
30%.
• Avoid intravascular volume and variceal overexpansion to prevent
rebleeding.
• Prevention of complications eg. hepatic encephalopathy, bronchial
aspiration, renal failure.
• It is important to monitor and correct electrolytes, urea/ creatinine,
clotting profile, fluid balance chart (input and output chart).
• All patients with cirrhosis and upper GIT bleeding are at high risk
of developing severe bacterial infections, which are associated with
early re- bleeding.
• The use of prophylactic antibiotics has been demonstrated to
decrease rate of bacterial infections and increase survival rate.
Broad-spectrum antibiotics such as ciprofloxacin and 3rd generation
cephalosporins are used.
Pharmacological therapy
• Somatostain is an endogenous hormone that decreases portal
blood flow by splanchnic vasoconstriction, without significant
 Medical Emergencies Guidebook

systemic adverse effect.

• Octeriotide is a synthetic analogue of somatostatin. It is
administered as a constant infusion at 50 mcg/h.
• Vasopressin is most potent splanchnic vasoconstrictor. Its use is
limited by systemic vasoconstriction, especially of the coronary
vessels. Continious infusion of 0.2-0.4 IU/min is recommended.
• Vasopressin always should be accompanied by intravenous
Nitro-glycerine at a dose of 40 mcg/min to maintain systolic blood
pressure greater than 90 mmHg.
• Terlipressin is a synthetic analogue of vasopressin that has longer
biological activity and significantly fewer adverse effects than
vasopressin.
Endoscopic therapy
• Has the advantage of allowing specific therapy at the time of
diagnosis.
• Efficacy in achieving hemostasis is higher than 80%.
• Failure of endoscopic treatments may be managed by a second
session of endoscopic treatment, but no more than 2 sessions should
be allowed before deciding to perform Transjugular Intrahepatic
Porto-systemic Shunt (TIPS) or surgery.
• Endoscopic injection sclerotherapy involves injecting a
sclerosant solution into the bleeding varix, obliterating the lumen
by thrombosis, or into the overlying submucosa, producing
inflammation followed by fibrosis.
• Sclerosant agents available are: 5% ethanolamine oleate and 1%
to 3% sodium tetradecyl sulphate. The typical volume used per
injection is 2-5ml of sclerosant, with total volume ranging from 20
to 30 ml.
• Complications of endoscopic injection sclerotherapy are related to
the toxicity of the sclerosant and include transient fever, stricture,
perforation (rarely), chest pain, mediastinitis, ulceration and pleural
effusion.
• Endoscopic Variceal Ligation (EVL) is achieved by a banding
device attached to the tip of the endoscope. The varix is aspirated
into the banding chamber, and a trip wire dislodges a rubber band
carried on the banding chamber, ligating the entrapped varix.
Leading to its thrombosis.
 • EVL is less prone to complications than injection sclerotherapy.
Other interventions:
• Balloon-tube tamponade is used temporally in massive bleeding
till a definite procedure is done. Ideally an endotracheal tube should
be placed to protect airways.
• Minnesota tube is a modification of Sengstaken-Blackmore (S-
B) tube; the difference is that the (S-B) tube does not have the
esophageal suction port to prevent aspiration.
• The Minnesota tube has 4 lumens, 1 for gastric aspiration, 2 to
inflate the gastric and esophageal balloons and 1 above esophageal
balloon for suction of secretions and prevent aspiration.
• The tube is inserted through the mouth; its position within the
stomach is checked by auscultation while injecting air through the
gastric lumen. Gastric balloon is inflated with 200 ml of air. Once
fully inflated, use approximately 0.5 kg of traction, compressing the
submucosal varices. The esophageal balloon is rarely is required.
• Endoscopic administration of Cyanoacrylate monomer
(superglue) in gastric varices is another intervention.

Primary prophylaxis:
Primary prophylaxis is administered to patients at high risk of bleeding.
These patients have (1) large varices, red wale markings on the varices at
endoscopy indicating thinning of varix wall due to high wall tension or (2)
severe liver failure as patients with Child-Pugh class B & C. (see table 1)
Beta-Blockers
• Beta-Blockers include Propranolol and Nadolol. They are non-
cardioselective reducing portal and collaterals blood flow. Reducing
cardiac output and causing splanchnic vasoconstriction.
• Propranolol is administered at a dose of 20mg every 12hrs, which
is increased or decreased every 3-4 days until a 25% reduction in
the resting heart rate occurs or the heart rate is down to 55 beats per
minute. Average dose is 40mg bid.
• Nadolol dosing is half the daily dose of propranolol, administered
once a day.
• Propranolol is contraindicated in patients with asthma, chronic
obstructive airway disease, heart block, intermittant claudication
 Medical Emergencies Guidebook

and psychosis. Side effects (S/E) include: fatigue, dyspnea on

exertion, bronchospasm, insomnia, impotence and apathy. Reducing
dose usually helps with the S/E
Vasodilators
• Isosorbide mononitrate (ISMN) is a vasodilator and has been
demonstrated to reduce hepatic venous pressure gradient. Patient
may develop tolerance to the drug.
• Available evidence does not support the use of ISMN as
monotherapy, even in patients with contraindications or intolerance
to beta-blockers.
• Combination therapy involves both beta-blockers and ISMN.
Unfortunately associated with increased side effects.
Note:
• Prophylactic sclerotherapy has no role in primary prophylaxis.
• Prophylactic endoscopic variceal ligation has been shown to have
an efficacy similar to beta-blockers in prevention of first variceal
bleed, but with increased adverse effects.
• EVL may be an option for patients with large varices who have
contraindication to or cannot tolerate beta-blockers.
Secondary prophylaxis
• Nonselective beta-blockers are as effective as sclerotherapy in
prevention of rebleed. They reduce mortality as well. Doses are
similar to those used in primary prophylaxis.
• Endoscopic sclerotherapy performed at weekly intervals. About
4-5 sessions are needed for eradication of varices, which is achieved
in nearly 70% of patients.
• Endoscopic variceal ligation (EVL) is associated with lower
rebleeding rates and lower frequency of esophageal strictures.
Fewer sessions are needed for variceal eradication compared with
sclerotherapy.
• EVL is the treatment of choice. Sessions are done every 1-2 weeks
intervals until variceal obliteration (usually 2-4 sessions).
• Combination of EVL and pharmacological therapy: recent
studies showed that EVL plus nadolol plus sucralfate is more
effective than EVL alone.
Surgical care:
Includes decompressive shunts, devascularization procedures and liver
transplantation.
• Surgery has no role in primary prophylaxis.
• The role of surgery in acute variceal bleeding is limited in view
of endoscopic therapy, which control bleeding in up to 90% of
patients.
• In those patients with failure of endoscopic therapy to control their
bleeding TIPS is an important option, as it is less invasive compared
to surgery (see below).
Trans-jugular Intra-hepatic Porto systemic Shunt (TIPS)
Technique:
Under local anesthesia with sedation via the internal jugular vein,
the hepatic vein is cannulated and a tract is created through the liver
parenchyma from the hepatic to portal vein with a needle. This is
performed under ultrasonographic and fluoroscopic guidance. The
tract is dilated; an expandable metal stent is introduced, connecting
hepatic and portal systems. Blood from hypertensive portal vein and
sinusoidal bed is shunted to the hepatic vein.

Indications:
• Uncontrolled variceal bleeding, despite emergency endoscopic
and/or pharmacological treatment.
• Recurrent variceal bleeding, despite adequate endoscopic
treatment.
• Isolated bleeding from fundal varices.
• Bleeding portal gastropathy.
• Budd Chiari syndrome.
• Bleeding ectopic varices.
• Refractory ascites.
• Hepatorenal syndrome.
• Protein loosing entropathy due to portal hypertension.
Causes of recurrent portal hypertension and bleeding after
TIPS:
1. Stent dysfunction (as many as 50% of shunts may occlude in
 Medical Emergencies Guidebook

1year) due to stenosis, thrombosis, retraction or displacement.

2. Persistant gastric varices associated with spontaneous splenorenal
collaterals or associated with massive splenomegaly.
Complication of TIPS related to technique:
1-neck hematoma, 2- cardiac arrhythmias, 3- perihepatic hematoma,
4- rupture of liver capsule, 5- extra hepatic puncture of portal vein, 6-
arterioportal fistula, and 7-portobiliary fistula.
Complication of TIPS related to porto-systemic shunting: 1-
hepatic encephalopathy (occurs in approximately 30%), 2- increased
susceptibility to bactremia, and 3- liver failure.
Other complications: 1-TIPS associated hemolysis (approximately
10%) and 2- infection of stent.

Drugs used in this section

Main
Drug Recommended dose
indication
20mg every 12hrs, which is increased
or decreased every 3-4 days until a 25%
Prophylaxis of
Propranolol reduction in the resting heart rate occurs
variceal bleeding
or the heart rate is down to 55 beats per
minute. Average dose is 40mg bid.

Regular tablet: 5-10 mg twice daily.

Extended release tablet: Initial: 30-60 mg
Isosorbide Prophylaxis of given in morning as a single dose; titrate
mononitrate variceal bleeding upward as needed, giving at least 3 days
between increases; maximum daily single
dose: 240 mg

I.V. bolus: 25-50 mcg followed by

Upper
Somatostatin continuous I.V. infusion of 25-50 mcg/
GI hemorrhage
hour
 Continuous I.V. infusion: 0.5 milliunits/kg/
hour (0.0005 unit/kg/hour); double dosage
as needed every 30 minutes to a maximum
Upper of 10 milliunits/kg/hour
Vasopressin
GI hemorrhage I.V.: Initial: 0.2-0.4 unit/minute, then titrate
dose as needed; if bleeding stops, continue
at same dose for 12 hours, taper off over
24-48 hours.

I.V.: Adults: 2 mg followed by 1 or 2 mg

Upper
Terlipressin every 4 hours until bleeding is controlled,
GI hemorrhage
for up to 36 hours

Table 1. Child-Pugh Classification of Cirrhosis*

Score
Variable
1 point 2 points 3 points
Mild/
Encephalopathy Absent Severe/ Coma
Moderate
Ascites Absent Slight Moderate
Serum Bilirubin (mg/dl) <2 2-3 >3
Serum Albumin (g/l) > 3.5 2.8- 3.5 < 2.8
Prothrombin time
1-4 4-6 >6
(seconds)
*If the total score is 5 or 6, the cirrhosis is class A; if the score is 7 to 9, the cirrhosis is class B, if the score is 10 or higher
the cirrhosis is class C. The prognosis is directly related to the score.

Appendix
• If endoscopy is not readily available, one has to resort to
pharmacotherapy in any suspected variceal bleeding, i.e. in patients
with hematemsis and signs of cirrhosis.
• Pharmacotherapy might be applied:
o As primary prophylaxis in a cirrhotic with signs of portal
hypertension (splenomegaly, thrombocytopenia) and/or
impaired liver function tests.
o As secondary prophylaxis in a cirrhotic with a history of
upper GI bleed.
 Medical Emergencies Guidebook

• If pharmacotherapy is also not available and variceal bleeding is

suspected, one must resort to general resuscitation measures with
the aid of balloon tamponade. The transfer of patient to an institution
where the necessary diagnostic/therapeutic means are available
should then be arranged.
Bleeding Esophageal Varices
 Medical Emergencies Guidebook

Lower Gastrointestinal Bleeding

Definition:
Lower gastrointestinal bleeding is defined as bleeding occurring from a site
below ligament of Trietze.
Presentation:
• Passage of fresh, bright red blood per rectum.
• Melena.
• Hematochezia (massive upper GIT bleeding).
• Symptoms of anemia (occult blood loss)
Causes:

Acute Chronic Rarer Causes

• Neoplasia • Massive upper GIT
• Diverticular Disease
(carcinoma, polyps) bleeding
• Angiodysplasia. • Hemorrhoids • Aortoenteric fistula.
• Ischaemic Colitis. • Fissure in ano
• Infective Colitis • Inflammatory bowel disease
• Radiation Colitis, proctitis
• Meckele’s Diverticulum

Assessement:
Important questions to be answered at presentation.
• Is the bleeding painful or painless?
• Colour (bright red or altered blood)?
• Relation to defecation (before or after?)
• Mixed with stool or not?
• Any associated abdominal pain?
• Any previous episodes?
Management:
1. Initial resuscitation .
2. Aim is to know site of bleeding:
• Proctoscopy (which is considered as part of clinical
examination).
• Upper GIT endoscopy is done first(see above
note.)
• Sigmoidoscopy. In about 10% of patients a lesion
causing lower GIT bleeding is encountered at
sigmoidoscopy. If this is negative then proceed to:
• Colonoscopy. If this is negative or the bleeding is
too brisk to detect the origin then two options are
there:
o Mesenteric angiography.Effective only if the bleeding is
greater than 1-2 ml/min.
o Technetium scan. It is very useful technique for localizing
site of bleeding (if it is available).
• Following identification of the site of bleeding, the
treatment may be through :
o Endoscopic intervention (such as adrenaline
injection and coagulation of bleeding vascular
lesion or polypectomy).
o Interventional radiology, as embolization of a
bleeding vessel.
o Surgical.
 Medical Emergencies Guidebook

Hepatic Encephalopathy and Fulminant Hepatic

Failure (FHF)
Definitions:
Hepatic Encephalopathy (HE)
This is a term that encompasses a wide spectrum of neuropychriatric
disturbances observed in patients with significant liver dysfunction. Three
main types are now recognized;
Type A Acute liver failure associated with normal liver function &
texture.
Type B HE associated with portosystemic bypass & no intrinsic liver
disease.
Type C HE in patients with chronic liver disease/ cirrhosis.
The syndrome is characterised by:
• Personality changes
• Intellectual impairment
• Depressed level of consciousness
Acute hepatic failure: [Fulminant Hepatic Failure (FHF)]
This describes the clinical syndrome of severe impairment of liver func-
tion (encephalopathy, coagulopathy and jaundice) within 6 months of the
onset of symptoms.
It is classified into:
• Hyperacute: Interval of jaundice to encephalopathy is < 7 days.
Cerebral oedema is common and prognosis is moderate.
• Acute: interval is 8-28 days, cerebral oedema is also common but
prognosis is poor.
• Sub acute: 29-12 weeks interval. Prognosis is poor.
Pathogenesis:
The encephalopaty in FHF is due to increased permeability of the blood brain
barrier and to impaired osmo-regulation within the brain. It is a common
cause of death. The encephalopathy in cirrhotics is due to neurotoxins as
ammonia, GABA, mercaptans, false neurotransmitters as tyramine and
octopamine. Here rarely we get brain edema.
Causes of Fulminant Hepatic Failure
Viral hepatitis:

• Hepatitis A, B, C, E, • Herpes viruses • CMV and EB virus

Delta agent

Toxic substances and drugs:

• Halothane • Rifampicin • NSAID’s
• Isoniazid • Mushroom poisoning • Some herbal medicines
• Valproic acid • Hydrocarbons • Amine oxidase inhibitors
• Disulfiram • Acetaminophen overdose • Carbon tetrachloride

Ischemic liver necrosis:

• Wilson’s disease with intra • Autoimmune • Acute Budd-Chiari

vascular hemolysis syndrome
• Hepatitis • Congestive • Heat stroke
heart failure
• Shock states.

