CAMBRIDGE

Emergency
medicine
SHORT NOTES
Essential Guide for Doctors
& Medical Students

1ST EDITION
Title: Cambridge Emergency Medicine Short Notes :
Essential Guide for Doctors and Medical Students
Edition : First Edition
Author: Dr. Rish T
Publisher: Cambridge Medical Books

Copyright © 2025 Dr. Rish T

All rights reserved.

No part of this publication may be reproduced, distributed, or

transmitted in any form or by any means without the prior
written permission of the publisher.

Disclaimer
The information provided in this book is for academic purposes
only and should not be used as a substitute for professional
medical advice, diagnosis, or treatment.

Acknowledgments
I would like to express my deepest gratitude to my colleagues
and mentors who provided invaluable insights and support
throughout the writing process. Special thanks to Dr. Mash for
her thorough review and constructive feedback. I also extend
my heartfelt thanks to my family for their patience and
understanding.
 Chapters
1. Cardiovascular Emergencies 4. Endocrine and Metabolic
Emergencies
• Myocardial Infarction (Heart Attack)
• Diabetic Ketoacidosis (DKA)
• Cardiac Arrest
• Hyperosmolar Hyperglycemic State
• Acute Heart Failure
(HHS)
• Hypertensive Crisis
• Hypoglycemia
• Aortic Dissection
• Adrenal Crisis
• Pulmonary Embolism
• Thyroid Storm
• Arrhythmias
• Myxedema Coma
• Electrolyte Imbalances (e.g.,
2. Respiratory Emergencies Hyperkalemia, Hyponatremia)
• Acute Asthma Exacerbation
• Chronic Obstructive Pulmonary 5. Gastrointestinal Emergencies
Disease (COPD) Exacerbation
• Upper GI Bleeding
• Pneumothorax
• Lower GI Bleeding
• Hemothorax
• Acute Pancreatitis
• Acute Respiratory Distress Syndrome
• Perforated Peptic Ulcer
(ARDS)
• Bowel Obstruction
• Foreign Body Aspiration
• Acute Appendicitis
• Mesenteric Ischemia
3. Neurological Emergencies
• Stroke (Ischemic and Hemorrhagic)
6. Toxicological Emergencies
• Seizures and Status Epilepticus
• Poisoning (e.g., Organophosphates,
• Traumatic Brain Injury
Carbon Monoxide)
• Meningitis and Encephalitis
• Drug Overdose (e.g., Opioids,
• Guillain-Barré Syndrome Benzodiazepines, Acetaminophen)
• Spinal Cord Injury • Alcohol Intoxication and Withdrawal
• Snake and Insect Bites
7. Trauma Emergencies 11. Environmental Emergencies
• Blunt and Penetrating Trauma • Hypothermia and Frostbite
• Fractures and Dislocations • Heatstroke and Heat Exhaustion
• Burns (Thermal, Electrical, Chemical) • Drowning and Near Drowning
• Crush Injuries • High-Altitude Illnesses
• Amputation • Snake Bites and Scorpion Stings

8. Infectious Emergencies 12. Psychiatric Emergencies

• Sepsis and Septic Shock • Acute Psychosis
• Necrotizing Fasciitis • Suicidal Ideation or Attempt
• Toxic Shock Syndrome • Agitated or Violent Behavior
• Acute Epiglottitis • Delirium and Acute Confusional State
• Infective Endocarditis with Embolic
Complications
13. Renal and Urological Emergencies
• Acute Kidney Injury (AKI)
9. Obstetric and Gynecological
• Urinary Retention
Emergencies
• Testicular Torsion
• Ectopic Pregnancy
• Ureteric Colic
• Postpartum Hemorrhage
• Preeclampsia and Eclampsia
14. Hematological Emergencies
• Placental Abruption
• Acute Anemia (e.g., Hemorrhage)
• Uterine Rupture
• Sickle Cell Crisis
• Disseminated Intravascular
10. Pediatric Emergencies
Coagulation (DIC)
• Pediatric Sepsis
• Hemophilia with Bleeding
• Croup and Epiglottitis
• Febrile Seizures
• Bronchiolitis
• Intussusception
1 Cardiovascular
Emergencies
• Myocardial Infarction (Heart Attack)
• Cardiac Arrest
• Acute Heart Failure
• Hypertensive Crisis
• Aortic Dissection
• Pulmonary Embolism
• Arrhythmias
✓ Atrial Fibrillation ✓ Ventricular
✓ Atrial Flutter, Fibrillation (VF)

✓ Paroxysmal ✓ Sinus Bradycardia

Supraventricular ✓ Heart Block
Tachycardia (PSVT) ✓ Bundle Branch
✓ Ventricular Blocks (BBB))
Tachycardia (VT)
Myocardial Infarction (Heart Attack)
Definition • Dyspnea
Myocardial infarction (MI) refers to
• Diaphoresis
irreversible myocardial necrosis due
to prolonged ischemia, typically • Nausea/vomiting
caused by acute coronary artery • Palpitations
occlusion.
• Syncope or sudden death in
severe cases
Types
• ST-Elevation MI (STEMI): Diagnosis
Complete occlusion of a
• ECG:
coronary artery
o STEMI: ST elevation ≥1 mm in
• Non-ST-Elevation MI (NSTEMI):
≥2 contiguous leads
Partial occlusion with
subendocardial infarction o NSTEMI: ST depression, T
wave inversion
Etiology/Risk Factors • Cardiac Biomarkers:
• Atherosclerosis (most common) o Troponin I/T: Most sensitive
• Thrombosis and specific (rise in 3–4 hrs,
peak in 24 hrs, lasts 7–10
• Coronary artery spasm (e.g.,
days)
Prinzmetal angina)
o CK-MB: Rises in 3–6 hrs,
• Risk factors: Hypertension,
peaks in 24 hrs, returns to
diabetes, smoking, dyslipidemia,
normal in 2–3 days
obesity, family history, sedentary
lifestyle • Echocardiography: Wall motion
abnormalities
Clinical Features • Coronary Angiography:
• Chest pain: Severe, crushing, Definitive for coronary anatomy
retrosternal, radiates to left
arm/jaw, >20 mins, not relieved
by rest
Initial Emergency Management Complications
(MONA-BASH)
• Arrhythmias (e.g., VF, VT, AF)
• Morphine: Pain relief • Cardiogenic shock
• Oxygen: If SpO₂ < 90%
• Heart failure
• Nitroglycerin: Sublingual, if no
• Pericarditis
hypotension
• Ventricular septal rupture
• Aspirin: 300 mg chewed
• Papillary muscle rupture
• Beta-blocker: If no
contraindications • Left ventricular aneurysm

• Antiplatelets: • Sudden cardiac death

Clopidogrel/ticagrelor
Secondary Prevention
• Statin: High-dose atorvastatin
• Lifestyle changes: Smoking
• Heparin:
cessation, diet, exercise
Unfractionated/LMWH
• Medications: Aspirin, statin,
beta-blocker, ACE inhibitor,
Definitive Management dual antiplatelet therapy (for at
• Reperfusion therapy: least 12 months post-MI)

o Primary PCI: Preferred

Mnemonic for Diagnosis
within 90 minutes of first
"CHEST PAIN"
medical contact
Chest discomfort
o Thrombolysis: If PCI Heart sounds (muffled if
unavailable within 120 complications)
minutes; best within 12 ECG changes
hours Shortness of breath
• NSTEMI: No thrombolysis; risk Troponin rise
stratification and early invasive Pulse irregularities
strategy if high risk Anxiety/sweating
Increased JVP (if RV infarct)
Nausea/vomiting
 Cardiac Arrest
Definition Recognition
Sudden cessation of effective
• Unresponsive
cardiac mechanical activity,
resulting in loss of circulation and • Not breathing or only gasping
consciousness. • No palpable pulse within 10
seconds

Causes (4 Hs & 4 Ts)

Hs: Initial Management (BLS & ALS)
Basic Life Support (BLS):
• Hypoxia
• Check responsiveness, call for
• Hypovolemia help
• Hypo-/Hyperkalemia (and • Start chest compressions
other metabolic (rate: 100–120/min, depth: 5–6
derangements) cm)
• Hypothermia • Give rescue breaths (30:2 ratio
if no advanced airway)
• Ts:
• Tension pneumothorax
• Tamponade (cardiac)
• Toxins
• Thrombosis (pulmonary or
coronary)
Advanced Life Support (ALS) Prognosis
• Attach monitor/defibrillator • Depends on duration and
• Rhythm check: Shockable cause of arrest, early
(VF/pVT) or Non-shockable defibrillation and quality
(PEA/asystole) CPR improve outcomes

• Immediate defibrillation for

VF/pVT (1 shock, then CPR Key Points
for 2 min) • Early recognition,
• 1 mg adrenaline IV every 3–5 immediate CPR, and rapid
min (after 2nd shock or defibrillation are critical
immediately in non- • Adrenaline improves
shockable) coronary and cerebral
• 300 mg amiodarone IV after perfusion
3rd shock, repeat 150 mg • Continuous high-quality
after 5th shock CPR with minimal
interruptions saves lives
Post-ROSC Care
• Airway protection and
oxygenation
• Hemodynamic support
• Identify and treat reversible
causes
• Targeted temperature
management if comatose
• Continuous cardiac
monitoring
 Acute Heart Failure
Definition • Cardiogenic shock – reduced
A rapid onset or worsening of cardiac output with end-organ
symptoms and signs of heart hypoperfusion
failure, requiring urgent medical
• Hypertensive AHF – high BP
intervention. It may be a new
with pulmonary congestion
presentation (de novo) or acute
decompensation of chronic heart • Right heart failure – RV
failure. dysfunction, often due to PE or
RV infarct

Causes
Clinical Features
• Cardiac: Acute MI, arrhythmias
(e.g., AF, VT), valvular disease • Dyspnea, orthopnea,
(e.g., acute MR, AR), paroxysmal nocturnal dyspnea
myocarditis • Cough with pink frothy sputum
• Non-cardiac: Hypertensive (pulmonary edema)
crisis, severe anemia, renal • Fatigue, confusion, cool
failure, infection/sepsis, peripheries, hypotension
pulmonary embolism, non- (shock)
compliance with medication or
• Raised JVP, peripheral edema,
dietary restrictions
hepatomegaly
• Crackles on lung auscultation,
Types S3 gallop
• Acute decompensated heart
failure (ADHF) – worsening of
chronic HF
• Pulmonary edema – fluid
accumulation in alveoli
Investigations • Inotropes (e.g., dobutamine,
milrinone): If cardiogenic
• ECG: Ischemia, arrhythmias
shock with low output
• CXR: Pulmonary congestion,
cardiomegaly • Morphine: Occasionally used
for anxiety and dyspnea relief
• Bloods: Troponins, BNP/NT-
• ACE inhibitors/ARBs: Once
proBNP, renal function,
stable
electrolytes, ABG
• Avoid beta-blockers in acute
• Echocardiography: LV
decompensation (unless
function, valvular lesions,
already on them and stable)
pericardial effusion
• Bedside: Pulse oximetry, BP Supportive Measures:
monitoring • Non-invasive ventilation
(CPAP/BiPAP) in pulmonary
edema
Management
• Mechanical ventilation if
General Principles:
respiratory failure
• Oxygen therapy if hypoxic
• ICU care if cardiogenic shock
• Monitor vitals, urine output,
Disposition:
cardiac rhythm
• Admit all cases to monitored
• Treat underlying cause (e.g.,
setting
MI, arrhythmia)
Pharmacologic: • Consider ICU/CCU if unstable
• Refer to cardiology for further
• Loop diuretics (e.g.,
evaluation and long-term HF
furosemide): For volume
management
overload
• Vasodilators (e.g.,
nitroglycerin): If BP >110
mmHg, to reduce
preload/afterload
 Hypertensive Crisis
Definition Target Organ Damage Features
A severe elevation in blood (Emergency)
pressure that may lead to acute
• Neurologic: Encephalopathy,
target organ damage. Categorized
stroke, seizures
into:
• Cardiac: MI, angina, heart
• Hypertensive Emergency: BP failure, pulmonary edema
≥180/120 mmHg with evidence
of acute target organ damage • Renal: Acute kidney injury

• Hypertensive Urgency: BP • Ocular: Papilledema, retinal

≥180/120 mmHg without acute hemorrhages
target organ damage • Pregnancy: Eclampsia, HELLP
syndrome

Causes
• Non-compliance with Clinical Features
antihypertensive medications • Severe headache, confusion
• Renovascular hypertension • Chest pain, dyspnea
• Pheochromocytoma • Visual disturbances
• Eclampsia • Nausea, vomiting
• Drugs: Cocaine, • Seizures, focal deficits
amphetamines, MAOIs with
tyramine
• Head trauma, stroke, CNS
tumors
• Autoimmune (e.g.,
scleroderma renal crisis)
Investigations • Avoid rapid overcorrection (risk
of ischemia)
• BP measurement in both arms
• ECG (ischemia, LVH) Hypertensive Urgency:
• No ICU admission usually
• Chest X-ray (pulmonary edema)
needed
• Urinalysis (proteinuria,
• Gradual BP reduction over 24–
hematuria)
48 hours
• Renal function tests
• Oral agents:
• Fundoscopy
o Captopril
• CT brain (if neuro signs)
o Clonidine
• Cardiac enzymes if chest pain
o Labetalol
Management • Close outpatient follow-up
Hypertensive Emergency:
• Admit to ICU Key Points
• Goal: Reduce MAP by no more • Differentiate emergency vs
than 25% in 1st hour, then to urgency by target organ damage
160/100-110 mmHg over next
• Never normalize BP rapidly in
2–6 hours
emergency – gradual reduction
• IV drugs: is safer
o Nitroprusside (rapid action, • Treat underlying cause if
titratable) identifiable
o Labetalol (preferred in • Monitor closely for
stroke, aortic dissection) complications
o Nicardipine
o Nitroglycerin (preferred in
ACS)
o Hydralazine (esp. in
pregnancy)
 Aortic Dissection
Definition Risk Factors
Aortic dissection is a life- • Hypertension (most
threatening condition where common)
there is a tear in the intimal
layer of the aorta, allowing • Connective tissue disorders
blood to enter the media and (e.g., Marfan, Ehlers-Danlos)
create a false lumen. • Bicuspid aortic valve
• Aortic aneurysm
Classification • Prior cardiac surgery
• Stanford Classification: • Trauma
o Type A: Involves
Clinical Features
ascending aorta (±
descending aorta) • Sudden, severe chest pain
radiating to back
o Type B: Involves
descending aorta only • Tearing or ripping in nature
• DeBakey Classification: • Pulse deficit or asymmetry
o Type I: Ascending + arch ± • Hypertension or hypotension
descending (if tamponade or rupture)
o Type II: Ascending only • Neurological deficits (stroke,
syncope, spinal cord
o Type III: Descending only
ischemia)
• Signs of organ ischemia (e.g.,
mesenteric ischemia, acute
renal failure)
Investigations Definitive treatment
• ECG: May be normal or show o Type A dissection: Emergency
ischemic changes surgical repair
• Chest X-ray: Widened o Type B dissection: Medical
mediastinum management unless
complications (e.g., rupture,
• CT Angiography (CTA): Gold
malperfusion) – then consider
standard in stable patients
endovascular (TEVAR) or
• TEE (Transesophageal Echo): surgical intervention
Useful in unstable patients
• MRI Angiography: Highly
accurate but not ideal in Complications
emergencies • Aortic rupture
• D-dimer: Can be elevated, • Cardiac tamponade
useful to rule out in low-risk
• Aortic regurgitation
cases
• Myocardial infarction
• Stroke
Management
• Acute kidney injury
Initial stabilization:
o Oxygen, IV access, monitoring
Key Points
o Control BP and HR:
• High index of suspicion in any
▪ Target SBP <120 mmHg, HR
patient with sudden
<60 bpm
chest/back pain and risk
▪ IV beta-blockers (e.g., factors
labetalol, esmolol) • Rapid imaging and blood
▪ Add vasodilators (e.g., pressure control are critical
nitroprusside) if needed
• Type A is a surgical emergency
– do not delay referral to
cardiothoracic surgery
Pulmonary Embolism (PE)
Definition Clinical Features
Obstruction of pulmonary artery or its
• Sudden onset dyspnea
branches by a thrombus, air, fat, or
amniotic fluid, most commonly from • Pleuritic chest pain
deep vein thrombosis (DVT) of lower • Tachypnea, tachycardia
limbs.
• Hemoptysis (in pulmonary
infarction)
Etiology • Syncope or hypotension (massive
• Thrombotic: DVT (most common) PE)

• Non-thrombotic: Fat (long bone • Signs of DVT (unilateral leg swelling,

fractures), air (central lines), tenderness)
amniotic fluid (obstetric
emergencies), tumor emboli Investigations
• ECG: Sinus tachycardia (most
common), S1Q3T3 pattern (classic
Risk Factors
but uncommon)
• Prolonged immobilization, recent
• CXR: Often normal, may show
surgery (especially orthopedic),
wedge-shaped infarct (Hampton
malignancy
hump), Westermark sign
• Pregnancy, OCP use, obesity,
• D-dimer: Elevated (nonspecific,
smoking
useful for ruling out PE in low-risk
• Inherited thrombophilias (e.g., patients)
Factor V Leiden)
• CT Pulmonary Angiography
• Previous VTE (venous (CTPA): Investigation of choice
thromboembolism)
• V/Q Scan: Used if CTPA
contraindicated
• Echocardiography: RV dysfunction
in massive PE
• Lower limb Doppler USG: To
detect DVT
Severity Classification Prevention
• Massive PE: Hypotension or • Early mobilization post-surgery
shock • DVT prophylaxis in high-risk
• Submassive PE: RV patients (LMWH, mechanical
dysfunction without compression devices)
hypotension
• Low-risk PE:
Key Points
Hemodynamically stable, no
RV dysfunction • Always consider PE in
unexplained dyspnea or chest
pain, especially with risk
Management factors
• Supportive: Oxygen, IV fluids, • CTPA is the diagnostic modality
hemodynamic stabilization of choice
• Anticoagulation: LMWH, UFH, • Prompt anticoagulation is
or DOACs lifesaving
• Thrombolysis: Indicated in • High index of suspicion is
massive PE or select crucial for early diagnosis and
submassive cases (e.g., treatment
alteplase)
• Embolectomy: Surgical or
catheter-directed in selected
cases
• IVC Filter: If anticoagulation
contraindicated or recurrent PE
despite treatment
 Atrial Fibrillation
Definition Clinical Features
o A common arrhythmia o Palpitations
characterized by rapid, o Fatigue
irregular atrial contractions.
o Dyspnea
o Atrial electrical activity
disorganized, leading to o Chest discomfort
ineffective atrial contraction. o Dizziness or syncope
o Reduced exercise tolerance
Epidemiology
o Prevalence increases with Diagnosis
age.
o Electrocardiogram (ECG)
o Higher incidence in patients showing absence of P waves,
with underlying heart disease. irregular R-R intervals.
o Holter monitor for
Etiology intermittent monitoring.

o Hypertension o Echocardiography to assess

underlying structural heart
o Coronary artery disease disease.
o Valvular heart disease
o Thyroid disorders
o Alcohol consumption
o Sleep apnea
o Stimulant use (e.g., caffeine,
nicotine)
Classification Complications
o Paroxysmal AF: Self- o Stroke: Higher risk due to stasis
terminating episodes lasting < 7 of blood in the atria.
days. o Heart failure exacerbation.
o Persistent AF: Sustained o Reduced exercise tolerance.
beyond 7 days, requiring
intervention for termination. o Impaired quality of life.

o Long-standing persistent AF:

Continuous AF lasting > 1 year. Prognosis
o Permanent AF: Decided upon o Depends on underlying
by patient and physician to not comorbidities and rate of
pursue rhythm control. complications.
o Early detection and appropriate
Management management improve
outcomes.
o Rate control: Beta-blockers,
calcium channel blockers,
digoxin. Follow-up
o Rhythm control: Antiarrhythmic • Regular monitoring for symptom
drugs, electrical cardioversion. control, rhythm assessment,
o Anticoagulation: Reduce risk of and anticoagulation
thromboembolic events (e.g., management.
stroke). • Patient education on symptom
o Catheter ablation: For recognition and importance of
symptomatic patients refractory adherence to medications.
to medications.
o Lifestyle modifications:
Alcohol cessation, weight loss,
sleep apnea management.
 Atrial Flutter
Definition Management
Rapid, regular atrial rhythm o Acute: Cardioversion if
characterized by a sawtooth hemodynamically unstable.
pattern on ECG. o Rate control: Beta-blockers,
calcium channel blockers,
Etiology digoxin.

Often associated with structural o Rhythm control: Antiarrhythmic

drugs (e.g., amiodarone,
heart disease (e.g., CAD, valve
flecainide), catheter ablation.
disorders), pulmonary embolism,
hyperthyroidism. o Anticoagulation: Assess stroke
risk using CHA2DS2-VASc
score; anticoagulate
Pathophysiology accordingly.
Reentrant circuit within atria leads
to rapid depolarization, causing
Complications
atrial contraction at rates of 250-
350 bpm. • Stroke (thromboembolism)
• Heart failure exacerbation,
Clinical Presentation • Tachycardia-induced
cardiomyopathy.
Palpitations, dizziness, dyspnea,
fatigue, chest discomfort.
Prognosis
ECG Findings Generally favorable with
appropriate management, but
Sawtooth "F waves" (atrial flutter
recurrence risk exists.
waves) with atrial rate typically
250-350 bpm and 2:1, 3:1, or
variable AV conduction.
 Paroxysmal Supraventricular
Tachycardia (PSVT)
Definition Management
PSVT is a rapid heart rate originating o Vagal maneuvers (Valsalva,
above the ventricles, often carotid sinus massage).
characterized by sudden onset and
o Adenosine for acute termination.
termination.
o Beta-blockers, calcium channel
blockers for rate control.
Etiology
o Catheter ablation for recurrent or
o Reentry circuit involving symptomatic cases.
atrioventricular (AV) node,
accessory pathway, or both.
Complications
o Triggers include stress, caffeine,
alcohol, and tobacco. o Hemodynamic compromise.
o Recurrent episodes may lead to
cardiomyopathy.
Clinical Features
o Palpitations, chest discomfort,
lightheadedness, and syncope. Prognosis

o Rapid regular heartbeat usually o Generally benign but can impact

between 150-250 bpm. quality of life.

o Often begins and ends suddenly. o Excellent prognosis with

appropriate management.

Diagnosis
Prevention
o Electrocardiogram (ECG) during
an episode. o Avoid triggers.

o Rule out other causes of o Long-term management with

tachycardia (e.g., atrial medications or catheter ablation
fibrillation, atrial flutter). when indicated.
 Ventricular Tachycardia (VT)
Definition Diagnosis
Rapid heart rhythm originating in o Electrocardiogram (ECG)
the ventricles with a rate showing wide QRS complexes
exceeding 100 beats per minute. (> 120 ms) with a rate > 100
bpm.

Etiology o 12-lead ECG for morphology

assessment.
o Structural heart disease (e.g.,
myocardial infarction,
cardiomyopathy) Management
o Electrolyte abnormalities (e.g., Stable VT
hypokalemia,
▪ Medications: Amiodarone,
hypomagnesemia)
procainamide, sotalol.
o Drug toxicity (e.g.,
▪ Electrical cardioversion if
antiarrhythmics, digitalis)
medications fail.
o Inherited arrhythmia syndromes
Unstable VT
(e.g., long QT syndrome,
Brugada syndrome) ▪ Immediate synchronized
cardioversion.
Recurrent VT
Clinical Features
▪ Consideration of antiarrhythmic
o Palpitations
therapy.
o Dizziness or syncope
▪ Implantable cardioverter-
o Hypotension defibrillator (ICD) for high-risk
patients.
o Cardiac arrest
Prognosis Follow-up
o Depends on underlying o Regular monitoring of
etiology and comorbidities. symptoms and ECG
o VT in the setting of acute findings.
myocardial infarction o Adjustment of medications
carries a worse prognosis. as needed.

Complications Education
o Hemodynamic compromise o Patient education on
leading to shock or cardiac recognizing symptoms and
arrest. seeking prompt medical
o Recurrent episodes may attention.
lead to ventricular o Counseling on lifestyle
fibrillation and sudden modifications and
cardiac death. adherence to medications.

Prevention
o Identification and
treatment of underlying
structural heart disease.
o Avoidance of triggers (e.g.,
electrolyte imbalances, QT-
prolonging medications).
 Ventricular Fibrillation (VF)
Definition Management
Rapid, irregular, and o Immediate Defibrillation:
ineffective heart rhythm Priority to restore normal
originating from the ventricles. rhythm and perfusion.
o CPR: Initiate chest
Etiology
compressions promptly to
Often precipitated by acute maintain blood flow.
myocardial infarction (AMI),
o Medications: Epinephrine
electrolyte imbalances, drug
and antiarrhythmic drugs
toxicity, or cardiac trauma.
like amiodarone may be
administered.
Pathophysiology
o Advanced Life Support
Chaotic electrical activity
(ALS) : Rapid transport to a
leads to uncoordinated
facility capable of
ventricular contractions,
advanced cardiac care.
compromising cardiac output.

Clinical Features Prognosis

Sudden loss of Without prompt intervention,
consciousness, absence of VF leads to cardiac arrest and
pulse, and absence of death within minutes.
effective circulation.

Diagnosis Prevention
ECG reveals irregular Emphasize public education
undulations without on CPR, early defibrillation,
discernible QRS complexes. and prompt medical response.
 Sinus Bradycardia
Definition Diagnosis
Heart rhythm characterized by Electrocardiogram (ECG)
a slow sinus rate, typically <60 showing regular P waves
beats per minute. originating from the sinus
node, with a heart rate <60
Etiology bpm.
• Physiological: Seen in
athletes, during sleep, and Management
in healthy individuals. • Treat the underlying cause.
• Pathological: May result • Consider discontinuation or
from intrinsic cardiac adjustment of medications
disorders (e.g., sick sinus contributing to bradycardia.
syndrome), increased vagal • In symptomatic patients,
tone, medications (e.g., particularly those with
beta-blockers, calcium hemodynamic compromise,
channel blockers), temporary pacing or
hypothyroidism, electrolyte permanent pacemaker
imbalances (e.g., implantation may be
hyperkalemia), or increased necessary.
intracranial pressure.
Prognosis
Clinical Features Generally good, especially if
• Often asymptomatic. the underlying cause is
• Symptoms may include reversible and promptly
fatigue, dizziness, syncope, addressed.
or angina in severe cases.
 Heart Block
Definition ▪ Clinical Significance: More serious;
can progress to complete block; often
Heart block, also known as
requires pacemaker.
atrioventricular (AV) block, is a condition
where the conduction of electrical 3. Third-Degree (Complete) AV Block
impulses through the AV node is impaired,
o Description: Complete absence of AV
resulting in delayed or blocked signals
conduction; atria and ventricles beat
between the atria and ventricles.
independently.
o ECG Findings: P waves and QRS
Classification complexes present but no relationship
between them.
1. First-Degree AV Block
o Clinical Significance: High risk of
o Description: Prolonged PR interval
asystole and sudden death; usually
(>200 ms) without missed beats.
requires pacemaker.
o ECG Findings: PR interval consistently
longer than 200 ms.
Etiology
o Clinical Significance: Often
asymptomatic; may indicate underlying • Intrinsic Causes:
heart disease or medication effect.
o Aging (degenerative changes)
2. Second-Degree AV Block
o Ischemic heart disease
Type I (Wenckebach/Mobitz I)
o Cardiomyopathies
▪ Description: Progressive lengthening
o Congenital heart defects
of PR interval until a beat is dropped.
• Extrinsic Causes:
▪ ECG Findings: Progressive PR
lengthening followed by a non- o Medications (beta-blockers, calcium
conducted P wave (dropped QRS). channel blockers, digoxin)
▪ Clinical Significance: Usually benign; o Electrolyte imbalances (hyperkalemia)
may cause occasional symptoms like
o Inflammatory diseases (myocarditis,
dizziness.
Lyme disease)
Type II (Mobitz II)
▪ Description: Intermittent non-
conduction of P waves without PR
interval prolongation.
▪ ECG Findings: Constant PR interval
with random dropped beats.
Clinical Presentation Management
• First-Degree: Usually • First-Degree and Second-Degree
asymptomatic. Type I:
• Second-Degree Type I: Generally o Often no treatment needed.
asymptomatic or mild symptoms
o Monitor for progression.
(dizziness, fatigue).
• Second-Degree Type II and Third-
• Second-Degree Type II and Third-
Degree:
Degree: More severe symptoms
(syncope, severe fatigue, heart o Pacemaker implantation is the
failure symptoms). primary treatment.
o Address underlying causes (e.g.,
discontinue causative
Diagnosis
medications).
• History and Physical Examination:
o Temporary pacing may be needed
Check for symptoms, medication
in emergency situations.
use, and underlying conditions.
• Electrocardiogram (ECG): Key
diagnostic tool to identify the type Prognosis
and degree of block. • First-Degree and Second-Degree
• Holter Monitoring: For intermittent Type I: Generally good with
blocks. monitoring.

• Electrophysiological Studies: In • Second-Degree Type II and Third-

complex cases to localize the block. Degree: Variable, depends on
timely intervention with pacemaker
and underlying health.

Key Points
• Early recognition and differentiation
of heart block types are crucial.
• Pacemaker therapy significantly
improves outcomes in higher-
degree AV blocks.
• Regular follow-up is necessary to
monitor for progression and
manage symptoms.
 Bundle Branch Blocks (BBB)
Definition Management
Interruption or delay in the conduction of o Treat underlying conditions if present.
electrical impulses through the bundle
o Close monitoring for progression or
branches of the heart.
development of associated cardiac
issues.
Types
o Right Bundle Branch Block (RBBB): Prognosis
Impaired conduction through the right
o Generally benign if isolated.
bundle branch.
o May indicate increased risk of
o Left Bundle Branch Block (LBBB):
arrhythmias or heart failure in certain
Impaired conduction through the left
contexts.
bundle branch.

Differential Diagnosis
Electrocardiogram (ECG) Findings
o Other causes of widened QRS complex
o RBBB: Wide QRS complex (>0.12
on ECG should be considered, such as
seconds), predominantly in V1 and V2.
ventricular tachycardia, electrolyte
o LBBB: Wide QRS complex (>0.12 abnormalities, or ventricular paced
seconds), predominantly in V5 and V6. rhythms.

