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MD Anaesthesiology Exam Notes

Approach Towards an Unconscious Patient

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1. DEFINITIONS & SPECTRUM OF CONSCIOUSNESS

Almost all coma traces to (1) widespread bihemispherical dysfunction or (2) suppression of the reticular activating system (RAS) in the upper brainstem/thalamus. — Harrison's Principles of Internal Medicine 22E

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2. IMMEDIATE PRIORITIES (BEFORE ANYTHING ELSE)

A–B–C–D–E: The Anaesthetist's Primary Survey

"It is never justified to delay attending to the basics of airway, breathing, and circulation while performing a more elaborate scoring evaluation." — Plum & Posner's Diagnosis and Treatment of Stupor and Coma

Empiric IV "coma cocktail" (when cause unknown and IV access secured):

• Dextrose 50% 50 mL IV (after checking glucose; treat hypoglycaemia empirically in resource-limited settings)
• Thiamine 100 mg IV (before or with dextrose to prevent Wernicke's encephalopathy)
• Naloxone 0.4–2 mg IV (if opioid overdose suspected)
• Flumazenil (if benzodiazepine overdose — use cautiously in polypharmacy/epilepsy)

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3. AIRWAY MANAGEMENT IN THE UNCONSCIOUS PATIENT

RSI Drug Sequence

1. Pre-oxygenate 3–5 min 100% O₂
2. Pre-treatment (optional): Fentanyl 1–3 µg/kg, Atropine in children/bradycardia
3. Induction: Ketamine 1–2 mg/kg (haemodynamically unstable) OR Thiopentone 3–5 mg/kg (raised ICP) OR Propofol 1–2 mg/kg (haemostable)
4. Cricoid pressure applied
5. Paralysis: Succinylcholine 1.5 mg/kg IV (preferred, fastest onset) OR Rocuronium 1.2 mg/kg (if succinylcholine contraindicated)
6. Laryngoscopy & intubation; confirm with waveform capnography
7. Release cricoid pressure after cuff inflation confirmed

Succinylcholine contraindications in unconscious patients: crush injuries >72 h, burns >72 h, denervation injuries, hyperkalemia, known malignant hyperthermia susceptibility.

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4. CLINICAL ASSESSMENT

4a. History (from relatives/witnesses/EMS)

• Onset: sudden (vascular/trauma) vs subacute (metabolic/infection)
• Preceding symptoms: headache, seizure, fever, focal deficit, vomiting
• Medical history: diabetes, epilepsy, liver/renal disease, hypertension, psychiatric illness
• Drug history: prescribed medications, recreational drugs, alcohol
• Circumstances: found alone, near medications, trauma scene, hospital setting

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4b. Level of Consciousness Scales

AVPU Scale (Rapid Bedside Tool)

• A — Alert and oriented
• V — Responds to Voice
• P — Responds to Pain
• U — Unresponsive

Glasgow Coma Scale (GCS)

• GCS ≤ 8 = severe brain injury → secure airway
• 9–12 = moderate; 13–15 = mild — Miller's Anesthesia 10e; Plum & Posner

FOUR Score (Full Outline of Unresponsiveness)

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4c. General Physical Examination

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4d. Neurological Examination

Pupils

CNS-depressant drugs lose corneal responses before pupils become unreactive to light. Preserved pupillary responses strongly suggest a metabolic cause. — Harrison's Principles of Internal Medicine 22E

Ocular Movements

Respiratory Patterns in Coma

Motor Examination

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5. DIFFERENTIAL DIAGNOSIS OF COMA

Mnemonic: "AEIOU TIPS"

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Formal Classification (Harrison's Principles of Internal Medicine 22E)

• Intoxications: alcohol, sedatives, opioids
• Metabolic: anoxia, hypoglycaemia, hyperglycaemia, hypo/hypernatraemia, hypercalcaemia, uraemia, hepatic failure, Addisonian crisis, thyroid disorders
• Severe systemic infection: septicaemia, pneumonia, typhoid, malaria
• Shock (any cause)
• Status epilepticus / post-ictal
• Hypertensive encephalopathy / PRES / eclampsia
• Hyperthermia / hypothermia
• Concussion, acute hydrocephalus