Acute steatosis syndromes:

• Reye’s syndrome • Dideoxyinosine • Acute fatty liver of
pregnancy

• Neoplastic • Tetracyclines

Malignant infiltration of the liver:

• Lymphoreticular • Acute phase of CML • Metastatic
liver disease
(lung, breast,
melanoma)
• Hodgkin’s and Non - • AML
Hodgkin’s lymphoa
 Medical Emergencies Guidebook

Diagnosis and investigation of FHF:

• Full Blood Count and Blood Group
• L.F.T.: Measure serum transaminases AST and ALT together with
Albumin and Bilirubin.
o In toxic or viral FHF, the serum transferases are significantly
elevated due to hepatocytes injury.
o In acute fatty and malignant infiltration the amino-
transferases are moderately elevated.
• RFT; S creatinine
• Hepatitis serology
• Clotting profile esp; PT & INR
• Random Blood Glucose
• Drug levels eg Paracetamol.
• S. copper and ceruloplasmin, 24hr urinary copper, when
appropriate.
• Electrolyts.
• Liver biopsy may be helpful, after correction of coagulopathy.
• CXR
• U/S abdomen and Doppler studies & EEG
• Blood cultures and septic screen
• S. amylase
Prognosis:
Depends on: (1) the ability of liver to regenerate (2) age of the patient
(3) cause of the acute liver failure (4) clinical course (5) occurrence of
secondary complications and (6) duration and severity of the coma.
Poor prognostic indicators are:
1- Prothrombin time greater than 100 seconds regardless of the stage
of encephalopathy.
2- Presence of any three of the following:
a. Arterial pH <7.3
b. Age <10 or > 40 yrs.
c. Jaundice > 7 days before onset of encephalopathy.
d. Prothrombin time >50 seconds
e. Serum bilirubin > 18mg/dl.
Causes of death in FHF:
• Neurological complications as brain edema causing brainstem
 herniation or intracranial bleed in 57%.
• Gastrointestinal hemorrhage in 13%
• Bacterial infection and sepsis in 13%
• Hemodynamic complications in 8%
• Progressive respiratory and renal failure.
• Hypoglycemia and hypokalemia.
Management of FHF:
General:
• Intensive care nursing.
• Monitor vital signs, urine output, regular neurological and full
physical examination.
• Monitor blood glucose, S.K+, FBC, Ur/Cr, Albumin and coagulation
and correct according to abnormality.
• Correct hypoglycemia with 10% up to 50% dextrose, depending on
its severity.
• Avoid intravenous saline give N- acetylcystine IV infusion if
available.
Encephalopathy:
• Limit oral protein to 0.5-1 g/kg/day.
• Lactulose 20-30ml t.d.s.
• Avoid sedation
Bleeding:
• Avoid arterial puncture.
• Fresh Frozen Plasma FFP, if bleeding occurs.
• Ranitidine 50mg in 20ml over 2min t.d.s.,to reduce stress ulcers.
Hypotension:
Difficult to treat. Use crystalloid or albumin infusion. If not corrected
can use vasoconstricters like noradrenaline.
Renal impairment:
• Urea is falsely low in severe liver disease so creatinine should be
measured.
• Correct hypovolemia.
• Avoid diuretics.
• Consider dopamine 2.5mcg/kg/min which is the renal dose.
• Hemofilteration or dialysis is indicated if serum potassium >6mmol,
HCO3+ < 15mmol/l or rising creatinine.
 Medical Emergencies Guidebook

Infection:
• Meticulous care of IV lines and urinary catheter.
• Full septic screen including blood, urine and catheter cultures are
taken before starting antibiotics.
• Broad-spectrum antibiotics are recommended because patients
are critically ill and common signs of sepsis are often absent.
IV Cefotaxime 1g twice daily is an appropriate broad-spectrum
antibiotic until culture results are available.
Cerebral edema:
• Occurs in 70-80% of patient with Grade 4 encephalopathy and is
often fatal.
• Features include paroxysmal hypertension, dilated pupils, sustained
ankle clonus. ICP can be monitored by epidural pressure transducer
used in specialized units.
• 20% Mannitol 0.5g/kg I.V. over 10 minutes provided urine out-put
is more than 30ml/hr. In patients with renal failure it can only be
used in combination with ultrafilteration to avoid hyperosmolality
& fluid overload.
Artificial hepatic support:
• Allows time for the massively damaged liver to regenerate and
resume normal function.
• Many different methods have been tried, including exchange blood
transfusions, & plasmapheresis.
Liver transplant:
• May be the only lifesaving procedure in FHF.
• In most centres worsening hepatic encephalopathy, clinical evidence
of cerebral edema and increasing prolongation of the prothrombin
time after 24 to 48 hrs. of intensive medical treatment are used as
the key factors for recommending liver transplantation.
• The 1-year survival rate for such patients after liver transplant is
65%
Clinical Features of Chronic Hepatic
Encephalopathy:
Can be subclinical, acute discrete episodes with full recovery within 4 weeks
precipitated or spontaneous or chronic with persistent symptoms. The later
group may respond to treatment but lapse into HE with cessation of therapy.
Patient can fluctuate between grades I-II & severe grades III – IV.
Grading of symptoms and signs of chronic hepatic encephalopathy is as
follows:
Grade 0:
• Minimal changes in memory, concentration, intellectual function
and coordination.
Grade 1:
• Mild confusion, euphoria or depression
• Decreased attention.
• Slowing of ability to perform mental tasks.
• Irritability.
• Disordered sleep pattern, such as inverted sleep cycle.
Grade 2:
• Drowsiness, lethargy.
• Gross deficit in performing mental tasks.
• Personality changes, inappropriate behaviour.
• Disorientation to time.
Grade 3:
• Somnolent but arousable
• Unable to perform mental tasks.
• Disorientation about time and place.
• Marked confusion.
• Occasional fits of rage (aggressiveness)
• Incomprehensible speech.
Grade 4:
• Coma (with or without response to painful stimuli)
Other important physical signs:
• Fetor hepaticus
• Asterixis (Flapping tremor)
• Fever and other signs of infection
• Jaundice (may be minimal in early stages)
• Liver size (usually small in cirrhosis and acute hepatic necrosis)
• Spleen: usually normal size.
• Ascites: develops or increase.
• Venous hum.
• Rectal examination for melena.
 Medical Emergencies Guidebook

Common Precipitants of Hepatic Encephalopathy in Liver

Cirrhosis
1. G.I.T.bleeding: presence of blood in upper gastrointestinal tract
results in increased ammonia and nitrogen absorption from the
gut.
2. Renal failure: this lead to decreased clearance of urea and other
nitrogenous compounds s.
3. Hypokalaemia
4. Infection: may predispose to renal impairment and to increased
tissue catabolism, both of which increase blood ammonia level.
5. Constipation: increases intestinal production and absorption of
ammonia.
6. Diuretic therapy: leads to hypokalemia and alkalosis both
facilitate the conversion of NH4+ to NH3+.
7. Medications: drugs acting in C.N.S. such as opiates,
benzodiazepines, antidepressants and antipsychotic agents may
worsen hepatic encephalopathy.
8. portsystemic shunt creation; e.g. TIPS
9. Non compliance with therapy.
10. Dietary protein overload: an infrequent precipitating factor of
hepatic encephalopathy.
Differential Diagnosis for Hepatic Encephalopathy
• Intracranial lesions: such as subdural hematoma, intracranial bleed,
stroke, tumor.
• Infections: such as meningitis, encephalitis and intracranial
abscess.
• Metabolic encephalopathy: such as hypoglycemia, electrolyte
imbalance, hypoxia, hypercapnia and uremia. Including zinc
deficiency.
• Hyperammonemia from any other cause such as inherited urea
cycle disorders or secondary to uretrosigmoidostomy.
• Toxic encephalopathy from alcohol intake, such as acute
intoxication, alcohol withdrawal and Wernicke’s encephalopathy.
• Toxic encephalopathy from drugs such as sedative hypnotics,
antidepressants, antipsychotic agents and salycylates.
• Post-seizure encephalopathy.
Management of Hepatic Encephalopathy
The following steps showed should be taken whenever possible:
• Precipitants of hepatic encephalopathy such as metabolic
disturbances, gastrointestinal bleeding, infection, sedative drugs
and constipation should be corrected.
• Lactulose (beta-galactosidofructose) is a nonabsorbable
disaccharide. It inhibit intestinal ammonia production by a number
of mechanisms:
1. Lactulose is degraded by colonic bacteria to lactic acid
and other acids with resulting acidification of intestinal
lumen. This favors conversion of NH4+ to NH3+ from
tissues into gut lumen.
2. Gut lumen acidification inhibits ammoniogenic
coliform bacteria.
3. Lactulose cause osmotic diarrhea, so reducing the
stasis of bacterial load.
Dose: start with 30ml Lactulose (orally or by nasogastric tube)
daily, twice or three times daily. Aim for 3-4 loose motions per
day.
S/E: diarrhea, abdominal cramps and bloating.(May consider
reducing dose)
Lactulose may be given through NG tube as well as enema to
comatose patients. Enema is warrented in patients with ileus or
bowel obstruction. In all patients an initial enema can be used to
begin bowel cleansing especially if they have hard stools on rectal
examination.
Dose: 300 ml Lactulose plus 700 ml water administered as retension
enema every 4 hours as needed.
• Neomycin and other antibiotics such as: oral vacomycin,
paromomycin, oral quinolones and metronidazole are administered
in an effort to reduce colonic ammoniogenic bacteria. Neomycin is
usually reserved as a second-line agent after lactulose.
Dose of Neomycin: 250mg orally 2-4 times /day. Doses as high as
4000mg /day may be given. Long term treatment with this amino
glycoside runs the risk of inducing ototoxicity and nephrotoxicity
because of some systemic absorption.
Oral Metronidazole can be given as second line treatment for a
 Medical Emergencies Guidebook

short period as 250 mg three times a day. It is not recommended

for long term use.
Other drugs used in encephalopathy:
• L-ornithine L-aspartate (LOLA) stimulate urea cycle, where
ammonia is used as a substrate.This drug is new and found effective
in a number of studies.
• Sodium benzoate interact with glycine to form hippurate.
The subsequent renal excretion of hippurate results in the loss
of ammonia ions.Dose: 5g twice daily. S/E: sodium retension,
unpleasant taste.
• Diet: Rarely one should restrict proteins to less than 0.5g-1g/kg
body weight in encepalopathy. Branched chain amino acid enriched
formulae can be used in patients with intolerance to oral protein.
Vegetable proteins tolerated better than animal proteins, especially
proteins derived from red meat.!
• Mannitol: acts by reducing brain edema, mainly in c fulminant
hepatic failure (FHF) rather than in cirrhotics.(see pathogenesis
above)
• Avoid nephrotoxic drugs; NSAID
• Patients with recurrent or intractable HE should go for liver
transplantation.
Drugs used in this section

Drug Main indication Recommended dose

Oral: 20-30 g (30-45 mL)
every 1-2 hours to induce rapid
laxation; adjust dosage daily to
produce 2-3 soft stools; doses of
Lactulose Hepatic encephalopathy 30-45 mL may be given hourly
to cause rapid laxation, then
reduce to recommended dose;
usual daily dose: 60-100 g (90-
150 mL) daily

Oral: 500-2000 mg every 6-

Neomycin Hepatic encephalopathy 8 hours or 4-12 g/day divided
every 4-6 hours for 5-6 days
 Medical Emergencies Guidebook

Pulmonary
Emergencies
Editor: Ala’Eldin Hassan Ahmed
 Medical Emergencies Guidebook

Management of Acute Asthma Exacerbations

in Adults
Definition:
Asthma is an inflammatory disorder of the airways associated with reversible
airflow obstruction. Airflow obstruction is assessed by measuring peak
expiratory flow (PEF). Clinically asthma presents as cough, and/or shortness
of breath, and/or wheeziness and/or chest tightness. The symptoms of asthma
tend to be variable, intermittent, worse at night, and provoked by triggers
including exercise; these features are helpful in reaching a diagnosis.
Differential diagnosis:
• Congestive heart failure.
• Pulmonary embolism.
• Chronic obstructive pulmonary disease.
• Acute pneumothorax
• Mechanical airway obstruction.
• Vocal cord dysfunction (rare).
Directed Approach to Acute Asthma Exacerbations:
History:
Determine how good or bad is the patient’s asthma control in the chronic
stable state
• Symptoms especially the presence of nocturnal symptoms
• Range of home peak expiratory flow rates (PEFs), if available
• Frequency of emergency department visits and ICU admissions.
• Long-term medications including oral steroid dependence
Evaluate the following concerning the current exacerbation:
• duration
• severity (see next)
• potential precipitants
• medications taken in response
Physical examination:
• Asses asthma severity: Features of severe asthma are: PEF < 50%
best or predicted; respirations >/= 25/min; pulse rate >/= 110 beats/
min; can’t complete sentences in one breath.
• Features of life threatening asthma are: SpO2 < 92%; silent
chest; cyanosis; poor respiratory effort; bradycardia; arrhythmia;
 hypotension; exhaustion; confusion; coma.
• These findings are not sensitive indicators of severe attacks; up
to 50 percent of patients with severe airflow obstruction will not
manifest many of these abnormalities.
• Look for signs of pneumothorax or pneumomediastinum.
Diagnostic studies:
1. PEF measurement:
• This is the best test for assessing the severity of an asthma attack.
• It is easy to perform and when repeated over time can be used to
monitor a patient's response to treatment.
• Predicted values for an individual differ with size, age, gender, and
ethnicity, but a peak flow rate below 200 L/min indicates severe
obstruction for all but unusually small adults.
2. Arterial blood gas (ABG) analysis:
• This is generally indicated only among patients with persistent
dyspnea (despite initial bronchodilator therapy) whose PEF is
below 33 percent of predicted or those with signs of life threatening
asthma.
3. Chest x-ray:
• Generally not recommended for all patients.
• It can be limited to patients with suspected complications such as
pneumothorax; pneumomediastinum; consolidation; those with
features of life threatening asthma; and those who fail to respond to
treatment satisfactorily.
For a stepwise approach for treating acute asthma exacerbations please
refer to the attached flowchart.
Notes:
• Give high flow oxygen to all patients with acute severe asthma.
• Ipratropium bromide provides greater bronchodilation for patients not
rapidly responding to initial beta agonist therapy.
• There is no evidence for any difference in efficacy between salbutamol or
terbutaline.
• Generally, avoid I.V. aminophylline if salbutamol is available. The
combination of salbutamol and intravenous aminophylline results in no
further bronchodilation than that achieved with nebulized beta agonists
alone and may lead to increased risk of toxicity.
 Medical Emergencies Guidebook

• Rarely, however, some patients with near fatal asthma or life threatening
asthma with poor response to inhaled therapy may gain additional benefit
from IV aminophylline 5 mg/kg loading dose over 20 minutes unless on
maintenance oral therapy then give infusion of 0.5 – 0.7 mg/kg/h.
• If PEF is < 50% on presentation prescribe prednisolone 40 – 50 mg/day.
Continue prednisolone 40 – 50 mg daily for at least five days or until
recovery. This should be followed by treatment with regular inhaled
corticosteroids.
• In the absence of vomiting, oral administration of corticosteroids can be
substituted for intravenous administration. Oral formulations are rapidly
absorbed and exhibit comparable efficacy.
• If a nebulizer is unavailable, salbutamol may be delivered via a metered
dose inhaler (MDI) with a spacer. The equivalent dose has not been
precisely defined, but four to six carefully administered inhalations from
an MDI with spacer have generally been found to equal one nebulizer
treatment.
• Routine prescription of antibiotics is not indicated for acute asthma.
Drugs used in this section:

Main
Drug Recommended dose
indication
Prednisolone Acute Oral: prednisolone 40 – 50 mg per
asthma day as single dose. Continue for at
least five days or until recovery

Hydrocortisone Acute asthma I.V. 100 mg 6 hourly is as effective

as higher doses
Salbutamol (via Acute Inhalation: 90 mcg/puff: 4 - 6 puffs
a nebulizer OR asthma every 20 minutes for up to 4 hours,
a metered dose then every 1 - 4 hours as needed.
inhaler with a Nebulization: 5 mg continuous
spacer) flow nebulization every 20 minutes
for three doses. May also give via
continuous nebulization, at rate of 5-
10 mg/hour.
Ipratropium Acute Nebulization: 500 mcg 4 times/day.
bromide asthma Metered dose inhaler: 2 inhalations
4 times/day,
Aminophylline Acute asthma I.V. loading dose (in patients
not currently receiving oral
aminophylline or theophylline): 5
mg/kg over 20 minutes (given in
normal saline or 5% dextrose)
I.V. maintenance dosage continuous
infusions in normal saline or
dextrose 5%: 0.5 – 0.7 mg/kg/hour.
Dosage should be adjusted according
to serum level measurement (if
available)

Magnesium Acute asthma IV. 1.2 – 2 grams infusion in normal

sulphate saline or 5% dextrose over 20
minutes (single dose)
 Medical Emergencies Guidebook

Management of Acute Severe

Asthma in Adults in Emergency Department
 Spontaneous Pneumothorax
Pneumothorax is defined as air in the pleural space. Primary pneumothoraces
arise in otherwise healthy people without lung disease. Secondary
pneumothoraces arise in subjects with underlying lung disease.
Differential diagnosis:
• Acute severe asthma.
• Acute pulmonary embolism.
• Acute left ventricular failure.
• Exacerbation of chronic obstructive pulmonary disease.
• Mechanical airway obstruction.
Directed Approach to Spontaneous Pneumothorax:
History:
There is no relationship between physical activity and onset of a
pneumothorax; most pneumothraces occur at rest. Smoking is a significant
risk factor. Remember that history is not a reliable indicator of the size of
a pneumothorax.
Physical examination:
• Look for signs of respiratory distress, cyanosis, and shock; if present
they indicate tension pneumothorax.
Diagnostic studies:
• Chest radiograph. Expiratory CXR is not recommended for the routine
diagnosis of a pneumothorax.
• A lateral chest or lateral decubitus radiograph should be performed if
the clinical suspicion is high but the PA film is normal.
• CT scan is only recommended when differentiating a pneumothorax
from complex bullous lung disease.
For a stepwise approach for management of spontaneous
pneumothorax (primary or secondary) refer to flowchart.