Clinical Significance Follow-Up

o Often incidental findings. o Regular monitoring of cardiac function
and ECG changes.
o Can indicate underlying heart disease,
particularly in older patients. o Educate patients about symptoms and
when to seek medical attention.
o May occur in conditions like myocardial
infarction, cardiomyopathy, and
electrolyte imbalances.
Conclusion
o Bundle Branch Blocks are common
Symptoms ECG findings.
o Often asymptomatic. o Understanding their significance and
implications for patient care is crucial
o Symptoms, if present, can include
in clinical practice.
palpitations, dizziness, or syncope.
 Respiratory
2 Emergencies
• Acute Asthma Exacerbation
• Chronic Obstructive Pulmonary
Disease (COPD) Exacerbation
• Pneumothorax
• Hemothorax
• Acute Respiratory Distress
Syndrome (ARDS)
• Foreign Body Aspiration
 Acute Asthma Exacerbation
Definition • Silent chest, cyanosis, altered
A sudden worsening of asthma consciousness → life-
symptoms due to increased airway threatening
inflammation,
bronchoconstriction, and mucus
production. Assessment (Severity)
• Mild: Talks in sentences, SpO₂
≥ 95%, PEFR > 75%
Triggers
• Moderate: Talks in phrases,
• Respiratory infections (most
SpO₂ 92–94%, PEFR 50–75%
common)
• Severe: Words only, SpO₂ <
• Allergen exposure 92%, PEFR < 50%, agitation
• Air pollution, smoke
• Life-threatening: Silent chest,
• Poor medication adherence confusion, exhaustion, SpO₂ <
90%, bradycardia
• NSAIDs, beta-blockers
• Exercise, cold air, emotional
stress Investigations
• SpO₂ monitoring (target ≥ 94%)
Clinical Features
• Peak Expiratory Flow Rate
• Dyspnea, wheezing, chest (PEFR)
tightness
• ABG if severe or deteriorating
• Cough, especially at night or may show normal/high PaCO₂ =
early morning bad sign
• Tachypnea, tachycardia • Chest X-ray if suspect
• Use of accessory muscles, pneumothorax, consolidation,
inability to speak in full or not improving
sentences
Emergency Management Monitoring
• Oxygen: High-flow O₂ to • Repeat PEFR, SpO₂ regularly
maintain SpO₂ ≥ 94% • Monitor for signs of fatigue or
• Bronchodilators: deterioration
o Nebulized Salbutamol 2.5–5 • Watch for response to
mg q20min × 3 doses, then bronchodilators
PRN
o Add Ipratropium Bromide 0.5 Disposition
mg q20min × 3 if severe
• Mild/Moderate: Observe 1–3
• Systemic Steroids:
hours post-treatment;
o Oral Prednisolone 40–50 mg discharge if stable
OR IV Hydrocortisone 100
• Severe/Life-threatening: Admit
mg
to ICU/HDU
• Magnesium Sulfate: • Ensure follow-up, inhaler
o IV 2 g over 20 min if poor technique review, and asthma
response or life-threatening action plan
• Consider IV Aminophylline or
SC/IM Adrenaline if severe or
Key Points
poor response
• Early steroids reduce admission
• Non-invasive or invasive risk
ventilation:
• "Silent chest" is an emergency
o If deteriorating, rising
CO₂, fatigue, or GCS drop • Rising PaCO₂ or fatigue =
impending respiratory failure
• Educate on inhaler use and
triggers before discharge
 Chronic Obstructive Pulmonary
Disease (COPD) Exacerbation
Definition Assessment
An acute worsening of respiratory
• ABCs and vital signs
symptoms in a patient with COPD,
beyond normal day-to-day • Pulse oximetry, ABG (check for
variation, requiring a change in hypoxia/hypercapnia)
treatment. • Chest X-ray (to rule out
pneumonia, pneumothorax)

Common Triggers • ECG (to rule out cardiac

causes)
• Respiratory infections (viral >
bacterial) • Blood tests: CBC, CRP,
electrolytes
• Environmental pollutants,
allergens • Sputum culture if infection
suspected
• Medication non-compliance
• Consider COVID-19 or
• Unknown (up to 30% of cases)
influenza testing

Clinical Features
Severity Classification
• Increased dyspnea
• Mild: Managed with increased
• Increased cough and/or bronchodilators only
sputum volume • Moderate: Requires systemic
• Purulent sputum corticosteroids and/or
antibiotics
• Wheeze, chest tightness
• Severe: Requires
• Fatigue, reduced exercise
hospitalization or ED visit
tolerance
• Hypoxia, tachypnea, use of
accessory muscles
Emergency Management Disposition
• Oxygen: Controlled O2 to • Discharge if mild/moderate
maintain SpO₂ 88–92% and good response to ED
• Bronchodilators: Nebulized treatment
salbutamol ± ipratropium • Admit if severe
(q20min x3 then PRN) exacerbation, hypoxia,
• Steroids: IV hydrocortisone hypercapnia, comorbidities,
100 mg or PO prednisolone or poor social support
30–40 mg daily (5–7 days) • ICU if requiring ventilatory
• Antibiotics: If increased support or unstable vitals
sputum purulence/volume
or fever (e.g., amoxicillin- Key Notes
clavulanate, azithromycin,
doxycycline) • Avoid over-oxygenation

• Non-Invasive Ventilation • Review inhaler technique

(NIV): Indicated if and adherence on discharge
respiratory acidosis (pH < • Arrange follow-up and
7.35, PaCO₂ > 45 mmHg) consider pulmonary rehab
• Intubation and mechanical referral
ventilation: If NIV fails or • Provide smoking cessation
patient deteriorates support if applicable
• Supportive care: IV fluids,
treat underlying cause
 Pneumothorax
Definition Clinical Features
Presence of air in the pleural • Sudden onset dyspnea
space causing partial or
complete lung collapse. • Pleuritic chest pain
• Decreased/absent breath
sounds on affected side
Types
• Hyperresonant percussion
• Spontaneous note
o Primary: No underlying • Tracheal deviation away
lung disease from the affected side (in
o Secondary: Underlying tension pneumothorax)
lung disease (e.g. • Hypotension, tachycardia,
COPD, TB, ILD) cyanosis (in tension
• Traumatic: Penetrating or pneumothorax)
blunt chest trauma
• Iatrogenic: Post-procedures
(e.g. central line insertion,
mechanical ventilation)
• Tension Pneumothorax:
Life-threatening; air enters
but cannot escape, leading
to increased intrathoracic
pressure
Diagnosis • Persistent air leak or
recurrent: Consider surgical
• Clinical diagnosis is critical in
intervention (e.g. VATS,
tension pneumothorax (do not
pleurodesis)
delay for imaging)
• Chest X-ray: Visible pleural
line, absence of lung markings Complications
peripherally
• Respiratory failure
• Ultrasound: Absence of lung
• Recurrence
sliding (“barcode sign” or
“stratosphere sign”) • Tension pneumothorax

• CT Chest: Most sensitive (used • Infection (empyema)

for complex/unclear cases)

Key Emergency Points

Management • Tension pneumothorax is a
• Tension Pneumothorax: clinical diagnosis—do not wait
Immediate needle for imaging
decompression • Needle decompression saves
o 14G needle in 2nd lives
intercostal space, • Always insert chest drain in safe
midclavicular line triangle to avoid injury
o Follow with chest tube
insertion
• Simple Pneumothorax:
o Small & asymptomatic:
Observe + O2
o Large/symptomatic:
Intercostal chest drain (tube
thoracostomy)
 Hemothorax
Definition • Hypotension, tachycardia
Accumulation of blood in the (signs of shock in massive
pleural space, usually due to hemothorax)
trauma. • Tracheal deviation (if tension
hemothorax)
Etiology
• Traumatic: Penetrating or Investigations
blunt chest trauma (most • Chest X-ray: Blunting of
common) costophrenic angle,
• Iatrogenic: Central line homogenous opacity
placement, thoracic surgery • Ultrasound (eFAST):
• Spontaneous: Ruptured Detects pleural fluid quickly
vascular malformations, in trauma
tumors (e.g. mesothelioma) • CT Chest: Precise
• Others: Anticoagulation, localization and cause
coagulopathies • Hemoglobin/Hematocrit:
May drop with ongoing
Clinical Features bleeding

• Chest pain, dyspnea,

tachypnea
• Dullness to percussion,
decreased breath sounds on
affected side
Management Complications
• ABC Stabilization • Retained hemothorax
• Oxygen, IV fluids, blood • Infection → Empyema
transfusion if needed • Fibrothorax
• Chest tube (intercostal • Respiratory distress
drainage)
o Inserted at 5th ICS, mid-
axillary line Key Points

o Immediate drainage; • Suspect in all chest trauma

>1.5 L or >200 mL/hr with signs of shock and
indicates surgery absent breath sounds

• Surgical Intervention • Prompt diagnosis and

chest tube placement are
o Thoracotomy if massive life-saving
bleeding, ongoing
drainage, or • Monitor for ongoing
hemodynamic bleeding and
instability complications

• Monitor: Vitals, drain

output, serial imaging
 Acute Respiratory Distress Syndrome
(ARDS)
Definition Berlin Definition of ARDS
ARDS is a form of acute, diffuse,
• Timing: Within 1 week of a
inflammatory lung injury leading
known insult or new/worsening
to increased pulmonary vascular
symptoms
permeability, loss of aerated lung
tissue, and severe hypoxemia. • Chest imaging: Bilateral
opacities not fully explained by
effusions, collapse, or nodules
Etiology
• Origin of edema: Respiratory
• Direct lung injury: Pneumonia,
failure not explained by cardiac
aspiration, pulmonary
failure/fluid overload
contusion, inhalation injury,
drowning • Oxygenation (on PEEP ≥5 cm
H₂O):
• Indirect lung injury: Sepsis,
pancreatitis, major trauma, o Mild: PaO₂/FiO₂ 200–300
transfusion-related acute lung mmHg
injury (TRALI), drug overdose, o Moderate: 100–200
burns mmHg
o Severe: <100 mmHg
Pathophysiology
• Alveolar-capillary membrane Clinical Features
damage → protein-rich edema →
• Dyspnea, tachypnea, hypoxia
decreased lung compliance
• Bilateral crackles
• Neutrophil activation and
cytokine release → diffuse • Cyanosis, respiratory distress
alveolar damage • May progress to respiratory
• Ventilation-perfusion (V/Q) failure requiring mechanical
mismatch and intrapulmonary ventilation
shunting → hypoxemia
Investigations o Conservative fluid
management after initial
• ABG: Hypoxemia, respiratory
resuscitation
alkalosis → respiratory acidosis
• Chest X-ray/CT: Bilateral Treat underlying cause
infiltrates Antibiotics for sepsis, control of
source, etc.
• Rule out cardiac causes with
echocardiography Adjuncts
• Identify underlying cause (blood Neuromuscular blockade (short-
cultures, inflammatory markers, term), ECMO in refractory cases
etc.)

Complications
Management
Barotrauma, ventilator-associated
Supportive Care: pneumonia (VAP), multiorgan
o Oxygen therapy; high-flow failure, long-term pulmonary
nasal cannula or non- fibrosis
invasive ventilation (early)
o Mechanical ventilation with Prognosis
lung-protective strategy:
• Mortality: 30–40%, higher with
▪ Low tidal volume (6 severe ARDS
mL/kg ideal body weight) • Survivors may have long-term
▪ Plateau pressure <30 cm respiratory and functional
H₂O impairments
▪ Moderate to high PEEP
▪ Permissive hypercapnia
o Prone positioning for
PaO₂/FiO₂ <150 mmHg
 Foreign Body Aspiration
Definition Phases
Inhalation of a solid or semi-solid
1. Choking phase: sudden
object into the respiratory tract,
coughing, gagging, distress
commonly affecting children aged
6 months to 5 years. 2. Asymptomatic phase: object
lodges, symptoms may
Etiology subside

• Common objects: nuts, seeds, 3. Complication phase:

toy parts, coins, food particles infection, obstruction,
atelectasis, pneumonitis
• Risk factors: age <5 years,
neurological impairment, poor
chewing/swallowing
coordination

Clinical Features
• Acute onset of choking,
coughing, gagging
• Stridor (upper airway) or
wheezing/decreased air entry
(lower airway)
• Cyanosis, respiratory distress
• Sudden onset unilateral
wheeze or decreased breath
sounds
• May be asymptomatic initially
(especially with partial
obstruction)
Diagnosis Treat complications
• History and clinical exam are antibiotics for post-obstructive
key pneumonia
• CXR: may be normal; look for
hyperinflation, mediastinal
Complications
shift, atelectasis
Airway edema, bronchiectasis,
• Inspiratory/expiratory films or
lung abscess, pneumothorax,
lateral decubitus views
death if not promptly treated
• CT chest if uncertain
• Rigid bronchoscopy:
Prevention
diagnostic and therapeutic
(gold standard) • Parent education
• Avoid small toys/foods in young
children
Management
• Supervision during eating
Initial
Ensure airway patency
Key Point
o Complete obstruction: back Always suspect foreign body
blows (infants) or Heimlich aspiration in any child with sudden
maneuver (older children) onset respiratory symptoms,
o Partial obstruction: avoid unilateral wheeze, or unexplained
blind finger sweeps; keep respiratory distress.
calm, give oxygen
Definitive
o Rigid bronchoscopy under GA
– preferred method of removal
o Flexible bronchoscopy – may
be diagnostic or therapeutic in
select cases
3 Neurological
Emergencies

• Ischemic Stroke
• Hemorrhagic Stroke
• Status Epilepticus
• Traumatic Brain Injury
• Meningitis
• Encephalitis
• Guillain-Barré Syndrome
• Spinal Cord Injury
 Ischemic Stroke
Definition Initial Assessment
Acute neurological deficit caused by
• ABCs, vital signs, rapid neurological
interruption of cerebral blood flow due
exam (NIH Stroke Scale)
to thrombotic or embolic occlusion of a
cerebral artery. • Blood glucose (rule out
hypoglycemia)
• CT head (non-contrast) to exclude
Etiology
hemorrhage
• Thrombotic: Atherosclerosis, small
• Labs: CBC, electrolytes,
vessel disease
coagulation profile, cardiac
• Embolic: Cardiac (e.g. atrial enzymes, ECG
fibrillation, valvular disease),
carotid artery atheroembolism
Emergency Management
• Other causes: Hypercoagulable
states, dissection, vasculitis • Time is brain: Identify onset time,
consider stroke code activation
• If within 4.5 hours: IV thrombolysis
Clinical Features
with alteplase (rTPA) after ruling out
• Sudden-onset focal neurological contraindications
deficits
• If within 6-24 hours and large
• Hemiparesis, hemisensory loss vessel occlusion: Consider
mechanical thrombectomy
• Dysarthria, aphasia
• Aspirin 300 mg (if thrombolysis not
• Visual field defects (e.g.
given or 24h post-thrombolysis)
homonymous hemianopia)
• BP management: Allow permissive
• Ataxia, vertigo (posterior
hypertension unless >185/110
circulation)
mmHg for thrombolysis
• Altered consciousness (in large
• Manage blood glucose,
strokes)
temperature, and oxygenation
Contraindications to Key Points
Thrombolysis (selected)
• Rapid recognition and imaging
• Intracranial hemorrhage are critical
• Recent surgery or trauma • Thrombolysis and
thrombectomy are time-
• Severe uncontrolled
sensitive
hypertension
• Manage comorbidities and
• Low platelet count, INR >1.7
prevent complications
• Stroke or head trauma in past 3
months • Multidisciplinary approach for
rehabilitation and secondary
prevention
Supportive Care
• NPO until swallow assessed
• DVT prophylaxis
• Monitor for complications:
cerebral edema, hemorrhagic
transformation, aspiration

Post-Acute Care
• Start secondary prevention:
antiplatelets, statins, BP and
glucose control
• Identify cause: cardiac
evaluation, carotid imaging
• Initiate rehabilitation early
 Hemorrhagic Stroke
Definition Clinical Features
Bleeding into the brain
• Sudden onset of severe
parenchyma (intracerebral
headache ("worst headache of
hemorrhage, ICH) or subarachnoid
life" in SAH)
space (subarachnoid hemorrhage,
SAH) due to vessel rupture, leading • Vomiting
to increased intracranial pressure • Altered mental status or coma
and brain damage.
• Focal neurological deficits (e.g.
hemiparesis, aphasia)
Etiology • Seizures
• Hypertension (most common • Signs of raised intracranial
cause of spontaneous ICH) pressure: bradycardia,
• Aneurysmal rupture (SAH) hypertension, irregular
respiration (Cushing’s triad)
• Arteriovenous malformations
(AVMs)
Diagnosis
• Trauma
• Non-contrast CT head: First-
• Anticoagulant use or
line, detects acute bleed
coagulopathy
• CT Angiography/MRI/MRA:
• Cerebral amyloid angiopathy
Evaluate aneurysm, AVM, or
(elderly)
underlying lesion
• Illicit drug use (e.g. cocaine,
• Lumbar puncture: If SAH
amphetamines)
suspected and CT negative
(look for xanthochromia)
• Labs: CBC, coagulation profile,
renal function, toxicology
screen if indicated
Emergency Management Prognosis
• Airway, breathing, High morbidity and mortality.
circulation – secure airway if Prognosis depends on
GCS <8 hemorrhage size, location, GCS
on admission, age, and
• Blood pressure control: comorbidities.
o Target SBP <140-160
mmHg (individualize; avoid
rapid drops) Key Points

o IV antihypertensives: • Rule out hemorrhagic stroke

labetalol, nicardipine before giving thrombolytics

• Reverse anticoagulation: • Early BP control and

Vitamin K, FFP, PCC, neurosurgical input crucial
idarucizumab, etc. • Rapid CT scan is the
• Seizure control: cornerstone of diagnosis
Benzodiazepines for acute • Monitor for complications:
seizures; avoid prophylaxis rebleeding, hydrocephalus,
unless seizures occur vasospasm (especially in
• Intracranial pressure (ICP) SAH)
management:
o Elevate head of bed 30°
o Mannitol or hypertonic
saline if signs of herniation
• Neurosurgical consult:
Hematoma evacuation, EVD,
aneurysm clipping/coiling
• ICU admission for monitoring
and supportive care
 Status Epilepticus
Definition Clinical Features
A seizure lasting >5 minutes or
• Continuous or repeated seizures
recurrent seizures without return to
baseline consciousness between • No recovery of consciousness
episodes. It is a neurological • May have tonic-clonic activity,
emergency requiring immediate subtle twitches, or just altered
intervention. mental status

Types
Initial Emergency Management
• Convulsive Status Epilepticus:
(ABCs first)
Generalized tonic-clonic seizures
1. Airway and oxygen
• Non-convulsive Status
Epilepticus: Altered mental 2. IV access and blood samples
status with subtle motor signs or (CBC, electrolytes, glucose,
no motor activity calcium, magnesium, renal/liver
function, toxicology)
Etiology (common causes) 3. Check blood glucose – correct
• Non-compliance with hypoglycemia if present
antiepileptic drugs 4. Benzodiazepines (first-line):
• CNS infections (e.g., meningitis, o Lorazepam 0.1 mg/kg IV
encephalitis) (max 4 mg)
• Stroke o Diazepam 0.15–0.2 mg/kg IV
• Head trauma (max 10 mg) or per rectum if
no IV access
• Metabolic disturbances (e.g.,
hyponatremia, hypoglycemia) o Midazolam
IM/buccal/intranasal if no IV
• Alcohol withdrawal
access
• Toxic ingestion
• Intracranial tumors
Second-line Management (if Complications
seizures persist after 5–10 min)
• Neuronal damage
• Phenytoin 20 mg/kg IV (infuse • Respiratory failure
slowly, monitor ECG)
• Arrhythmias
• Alternatives: Fosphenytoin,
Valproate, Levetiracetam • Death

Key Points

Third-line Management • Time is brain – early treatment

(Refractory SE) reduces morbidity and
mortality
• ICU admission, intubation,
continuous EEG • Always search for and address
the underlying cause
• General anesthesia:
Midazolam, Propofol, or • Consider non-convulsive
Pentobarbital infusion status in patients with altered
consciousness without
obvious seizures
Monitoring and Support
• Continuous cardiorespiratory
monitoring
• Monitor for complications:
hypoxia, aspiration,
hypotension, rhabdomyolysis
• Treat underlying cause
Traumatic Brain Injury (TBI)
Definition Mechanisms of Injury
TBI refers to an alteration in • Acceleration-deceleration
brain function or other evidence
of brain pathology caused by an • Blunt trauma
external force (e.g., blow to the • Penetrating trauma
head, penetrating injury).
• Blast injury

Classification Clinical Features

• Mild TBI: GCS 13–15 • Altered level of consciousness

• Moderate TBI: GCS 9–12 • Headache, vomiting

• Severe TBI: GCS ≤8 • Seizures

• Focal neurological deficits

Primary vs Secondary Injury • Signs of raised ICP:

bradycardia, hypertension,
• Primary injury: Occurs at the
irregular respiration (Cushing’s
time of trauma (e.g.,
triad)
contusions, lacerations,
hematomas) • CSF rhinorrhea/otorrhea,
raccoon eyes, Battle’s sign
• Secondary injury: Due to
(base of skull fracture)
subsequent factors like
hypoxia, hypotension, raised
Assessment
ICP
• ABCDE approach
• GCS score
• Pupil assessment
• Neurological exam
Investigations Indications for Neurosurgical
Referral/Intervention
• Non-contrast CT brain (initial
imaging of choice) • GCS ≤8
• X-rays (cervical spine if • Deteriorating neurological
suspected injury) status
• Labs: electrolytes, coagulation • Significant hematoma/midline
profile, ABG, blood glucose shift
• Open or depressed skull
Management fracture
• Penetrating brain injury
• Initial Resuscitation: Airway
protection, oxygenation,
maintain BP Monitoring
• Prevent secondary injury: • Serial GCS, pupil
Avoid hypoxia and hypotension size/reactivity, vital signs
• ICP management: Elevate • ICP monitoring in severe TBI
head, mannitol/hypertonic
saline, sedation, ventilation, Complications
surgical decompression if
needed • Raised ICP, herniation

• Seizure prophylaxis: • Post-traumatic seizures

Levetiracetam or phenytoin • Hydrocephalus
• Surgery: Evacuation of • Cognitive, behavioral, and
hematomas (e.g., EDH, SDH), motor deficits
decompressive craniectomy if
refractory ICP Disposition
• Mild TBI: Discharge if normal
CT and no risk factors
• Moderate/Severe TBI: Admit,
often ICU, neurosurgical care
 Meningitis
Definition Clinical Features
Acute inflammation of the
• Fever, headache, neck
meninges (pia and arachnoid
stiffness
mater) surrounding the brain and
spinal cord. • Photophobia, vomiting
• Altered mental status,
irritability
Etiology
• Seizures, focal deficits
• Bacterial: Neonates: Group B
Streptococcus, E. coli, Listeria • Bulging fontanelle (infants),
Children/adults: poor feeding, lethargy
Streptococcus pneumoniae, • Kernig’s and Brudzinski’s signs
Neisseria meningitidis, (often absent in young
Haemophilus influenzae type b children)
• Viral: Enteroviruses, HSV, VZV,
mumps
Red Flags
• Fungal: Cryptococcus (mainly
• Rapid deterioration in
in immunocompromised)
consciousness
• TB meningitis: Seen in
• Seizures or focal neurological
endemic areas, subacute
signs
course
• Signs of raised ICP
• Non-infectious: Drug-
(papilledema, bradycardia,
induced, autoimmune
hypertension)
• Petechial rash (suggests
meningococcemia)
Diagnosis Adjunctive Treatment
• Lumbar Puncture (LP): • Dexamethasone before/with 1st
Contraindicated if raised ICP, dose of antibiotics (mainly for
shock, or focal deficits Hib/S. pneumoniae)
o Bacterial: ↑WBC • Seizure control
(neutrophilic), ↓glucose,
• Supportive care: Fluids,
↑protein, ↑opening pressure
antipyretics, ICU monitoring if
o Viral: ↑WBC (lymphocytic), severe
normal glucose, mild
↑protein
Complications
• Blood cultures
• Hearing loss, hydrocephalus
• CT/MRI Brain: If LP
contraindicated • Cerebral infarction, SIADH

• CSF PCR/Gram stain/culture • Cognitive deficits, seizures

• Death if untreated or delayed

Empirical Antibiotic Therapy

• Neonates: Ampicillin + Prevention
cefotaxime/gentamicin • Vaccination: Hib, Pneumococcal,
• Infants/children: Meningococcal
Ceftriaxone/cefotaxime + • Prophylaxis for close contacts
vancomycin (e.g. rifampicin for
• Adults: Ceftriaxone + meningococcal exposure)
vancomycin ± ampicillin (for
Listeria >50 yrs)
Key Points
• Immunocompromised: Add
• Don’t delay antibiotics for LP
ampicillin + consider
antifungals/antivirals • Always assess for
contraindications to LP
• TB meningitis: Anti-TB therapy +
steroids • High suspicion needed in infants
and altered mental status cases
 Encephalitis
Definition • Behavioral changes,
Acute inflammation of the brain hallucinations (especially in
parenchyma, commonly due to HSV)
viral infections.
• Signs of raised ICP

Etiology
Diagnosis
• Viral: HSV-1 (most common),
• Clinical suspicion in febrile
HSV-2 (neonates), VZV, CMV,
patients with altered sensorium
EBV, Enteroviruses, Japanese
or seizures
encephalitis, Rabies
• CSF analysis: lymphocytic
• Bacterial: TB, Listeria pleocytosis, elevated protein,
• Autoimmune: Anti-NMDA normal glucose
receptor encephalitis
• CSF PCR: for HSV,
• Post-infectious: ADEM (Acute enteroviruses, others
Disseminated
• Neuroimaging (MRI): temporal
Encephalomyelitis)
lobe involvement in HSV
• EEG: diffuse slowing,
Clinical Features epileptiform discharges
• Fever, headache • Serology/Autoantibodies: if
autoimmune suspected
• Altered mental status:
confusion, lethargy, coma
• Seizures (focal/generalized)
• Focal neurological deficits:
hemiparesis, cranial nerve
palsies
Differential Diagnosis Key Points
• Meningitis • Always consider HSV in
• Sepsis with encephalopathy encephalitis – initiate acyclovir
early
• Metabolic encephalopathy
• MRI and CSF PCR are
• Drug/toxin-induced diagnostic cornerstones
• Intracranial bleed or mass • Early treatment reduces
mortality and improves
outcomes
Management
• Supportive: airway protection,
antipyretics, fluids, seizure
control (benzodiazepines,
levetiracetam)
• Empiric antiviral: IV Acyclovir
(10 mg/kg q8h) for suspected
HSV until ruled out
• Steroids: if ADEM or
autoimmune suspected
• ICU care: if coma, seizures,
raised ICP

Complications
• Seizures/status epilepticus
• Cerebral edema, herniation
• Long-term neurological
sequelae (cognitive/behavioral)
• Mortality if untreated
(especially HSV)
 Guillain-Barré Syndrome (GBS)
Definition Pathophysiology
GBS is an acute inflammatory • GBS is an autoimmune disorder
polyneuropathy characterized by where the immune system attacks
progressive muscle weakness and the peripheral nervous system,
areflexia, often following an infection. It specifically the myelin sheath (or
is considered a medical emergency due sometimes axons) of peripheral
to the rapid progression that can lead to nerves.
respiratory failure and autonomic
• This results in demyelination,
instability.
impairing nerve signal transmission,
causing weakness, sensory loss, and
other neurological deficits.
Etiology
• Often follows viral or bacterial
infections, such as: Clinical Features
o Campylobacter jejuni (most • Progressive motor weakness: Starts
common) in the lower limbs and ascends
upward (ascending paralysis).
o Cytomegalovirus (CMV)
• Paresthesia: Often begins in the feet
o Epstein-Barr virus (EBV)
and hands.
o Influenza
• Areflexia: Loss of deep tendon
o Zika virus reflexes is characteristic.
o Mycoplasma pneumoniae • Autonomic dysfunction: Includes
• Rarely, it can occur after vaccinations fluctuations in heart rate, blood
or as a result of surgery. pressure, and respiratory failure in
severe cases.
• Respiratory involvement: In severe
cases, respiratory muscles are
affected, leading to respiratory
failure. Intubation and ventilation
may be required.
• Pain: Muscle aches or cramps can be
present.
Diagnosis Prognosis
• Clinical presentation: Progressive • Most patients experience partial or
ascending weakness with areflexia. complete recovery, with some
remaining with mild residual
• Lumbar puncture: Shows
weakness.
albuminocytologic dissociation
(elevated protein levels with normal • The recovery period can take
white cell count). months, and in severe cases, full
recovery may take up to a year.
• Electromyography (EMG): Reveals
demyelination with conduction block • A small percentage may have
or slowing. permanent disability or
complications like respiratory failure
• Nerve conduction studies: Show
or cardiovascular instability.
prolonged latencies, slowed
conduction velocities, and
decreased amplitude of the
Complications
compound muscle action potentials.
• Respiratory failure
Management • Autonomic instability
• Supportive care: Includes • DVT/PE
monitoring for respiratory failure,
• Pressure ulcers
autonomic dysfunction, and
preventing complications like deep • Chronic fatigue and mild residual
vein thrombosis (DVT) and pressure neurological deficits
ulcers.
• Plasmapheresis or IV
Key Points
immunoglobulin (IVIG): First-line
treatments to reduce the • Early recognition and intervention
autoimmune response. are crucial.

• Mechanical ventilation: For patients • Close monitoring of respiratory and

with respiratory failure. autonomic function is essential.

• Pain management: For neuropathic • Plasmapheresis and IVIG are the

pain, often requiring gabapentinoids cornerstone treatments.
or opioids.
• Physical therapy: Early mobilization
to prevent muscle atrophy and
contractures.
 Spinal Cord Injury (SCI)
Definition Mechanism of Injury
Spinal cord injury is any damage to the
• Primary injury: Direct trauma to the
spinal cord that results in a loss of
spinal cord (compression, contusion,
function, such as mobility or sensation. It
laceration).
can occur due to trauma (e.g., motor
vehicle accidents, falls) or non-traumatic • Secondary injury: Cascade of
causes (e.g., tumors, infections, biological events that occur post-injury
degenerative diseases). (ischemia, inflammation, oxidative
stress).