• Basal ganglia/thalamic haemorrhage, large MCA infarction
• Basilar artery thrombosis
• Brainstem infarction
• Brain abscess, subdural empyema
• Epidural/subdural haemorrhage, cerebral contusion
• Brain tumour with oedema
• Cerebellar/pontine haemorrhage or infarction
• Diffuse traumatic brain injury

• Subarachnoid haemorrhage (sudden severe headache + collapse)
• Bacterial meningitis, encephalitis
• Paraneoplastic/autoimmune encephalitis
• Carcinomatous meningitis

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6. INVESTIGATIONS

Immediate (Bedside/Point-of-Care)

• Blood glucose (fingerprick — treat hypoglycaemia immediately)
• SpO₂, ABG (acid-base, PaO₂, PaCO₂)
• ECG (arrhythmia, ischaemia)
• 12-lead ECG + continuous monitoring

Urgent Bloods

• Full blood count (infection, anaemia)
• Urea, creatinine, electrolytes (Na⁺, K⁺, Ca²⁺, Mg²⁺, phosphate)
• Liver function tests + ammonia
• Blood glucose, HbA1c
• Thyroid function (TFTs)
• Serum osmolality
• Coagulation (PT, APTT, INR)
• Blood cultures (if febrile)
• Toxicology screen (blood + urine)
• Cortisol (if Addisonian crisis suspected)
• Lactate

Neuroimaging

• CT head (non-contrast) — FIRST LINE: haemorrhage, mass lesion, herniation, hydrocephalus
  • Normal CT does not exclude: early bilateral infarction, brainstem infarction, encephalitis, axonal shearing, hypoxic injury, isodense subdural
• MRI Brain (+ DWI) — superior for posterior fossa, early ischaemia, diffuse axonal injury
• CT Angiography — if posterior circulation stroke suspected

CSF Analysis (Lumbar Puncture)

• Indicated: meningism, fever + no focal signs, SAH with normal CT
• Contraindicated: mass lesion / raised ICP, coagulopathy, overlying skin infection
• Test: opening pressure, cells (WBC/RBC), protein, glucose (paired serum glucose), Gram stain, culture, xanthochromia

EEG

• Essential for non-convulsive status epilepticus (NCSE)
• Metabolic coma: generalised slow δ or triphasic waves (frontal in hepatic failure)
• Sedative OD: diffuse fast β activity
• Herpes encephalitis: periodic lateralised epileptiform discharges (PLEDs)
• "Alpha coma" (unresponsive α): post-cardiac arrest, brainstem infarction — poor prognosis

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7. HERNIATION SYNDROMES

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8. RAISED INTRACRANIAL PRESSURE (ICP) MANAGEMENT

Cushing's Triad: Hypertension + Bradycardia + Irregular respiration → sign of impending herniation

Principles

• Cerebral Perfusion Pressure (CPP) = MAP − ICP; target CPP 60–70 mmHg
• Normal ICP: ≤ 15 mmHg; treat if > 20–22 mmHg

Immediate Measures

1. HOB 30°, head in neutral position
2. Ensure adequate oxygenation/ventilation; target PaO₂ > 60 mmHg, PaCO₂ 35–40 mmHg (avoid hypercapnia)
3. Avoid hypotension — maintain adequate MAP
4. Treat hyperthermia, seizures, pain/agitation
5. Mannitol 20% 0.25–1 g/kg IV bolus (osmotic agent)
6. Hypertonic saline 3% NaCl (alternative to mannitol)
7. Avoid glucose-containing fluids (worsen cerebral oedema)
8. Dexamethasone (only for oedema around tumours/abscesses; NOT for TBI or stroke)
9. Hyperventilation to PaCO₂ 30–35 mmHg — temporising only (causes vasoconstriction)
10. CSF drainage via external ventricular drain (EVD) if available
11. Decompressive craniectomy (surgical option)

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9. CEREBRAL AUTOREGULATION

• Normal range: MAP 50–150 mmHg — CBF remains constant
• Chronic hypertension: autoregulatory curve shifts right → risk of ischaemia at "normal" blood pressures
• Below lower limit → CBF ∝ MAP → ischaemia
• Above upper limit → hyperaemia → hypertensive encephalopathy, PRES