Notes:
• If tension pneumothorax is present a cannula of adequate length should
be promptly inserted into the second intercostal space in the mid
clavicular line and left in place until a functioning intercostals tube can
be positioned.
 Medical Emergencies Guidebook

• The size of a pneumothorax is divided into small or large depending

on the presence of a visible rim of < 2 cm or ≥ 2 cm between the lung
margin and the chest wall respectively.
• If a patient with a pneumothorax is admitted for observation, high flow
oxygen (10 L/min) should be given.
• All breathless patients should not be left without intervention regardless
of the size of the pneumothorax.
• If > 2.5 L. of air were aspirated and the lung is not fully expanded
(as indicated by cessation of air coming out) the procedure should be
abandoned and regarded unsuccessful.
• There is no evidence that large tubes (20 – 24 F) are better than small
tubes (10 – 14 F). The initial use of large tubes is not recommended.
• A bubbling chest tube should never be clamped or removed.
• If possible, pneumothorax patient should be admitted under the care of
a respiratory physician.
Recommended Algorithm For The Treatment of
Primary Spontaneous Pneumothorax
 Medical Emergencies Guidebook

Recommended Algorithm For The Treatment of

Spontaneous Secondary Pneumothorax
 Acute Pulmonary Embolism
Consider pulmonary embolism as a possible diagnosis in any patient
presenting with acute shortness of breath.
Differential diagnosis:
• Acute severe asthma.
• Acute left ventricular failure.
• Tension pneumothorax.
• Exacerbation of chronic obstructive pulmonary disease.
• Mechanical airway obstruction.
Directed Approach to Acute Pulmonary Embolism:
History:
Clinical presentation of pulmonary embolism may be subtle, atypical or
obscured by other coexisting diseases. In a patient with suspected pulmonary
embolism determine the risks of pulmonary embolism (see table)
Physical examination:
• Assess hemodynamic instability: low blood pressure or the presence of
acute right heart failure.
Diagnostic studies:
See figures
For a stepwise approach for diagnosing pulmonary embolism please
refer to attached table (rules for predicting the probability of embolism)
and flowchart.
Notes:
• If the diagnosis of pulmonary embolism is strongly suspected, start
treatment immediately (before investigations are done or their results
are available). See table: drug treatment of acute pulmonary embolism
for drugs used.
• Intravenous unfractionated heparin is as effective as low-molecular-
weight heparin.
• For patients with severe renal failure unfractinated heparin is preferred
over low-molecular-weight heparin as low-molecular-weight heparin
dose need to be monitored.
• Begin oral anticoagulation therapy within 24 hours of starting heparin.
• Discontinue heparin when the INR has been >/= 2 for two consecutive
days.
 Medical Emergencies Guidebook

• Thrombolytic therapy has not been shown to be superior to

anticoagulation in the management of pulmonary embolism.
• Thrombolytic therapy may be considered for patients who are
hemodynamically unstable.
• Thrombolytic therapy may also be considered for patients who are
normotensive but have acute right ventricular dysfunction either
clinically or on echocardiography.
Drug treatment of acute pulmonary embolism

Main
Drug Recommended dose
indication
Give bolus dose of 5000 units IV (or 80U/
kg bolus). Followed by continuous infu-
Acute sion (in 5% dextrose or normal saline) of at
Unfractionated
pulmonary least 30,000 units for the first 24 hours (18
heparin
embolism U/kg/h.). Subsequent dosing should main-
tain an aPTT value of 1.5 to 2.5 times the
control value.

Can be used as an alternative to unfraction-

Acute ated heparin. Body weight adjusted doses
Low molecular pulmonary should be administered subcutaneously
weight heparin embolism once or twice daily without laboratory
monitoring. Follow manufacturers’ recom-
mendations for dosing.

May be given to patients who are hemody-

namically unstable, or those with acute right
Acute ventricular dysfunction (see text). Dose
pulmonary 250,000 units IV infusion ((in 5% dextrose
Streptokinse
embolism or normal saline) over 30 minutes. Should
be followed by unfractionated heparin infu-
sion as above, or SC low molecular weight
heparin as above.

Acute
Given orally as a single daily dose to main-
Warfarin pulmonary
tain an INR between 2.0 to 3.0.
embolism
Rules for predicting the probability of pulmonary embolism

No of
Variable
points
Risk factors
Clinical signs and symptoms of venous thrombosis 3
An alternative diagnosis deemed less likely than P.E. 3
Heart rate > 100 beats per minute 1.5
Immobilisation or surgery in the past 4 weeks 1.5
Previous deep vein thrombosis or P.E. 1.5
Hemoptysis 1
Cancer receiving treatment or treated past 6 months 1

Clinical probability
Low < 2.0
Intermediate 2.0 – 6.0
High > 6.0
 Medical Emergencies Guidebook

Diagnostic Approach to a Patient with Low Clinical

Probability Pulmonary Embolism
Diagnostic Approach to a Patient with High or Moderate
Clinical Probability of PE
 Medical Emergencies Guidebook

Renal, Hypertensive and

Electrolyte Emergencies

Editor: Elwaleed Ali Mohamed Elhassan

 Medical Emergencies Guidebook

Acute Renal Failure

Definition:
Acute renal failure (ARF) is defined as a rapid (over hours to weeks) decrease
in renal function sufficient to increase the concentration of nitrogenous
wastes in the blood.
It is usually manifested by a rise in serum creatinine of ≥ 0.5 mg/dl or 50%
or a GFR reduction by >50%.
In ARF, reduction of urine output is often seen:
• Oliguria, a decrease of urine output to less than 500 ml/day.
• Anuria is reduction of urine output to less than 100 ml/day.
Etiology:
Category Etiologies
Pre-renal • Hypovolemia; hemorrhage, vomiting, diarrhea,
(Decreased renal inappropriate diuresis, burns, cardiogenic shock,
blood flow) distributive shock (sepsis, anaphylaxis), ACE
inhibitors, NSAIDs, contrast dye, cyclosporine
• Decreased effective arterial volume: heart failure,
nephrotic syndrome, cirrhosis (hepatorenal
syndrome)
Renal • Acute tubular necrosis (ATN)
intrinsic renal pa- o Ischemic: progression of any pre-renal process
thology) o Toxins
o Drugs: aminoglycosides, amphoterecin, contrast
dye (usually only in setting of baseline renal
disease), pigments (myoglobin, Hb), crystals
(uric acid) or proteins (Ig light chains)
• Acute interstitial nephritis (AIN)
o Allergic: beta-lactam antibiotics, sulfa drugs,
NSAIDs
o Infection
• Infiltration (e.g. sarcoid, lymphoma)
• Autoimmune disease (e.g. SLE)
• Vascular: renal artery stenosis (esp. bilateral + ACE
inhibitors), thrombosis, hypertensive crisis,
scleroderma renal crisis, cholesterol emboli, HUS/
TTP
• Acute glomerulonephritis (AGN)
 • Bladder neck: BPH, prostate cancer, neuropathies,
anticholinergic drugs
Post- renal (obstruc-
• Ureteral: malignancy, lymphadenopathy, retroperitoneal
tion of urine)
fibrosis
• Tubular: precipitation of crystals

Clinical presentation:
• Patients may present with non-specific symptoms due to azotemia and
the underlying cause of acute renal failure.
• Azotemia can cause malaise, nausea, vomiting, seizures, nonspecific
abdominal pain and platelet dysfunction which may lead to bleeding.
• Enquire about recent procedures and medications.
Physical examination:
• Obtain vital signs, assess volume status. Look for signs of obstruction,
pericardial effusion or rub, vascular or systemic disease.
• Lung examination may reveal crackles due to fluid overload.
• Neurological examination may show altered sensorium and asterixis.

Workup:
Send blood samples for:
• BUN, s.creatinine, electrolytes including Ca and phosphorus. Obtain
HCO³ and Chloride for anion gap determination.
• CBC, uric acid and RBS.
• If diagnosis uncertain or clinical setting appropriate; obtain complement
levels (C3/C4), ANA, Anti double-stranded DNA, ANCA, ASO titer,
blood cultures and Bence Jones proteins in urine

Evaluate urine:
• Observe output.
• Get a sample for urinalysis, urine sediments, electrolytes and
osmolality.
• Calculate the fractional excretion of Na (FE Na) = (Urine Na/Plasma
Na) / (Urine creatinine/Plasma creatinine):
o Concentration ability preserved: urine osmolality >500 mOsm,
specific gravity > 1.025, decreased urine Na: < 20 meq/L, FE
Na < 1% (e.g. pre-renal, contrast and pigment nephrotoxicity,
 Medical Emergencies Guidebook

AGN, early post-renal)

o Concentration ability impaired: urine osmolality <350 mOsm,
specific gravity < 1.015, increased urine Na > 20 meq/L, FE Na
> 1% (e.g. ATN, AIN, late pre-renal)

Etiology Sediment
Pre-renal Bland, few hyaline casts

Intrinsic
• ATN: pigmented granular casts
• AIN: WBCs and WBC casts; ± RBCs
• Vascular: bland, RBCs if necrosis
• AGN: dysmorphic RBCs and RBC casts

Post-renal ± RBCs, WBCs, crystals

Renal ultrasound:
Is useful to rule out obstruction and evaluate kidney size to estimate
chronicity of renal failure.
Renal biopsy:
Consider renal biopsy if AGN or AIN suspected.
Treatment:
• Treat underlying disorder e.g. relieve obstruction if present, discontinue
culprit medications.
• Optimize volume status:
o Give I.V crystalloids if suspected or established volume-
depletion
o If the patient appears fluid-overloaded and is oliguric, diuretics
may be employed to attempt conversion to nonoliguric state.
Furosemide may be administered intravenously (100-200 mg)
slowly. If no favorable response, dose may be repeated or doubled
in 2 hours. It may be given in combination with metolazone. It
may also be given in a continuous I.V. infusion of 10-40 mg/hr
(max 1000 mg/day).
o Support hemodynamics with pressors, inotropes if needed.
 o Dialysis
• Electrolytes disorders:
o Hyperkalemia:
§ (See Hyperkalemia section); decreased K intake,
cation-exchange resin, dialysis
o Hyperphosphatemia: may use phosphates binders
• Correct drug doses for degree of renal insufficiency
• Fluid intake:
o After normal volume has been restored, restrict fluid intake
to an amount equal to urinary and other losses plus insensible
losses of 300-500 ml/day.
o In oliguric patients daily fluid intake may need to be restricted
to less than 1 L/day.
• Nutritional support:
o High biologic value protein intake of 0.6 mg/kg/day.
o A daily diet comprising about 2 g of sodium, 40-60 mg of
potassium and at least 35 kcal/kg of non-protein calories.
• Most patients with ATN spontaneously recover renal function. Recovery
is usually heralded by an increase in urine output and a gradual return
of the BUN and serum creatinine concentration to or very near the
previous baseline level. There are no specific proven treatments to
achieve reversal of ATN or alter its final outcome (i.e. no proven benefits
for dopamine, furosemide or mannitol)

Indications for urgent dialysis (when condition refractory to

conventional treatment)
o Persistent severe acedemia with (pH less than 7.2)
o Life threatening electrolyte disturbances: e.g. hyperkalemia
o Intoxication: methanol, ethylene glycol
o Overload of volume unresponsive to diuresis
o Uremia: pericarditis, encephalopathy, seizures
 Medical Emergencies Guidebook

Drugs used in this section:

Drug Main indication Recommended dose

Furosemide Augmenting diuresis I.V.: 100-200 mg/dose, may be
in acute renal failure repeated or doubled in 1-2 hours
as needed up to 1000 mg/day.
I.V. injections should be given
slowly. In adults, undiluted di-
rect I.V. injections may be ad-
ministered at a rate of 40 mg
over 1-2 minutes.
Continuous I.V. infusion: Initial
I.V. bolus dose of 0.1 mg/kg fol-
lowed by continuous I.V. infu-
sion doses of 0.1 mg/kg/hour
doubled every 2 hours to a maxi-
mum of 0.4 mg/kg/hour if urine
output is < 1 mL/kg/hour have
been found to be effective and
result in a lower daily require-
ment of furosemide than with
intermittent dosing.
Metolazone Augmenting diuresis Oral: 5-20 mg/dose every
in acute renal failure 24 hours.
 Severe Hypertension
Definition:
• Severe Hypertension is defined as marked elevation in blood pressure
(BP) with the diastolic BP usually above 120 mmHg.
• It may be viewed as:

o Hypertensive emergencies, whereby there is evidence of ongoing

end-organ damage. Parenteral treatment is usually needed.
o Hypertensive urgency, which is seen in the majority of patients,
who have similar BP elevations, but exhibit no such features of
ongoing end-organ damage. Oral therapy is employed
Hypertensive Emergency
This is defined by a significant elevation in BP associated with ongoing
vascular damage symptoms or signs of neurological, renal, cardiac or
retinal dysfunction.
Hypertensive emergencies include severe hypertension in the following
settings:
• Hypertensive encephalopathy (headache, irritability, and altered mental
status due to cerebral vasospasm).
• Malignant hypertension:
o Marked hypertension with new retinal hemorrhages, exudates,
or papilledema.
o There may also be renal involvement, called malignant
nephrosclosis and manifests as hematuria, proteinuria and
progressive renal dysfunction (by comparing the presenting s.
creatinine with a recent measurement) due to arteriolar necrosis
and intimal hyperplasia of the interlobular arteries.
• Aortic dissection
• Acute left ventricular failure and pulmonary edema.
• Unstable angina or acute myocardial infarction.
• Acute increase in sympathetic activity which can lead to severe
hypertension in conditions like: (1) pheochromocytoma; (2) autonomic
dysfunction, as in the Guillain-Barré syndrome; (3) renovascular
disease (4) post-spinal cord injury
• Eclampsia and pre-eclampsia
 Medical Emergencies Guidebook

Treatment
• Parenteral treatment is usually indicated.
• Aim initially at rapidly lowering the diastolic BP to about 100 to 105
mmHg (or a reduction in 25 percent of the presenting value, whichever
is higher); this goal should be achieved within two to six hours.
• Excessive reduction may precipitate coronary, cerebral or renal
ischemia. Therefore agents with a predictable, dose-dependant and
transient effect are employed.

Best Practice Pharmacologic Management:

Nitroprusside sodium:
• Is the agent of choice in almost all hypertensive emergencies (except
myocardial ischemia, renal impairment or pregnancy)
• It is a combined arteiolar and venodilator reducing both afterload and
preload.
• It is given as an intravenous infusion. Initial dose: 0.25 to 0.5 µg/kg
per min; maximum dose: 8 to 10 µg/kg per min. Nitroprusside acts
within seconds and has duration of action of only two to five minutes.
Thus, hypotension can be easily reversed by temporarily discontinuing
the infusion, providing an advantage over the drugs listed below.
However, the potential for cyanide toxicity limits the prolonged use of
nitroprusside, particularly in patients with renal insufficiency. In most
hospitals nitroprusside is only given in an ICU with an arterial line in
place to contiuosly monitor the BP.
Labetalol:
• An alpha- and beta-adrenergic blocker, given as an intravenous bolus or
infusion.
• Bolus: 20 mg initially, followed by 20 to 80 mg every 10 minutes to a
total dose of 300 mg. Infusion: 0.5 to 2 mg/min.
Nicardipine:
• A nondihydropyridine calcium channel blocker acting as an arteriolar
dilator.
• Is given as an intravenous infusion. Initial dose: 5 mg/h; maximum
dose: 15 mg/h
Enalaprilat:
• Is an angiotensin converting enzyme inhibitor and an ideal choice for
patients with heart failure.
• Is given as an intravenous bolus. Dose: 1.25 mg every six hours which
might be increased to 5 mg every six hours.