Classification of SCI Signs and Symptoms

1. Complete SCI: Total loss of motor and • Motor dysfunction: Paralysis or
sensory function below the level of weakness (tetraplegia or paraplegia).
injury.
• Sensory dysfunction: Loss of
2. Incomplete SCI: Partial loss of motor sensation below the level of injury
and/or sensory function below the (numbness, tingling).
injury site.
• Autonomic dysfunction: Bradycardia,
hypotension, loss of thermoregulation,
Levels of Injury and bowel/bladder dysfunction.

• Cervical (C1-C8): Paraplegia or • Pain: Acute, localized pain from injury

quadriplegia. Loss of function in arms, site or referred pain.
legs, and respiratory muscles (C4 and • Respiratory compromise: Due to
above may cause respiratory failure). cervical injuries (especially above C4).
• Thoracic (T1-T12): Paraplegia. Loss of
motor and sensory function in legs and Assessment
trunk.
1. History: Mechanism of injury (trauma
• Lumbar (L1-L5) and Sacral (S1-S5): or non-trauma), time of injury,
Paraplegia. Loss of function in legs, associated injuries.
possibly affecting bowel and bladder
2. Physical examination: Thorough
control.
neurological examination to assess
motor and sensory function.

3. ASIA scale: Used to assess the

severity and completeness of the injury
(American Spinal Injury Association).
Diagnosis Complications
• Clinical assessment supported by • Neurogenic shock: Due to disruption
imaging (X-ray, MRI, CT scan) to of sympathetic nervous system
evaluate the level and extent of function; hypotension, bradycardia,
damage. and warm, dry skin.
• MRI: Gold standard for detecting soft • Spinal shock: Temporary loss of all
tissue damage, including the spinal spinal cord activity below the injury
cord. level, including motor, sensory, and
reflexes.

• Deep vein thrombosis (DVT): Due to

Management
immobility.
Initial Care (ABCDE approach):
• Pressure ulcers: Due to prolonged
o Airway and breathing: Ensure airway immobility.
stability; if cervical injury is
• Autonomic dysreflexia: In patients
suspected, use jaw-thrust maneuver
with injuries above T6, causing
to avoid neck movement.
dangerous hypertension.
o Circulation: Manage hypotension,
stabilize with fluids, and consider
vasopressors if needed. Rehabilitation

o Immobilization: Spine precautions • Early mobilization, physical therapy,

(manual in-line stabilization, cervical and occupational therapy.
collar, spinal board). • Psychological support for the patient
Surgical intervention: and family.

Indicated for unstable fractures, spinal

Prognosis
cord compression, or to decompress the
cord. Varies depending on the level and
completeness of injury. Higher injuries
Medications:
generally have poorer outcomes. Early
o Methylprednisolone: Given within 8 intervention and rehabilitation can
hours post-injury to reduce improve functional recovery.
secondary damage (controversial in
use).
Prevention
o Pain management: Opioids and
adjunctive medications as necessary. • Proper use of safety gear (helmets,
seatbelts).
o Antibiotics: For associated open
fractures or infections. • Public awareness and education on
spinal cord injury prevention.
 Endocrine and
4 Metabolic
Emergencies

• Diabetic Ketoacidosis (DKA)

• Hyperosmolar Hyperglycemic
State (HHS)
• Hypoglycemia
• Adrenal Crisis
• Thyroid Storm
• Myxedema Coma
• Electrolyte Imbalances
• Hyperkalemia • Hypercalcemia
• Hypokalemia • Hypocalcemia
• Hypernatremia
• Hyponatremia
 Diabetic Ketoacidosis (DKA)
Definition Clinical Features
A life-threatening complication of
• Polyuria, polydipsia, dehydration
diabetes mellitus (mostly Type 1)
characterized by hyperglycemia, • Vomiting, abdominal pain
metabolic acidosis, and ketonemia. • Kussmaul respiration (deep, rapid
breathing)

Etiology/Precipitating Factors • Fruity (acetone) breath

• Infection (most common) • Altered mental status to coma

• Missed insulin doses • Signs of dehydration (tachycardia,

hypotension, dry mucosa)
• New-onset diabetes
• Myocardial infarction, stroke
Investigations
• Drugs (e.g., corticosteroids,
thiazides) • Blood glucose: >250 mg/dL

• Trauma, surgery, emotional stress • Arterial/venous blood gas: pH

<7.3, HCO₃ <18 mEq/L
• Serum/urine ketones: positive
Pathophysiology
• Anion gap: increased
• Insulin deficiency + excess
counter-regulatory hormones → • Electrolytes: low Na⁺ (pseudo-
lipolysis hyponatremia), K⁺ variable

• Free fatty acids converted to • CBC, blood cultures (if infection

ketones (acetoacetate, β- suspected)
hydroxybutyrate) → metabolic • ECG (to monitor K⁺ effects)
acidosis
• Hyperglycemia → osmotic diuresis
→ dehydration, electrolyte loss
Management Complications
Fluid Resuscitation • Cerebral edema (especially in
children)
o Isotonic saline (0.9% NaCl): 15-
20 mL/kg in 1st hour • Hypoglycemia, hypokalemia
o Switch to 0.45% NaCl if needed • ARDS, acute kidney injury
based on corrected Na⁺
• Thromboembolism
Insulin Therapy
o Regular insulin IV bolus (0.1
Prevention
units/kg), then infusion (0.1
units/kg/hr) • Patient education on insulin
adherence
o Aim: Decrease glucose by 50–
70 mg/dL/hr • Sick day rules (insulin
adjustment, hydration)
o Add dextrose (5% or 10%) when
glucose <200–250 mg/dL • Early recognition of warning
signs
Potassium Replacement
o If K⁺ <3.3 mEq/L: hold insulin,
give K⁺
o If K⁺ 3.3–5.3: start K⁺ with
fluids/insulin
o If K⁺ >5.3: monitor closely
Bicarbonate
o Only if pH <6.9
Monitor Closely
o Glucose, electrolytes, ABG,
ketones, vitals, fluid
input/output
Hyperosmolar Hyperglycemic State (HHS)
Definition Clinical Features
A life-threatening complication of type
• Gradual onset (over days)
2 diabetes mellitus characterized by
severe hyperglycemia, • Polyuria, polydipsia
hyperosmolarity, and dehydration • Severe dehydration signs (dry
without significant ketoacidosis. mucosa, poor skin turgor,
hypotension, tachycardia)

Etiology/Precipitating Factors • Altered sensorium, confusion,

seizures, coma
• Infections (most common, e.g.,
pneumonia, UTI) • No or mild Kussmaul breathing or
abdominal pain (contrast with DKA)
• Non-compliance with antidiabetic
therapy
• New-onset diabetes Diagnostic Criteria (typical values)

• Myocardial infarction, stroke • Plasma glucose > 600 mg/dL

• Medications (e.g., steroids, • Serum osmolality > 320 mOsm/kg

thiazides, antipsychotics) • Arterial pH > 7.3
• Serum bicarbonate > 15 mEq/L
Pathophysiology • Absent/mild ketonemia/ketonuria
• Relative insulin deficiency → • Altered mental status
hyperglycemia
• Osmotic diuresis → profound
dehydration Investigations

• Minimal ketosis due to residual • CBC, renal function, electrolytes

insulin activity • Blood glucose, serum ketones
• Hyperosmolarity impairs • Serum osmolality
consciousness
• Arterial blood gas
• ECG, chest X-ray, urinalysis,
cultures (identify precipitant)
Management Monitoring
Fluid Replacement o Hourly glucose
o Start with isotonic saline o Frequent electrolytes,
(0.9% NaCl) osmolality, and vitals
o Switch to 0.45% NaCl based
on sodium level
Complications
o Correct over 24–48 hours • Cerebral edema (rare but
Insulin Therapy serious)
o IV insulin after partial fluid • Hypoglycemia, hypokalemia
replacement
• Thromboembolism
o Bolus may be given followed
by continuous infusion
Prognosis
o Target glucose reduction: 50–
75 mg/dL/hour • Mortality higher than DKA (10–
20%)
o Add dextrose once glucose <
300 mg/dL • Poor prognosis with advanced
age, comorbidities, delayed
Electrolyte Correction treatment
o Monitor and correct
potassium (usually low
despite high serum K) Key Differences from DKA

o Replace aggressively once • Type 2 DM vs. Type 1 DM

urine output is adequate • Minimal/no ketosis
Identify and Treat Underlying • Higher glucose and osmolality
Cause
• More profound dehydration
o Start empirical antibiotics if
• Slower onset
infection suspected
 Hypoglycemia
Definition Diagnosis
Blood glucose <70 mg/dL (3.9 • Check capillary blood
mmol/L); clinically significant glucose
hypoglycemia usually <54
mg/dL (3.0 mmol/L) • Confirm with lab plasma
glucose
• Whipple’s triad: symptoms +
Causes low plasma glucose +
• Diabetic patients: excess symptom resolution after
insulin or oral hypoglycemics, glucose correction
missed meals, exercise,
alcohol
• Non-diabetic: sepsis,
adrenal insufficiency,
insulinoma, liver failure,
malnutrition, critical illness,
dumping syndrome

Symptoms (Adrenergic and

Neuroglycopenic)
• Adrenergic: tremor,
palpitations, sweating,
anxiety, hunger
• Neuroglycopenic: confusion,
dizziness, blurred vision,
seizures, loss of
consciousness, coma
Management Disposition
• Conscious patient: oral • Stable and cause known:
glucose (15–20 g) – glucose discharge with education
tablets, juice, sugar • Recurrent, unexplained, or
• Unconscious or unable to severe: admit for evaluation
swallow:
o IV dextrose: 25–50 mL of Key Points
50% dextrose (D50)
bolus in adults • Always rule out
hypoglycemia in altered
o Children: 2 mL/kg of mental status
D10 or 1 mL/kg of D25
• Educate diabetic patients
o If IV access not on prevention and
available: IM glucagon recognition
(1 mg adults/children
>25 kg; 0.5 mg <25 kg) • Frequent glucose
monitoring essential after
correction
Monitor
• Repeat glucose in 15 min
• Re-treat if <70 mg/dL
• Identify and treat underlying
cause
 Adrenal Crisis
Definition Precipitating Factors
Acute, life-threatening • Infection (especially
deficiency of cortisol (± gastroenteritis)
aldosterone) due to adrenal
insufficiency. • Surgery, trauma
• Non-compliance with steroid
therapy
Causes
• Sudden cessation of steroids
• Primary adrenal
insufficiency (Addison’s
Clinical Features
disease): autoimmune, TB,
metastases, hemorrhage • Hypotension (often
(Waterhouse–Friderichsen refractory to fluids)
syndrome) • Shock, collapse
• Secondary adrenal • Hypoglycemia
insufficiency: sudden
• Vomiting, abdominal pain,
withdrawal of long-term
nausea
steroids, pituitary disease
• Confusion, lethargy, coma
• Stress (e.g. infection,
surgery, trauma) in known • Dehydration
adrenal insufficiency • Hyperpigmentation (in
chronic/primary cases)
• Hyponatremia, hyperkalemia
(esp. in primary adrenal
insufficiency)
Investigations Follow-Up
• Electrolytes: hyponatremia, • Taper steroids to maintenance
hyperkalemia, hypoglycemia dose over 1–3 days
• Serum cortisol (low) • Fludrocortisone if primary
adrenal insufficiency
• ACTH (high in primary, low in
secondary) • Educate patient on stress
dosing, emergency steroid use
• Short Synacthen test (if
diagnosis unclear and patient • Medic alert bracelet
stable) recommended

Management Key Points

Immediate (do not wait for
• Life-threatening emergency
Investigations)
• Treat first, investigate later
• Hydrocortisone 100 mg IV
bolus, then 50–100 mg IV 6- • Always suspect in patients with
hourly or 200 mg/day known adrenal insufficiency
continuous infusion who present unwell or in shock

• IV fluids: 0.9% saline ± 5%

dextrose for volume and
glucose replacement
• Treat precipitating cause (e.g.
antibiotics for sepsis)
• Monitor vitals, electrolytes,
glucose
 Thyroid Storm
Definition • CNS: Agitation, delirium,
A life-threatening exacerbation of psychosis, seizures, coma
thyrotoxicosis with systemic
• GI: Nausea, vomiting, diarrhea,
decompensation. Medical
abdominal pain, jaundice
emergency with high mortality if
untreated. • CVS: Heart failure,
hypotension, shock

Etiology / Triggers • Others: Goiter, exophthalmos

(if Graves’ disease)
• Infection (most common)
• Surgery (especially thyroid
surgery) Diagnosis

• Trauma • Clinical diagnosis – labs may be

similar to regular thyrotoxicosis
• Diabetic ketoacidosis
• Burch-Wartofsky score can
• Myocardial infarction help assess probability (>45 =
• Parturition thyroid storm)
• Sudden withdrawal of • Labs: ↑ Free T4, ↑ Free T3, ↓
antithyroid drugs TSH; CBC, LFTs, glucose,
cardiac markers as needed
• Iodine load (e.g., contrast
agents, amiodarone) • Rule out infection, MI, sepsis,
etc.
Clinical Features
• Fever (often > 38.5°C, may
exceed 40°C)
• Tachycardia (out of proportion
to fever), arrhythmias (esp.
atrial fibrillation)
Management Control Symptoms
Supportive Care o Propranolol 60–80 mg
• Admit to ICU orally q6h or 1–2 mg IV
• IV fluids, cooling, oxygen q10–15 min

• Treat precipitating cause o Caution in heart failure –

(e.g., antibiotics for infection) use esmolol if needed

Definitive Therapy Prognosis

Block Hormone Synthesis • Mortality up to 20–30%

without prompt treatment
o Propylthiouracil (PTU)
500–1000 mg loading • Early aggressive therapy
dose, then 250 mg q4–6h improves outcomes

o Alternatively:
Methimazole 20–30 mg Key Points
q6–8h (if PTU unavailable) • Always consider thyroid
Block Hormone Release storm in febrile, delirious
(1 hour after antithyroid drug) patients with tachycardia and
known hyperthyroidism
o Iodine (e.g., Lugol’s
iodine, sodium iodide) • Initiate treatment based on
clinical suspicion—do not
Block Peripheral Conversion wait for lab confirmation
of T4 to T3
o Hydrocortisone 100 mg IV
q8h
o Also prevents adrenal
insufficiency
 Myxedema Coma
Definition Clinical Features
Myxedema coma is a rare, life- • Altered mental status:
threatening emergency due to confusion to coma
severe, untreated
hypothyroidism. Despite the • Hypothermia
name, coma is not always • Bradycardia
present.
• Hypotension
• Hypoventilation
Etiology/Precipitating Factors
• Generalized non-pitting edema
• Long-standing untreated
• Dry, coarse skin and hair
hypothyroidism
• Macroglossia, hoarseness
• Infections (most common
trigger) • Hypoglycemia, hyponatremia

• Cold exposure • Pericardial/pleural effusions

• Trauma
Investigations
• Surgery
• TSH ↑, Free T4 ↓ (primary
• CNS depressants (e.g., hypothyroidism)
sedatives, opioids)
• Hyponatremia, hypoglycemia
• Stroke or myocardial infarction
• ABG: respiratory acidosis
• Non-compliance with thyroid
• CBC, cultures (to detect
hormone therapy
infection)
• ECG: bradycardia, low voltage
complexes
• CXR, echocardiography if
effusions suspected
Management Key Points
• Airway & Breathing: May require • Suspect in elderly with altered
intubation and mechanical consciousness, hypothermia,
ventilation and known/possible
• Circulation: IV fluids cautiously hypothyroidism
(risk of fluid overload) • Start treatment based on clinical
suspicion—do not wait for lab
• Thyroid hormone replacement:
confirmation
o IV levothyroxine (T4): 200–
• Multidisciplinary ICU care often
400 mcg loading dose,
required
then 50–100 mcg daily
o Some recommend adding
IV liothyronine (T3) in
critical cases
• Steroids: IV hydrocortisone 100
mg 8 hourly (until adrenal
insufficiency excluded)
• Rewarming: Passive only (avoid
active warming due to risk of
vasodilation and collapse)
• Treat underlying cause:
Antibiotics for infection, manage
precipitating factors

Prognosis
High mortality rate (30–60%); early
recognition and prompt treatment
improve outcomes
 Hyperkalemia
Definition ECG Changes
Serum potassium >5.5 mmol/L
(progressive with increasing K+)
Severe: >6.5 mmol/L or presence of
ECG changes • Peaked T waves
• Widened QRS

Causes • Flattened P waves

• Increased intake: Rare unless renal • PR prolongation

impairment • Sine wave → VF/asystole
• Decreased excretion: CKD, AKI,
hypoaldosteronism, K+-sparing
Emergency Management
diuretics (e.g. spironolactone),
ACEi/ARBs, NSAIDs 1. Cardiac membrane stabilization

• Redistribution: Acidosis, insulin o Calcium gluconate 10 mL of 10%

deficiency, beta-blockers, IV over 5–10 min
rhabdomyolysis, tumor lysis, burns, o Onset: immediate; duration: ~30–
crush injuries 60 min
• Pseudohyperkalemia: Hemolysis 2. Shift K+ into cells
during sample collection
o Insulin + glucose: 10 units
Actrapid IV + 50 mL of 50%
Clinical Features dextrose

• Often asymptomatic o Salbutamol: 10–20 mg nebulized

• Neuromuscular: Weakness, flaccid o Sodium bicarbonate: 50 mmol IV

paralysis, paresthesia if acidotic

• Cardiac: Palpitations, syncope, 3. Remove K+ from the body

arrhythmias o Loop diuretics: if volume
overloaded
o Sodium polystyrene sulfonate
(slow)
o Dialysis: if severe or refractory
Monitoring Mnemonic
• Continuous ECG C BIG K Drop
• Repeat K+ every 1–2 hours • Calcium
• Monitor glucose (risk of • Bicarbonate
hypoglycemia post-insulin)
• Insulin
• Glucose
Disposition
• Kayexalate
• Admit if moderate/severe, ECG
• Diuretics/Dialysis
changes, or ongoing cause
• Dialysis if ESRD or refractory
hyperkalemia
 Hypokalemia
Definition Clinical Features
Hypokalemia is a low level of
• Neuromuscular: weakness,
potassium in the blood serum.
fatigue, cramps, hyporeflexia,
Serum potassium <3.5 mmol/L
paralysis (severe)
• Cardiac: arrhythmias
Causes (especially with digoxin),
palpitations
• Increased loss:
• GI: ileus, constipation
o GI losses: vomiting, diarrhea,
NG suction
o Renal losses: diuretics ECG Changes
(especially loop/thiazide),
o Flattened/inverted T waves
hyperaldosteronism,
Cushing’s syndrome, renal o ST depression
tubular acidosis o Prominent U waves
o Excessive sweating o Prolonged QT
• Intracellular shift: o PVCs, VT/VF (severe cases)
o Alkalosis
o Insulin or β-agonist therapy
o Refeeding syndrome
o Hypokalemic periodic
paralysis
• Inadequate intake (rare):
starvation, alcoholism
Severity Classification Complications
• Mild: 3.0–3.5 mmol/L • Life-threatening arrhythmias
• Moderate: 2.5–3.0 mmol/L • Respiratory muscle weakness
• Severe: <2.5 mmol/L • Rhabdomyolysis (rare)

Management Key Emergency Points

• Identify and treat underlying • Always check ECG
cause
• Treat K⁺ <2.5 mmol/L urgently,
• Potassium replacement: especially with
o Oral K⁺ preferred if mild and symptoms/ECG changes
asymptomatic • Consider concurrent Mg²⁺
deficiency
o IV K⁺ for moderate–severe or
symptomatic cases • Monitor K⁺ levels frequently
during replacement
▪ Peripheral line: max 10
mmol/hr
▪ Central line: up to 20
mmol/hr with ECG
monitoring
• Magnesium replacement:
correct concomitant
hypomagnesemia
• Cardiac monitoring: if K⁺ <2.5
mmol/L or symptomatic/ECG
changes
• Avoid glucose-containing
fluids (can worsen
hypokalemia via insulin
release)
 Hypernatremia
Definition Clinical Features
Hypernatremia is a common • Mild: Lethargy, weakness,
electrolyte problem that is irritability
defined as a rise in serum
sodium concentration to a value • Moderate-severe: Confusion,
exceeding 145 mmol/L. seizures, coma
• Signs of volume status:

Etiology o Hypovolemia: Dry mucous

membranes, hypotension,
• Water loss (most common): tachycardia
o Insensible losses (fever, o Euvolemia: Often in
burns) diabetes insipidus
o GI losses (diarrhea, o Hypervolemia: Edema,
vomiting) hypertension
o Diabetes insipidus
(central/nephrogenic)
Investigations
o Osmotic diuresis (e.g.
hyperglycemia) • Serum Na+, osmolality

• Sodium gain (less common): • Urine Na+ and osmolality

o Iatrogenic (hypertonic • Assess fluid status

saline, sodium bicarbonate) • Blood glucose, urea,
o Salt poisoning creatinine
• Consider cortisol, ADH, and
water deprivation test if DI
suspected
Management Principles Monitoring
• Identify and treat underlying • Serum Na+ every 2–4 hours
cause during correction
• Fluid replacement • Strict fluid balance charting
(mainstay): • Neurological status
o Hypovolemic: Start with monitoring
isotonic saline, then switch
to hypotonic fluids (e.g. 5%
dextrose or 0.45% saline) Complications

o Euvolemic/DI: Free water • Seizures, coma

replacement + • Intracerebral hemorrhage
desmopressin (for central • Osmotic demyelination (rare
DI) in hypernatremia)
o Hypervolemic: Diuretics +
• Cerebral edema with rapid
hypotonic fluids correction

Correction Rate
Key Points
• Chronic (>48h): Correct
• Always assess volume status
slowly – max 10 mmol/L/day first
• Acute (<48h): May correct • Rapid correction is dangerous
faster but monitor closely
• Tailor fluid type and rate to
• Rapid correction can cause etiology and volume status
cerebral edema
 Hyponatremia
Definition • Euvolemic: Normal volume;
Hyponatremia is a low excess free water
concentration of sodium in the o Causes: SIADH,
blood. Serum sodium <135 hypothyroidism,
mmol/L psychogenic polydipsia,
drugs (SSRIs,
Classification by Serum Na+ carbamazepine)
Level • Hypervolemic: Na+ and
• Mild: 130–134 mmol/L water gain; more water
retained
• Moderate: 125–129 mmol/L
o Causes: Heart failure,
• Severe: <125 mmol/L cirrhosis, nephrotic
syndrome, CKD
Classification by Duration
• Acute: <48 hours Symptoms (related to rate and
severity):
• Chronic: >48 hours
• Mild: Often asymptomatic

Classification by Volume • Moderate: Nausea,

Status headache, confusion
• Severe/acute: Vomiting,
• Hypovolemic: Na+ and water
loss; more Na+ lost seizures, coma, respiratory
arrest
o Causes: GI loss (vomiting,
diarrhea), diuretics,
adrenal insufficiency
Emergency Assessment Avoid Rapid Correction
• ABCs • Risk of osmotic demyelination
• Neurological exam syndrome (central pontine
myelinolysis)
• Volume status (clinical exam)
• Especially in chronic
• Serum electrolytes, osmolality hyponatremia
• Urine Na+ and osmolality
• Blood glucose, cortisol, thyroid Key Emergency Takeaways
function tests
• Treat acute symptomatic cases
urgently with controlled
Management Principles
hypertonic saline
Symptomatic or severe (<120
• Determine and address
mmol/L or seizures/coma):
underlying cause
o Hypertonic saline (3%) 100 mL
• Avoid overcorrection – monitor
bolus over 10 min; repeat up to
serum Na+ closely during
3 times if needed
treatment
o Aim: Increase serum Na+ by 4–
6 mmol/L in first 6 hrs (not more
than 10–12 mmol/L in 24 hrs)
Asymptomatic or
mild/moderate:
o Treat underlying cause
o Fluid restriction for SIADH
o Salt tablets, loop diuretics with
saline in some cases
o Demeclocycline or vasopressin
antagonists (tolvaptan) for
refractory SIADH
 Hypercalcemia
Definition • Others – prolonged
Serum calcium >10.5 mg/dL immobilization, milk-alkali
(2.6 mmol/L); severe if >14 syndrome, familial
mg/dL (3.5 mmol/L) hypocalciuric
hypercalcemia

Causes
• Primary Clinical Features
hyperparathyroidism – • Neurological: fatigue,
most common outpatient confusion, lethargy, coma
cause • Gastrointestinal: nausea,
• Malignancy – most vomiting, constipation,
common inpatient cause pancreatitis
(PTHrP-secreting tumors, • Renal: polyuria, polydipsia,
bone metastases, dehydration,
myeloma) nephrolithiasis, renal failure
• Drugs – thiazides, lithium, • Cardiac: shortened QT,
vitamin D/A toxicity, arrhythmias, hypertension
theophylline
• Bones: bone pain, fractures
• Endocrine – thyrotoxicosis, (increased resorption)
adrenal insufficiency,
pheochromocytoma
• Granulomatous diseases –
sarcoidosis, TB (↑1α-
hydroxylase activity)
ECG Changes Disposition
• Shortened QT interval • Admit moderate to severe
• Possible arrhythmias (e.g., cases
heart block, bradycardia) • Monitor electrolytes, renal
function, cardiac rhythm
• Follow up for underlying
Emergency Management
diagnosis (e.g., malignancy
1. ABC + Cardiac monitoring workup, PTH level)
2. IV fluids – normal saline 200–
300 mL/h; correct volume
Key Point
depletion
Severe hypercalcemia is a medical
3. Loop diuretics (e.g., emergency due to risk of
furosemide) – after arrhythmias, renal failure, and
rehydration, promote coma.
calciuresis
4. IV bisphosphonates (e.g.,
zoledronic acid, pamidronate)
– inhibit bone resorption;
onset: 24–48 hrs
5. Calcitonin – rapid onset but
short-lived; adjunct therapy
6. Glucocorticoids – useful in
vitamin D-mediated
hypercalcemia (e.g.,
sarcoidosis)
7. Dialysis – for
severe/refractory cases or
renal failure
8. Treat underlying cause
 Hypocalcemia
Definition Clinical Features
Serum calcium <8.5 mg/dL (2.1 • Neuromuscular irritability:
mmol/L) or ionized calcium <1.1
mmol/L (adjusted for albumin). o Perioral numbness,
paresthesias (hands/feet)
o Muscle cramps,
Causes carpopedal spasm
• Hypoparathyroidism (post- o Tetany, laryngospasm
thyroidectomy, autoimmune)
o Seizures
• Vitamin D deficiency
(malnutrition, malabsorption, • Signs:
CKD) o Chvostek’s sign: facial
• Chronic kidney disease (↓ twitching on tapping facial
1,25(OH)₂D, nerve
hyperphosphatemia) o Trousseau’s sign: carpal
• Acute pancreatitis spasm with BP cuff
inflation
• Sepsis
• Cardiac: prolonged QT
• Massive transfusion (citrate interval, arrhythmias
binds calcium)
• Chronic features (in long-
• Drugs: bisphosphonates, standing cases): brittle nails,
loop diuretics, phenytoin, dry skin, cataracts
calcitonin
• Magnesium deficiency
(impairs PTH secretion)
Investigations Chronic/Asymptomatic
• Serum total and ionized Management
calcium • Oral calcium supplements
• Serum phosphate, • Vitamin D (cholecalciferol
magnesium, PTH, vitamin D or calcitriol)
• Renal function, LFTs • Monitor for recurrence or
• ECG: prolonged QT, overcorrection
possible arrhythmias (hypercalcemia)

Emergency Management Key Points

• Symptomatic or severe • Always check and correct

(<1.9 mmol/L ionized magnesium in refractory
calcium): cases

o IV calcium gluconate 10 • Calcium chloride is more

mL of 10% solution over potent but irritant – use via
10 minutes central line if needed

o Repeat if symptoms • Prolonged QT may lead to

persist; follow with torsades de pointes –
continuous infusion if monitor ECG closely
needed
• Correct magnesium
deficiency
• Treat underlying cause
• Monitor: ECG, calcium
levels, symptoms
5 Gastrointestinal
Emergencies

• Upper GI Bleeding
• Lower GI Bleeding
• Acute Pancreatitis
• Perforated Peptic Ulcer
• Bowel Obstruction
• Acute Appendicitis
• Mesenteric Ischemia
 Upper GI Bleeding
Definition Initial Assessment &
Bleeding originating proximal to Resuscitation
the ligament of Treitz (esophagus,
• ABC approach
stomach, duodenum)
• Secure airway if altered
Common Causes sensorium or active vomiting
• Esophageal: Varices, Mallory- • IV access – two large-bore
Weiss tear, esophagitis cannulas
• Gastric: Peptic ulcer (most • Fluid resuscitation: crystalloids
common), erosive gastritis, • Blood transfusion if
gastric cancer hemodynamically unstable or
• Duodenal: Duodenal ulcer Hb <7 g/dL (target Hb ~7–8 g/dL)
• Others: Dieulafoy’s lesion, • Monitor vitals, urine output
angiodysplasia, aorto-enteric • Risk stratification: Rockall or
fistula (rare) Glasgow-Blatchford score

Clinical Features
• Hematemesis (vomiting of fresh
blood or coffee-ground
material)
• Melena (black, tarry stools)
• Hematochezia (if brisk upper GI
bleed)
• Features of shock: tachycardia,
hypotension, pallor, altered
sensorium
• History of NSAID/alcohol use,
liver disease
Investigations Disposition
• CBC, PT/INR, LFT, RFT, blood • Admit high-risk patients to ICU
group & crossmatch • Monitor for rebleeding
• Upper GI endoscopy (diagnostic
• Address underlying cause (e.g.,
& therapeutic) – within 24 hrs
H. pylori eradication, alcohol
• ECG, troponins in elderly/at-risk cessation, stop NSAIDs)
patients

Management
Pharmacologic:
o IV PPI (e.g., pantoprazole 80
mg bolus + infusion)
o Octreotide (especially in
suspected variceal bleeding)
o Antibiotics in cirrhotics (e.g.,
ceftriaxone)
Endoscopic Therapy:
o Thermal coagulation, clipping,
injection therapy for ulcers
o Band ligation or sclerotherapy
for varices
Other Options:
o Sengstaken-Blakemore tube
(temporary variceal control)
o TIPS for refractory variceal
bleeding
o Angiographic embolization or
surgery in unstable patients or
failed endoscopy
 Lower GI Bleeding
Definition • Ischemic colitis
Bleeding originating distal to the
• Infectious colitis
ligament of Treitz (i.e., from the
small intestine, colon, rectum, or • Post-polypectomy bleeding
anus)

Initial Assessment
Clinical Presentation • ABCs (Airway, Breathing,
• Hematochezia (bright red or Circulation)
maroon blood per rectum) • IV access ×2 large bore
• Melena (if slow, proximal bleed) • Monitor vitals, urine output
• Abdominal pain, tenesmus, • Bloods: CBC, coagulation
diarrhea profile, renal function, LFTs,
• Signs of shock (tachycardia, type & crossmatch
hypotension, pallor, syncope) • Rectal exam, proctoscopy if
hemorrhoids/fissures
suspected
Common Causes
• Diverticular disease (most
common in elderly)
• Angiodysplasia
• Hemorrhoids
• Anal fissures
• Colorectal cancer or polyps
• Inflammatory bowel disease
(IBD)
Resuscitation Management
• Fluid resuscitation with • Supportive care and
crystalloids monitoring
• Blood transfusion if • Endoscopic therapy: clipping,
hemodynamically unstable or cautery, injection (epinephrine)
Hb < 7–8 g/dL
• Angiographic embolization for
• Correct coagulopathy if active bleeding sites
present
• Surgery (segmental colectomy)
• NPO (nil per os) status if refractory or life-threatening
bleeding

Diagnostic Approach Disposition

• Colonoscopy (diagnostic and • Admit to monitored setting
therapeutic) (ICU if unstable)
• CT angiography (if ongoing • Serial hemoglobin monitoring
bleeding and hemodynamically
• Consider GI/surgical
stable)
consultation early
• Radionuclide scan (for
intermittent/slow bleeds) Key Points
• Surgical exploration (if • Hematochezia can rarely
massive bleeding not originate from an upper GI
controlled) source – consider NG tube
aspiration if in doubt
• Early colonoscopy within 24
hours improves diagnostic
yield and reduces recurrence
• Ongoing bleeding despite
endoscopic or angiographic
therapy warrants surgical
evaluation
 Acute Pancreatitis
Definition Clinical Features
Acute inflammation of the
• Severe epigastric pain radiating
pancreas due to premature
to back
activation of pancreatic enzymes,
leading to autodigestion. • Nausea, vomiting
• Fever

Causes • Abdominal tenderness,

guarding
(GET SMASHED mnemonic)
• Hypotension (if severe)
• Gallstones
• Cullen’s sign (periumbilical
• Ethanol (alcohol)
discoloration)
• Trauma
• Grey Turner’s sign (flank
• Steroids discoloration)
• Mumps (and other infections)
• Autoimmune diseases
• Scorpion sting
• Hyperlipidemia/hypercalcemia
• ERCP
• Drugs (e.g., azathioprine,
thiazides, valproate)
Diagnosis Management
• Serum amylase and lipase: • Supportive care (mainstay):
>3x upper limit (lipase more o IV fluids (aggressive
specific) hydration)
• Imaging: o NPO → then gradual
o USG: to detect gallstones refeeding
o CT abdomen (contrast- o Analgesia (e.g., opioids)
enhanced): for diagnosis o Oxygen if needed
and severity
• Antibiotics: Only if infected
• Ranson’s criteria or necrosis
Modified Glasgow score for
severity assessment • ERCP: If gallstones with
cholangitis
• CRP: marker of severity
(>150 mg/L after 48 hrs) • Surgery/intervention: For
complications like infected
necrosis or pseudocyst
Complications
• Local: Pseudocyst, necrosis,
abscess, hemorrhage
Disposition
• Systemic: ARDS, shock,
renal failure, DIC, sepsis • Mild: Admit to ward,
supportive care
• Severe: ICU care with organ
support if needed
 Perforated Peptic Ulcer
Definition Clinical Features
A perforated peptic ulcer is a full-
• Sudden onset severe epigastric
thickness defect in the wall of the
pain
stomach or duodenum due to
peptic ulcer disease, leading to • Pain may radiate to the
leakage of gastric or duodenal shoulder (diaphragmatic
contents into the peritoneal cavity. irritation)
• Board-like abdominal rigidity
(peritonitis)
Etiology
• Nausea, vomiting
• Helicobacter pylori infection
• Hypotension, tachycardia
• NSAID use (signs of shock)
• Smoking and alcohol
• Reduced or absent bowel
• Stress-related mucosal damage sounds
• Zollinger-Ellison syndrome
Investigations
Sites • Erect abdominal X-ray: Free air
under diaphragm
• Duodenum (most common)
(pneumoperitoneum)
• Gastric antrum
• CT abdomen: Most sensitive
• Lesser curvature of the for detecting perforation
stomach
• Blood tests: Leukocytosis,
elevated serum amylase,
deranged electrolytes
• Endoscopy: Not done in acute
setting
Management Complications
Initial Resuscitation:
• Generalized peritonitis
• NPO • Septic shock
• IV fluids
• Intra-abdominal abscess
• Broad-spectrum antibiotics
• Fistula formation
• Nasogastric tube • Recurrent ulcer disease
• Proton pump inhibitors
• Analgesia
Prognostic Factors
Surgical Treatment: • Age >70 years
• Graham patch repair (omental
• Delay in surgery >24 hours
patch): Common procedure
• Coexisting medical illnesses
• Definitive anti-ulcer surgery
(e.g., vagotomy ± drainage • Presence of shock or sepsis on
procedure): Rarely done presentation
nowadays
• Laparoscopic repair:
Increasingly preferred
• Peritoneal lavage to clear
contamination
Post-op Care:
• Continue PPI
• H. pylori eradication therapy if
positive
• Avoid NSAIDs, smoking, alcohol
• Regular follow-up for
recurrence
 Bowel Obstruction
Definition o Ileus: Lack of peristalsis, often post-
surgery or due to electrolyte
Bowel obstruction refers to a blockage
imbalance.
that prevents the normal movement of
contents through the intestines. It can
occur in the small or large bowel and can
Clinical Features
be partial or complete.
• Pain: Colicky abdominal pain,
Causes intermittent in nature, worsening
over time.
Mechanical Obstruction:
• Distension: Abdominal bloating or
o Adhesions (post-surgical): Most
visible distension.
common cause in developed
countries. • Vomiting: Early in small bowel
obstruction, may be bile-stained;
o Hernias: Intestinal contents pushed
later, feculent.
through a weak spot in the
abdominal wall. • Constipation/Absence of stool or
gas: Incomplete obstruction may
o Intussusception: One part of the
allow some passage of stool.
intestine slides into the next,
common in children. • Signs of Dehydration: Dry mucous
membranes, tachycardia,
o Volvulus: Twisting of the intestine,
hypotension.
causing obstruction.
o Tumors: Benign or malignant
growths obstructing the bowel Physical Examination
lumen. • Inspection: Visible bowel loops,
o Gallstones: Can cause obstruction if abdominal distension.
they pass into the intestines. • Palpation: Tenderness, possibly a
o Incarcerated or strangulated palpable mass or hernia.
hernias: Can lead to tissue ischemia • Auscultation: High-pitched bowel
and necrosis. sounds early, followed by absent
Non-Mechanical (Functional) bowel sounds in late obstruction.
Obstruction: • Percussion: Tympany due to trapped
o Neurogenic causes: Spinal cord air.
injury, diabetic neuropathy.
Diagnosis Surgical:
• Clinical Examination: History Indicated if:
and physical exam. o Complete obstruction or
• Imaging: bowel ischemia is suspected.
o X-ray (Abdominal): May o Incarcerated hernia or
show dilated loops of bowel, strangulation.
air-fluid levels.
o Failed conservative
o CT scan: More sensitive, management.
identifying location, cause, Antibiotics:
and complications (e.g.,
strangulation). Administered if perforation or
bowel ischemia is suspected.
o Ultrasound: Useful for
pediatric cases or in
diagnosing intussusception. Complications
• Bowel perforation: Can lead to
Management peritonitis.

Conservative: • Strangulation: Leads to bowel

ischemia and necrosis.
o Nasogastric Tube: For
decompression and to reduce • Dehydration and electrolyte
vomiting. imbalance.

o IV Fluids: Correct dehydration • Sepsis: Particularly if

and electrolyte imbalance. perforation occurs.

o Monitoring: Regular
monitoring of vital signs and Prevention
fluid balance.
Early diagnosis and management
o Foley catheter: For of risk factors, such as hernia
monitoring urinary output. repair and post-operative care to
avoid adhesions.
 Acute Appendicitis
Definition o Progression: Pain localizes to
the right lower quadrant (RLQ)
Inflammation of the appendix, a
(somatic pain) after 6–12
small tubular structure attached
hours.
to the cecum, typically caused by
obstruction of the appendiceal o Signs:
lumen. ▪ McBurney's Point
Tenderness: 1/3 distance
from the anterior superior
Etiology
iliac spine (ASIS) to the
Most commonly due to fecaliths umbilicus.
(hardened stool), lymphoid
▪ Rovsing's Sign: Pain in
hyperplasia, or foreign bodies. It
the RLQ when palpating
can also result from infection or
the left lower quadrant.
tumors.
▪ Psoas Sign: Pain on
extension of the right hip
Pathophysiology (suggests retrocecal
Obstruction leads to increased appendix).
intraluminal pressure, ischemia, ▪ Obturator Sign: Pain on
bacterial overgrowth, and internal rotation of the
eventually perforation if untreated. right hip (suggests pelvic
appendix).

Clinical Features o Systemic Signs: Fever,

elevated white blood cell
o Initial Symptoms:
count (WBC), and mild
Periumbilical pain (visceral),
tachycardia.
nausea, vomiting, and
anorexia.
Differential Diagnosis Surgical:
o Gastroenteritis, urinary tract Appendectomy (open or
infection (UTI), ectopic laparoscopic). Delayed surgery
pregnancy, ovarian torsion, may be required in cases of
mesenteric adenitis, and perforation with abscess
Crohn’s disease. formation.
Antibiotics:
Investigations
Preoperative broad-spectrum
o Physical Examination: Focus antibiotics, typically covering
on tenderness, guarding, and Gram-negative and anaerobic
rebound tenderness. organisms (e.g., ceftriaxone +
o Laboratory Tests: Elevated metronidazole).
WBC, with a left shift
indicating bacterial infection.
Complications
o Imaging:
o Perforation: Leads to
▪ Ultrasound: First-line in peritonitis and widespread
children and pregnant sepsis.
women.
o Abscess Formation: Often
▪ CT Scan: Gold standard requires drainage.
in adults, particularly for
o Postoperative: Wound
atypical presentations.
infection, ileus, and rarely,
▪ MRI: Used in pregnant bowel obstruction.
women when CT is
contraindicated.
Prognosis
Management Generally excellent with timely
Conservative: surgical intervention. Mortality
increases with delayed diagnosis,
o Antibiotics if the diagnosis is
perforation, and sepsis.
uncertain or in patients who
are unfit for surgery.
 Mesenteric Ischemia
Definition • Venous thrombosis: Clot
Mesenteric ischemia is a condition formation in the mesenteric veins,
caused by inadequate blood flow to often associated with
the small or large intestines, hypercoagulable states.
resulting in tissue damage. It can be
• Hypoperfusion: Decreased blood
acute or chronic.
flow due to shock or cardiac
failure.
Types
1. Acute mesenteric ischemia Risk Factors
(AMI): Sudden onset, often life-
• Atherosclerosis, atrial fibrillation,
threatening, caused by arterial
heart failure, hypercoagulable
occlusion or venous thrombosis.
states, recent surgeries, or
2. Chronic mesenteric ischemia trauma.
(CMI): Gradual reduction in
• Risk factors for venous
blood flow, typically due to
thrombosis include malignancy,
atherosclerosis or narrowing of
hypercoagulable disorders, and
mesenteric arteries.
intra-abdominal infections.
3. Mesenteric venous thrombosis:
Blood clot in the mesenteric
veins leading to impaired venous Clinical Features
drainage and intestinal ischemia. • Acute mesenteric ischemia:
Severe, sudden abdominal pain
out of proportion to physical
Etiology
findings, vomiting, diarrhea,
• Arterial occlusion: Embolic bloody stools (late sign),
(most common, e.g., from heart), hypotension, tachycardia.
thrombotic (due to
• Chronic mesenteric ischemia:
atherosclerosis), or non-occlusive
Postprandial abdominal pain
(related to low perfusion states
(intestinal angina), weight loss,
like shock).
diarrhea, nausea, bloating.
Diagnosis o Endovascular treatment:
Angioplasty or stenting in some
• Clinical suspicion is key,
cases.
especially in patients with known
risk factors. Chronic mesenteric ischemia:
• Imaging studies: o Revascularization: Surgical
bypass or angioplasty/stenting
o CT angiography: Gold
for arterial narrowing.
standard for diagnosing arterial
occlusion. o Supportive care: Nutritional
support and management of
o MRI angiography: Alternative
symptoms.
for arterial studies.
o Doppler ultrasound: Can
assess mesenteric artery Prognosis
blood flow.
• Poor in acute cases if not treated
o Mesenteric angiography: promptly (mortality rate >60%).
Used in the evaluation of both
• Chronic mesenteric ischemia has
diagnosis and intervention.
a better prognosis with timely
• Lab tests: Leukocytosis, lactate intervention.
elevation, metabolic acidosis (in
severe cases).
Key Points
• Early diagnosis is critical; patients
Management
with acute mesenteric ischemia
Acute mesenteric ischemia: can deteriorate rapidly.
o Resuscitation: IV fluids, • Surgical and endovascular
broad-spectrum antibiotics if interventions are often required
bowel necrosis is suspected. for arterial occlusion.
o Surgical intervention: • Chronic mesenteric ischemia
Embolectomy or requires revascularization to
thrombectomy for arterial prevent further bowel injury and
occlusion, resection of improve quality of life.
necrotic bowel.
6 Toxicological
Emergencies
• Acetaminophen (Paracetamol) Toxicity
• Opioid Poisoning (including heroin,
fentanyl, etc.)
• Carbon Monoxide Poisoning
• Organophosphate Poisoning
• Alcohol Poisoning (Ethyl and Isopropyl)
• Aspirin (Salicylate) Poisoning
• Benzodiazepine Overdose
• Iron Toxicity
• Snake
• Insect Bites
 Acetaminophen (Paracetamol) Toxicity

Introduction o Peak Symptoms (24-72 hours):

Symptoms can progress to liver
Acetaminophen (also known as
dysfunction, jaundice,
paracetamol) is a widely used
coagulopathy, and renal failure.
analgesic and antipyretic. Toxicity is
Elevated liver enzymes (AST, ALT)
one of the most common causes of
and bilirubin levels are seen.
drug-induced liver failure.
o Late Symptoms (3-7 days): Severe
cases may progress to acute liver
Mechanism of Toxicity failure with encephalopathy,
o Under normal circumstances, coagulopathy, and multi-organ
acetaminophen is metabolized in failure, requiring liver
the liver via conjugation with sulfate transplantation in some cases.
and glucuronide, forming non-toxic
metabolites. A small fraction is
Diagnosis
metabolized by the cytochrome
P450 enzyme system into a highly o History: Obtain a detailed history of
reactive intermediate, NAPQI (N- acetaminophen ingestion,
acetyl-p-benzoquinone imine). At including time and dose.
therapeutic doses, this is detoxified
o Laboratory Tests: Liver function
by glutathione.
tests (AST, ALT, bilirubin),
o In overdose, glutathione stores are prothrombin time (PT), and renal
depleted, and excess NAPQI binds function tests.
to cellular proteins, leading to
o Acetaminophen Levels:
hepatocellular injury, inflammation,
Measurement of plasma
and eventually liver failure.
acetaminophen concentration is
critical. The Rumack-Matthew
nomogram can help predict the risk
Presentation
of hepatotoxicity based on plasma
o Early Symptoms (0-24 hours): acetaminophen levels and the time
Initially, patients may be elapsed since ingestion.
asymptomatic or have nonspecific
symptoms like nausea, vomiting,
malaise, and abdominal pain.
Management Prevention
o Early Intervention: Activated o Advise patients to adhere to the
charcoal can be administered if recommended dose of
the ingestion occurred within 1- acetaminophen and avoid
2 hours to reduce absorption. concomitant use of alcohol or
o N-acetylcysteine (NAC): The other hepatotoxic drugs.
antidote of choice for o Educate patients regarding the
acetaminophen toxicity. NAC potential risks of exceeding the
works by replenishing maximum daily dose.
glutathione stores and
preventing further liver damage.
It should be administered as Prognosis
soon as possible, ideally within o In mild to moderate cases, with
8 hours of ingestion, though it early NAC administration, the
can still be effective if given prognosis is generally good.
later.
o In severe cases (acute liver
o Supportive Care: In addition to failure), the prognosis is
NAC, management may include guarded, with a high risk of
IV fluids, electrolyte correction, mortality without a liver
and monitoring for signs of liver transplant.
failure.
o Liver Transplantation:
Indicated in cases of acute liver
failure with complications such
as coagulopathy,
encephalopathy, and renal
failure, or when liver
transplantation is the only
option for survival.
Opioid Poisoning (Heroin, Fentanyl, etc.)
Definition Clinical Features
Opioid poisoning occurs due to the • CNS depression: Sedation,
overdose of opioid drugs, including drowsiness, confusion, or coma.
heroin, fentanyl, morphine, oxycodone,
• Respiratory depression:
hydrocodone, and prescription painkillers,
Hypoventilation, shallow breathing, or
leading to potentially life-threatening
apnea (most critical sign).
respiratory depression, altered mental
status, and other systemic effects. • Miosis: Pinpoint pupils (classic sign
but not always present, especially with
fentanyl overdose).
Mechanism of Action
• Hypotension: Often secondary to
Opioids bind to opioid receptors (mu, respiratory depression and decreased
kappa, delta) in the central nervous systemic vascular resistance.
system and peripheral tissues, producing
• Bradycardia: Common, especially
analgesia, sedation, euphoria, and
with severe respiratory depression.
respiratory depression. Overdose results
in exaggerated pharmacological effects, • Hypothermia: May be noted in severe
primarily respiratory depression. cases.

• Pulmonary edema: Can develop due

to respiratory failure.
Causes

• Heroin: Illicitly used opioid with high

potential for overdose, especially due Diagnosis
to variability in purity. • Clinical suspicion: History of opioid
• Fentanyl: Synthetic opioid 50-100 use or suspected overdose.
times more potent than morphine. • Physical exam: Look for signs of CNS
Overdose is common due to its depression, respiratory rate, and pupil
potency and the presence of fentanyl- size.
laced heroin.
• Toxicology screening: Urine drug
• Prescription opioids: Misuse of pain screen can confirm presence of
medications such as oxycodone, opioids, but it may not detect synthetic
hydrocodone, and morphine. opioids like fentanyl or carfentanil.
• Other synthetic opioids: Carfentanil, Confirmation by specific tests may be
tramadol, etc., may also lead to needed.
overdose.
Management Complications
• Airway and Breathing: Ensure • Respiratory failure: Leading to
airway protection. Provide hypoxia, brain injury, or death if
supplemental oxygen, consider untreated.
intubation if necessary.
• Cardiac arrest: Due to profound
• Naloxone (Narcan): Opioid respiratory depression.
antagonist that can rapidly reverse
• Pulmonary edema: Secondary to
the effects of opioid overdose.
hypoxic injury.
Administer intravenously (0.4–2
mg), intramuscularly, or • Coma: Prolonged due to severe
intranasally (4 mg). Repeat doses overdose.
every 2–3 minutes as needed.
Prevention
• Monitor: Continuous monitoring
of respiratory and cardiovascular • Public education: Raise
status. If respiratory depression awareness about the risks of
persists despite naloxone, opioid misuse, including heroin
additional doses may be required. and fentanyl.

• Supportive care: IV fluids for • Opioid stewardship: Prescribe

hypotension and hypoperfusion, opioids judiciously and monitor for
and sedation for agitation. signs of misuse.

• Fentanyl overdose: Higher doses • Naloxone availability: Ensure

of naloxone (up to 10 mg or more) naloxone access to at-risk
may be required. Continuous individuals, including first
monitoring for several hours is responders, family members, and
essential due to the prolonged people using opioids.
effect of fentanyl.
Prognosis
With prompt and appropriate
treatment (especially naloxone
administration), the prognosis is
generally good. However, delays in
treatment or multiple drug overdoses
may increase the risk of morbidity
and mortality.
 Carbon Monoxide Poisoning
Definition Clinical Features
Carbon monoxide (CO) poisoning
• Mild poisoning: Headache,
occurs when CO, a colorless,
dizziness, nausea, vomiting, and
odorless gas, is inhaled, leading to
fatigue.
hypoxia due to its binding with
hemoglobin, forming • Moderate poisoning: Confusion,
carboxyhemoglobin (COHb). dyspnea, tachypnea, chest pain,
and weakness.
• Severe poisoning: Loss of
Pathophysiology
consciousness, seizure,
CO has a 200-250 times higher
arrhythmias, hypotension, and
affinity for hemoglobin than oxygen,
coma.
reducing the oxygen-carrying
capacity of blood. It also disrupts • Chronic exposure: Memory
cellular respiration by binding to deficits, irritability, and cognitive
cytochrome c oxidase in dysfunction.
mitochondria, leading to cellular
hypoxia. Symptoms arise due to Diagnosis
tissue hypoxia, particularly in the • Clinical suspicion based on
brain and heart. exposure history.
• Carboxyhemoglobin levels
Sources of CO (normal: <3% in non-smokers,
<10% in smokers). Levels above
• Motor vehicle exhaust 25-30% are typically
• Faulty gas heaters, stoves, and symptomatic.
boilers • Pulse oximetry can be
• Wood-burning stoves and misleading as it cannot
fireplaces differentiate COHb from
oxyhemoglobin.
• Smoke inhalation during fires
• ABG (arterial blood gas) may
show a normal oxygen saturation
with high COHb levels.
Management Prevention
• Immediate removal from Regular maintenance of
exposure to CO source. appliances that burn fuel, proper
• Oxygen therapy: High-flow ventilation in homes, and
oxygen via a non-rebreather installation of CO detectors.
mask is the first step. This
reduces COHb half-life from 4-
Key Points
6 hours (room air) to 1-2 hours
(100% oxygen). • CO poisoning is a medical
emergency; early recognition
• Hyperbaric oxygen (HBO):
and treatment are critical.
Indicated for severe cases (e.g.,
coma, neurological symptoms, • Always consider CO poisoning
or high COHb levels >25%) or in patients with unexplained
pregnancy. neurological symptoms,
especially after exposure to
• Supportive care: IV fluids, potential sources of CO.
monitoring of vitals, and
management of arrhythmias if
necessary.

Prognosis
• Good in mild cases: Complete
recovery expected with prompt
treatment.
• Poor in severe cases:
Neurological sequelae (e.g.,
cognitive dysfunction,
movement disorders) may
persist, and death can occur
without treatment.
Organophosphate Poisoning
Introduction Nicotinic Effects:
Organophosphates (OPs) are
o Muscle twitching
commonly used as pesticides and
insecticides, which can cause toxic o Weakness, paralysis (especially
effects when absorbed into the body. respiratory muscles)
They inhibit acetylcholinesterase, o Fasciculations
leading to an accumulation of
Central Nervous System (CNS):
acetylcholine at cholinergic synapses.
o Anxiety, confusion
o Seizures
Pathophysiology
OPs bind irreversibly to o Coma
acetylcholinesterase at nerve
endings, preventing the breakdown of
acetylcholine. This results in Diagnosis
continuous stimulation of cholinergic • History: Exposure to
receptors, leading to overstimulation organophosphates (pesticide,
of muscarinic and nicotinic receptors. insecticide).
• Clinical Features: Presence of
Clinical Features cholinergic symptoms.

Muscarinic Effects (SLUDGE): • Laboratory Tests:

o Salivation o Measurement of plasma or

red blood cell
o Lacrimation
acetylcholinesterase activity
o Urination (decreased activity).
o Defecation o OPs or their metabolites in
urine (confirmatory).
o Gastrointestinal distress
• Additional tests: Arterial blood gas
o Emesis (vomiting)
(ABG) to assess respiratory status.
o Bradycardia, hypotension
o Miosis (pinpoint pupils)
Management Monitoring:
Decontamination: o Continuous monitoring of vital
o Remove contaminated signs (heart rate, blood
clothing, wash skin with soap pressure, respiratory rate).
and water. o Electrocardiogram (ECG) for
arrhythmias.
o Irrigate eyes if exposed.
o Repeat blood gas and
Antidote Administration:
electrolytes as needed.
o Atropine: A muscarinic
antagonist that reverses the
effects of acetylcholine Prognosis
excess. Start with high doses
Early and aggressive treatment
and titrate to effect (usually
improves outcomes. Delayed
until drying of secretions and
treatment or severe exposure can
normalization of heart rate).
lead to respiratory failure,
o Pralidoxime (2-PAM): A seizures, and death. Recovery can
cholinesterase reactivator, take weeks, and long-term
effective if administered early neurological effects may occur in
(within 24 hours). It reverses severe cases.
both muscarinic and nicotinic
effects by reactivating
acetylcholinesterase. Prevention

o Diazepam: For seizure • Proper use of personal

control. protective equipment (PPE)
when handling
Supportive Care:
organophosphates.
o Maintain airway, breathing,
• Avoiding exposure, especially
and circulation (ABCs).
for agricultural workers.
o Intubation and mechanical
ventilation may be required for
respiratory failure.
o IV fluids for hypotension.
Alcohol Poisoning (Ethyl and Isopropyl)
Etiology and Pathophysiology • Isopropyl Alcohol Poisoning:
Causes more pronounced CNS
• Ethyl alcohol (ethanol) and
depression than ethanol, with
isopropyl alcohol (isopropanol)
symptoms like dizziness,
are common causes of alcohol
hypotension, bradycardia, and
poisoning.
respiratory depression.
• Ethanol is found in alcoholic Respiratory alkalosis is often
beverages, while isopropanol is seen.
used in household products like
rubbing alcohol.
Diagnosis
• Both alcohols are CNS
depressants, causing respiratory • History and Clinical
depression, hypotension, and Examination: Important in
altered mental status. suspecting alcohol poisoning.
• Ethanol is metabolized by alcohol • Blood Alcohol Concentration
dehydrogenase to acetaldehyde (BAC): Ethanol poisoning is
and then to acetic acid. diagnosed by a high BAC, but BAC
Isopropanol is metabolized to does not correlate with severity in
acetone, which can have toxic all cases.
effects.
• Toxicology Screen: Confirm
presence of alcohol in the blood.
For isopropyl alcohol, blood tests
Clinical Features
will show elevated acetone levels.
• Ethanol Poisoning: Symptoms
• Arterial Blood Gas (ABG): Check
depend on the level of
for metabolic acidosis (from
intoxication: mild (slurred speech,
ethanol) or respiratory alkalosis
ataxia, dizziness), moderate
(from isopropanol).
(nausea, vomiting, confusion,
hypotension), and severe (coma, • Other Lab Tests: Check glucose
respiratory depression, levels, liver and renal function,
hypothermia, seizures). and electrolytes.
Management Complications
General Supportive Care: • Ethanol: Seizures, respiratory
depression, aspiration pneumonia,
ABCs (airway, breathing, circulation),
hypothermia, arrhythmias, and
monitor vitals, and manage hypoxia with
Wernicke-Korsakoff syndrome.
oxygen if necessary.
• Isopropanol: Hypotension,
Ethanol Poisoning:
arrhythmias, CNS depression,
o Gastric Decontamination: If within 1 respiratory depression, and acetone
hour, activated charcoal can be given. toxicity (causing breath odor).
Avoid gastric lavage unless indicated.
o IV Fluids: Correct dehydration and
Prognosis
electrolyte imbalances.
• Ethanol Poisoning: Generally good
o Thiamine (Vitamin B1): Administer to
with prompt treatment, but the risk
prevent Wernicke-Korsakoff
increases with delayed intervention
syndrome.
or severe intoxication.
o Correction of Hypoglycemia:
• Isopropanol Poisoning: Can be more
Administer glucose if hypoglycemia is
severe, especially in cases with high
suspected.
levels of acetone, but the prognosis is
o Alcohol Dehydrogenase Inhibition: also generally good with treatment.
Administer fomepizole or ethanol in
severe cases to prevent metabolism
of ethanol to toxic metabolites. Prevention
o Hemodialysis: Indicated in severe • Educate patients about the dangers
cases (e.g., coma, respiratory failure, of excessive alcohol consumption
or extremely high BAC). and the proper use of products
containing isopropanol.
Isopropyl Alcohol Poisoning:
• Enforce measures to prevent access
o Supportive Care: IV fluids, monitor
to harmful alcohol-containing
vitals, and oxygen supplementation if
substances, especially in vulnerable
needed.
populations (e.g., children).
o Correction of Acidosis: Bicarbonate
may be used to treat metabolic
acidosis.
o Avoid Dialysis: Isopropanol is less
effectively removed by dialysis than
ethanol.
Aspirin (Salicylate) Poisoning
Introduction Severe Poisoning:
Aspirin poisoning occurs when there is
o Respiratory distress or failure
an overdose of acetylsalicylic acid
(ASA), a nonsteroidal anti-inflammatory o Seizures
drug (NSAID), leading to toxicity. It can o Coma
result from acute or chronic overdose
and is common in both pediatric and o Cardiovascular instability
adult populations. (hypotension, arrhythmias)
o Renal failure