Alternative Drugs:
Hydralazine:
• Is a direct arteriolar dilator which causes reflex sympathetic stimulation
of the heart. Precautions are needed in patients with underlying
coronary disease or an aortic dissection, and a ß-blocker should be
given concurrently to minimize the effect on the heart.
• It is given in intravenous or intramuscular boluses. However, its effect
is less predictable than other agents.
• Initial dose: 10-20 mg/dose every 2-4 hours as needed. May increase
to 40 mg/dose; change to oral therapy as soon as possible.

Nitroglycerin
• Mainly is a venous dilator, given as an intravenous infusion. Is the drug
of choice for hypertensive emergencies with coronary ischemia.
• Disadvantages include being unstable in solution, tolerance with
prolonged use and profound headaches.
• Initial dose: 15 µg IV bolus, then 5-100 µg/min (50 mg in 250 mL
D5W); maximum dose: 100 µg/min.
Hypertensive Urgency
Is severe asymptomatic elevation of blood pressure (systolic >180 Hg, or
a diastolic >120 mmHg) in the absence of indicators of acute end-organ
damage.
Management:
• In all patients presenting with severe hypertension, repeat the blood
pressure measurement, with a proper technique, after rest in a quiet
room.
• The initial goal should be a reduction in blood pressure to 160/100
over several hours to days with conventional oral therapy. This is based
on the adverse effects observed with faster correction and/or lower
 Medical Emergencies Guidebook

achieved blood pressures

• Sublingual or oral fast-acting nifedipine is best avoided. Serious
adverse ischemic events have been reported in relation to its use.
Previously treated hypertension:
In patients previously treated for hypertension do one of the following:
• Increase the dose of existing antihypertensive medications or
• Add another agent (a diuretic if not previously included) and reinforce
dietary sodium restriction or
• Reinstitute medications in non-adherent patients
Previously untreated hypertension:
For previously untreated patients:
• Administer oral furosemide (if the patient is not volume depleted) at a
dose of 20 mg (or higher if the renal function is not normal) or a small
dose of oral captopril (12.5 or 25 mg). This can achieve relatively rapid
initial blood pressure reduction (over several hours).
• Following that, observe the patient for a few hours to ascertain a
reduction in blood pressure of 20 to 30 mmHg. Thereafter, prescribe a
longer acting agent and send the patient home to follow up within a few
days:
• A calcium channel blocker (e.g. oral amlodipine or felodipine 5 mg once
daily or long-acting nifedipine 20 mg once or twice daily) or,
• A beta blocker ( e.g oral atenolol 50 mg daily, or metoprolol 50 mg twice
daily)
• ACE inhibitor (e.g. enalapril 5 mg twice daily or lisinoprol 5 mg daily).
• Almost all patients with persistently high BP (> 160/100 [stage
2 hypertension]) will eventually require therapy with at least two
antihypertensive medications to achieve goal blood pressure.
• The choice of agent should take into consideration patient characteristics
and comorbid conditions, which influence optimal long-term therapy.
• Over subsequent weeks and months, the dose and selection of medications
should be adjusted as needed to achieve desired goals (eg, <140/90 or
<130/80 mmHg, as appropriate), preferably with longer acting agents. A
diuretic with another drug is reasonable.
Emergency Treatment of Hypertension (1)
 Medical Emergencies Guidebook

Emergency Treatment of Hypertension (2)

Drugs used in this section:

Drug Main Indication Recommended Dose

Nitroprusside Initial dose: 0.25 to 0.5 µg/kg per
Hypertensive
sodium IV min; maximum dose: 8 to 10 µg/kg
emergency
infusion per min
Bolus: 20 mg initially, followed by
Hypertensive 20 to 80 mg every 10 minutes to a
Labetalol IV
emergency total dose of 300 mg. Infusion: 0.5
to 2 mg/min

Nicardipine IV Hypertensive Initial dose: 5 mg/h; maximum

infusion emergency dose: 15 mg/h IV infusion
1.25 mg every six hours which
Hypertensive
Enalaprilat IV might be increased to 5 mg every
emergency
six hours
Initial dose: 10-20 mg/dose every 2-
Hypertensive 4 hours as needed. May increase to
Hydralazine
emergency 40 mg/dose; change to oral therapy
as soon as possible
15 µg IV bolus, then 5-100 mcg/min
Nitroglycerin IV Hypertensive
(50 mg in 250 mL D5W); maximum
infusion emergency
dose: 100 µg/min
20 mg if renal function is normal
Hypertensive
Furosemide PO and higher if renal insufficiency is
urgency
present

Labetalol Hypertensive 200-400 mg, may be repeated every

PO urgency 2-3 hrs.

Hypertensive 12.5-25 mg every, may be repeated

Captopril PO
urgency 1-2 hrs

Hypertensive
Felodipine PO 5 mg orally
urgency

Hypertensive
Amlodipine 5 mg orally
urgency
 Medical Emergencies Guidebook

Hypokalemia

Definition:
• Hypokalemia is defined by serum potassium (K+) less than 3.5 meq/L.
Etiology:
• The commonest cause of hypokalemia is loss of potassium from the
gastrointestinal or urinary systems when replacement is not adequate.
• However, hypokalemia can be transiently induced by the entry of
potassium into the cells (for example with severe hypoglycemia or
salbutamol overdose).
Presentation:
• Muscular weakness, fatigue and muscle cramps are frequent complaints
in mild to moderate hypokalemia.
• Smooth muscle involvement may result in constipation or ileus. Flaccid
paralysis, hyporeflexia, tetany and rhabdomyolysis may be seen with
severe hypokalemia. (< 2.5 meq/L).
• The ECG shows decreased amplitude and broadening of T waves,
prominent U waves, premature ventricular complexes and depressed
ST segments.
Workup:
• Rule out trans-cellular shifts: alkalemia, insulin, catecholamines,
hypokalemic periodic paralysis.
• Determine whether K+ depletion is due to gastro-intestinal (urine K+
< 15meq/L) or renal (urine K+ >15 meq/L) losses. If renal losses,
determine blood pressure and acid-base status:
Gastro-intestinal (G.I.) losses: (urine K+ < 15 meq/L or 25 meq/d)
• G.I. losses plus acidosis: diarrhea, laxative abuse, villous adenoma
• Vomiting and nasogastric tube drainage usually manifest as renal losses
due to increased aldosterone and metabolic alkalosis.
Renal losses: (urine K+ > 30 meq/d or 15 meq/L)
• Hypo- or normotensive:
o Acidosis: DKA, RTA
o Variable acid-base: Mg depletion
o Alkalosis: diuretics, vomiting, nasogastric drainage, Bartter’s
syndrome. Gitelman’s syndrome.
• Hypertensive
o Primary aldosteronism (Conn’s syndrome)
o Secondary aldosteronism (i.e. high renin states) renal artery
stenosis, rennin secreting tumors
o Pseudohyperaldosteronism: licorice ingestion, Cushing’s
syndrome, Liddle’s syndrome.
Management:
• Optimal therapy is dependent upon the severity of the potassium
deficit.
Evaluating the Potassium Deficit:
• The total potassium deficit in patients with hypokalemia due to
potassium loss can only be approximated, since there is no strict
correlation between the plasma potassium concentration and total body
potassium stores.
• In general, the loss of 200 to 400 meq of potassium is required to lower
the plasma potassium concentration by 1.0 meq/L. Continued potassium
losses below a serum level of 2 meq/L will not produce much more
hypokalemia due to release of potassium from the cell stores.
Potassium Replacement:
• An intravenous or oral potassium chloride preparation is generally
preferred in the treatment of hypokalemia.
• Oral replacement is safer because it is associated with less risk of
hyperkalemia. A dose of 40 meq every 4-6 hours may be employed
with frequent checking of serum K+.
• Use I.V. Potassium chloride should be reserved for patients:
o who are unable to eat
o who have severe or symptomatic hypokalemia
o whose GI tract absorption is impaired.
• In general, potassium can be safely given through a peripheral line in
a concentration that should not exceed 40 meq/L at rates of up to 10
meq/hr. A saline rather than a dextrose solution is preferred for therapy
as dextrose may promote potassium entry into cells through stimulation
of endogenous insulin release.
• If more rapid replacement is necessary, then 40 meq/hr can be
administered through a central venous catheter, but simultaneous ECG
monitoring should be used.
 Medical Emergencies Guidebook

• The underlying cause should be treated whenever possible, for example

patients with diuretic-induced hypokalemia may be re-evaluated for
their need of diuretics or a potassium-sparing diuretic might be added.
• Hypomagnesemia may lead to refractory hypokalemia. Patients with
unexplained hypokalemia or with diuretic-induced hypokalemia should
have their magnesium checked and repleted as necessary.
Drugs used in this section:
Main
Drug Recommended Dose
Indication
Potassium Hypokalemia Potassium >2.5 mEq/L:
cholride • Oral: 60-80 mEq/day plus additional amounts
oral/I.V. if needed
• I.V.: 10 mEq over 1 hour with additional
doses if needed. Maximum infusion rate:
10 mEq/hour; maximum concentration: 40
mEq/L; maximum 24-hour dose: 200 mEq
Potassium <2.5 mEq/L:
• Oral: Up to 40-60 mEq initial dose, followed
by further doses based on lab values
• I.V.: Up to 40 mEq over 1 hour, with doses
based on frequent lab monitoring; deficits at
a plasma level of 2 mEq/L may be as high
as 400-800 mEq of potassium. Maximum
infusion rate: 40 mEq/hour; maximum
concentration: 80 mEq/L (via central line);
maximum 24-hour dose: 400 mEq
 Hyperkalemia
Definition:
Hyperkalemia is defined as serum potassium (K+) of more than 5.5 meq/l in
the absence of hemolysis in the blood sample taken.
Etiology:
The major causes of hyperkalemia are:
1. Decreased excretion e.g. with renal insufficiency,
2. Trans-cellular shifts as in metabolic acidosis,
3. Hemolysis and rhabdomyolysis
4. As an adverse effect of drugs (e.g. ACE-inhibitors, NSAIDs,
spiranolactone and cyclosporine.
Presentation:
• An elevated potassium (K+) concentration interferes with normal
neuromuscular function to produce muscle weakness and, rarely, flaccid
paralysis. Abdominal distension and diarrhea may occur.
• ECG is not a sensitive method for detection of hyperkalemia. However
the first observed change is peaking of the T waves (see figure) followed
by flattening of P wave, prolongation of PR then QRS intervals leading
eventually to sine wave pattern.
V3 V4

Hyperkalemia A tall peaked and symmetrical T wave is the first change seen on the ECG in a
patient with hyperkalemia

Workup:
• Rule out trans-cellular shifts: acidosis, β-blockers, insulin deficiency
(untreated insulin-dependent diabetes), digoxin intoxication, massive
cellular necrosis, hyperkalemic periodic paralysis.
• Determine whether severely decreased GFR or normal GFR.
• If normal GFR determine why there is decreased effective aldosterone
function.
 Medical Emergencies Guidebook

Decreased GFR:
• Any cause of oligo- or anuric renal failure or any cause of end stage
renal disease
Normal GFR (i.e. hypoaldosteronism)
• Hyporeninemic (i.e. type 4 renal tubular acidosis usually secondary to
diabetic nephropathy, ACE-inhibitors, NSAIDs)
• Primary adrenal: Addison’s disease, congenital adrenal hyperplasia,
heparin.
• Renal tubular disorders: K-sparing diuretics, cyclosporine, SLE,
multiple myeloma, amyloid.
Treatment:
• Treatment of hyperkalemia is divided into:
1. Emergency interventions aimed at stabilizing the membranes and
shift serum (K+) inside the cells.
2. Non-emergent, more definitive measures that decrease total body
(K+) content.
• The selection of the treatment approach depends on the clinical
manifestations, the serum (K+) level and the ECG changes:
1. Plasma potassium concentrations above 7.0 meq/L or greater,
severe muscle weakness, or marked electrocardiographic changes
are potentially life-threatening and require emergency treatment.
2. An asymptomatic patient with a plasma potassium concentration
of 6.5 meq/L or less whose ECG does not manifest signs of
hyperkalemia can be treated only with a cation exchange resin.
3. Patients with a value below 6 meq/L can often be treated with a
low potassium diet and diuretics. In addition any potentiating
drugs (such as nonsteroidal anti-inflammatory drugs or angiotensin
converting enzyme inhibitors) should be discontinued.
For a stepwise approach for treating hyperkalemia please refer to the attached
flowchart.
Hyperkalemia (Serum (K+) >5.5 Meq/L in The Absence
of Hemolysis in The Blood Sample Taken)
 Medical Emergencies Guidebook

The following tables illustrate the different drugs used for treating hyperkalemia
and their modes of actions:
Emergent Treatment of Hyperkalemia

Modality Mechanism Onset Duration Prescription (K+)

of Action Removed
From
Body
Calcium Antagonizes 0-5 1 hour Calcium Gluco- 0
cardiac minutes nate 10%, 5-30
conduction ml IV; or Cal-
abnormailty cium Chloride
5%, 5-30 ml IV

Bicarbonate Distributes 15-30 1-2 hours NaHCO3, 44- 0

(K+) into cells minutes 88 meq (1-2
ampules)IV
Insulin Distributes 15-60 4-6 hours Regular insulin, 0
(K+) into cells minutes 5-10 units, plus
dextrose 50%,
50 ml if plasma
glucose is < 250
mg/dl

Salbutamol Distributes 15-30 2-4 hours Nebulized sal- 0

(K+) into cells minutes butamol, 10-20
mg in 4 ml
normal saline,
inhaled over 10
minutes

Non-emergent Treatment of Hyperkalemia

Modality Mechanism Onset Prescription (K+) Removed
of Action From Body

Loop Diuretic Enhances Renal (K+) 0.5-2 hours Furosemide, Variable

excretion 40-160 mg IV
or orally
Sodium Ion exchange resin 1-3 hours Oral: 15-30 g 0.5-1 meq/g
Polystyrene binds (K+) in 20% sorbitol
sulfonate (50-100ml)
(Kayxalate) Rectal: 50 g
in 20%
sorbitol