Pathophysiology
Aspirin toxicity leads to metabolic Diagnosis
acidosis and respiratory alkalosis.
• Clinical History: History of aspirin
Salicylates uncouple oxidative
ingestion (acute or chronic)
phosphorylation in mitochondria,
leading to increased heat production, • Blood Tests:
increased oxygen consumption, and o Serum salicylate levels: Critical
the production of lactic acid, causing levels are > 40 mg/dL
metabolic acidosis. They also stimulate
the respiratory center, causing o ABG (arterial blood gas):
hyperventilation, which results in Metabolic acidosis and
respiratory alkalosis. respiratory alkalosis
o Electrolytes: Hypokalemia,
hypoglycemia
Clinical Features
o Renal function tests (creatinine,
Early Symptoms: BUN) for renal failure
o Nausea, vomiting, abdominal pain assessment

o Tinnitus (ringing in the ears) • Urinary pH: Alkaline urine can

enhance salicylate elimination.
o Hyperventilation (due to
respiratory alkalosis)
o Sweating and dehydration
o Dizziness, confusion, agitation
Management Complications
Initial Stabilization: • Respiratory failure
o Assess airway, breathing, and • Seizures
circulation (ABC)
• Renal failure
o Administer oxygen if hypoxia is
• Cerebral edema
present
• Cardiac arrhythmias
o IV fluids for hydration and
correction of electrolyte
imbalances Prevention
Decontamination: • Proper storage of aspirin to prevent
o Activated charcoal (if within 1–2 pediatric ingestion
hours of ingestion) • Awareness of potential overdose in
o Gastric lavage (if large overdose and adults, especially in cases of
within 1 hour) chronic use for pain or
inflammation
Enhanced Elimination:
o Alkalinization of urine: Sodium
bicarbonate (IV) is used to increase Prognosis
renal elimination of salicylates by The prognosis depends on the timing of
alkalinizing urine. treatment and the severity of poisoning.
With early intervention, the prognosis is
o Hemodialysis: Indicated for severe
generally good. However, severe
cases (levels > 100 mg/dL), or if
poisoning, particularly in the presence
there is refractory acidosis, renal
of renal failure or CNS involvement,
failure, or CNS involvement.
carries a higher risk of mortality.
Symptomatic Management:
o Benzodiazepines for seizures or
agitation
o Monitor and correct electrolyte
imbalances (hypokalemia,
hypoglycemia)
o Supportive care (intensive
monitoring in severe cases)
Benzodiazepine Overdose
Overview Diagnosis
Benzodiazepines are commonly
• Clinical History: Assessment
used for their anxiolytic, sedative,
of drug history, time of
and muscle-relaxant properties.
ingestion, and potential co-
Overdose typically results from
ingestion (e.g., alcohol or
intentional or accidental
opioids).
ingestion, leading to CNS
depression. Common agents • Physical Examination: Vital
include diazepam, lorazepam, signs, neurological status, and
alprazolam, and clonazepam. respiratory function.
• Toxicology Screening: Urine
toxicology tests may detect
Clinical Features
benzodiazepines, but they do
• Central Nervous System: not quantify the level of
Drowsiness, confusion, ataxia, intoxication.
slurred speech, impaired
coordination, respiratory
depression, coma,
hypoventilation.
• Cardiovascular: Hypotension,
bradycardia.
• Other: Nausea, vomiting,
dizziness, myoclonus, and
rarely, seizures (particularly in
withdrawal or in combination
with other substances).
Management Prognosis
Most benzodiazepine overdoses
1. Airway Protection: Ensure a
are self-limited and resolve with
patent airway. If the patient is
supportive care. Severe cases may
drowsy or comatose, consider
require prolonged ventilation or
intubation if there is respiratory
critical care monitoring.
depression.
Flumazenil can be helpful, but the
2. Supportive Care: Provide risk of seizure or withdrawal in
oxygen, monitor vital signs, and dependent individuals must be
establish intravenous access. considered.
3. Flumazenil (Benzodiazepine
Antagonist): Administered
Prevention
intravenously in severe cases of
overdose, especially if the • Educate patients about proper
diagnosis is unclear. It can use, especially in combination
rapidly reverse sedation, but with other CNS depressants.
may precipitate withdrawal
• Monitor for signs of misuse or
symptoms or seizures in
overdose in patients on long-
chronic users or if co-ingested
term benzodiazepine therapy.
with other substances like
tricyclic antidepressants. Use
with caution.
4. Activated Charcoal: Consider
within 1 hour of ingestion in
alert patients with a known
overdose to reduce absorption.
5. Intravenous Fluids: Correct
hypovolemia and hypotension
with IV fluids.
 Iron Toxicity (Iron Overdose)
Introduction • Phase 3 (12-48 hours):
Iron toxicity occurs when there is an This phase is marked by systemic
excessive accumulation of iron in the toxicity, including metabolic
body, often due to the ingestion of a acidosis, shock, liver failure
large quantity of iron supplements. It (jaundice, coagulopathy), and
can lead to severe organ damage, cardiac dysrhythmias.
particularly in children, and requires
• Phase 4 (2-4 weeks):
prompt medical intervention.
Chronic effects may include liver
cirrhosis, gastrointestinal
scarring, and growth retardation,
Pathophysiology
particularly in children.
Excess iron in the body leads to the
formation of free radicals, which can
cause cellular damage, especially in
Diagnosis
the gastrointestinal system, liver, and
heart. The iron overload causes • History: Recent ingestion of iron-
oxidative stress, damaging tissues containing substances, especially
and leading to multi-organ failure. in children.
• Serum Iron Levels: Levels greater
than 500 mcg/dL are suggestive of
Clinical Features
toxic ingestion.
• Phase 1 (0-6 hours):
• Other Laboratory Tests:
Initial symptoms are non-specific
and include nausea, vomiting, o Complete blood count (CBC)
diarrhea, abdominal pain, and may show a leukocytosis in
lethargy. severe toxicity.

• Phase 2 (6-24 hours): o Liver function tests and

Improvement or apparent clinical coagulation profiles may
stability may occur, but iron indicate liver damage.
toxicity can still progress to
severe outcomes.
Management Prognosis
Prognosis depends on the timing of
• Decontamination:
intervention. Early recognition and
If the ingestion was within 1-2
treatment are critical to reducing
hours, activated charcoal may
mortality and long-term
not be effective. Gastric lavage
complications. With prompt
can be considered in severe
treatment, most patients recover
cases. Whole bowel irrigation
without permanent organ damage.
may be used for large
ingestions.
• Iron Chelation Therapy: Prevention
Deferoxamine is the mainstay
• Keep iron-containing
of treatment. It binds free iron,
supplements out of reach of
forming a complex that is
children.
excreted in the urine. It is
typically used when serum iron • Educate caregivers on the
levels are high or when dangers of iron toxicity and
symptoms are severe. proper storage of medications.

• Supportive Care:
o IV fluids for shock Key Points
management. • Iron toxicity is more common in
o Correct metabolic acidosis. children, often due to accidental
ingestion.
o Monitor for organ
dysfunction and provide • It has a biphasic course, with
treatment accordingly (e.g., initial non-specific symptoms
dialysis in severe renal followed by a critical phase with
failure). possible multi-organ failure.

• Hemodialysis: • Early diagnosis and treatment

May be used in severe cases to with iron chelation
remove iron and deferoxamine (deferoxamine) can prevent
complexes, particularly if renal severe outcomes.
failure is present.
 Snake Bite
Types of Snakes o Renal effects: Acute
• Venomous snakes: Elapidae kidney injury due to
(cobras, kraits, mambas), hemolysis or direct
Viperidae (vipers, pit vipers), venom effects.
and Hydrophidae (sea o Myotoxic effects: Muscle
snakes). weakness, pain, and
• Non-venomous snakes: rhabdomyolysis.
Usually pose little threat;
bites are more of a Diagnosis
mechanical injury.
• Clinical suspicion: History of
snake exposure,
Clinical Features characteristic bite marks.
• Local effects: Immediate • Laboratory tests: Blood
pain, swelling, redness, and coagulation profile (PT, APTT),
bleeding at the bite site. complete blood count (CBC),
Necrosis and blistering may renal function tests (BUN,
occur. creatinine), and urine
• Systemic effects: myoglobin levels.

o Neurotoxic effects: • Serum venom detection:

Ptosis, difficulty Available in some settings.
swallowing, respiratory
distress.
o Hemotoxic effects:
Coagulopathy, bleeding,
hemolysis, and organ
failure.
Management Prevention
Initial management: Avoidance of snake-prone areas,
o Resuscitation: ABC (airway, wearing protective clothing, and
breathing, circulation), IV using snake repellents.
fluids for shock.
o Wound care: Clean the bite Prognosis
site with soap and water, Depends on the species,
avoid tourniquets, and do amount of venom injected, and
not try to suck out venom. time to medical intervention.
o Antivenom: Administer as Early administration of
soon as possible in cases of antivenom improves survival
severe envenomation or if rates.
symptoms worsen. Specific
antivenom for the species is
preferred.
o Analgesia: Pain control with
opioids or NSAIDs.
Monitoring:
Close observation for signs of
progression of symptoms (e.g.,
respiratory failure, renal failure,
coagulopathy).
Supportive care:
Intubation if respiratory distress
occurs, dialysis in case of renal
failure, blood products for
coagulopathy.
 Insect Bites
Introduction Clinical Presentation
Insect bites are common in everyday
Local Reactions:
clinical practice, with symptoms ranging
from mild irritation to severe allergic o Redness, swelling, and itching at the
reactions. Proper diagnosis and site of the bite.
management are essential to avoid o Pain or burning sensation
complications. (particularly from bee or wasp stings).
o Papules or wheals (mosquito bites,
Types of Insects Involved flea bites).

1. Mosquitoes: Can transmit diseases like Systemic Reactions:

malaria, dengue, Zika, and o Anaphylaxis (most common with bee
chikungunya. or wasp stings).
2. Bees/Wasps: Stings cause pain, o Fever, chills, and malaise (associated
swelling, and can trigger allergic with tick bites or mosquito-borne
reactions (anaphylaxis). diseases).
3. Ants: Some species, like fire ants, can o Secondary infections due to
cause severe reactions due to venom. scratching.
4. Fleas: Bites typically cause itching and
irritation; can lead to secondary Diagnosis
bacterial infections. • History: Inquire about the type of
5. Ticks: Can transmit Lyme disease, insect, timing of exposure, and
Rocky Mountain spotted fever, and geographic location (for disease-related
other infections. risks).

6. Bedbugs: Cause localized itching and • Clinical Examination: Assess for signs
redness, often in clusters or lines. of infection, systemic reactions, or
unusual findings (e.g., ticks attached to
the skin).
• Investigations:
o Blood tests (in cases of systemic
illness, e.g., malaria, dengue).
o Skin tests (for suspected allergy).
o Culture if infection is suspected.
Management Prevention
Mild Reactions: • Use insect repellent (DEET,
picaridin).
o Antihistamines (oral or topical) for
itching and swelling. • Wear protective clothing when in
areas with high insect activity.
o Topical corticosteroids for
inflammation. • Avoid peak insect activity times
(dawn and dusk).
o Ice packs for pain relief and to
reduce swelling. • Take antimalarial medications
when traveling to endemic areas.
Severe Reactions/Anaphylaxis:
• Remove standing water to reduce
o Immediate administration of
mosquito breeding sites.
epinephrine (adrenaline).
o Oxygen therapy and airway
management if required. Key Points
o Hospitalization for observation • Most insect bites are self-limiting,
and further treatment (e.g., but some can cause significant
antihistamines, corticosteroids). systemic reactions.
Infections: • Early recognition of severe
reactions (e.g., anaphylaxis) is
o For secondary bacterial
critical for patient management.
infections, consider oral
antibiotics. • Appropriate prevention strategies
can significantly reduce the
o Tetanus prophylaxis if there is a
incidence of insect bites and
puncture wound.
associated diseases.
Ticks:
o Remove the tick carefully with
fine-tipped tweezers.
o Disinfect the bite site.
o If the tick is attached for an
extended period, consider
prophylactic antibiotics to prevent
Lyme disease, especially in
endemic areas.
7 Trauma
Emergencies

• Blunt Trauma
• Penetrating Trauma
• Fractures
• Dislocations
• Burns (Thermal, Electrical,
Chemical)
• Crush Injuries
• Amputation
 Blunt Trauma
Definition Primary Survey Goals
Injury caused by non-penetrating
• Identify and treat life-threatening
force resulting in damage to internal
conditions
organs, bones, or soft tissues
without an open wound. • Rapid assessment and
resuscitation

Common Mechanisms
Secondary Survey
• Road traffic accidents
• Detailed head-to-toe evaluation
• Falls
• History (AMPLE: Allergies,
• Assaults
Medications, Past history, Last
• Sports injuries meal, Events leading to injury)
• Blast injuries (secondary blunt
effects)
Common Injuries
• Head: Concussion, skull fracture,
Initial Assessment (ABCDE intracranial hemorrhage
Approach)
• Chest: Rib fractures, pulmonary
A – Airway with cervical spine
contusion, pneumothorax,
protection
hemothorax, cardiac tamponade
B – Breathing and ventilation
C – Circulation with hemorrhage • Abdomen: Solid organ injury
control (spleen, liver, kidney), hollow
D – Disability (neurological status: viscus injury
AVPU, GCS) • Pelvis: Fractures with high risk of
E – Exposure and environmental bleeding
control
• Extremities: Long bone fractures,
compartment syndrome
• Spine: Vertebral fractures, spinal
cord injury
Investigations Complications
• FAST (Focused Assessment • Hemorrhagic shock
with Sonography in Trauma) • Organ failure
• X-rays (CXR, pelvis, limbs)
• Sepsis
• CT scan (especially for head,
• ARDS
chest, and abdominal injuries)
• DIC
• Blood tests (CBC, crossmatch,
lactate, coagulation profile) • Missed injuries

Management Principles Key Points

• Resuscitate per ATLS protocol • Blunt trauma may have hidden

internal injuries
• Control external bleeding
• Hypotension in blunt trauma =
• Stabilize fractures
assume bleeding until proven
• Monitor vitals, urine output, and otherwise
neurological status • Continuous reassessment is
• Early surgical consultation if vital
internal bleeding suspected
• Tertiary survey to identify
• Definitive management missed injuries
depends on injury severity and
site
 Penetrating Trauma
Definition Immediate Priorities
Penetrating trauma occurs when an
• Control bleeding (direct pressure,
object pierces the skin and enters
tourniquets if needed)
the body, creating an open wound
and potentially damaging internal • Prevent contamination (cover with
organs, vessels, and tissues. sterile dressing)
• Avoid removing embedded
Common Causes objects in pre-hospital/ED setting
• Stab wounds (knives, sharp • Ensure rapid IV access and initiate
objects) fluid resuscitation if hypotensive
• Gunshot wounds
• Impalement injuries Investigations
• Blast injuries with embedded • Blood tests: CBC, crossmatch,
fragments coagulation profile

Initial Assessment (ATLS • Imaging: FAST, X-ray

approach): (chest/abdomen), CT scan if
stable
Primary Survey (ABCDE)
• E-FAST: To detect pneumothorax,
o Airway: Assess patency, look for
hemothorax, pericardial effusion,
obstruction or injury
intra-abdominal bleeding
o Breathing: Check for
pneumothorax, hemothorax,
sucking chest wound
o Circulation: Control external
bleeding, assess for shock
o Disability: Rapid neurological
assessment (GCS)
o Exposure: Fully expose to
assess all injuries
Management Antibiotics
• Chest injuries: Tube • Broad-spectrum antibiotics for
thoracostomy for open wounds, contaminated or
pneumothorax/hemothorax; intra-abdominal injuries
surgical intervention if massive
bleeding or cardiac tamponade
Definitive Care
• Abdominal injuries: Exploratory
laparotomy if unstable or signs of • Often requires surgical
peritonitis intervention

• Neck injuries: Evaluate zones I– • May involve trauma team, general

III; surgical exploration if hard surgery, orthopedics,
signs of vascular/airway injury neurosurgery, or cardiothoracic
surgery
• Extremity injuries: Assess
neurovascular status; surgical
repair as needed Disposition
• Head injuries: CT brain; • Admit to ICU/ward depending on
neurosurgical intervention if stability
required
• Ongoing monitoring and
supportive care
Signs of Life-Threatening Injuries
• Hemodynamic instability
Key Points
• Airway compromise
• Always assume underlying organ
• Evisceration injury in penetrating trauma
• Expanding hematoma • Early recognition and rapid
• Active bleeding despite pressure surgical consultation are critical

• Neurological deficit • Follow structured trauma

protocols (ATLS principles)
Tetanus Prophylaxis
• Administer according to
immunization status and wound
type
 Fractures
Definition • Abnormal mobility
Break or disruption in the
• Open wound in compound
continuity of a bone, typically due
fractures
to trauma.
• Neurovascular compromise
Classification (assess distal pulses, capillary
refill, sensation, movement)
By skin involvement:
o Closed (simple) – skin intact
Special Considerations
o Open (compound) – bone
pierces skin, risk of infection • Pediatric fractures – risk of
growth plate involvement
By pattern:
(Salter-Harris classification)
o Transverse, oblique, spiral,
• Elderly patients – high risk of
comminuted, impacted,
hip fractures, consider
greenstick (children)
osteoporosis
By displacement:
• Open fractures – urgent
o Displaced vs. Non-displaced debridement, IV antibiotics,
By location: orthopedic consult

o Diaphyseal, metaphyseal, • Compartment syndrome –

epiphyseal, intra-articular monitor for pain out of
proportion, tense limb,
Clinical Features paresthesia, pallor,
• Pain and tenderness pulselessness

• Swelling • Fat embolism syndrome –

especially in long bone
• Deformity fractures (triad: hypoxia,
• Loss of function neurological symptoms,
petechial rash)
• Crepitus
Initial Emergency Management (ATLS Definitive Management
approach)
• Depends on fracture type and
1. Primary survey – ABCDE location
2. Immobilize the fracture • Options:
o Splint the limb in position found o Conservative: immobilization
with cast/splint
o Avoid unnecessary manipulation
o Surgical: external fixation,
3. Control bleeding
internal fixation (plates, screws,
o Apply direct pressure nails)
o Avoid tourniquets unless life-
threatening
Disposition
4. Neurovascular assessment
• Most closed fractures: discharge with
o Reassess after splinting follow-up
5. Pain management • Open, displaced, neurovascularly
o IV analgesia preferred compromised, or complex fractures:
admit and refer to orthopedics
6. Tetanus prophylaxis for open urgently
fractures
7. Antibiotics for open fractures (e.g.,
IV cefazolin ± gentamicin)
8. Imaging
o X-rays: at least two views (AP
and lateral)
o CT/MRI if needed
 Dislocations
Definition Clinical Features
Displacement of bones at a joint • Severe pain
from their normal anatomical • Deformity
position.
• Swelling
• Loss of function
Common Sites
• Joint held in a fixed position
• Shoulder (most common)
• Possible associated
• Elbow
neurovascular injury (check
• Fingers distal pulses and nerve
function)
• Hip
• Knee (less common)
Diagnosis
• Ankle
• Clinical examination

Causes • Confirm with X-ray (AP and

lateral views)
• Trauma (falls, accidents)
• CT/MRI if fracture-dislocation
• Sports injuries or recurrent cases suspected
• Congenital or pathological joint
laxity
Emergency Management Red Flags
• Do not attempt reduction • Open dislocation
without imaging unless limb- • Suspected vascular
threatening situation compromise
• Analgesia and sedation
• Associated fracture
• Prompt closed reduction (e.g.
• Irreducible dislocation
Hippocratic or Kocher’s for
shoulder)
• Post-reduction X-ray to confirm Follow-up
alignment • Orthopedic evaluation
• Neurovascular reassessment • Physiotherapy for joint strength
after reduction and mobility
• Immobilization with splint or • Surgical stabilization if
sling recurrent
• Orthopedic referral

Complications
• Recurrent dislocation
• Neurovascular injury (e.g.
axillary nerve in shoulder
dislocation)
• Associated fractures
• Joint stiffness
• Avascular necrosis (especially
in hip dislocation)
Burns (Thermal, Electrical, Chemical)
Classification by Depth • Moderate burns: 10–20% TBSA
• Superficial (1st degree): • Major burns: >20% TBSA or
Epidermis only; red, painful, no involving face, hands, feet,
blisters; heals in 3–6 days perineum, or inhalation injury
• Partial thickness (2nd degree):
Thermal Burns
o Superficial: Epidermis + upper
dermis; blisters, moist, very • Cause: Flame, scald, contact
painful with hot objects
o Deep: Deeper dermis; less • Features: Local tissue damage
pain, dry or waxy; may need depending on temperature &
grafting duration
• Full thickness (3rd degree): • Management:
Entire dermis; painless, leathery, o Stop the burning process
charred; requires grafting
o Cool with running water (not
• Fourth degree: Extends to ice)
muscle/bone
o Pain control
o Fluid resuscitation (if >10%
Classification by Extent – TBSA
TBSA in children or >15% in
(Total Body Surface Area)
adults)
• Rule of 9s (Adults): Head 9%,
o Parkland Formula: 4 mL ×
each arm 9%, each leg 18%,
body weight (kg) × TBSA%
front of trunk 18%, back 18%,
(Half in first 8 h, rest over 16 h)
perineum 1%
o Tetanus prophylaxis, wound
• Lund and Browder chart: More
care, consider escharotomy
accurate in children
for circumferential burns
• Minor burns: <10% TBSA in
adults
Electrical Burns • Management:
• Cause: Contact with electrical o Immediate and prolonged
current (low or high voltage) irrigation with water (at least
• Features: Entry and exit 30 min)
wounds; deep tissue injury may o Brush off dry powders before
be worse than visible damage; irrigation
risk of arrhythmias,
o Avoid neutralizing agents
rhabdomyolysis
o Identify chemical if possible
• Complications: Cardiac
(MSDS)
arrhythmias (monitor ECG),
compartment syndrome, acute o Treat systemic toxicity if
kidney injury from myoglobinuria present (e.g., hydrofluoric
acid – calcium gluconate)
• Management:
o Ophthalmology review if eye
o ABCs and cardiac monitoring
involvement
o Aggressive IV fluids (target
high urine output to prevent
myoglobin nephropathy) General Emergency Approach

o Monitor CK, renal function, • Primary survey (ABCDE)

urine color • Remove clothing/jewelry
o Fasciotomy if compartment • Ongoing monitoring: vitals, urine
syndrome suspected output
• Inhalation injury: Suspect with
Chemical Burns facial burns, singed nasal hairs,
• Cause: Acids (coagulative hoarseness; may need early
necrosis), alkalis (liquefactive intubation
necrosis – deeper), industrial • Referral to burn center: Major
agents burns, inhalation injury,
• Features: Severity depends on circumferential burns,
agent, concentration, duration of electrical/chemical burns,
contact children, comorbidities
 Crush Injuries
Definition Clinical Features
Crush injury refers to damage
• Swollen, tense, tender limb
resulting from prolonged
compressive force to a body part, • Skin changes: bruising,
commonly the limbs. It may lead to blistering, pallor
local tissue damage and systemic • Loss of sensation, motor
complications, especially if weakness
compression exceeds 1 hour.
• Compartment syndrome signs
• Systemic: hypotension,
Causes tachycardia, hematuria
• Road traffic accidents (myoglobinuria), metabolic
acidosis
• Building collapses
• Industrial/workplace accidents
Complications
• Natural disasters (e.g.,
earthquakes) • Crush syndrome (traumatic
rhabdomyolysis): AKI,
hyperkalemia, DIC
Pathophysiology
• Compartment syndrome
• Prolonged compression →
• Sepsis, multiorgan failure
muscle ischemia → necrosis
• Limb ischemia/gangrene
• Release of intracellular contents
(K⁺, myoglobin, phosphate, uric
acid)
• Reperfusion injury on removal of
compression
• Can lead to crush syndrome
(systemic complications)
Investigations • Debridement/amputation if
needed
• CBC, renal function tests,
electrolytes • Dialysis for renal failure
• Serum creatine kinase (↑) • Tetanus prophylaxis, antibiotics
if contaminated
• Urinalysis (myoglobinuria)
• ECG (hyperkalemia signs)
• Imaging: X-ray (fracture), Key Points
USG/Doppler if vascular injury • Early fluid resuscitation is life-
suspected saving
• Monitor for crush syndrome and
Management compartment syndrome
Prehospital:
• Anticipate and treat
• Early fluid resuscitation (before hyperkalemia promptly
release of compression)
• Multidisciplinary care often
• Avoid tourniquet unless needed (surgery, nephrology,
uncontrolled bleeding critical care)
Emergency Department:
• High-flow oxygen
• Aggressive IV fluids (NS or RL)
to prevent AKI
• Correct electrolyte imbalances
(especially hyperkalemia:
calcium gluconate, insulin +
dextrose, bicarbonate)
• Monitor urine output (>1
mL/kg/hr); consider mannitol or
diuretics
• Fasciotomy if compartment
syndrome
 Amputation
Definition Levels of Amputation
Surgical removal of all or part of a
• Upper limb: Finger, hand,
limb or extremity.
forearm, above elbow
• Lower limb: Toe, foot, below
Types
knee (BKA), above knee (AKA),
• Traumatic amputation – Due to hip disarticulation
injury (e.g., industrial, road
traffic accidents)
Initial Management in Traumatic
• Surgical amputation –
Amputation
Performed intentionally due to
non-salvageable limb (e.g., • ABCs (Airway, Breathing,
gangrene, severe infection) Circulation)
• Control hemorrhage (direct
Indications for Emergency pressure, tourniquet if
Amputation necessary)
• Life-threatening sepsis (e.g., wet • IV access, fluid resuscitation
gangrene, necrotizing fasciitis)
• Pain management
• Irreversible ischemia (e.g., acute
• Broad-spectrum IV antibiotics
limb ischemia, frostbite)
• Tetanus prophylaxis
• Crush injuries with non-viable
limbs • Preserve amputated part (wrap
in moist gauze, place in sterile
• Malignancy (if rapidly
bag, keep cool—not directly on
progressing with systemic
ice)
effects)
• Failed revascularization
attempts
Surgical Principles Key Points
• Remove all devitalized tissue • Life and limb-saving priorities
• Ensure adequate stump dictate emergency amputation
coverage and vascularity • Preserve function and facilitate
rehabilitation
• Shape stump for prosthesis
• Multidisciplinary approach
• Wound may be closed
improves outcomes
primarily or delayed (in case of
infection)

Complications
• Bleeding, infection, stump
necrosis
• Phantom limb pain
• Contractures
• Psychological impact

Postoperative Care
• Pain control
• Wound care
• Early physiotherapy
• Psychological support
• Planning for prosthesis fitting
and rehabilitation
8 Infectious
Emergencies

• Sepsis and Septic Shock

• Necrotizing Fasciitis
• Toxic Shock Syndrome
• Acute Epiglottitis
• Infective Endocarditis with
Embolic Complications
 Sepsis and Septic Shock
Definition Risk Factors

• Sepsis: A life-threatening organ • Extremes of age (neonates, elderly)

dysfunction caused by a dysregulated
• Immunocompromised states (e.g.,
host response to infection.
diabetes, cancer, HIV, post-
• Septic Shock: A subset of sepsis with transplantation)
persistent hypotension despite adequate
• Chronic illnesses (e.g., cirrhosis, renal
fluid resuscitation, associated with
failure)
increased mortality.
• Invasive devices (e.g., catheters,
ventilators)
Pathophysiology
• Recent surgeries or trauma
• Sepsis is initiated by infection, leading to
an exaggerated immune response with
the release of pro-inflammatory Clinical Features
mediators (e.g., cytokines, TNF-α, IL-6).
Sepsis:
• These mediators cause widespread
o Fever or hypothermia
endothelial dysfunction, vasodilation,
increased vascular permeability, and o Tachycardia, tachypnea
coagulation abnormalities.
o Hypotension (early stages)
• Septic shock occurs when this response
o Altered mental status (confusion,
causes profound circulatory failure,
agitation)
leading to inadequate tissue perfusion
and oxygenation. o Oliguria or anuria

o Warm or cold extremities (depends on

phase)
Causes
Septic Shock:
• Bacterial infections: Most common (e.g.,
pneumonia, urinary tract infections, intra- o Persistent hypotension despite fluid
abdominal infections). resuscitation

• Fungal infections: Common in o Cold extremities, weak pulse, mottling

immunocompromised patients. (late stage)

• Viral infections: Less common, but can o Multi-organ dysfunction (renal failure,
cause sepsis in immunocompromised hepatic failure, coagulopathy)
individuals.

• Other: Parasitic infections, infections due

to medical devices.
Diagnosis o Vasopressors (e.g., norepinephrine)
for hypotension unresponsive to
• Clinical Diagnosis: Based on the
fluids.
presence of infection and signs of organ
dysfunction. o Inotropes (e.g., dobutamine) if
cardiac output is low.
• SIRS Criteria: Sepsis is suspected with
two or more of the following: Source Control
o Temperature >38°C or <36°C Surgical drainage or removal of infected
devices.
o Heart rate >90 bpm
o Respiratory rate >20/min or Prognosis
PaCO2 <32 mmHg
• Early recognition and treatment are
o White blood cell count >12,000 or critical. Mortality is high in septic shock
<4,000 cells/μL (30-50%) and increases with age,
• Sepsis-3 Criteria: comorbidities, and delayed
intervention.
o SOFA (Sequential Organ Failure
Assessment) score ≥2, indicating • Organ dysfunction and multi-organ
organ dysfunction. failure are common in severe sepsis or
septic shock, leading to prolonged
o Lactate >2 mmol/L (marker of recovery.
poor perfusion).

• Blood Cultures: Obtained before Prevention

antibiotics, if possible.
• Hand hygiene, vaccination
• Imaging: To identify the source of (pneumococcal, influenza), and
infection. appropriate use of antibiotics in at-risk
populations.
Management
• Careful management of invasive
Initial Resuscitation: devices to prevent hospital-acquired
infections.
o Early goal-directed therapy (within 3
hours): administer broad-spectrum
antibiotics, IV fluids (30 mL/kg), and Key Points
vasopressors if hypotension persists. • Sepsis is a medical emergency
o Antibiotics: Broad-spectrum empiric requiring immediate intervention to
antibiotics within 1 hour, adjusted prevent organ failure and death.
based on culture results. • The key to survival in septic shock is
Supportive Therapy: early recognition, rapid antibiotic
administration, and aggressive
o Oxygen supplementation to maintain supportive care.
oxygen saturation >90%.
 Necrotizing Fasciitis (NF)
Definition Risk Factors
Necrotizing fasciitis is a severe, Diabetes, immunocompromised
rapidly progressive soft tissue states (e.g., cancer, HIV,
infection characterized by corticosteroid therapy), trauma,
widespread tissue necrosis, often surgery, intravenous drug use,
involving the fascial plane, poor vascular supply, and chronic
subcutaneous tissues, and wounds.
muscles. It is a life-threatening
condition requiring urgent
intervention. Clinical Features
• Early Symptoms: Sudden
onset of pain, fever, and
Etiology
swelling at the site of infection.
• Bacterial Causes: Pain is disproportionate to the
o Group A Streptococcus visible signs of infection.
(GAS), Clostridium • Progression: Rapid worsening
perfringens, with erythema, warmth, and
Staphylococcus aureus marked tenderness. Skin
(including MRSA), changes include blistering,
Escherichia coli, discoloration (cyanosis,
Bacteroides, Vibrio mottling), and skin necrosis.
vulnificus.
• Signs of Systemic Toxicity:
• Polymicrobial Infections: Sepsis, hypotension, multi-
Common, with both aerobic organ failure.
and anaerobic organisms
• Classic Features: Crepitus
involved.
(gas in the tissue), foul-smelling
discharge, and shock in
advanced stages.
Diagnosis o For specific pathogens
(e.g., Vibrio or Clostridium),
• Clinical Diagnosis: High index
tailored therapy is needed.
of suspicion based on rapid
progression and severity of • Supportive Care: Fluid
symptoms. resuscitation, vasopressors for
• Imaging: X-ray, CT scan, or MRI shock, and intensive care
to assess gas within tissues or support for organ dysfunction.
extent of fascial involvement.
• Laboratory: Blood cultures, Prognosis
wound cultures, and laboratory
• Mortality rate remains high,
findings indicating severe
especially if diagnosis is
infection (e.g., elevated white
delayed.
blood cell count, metabolic
acidosis). • Prognosis depends on the
speed of intervention, the
Management patient's underlying health, and
the extent of tissue
• Surgical Intervention: Urgent involvement.
debridement of necrotic tissue
is the cornerstone of treatment.
Multiple surgeries may be Prevention
required.
• Early recognition and treatment
• Antibiotic Therapy: Broad- of infections, especially in high-
spectrum antibiotics should be risk individuals.
initiated immediately, targeting
• Proper wound care and hygiene
both gram-positive, gram-
to reduce the risk of soft tissue
negative, and anaerobic
infections.
organisms. Typical regimen:
o Penicillin (for GAS) plus
Clindamycin plus
Gentamicin or
Metronidazole for
anaerobes.
 Toxic Shock Syndrome (TSS)
Definition • It can result in multi-organ
dysfunction due to the systemic
Toxic Shock Syndrome (TSS) is a
inflammatory response.
severe, life-threatening condition
caused by bacterial toxins, most
commonly Staphylococcus aureus
Clinical Features
and Streptococcus pyogenes. It is
characterized by rapid onset of fever, • Fever: High-grade, sudden onset.
rash, hypotension, and multi-organ • Rash: Diffuse erythematous rash,
involvement. resembling sunburn, often
peeling after a few days.
Etiology • Hypotension: Marked, leading to
• Most cases are associated with shock.
Staphylococcus aureus • Multisystem Involvement:
(produces toxic shock syndrome
o Renal: Acute renal failure.
toxin-1, TSST-1) or Streptococcus
pyogenes (produces pyrogenic o Hepatic: Hepatic
exotoxins). dysfunction (elevated liver
enzymes).
• Risk factors include tampon use,
surgical wounds, skin infections, o Cardiovascular: Myocardial
post-partum period, and any dysfunction.
foreign body like nasal packing or o Gastrointestinal: Nausea,
surgical drains. vomiting, diarrhea.
o Neurological: Confusion,
Pathophysiology seizures, or coma in severe
• Bacterial toxins act as cases.
superantigens, triggering a
massive release of cytokines,
leading to widespread
inflammation, vasodilation, and
shock.
Diagnosis • Surgical intervention:
Drainage of infected wounds or
• Clinical diagnosis based on
abscesses.
major criteria (fever, rash,
hypotension, multi-organ
involvement) and minor criteria Prognosis
(e.g., gastrointestinal
symptoms, liver dysfunction). With prompt treatment, the
prognosis can be good, though
• Laboratory tests: Positive
mortality rates remain significant
cultures for Staphylococcus
(up to 30% in severe cases).
aureus or Streptococcus
Delayed diagnosis and treatment
pyogenes, or detection of toxin
increase the risk of fatality.
in blood or exudate.

Prevention
Management
• Proper hygiene, especially in
• Supportive care: IV fluids,
post-operative and post-
vasopressors, and intensive
partum care.
monitoring.
• Avoid prolonged use of
• Antibiotics: Empiric broad-
tampons or foreign body
spectrum antibiotics, typically
insertion.
vancomycin or clindamycin, to
target Staphylococcus aureus • Early recognition and treatment
and Streptococcus pyogenes. of soft tissue infections can
Clindamycin helps inhibit toxin help prevent progression.
production.
• Toxin neutralization: IV
immunoglobulin (IVIG) may be
used in severe cases.
 Acute Epiglottitis
Definition • Tripod position: Sitting upright
Acute epiglottitis is a potentially life- with the neck extended to improve
threatening condition characterized airflow.
by rapid inflammation and swelling
• Voice changes: Muffled or hoarse
of the epiglottis, leading to airway
voice (dysphonia).
obstruction. It commonly affects
children but can also occur in adults. • Anxiety and agitation in children
due to difficulty breathing.
• Cyanosis in severe cases.
Etiology
• Most commonly caused by
Haemophilus influenzae type b Diagnosis
(Hib) infection, though it can also • Clinical Diagnosis: History and
be caused by other bacteria such physical examination.
as Streptococcus pneumoniae,
• Laryngoscopy (if performed
Staphylococcus aureus, and
cautiously) may reveal a swollen,
Group A Streptococcus.
erythematous epiglottis.
• Viral infections, trauma, or burns
• X-ray of the neck (lateral view):
can also contribute to epiglottitis.
Shows a "thumbprint sign,"
indicating an enlarged epiglottis.
Clinical Features • Blood cultures or throat swabs
• Rapid onset of fever, sore throat, may identify the causative
and difficulty swallowing organism.
(dysphagia).
• Stridor (high-pitched wheezing)
and respiratory distress.
• Drooling due to difficulty
swallowing.
Management Prevention
• Airway Management: • Hib Vaccination: The
Immediate attention to airway widespread use of the Hib
patency is critical. If airway vaccine has significantly
compromise is severe, reduced the incidence of
intubation or emergency epiglottitis caused by
tracheostomy may be required. Haemophilus influenzae type b.
• Antibiotic Therapy: Empiric • Post-exposure Prophylaxis:
broad-spectrum IV antibiotics Rifampin for close contacts of
(e.g., ceftriaxone or cefotaxime children diagnosed with Hib
plus clindamycin) to cover epiglottitis.
bacterial pathogens, with
adjustment based on culture
results. Prognosis

• Corticosteroids: May be • With prompt recognition and

administered to reduce management, the prognosis is
inflammation, although the role generally good, though it
remains debated. remains a medical emergency
due to the potential for rapid
• Hydration and supportive airway obstruction.
care: IV fluids and monitoring
of vital signs. • Mortality rates have
significantly decreased due to
vaccination and improved
management, but it remains a
critical condition in the
absence of intervention.
 Infective Endocarditis
Definition • Vegetations can embolize to distant
organs via the bloodstream, leading
Infective endocarditis (IE) is an
to complications such as stroke,
infection of the endocardial surface of
renal infarction, or pulmonary
the heart, often involving heart valves.
embolism.
Embolic complications occur when
infected material, such as fragments of
thrombi or infected valve vegetations,
Clinical Features
break off and travel through the
bloodstream to distant organs. • Fever: Common symptom, but may
be absent in some cases
(especially in
Etiology immunocompromised patients).
• Microorganisms: The majority of • Murmur: New or changing heart
cases are caused by bacteria, most murmur, often heard in the mitral or
commonly Streptococcus and aortic valve.
Staphylococcus species. Fungal
• Embolic Events: Symptoms
and other pathogens can also
depend on the organ affected (e.g.,
cause IE.
stroke, limb ischemia, or
• Risk Factors: Valvular heart abdominal pain from renal
disease, prosthetic heart valves, infarction).
intravenous drug use (IVDU),
• Osler's Nodes: Painful, raised
immunocompromised states,
lesions on fingers or toes.
diabetes, and congenital heart
defects. • Janeway Lesions: Painless,
erythematous lesions on palms or
soles.
Pathophysiology
• Roth Spots: Retinal hemorrhages
• Infection starts on the heart valve with pale centers.
or endocardial surface.
• Splenomegaly: Enlargement of the
• Formation of a vegetation (mass of spleen due to emboli.
microorganisms, platelets, fibrin)
on the valve.
Diagnosis Embolic Complications
• Blood Cultures: Essential for • Neurological: Stroke is the most
identifying causative organisms. At common embolic complication,
least 3 sets should be obtained resulting from emboli traveling to the
before starting antibiotics. brain. Symptoms include sudden-
onset weakness, confusion, or
• Echocardiogram: Transesophageal
speech disturbances.
echocardiography (TEE) is more
sensitive than transthoracic • Renal: Embolism to the kidneys can
echocardiography (TTE) in detecting cause renal infarction, presenting as
vegetations and valve involvement. flank pain, hematuria, or acute renal
failure.
• Modified Duke Criteria: Used for
diagnosing IE, based on clinical, • Pulmonary: Embolic material can
microbiological, and lodge in the lungs, causing
echocardiographic findings. pulmonary embolism or infarction,
leading to pleuritic chest pain,
shortness of breath, or hemoptysis.
Management
• Peripheral Vascular: Limb ischemia
• Antibiotics: Empiric antibiotic or gangrene may occur due to
therapy should be initiated emboli traveling to the arteries.
immediately after blood cultures are
obtained. Common regimens
include a combination of Prognosis
ceftriaxone or vancomycin and
• Mortality rates can be high,
gentamicin. The regimen is adjusted
especially in those with prosthetic
based on culture results.
valves, heart failure, or severe
• Surgical Intervention: Indicated in embolic complications.
cases of large vegetations,
• Early diagnosis and treatment
persistent infection despite
improve outcomes significantly.
antibiotics, heart failure due to valve
destruction, or major embolic
events.
• Anticoagulation: Contraindicated in
cases of infective endocarditis with
active embolic events due to the risk
of worsening embolism.
 Obstetric and
9 Gynecological
Emergencies

• Ectopic Pregnancy
• Postpartum Hemorrhage
• Preeclampsia and Eclampsia
• Placental Abruption
• Uterine Rupture
 Ectopic Pregnancy (EP)
Definition Severe symptoms (ruptured
Ectopic pregnancy occurs when a ectopic):
fertilized egg implants and grows
o Acute onset of sharp
outside the uterine cavity, most
abdominal pain
commonly in the fallopian tubes.
o Shoulder tip pain (due to
diaphragmatic irritation)
Risk Factors
o Hypotension, tachycardia
• Previous ectopic pregnancy
o Signs of shock (pallor, fainting,
• Pelvic inflammatory disease (PID) dizziness)
• Tubal surgery
• Intrauterine device (IUD) use Diagnosis
• Assisted reproductive techniques • History & Physical Exam: A high
(ART) index of suspicion in a patient with
risk factors and abdominal pain.
• Endometriosis
• Transvaginal Ultrasound (TVUS):
• Smoking
Main diagnostic tool; may show an
• Age > 35 years empty uterus with a mass in the
• History of tubal surgery or adnexa.
sterilization • Serum hCG levels: Can help in
diagnosis when compared to
normal intrauterine pregnancy
Clinical Features
levels. A rising hCG should
Early symptoms: correlate with a developing
o Amenorrhea (missed period) pregnancy inside the uterus.

o Abdominal pain (usually • Culdocentesis: In cases of

unilateral) suspected rupture with internal
bleeding, aspiration of blood from
o Vaginal bleeding (spotting to the pouch of Douglas can confirm
heavy) hemoperitoneum.
Management • Recurrent ectopic pregnancy:
Risk increases after a previous
Stable patient (non-ruptured,
ectopic.
early diagnosis):
o Medical treatment with
methotrexate, which inhibits Prevention
cell division and resolves the
• Early diagnosis and treatment of
pregnancy.
pelvic infections (e.g., PID).
o Close follow-up of hCG levels
• Counseling on contraceptive
until they return to normal.
use, including options that
Unstable patient (ruptured prevent tubal pregnancy (e.g.,
ectopic or ongoing hemorrhage): IUD).
o Immediate surgical
intervention via laparoscopy
Prognosis
or laparotomy.
• With prompt diagnosis and
o Salpingectomy (removal of the
treatment, the prognosis is
fallopian tube) or
good. However, delayed
salpingostomy (removal of the
diagnosis and rupture increase
ectopic pregnancy while
morbidity and mortality.
preserving the tube).
o Blood transfusion if
necessary.

Complications
• Rupture: Can lead to massive
internal bleeding and life-
threatening hemorrhagic shock.
• Infertility: Scarring of the
fallopian tube may result in
future fertility issues.
 Postpartum Hemorrhage (PPH)
Definition 4.Coagulation Disorders:
Excessive bleeding following
o Conditions like disseminated
childbirth, usually defined as a blood
intravascular coagulation (DIC)
loss of more than 500 mL after
or inherited clotting disorders.
vaginal delivery or more than 1000
mL after cesarean section. o Can be secondary to pregnancy-
related conditions such as
preeclampsia.
Causes
1.Uterine Atony (most common) Risk Factors
o Lack of uterine contraction after • Previous PPH
delivery, leading to failure of
• Multiple pregnancies (multiparity)
blood vessels to constrict.
• Prolonged or rapid labor
o Risk factors: prolonged labor,
overdistended uterus (e.g., • Use of forceps or vacuum
multiple gestation), use of extraction
anesthesia. • Placenta previa or placental
2. Trauma: abruption

o Lacerations or tears in the • Retained placenta

cervix, vagina, or perineum
during delivery. Clinical Presentation
o Uterine rupture or inversion. • Excessive bleeding (visible or
3. Retained Placenta: concealed).
o Part of the placenta or • Hypotension, tachycardia.
membranes remain in the • Pallor, dizziness, confusion, or
uterus, preventing uterine fainting.
contraction and leading to
hemorrhage. • Uterus may be soft, boggy, or
enlarged if atony is present.
Management Surgical Interventions
1. Initial Resuscitation (ABC): • Bimanual compression of the uterus.
o Ensure airway, breathing, and • Balloon tamponade (e.g., Bakri
circulation. balloon).
o Establish large-bore IV access. • Hysterectomy (in cases of severe,
unmanageable hemorrhage).
o Administer crystalloid fluids and
blood products if needed (e.g.,
RBCs, FFP).
Complications
2. Uterine Atony Treatment:
• Hypovolemic shock.
o Fundal massage to stimulate
• Organ failure (due to hypoperfusion).
contraction.
• Anemia and need for transfusion.
o Oxytocin infusion (first-line).
• Coagulopathy.
o Other uterotonic agents:
Misoprostol, ergometrine,
prostaglandins (e.g., carboprost). Prevention
3. Trauma Management: • Active management of the third stage
o Examine for lacerations and repair of labor (oxytocin administration after
them under anesthesia. delivery, controlled cord traction).

o Consider surgical intervention if • Proper antenatal care to manage risk

the trauma is extensive (e.g., factors (e.g., iron supplementation,
uterine rupture). managing placental abnormalities).

4. Retained Placenta Management: • Timely identification and

management of complications during
o Manual removal of placenta under
labor.
anesthesia.
o Curettage if necessary.
Prognosis
o Hysterectomy may be required if
With prompt and appropriate
bleeding persists.
management, most women recover
5. Coagulation Disorder Management: without long-term complications.
However, delays in treatment can lead to
o Correct underlying coagulopathy
severe morbidity and mortality.
(e.g., FFP, platelet transfusions).
o Consider antifibrinolytics (e.g.,
tranexamic acid) for severe cases.
 Preeclampsia
Definition Clinical Features
Preeclampsia is a pregnancy-
• Headache
specific hypertensive disorder
characterized by new-onset • Visual disturbances (e.g., blurred
hypertension (≥140/90 mmHg) after vision, scotomas)
20 weeks gestation, with proteinuria • Epigastric/RUQ pain
and/or signs of organ dysfunction.
• Edema (especially face/hands)
• Hypertension (≥140/90 mmHg
Etiology/Risk Factors on 2 occasions ≥4 hours apart)
• Primigravida • Proteinuria (≥300 mg/24h or
• History of preeclampsia protein/creatinine ratio ≥0.3)

• Chronic hypertension • Signs of end-organ damage:

elevated liver enzymes,
• Diabetes mellitus
thrombocytopenia, renal
• Renal disease insufficiency
• Multiple gestation
• Autoimmune disorders (e.g., Severe Features
SLE, antiphospholipid
• BP ≥160/110 mmHg
syndrome)
• Thrombocytopenia
• Obesity, advanced maternal age
(<100,000/mm³)
• Impaired liver function (AST/ALT
>2× normal)
• Renal insufficiency (creatinine
>1.1 mg/dL or doubling)
• Pulmonary edema
• New-onset cerebral/visual
symptoms
Complications Delivery
• Eclampsia (seizures) Definitive treatment—timing
• HELLP syndrome (Hemolysis, based on severity and
Elevated Liver enzymes, Low gestational age
Platelets) o Immediate delivery if ≥37
weeks or if maternal/fetal
• Placental abruption
condition deteriorates
• DIC
o Corticosteroids if <34 weeks
• Acute renal failure to promote fetal lung
• Fetal growth restriction, maturity
preterm birth, intrauterine fetal
demise
Postpartum
• Monitor for resolution (usually
Emergency Management within 48h)
• Admit for monitoring and • Continue magnesium sulfate
management for 24h postpartum if severe
• Control BP: Labetalol IV, features
Hydralazine IV, or Nifedipine • Antihypertensives as needed
PO
• Long-term follow-up for
• Prevent seizures: Magnesium cardiovascular risk
sulfate IV/IM (monitor for
toxicity—loss of reflexes,
respiratory depression) Key Point
Preeclampsia can rapidly
• Monitor: BP, urine output, fetal
progress—early recognition, blood
well-being, labs (CBC, LFTs,
pressure control, seizure
renal function)
prophylaxis, and timely delivery
are critical.
 Eclampsia
Definition Complications
Eclampsia is the occurrence of
• Maternal: aspiration, cerebral
generalized tonic-clonic seizures
hemorrhage, DIC, renal failure,
in a pregnant woman with
pulmonary edema
preeclampsia (hypertension +
proteinuria ± edema), not • Fetal: hypoxia, intrauterine
attributable to other causes. growth restriction, preterm
birth, death

Epidemiology
• Typically occurs after 20 weeks
gestation, during labor, or
postpartum (up to 6 weeks)
• More common in primigravida

Clinical Features
• Seizures: tonic-clonic, may be
preceded by headache, visual
disturbances, epigastric pain,
or altered mental status
• Hypertension (SBP ≥140
mmHg or DBP ≥90 mmHg)
• Proteinuria (>300 mg/24h or
≥1+ on dipstick)
• Edema (face, hands, feet)
• May progress to coma
Emergency Management D. Delivery of Fetus
A. Initial Stabilization (ABCs)
• Definitive treatment = delivery
• Airway protection, oxygen via after maternal stabilization
mask • Mode: Vaginal preferred if no
• IV access, monitor vitals, urine obstetric contraindications
output (Foley catheter)
• C-section if fetal distress or
• Prevent maternal injury during failed induction
seizure
B. Control Seizures Postpartum Care
Magnesium sulfate (drug of
• Continue MgSO₄ for 24 hrs
choice)
post-seizure
o Loading dose: 4 g IV over 5–
• Monitor BP and urine output
10 min, then
• Monitor for recurrence and
o Maintenance: 1 g/hr IV complications
infusion for 24 hrs after last
seizure
o Monitor for signs of toxicity: Key Notes
↓RR, ↓reflexes, ↓urine • Eclampsia can occur without
output prior diagnosis of preeclampsia
o Antidote: 10 mL of 10% • Avoid diazepam unless MgSO₄
calcium gluconate IV is contraindicated or
C. Control BP (if BP ≥160/110 unavailable
mmHg) • Multidisciplinary approach
• Labetalol 20 mg IV, repeat every (Obstetrics + Medicine/ICU)
10–20 min (max 300 mg) OR essential

• Hydralazine 5–10 mg IV every

20–30 min OR
• Nifedipine 10 mg PO (if no IV
access)
 Placental Abruption
Definition Classification
Placental abruption is the premature
• Grade 1 (Mild): Small separation
separation of the placenta from the
with minimal bleeding,
uterine wall, occurring after 20
asymptomatic or mild
weeks of gestation. It can result in
symptoms.
maternal hemorrhage and fetal
distress or death. • Grade 2 (Moderate): Partial
placental separation with
moderate bleeding, maternal
Etiology symptoms (e.g., abdominal pain).
• Trauma (e.g., motor vehicle • Grade 3 (Severe): Complete
accidents, falls) separation with significant
bleeding, fetal distress, and
• Hypertension (chronic or
potential maternal shock.
pregnancy-induced)
• Pre-eclampsia or eclampsia
Clinical Features
• Smoking and drug use (especially
• Sudden onset of severe
cocaine)
abdominal pain, often with a
• Advanced maternal age board-like abdomen
• Previous history of placental • Vaginal bleeding (may be
abruption concealed or overt)
• Multiple gestation • Uterine tenderness or
• Short umbilical cord contractions

• Uterine abnormalities (fibroids, • Fetal heart rate abnormalities

scars from previous surgery) (e.g., bradycardia or
decelerations)
• Shock (in severe cases, from
blood loss)
• Possible uterine rigidity
Diagnosis • Pain relief: Analgesia as
needed, often epidural or
• Clinical presentation is key,
systemic opioids
supported by ultrasound if
necessary • Postpartum care: Monitor for
• Ultrasound may not always complications such as
detect abruption, particularly in disseminated intravascular
cases of concealed bleeding coagulation (DIC), renal failure,
or infection
• CTG (Cardiotocography) to
monitor fetal heart rate and
uterine contractions Complications
• Maternal hemorrhage, shock,
Management DIC
• Fetal complications, including
• Stabilize the mother: IV
preterm birth, hypoxia, and
access, blood transfusions as
death
needed, oxygen administration
• Risk of recurrence in
• Monitoring: Continuous fetal
subsequent pregnancies
monitoring for distress
• Delivery:
Prognosis
o In cases of mild abruption, if
the fetus is stable, consider • Dependent on the severity of the
conservative management abruption and timeliness of
with close monitoring. intervention. Severe cases carry
high maternal and fetal
o For moderate to severe
morbidity and mortality.
cases, delivery should be
expedited (vaginal or
cesarean, depending on the
condition of the mother and
fetus).
 Uterine Rupture
Definition Risk Factors
Uterine rupture is a tear in the wall • Previous uterine scar (most
of the uterus, often occurring during significant)
labor, particularly in the setting of a
• Previous uterine surgery (e.g.,
previous cesarean section or other
myomectomy)
uterine scars.
• Multiple gestations or
polyhydramnios
Etiology
• Induced labor with high-dose
• Previous cesarean section (most oxytocin
common)
• Advanced maternal age
• Uterine trauma (e.g., surgery,
• Trauma (e.g., motor vehicle
accidents)
accidents)
• Overdistended uterus (e.g.,
multiple pregnancies, Clinical Features
polyhydramnios)
• Sudden, severe abdominal pain
• Uterine abnormalities (e.g.,
• Fetal heart rate abnormalities
fibroids)
(variable decelerations or absent
• Use of uterotonic drugs (e.g., fetal heart tones)
oxytocin, prostaglandins)
• Vaginal bleeding (may be absent
• High parity if rupture is confined to the
• Prolonged or obstructed labor uterus)

• Malpresentation (e.g., breech) • Loss of uterine contractions or

abnormal uterine tone
• Hemodynamic instability
(tachycardia, hypotension, shock)
• Palpable fetal parts in the
abdomen (if rupture is complete)
Diagnosis Complications
• Clinical suspicion based on risk • Fetal death or injury
factors and presenting symptoms
• Maternal hemorrhage and shock
• Ultrasound (if available) may
• Infection (endometritis,
show free fluid in the abdomen or
peritonitis)
abnormal fetal positioning
• Renal failure due to
• CT scan may show signs of
hypoperfusion
rupture but is not always
necessary • Hysterectomy in severe cases

• Immediate assessment of fetal

heart rate and maternal Prognosis
hemodynamics
Uterine rupture carries high
maternal and fetal mortality if not
Management treated promptly. Early recognition
and surgical intervention are crucial
• Immediate surgical intervention
for improving outcomes.
is required (laparotomy and
repair or hysterectomy if
necessary)
• Resuscitation with IV fluids and
blood products (if hemorrhagic
shock is present)
• Monitoring of fetal well-being and
maternal vitals
• In cases with fetal distress, rapid
delivery is necessary
• Broad-spectrum antibiotics to
prevent infection
• Post-operative care for maternal
recovery (monitor for signs of
infection or hemorrhage)
10 Pediatric
Emergencies

• Pediatric Sepsis
• Croup and Epiglottitis
• Febrile Seizures
• Bronchiolitis
• Intussusception
 Pediatric Sepsis
Definition Clinical Features

Sepsis in children is a life-threatening • Early signs: Fever, tachycardia,

condition that arises when the body’s tachypnea, hypothermia (especially in
response to an infection causes neonates), irritability, lethargy, poor
widespread inflammation, leading to organ feeding, vomiting, abdominal pain, or
dysfunction and potentially organ failure. diarrhea.

• Progressive signs: Hypotension,

altered mental status, poor perfusion
Etiology
(cold extremities, delayed capillary
• Most common causes are bacterial refill, weak pulses), respiratory
infections, though viral, fungal, and distress (including hypoxemia),
parasitic infections can also lead to oliguria or anuria, cyanosis.
sepsis.
• Severe sepsis: Organ dysfunction
• Common pathogens in neonates: (renal failure, respiratory failure,
Group B Streptococcus, Escherichia cardiovascular collapse),
coli, Listeria monocytogenes, disseminated intravascular
Klebsiella. coagulation (DIC), and multi-organ
• In older children, Streptococcus failure.
pneumoniae, Neisseria meningitidis,
Staphylococcus aureus (including
Diagnosis
MRSA), and Haemophilus influenzae
are frequent pathogens. • Clinical suspicion is critical in a child
with signs of infection and systemic
illness.
Risk Factors
• Blood cultures, urine cultures, and
• Prematurity, low birth weight, or other relevant cultures (e.g., CSF,
chronic conditions like congenital wound, stool) should be obtained.
heart disease, immunodeficiency, or
• Laboratory tests: Elevated white blood
invasive devices (e.g., central lines,
cell count, thrombocytopenia,
endotracheal tubes).
elevated lactate, metabolic acidosis,
• Invasive procedures or post-surgical and abnormal liver or renal function
states. tests.
• Underlying conditions such as cancer, • Imaging may be indicated based on
metabolic disorders, or asplenia. suspected focus of infection.
Management Monitoring
• Initial Resuscitation: Early • Frequent reassessment of vital signs,
identification and prompt treatment urine output, and mental status.
are key to improving outcomes.
• Regular laboratory monitoring (e.g.,
o Fluid resuscitation: Administer blood gases, lactate levels, renal and
isotonic fluids (e.g., 20 mL/kg liver function tests).
boluses of normal saline) to
• Consider transfer to a pediatric
correct hypovolemia and
intensive care unit (PICU) if signs of
improve perfusion.
shock or organ dysfunction are
o Antibiotics: Empiric broad- present.
spectrum antibiotics should be
started as soon as sepsis is Prognosis
suspected, ideally within the
• The prognosis depends on the
first hour.
severity of sepsis, the age and
o Oxygen therapy: Administer underlying health of the child, and
oxygen to maintain adequate the timeliness of treatment.
oxygenation, especially if
• Early recognition and prompt,
respiratory distress or
aggressive treatment improve
hypoxemia is present.
outcomes.
• Vasopressors: If hypotension
• Long-term complications may
persists despite adequate fluid
include neurological deficits,
resuscitation, initiate vasopressors
developmental delay, or growth
(e.g., norepinephrine or dopamine) to
disturbances, particularly if there is
maintain adequate blood pressure.
significant organ damage.
• Source Control: Identify and treat
the source of infection (e.g., drainage Prevention
of abscesses, removal of infected
devices). • Immunization against preventable
infections (e.g., pneumococcus,
meningococcus, Haemophilus
influenzae).
• Prompt management of infections,
particularly in high-risk children.
• Proper hygiene and infection control
practices in healthcare settings.
 Croup
Definition Clinical Features
Croup (laryngotracheobronchitis) • Barking cough (seal-like)
is a common viral upper airway
infection in children • Inspiratory stridor
characterized by inflammation of • Hoarseness
the larynx, trachea, and bronchi, • Respiratory distress
leading to airway obstruction. (retractions, tachypnea)
• Often preceded by coryza,
Age Group low-grade fever
Common in children 6 months to
• Symptoms worse at night
3 years (peak at 1–2 years)

Severity Assessment
Etiology
• Mild: Occasional barking
• Most common: Parainfluenza
cough, no stridor at rest
virus type 1
• Moderate: Frequent barking
• Others: RSV, influenza A & B, cough, stridor at rest, mild
adenovirus, rhinovirus, retractions
coronavirus, measles
• Severe: Stridor at rest, marked
retractions, agitation, hypoxia
• Impending respiratory
failure: Fatigue, decreased
consciousness, cyanosis,
silent chest
Investigations Disposition
• Clinical diagnosis • Mild: Discharge with follow-up
• X-ray (not routinely needed): • Moderate/Severe: Observe ≥2–
“Steeple sign” on neck AP view 4 hrs post-nebulization
(subglottic narrowing)
• Admit if persistent stridor at
• Avoid agitating procedures in rest, respiratory distress, poor
moderate/severe cases oral intake, or need for repeat
nebulizations

Management
Differentials
• General: Keep child calm,
oxygen if needed • Epiglottitis
• Mild: Single dose oral • Bacterial tracheitis
dexamethasone (0.15–0.6 • Foreign body aspiration
mg/kg)
• Allergic reaction
• Moderate/Severe:
• Retropharyngeal abscess
o Nebulized epinephrine (0.5
mL/kg of 1:1000 solution,
max 5 mL)
o Dexamethasone
(oral/IM/IV)
o Observe for recurrence of
symptoms after
epinephrine wears off
(rebound stridor)
• Impending failure: Prepare for
airway management/intubation
in controlled setting
 Epiglottitis
Definition Clinical Features
Acute inflammation of the • Rapid onset high fever
epiglottis and surrounding
supraglottic structures, • Severe sore throat, dysphagia,
potentially life-threatening due odynophagia
to risk of sudden airway • Drooling, muffled “hot potato”
obstruction. voice
• Inspiratory stridor
Etiology • Sitting in “tripod” position to
• Most common: Haemophilus ease breathing
influenzae type B (HiB) • Irritability, anxiety
(especially in unvaccinated
• May progress to complete
children)
airway obstruction
• Others: Streptococcus
pneumoniae, Streptococcus
pyogenes, Staphylococcus
aureus, viruses, fungi
(immunocompromised)

Epidemiology
• Peak incidence: 2–7 years (but
can occur in adults)
• Reduced incidence due to HiB
vaccination
Diagnosis Management
• Clinical diagnosis; avoid • Airway first: Secure airway in
distressing the child OT/ICU; intubation may be
• Thumb sign on lateral neck X- needed
ray (enlarged epiglottis) • Avoid agitating the patient (no
• Definitive diagnosis by IV lines or throat exam until
laryngoscopy (done in airway secured)
controlled setting like • Oxygen by blow-by if
OT/ICU) tolerated
• Avoid throat examination • IV antibiotics: Ceftriaxone or
unless airway secured cefotaxime
• Consider dexamethasone (to
Differential Diagnosis reduce edema)

• Croup • ICU monitoring

• Retropharyngeal abscess
• Peritonsillar abscess Prevention

• Foreign body aspiration HiB vaccination as part of

routine immunization
• Angioedema

Key Point
Epiglottitis is a true airway
emergency; prioritize airway
management and minimize
interventions until airway is
secured.
 Febrile Seizures
Definition • High fever, especially if it rises quickly.
Febrile seizures are seizures triggered by • Low-grade fever in the early stage of
fever in children, typically between 6 illness.
months and 5 years of age. They are the
most common type of seizure in this age
group and are usually benign. Pathophysiology
The rapid rise in body temperature is
thought to lower the threshold for
Types
neuronal excitability, leading to seizure
1. Simple Febrile Seizure: Generalized activity.
tonic-clonic seizure lasting less than
15 minutes and not recurring within
24 hours. Clinical Presentation

2. Complex Febrile Seizure: Focal • Sudden onset of generalized tonic-

seizure or one lasting more than 15 clonic movements, loss of
minutes or recurring within 24 hours. consciousness, and postictal
confusion.
• May be preceded by fever or signs of
Etiology
an infection.
• Often triggered by viral infections
• Duration typically under 5 minutes,
(e.g., respiratory or gastrointestinal
with the child often regaining
infections).
consciousness within 15-20 minutes.
• Can also be caused by bacterial
infections, including otitis media or
urinary tract infections. Differential Diagnosis

• Genetic factors may predispose • Meningitis or encephalitis (especially

certain children. in complex febrile seizures).
• Hypoglycemia.
Risk Factors • Electrolyte imbalances (e.g.,
• Family history of febrile seizures or hyponatremia).
epilepsy. • Non-epileptic events like breath-
• Age: More common in children 6 holding spells.
months to 3 years old.
Management Prognosis
Initial Management: • Simple febrile seizures generally have
an excellent prognosis, with no long-
o Ensure safety: Prevent injury during the
term neurological consequences.
seizure by positioning the child on their
side and protecting the head. • The recurrence rate is around 30-40%,
but most children outgrow febrile
o Do not attempt to restrain or place
seizures by age 5.
objects in the mouth.
• A history of febrile seizures increases
o Administer antipyretics (e.g.,
the risk of developing epilepsy later in
paracetamol or ibuprofen) to reduce
life, but the risk is still low.
fever.
o Oxygen is not required unless there is
respiratory compromise. Prevention
Post-Seizure Care: • Antipyretics may help control fever, but
there is no proven method to prevent
o Monitor the child until fully recovered.
febrile seizures.
o Reassure parents or caregivers about
• Prophylactic treatment with
the benign nature of most febrile
anticonvulsants is not routinely
seizures.
recommended.
Pharmacologic Intervention:

o For seizures lasting longer than 5

Key Points
minutes, administer benzodiazepines
(e.g., lorazepam or diazepam). • Febrile seizures are typically benign
and self-limited.
o Consider anticonvulsants (e.g.,
phenytoin or valproate) if seizures • Simple febrile seizures require minimal
persist despite benzodiazepine intervention and have a good
administration. prognosis.