Hemodialysis Extracorporeal (K+) 48 hours Blood flow ≥ 200-300 meq

removal 200-300 ml/
min. Dialysate
[K+] ≈ 0

Peritoneal Peritoneal (K+) 48 hours Fast exchanges 200-300 meq

Dialysis removal 3-4 L/h
 Medical Emergencies Guidebook

Hyponatremia
Definition:
Hyponatremia is defined by low serum sodium concentration (less than 130
meq/L) due to excess water relative to sodium.
It is almost always due to excessive ADH secretion. This may either be:
• Appropriate: as in hypovolemia or hypervolemia but with decreased
effective arterial volume.
• Inappropriate: seen in the syndrome of inappropriate ADH secretion
(SIADH).
Workup:
Determine serum osmolality (normal being 280-295 mosm/Kg H2O):
• Isotonic hyponatremia: a normal plasma osmolality is seen as a rare
laboratory artifact due to hyperlipidemia or hyperproteinemia.
• Hypertonic hyponatremia with a high osmolality is due to the presence
of another effective osmole (e.g. glucose or mannitol).
• Hypotonic hyponatremia: due to true excess of water relative to sodium.
This is the case in the majority of patients with hyponatremia.
Hypotonic Hyponatremia:
• Determine volume status (vital signs with orthostatic measurements,
skin turgor, mucous membranes, JVP, peripheral edema, urine output,
BUN, Cr. and uric acid). Determine whether hypovolemic, euvolemic
or hypervolemic.
• Obtain urine Na concentration.
• Refer to figure below for further diagnostic clues.
Treatment:
Hypovolemic hyponatremia:
Volume replacement with isotonic (0.9%) saline.
Hypervolemic hyponatremia:
Water restriction (1-1.5 L/d) and diuretics.
Euvolemic Hyponatremia:
Symptomatic:
Is usually seen with Na+ of <120 meq/L. If there are central nervous
symptoms, hyponatremia should be rapidly treated at any level of serum
sodium concentration.
Rate of correction:
• In chronic hyponatremia, brain cells secrete osmoles to minimize
intracellular swelling. Too rapid correction leads to raised serum
osmolality in the setting of low brain osmolality. This results in rapid
water egress leading to acute brain demylination (central pontine
myelinosis).
• However, acute symptomatic hyponatremia, especially associated with
seizures or other neurologic manifestations, and developing in less
than 48 hours should be treated promptly as the risk of brain edema far
exceeds that of osmotic demyelination.
• A reasonable approach is to increase the serum sodium concentration
by no more than 1-2 meq/L/h and not more than 25-30 meq/L in the
first two days; the rate should be reduced to 0.5-1 meq/L/h as soon as
neurologic symptoms improve.
• The initial goal is to achieve a serum sodium concentration of 125-130
meq/L, guarding against overcorrection.
Hypertonic Saline with Furosemide:
1. Calculate Na deficit that needs to be repleted to achieve Na+ of 120 meq/
L:
Na+ deficit = 0.6 x ideal body weight x (120 – measured Na) (x 0.85 in
females).
E.g. in a 70 kg man with a Na of 110 meq/L, must replete 0.6 x 70 x (120-
110) = 420 meq of Na+.
2. Calculate the number of liters of 3% saline (513 meq Na/L) needed to
replete Na deficit, e.g. to replete 420 meq of Na+ needs (420 meq Na)/
(513 meq Na/L) = 820 ml of 3% saline.
3. Calculate rate of infusion to achieve replacement at 1 meq/L/h e.g. to
have serum sodium go from 110 to 120 at a rate of 1 meq/L/h, infuse at
820 ml/10 hours = 82 ml/hr. Decrease the infusion rate to 0.5 me/L/h as
soon as neurologic symptoms improve.
These calculations are only approximation and careful follow-up of serum
Na and infusion adjustments are essential.
 Medical Emergencies Guidebook

Asymptomatic:
• In these cases the rate of correction need be no more than 0.5 meq/L/
h.
• Water restriction, normal saline with furosemide and demeclocycline
may be employed.
• Demeclocycline (300-600 mg twice per day) is useful in patients who
cannot adhere to water restriction or need additional therapy. It inhibits
the effect of ADH on the distal tubule. Onset of action may require one
week and concentration may be permanently impaired.

Drugs used in this section:

Drug Main Indication Recommended Dose
Demeclocycline SIADH 900-1200 mg/day or 13-15 mg/
kg/day divided every 6-8 hours
initially, then decrease to 600-900
mg/day

Hypertonic saline Hypotnic See text

3% hyponatremia
Hypernatremia
 Medical Emergencies Guidebook

Hypercalcemia
Definition:
• Hypercalcemia is defined as a serum calcium level above the normal
range of 8.5-10.5 mg/dl (2.1-2.6 mmol/L).
Clinical Presentation:
• Constipation and polyuria are syptoms of hypercalcemia irrespective of
cause (see notes below), they usually occur if the serum calcium is >12
mg/dl and tend to be more severe if hypercalcemia develops acutely.
• Stupor, coma and azotemia may develop in severe hypercalcemia.
Ventricular extrasystoles and idioventricualr rhythm may also develop
and can be accentuated with digitalis.
• The focus of the history and physical examination should be on the
duration of the process of hypercalcemia and evidence for a neoplasm.
Workup:
• Obtain blood samples for serum calcium, phosphorus and albumin.
When a significant elevation of serum calcium is seen, it must be
interpreted in relation to the serum albumin level. Serum phosphate
may or may not be low depending on the cause.
• The ECG shows a shortened QT interval.
• If feasible, measurements of 24 hr urinary calcium, PTH and PTH-
related protein help distinguish between malignancy-associated
hypercalcemia and hyperparathyroidism.
Best Practice Treatment Algorithm:
The most effective therapy depends mostly upon the cause of the
hypercalcemia:
• Until the primary cause can be brought under control, renal excretion of
calcium with resultant decrease in serum calcium is promoted.
• For mild cases (s. calcium concentrations 11-12 mg/dL):
o Encourage oral hydration and eating a high-salt diet.
o Glucocorticoids can be used for granulomatous causes of
hypercalcemia.
o Oral phosphate (1 to 3 g/day) can also be considered, as long as
serum phosphate concentrations do not exceed 4 mg/dL (1.3
mmol/L). Oral phosphate usually lowers the serum calcium
concentration by 0.5 to 1.0 mg/dL (0.1 to 0.3 mmol/L)
• Acute therapy of patients with more severe or symptomatic
hypercalcemia, (i.e. , s. calcium concentrations exceeding 12 mg/dL)
consists of a three-pronged approach:
1. Expand volume with isotonic saline at an initial rate of 200 to 300
ml/hr that is then adjusted to maintain the urine output at 100 to
150 ml/hr. Give Furosemide to patients who are, or who get fluid-
overloaded on this regimen. Frequent checking and repleting for
electrolytes is needed if diuretics are employed.
2. Administer salmon calcitonin (4 IU/kg), remeasure s. calcium in
several hours. If a hypocalcemic response is noted, then the patient
is calcitonin-sensitive and the calcitonin can be repeated every six
to 12 hours.
3. Administer a bisphosphonate: zoledronic acid (4 mg IV over
15 minutes) or pamidronate (60 to 90 mg over two hours). The
bisphosphonates will be effective by the second to fourth day,
thereby maintaining control of the hypercalcemia.
• Follow-up therapy is aimed at preventing recurrence of
hypercalcemia.
• Tumors may respond to chemotherapy or radiation therapy leading to
resolution of the hypercalcemia.
• Additional more aggressive measures are necessary in the rare patient
with severe, symptomatic hypercalcemia.
• Hemodialysis with little or no calcium in the dialysis fluid and
peritoneal dialysis (though it is slower) are both effective therapies for
Hypercalcemia.
• Dialysis may be indicated in patients with severe malignancy-
associated hypercalcemia and renal insufficiency or heart failure, in
whom hydration cannot be safely administered
 Medical Emergencies Guidebook

Notes:
Causes of Hypercalcemia:

Increased bone Increased intestinal Miscellaneous

resorption calcium absorption

• Primary and secondary • Increased calcium intake • Chronic lithium intake

hyperparathyroidism • Renal failure (often with • Thiazide diuretics
• Malignancy vitamin D supplimentation) • Pheochromocytoma
• Hyperthyroidism • Milk-alkali syndrome • Adrenal insuffeciency
• Other: Paget’s • Hypervitaminosis D • Rhabdomyolysis and
disease, estrogens • Enhanced intake of acute renal failure
and antiestrogens in vitamin D or metabolites • Familial hypocalciuric
metastatic breast cancer, • Chronic granulomatous hypercalcemia
hypervitamiosis A, diseases (e.g. sarcoidosis) • Immobilzation
retinoic acid • Malignant lymphoma
• Acromegaly
Emergency Treatment of Hypercalcemia (1)
 Medical Emergencies Guidebook

Emergency Treatment of Hypercalcemia (2)

Drugs used in treatment of hypercalcemia:

Main
Drug Recommended dose
indication
Calcitonin Severe or I.M., Sub-Q: Initial: 4 units/kg every
symptomatic 12 hours; may increase up to 8 units/
hypercalcemia kg every 12 hours to a maximum of
every 6 hours
Zoledronic acid Severe of 4 mg (maximum) given as a
symptomic single dose infused over no less
hypercalemia than 15 minutes; patients should
be adequately hydrated prior to
treatment (restoring urine output
to ~2 L/day). Monitor serum
calcium and wait at least 7 days
before considering retreatment.
Dosage adjustment may be needed
in patients with decreased renal
function following treatment.
Pamidronate Severe of 60-90 mg, as a single dose, given
symptomic as a slow infusion over 2-24 hours;
hypercalemia dose should be diluted in 1000 mL
0.45% NaCl, 0.9% NaCl, or D5W
 Medical Emergencies Guidebook

Neurologic
Emergencies*
Editor: Elwaleed Ali Mohamed Elhassan

* Acknowledgement: many thanks to: Dr. Eldirdiry Mohamed Elamin FRCP, FAAN, CCST, consultant
neurologist at the National Ribat University Hospital for his kind review and invaluable comments on
this chapter
 Medical Emergencies Guidebook

Stroke (Cerebrovascualr Accident)

Definition:
The following are the common features of a stroke:
• Characteristically, there will be sudden onset of neurological deficit
• The patient often has history of hypertension, diabetes mellitus, obesity,
valvular heart disease or atherosclerosis.
• In young adult patients rare causes may be related, these include vasculitis,
anti-phospholipid antibody syndrome, hyperhomocysteinemia and drug
abuse.
• Often there are distinctive neurological signs reflecting the region of
the brain involved.
Stroke can be broadly divided into ischemic (thromboembolic) or
hemorrhagic stroke. Approximately 80 percent of strokes are due to
ischemic cerebral infarction and 20 percent to brain hemorrhage.
The following is the differential diagnosis for acute stroke:
o Complicated migraine
o Head trauma
o Todd’s paralysis (a deficit occurring after a seizure episode)
o Septicemia
o Toxic metabolic disturbances (hypoglycemia, acute renal or hepatic
insufficiency, drug intoxication)
o Conversion reaction
Key Management Steps*
• Ensure a patent airway and adequate respiration. Intubation may be
necessary to restore adequate ventilation and to protect the airway
from aspiration, especially in the presence of vomiting, which occurs
commonly with increased intracranial pressure (ICP). Check the oxygen
saturation and administer supplemental oxygen if patient is hypoxic.
• Blood pressure management (see below)
• Most patients are treated initially with intravenous fluids. Premature
insertion of a feeding tube may be hazardous and should be avoided in
patients with altered consciousness who may not be able to cooperate
adequately with swallowing or indicate inadvertent misplacement of the
* Guidelines for the Early Management of Adults with Ischemic Stroke: A Guideline From the American
Heart Association/American Stroke Association Stroke Council, endorsed by the American Academy of
Neurology. H. P. Adams Jr et al. Circulation, May 22, 2007; 115(20): e478 - e534
 tube into the trachea. It is also associated with higher risk of aspiration
pneumonia.
• Subsequently, if the patient remains unable to be fed orally, a feeding
tube may be carefully inserted. Ascertaining proper gastric placement
is recommeded clinically and radiologically.
• Bowel management to avoid constipation and fecal impaction or
diarrhea also is a component of supplementary care.
• Some patients, with major impairments, are at high risk for urinary
incontinence. To ease care and to avoid skin complications, some
patients will need an indwelling bladder catheter. Whenever possible,
prolonged use of an indwelling catheter should be avoided because
of the attendant increased risk of urinary infections. Intermittent
catheterization may be needed.
• Pneumonia, which is most likely to occur in seriously affected,
immobile patients and those who are unable to cough, is an important
cause of death after stroke. The appearance of fever after stroke should
prompt a search for pneumonia, and appropriate antibiotics should
be administered. Protection of the airway and suctioning, measures
to treat nausea and vomiting may help to lower the risk of aspiration.
Exercise and encouragement to take deep breaths may help to lessen
the development of atelectasis.
• The risk of deep vein thrombosis (DVT) is highest among immobilized
and older patients with severe stroke. It may lead to a life-threatening
pulmonary embolism. The options for lowering the risk of DVT include
early mobilization, anticoagulants, and the use of external compression
stockings and devices. Patients with hemorrhagic stroke may have low-
dose LMW or unfracionated heparin after documentation of cessation
of bleeding, and after 3 to 4 days from onset.
• After stabilization of the patient’s condition, rehabilitation, measures
to prevent long-term complications, patient and family education, and
family support may be started
• Specific stroke management approach is three-pronged:
1. Sorting out the cause
2. Practical management of the acute stroke patient
3. Secondary prevention
Sorting Out the Cause
• Get history from the patient or a relative regarding the onset and
 Medical Emergencies Guidebook

progression of the event. Subacute onset (occurring over minutes to a

few hours) is characteristic of thrombotic episode.
• The presence of headache at the onset and vomiting favor the diagnosis
of hemorrhagic compared with a thromboembolic stroke while an
abrupt onset of cerebral dysfunction without focal symptoms or signs
favor the diagnosis of subarachnoid hemorrhage (SAH).
• Ask whether the patient takes insulin or oral hypoglycemic agents, has
history of a seizure disorder or drug overdose or abuse. Enquire about
medications on admission, or recent trauma.
• Enquire about atherosclerotic risk factors or a relevant cardiac history.
• Look for signs of endocarditis, bleeding tendency, valvular cardiac
lesions or irregular rhythm.
• Examine the neck and retroorbital regions for vascular bruits. Examine
the fundus for papilledema or cholesterol emboli.
• Examine the head for trauma and tongue for lacerations that might
indicate seizures.
• Perform a screening neurological examination to define the extent of
the deficit.
Practical Management of the Acute Stroke
Immediate Laboratory Studies:
• Electrocardiogram.
• Oxygen saturation if hypoxia is suspected. Chest radiography is
indicated if lung or heart disease is suspected.
• Chest radiography, urinalysis and blood cultures are indicated if fever is
present.
• Blood samples for the following studies:
o Finger stick and serum glucose as hypoglycemia can present
with focal neurologic deficits. This is important if patient is
diabetic, taking insulin or oral hypoglycemic medications.
o Complete blood count including platelets and an ESR (an
elderly patient with high ESR may have cranial arteritis)
o Electrolytes, urea nitrogen, creatinine (hyponatremia may
present with focal neurologic deficits)
o Prothrombin time and partial thromboplastin time
o Blood for type and cross match in case fresh frozen is needed
to reverse a coagulopathy if intracranial hemorrhage (ICH) is
 present
o Consider evaluation for hypercoagulable state in young patients
without apparent stroke risk factors
Radiological Studies:
• The patient should be sent for imaging studies once hemodynamics
and respiratory status are stabilized (see below).
• Emergent non-contrast brain CT is important in excluding cerebral
hemorrhage. In the hyperacute stage a cerebral infarct will not show
on non-contrast CT while a hemorrhagic lesion will manifest with
evidence of a lesion sometimes with mid-line shift. If feasible, it
should be obtained as soon as the patient is medically stabilized.
• In selected patients, a carotid duplex study, MRI and MR angiography
may also be necessary. Diffusion-weighted MRI is more sensitive than
standard MRI in detecting ischemia.
Specific Treatments8
• Early treatment of a completed stroke (see note below for a brief
classification of stroke) consists of attention to general supportive
measures. This includes ensuring a patent airway and adequate
respiration, keeping the patient on nil by mouth until swallowing
competency is verified and caring for the sphincters and skin.
Blood pressure management:
Acute management of blood pressure (BP) may vary according to the type
of stroke. An effort should be made to determine the type of stroke based
on history and CT scan.
Acute Ischemic (Thromboembolic) Stroke:
• Lowering the BP in the acute phase should generally be avoided as there
is loss of the cerebral autoregulation. Lowering the BP may further
compromise ischemic areas.
• High blood pressure should only be acutely treated if:
o Extreme elevation (diastolic BP above 120 mmHg and/or
systolic BP above 220 mmHg)
o the patient has active ischemic coronary disease, heart failure,
or aortic dissection
• In the absence of those conditions, antihypertensive therapy may be
* Guidelines for the Early Management of Adults with Ischemic Stroke: A Guideline From the American
Heart Association/American Stroke Association Stroke Council, endorsed byt the American Academy
of Neurology. H. P. Adams Jr et al. Circulation, May 22, 2007; 115(20): e478 - e534
 Medical Emergencies Guidebook

withheld for at least 10 days after a thromboembolic stroke

• If pharmacologic therapy is given, intravenous labetalol is the drug of
choice.
Acute Hemorrhagic Stroke:
• Reducing the BP in patients with either intracranial (ICH) or
subarachnoid hemorrhage (SAH) may be beneficial by minimizing
further bleeding and continued vascular damage. However, it may
adversely affect the cerebral perfusion pressure needed to counteract
the raised intracranial pressure caused by the bleed.
• With ICH, intravenous treatment should be given if the systolic pressure
is above 170 mmHg. The goal is to maintain the systolic pressure
between 140 and 160 mmHg and to carefully monitor the patient for
signs of cerebral hypoperfusion induced by the fall in blood pressure.
• With SAH, in the absence of ICP measurement, antihypertensive
therapy is often withheld unless there is a severe elevation in blood
pressure. see notes below
Best Practice Drug Treatment:
• Intravenous labetalol is the first drug of choice because of easy titration
and limited effect on cerebral vessels.
• Dose: I.V. bolus: 20 mg or 1-2 mg/kg whichever is lower, I.V. over 2
minutes, may give 40-80 mg at 10-minute intervals, up to 300 mg total
dose
• I.V. infusion: Initial: 2 mg/minute; titrate to response up to 300 mg total
dose. Administration requires the use of an infusion pump.
Alternative Blood Pressure Medications:
• Please refer to “Hypertensive Crises” section.
• Sublingual nifedipine should be avoided as it may precipitously drop
BP and extend ischemia.
Other Treatments*
Thrombolytic Therapy for Acute Ischemic Stroke (in tertiary care centers):
• I.V. thrombolytic therapy with recombinant tissue plasminogen activator
(rt-PA) (0.9 mg/kg to a maximum of 90 mg, with 10% given as a bolus
over 1 minute and the remainder over 1 hour) is effective in reducing
* Guidelines for the Early Management of Adults with Ischemic Stroke: A Guideline From the American
Heart Association/American Stroke Association Stroke Council, endorsed byt the American Academy of
Neurology. H. P. Adams Jr et al. Circulation, May 22, 2007; 115(20): e478 - e534
 the neurological deficit in selected patients when given within 3 hours.
• Prerequisites include:
o Lack of CT evidence of ICH
o Absence of contraindications
Systemic Anticoagulation
• In general, early systemic anticoagulation is not recommended for
unselected patients with acute ischemic stroke as the risk of bleeding
outweighs the benefit of protecting from recurrence.
• Systemic anticoagulation may be warranted for treatment of acute cardio-
embolic (such as from an established intracardiac thrombus associated
with significant valvular disease, severe congestive heart failure, or
mechanical heart valves), stroke due to large artery atherosclerotic
stenosis with documented intraluminal thrombus, or dissection of a
cervical or intracranial large artery, and progressing stroke. However,
this is controversial as there is insufficient data to support acceptable
efficacy and lack of significant bleeding complications. In the selected
patients who receive heparin in the acute stroke setting, a bolus is not
administered.
• Anticoagulation may only be considered after a brain imaging study
has excluded hemorrhage and estimated the size of the infarct. Early
anticoagulation should be avoided when potential contraindications
to anticoagulation are present, such as a large infarction (based upon
clinical syndrome or brain imaging findings), uncontrolled hypertension,
or other bleeding conditions.
For embolic stroke due to atrial fibrillation (AF)*
o Heparin should not be used in patients with atrial fibrillations
presenting with acute ischemic stroke.
o Warfarin (goal INR 2.0 to 3.0) can be initiated as soon as the patient
is medically and neurologically stable.
o In patients with large infarcts and those with poorly controlled
hypertension the initiation of warfarin therapy should be delayed
for two weeks because of the potential risk of hemorrhagic
transformation.
o Aspirin: a dose of 325 mg/day may be administered until warfarin
is therapeutic.
 Medical Emergencies Guidebook

Secondary Ischemic Stroke Prevention*

Antithrombotic Therapy
• The oral administration of aspirin (initial dose is 325 mg) within 24
to 48 hours after stroke onset is recommended for treatment of most
patients.
• Subsequently, patients may be maintained on smaller doses (75-100
mg/day) as fewer gastrointestinal side effects and bleeding occur with
lower doses.
• Clopidogrel (75 mg/day) is an alternative for patients who cannot tolerate
aspirin. Aspirin and clopidogrel should not be used in combination for
stroke prevention, given the apparent lack of greater efficacy compared
with clopidogrel alone and the substantially increased risk of bleeding
complications
Blood Pressure Reduction
• Patients who are hypertensive at baseline should be treated to a goal
of <130/80 mmHg. The blood pressure should be lowered gradually
over several months to minimize side effects including hypotensive
symptoms due to failure of autoregulation of cerebral blood flow.
Antihypertensive treatment options should be individualized.
Glucose Control
• Diabetics need to get glucose control to near normoglycemic levels.
Diet, exercise, oral hypoglycemic drugs, and insulin are proven methods
to achieve glycemic control. The recommended goal for hemoglobin
A1C is 7 percent.
Cholesterol and Statin Therapy
• Statin therapy is recommended for patients with TIA, ischemic stroke
who have a baseline LDL >100 mg/dL to an LDL goal of <100 mg/
dL. More aggressive LDL lowering (<70 mg/dL) may be warranted for
those patients at very high cardiovascular risk (those who have at least
one of the following criteria: diabetes, continued smoking, multiple
components of the metabolic syndrome, especially high triglycerides
200 mg/dL (5.2 mmol/L) plus non-HDL-C 130 mg/dL (3.4 mmol/
L) with low HDL-C <40 mg/dL (1.0 mmol/L) and acute coronary
syndromes.
* Guidelines for Prevention of Stroke in Patients with Ischemic Stroke or Transient Ischemic Attack:
American Heart Association/American Stroke Association Council on Stroke/ American Academy of
Neurology. Sacco RL et al. Stroke. 2006 Feb;37(2):577-617
Lifestyle Modification
• Reduction of dietary saturated fat and cholesterol intake, cessation
of smoking and alcohol consumption, weight control (to maintain a
body mass index (BMI) between 18.5 and 24.9 kg/m2 and a waist
circumference for men and women of (< 102 cm and < 88 cm,
respectively), regular aerobic physical activity for those capable
(moderate intensity physical exercise most days of the week for at least
30 minutes), and a diet that is rich in fruits, vegetables, and low-fat
dairy products
Notes:
Definitions:
• A completed stroke is a neurological deficit referable to a vascular
territory which has reached its maximum beyond 24 hours.
• A stroke in evolution is a progressive neurological deficit that has not
reached its maximum yet.
• A transient ischemic attack (TIA) is a focal neurological deficit of acute
onset that resolves completely within 24 hours.
• Subarachnoid hemorrhage refers to bleeding into the subarachnoid
space. It is usually caused by rupture of an aneurysm or an arteriovenous
malformation
• The morbidity and mortality in SAH is related to two processes;
o Recurrent bleeding: early surgery (clipping or endovascular
therapy) is advocated for low grade SAH on Hunt and Hess
classification. This is best guided by a cerebral angiogram to
define the bleeding vessel.
o Vasospasm: this causes ischemia which is responsible for
neurological deficits in SAH. It is attenuated by the calcium
channel blocker nimodipine which has a preferential vasodilator
effect on the cerebral vessels. It is routinely used in SAH; the
dose is 60 mg every 4 hours for 21 days, start therapy within 96
hours after the bleed.
 Medical Emergencies Guidebook

Table of drugs used in this section:

Main
Drug Recommended dose
indication
Labetalol Acute lowering of I.V. bolus: 20 mg I.V. over 2 minutes, may
blood pressure in give 40-80 mg at 10-minute intervals, up to
acute stroke when 300 mg total dose.
indicated I.V. infusion: Initial: 2 mg/minute; titrate
to response up to 300 mg total dose.
Administration requires the use of an
infusion pump.
Alteplase Acute ischemic I.V.: Doses should be given within the
(recombinant stroke first 3 hours of the onset of symptoms;
tissue recommended total dose: 0.9 mg/kg
(maximum dose should not exceed 90 mg)
plasminogen infused over 60 minutes.
activator)
Load with 0.09 mg/kg (10% of the 0.9
mg/kg dose) as an I.V. bolus over 1 minute,
followed by 0.81 mg/kg (90% of the 0.9
mg/kg dose) as a continuous infusion over
60 minutes. Heparin should not be started
for 24 hours or more after starting alteplase
for stroke.
Warfarin Acute embolic Start 5-10 mg daily for 2 days. Adjust
stroke due dose according to INR results; usual
to atrial maintenance dose ranges from 2-10 mg
daily
fibrillations
Aspirin Acute ischemic 160-325 mg/day, initiated within 48
stroke hours (in patients who are not candidates
for thrombolytics and are not receiving
systemic anticoagulation.
Clopidogrel Acute ischemic 75 mg daily
stroke
Aspirin and Acute ischemic 25/200 twice daily
extended- stroke
release
dipyridamole
Nimodipine Subarachnoid 60 mg every 4 hours for 21 days, start
hemorrhage therapy within 96 hours after the bleed.
Approach to Suspected Stroke
 Medical Emergencies Guidebook

Status Epilepticus
Definition:
• Status epilepticus refers to the occurrence of a single unremitting
seizure or frequent clinical (or subclinical) seizures without an interim
return to normal consciousness.
• Any type of seizures can present in status epilepticus but the most
serious is tonic-clonic status.
• It is a life-threatening emergency which can be complicated by
rhabdomyolysis, lactic acidosis, aspiration pneumonitis, neurogenic
pulmonary edema, respiratory failure and neuronal death from ischemia
and hypoxia.
Predisposing factors:
• Withdrawal syndromes associated with the sudden discontinuation of
anticonvulsants, alcohol, barbiturates, or benzodiazepines.
• Acute inflammatory or structural insult (e.g., encephalitis, cerebral
malaria, stroke, head trauma, subarachnoid hemorrhage, cerebral
anoxia)
• Remote or longstanding structural injury (e.g., prior head injury,
cerebral palsy, previous neurosurgery, perinatal cerebral ischemia,
arteriovenous malformations)
• Metabolic abnormalities (e.g., hypoglycemia, hepatic encephalopathy,
uremia, pyridoxine deficiency, hyponatremia, hyperglycemia,
hypocalcemia, hypomagnesemia)
• Use of, or overdose with drugs that lower the seizure threshold
(e.g., theophylline, high dose penicillin G, quinolone antibiotics,
metronidazole, isoniazid and cyclosporine).
• Advanced neurodegenerative and neurometabolic inherited disorders.
Management Steps
Assessment and support:
• Promptly assess the patient with particular attention to respiratory and
circulatory status, offer supportive therapy (e.g., oxygen, mechanical
ventilation) as needed.
• Treat hyperthermia promptly with passive cooling. It occurs relatively
frequently during status epilepticus and in many cases is primarily a
manifestation of the seizures rather than evidence of infection.
• Perform a rapid neurologic examination to provide a preliminary
classification of the type of status epilepticus and its probable etiology.
• Insert IV catheters, give 50 ml of 50% glucose and start a saline drip.
• Obtain blood for electrolyte, serum glucose, blood film for malaria,
toxicology studies, CBC, and rapid finger-stick glucose.
• Frequent measurement of blood pressure (BP), and pulse oximetry
should be instituted. Cardiac monitoring is advisable.
Best Practice Initial pharmacologic therapy
Lorazepam or Diazepam:
Lorazepam: administer 4 mg I.V. dose slowly over 2-5 minutes; may repeat
in 10-15 minutes; usual maximum dose: 8 mg. The clinical advantage of
lorazepam is a longer duration of action because of its less pronounced
redistribution into adipose tissue.
Diazepam: 5-10 mg slowly over 2 minutes every 10-20 minutes, up to 30
mg in an 8-hour period.
If IV route is not immediately accessible a rectal diazepam gel formulation
may be used, the dose is 0.2 mg/kg.
Phenytoin:
• If seizures continue place a second intravenous catheter in order
to begin a concomitant phenytoin loading infusion. Phenytoin and
benzodiazepines are incompatible and will precipitate if infused through
the same line.
• Start phenytoin infusion of 20 mg/kg at 20-50 mg/min. Flush the vein
with normal saline after the infusion to prevent irritation.
• It is imperative to connect the patient to a cardiac monitor because
hypotension and serious arrhythmias may occur with infusion. Their
risk increase with higher infusion rates, reduce the rate if significant
adverse effects are seen.
• If a monitor is not available, keep checking the pulse and BP manually
frequently.
• Although approved for I.M. use, I.M. administration is not recommended
due to erratic absorption and pain on injection.
 Medical Emergencies Guidebook

Treatment of refractory seizures

• If seizures continue, infuse another 10 mg/kg of phenytoin, review
metabolic derangements from initial laboratory studies and treat
appropriately.
• Intubate and ventilate patient; admit to intensive care unit.
• Electroencephalographic (EEG) monitor, pulse oximetry and arterial
catheter for blood pressure monitoring are desirable.
• Further pharmacologic therapy at this point is based primarily upon the
patient's hemodynamic stability:

Hemodynamically stable patients:

Phenobarbital:
• 20 mg/kg by slow infusion with a pump or intermittent injections (90-
120) mg/dose every 5-10 minutes) to a maximum of 1 gm at a rate of
50 mg/minute
• If seizures continue, infuse another dose of 10 mg/kg of while paying
careful attention to the EEG and hemodynamic status.
• Additional doses of pentobarbital at rates up to 100 mg/min should be
infused until all seizures stop.
• Almost all patients at this point will require vasopressor support
(typically phenylephrine or dopamine) as well as crystalloid infusions.
If seizures not yet controlled proceed to the following options.
• If seizures are terminated with pentobarbital, then an infusion at 1 to 4
mg/kg per hour should be maintained for 24 hours and tapered over the
following 24 hours.

Hemodynamically unstable patients:

Midazolam:
• 0.2 mg/kg bolus, followed by a continuous infusion of 0.05 to 0.5 mg/
kg per hour. If this is unsuccessful within 45 to 60 minutes, a propofol
infusion should be started.
Propofol:
• Loading dose 1-2 mg/kg followed by 2 mg/kg/hr, titrate to 10 mg/kg/hr.
Adjust dose to achieve seizure-free status on EEG.
• After seizures have been controlled for 12 hours, infusion of the
anesthetic should be slowly reduced and discontinued to allow for
 neurologic assessment. The drug infusion should be resumed if epileptic
activity is observed.
• An EEG showing burst suppression pattern indicates adequate
anticonvusants.
Long-term seizure control:
• A long acting anticonvulsant may be added once the status is
controlled.
• Whenever feasible, dose adjustments are best determined by the clinical
response and serum drug levels.

Best practice options for generalized tonic-clonic seizures:

Phenytoin:
§ Begin maintenance dose 12 hours after loading dose.
§ Maintenance dose: 300 mg/day or 5-6 mg/kg/day in 3 divided doses
or 1-2 divided doses using extended release tablets.
§ If unable to swallow may give the same dose intravenously daily.
Valproate:
§ Initial: 10-15 mg/kg/day in 1-3 divided doses
§ Increase by 5-10 mg/kg/day at weekly intervals until therapeutic
levels are achieved; maintenance: 30-60 mg/kg/day.
§ Adult usual dose: 1000-2500 mg/day.
Carbamazepine:
§ 200 mg twice daily to start
§ Increase by 200 mg/day at weekly intervals until therapeutic levels
achieved
§ Usual dose: 800-1200 mg/day in 3-4 divided doses; some patients
have required up to 1.6-2.4 g/day
Alternatively:
Phenobarbital:
§ Oral, I.V.: 1-3 mg/kg/day in divided doses or 50-100 mg 2-3 times/
day
 Medical Emergencies Guidebook

Initial Management of Status Epilepticus

 Antiepileptic Drug Therapy for Status Epilepticus*
The horizontal bars indicate the approximate duration of drug infusions.