Further Evaluation: • In cases of prolonged or complex

seizures, further investigation is
o For simple febrile seizures, no further
warranted to rule out other causes.
investigations are typically needed
unless there are atypical features.
o In cases of complex febrile seizures,
perform a full evaluation (e.g., blood
cultures, lumbar puncture if meningitis
is suspected, or imaging if there are
focal signs).
 Bronchiolitis
Definition Clinical Features
Acute viral lower respiratory tract o Initial: Rhinorrhea, low-grade
infection primarily affecting infants fever, cough, sneezing.
and young children, leading to o Progression: Respiratory
inflammation and obstruction of distress (tachypnea, wheezing,
the bronchioles. retractions), crackles,
prolonged expiration, and
hypoxia.
Etiology
o Severe cases: Cyanosis,
Most commonly caused by
apneic episodes, exhaustion.
Respiratory Syncytial Virus (RSV),
but also by other viruses like
rhinovirus, adenovirus, influenza, Diagnosis
and parainfluenza.
o Clinical Diagnosis: Based on
history and physical
Risk Factors examination.
Prematurity, age < 6 months, o Laboratory Tests:
congenital heart disease, chronic Nasopharyngeal swab for viral
lung disease, identification (RSV antigen test
immunocompromised status, and or PCR).
lack of breastfeeding. o Chest X-ray: May show
hyperinflation and
peribronchial cuffing.
Management Prevention
Supportive Care: o RSV Prophylaxis: Palivizumab
▪ Oxygen therapy if hypoxic (monoclonal antibody) for high-
(target SpO2 > 90%). risk infants.
o Hand hygiene and avoiding
▪ Hydration (oral or IV fluids as
exposure to sick contacts.
needed).
o Vaccination strategies (e.g.,
▪ Nasal saline drops and
maternal vaccination to reduce
suctioning to clear the airway.
risk of severe disease).
▪ Monitoring for respiratory
distress and need for invasive
support. Prognosis
Ventilatory Support: o Most children recover in 1-2
weeks with supportive care.
▪ Non-invasive ventilation (e.g.,
CPAP or BiPAP) if severe o A small percentage may require
respiratory distress. hospitalization due to
▪ Intubation and mechanical respiratory failure.
ventilation in cases of acute o Rare long-term effects, but
respiratory failure. recurrent wheezing may occur
in some children.
Medications:
▪ Bronchodilators: Limited role,
only in those with history of
wheezing (not routinely
recommended).
▪ Corticosteroids: Not
recommended in the
management of bronchiolitis.
▪ Ribavirin: Reserved for severe
cases or immunocompromised
children.
 Intussusception
Definition Clinical Presentation
Intussusception is a condition • Classic Triad:
where a part of the intestine folds o Abdominal pain
into the section next to it, leading (intermittent, severe,
to obstruction and decreased colicky).
blood flow. It is most common in
infants and young children. o Vomiting (often bilious).
o Redcurrant jelly stools
(blood and mucus).
Pathophysiology
• Lethargy, irritability, and
A segment of the bowel, often the abdominal distension.
ileum, telescopes into the
adjacent part of the bowel (usually • In infants: The child may
the cecum). This causes present with sudden onset of
obstruction, ischemia, and crying episodes and drawing
inflammation. up of legs.

Causes Diagnosis

• Primary: Idiopathic (most • Ultrasound: The "target" or

common). "doughnut" sign is seen,
indicating a bowel within a
• Secondary: Infections (e.g.,
bowel appearance.
rotavirus), tumors, Meckel's
diverticulum, polyps, and other • X-ray: May show signs of bowel
anatomical anomalies. obstruction.
• CT scan: More accurate in
adults, showing the
intussuscepted bowel.
Management Prognosis
Non-surgical: Early diagnosis and intervention
o Hydrostatic reduction (using have excellent outcomes, with the
contrast or saline via the majority of children recovering
rectum). fully. Delayed treatment increases
the risk of complications.
o Pneumatic reduction (using
air insufflation via the rectum).
Both are successful in most Differential Diagnosis
cases in children.
• Acute gastroenteritis.
Surgical: • Appendicitis.
o If non-surgical reduction fails
• Gastrointestinal volvulus.
or complications like
perforation or ischemia occur, • Constipation.
surgery is required.
o Involves manual reduction or
resection of the affected
bowel.

Complications
• Bowel perforation.
• Peritonitis.
• Shock.
• Long-term bowel dysfunction if
untreated.
11 Environmental
Emergencies

• Hypothermia
• Frostbite
• Heatstroke
• Heat Exhaustion
• Drowning and Near Drowning
• High-Altitude Illnesses
 Hypothermia
Definition Clinical Features
Hypothermia occurs when the body Shivering, slurred speech, confusion,
temperature falls below 35°C (95°F) bradycardia, hypotension,
due to prolonged exposure to cold hypoventilation, and ultimately coma
environments. and death in severe cases.

Types Management

o Mild: 32-35°C (shivering, o Initial: Remove from the cold,

confusion, tachycardia). remove wet clothing, and
rewarm with blankets or dry
o Moderate: 28-32°C (drowsiness,
clothing.
slurred speech, weak pulse).
o Moderate Hypothermia: Passive
o Severe: <28°C
rewarming (e.g., warm
(unconsciousness, absent pulse,
environment, heated blankets),
respiratory failure).
active rewarming (e.g., warm
fluids, heated air).
Pathophysiology
o Severe Hypothermia: Active
Core body temperature drops, core rewarming (e.g., warm
causing vasoconstriction, shivering, intravenous fluids, peritoneal or
and reduced blood flow to peripheral pleural lavage), cardiopulmonary
tissues. The body's metabolic bypass in extreme cases.
processes slow down, and vital
o Supportive Care: Oxygen, fluid
organs are at risk of failure.
resuscitation, and monitoring of
cardiac rhythms (risk of
Risk Factors arrhythmias).
Prolonged exposure to cold, wet
clothing, alcohol or drug use, elderly, Prevention
infants, malnutrition, and certain Proper clothing, staying dry, avoiding
medical conditions like alcohol, and adequate nutrition.
hypothyroidism.
 Frostbite
Definition Management
Frostbite is a cold-induced injury o Initial: Move to a warm environment.
resulting from exposure to freezing Avoid rubbing or massaging the
temperatures, leading to tissue damage affected area as it may cause further
and cell death due to ice crystal injury.
formation within cells.
o Rewarming: Immerse the affected
areas in warm (not hot) water (37-
Risk Factors
39°C) or use warm, dry compresses.
Cold, wind, wet conditions, poor Avoid direct heat sources like stoves
circulation, alcohol use, smoking, and or heating pads.
certain medical conditions (e.g.,
o Medications: Analgesia for pain
Raynaud's disease).
relief, tetanus prophylaxis, and
possibly thrombolytics in severe
Classification
cases (e.g., tissue perfusion
o First Degree (Frostnip): Mild form, restoration).
affects the skin causing numbness
o Wound Care: For blisters, avoid
and redness. No permanent damage.
rupturing; if ruptured, keep the area
o Second Degree: Blisters with clear clean and covered. Surgical
fluid form after rewarming, with intervention may be necessary in
partial-thickness tissue damage. severe cases to debride necrotic
tissue.
o Third Degree: Full-thickness tissue
damage, leading to hard, blackened o Prevention: Proper insulation,
tissue (eschar) and deep tissue avoiding prolonged exposure to cold,
injury. and keeping extremities dry and well-
protected.
o Fourth Degree: Involves muscle and
bone, leading to permanent tissue
necrosis and potential amputation.
Complications

Clinical Features Infection, gangrene, long-term nerve

damage, and potential need for
Initially, the skin feels cold and numb,
amputation in severe cases.
followed by a prickling or burning
sensation. In more severe forms, the skin
appears pale, hard, and waxy.
 Heatstroke
Definition Management
A life-threatening condition o Immediate cooling: Rapid
characterized by a core body cooling is the priority (e.g., cold
temperature >40°C (104°F) with water immersion, ice packs,
central nervous system evaporative cooling).
dysfunction due to excessive heat o Hydration: IV fluids (normal
exposure. saline or lactated Ringer's
solution) for rehydration if
hypotensive or in shock.
Causes
o Monitoring: Continuous
Prolonged exposure to high
monitoring of core temperature,
temperatures, especially in hot,
vital signs, and organ function.
humid environments; vigorous
physical activity (e.g., exercise, o Medications: Benzodiazepines
sports); dehydration; wearing for seizures, and possibly
excessive clothing; and certain antipyretics if fever persists
medications (e.g., diuretics). despite cooling.

Complications
Symptoms
Multi-organ failure,
High fever, altered mental status rhabdomyolysis, renal failure,
(confusion, agitation, delirium, or disseminated intravascular
coma), hot, dry skin (anhidrosis), coagulation (DIC), and death.
tachycardia, hypotension, and
respiratory distress. Prevention
Adequate hydration, avoiding
strenuous activity in extreme heat,
wearing lightweight clothing, and
acclimatization to heat.
 Heat Exhaustion
Definition Management
A milder form of heat-related o Cooling: Move the patient
illness due to excessive heat to a cool environment and
and dehydration, typically remove excess clothing.
presenting with weakness and o Hydration: Oral
fatigue. rehydration with electrolyte
solutions or IV fluids (if the
Causes patient is unable to drink).

Prolonged exposure to high o Rest: Rest and recovery in

environmental temperatures, a comfortable
dehydration, and physical environment.
exertion, especially in hot,
humid conditions. Complications
If left untreated, heat
Symptoms exhaustion can progress to
Heavy sweating, weakness, heatstroke.
dizziness, nausea, vomiting,
headache, muscle cramps, Prevention
fatigue, and mild confusion.
Skin may be cool and moist. Adequate hydration, taking
breaks during heat exposure,
and wearing appropriate
clothing.
Drowning and Near Drowning
Definition Pathophysiology

Drowning is defined as the process of • Submersion leads to water entering the

experiencing respiratory impairment from airways and impairing normal gas
submersion/immersion in liquid, which may exchange.
result in death. Near drowning refers to a
• Initial stage: Struggling, hyperventilation,
survival event in which a person has
and gasping for air.
experienced submersion or immersion but
survived, often requiring medical intervention. • Laryngospasm: The body may attempt to
protect the airway, causing temporary
closure of the larynx.
Etiology and Risk Factors
• Aspiration: In cases of water entering the
• Age: Children and elderly individuals are lungs, it leads to pulmonary edema and
more prone due to lack of supervision, hypoxemia.
impaired mobility, and weakened
• Pulmonary damage: Can lead to ARDS
respiratory mechanisms.
(acute respiratory distress syndrome) in
• Alcohol consumption: Increases risk of severe cases.
drowning due to impaired judgment and
• Metabolic and electrolyte imbalances:
motor skills.
Resulting from aspiration of water
• Seizure disorders: Increased risk in water (hypothermia or hyperthermia depending
due to potential loss of consciousness or on water temperature).
control.

• Water-related activities: Swimming, Clinical Features of Near Drowning

boating, and diving accidents are common
• Respiratory distress: Tachypnea,
causes.
cyanosis, or labored breathing.
• Mental health issues: Suicide attempts
• Altered consciousness: Ranging from
or self-harm in water bodies.
confusion to coma.
• Underlying medical conditions:
• Coughing and sputum production: Often
Cardiovascular or respiratory conditions
with frothy sputum.
can predispose to drowning.
• Hypothermia: Due to prolonged
immersion in cold water.

• Pulmonary edema: Can cause crackles

and decreased breath sounds.

• Cardiovascular instability: Tachycardia,

hypotension, or arrhythmias.
Management Prevention
• Initial Assessment: A-B-C (Airway, • Supervision: Constant supervision
Breathing, Circulation). Prioritize of children near water.
airway management and respiratory
• Education: Promote water safety,
support.
swimming lessons, and
• Resuscitation: Begin CPR if the understanding of water hazards.
patient is unresponsive and not
• Safety equipment: Use of life
breathing. Consider advanced
jackets, especially in boating or
airway management if necessary.
water sports.
• Oxygen therapy: Administer high-
• Avoid alcohol: Prevent alcohol
flow oxygen, and consider
consumption when near water.
mechanical ventilation in cases of
respiratory failure or severe • Rescue training: First aid and CPR
pulmonary edema. training for individuals who frequent
water-related activities.
• Rewarming: If hypothermic, rewarm
the patient gradually to avoid shock.
• Fluid management: Correct any Key Points
fluid or electrolyte imbalances and • Drowning is a preventable cause of
treat hypotension or shock with IV death that requires rapid recognition
fluids. and immediate intervention.
• Monitoring: Continuous monitoring • Near drowning can result in
of oxygen saturation, respiratory prolonged morbidity, even if the
rate, and heart rate. Watch for signs individual survives the initial event.
of ARDS, cardiac arrhythmias, or
seizures. • Timely resuscitation, adequate
respiratory support, and monitoring
for complications are crucial in the
Prognosis management of these cases.

The prognosis depends on the

duration of submersion, the water
temperature, and the immediate
medical response. If the patient is
rescued early and resuscitated
effectively, the outcomes improve,
especially if there is minimal
aspiration of water.
 High-Altitude Illnesses
Overview ▪ Symptoms: Shortness of
High-altitude illnesses are medical breath, cough (may be
conditions caused by exposure to productive with pink frothy
reduced oxygen levels at high sputum), chest tightness,
altitudes (usually above 2,500 cyanosis, and rapid breathing.
meters). The risk increases with
▪ Management: Descent to lower
elevation and the speed of ascent.
altitude, supplemental oxygen,
nifedipine (to reduce pulmonary
vasoconstriction), and if severe,
Types of High-Altitude Illnesses
mechanical ventilation.
Acute Mountain Sickness (AMS)
High-Altitude Cerebral Edema
▪ Pathophysiology: Occurs due (HACE)
to hypoxia (low oxygen levels).
▪ Pathophysiology: Swelling of
Symptoms start 6-12 hours
the brain caused by hypoxia and
after ascent.
changes in blood-brain barrier
▪ Symptoms: Headache, permeability.
nausea, vomiting, fatigue,
▪ Symptoms: Severe headache,
dizziness, insomnia.
confusion, ataxia,
▪ Management: Acclimatization hallucinations, and coma.
(gradual ascent), hydration,
▪ Management: Immediate
pain relief (NSAIDs), and if
descent to lower altitude,
symptoms worsen, descent to a
supplemental oxygen, and
lower altitude.
steroids (dexamethasone) to
High-Altitude Pulmonary Edema reduce brain edema.
(HAPE)
▪ Pathophysiology: Fluid
accumulation in the lungs due
to hypoxic pulmonary
vasoconstriction and capillary
leakage.
Risk Factors Complications
Rapid ascent, lack of o Progression of AMS to HAPE or
acclimatization, previous history HACE if untreated.
of altitude illness, younger age, o Fatalities can occur in severe
dehydration, and underlying cases, particularly if descent
medical conditions (e.g., is not initiated promptly.
cardiovascular diseases,
pulmonary disorders).
Prognosis

Prevention o With appropriate

management, most cases of
o Gradual ascent (e.g., 300-500 AMS resolve. However,
meters/day above 3,000 untreated severe HAPE or
meters). HACE can be fatal.
o Adequate hydration, balanced
diet, and rest.
Treatment Summary
o Acetazolamide (250 mg twice
daily) to prevent AMS. o AMS: Rest, hydration, and
gradual ascent.
o Dexamethasone (4 mg every 6 Acetazolamide for prevention.
hours) as prophylaxis for
severe cases. o HAPE: Descent, oxygen, and
nifedipine.
o HACE: Descent, oxygen, and
Diagnosis
steroids (dexamethasone).
o Primarily clinical, based on
symptoms and exposure to
high altitude.
o Imaging or laboratory tests are
usually not necessary unless
complications like HAPE or
HACE are suspected.
12 Psychiatric
Emergencies

• Acute Psychosis
• Suicidal Ideation or Attempt
• Agitated or Violent Behavior
• Delirium and Acute
Confusional State
• Post partum psychosis
 Acute Psychosis
Definition Psychotic Symptoms in Acute Medical
Acute psychosis is a mental state Conditions:
characterized by a loss of touch with reality,
o Hypoxia
leading to significant impairments in thought
processes, perception, emotional regulation, o Hyperthyroidism
and behavior. It can manifest as delusions,
o Hypoglycemia
hallucinations, disorganized speech, or severe
disturbances in behavior. Neurodegenerative Disorders:

o Alzheimer's, Parkinson's, Huntington's

disease
Causes

Primary Psychiatric Disorders:

Clinical Features
o Schizophrenia
Positive Symptoms:
o Bipolar disorder (mania with psychotic
features) o Hallucinations (auditory, visual, tactile)

o Severe depression (with psychotic o Delusions (paranoid, grandiose,

features) religious)

Substance-Induced: o Disorganized speech (incoherent,

tangential, circumstantial)
o Alcohol intoxication or withdrawal
o Disorganized or catatonic behavior (e.g.,
o Illicit drug use (e.g., cocaine,
agitated, inappropriate, lack of
amphetamines, hallucinogens)
movement)
o Medication-induced (e.g.,
Negative Symptoms:
corticosteroids, anticholinergics,
hallucinogens) o Affective flattening

Medical Conditions: o Social withdrawal

o Brain infections (meningitis, encephalitis) o Lack of motivation

o Seizure disorders (postictal psychosis) o Reduced speech output (alogia)

o Metabolic disturbances (e.g., Cognitive Symptoms:

hyponatremia, hypercalcemia)
o Impaired attention and concentration
o Stroke, traumatic brain injury
o Memory impairment
o Hepatic or renal encephalopathy
o Poor executive functioning
Assessment Pharmacologic Treatment:

History and Mental Status Examination: o Antipsychotics:

o Onset, duration, and progression of ▪ First-generation (e.g., haloperidol) for

symptoms acute psychosis

o Substance use and medication history ▪ Second-generation (e.g., risperidone,

olanzapine) for fewer extrapyramidal
o Presence of medical conditions
side effects
o Family psychiatric history
o Benzodiazepines:
Physical Examination:
▪ Lorazepam or diazepam for agitation,
o Vital signs, neurologic status anxiety

o Signs of trauma, infection, or metabolic o Mood stabilizers/antidepressants:

imbalance
▪ For psychosis associated with mood
Laboratory and Diagnostic Tests: disorders

o Basic metabolic panel, liver and kidney Supportive Care:

function tests
o Hydration, nutrition, and monitoring of
o Toxicology screen for drugs/alcohol vital signs

o CT/MRI of the brain (if focal neurologic o Psychological support and environment
signs or suspected brain lesion) modification (quiet room, de-escalation
techniques)
o Electroencephalogram (EEG) for
suspected seizure activity Referral:

o Thyroid function tests and other o Psychiatric evaluation for long-term care
metabolic screens
o Hospitalization if the patient poses a
danger to themselves or others or if there
is an underlying medical condition
Management
requiring urgent attention
Stabilization:

o Ensure safety of the patient and others

Prognosis
(restrictive measures if needed)
• Prognosis depends on the underlying
o Address underlying medical or psychiatric
cause, timeliness of intervention, and
causes (e.g., correcting metabolic
patient's response to treatment.
imbalances, managing substance
withdrawal) • If psychosis is due to a primary psychiatric
disorder, long-term psychiatric care may
o Treat acute agitation or violent behavior
be necessary.
(benzodiazepines, antipsychotics)
• If secondary to medical conditions,
prognosis improves with treatment of the
underlying cause.
 Suicidal Ideation or Attempt
Definition Signs & Symptoms
Suicidal ideation refers to thinking about,
• Verbal cues: Direct or indirect statements
considering, or planning suicide, while a
like "I want to die" or "I can't take it
suicidal attempt involves engaging in an
anymore."
intentional act of self-harm with the intention
of ending one's life. Suicidal behaviors are • Behavioral signs: Withdrawal, changes in
often a manifestation of underlying behavior, neglect of personal care, and
psychological distress or mental health giving away possessions.
disorders.
• Psychological distress: Feelings of
hopelessness, worthlessness, guilt, or
anger.
Risk Factors
• Changes in mood: Severe depression,
• Psychiatric disorders: Depression,
anxiety, irritability, or agitation.
bipolar disorder, schizophrenia, anxiety
disorders, and borderline personality • Physical signs: Unexplained injuries or
disorder. frequent visits to the emergency
department.
• Previous suicide attempt: A strong
predictor of future attempts.
Types of Suicidal Ideation
• Family history: Genetics and family
history of suicide or mental illness.
• Passive suicidal ideation: Thoughts of
death without an intention to act on them.
• Substance abuse: Alcohol or drug misuse
increases risk.
• Active suicidal ideation: Specific plans or
intentions to harm oneself.
• Chronic illness or pain: Particularly in
cases of terminal illness. Diagnosis
• Social isolation: Lack of social support, • Clinical assessment: History-taking,
loneliness, and recent loss. including psychiatric, social, and family
• Recent trauma or stress: Loss of job, background.
relationship breakdown, financial • Suicide risk assessment: Evaluating
problems. ideation, intent, and the presence of a
• Adverse childhood experiences: Abuse, plan.
neglect, or other trauma. • Mental status examination: Assessing
• Cultural or religious factors: Stigma mood, thought content, and cognitive
around seeking help or discussing suicidal function.
thoughts. • Screening tools: Use of scales like the
Columbia-Suicide Severity Rating Scale
(C-SSRS) or the Beck Depression Inventory
(BDI).
Management Complications

• Immediate safety: Ensuring the patient's • Permanent physical injury or death.

safety, especially if there is a high risk of
• Psychiatric complications: Worsening of
imminent harm.
mental health disorders, including
• Hospitalization: Required in cases of high depression and PTSD.
risk, especially if there is a suicide plan or
• Emotional impact on families and
previous attempts.
friends: Long-term effects on loved ones,
• Psychiatric evaluation: Comprehensive including guilt and trauma.
assessment by a mental health
professional.
Prognosis
• Crisis intervention: Short-term, goal-
The prognosis depends on the severity of the
directed therapy to reduce immediate
ideation, underlying mental health conditions,
suicidal thoughts.
and the timeliness of intervention. With
• Psychotherapy: Cognitive-behavioral appropriate treatment and support, many
therapy (CBT), dialectical behavior therapy individuals recover and go on to lead fulfilling
(DBT), and other approaches. lives.

• Medication: Antidepressants (SSRIs,

SNRIs) and antipsychotics may be
Conclusion
indicated in cases of underlying mood
Suicidal ideation and attempts are significant
disorders or psychosis.
medical emergencies. Early identification,
• Follow-up: Regular monitoring and long- proper risk assessment, and timely
term therapy for patients at risk. intervention are essential in reducing the risk
of death or further harm. Multidisciplinary
approaches involving medical, psychiatric,
Prevention
and social support are key to successful
• Early intervention: Identifying at-risk management and recovery.
individuals and offering counseling,
therapy, and medication.

• Social support: Encouraging engagement

in supportive relationships and
communities.

• Education: Raising awareness about

mental health and reducing the stigma
surrounding seeking help.

• Crisis helplines: Offering immediate

support for those in distress (e.g., suicide
hotlines).

• Strengthening coping mechanisms:

Teaching stress management techniques
and problem-solving skills.
 Agitated or Violent Behavior - Emergency
Management
Definition Management
Agitated or violent behavior refers to
• Initial approach: Ensure safety of the
extreme, disruptive, or aggressive actions
patient and healthcare providers.
that can cause harm to oneself or others. It
Secure environment, use of personal
may present as physical violence, verbal
protective equipment, and control of
threats, or destructive actions.
weapons or harmful objects.

Causes • De-escalation techniques: Approach

calmly, maintain a safe distance, use
• Medical causes: Hypoglycemia,
non-threatening body language, and
hypoxia, delirium, seizures, brain injury,
speak in a calm and clear voice.
infections (e.g., meningitis), stroke,
intoxication (alcohol, drugs), • Pharmacological intervention:
withdrawal (e.g., benzodiazepines, o Sedation: Benzodiazepines (e.g.,
opioids), metabolic disturbances. lorazepam) or antipsychotics
• Psychiatric causes: Acute psychosis (e.g., haloperidol) for agitation.
(schizophrenia, bipolar disorder), o For medical causes: Treat
anxiety disorders, mood disorders, underlying conditions (e.g.,
personality disorders, PTSD. glucose for hypoglycemia, oxygen
• Environmental causes: Stress, lack of for hypoxia).
sleep, fear, external threats, noise, o For psychiatric causes:
overcrowding. Antipsychotic medications (e.g.,
olanzapine, quetiapine) may be
Assessment used.
• History: Assess for underlying medical • Restraints: Should be used as a last
conditions, psychiatric history, recent resort and under strict medical
substance use, and precipitating supervision. Ensure proper
factors. documentation and continuous
• Physical exam: Check for signs of monitoring.
injury, intoxication, or medical
conditions (e.g., altered vital signs,
neurological deficits).
• Mental status exam: Assess for signs
of psychosis, delirium, and cognitive
function.
Complications Key Points
• Physical harm: Injuries to the • Always prioritize safety.
patient, staff, or bystanders • Use de-escalation techniques
due to aggressive behavior. whenever possible.
• Psychological harm: Long-
• Consider both medical and
term trauma to the patient or
psychiatric causes.
healthcare providers.
• Pharmacological intervention
• Legal implications:
should be tailored to the
Documentation of restraints,
underlying cause.
sedation, and the rationale for
actions taken. • Restraints should be used
judiciously and with
appropriate monitoring.
Disposition
• Inpatient care: If psychiatric
evaluation and treatment are
needed, or if medical
conditions require
hospitalization.
• Psychiatric referral: For
ongoing psychiatric care,
including observation and
treatment in a psychiatric unit if
necessary.
• Follow-up care: Ensure
appropriate follow-up for
patients with psychiatric or
medical conditions that
contributed to the behavior.
Delirium and Acute Confusional State
Definition Clinical Features
Delirium, also known as Acute
• Acute onset and fluctuating course.
Confusional State (ACS), is an acute
disturbance in attention, awareness, and • Reduced ability to focus, sustain, or
cognition. It commonly develops over shift attention.
hours to days and is usually reversible • Disorganized thinking, impaired
with appropriate treatment. judgment.