* After N Engl J Med 1998; 338:970-976

 Medical Emergencies Guidebook

Table of drugs used in this section:

Drug Main Indication Recommended Dose
Lorazepam Status epilepticus I.V.: 4 mg/dose given slowly over 2-5
minutes; may repeat in 10-15 minutes;
usual maximum dose: 8 mg
Diazepam Status epilepticus I.V.: 5-10 mg every 10-20 minutes,
up to 30 mg in an 8-hour period; may
repeat in 2-4 hours if necessary

Phenytoin Status epilepticus I.V.: Loading dose: 20 mg/kg;

maintenance dose: 300 mg/day or 5-6
mg/kg/day in 3 divided doses or 1-2
divided doses using extended release
Phenobarbital Status epilepticus Loading dose: I.V.: 300-800 mg
initially followed by 120-240 mg/dose
at 20-minute intervals until seizures are
controlled or a total dose of 1-2 g
Midazolam Status epilepticus I.V. bolus: 0.2 mg/kg followed by
continuous infusion at rates of 0.75 to
10 µg/kg per minute
Propofol Status epilepticus I.V.: 2 mg/kg over 10 minutes. If the
seizures stop prior to the infusion of
the entire bolus, the bolus should be
discontinued and a continuous infusion
begun at 4 to 12 mg/kg per hour. This
infusion should be titrated over the
next 20 to 60 minutes to maintain a
seizure-free state and burst suppression
on the EEG.
Keep pressors at bedside and
continuously monitor BP and EEG.
 Medical Emergencies Guidebook

Psychiatric
Emergencies
Edited by: A.E. Abdelghani
 Medical Emergencies Guidebook

Psychiatric Emergencies
Problem-Based Approach

1. The violent aggressive patient

2. The suicidal patient
3. The unresponsive patient
4. Neuroleptic Malignant Syndrome
5. Other Neuroleptic Induced Problems
6. Medications Chart

Management of Aggressive Violent Patients

Introduction
The threat of violence is an increasing concern in all branches of clinical
medicine however the out-patient clinics and emergency units in addition
to psychiatric units and hospitals are areas of high risk for violence (10% of
patients in general psychiatric units have a history of violence). The hostile
patient may be actively violent, threatening violence, or have been violent.
The aim is to gain control of the situation quickly by an accurate assessment
to ensure safety. The patient should be offered or given the best available
treatment.
Definitions
• Violence is an act leading to physical injury or destruction to property.
• Aggression is any hostile or destructive behaviour or action directed
towards others, objects or self. It can be verbal, physical or sexual.
Presentation
• Acutely disturbed patient (excitement – agitation).
• Patient carrying weapons.
• Verbally aggressive and threatening patient.
• Physically aggressive patient.
• Escorted by police.
• Disinhibited patient.
Differential diagnosis
When dealing with hostile or violent patient, the most important task is to
differentiate between organic (physical) mental disturbances and functional
psychiatric disorders.
A-Psychiatric / functional disorders
* Schizophrenia (especially paranoid type).
* Mania (excited states).
* Delusional disorders.
* Personality disorders: antisocial/ borderline / intermittent
explosive.
* Depression (agitated).
* Post-traumatic stress disorder.
* A cute reaction to stress.
* Learning disabilities (mental retardation).
B-physical / organic causes
Violence may occur during delirious states or organic psychosis due to
various physical causes:
1 - systemic disorders
* Systemic infection.
* Hypoglycemia.
* Hepatic / renal impairment.
* Endocrine.
* Electrolyte imbalance.
* Intoxication (heavy metals, poisons etc).
2 - Primary diseases of the brain
* Infection.
* Trauma.
* Epilepsy.
* Cerebro-vascular.
* Tumors.
* Dementia.
* Degenerative.
3 - Drug intoxication / withdrawal
* Alcohol.
* Benzodiazepines.
* Amphetamines.
 Medical Emergencies Guidebook

* Opioiods.
* Volatile substances (glue, benzene).
Assessment / work-up
* Take as many details as you can to make a quick assessment.
* Skilled multidisciplinay intervention can prevent or minimise violence.
* For a rapid screening the presence of any of the following is an indicator
for:
Delirium
* Sudden onset.
* Cognitive impairment (impaired consciousness, disorientation).
* Hallucinations (visual / auditory).
* Known medical illness (DM, Hypertension).
Drug intoxication / withdrawal
* Physical signs of intoxication (smell of alcohol, glue, benzene, needle
marks etc)
* Impairment of consciousness.
* Tremor, ataxic gait, pupillary changes, nystagmus, slurred speech.
* History of alcohol or drug abuse.
Schizophrenia / mania
* No impairment of consciousness.
* Intact orientation.
* Hallucinations.
* Delusions (paranoid/grandiosity).
* Thought disorder (disorganised, flight of ideas, etc).
* Mood disturbance (mania).
* Known psychiatric patient.
Personality disorders
* No impairment (of consciousness or orientation).
* No hallucinations or delusions.
* History of antisocial behaviour (aggression, stealing, frequent fights,
drug abuse).
* History of impulsive behaviour.
Investigations
If possible:
* Quick physical examination
* Mental state examination
* Lab investigations to rule out life threatening medical illness: complete
hemogram, glucose, urinalysis, urea, electrolytes, LFT.
* Other investigations: TFT, drugs and alcohol screening, ECG, CXR,
EEG, lumbar puncture, CT, MRI.
Management
When dealing with a violent patient, there are important points to
consider:
* Safety of staff including yourself.
* Safety of the patient.
* Safety of the environment.
* Ethical, legal, and, cultural issues.
The best setup for the interview office:
* It should be properly equipped with solid furniture that is difficult to
move, light chair as a shield, and alarms.
* It should be spacious, neither the patient nor the doctor should feel
trapped. It should preferably have two exits, but if one exit is available
then the doctor should be near the door and staff should be available for
intervention.
 Medical Emergencies Guidebook

Immediate Management of Aggressive Violent Patients

Non Pharmacolgical Management
 Immediate Management of Aggressive Violent Patients
Non Pharmacolgical Management

Important notes:
1-Verbal diffusion (talking the patient down)
* Maintain adequate distance at least two meters away from patient, avoid
corners.
* Identify yourself, be calm, confident and attentive, speak softly in non
provocative way, avoid intense eye contact, be neutral and concrete, and
address the patient with respect using his name.
* Hands should be kept in the midline avoid folded arms or having kept
hands in hips or pockets to avoid threatening gesture .Don’t turn away
from the patient , turn sideways, move backward if required.
* Engage in conversation, explain your intention, and acknowledge the
patient’s concerns and feelings.
* Listen to the patient, ask what is troubling him, help him talking about
problems, reassure avoid expressing contrary views at this stage avoid
giving promises.
 Medical Emergencies Guidebook

* Offer cold drinks if possible (avoid hot drinks).

* If the patient is armed, ask for weapon to be put down (not handed) and
call for the police.
2-Physical control and restraint
* Avoid force if possible and use minimum force and restraint necessary
to prevent the harm and release once the threat is over.
* Physical restraint should be used as a last resort.
* Secure adequate numbers of experienced staff trained in control and
restrain techniques, which approach the patient from behind, there
should be one person for each limb and one for the head the doctor
administer the medications to immobilise the patient swiftly.
* Don’t slap, kick or punch, ensure cultural and gender sensitivity in
addition to privacy and dignity of the patient.
3-Seclusion
* This is a supervised confinement of a patient alone in a room which is
locked for the protection of others, from significant harm.
* Should be used as little as possible for the shortest possible time.
* Should not be used as punishment of the patient or convenience of the
staff.
* Contra-indicated in delirious unstable or unknown medical status of the
patient.
4-Rapid tranquilization
Refers to the process of calming or sedating the patient in order to create a
safer environment both for the patient and for others.
* Offer oral medications initially.
* Don’t give i/m diazepam use i/v route.
* Most patients respond in 20-40 mins.
* Reassess every 30 mins.
* In elderly or physically ill patients, give half doses.
* Monitor vital signs, check for possible respiratory depression, and
dystonic reactions or any other side effects of meds.
* Zuclopenthixol acqua phase has duration of action 2-3 days, should not
be repeated until after 48-72 hrs. Never give to psychotropic- naïve
patient.
 The Suicidal Patient
Definitions
Suicidality
Refers to deliberate and potentially fatal acts of self harm.
Suicidal attempts and deliberate self harm (DSH)
A deliberate nonfatal acts whether physical, drug overdose, or poisoning
done in the knowledge that it was potentially harmful.
Any patients presents with suicidal attempt (DSH) or intention should be
considered as psychiatric emergency.
Presentation
• Patient with self inflicted physical injuries e.g., cutting hands or throat,
hanging marks, drug overdose…etc.
• Patient with depressed mood, psychomotor retardation, agitation,
irritability, worthlessness, hopelessness, guilt feelings, death wishes or
communicating clear suicidal intention
• Psychotic patient with nihilistic delusions, delusions of guilt or
distressing auditory hallucinations.
• Impulsive, emotionally unstable personality.
Differential Diagnosis
Suicidal attempts, intention or thoughts are usually part of depressive
disorder but can arise in any other psychiatric disorders. The most
common causes:
• Depressive disorders
• Alcohol and drug abuse
• Psychotic disorders.
• Personality disorders.
• Chronic physical illness (pain, loss of limbs, terminal illness).
Management
The assessment and management of suicidal risk is one of the most
fundamental tasks in emergency psychiatry. When suspecting a suicidal
risk immediate management involves the following (see chart):
 Medical Emergencies Guidebook

Management of Suicidal Patient

 The Unresponsive Patient (Stupor)
Definition
Psychological stupor is defined as mutism, immobility and no response to
external stimuli, without impairment of consciousness.
Stuporose patients usually display negativistic behavior, refusing fluids and
food intake which endangers patient’s life and is considered as psychiatric
emergency.
Presentation
It is important to differentiate psychological stupor (no impairment of
consciousness) from neurological stupor (medical emergency) which is
characterized by impairment of consciousness. The stuporose patient due
to psychiatric disorder appears alert because of eye movements as if awake
but does not respond to stimuli. All vital signs are stable and there is no
evidence of focal neurological signs.
Differential diagnosis
Psychiatric
• Catatonia
• Depression
• Dissociative
• Manic
Organic
• Delirium
• Head injury
• Epilepsy
• Electrolyte and endocrine imbalance
• Space-occupying CNS lesions
• Drug induced
Management: see chart
 Medical Emergencies Guidebook

Management of The Unresponsive Patient

(Stuporous)
 Neuroleptic Malignant Syndrome (NMS)
Definition
This is a rare but potentially serious, even fatal neuroleptic-induced
movement disorder which represents a psychiatric emergency of mortality
rate as high as 20% that can be reduced to less than 5% with early recognition
and intervention.
Presentation
Onset is acute, usually 2-28 days after taking neuroleptic drugs. The
following are the essential features:
• Hyperpyrexia
• Muscle rigidity, tremors, dysphagia
• Akinesia and mutism
• Clouded consciousness, confusion, coma
• Autonomic changes: tachycardia, increased respiration, elevated or
labile BP, sweating, pallor, and incontinence
Laboratory abnormalities
• Neutrophilia, raised CPK, raised K
• Altered liver enzymes
• Excess slow waves on EEG
• LP and MRI scan are negative
Differential diagnosis
• Infection
• Malignant hyperpyrexia
• Extra pyramidal disorder
• Lethal catatonia
Management: see chart
 Medical Emergencies Guidebook

Management of The Neuroleptic

Malignant Syndrome (NMS)
 Other Neuroleptic-Induced Problems
Extrapyramidal side effects of neuroleptic drugs are common, although
they are not life-threatening, but are usually presenting to the emergency
department because of their distressing nature to both the patient and his
family.
Acute dystonias
Can present as emergency because it can be painful and very frightening.
1. Occulogyric crisis: Muscle spasm causing eye rolling upwards.
2. Torticollis: Muscle spasm causing head and neck twisted to the side,
the patient may be unable to swallow or speak clearly. In extreme cases
the back may arch (opisthotonous) or jaw dislocates.
Management
Anticholinergic drugs given orally, i/m, or i/v depending on the severity.
1. Benzhexol 5-10mg.
2. Procyclidine 5-10mg.
Akathisia (restlessness)
This is a subjective unpleasant state of inner restlessness when there is a
strong desire or compulsion to move e.g. constantly pacing up and down,
rocking, and foot stamping when seated. Akthisia can be mistaken for
psychotic agitation and has been linked with suicide and aggression.
Management
1. Reduce the antipsychotic dose.
2. Change to an atypical.
3. Propranolol 20-40mg/day.
4. Anticholinergics are generally unhelpful.
 Medical Emergencies Guidebook

Drugs used in psychiatric emergencies

Recommended
Medication Main Psych Indication
Doses
Haloperidol Psychosis,excitement,aggression, 5-30mg/day
Agitation.
Chlorpromazine Psychosis,excitement,aggression, 200-1000mg/day
Agitation.

Zuclopenthixol Psychosis,excitement,aggression, 50-150mg/day

Agitation.
Diazepam Hypnotic, sedative, anxiolytic. 5-60mg/day

Lorazepam Hypnotic, sedative, anxiolytic. 2-6mg/day

Benzhexol Drug-Induced extrapyramidal symptoms 5-15mg/day

Procyclidine Drug-induced extrapyramidal symptoms 7.5-30mg/day
Dantrolene Muscle spasticity, malignant 25-400mg/day
hyperthermia
Bromocriptine Neuroleptic malignant syndrome 10-60mg/day
Appendix : 1
 Medical Emergencies Guidebook

Appendix : 2
Table of Drugs Used in This Guidebook

Main Recommended
Drug indication dose
Acyclovir HSV encephalitis I.V.: 10 mg/kg/dose every 8 hours for
10-15 days

Alteplase Acute Coronary 15 mg IV bolus, then 0.75 mg/kg over

Syndrome 30 min(max 50 mg) then 0.5 mg/kg
over 60 min (not to exceed 35 mg) (see
section on Acute Coronary Syndrome)

Aminophylline Acute asthma I.V Loading dose (in patients not

currently receiving aminophylline or
theophylline): 6 mg/kg over 20-30
minutes; administration rate should not
exceed 25 mg/minute
Approximate I.V. maintenance dosages:
Based upon continuous infusions:
smoker: 0.8 mg/kg/hour, nonsmoker: 0.5
mg/kg/hour, older patients and patients
with cor pulmonale: 0.3 mg/kg/hour,
patients with congestive heart failure:
0.1-0.2 mg/kg/hour. Dosage should
be adjusted according to serum level
measurement (if available)

Amlodipine Hypertensive 5 mg orally

urgency

Amoxicillin Susceptible 500-1000 mg every 8 hours

respiratory and
urinary tract
infections and
enteric fever

Amoxicillin-cla- Susceptible 1 gram every 8 hours

vulanate respiratory tract
infections
Aspirin Acute ischemic 160-325 mg/day, initiated within 48
stroke hours (in patients who are not candidates
for thrombolytics and are not receiving
systemic anticoagulation.

Aspirin Acute coronary ACS: Initial dose 300 mg (nonenteric

syndrome (ACS), formulation) followed by 100 mg/day.
acute ischemic AIS: 60-325 mg/day, initiated within 48
stroke (AIS) hours (in patients who are not candidates
for thrombolytics and are not receiving
systemic anticoagulation.

Aspirin and ex- Acute ischemic 25/200 twice daily

tended-release stroke
dipyridamole

Benzhexol Drug-Induced 5-15mg/day

extrapyramidal
symptoms.

Benzylpenicillin Susceptible I.M., I.V.: 2-24 million units/day in

respiratory divided doses every 4 hours depending
infections and on sensitivity of the organism and
meningitis severity of the infection

Bromocriptine Neuroleptic 10-60mg/day

malignant
syndrome.

Calcitonin Severe or I.M., Sub-Q: Initial: 4 units/kg every

symptomatic 12 hours; may increase up to 8 units/kg
hypercalcemia every 12 hours to a maximum of every
6 hours

Calcium Chloride Emergency 5-30 ml IV

5%, treatment of
hyperkalemia

Calcium Gluco- Emergency 5-30 ml IV

nate 10% treatment of
hyperkalemia
 Medical Emergencies Guidebook

Ceftriaxone Urinary tract 1 gram IV daily

infection

Meningitis 2 g every 12 hours for 7-14 days (longer

courses may be necessary for selected
organisms

Pneumonia, I.V.: 2 g once daily; >65 years of age: 1

community- g once daily
acquired

Cefuroxime Susceptible I.M., I.V.: 0.75-1.5 g every 8 hours (up

respiratory to 1.5 g every 6 hours in life-threatening
infections infections)

Chlorpromazine Psychosis, 200-1000mg/day

excitement,
aggression,
Agitation.

Ciprofloxacin Urinary tract Mild/moderate: oral 250 mg every

infection and 12 hours for 7-14 days, I.V.: 200 mg
enteric fever every 12 hours for 7-14 days. Severe/
complicated: oral 500 mg every 12 hours
for 7-14 days, I.V.: 400 mg every 12
hours for 7-14 days

Clarythromycin Susceptible Oral: 250-500 mg every 12 hours for

respiratory tract 7-14 days
infections

Clopidogrel Acute coronary 75 mg/d; for acute coronary syndrome, a

(Plavix) syndrome, acute loading dose of 4-8 tablets (300-600mg)
ischemic stroke can be used for rapid action.
(Use if ASA is
contraindicated)

Dantrolene Muscle spasticity, 25-400mg/day

malignant
hyperthermia.
Demeclocycline Syndrome of 900-1200 mg/day or 13-15 mg/kg/day
inappropriate divided every 6-8 hours initially, then
ADH secretion decrease to 600-900 mg/day

Desmopressin Central diabetes I.V., Subcutaneous: 2-4 mcg/day (0.5-1

insipidus mL) in 2 divided doses or 1/10 of the
maintenance intranasal dose
Intranasal (100 mcg/mL nasal solution):
10-40 mcg/day (0.1-0.4 mL) divided 1-3
times/day; adjust morning and evening
doses separately for an adequate diurnal
rhythm of water turnover
Oral: Initial: 0.05 mg twice daily;
total daily dose should be increased or
decreased as needed to obtain adequate
antidiuresis (range: 0.1-1.2 mg divided
2-3 times/day)

Diazepam Status epilepticus I.V.: 5-10 mg every 10-20 minutes, up to

30 mg in an 8-hour period; may repeat in
2-4 hours if necessary

Diazepam Hypnotic, 5-60mg/day

sedative,
anxiolytic.
 Medical Emergencies Guidebook

Dopamine Hemodynamic I.V. infusion: 1-5 mcg/kg/minute up

support in shock to 50 mcg/kg/minute, titrate to desired
response; infusion may be increased by
1-4 mcg/kg/minute at 10- to 30-minute
intervals until optimal response is
obtained
Note: If dosages >20-30 mcg/kg/minute
are needed, a more direct-acting
vasopressor may be more beneficial (i.e.,
epinephrine, norepinephrine).
Hemodynamic effects of dopamine are
dose dependent:
• Low-dose: 1-5 mcg/kg/minute,
increased renal blood flow and urine
output
• Intermediate-dose: 5-15 mcg/kg/
minute, increased renal blood flow,
heart rate, cardiac contractility, and
cardiac output
• High-dose: >15 mcg/kg/minute,
alpha-adrenergic effects begin to
predominate, vasoconstriction,
increased blood pressure

Enalaprilat Hypertensive 1.25 mg every six hours which might be

emergency increased to 5 mg every six hours

Enoxaparin Acute coronary 10 U (1 mg)/kg SC twice daily. An

syndrome initial bolus 30 mg IV can be given.

Erythromycin Susceptible Oral: base: 250-500 mg every 6-12

respiratory tract hours
infections

Erythromycin Susceptible Oral: base: 250-500 mg every 6-12

respiratory tract hours
infections

Felodipine Hypertensive 5 mg orally

urgency
Furosemide Augmenting I.V.: 100-200 mg/dose, may be repeated
diuresis in acute or doubled in 1-2 hours as needed up to
renal failure 1000 mg/day. I.V. injections should be
given slowly. In adults, undiluted direct
I.V. injections may be administered at a
rate of 40 mg over 1-2 minutes
Continuous I.V. infusion: Initial I.V.
bolus dose of 0.1 mg/kg followed by
continuous I.V. infusion doses of 0.1
mg/kg/hour doubled every 2 hours to
a maximum of 0.4 mg/kg/hour if urine
output is <1 mL/kg/hour have been
found to be effective and result in a
lower daily requirement of Furosemide
than with intermittent dosing.

Furosemide Hypertensive 20 mg orally if renal function is normal

urgency and higher if renal insufficiency is
present

Gentamicin Septic shock Susceptible systemic infections: I.M.,

I.V.: Severe life-threatening infections:
2-2.5 mg/kg/dose every 8 hours
Note: High-dose, once daily regimens:
Some clinicians suggest 4-7 mg/kg (as
a single daily dose) for all patients with
normal renal function. This dose is at
least as efficacious with similar, if not
less, toxicity than conventional dosing.

Glyceryl trini- Acute coronary Sublingual: 0.5 mg every 5 min as

trate syndrome needed x 3 doses.
IV: 10-200µg/min

Haloperidol Psychosis, 5-30mg/day

excitement,
aggression,
Agitation.
 Medical Emergencies Guidebook

Hydralazine Hypertensive Initial dose: 10-20 mg/dose every 2-4

emergency hours as needed. May increase to 40
mg/dose; change to oral therapy as soon
as possible

Hydrocortisone Acute asthma I.V. (succinate): 1-2 mg/kg/dose every 6

hours for 24 hours, then maintenance of
0.5-1 mg/kg every 6 hours

Hypertonic Hypotonic See section on “Hyperkalemia”

saline 3% hyponatremia

Insulin Emergency Regular insulin, 5-10 units, plus dextrose

treatment of 50%, 50 ml if plasma glucose is < 250
hyperkalemia mg/dl

Ipratropium Acute asthma Nebulization: 500 mcg (one unit-dose

bromide vial)
3-4 times/day with doses 6-8 hours apart
Metered dose inhaler: 2 inhalations 4
times/day, up to 12 inhalations/24 hours

Isosorbide Acute coronary Sublingual: 5mg as needed. Repeat

dinitrate syndrome every 5 min X 3 doses.
Oral: 10 -20 mg BD or TDS
IV: Mix with D5w. 1-10 mg/hr

Isosorbide mono- Prophylaxis of Regular tablet: 5-10 mg twice daily.

nitrate variceal bleeding Extended release tablet: Initial: 30-60
mg given in morning as a single dose;
titrate upward as needed, giving at least
3 days between increases; maximum
daily single dose: 240 mg

Labetalol Hypertensive Bolus: 20 mg initially, followed by 20 to

emergency 80 mg every 10 minutes to a total dose
of 300 mg. Infusion: 0.5 to 2 mg/min

Labetalol Hypertensive Orally: 200-400 mg, may be repeated

urgency every 2-3 hrs.
Labetalol Acute lowering of I.V. bolus: 20 mg I.V. over 2 minutes,
blood pressure in may give 40-80 mg at 10-minute
acute stroke when intervals, up to 300 mg total dose.
indicated I.V. infusion: Initial: 2 mg/minute; titrate
to response up to 300 mg total dose.
Administration requires the use of an
infusion pump.

Lactulose Hepatic Oral: 20-30 g (30-45 mL) every 1-2

encephalopathy hours to induce rapid laxation; adjust
dosage daily to produce 2-3 soft stools;
doses of 30-45 mL may be given hourly
to cause rapid laxation, then reduce to
recommended dose; usual daily dose:
60-100 g (90-150 mL) daily

Lorazepam Status epilepticus I.V.: 4 mg/dose given slowly over 2-5

minutes; may repeat in 10-15 minutes;
usual maximum dose: 8 mg

Lorazepam Hypnotic, 2-6mg/day

sedative,
anxiolytic.

Methylpredniso- Acute asthma I.V. (sodium succinate): Loading dose:

lone 2 mg/kg/dose, then 0.5-1 mg/kg/dose
every 6 hours for up to 5 days

Methylpredniso- Acute asthma I.V. (sodium succinate): Loading dose:

lone 2 mg/kg/dose, then 0.5-1 mg/kg/dose
every 6 hours for up to 5 days

Metolazone Augmenting Oral: 5-20 mg/dose every 24 hours.

diuresis in acute
renal failure

Metronidazole Amebiasis and Oral: 500-750 mg every 8 hours for

amebic liver 5-10 days
abscess

Midazolam Status epilepticus I.V. bolus: 0.2 mg/kg followed by

continuous infusion at rates of 0.75 to 10
µg/kg per minute
 Medical Emergencies Guidebook

Neomycin Hepatic Oral: 500-2000 mg every 6-8 hours or

encephalopathy 4-12 g/day divided every 4-6 hours for
5-6 days

Nicardipine Hypertensive Initial dose: 5 mg/h; maximum dose: 15

emergency mg/h IV infusion

Nimodipine Subarachnoid 60 mg every 4 hours for 21 days, start

hemorrhage therapy within 96 hours after the bleed.

Nitrofurantoin Urinary tract Oral: 50-100 mg/dose every 6 hours (not

infection to exceed 400 mg/24 hours)

Nitroglycerin Hypertensive 15 µg IV bolus, then 5-100 mcg/min (50

emergency mg in 250 mL D5W); maximum dose:
100 µg/min

Nitroprusside Hypertensive Initial dose: 0.25 to 0.5 µg/kg per min;

sodium emergency maximum dose: 8 to 10 µg/kg per min

Norepinephrine Hemodynamic Continuous I.V. infusion:

support in shock Adults: Initial: 0.5-1 mcg/minute and
titrate to desired response; 8-30 mcg/
minute is usual range;
ACLS dosing range: 0.5-30 mcg/minute
Rate of infusion: 4 mg in 500 mL D5W
• 2 mcg/minute = 15 mL/hour
• 4 mcg/minute = 30 mL/hour
• 6 mcg/minute = 45 mL/hour
• 8 mcg/minute = 60 mL/hour
• 10 mcg/minute = 75 mL/hour

Norfloxacin Urinary tract Oral: 400 mg twice daily for 3-21 days
infection depending on severity of infection or
organism sensitivity; maximum: 800
mg/day

Octreotide Upper GI I.V. bolus: 25-50 mcg followed by

hemorrhage continuous I.V. infusion of 25-50 mcg/
hour
Pamidronate Hypercalcemia 60-90 mg, as a single dose, given as
a slow infusion over 2-24 hours; dose
should be diluted in 1000 mL 0.45%
NaCl, 0.9% NaCl, or D5W

Paracetamol Pain or fever Oral, 1000 mg 3-4 times /day; rectal:

325-650 mg every 4-6 hours, do not
exceed 4 g/day.

Phenobarbital Status epilepticus Loading dose: I.V.: 300-800 mg initially

followed by 120-240 mg/dose at 20-
minute intervals until seizures are
controlled or a total dose of 1-2 g

Phenylephrine Hemodynamic I.M., S.C. : 2-5 mg/dose every 1-2 hours

support in shock as needed (initial dose should not exceed
5 mg)
I.V. bolus: 0.1-0.5 mg/dose every 10-15
minutes as needed (initial dose should
not exceed 0.5 mg)
I.V. infusion: 10 mg in 250 mL D5W or
NS (1:25,000 dilution) (40 mcg/mL);
start at 100-180 mcg/minute (2-5 mL/
minute; 50-90 drops/minute) initially;
when blood pressure is stabilized,
maintenance rate: 40-60 mcg/minute
(20-30 drops/minute); rates up to 360
mcg/minute have been reported; dosing
range: 0.4-9.1 mcg/kg/minute

Phenytoin Status epilepticus I.V.: Loading dose: 20 mg/kg;

maintenance dose: 300 mg/day or 5-6
mg/kg/day in 3 divided doses or 1-2
divided doses using extended release
 Medical Emergencies Guidebook

Potassium chol- Hypokalemia Potassium >2.5 mEq/L:

ride oral/I.V. Oral: 60-80 mEq/day plus additional
amounts if needed
I.V.: 10 mEq over 1 hour with additional
doses if needed. Maximum infusion rate:
10 mEq/hour; maximum concentration:
40 mEq/L; maximum 24-hour dose: 200
mEq
Potassium <2.5 mEq/L:
Oral: Up to 40-60 mEq initial dose,
followed by further doses based on lab
values
I.V.: Up to 40 mEq over 1 hour, with
doses based on frequent lab monitoring;
deficits at a plasma level of 2 mEq/L
may be as high as 400-800 mEq of
potassium. Maximum infusion rate: 40
mEq/hour; maximum concentration: 80
mEq/L (via central line); maximum 24-
hour dose: 400 mEq

Prednisolone Acute asthma Oral: 1-2 mg/kg/day in divided doses 1-

2 times/day for 3-5 days; most effective
if ingested at about 3 pm

Procyclidine Drug-induced 7.5-30mg/day

extrapyramidal
symptoms.

Propofol Status epilepticus I.V.: 2 mg/kg over 10 minutes. If the

seizures stop prior to the infusion of
the entire bolus, the bolus should be
discontinued and a continuous infusion
begun at 4 to 12 mg/kg per hour. This
infusion should be titrated over the next
20 to 60 minutes to maintain a seizure-
free state and burst suppression on the
EEG.
Keep pressors at bedside and
continuously monitor BP and EEG.
Propranolol Acute coronary 10-80(usually 20-40 mg) mg orally 2-3
syndrome times daily. For IV use give 0.5-1 mg IV
followed 2 hrs later with the oral dose.

Prophylaxis of 20mg every 12hrs, which is increased

variceal bleeding or decreased every 3-4 days until a 25%
reduction in the resting heart rate occurs
or the heart rate is down to 55 beats per
minute. Average dose is 40mg bid.

Reteplase Acute Coronary 10 units IV over 2 min then 30 min

Syndrome later another 10 units IV over 2
min (see section on Acute Coronary
Syndrome)
Rifampicin Meningococcal Oral: 600 mg every 12 hours for 2 days
meningitis <1 month: 10 mg/kg/day in divided
prophylaxis doses every 12 hours for 2 days
Infants and Children: 20 mg/kg/day in
divided doses every 12 hours for 2 days

Salbutamol Emergency Nebulized salbutamol, 10-20 mg in 4 ml

treatment of normal saline, inhaled over 10 minutes
hyperkalemia

Salbutamol (via Acute asthma Inhalation: 90 mcg/puff: 4-6 puffs every

a nebulizer OR 20 minutes for up to 4 hours, then every
a metered dose 1-4 hours as needed.
inhaler with a Nebulization: 2.5 mg diluted to a total
spacer) of 3 mL by continuous flow nebulization
every 20 minutes for three doses. May
also give via continuous nebulization,
administering approximately 10 mg over
one hour.

Sodium Emergency 44-88 meq (1-2 ampoules) IV

bicarbonate treatment of
hyperkalemia

Streptokinase Acute Coronary 1.5 million units IV over 30-60 min (see
Syndrome section on Acute Coronary Syndrome)
 Medical Emergencies Guidebook

Terlipressin Upper GI I.V.: Adults: 2 mg followed by 1 or

hemorrhage 2 mg every 4 hours until bleeding is
controlled, for up to 36 hours

Trimethoprim- Urinary tract Oral: 1 double strength tablet every 12

sulfamethoxazole infection, hours for 10-14 days
bacillary
dysentery
Unfractionated Acute coronary 60 U/kg IV bolus (max 5000 U)
Heparin syndrome followed by 15 U/kg/hr (max 1000/hr).
Adjust rate to aPTT 60-80s.

Vasopressin Upper GI Continuous I.V. infusion: 0.5 milliunits/

hemorrhage kg/hour (0.0005 unit/kg/hour); double
dosage as needed every 30 minutes to a
maximum of 10 milliunits/kg/hour
I.V.: Initial: 0.2-0.4 unit/minute, then
titrate dose as needed; if bleeding stops,
continue at same dose for 12 hours, taper
off over 24-48 hours.

Warfarin Acute embolic Start 5-10 mg daily for 2 days. Adjust

stroke due to dose according to INR results; usual
atrial fibrillations maintenance dose ranges from 2-10 mg
daily

Zoledronic acid Severe or 4 mg (maximum) given as a single

symptomatic dose infused over no less than 15
hypercalcemia minutes; patients should be adequately
hydrated prior to treatment (restoring
urine output to ~2 L/day). Monitor
serum calcium and wait at least 7 days
before considering retreatment. Dosage
adjustment may be needed in patients
with decreased renal function following
treatment.
Zuclopenthixol Psychosis, 50-150mg/day
excitement,
aggression,
Agitation.