Etiology • Cognitive disturbances (e.g., memory

deficits, disorientation).
• Medical conditions: Infections (e.g.,
UTI, pneumonia), sepsis, metabolic • Perceptual disturbances (e.g.,
disturbances (e.g., electrolyte hallucinations, delusions).
imbalances, dehydration), organ • Sleep-wake cycle disturbances.
failure (e.g., liver, renal), hypoxia,
• Emotional lability (e.g., anxiety,
hypoglycemia, vitamin deficiencies
agitation, or apathy).
(e.g., B12), and endocrine disorders.
• Medications: Anticholinergics,
sedatives, opioids, benzodiazepines, Classification
steroids, and others.
• Hyperactive: Increased activity,
• Neurological conditions: Stroke, agitation, restlessness,
seizures, dementia, or brain injury. hallucinations, and combativeness.
• Toxins: Alcohol withdrawal, drug • Hypoactive: Reduced activity,
overdose, environmental toxins. lethargy, or stupor, often mistaken for
depression.
• Post-surgical: Common in the elderly
following major surgery. • Mixed: A combination of both
hyperactive and hypoactive
symptoms.
Risk Factors
• Age (elderly), pre-existing cognitive
impairment (e.g., dementia), sensory
impairment, severe illness, recent
surgery, polypharmacy, alcohol or
drug abuse, ICU admission, and
immobility.
Diagnosis Prognosis
Delirium is often reversible once the
• Clinical diagnosis based on history
underlying cause is treated, though
and examination.
recovery can be delayed in older adults
• Cognitive testing (e.g., Mini-Mental or those with pre-existing cognitive
State Examination - MMSE) may help impairments. Long-term cognitive
in identifying cognitive impairment. decline may occur in some cases,
• Lab investigations: CBC, electrolytes, particularly in the elderly.
renal and liver function tests, glucose
levels, ABG, urine analysis, and
Prevention
imaging (CT/MRI) if neurological cause
is suspected. • Early identification of at-risk patients.
• Assess underlying causes (e.g., • Avoidance of unnecessary
infection, dehydration, medications). medications, particularly
anticholinergics and sedatives.
• Ensuring adequate hydration,
Management
nutrition, and sleep.
• Identify and treat the underlying
• Minimizing ICU and hospital-induced
cause: Address infections, metabolic
delirium through orientation
imbalances, withdrawal syndromes,
strategies and mobilization.
and other medical conditions.
• Pharmacologic treatment:
Antipsychotics (e.g., haloperidol, Key Points
olanzapine) may be used for agitation
• Delirium is a common and serious
or psychotic symptoms.
condition in acute care settings.
Benzodiazepines may be indicated for
alcohol withdrawal delirium. • Early recognition and treatment of the
underlying cause are essential.
• Non-pharmacologic management:
Re-orientation (e.g., use of clocks, • Multidisciplinary management
calendars), proper lighting, ensuring involving physicians, nurses, and
adequate hydration and nutrition, family is crucial for recovery.
sleep hygiene, minimizing noise, and • Prevention and minimizing risk factors
addressing sensory deficits (e.g., can help reduce incidence, especially
glasses, hearing aids). in vulnerable populations.
• Monitoring: Continuous monitoring in
a hospital setting, especially in high-
risk patients.
 Postpartum Psychosis
Definition Clinical Features
A severe mental illness that o Psychotic Symptoms:
occurs in the first few weeks Delusions (e.g., paranoid or
after childbirth, characterized grandiose beliefs),
by psychotic symptoms such as hallucinations (auditory or
delusions, hallucinations, visual), and disorganized
disorganized thinking, and speech or behavior.
severe mood disturbances. o Mood Symptoms: Severe
mood swings, depression,
Epidemiology or mania.

A rare condition, affecting 1–2 in o Cognitive Impairment:

1,000 women after childbirth. It Confusion, inability to
typically presents within the first concentrate, and poor
2 weeks postpartum, although it judgment.
can occur up to 6 weeks after o Behavioral Symptoms:
delivery. Agitation, hyperactivity, and
risk of self-harm or harm to
the infant.
Risk Factors
Previous psychiatric history
(especially bipolar disorder or
schizophrenia), family history of
psychiatric disorders, traumatic
childbirth, sleep deprivation,
stress, hormonal fluctuations,
and lack of social support.
Differential Diagnosis o Supportive Care: Involve a
multidisciplinary team,
o Postpartum depression (which
including obstetricians,
has more mood-related
psychiatrists, and social
symptoms without psychosis).
workers.
o Bipolar disorder with psychotic
features.
Prognosis
o Schizophrenia.
With early diagnosis and
o Organic causes (e.g., brain
treatment, most women recover
infections, metabolic
fully, though there is a higher risk
disturbances).
of recurrence in subsequent
pregnancies or postpartum
Management periods. Severe cases may lead to
long-term psychiatric disorders.
o Immediate Psychiatric
Intervention: Hospitalization is
usually necessary for both Prevention
safety and intensive treatment.
Women with a history of bipolar
o Pharmacological Treatment: disorder or psychotic illness may
Antipsychotics (e.g., benefit from close monitoring,
haloperidol, olanzapine) and prophylactic psychiatric care, or
mood stabilizers (e.g., lithium) medications during the
may be used, depending on the postpartum period.
severity and type of symptoms.
o Psychotherapy: Cognitive-
behavioral therapy (CBT) and
family therapy are essential for
long-term recovery and to
provide emotional support.
 Renal and
13 Urological
Emergencies

• Acute Kidney Injury (AKI)

• Urinary Retention
• Testicular Torsion
• Ureteric Colic
• Pyelonephritis
 Acute Kidney Injury (AKI)
Definition Clinical Features
AKI is a rapid decline in kidney function, • Oliguria or anuria
resulting in the accumulation of waste
• Edema, especially in lower extremities
products, fluid, and electrolyte
imbalances. It is commonly • Fatigue, confusion (due to uremia)
characterized by an increase in serum • Nausea, vomiting, anorexia
creatinine or a decrease in urine output.
• Hypertension (in cases of fluid
retention)
Etiology
• Prerenal: Due to decreased renal
perfusion (e.g., hypovolemia, shock, Diagnosis
sepsis, heart failure, or renal artery
• History and Physical Examination:
stenosis).
Identify underlying cause (e.g., recent
• Intrinsic (Renal): Involves damage to surgeries, trauma, or medication use).
kidney parenchyma (e.g., acute
• Urine Output Measurement: Oliguria
tubular necrosis (ATN),
(less than 0.5 mL/kg/hour) or anuria.
glomerulonephritis, interstitial
nephritis, and vasculitis). • Blood Tests: Serum creatinine and
blood urea nitrogen (BUN) levels. A
• Postrenal: Caused by obstruction of
rise in serum creatinine is indicative of
urine flow (e.g., kidney stones,
AKI.
enlarged prostate, tumors, or ureteral
obstruction). • Urinalysis: Can show proteinuria,
hematuria, or cast formation (e.g.,
Pathophysiology muddy brown casts in ATN).

• Prerenal: Reduced blood flow leads to • Imaging: Renal ultrasound to rule out
ischemia and subsequent cellular postrenal causes (obstructions).
injury in the kidneys. • Fractional Excretion of Sodium
• Intrinsic: Direct damage to kidney (FENa): Helps differentiate prerenal
structures (e.g., tubules or glomeruli) from intrinsic causes (FENa <1%
causes dysfunction. suggests prerenal cause, >2%
suggests intrinsic).
• Postrenal: Obstruction results in
increased pressure within the kidneys,
leading to damage.
Management Prevention
• Prerenal: Treat the underlying • Adequate hydration, especially
cause (e.g., fluid resuscitation, in high-risk patients (e.g., during
correcting hypotension, and surgery or after trauma).
improving renal perfusion). • Avoid nephrotoxic drugs or use
• Intrinsic: Manage the them cautiously.
underlying pathology (e.g., treat
• Monitor renal function in high-
infection, discontinue
risk patients (e.g., those with
nephrotoxic drugs, or initiate
diabetes, heart failure).
dialysis if necessary).
• Postrenal: Relieve obstruction
(e.g., catheterization, surgery, Prognosis
or stone removal). • Dependent on the underlying
• General Measures: Fluid cause and the severity of kidney
management, electrolytes injury.
correction, and avoiding • Can range from complete
nephrotoxic medications. recovery to progression to
• Dialysis: Indicated in severe chronic kidney disease or end-
cases of AKI with refractory fluid stage renal failure.
overload, severe electrolyte
disturbances, or uremia.
Key Points
• AKI is a reversible condition if
Complications treated early.
• Hyperkalemia • Identifying and addressing the
• Pulmonary edema underlying cause is crucial for
effective management.
• Metabolic acidosis
• Monitoring kidney function in
• Uremic syndrome (e.g.,
at-risk populations is essential
pericarditis, encephalopathy)
for prevention.
 Urinary Retention
Definition o Post-surgical complications (e.g.,
Urinary retention is the inability to pelvic surgery)
empty the bladder completely, leading
o Urinary tract infections (UTIs)
to the accumulation of urine in the
bladder. It can be acute or chronic. o Diabetes (due to neuropathy)

Types Symptoms
1. Acute Urinary Retention (AUR): • Difficulty or inability to urinate
Sudden and painful inability to pass
urine. Requires immediate • Severe suprapubic pain and
intervention. discomfort

2. Chronic Urinary Retention (CUR): • Distended bladder

Gradual onset with symptoms of • Urinary frequency and urgency (in
incomplete voiding, may be chronic cases)
asymptomatic or cause discomfort
• Incomplete voiding sensation
over time.

Causes Diagnosis
Obstructive: • Clinical evaluation: Patient history
o Benign prostatic hyperplasia (BPH) (medications, recent surgeries,
in men comorbid conditions).

o Urethral stricture • Physical examination: Palpation for

bladder distension, perineal exam.
o Bladder stones
• Bladder scan: Ultrasound to assess
o Pelvic masses (e.g., fibroids, bladder volume and post-void
tumors) residual (PVR).
o Neurogenic bladder (e.g., spinal • Urine analysis: To rule out
cord injury, multiple sclerosis) infections or other causes.
Non-obstructive: • Urodynamic studies: If chronic
o Medications (e.g., anticholinergics, retention is suspected to evaluate
opioids, diuretics) bladder function.
Management Complications
Acute Urinary Retention: • Infection: Urinary tract
o Immediate catheterization infections due to prolonged
(indwelling Foley catheter or catheterization.
suprapubic catheter) to relieve • Bladder damage:
distension. Overdistension of the bladder
can lead to permanent bladder
o Medications: Alpha-blockers
dysfunction.
(e.g., tamsulosin) for BPH,
anticholinergics for neurogenic • Renal damage: Prolonged
bladder. retention can lead to back
pressure on the kidneys,
o Treat underlying causes (e.g.,
causing hydronephrosis.
surgery for obstruction,
antibiotics for infection).
Chronic Urinary Retention: Key Points
o Manage underlying cause (e.g., • Emergency: Acute urinary
treat BPH with medication, retention is a medical
surgical intervention for emergency and requires
obstruction). immediate intervention to
avoid complications like renal
o Clean intermittent
failure or bladder damage.
catheterization (CIC) or
indwelling catheter for long- • Catheterization: The
term management. cornerstone of management in
o Neuromodulation therapy or acute retention.
bladder training for neurogenic • Chronic management:
bladder. Depends on the underlying
cause and may require surgical
intervention or long-term
catheterization.
 Testicular Torsion
Definition Diagnosis
Testicular torsion occurs when the o Clinical assessment is crucial,
spermatic cord twists, cutting off blood including the history and physical
supply to the testicle, leading to exam.
ischemia and potentially irreversible
o Ultrasound with Doppler: shows
damage.
reduced or absent blood flow to
the affected testicle.
Etiology o Urine analysis to rule out
infection.
It is most common in adolescent
males (ages 12-18) but can occur at o Surgical exploration may be
any age. It may be caused by needed if diagnosis is uncertain.
congenital malformation (bell clapper
deformity), trauma, or sometimes
occurs without any precipitating event.

Symptoms
o Sudden onset severe scrotal pain
(often unilateral)
o Swelling and erythema of the
scrotum
o Nausea and vomiting (due to pain)
o Absent cremasteric reflex on
examination
o High-riding testicle or abnormal
position (horizontal lie)
o Pain may radiate to the lower
abdomen or groin.
Management Prognosis
o Urgent surgery (orchiopexy or Prognosis is excellent if treated
orchiectomy) is the definitive within 6 hours. The longer the
treatment. Testicular salvage torsion persists, the higher the
is best if performed within 6 likelihood of testicular loss and
hours of symptom onset. infertility.
o Manual detorsion can be
attempted as an interim
measure before surgery. This
is done by rotating the testicle
externally (counterclockwise
in the right testicle and
clockwise in the left).
o If detorsion is successful,
surgery is still necessary to
prevent recurrence.

Complications
o Testicular necrosis and loss of
the testicle if not treated
promptly.
o Infertility if both testes are
lost.
 Ureteric Colic
Definition Clinical Features
Ureteric colic refers to severe pain caused by
• Pain: Severe, colicky pain that comes in
the obstruction of the ureter, typically due to
waves. The pain typically begins suddenly
the presence of a kidney stone, leading to
in the flank and radiates to the lower
distension and spasm of the ureter.
abdomen and groin.

• Hematuria: Blood in the urine, which may

Etiology be microscopic or grossly visible.

• Kidney stones: The most common cause, • Nausea and vomiting: Common due to
with stones typically passing from the the intensity of the pain.
renal pelvis to the ureter.
• Dysuria or frequent urination: If the stone
• Blood clots: Can obstruct the ureter, is near the bladder.
leading to similar symptoms.
• Restlessness: The patient often has
• Strictures: Ureteric strictures or scarring difficulty finding a comfortable position
due to previous infections, surgery, or due to the pain.
congenital abnormalities.

• Infections: Rarely, infections can cause

Diagnosis
edema or pus, leading to blockage.
• History and Physical Examination: The
classic presentation of sudden onset
Pathophysiology severe flank pain radiating to the groin,
with possible hematuria, is suggestive.
• Obstruction causes a backup of urine,
leading to increased pressure in the • Urinalysis: Microscopic hematuria is
affected kidney. common.

• The distension of the renal pelvis triggers • Imaging:

intense pain, which is classically colicky in
o Non-contrast CT scan of the
nature and radiates from the flank to the
abdomen: Gold standard for detecting
groin.
kidney stones and identifying the
• Spasm of the smooth muscle in the ureter location of obstruction.
contributes to the pain, often described as
o Ultrasound: Useful in pregnant
one of the worst types of pain.
patients or those who should avoid
radiation, but less sensitive than CT.

o X-ray KUB (Kidney, Ureter, Bladder):

Can detect radiopaque stones but
may miss smaller stones or those in
the ureter.
Management • Infection: Pyelonephritis or sepsis,
particularly if there is a delay in
• Pain Relief:
management.
o NSAIDs (e.g., ibuprofen) or
• Hydronephrosis: Enlargement of
opioids for severe pain.
the kidney due to retained urine.
o Alpha-blockers (e.g.,
tamsulosin) can help relax the Prognosis
smooth muscle of the ureter and
• Most small stones pass
facilitate stone passage.
spontaneously with adequate pain
• Hydration: Ensure adequate fluid management and hydration.
intake to encourage stone passage.
• Larger stones may require
• Observation: Small stones (less intervention, but the prognosis is
than 5mm) often pass generally good with appropriate
spontaneously with supportive treatment.
management.
Prevention
• Surgical Interventions:
• Increase fluid intake: Helps prevent
o Extracorporeal shock wave
stone formation.
lithotripsy (ESWL): For larger
stones or those that do not pass. • Dietary changes: Depending on the
type of stone (e.g., reducing oxalate-
o Ureteroscopy with stone
rich foods for calcium oxalate
extraction: For stones that are
stones).
too large or if ESWL is ineffective.
• Medications: Thiazide diuretics,
o Percutaneous
potassium citrate, or other agents
nephrolithotomy: In cases of
may be prescribed for recurrent
very large or complicated stones.
stone formation.
• Antibiotics: If there is associated
infection (e.g., pyelonephritis), Key Points
antibiotics are indicated.
• Sudden, severe, colicky pain in the
flank radiating to the groin is
characteristic.
Complications
• Non-contrast CT scan is the
• Acute renal failure: Due to
diagnostic tool of choice.
prolonged obstruction and pressure
buildup. • Pain management and hydration are
crucial in the initial treatment.
 Acute Pyelonephritis
Definition Clinical Features
Acute pyelonephritis is a sudden • Fever (often high)
bacterial infection of the kidney,
• Flank pain (often unilateral)
usually affecting one kidney. It is a
common cause of upper urinary tract • Dysuria, frequency, and urgency
infection (UTI) and can lead to • Nausea and vomiting
significant morbidity if untreated.
• Malaise, chills
• Costovertebral angle tenderness
Etiology
(positive Murphy's sign)
Most commonly caused by
• Tachycardia
Escherichia coli (80-90%), but other
organisms include Klebsiella,
Proteus, Enterococcus, and Diagnosis
Pseudomonas species. It often
• Clinical suspicion based on
arises from ascending infection from
symptoms
the lower urinary tract.
• Urine analysis: Pyuria,
bacteriuria, and sometimes
Risk Factors
hematuria
• Female gender (due to shorter
• Urine culture: Identifies the
urethra)
causative organism
• Urinary tract obstruction (e.g.,
• Blood culture: Positive in severe
kidney stones, pregnancy)
cases or bacteremia
• Catheterization or recent urinary
• Imaging: Ultrasound or CT may be
tract instrumentation
needed to rule out complications
• Diabetes mellitus like abscess, obstruction, or
• Immunocompromised states hydronephrosis.
(e.g., HIV, corticosteroid therapy)
• History of recurrent UTIs
Differential Diagnosis 5. Surgical intervention:
• UTI (lower tract infection) o If there is an abscess,
• Renal stones obstruction, or other
complications
• Appendicitis
• Ectopic pregnancy
Complications
• Pelvic inflammatory disease
• Renal abscess
• Sepsis or septic shock
Management
• Chronic kidney disease (if
1. Antibiotic therapy: recurrent or untreated)
o Empiric therapy (e.g., IV • Acute kidney injury
ceftriaxone, cefepime, or
piperacillin-tazobactam)
pending culture results Prognosis

o Adjust antibiotics based on • With prompt antibiotic

culture and sensitivity treatment, prognosis is generally
good.
o Duration typically 7-14 days,
longer for complicated cases • Mortality is rare but can increase
in immunocompromised
2. Fluids: Rehydration, especially patients or those with delayed
in febrile or vomiting patients treatment.
3. Analgesia: For pain
management (e.g.,
Prevention
acetaminophen or NSAIDs)
• Adequate hydration
4. Hospitalization:
• Proper hygiene, especially for
o Required for severely ill
women (wipe front to back)
patients, those with
comorbidities, or if oral • Prophylactic antibiotics in high-
antibiotics are not tolerated risk patients (e.g., pregnant
women, recurrent infections)
14 Hematological
Emergencies

• Acute Anemia (e.g., Hemorrhage)

• Sickle Cell Crisis
• Disseminated Intravascular
Coagulation (DIC)
• Hemophilia with Bleeding
 Acute Anemia (e.g., Hemorrhage)
Definition Clinical Features
Acute anemia refers to a rapid • Symptoms: Pallor, dizziness,
decrease in red blood cell mass or weakness, fatigue, confusion,
hemoglobin, often due to sudden blood shortness of breath, chest pain, or
loss or hemolysis, leading to syncope (fainting).
inadequate oxygen delivery to tissues.
• Signs: Tachycardia, hypotension,
cool extremities, increased
respiratory rate, diminished
Causes
peripheral pulses, and hypovolemic
• Trauma: External or internal bleeding shock (if severe).
due to accidents, fractures, or
lacerations. Diagnosis
• Gastrointestinal Bleeding: Peptic • History: Focus on trauma, surgery,
ulcers, esophageal varices, GI symptoms (e.g., hematemesis,
diverticulosis, or malignancies. melena), or obstetric history.
• Obstetric Hemorrhage: Postpartum • Physical Examination: Assess for
hemorrhage, ectopic pregnancy, signs of shock, hemorrhage, or other
placenta previa, or abruptio underlying causes.
placenta.
• Laboratory Tests:
• Surgical Bleeding: Postoperative
bleeding or bleeding due to o CBC: Low
complications of surgery. hemoglobin/hematocrit levels.

• Coagulopathies: Hemophilia, o Reticulocyte Count: Elevated in

disseminated intravascular response to acute blood loss.
coagulation (DIC), or anticoagulant o Coagulation Profile: To rule out
therapy. coagulopathies.
• Ruptured Aneurysm: Aortic or o Blood Type and Crossmatch:
splenic rupture. Important if transfusion is
anticipated.
o Serum Electrolytes and Renal
Function: To assess for shock-
related complications.
Management Monitoring
Resuscitation: • Monitor vital signs (heart rate,
o Airway, Breathing, blood pressure, oxygen
Circulation (ABC): Ensure saturation) and urinary output.
adequate oxygenation and • Repeat CBC and coagulation
circulation. profile to assess response to
treatment.
o IV Access: Establish 2 large-
bore IVs for fluid resuscitation
and blood transfusion if Complications
needed.
• Hypovolemic Shock: May
o Fluid Resuscitation: progress to multi-organ failure if
Crystalloid solutions (e.g., untreated.
normal saline or Ringer’s
• Acute Renal Failure: Due to low
lactate) to restore circulating
perfusion from hypovolemia.
volume.
• Cardiovascular
o Blood Transfusion: If
Complications:
significant blood loss
Tachyarrhythmias or myocardial
(typically >30-40% blood
infarction due to the increased
volume), administer packed
workload on the heart.
red blood cells (PRBCs).
• Disseminated Intravascular
Treatment of Underlying Cause:
Coagulation (DIC): In cases of
o Surgical intervention: For severe trauma or sepsis.
active bleeding or ruptured
organs.
Prognosis
o Medications: Use of
Depends on the severity of blood
procoagulants in cases of
loss, the underlying cause, and the
coagulopathy.
speed of intervention. Timely
o Oxygen Therapy: In severe resuscitation and correction of the
cases of anemia or shock. cause generally lead to good
outcomes.
 Sickle Cell Crisis
Definition 5. Hemolytic Crisis:
A sickle cell crisis is an acute An accelerated breakdown of red
complication of sickle cell disease blood cells, leading to anemia and
(SCD) characterized by the sudden jaundice, often precipitated by
onset of severe pain due to sickle- infection or stress.
shaped red blood cells obstructing
blood flow, leading to ischemia and
infarction of tissues. Clinical Features
• Severe pain in affected areas (e.g.,
bones, joints, chest)
Types of Sickle Cell Crisis
• Swelling in affected organs (e.g.,
1. Pain Crisis (Vaso-occlusive crisis):
spleen)
The most common form, resulting
from blockages in small blood • Fever, tachycardia, and signs of
vessels, causing pain in bones, systemic inflammation
joints, chest, abdomen, or other • Shortness of breath (in ACS)
areas.
• Jaundice (in hemolytic crisis)
2. Acute Chest Syndrome (ACS):
A life-threatening complication • Signs of hypovolemia (in splenic
involving lung infarction, sequestration)
pneumonia, or fat embolism,
presenting with chest pain, fever,
Indications for Hospitalization
and respiratory distress.
• Severe or unmanageable pain
3. Splenic Sequestration Crisis:
Rapid pooling of blood in the • Acute chest syndrome
spleen, leading to splenomegaly, • Signs of organ failure (e.g.,
hypovolemia, and shock. More respiratory distress, shock)
common in young children.
• Recurrent crises with inadequate
4. Aplastic Crisis: outpatient management.
Characterized by severe anemia due
to temporary cessation of red blood
cell production, often triggered by
parvovirus B19 infection.
Management Complications
Pain Management: • Organ damage (e.g., stroke, renal
High-dose opioids and non-opioid failure, heart failure)
analgesics for pain relief. Hydration
• Sepsis (due to splenic dysfunction)
with IV fluids to reduce blood
viscosity and improve circulation. • Chronic pain and disability

Hydration: • Increased risk of infection

IV fluids (e.g., normal saline or
Ringer’s lactate) to improve perfusion
Prevention
and prevent dehydration.
• Regular blood transfusions in high-
Oxygen Therapy:
risk patients to reduce the
For patients with low oxygen
frequency of crises
saturation or respiratory distress.
• Use of hydroxyurea to increase fetal
Antibiotics:
hemoglobin production and reduce
Empiric broad-spectrum antibiotics if
the occurrence of vaso-occlusive
infection is suspected, particularly for
episodes
acute chest syndrome.
• Vaccination against
Transfusion Therapy:
pneumococcus, Haemophilus
In cases of severe anemia, aplastic
influenzae type b (Hib), and other
crisis, or acute chest syndrome, red
pathogens due to splenic
blood cell transfusions may be
dysfunction
indicated.
• Preventive care, including pain
Supportive Care:
management plans and regular
Monitor vital signs, organ function,
medical check-ups.
and oxygenation. Provide
psychosocial support, especially in
recurrent crises. Differential Diagnosis
• Acute osteomyelitis
• Gallstones
• Infections (e.g., pneumonia, urinary
tract infection)
• Acute abdominal conditions (e.g.,
appendicitis, pancreatitis).
Disseminated Intravascular Coagulation (DIC)

Definition Pathophysiology
DIC is a complex, acquired • Activation of the clotting
disorder characterized by cascade leads to formation of
widespread activation of the fibrin clots in microcirculation.
coagulation system, leading to • As clotting factors and
both microvascular thrombosis platelets are consumed, there
and bleeding due to consumption is a paradoxical bleeding
of clotting factors and platelets. tendency.
• Endothelial injury contributes
Etiology to the activation of coagulation
pathways.
• Infections: Sepsis, particularly
from gram-negative bacteria.
• Trauma: Severe tissue injury, Clinical Features
burns, or head injury.
• Thrombotic manifestations:
• Obstetric complications: Skin necrosis, multi-organ
Placental abruption, amniotic failure (renal, hepatic,
fluid embolism, preeclampsia. pulmonary), seizures, altered
mental status, and gangrene.
• Malignancy: Acute
promyelocytic leukemia, • Bleeding manifestations:
metastatic cancer. Petechiae, ecchymoses,
• Other causes: Severe liver gastrointestinal bleeding,
disease, transfusion reactions, hematuria, oozing from
snake bites. injection sites, and prolonged
bleeding times.
• Symptoms vary depending on
the underlying cause and
extent of DIC.
Diagnosis • Blood products:
• Laboratory tests: o Platelets and fresh frozen
o Prolonged PT (Prothrombin plasma (FFP) if bleeding is
Time) and aPTT (Activated significant.
Partial Thromboplastin o Cryoprecipitate if
Time). fibrinogen levels are low.
o Low platelet count o Heparin in certain cases
(thrombocytopenia). (e.g., if thrombosis is
predominant and the
o Elevated fibrin degradation
underlying cause is not
products (FDP) and D-
bleeding).
dimers.
o Decreased fibrinogen
levels. Prognosis
• Clinical diagnosis requires the • The prognosis depends on the
presence of a triggering event underlying condition, the
with supporting laboratory speed of treatment initiation,
findings. and the severity of coagulation
abnormalities.

Management • Mortality rates are high in

severe DIC, particularly if it
• Treat the underlying cause: occurs with multiorgan failure
Prompt identification and or uncontrolled bleeding.
treatment of the triggering
condition (e.g., antibiotics for
sepsis, removal of the placenta
in obstetric cases).
• Supportive care: Fluid
resuscitation, organ support
(e.g., mechanical ventilation for
respiratory failure).
 Hemophilia with Bleeding
Definition Clinical Features
Hemophilia is an inherited bleeding • Spontaneous Bleeding: Common
disorder caused by a deficiency in in joints (hemarthrosis), muscles,
clotting factors, most commonly and soft tissues.
factor VIII (Hemophilia A) or factor IX
• Delayed Bleeding: After minor
(Hemophilia B). This leads to
trauma or surgery.
prolonged bleeding episodes after
trauma or surgery. • Hemarthrosis: Common
presenting sign; can lead to joint
deformity over time.
Types
• Soft Tissue Hematomas: Swelling
1. Hemophilia A: Deficiency of and pain in muscles.
Factor VIII (most common, ~80%
• Bleeding After Circumcision or
of cases).
Dental Procedures: May be first
2. Hemophilia B: Deficiency of sign in infants.
Factor IX.
3. Hemophilia C: Deficiency of
Diagnosis
Factor XI (less common and
usually milder). • Coagulation Profile:
o Prolonged activated partial
thromboplastin time (aPTT).
Etiology
o Normal prothrombin time (PT)
Hemophilia is X-linked recessive.
and platelet count.
Males are affected, and females are
typically carriers. o Low levels of Factor VIII
(Hemophilia A) or Factor IX
(Hemophilia B) on specific
assays.
• Genetic Testing: Confirmatory for
hemophilia and carrier detection.
Management Complications
• Factor Replacement Therapy: • Inhibitors: Development of
antibodies against the infused
o Hemophilia A: Factor VIII
clotting factors.
concentrates.
• Joint Damage: Repeated
o Hemophilia B: Factor IX
hemarthrosis can lead to joint
concentrates.
deformities and disability.
o Administered prophylactically or
• Intracranial Hemorrhage: A life-
on-demand during bleeding
threatening complication, especially
episodes.
after head trauma.
• Desmopressin (DDAVP): For mild
Hemophilia A, stimulates release of
stored Factor VIII. Prevention
• Antifibrinolytics: To reduce • Prophylaxis: Regular factor infusion
bleeding, used for oral or nasal to prevent spontaneous bleeding
bleeding. episodes.
• Cryoprecipitate: An alternative • Patient Education: Avoidance of
source of fibrinogen and clotting high-risk activities and trauma.
factors in emergencies.
• Emergency Plan: Ensure availability
of factor replacement therapy at all
times.
Emergency Management
• Active Bleeding: Immediate factor
replacement therapy to control Key Points for Emergency Care
bleeding.
1. Rapid Factor Replacement:
• Joint Bleeding (Hemarthrosis): Essential for bleeding control.
Rest, ice, compression, and
2. Prophylactic Treatment: For
elevation (R.I.C.E.), and factor
patients at high risk of bleeding,
replacement.
start early factor infusions.
• Trauma: If severe trauma occurs,
3. Avoid NSAIDs and Aspirin: These
initiate factor replacement therapy
medications worsen bleeding risk.
and manage symptoms according to
severity. 4. Monitor for Complications: Joint
bleeds, inhibitors, and internal
bleeding need close monitoring.
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