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10. SPECIFIC CAUSES — ANAESTHETIC MANAGEMENT PEARLS

Hypoglycaemia

• BGL < 3 mmol/L: 50% dextrose 50 mL IV → recheck
• Follow with 10% dextrose infusion; monitor regularly

Opioid Overdose

• Miosis, respiratory depression, bradycardia
• Naloxone 0.4–2 mg IV (q2–3 min, titrate); short half-life → repeat doses/infusion needed
• Airway support/intubation if severe

Benzodiazepine Overdose

• Flumazenil 0.2 mg IV (q1 min up to 1 mg) — caution in epileptics, chronic BZD users (precipitates seizures)

Status Epilepticus / NCSE

• Lorazepam 0.1 mg/kg IV OR diazepam 0.1–0.2 mg/kg IV
• If refractory: phenytoin/fosphenytoin, levetiracetam, sodium valproate
• Refractory SE: ICU admission, propofol/midazolam/thiopentone infusion
• EEG monitoring mandatory in intubated patients

Hepatic Encephalopathy

• Avoid hepatotoxic drugs; reduce nitrogen load (lactulose, rifaximin)
• Correct precipitants (GI bleed, infection, electrolyte disturbance)
• Airway protection often required in Grade III–IV

Meningitis/Encephalitis

• Dexamethasone 0.15 mg/kg IV then empiric antibiotics (ceftriaxone ± ampicillin ± acyclovir)
• Do NOT delay antibiotics for CT/LP if high suspicion

Diabetic Ketoacidosis / HHS

• Fluid resuscitation first (0.9% NaCl)
• Insulin infusion, electrolyte replacement
• Avoid rapid correction of glucose/sodium (cerebral oedema risk)

Eclampsia

• MgSO₄ 4–6 g IV loading, 1–2 g/hr maintenance
• Control BP: labetalol, hydralazine, nifedipine
• Airway: RSI with thiopentone, suxamethonium
• Deliver fetus

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11. BRAIN DEATH

Prerequisites (confounders must be excluded)

• Core temperature > 36°C
• No drug/sedative effect
• No metabolic derangement (Na⁺, glucose, acid-base)
• No neuromuscular blocking agents
• Circulatory stability

Clinical Criteria

1. Deep coma: unresponsive to all stimuli
2. Fixed dilated pupils (usually mid-sized; may be dilated)
3. Absent corneal reflexes bilaterally
4. Absent oculovestibular reflexes (caloric testing)
5. Absent gag and cough reflexes
6. Apnoea test: PaCO₂ rises to >60 mmHg (>8 kPa) with no respiratory effort
   • Pre-oxygenate 100% O₂; disconnect ventilator; deliver O₂ at 6 L/min via catheter
   • PaCO₂ rises ~2–3 mmHg/min; observe for 8–10 minutes

Ancillary Tests (where clinical testing incomplete)

• EEG (isoelectric/electrocerebral silence)
• Cerebral angiography (no intracranial flow)
• CT/MRI angiography
• Transcranial Doppler (absent flow/reverberant pattern)
• Nuclear scan (no cerebral perfusion)

"Brain death is the only type of brain damage recognised as morally, ethically, and legally equivalent to death." — Harrison's Principles of Internal Medicine 22E

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12. MONITORING IN THE UNCONSCIOUS PATIENT (ANAESTHETIC/ICU)

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13. FLOWCHART SUMMARY

UNCONSCIOUS PATIENT
        │
        ▼
   CALL FOR HELP + START TIMER
        │
        ▼
   PRIMARY SURVEY (ABCDE)
   ├─ Airway: Open + protect (intubate if GCS ≤ 8)
   ├─ Breathing: O₂, ventilation
   ├─ Circulation: IV access, fluids, monitoring
   ├─ Disability: GCS, pupils, BGL
   └─ Exposure: trauma signs, temp, rash
        │
        ▼
   EMPIRICAL TREATMENT
   (Dextrose + Thiamine + Naloxone)
        │
        ▼
   HISTORY + EXAMINATION
   (Focused neurological exam)
        │
        ▼
   INVESTIGATIONS
   (Bloods + CT head ± LP ± EEG)
        │
        ▼
   DIAGNOSIS → SPECIFIC TREATMENT
   (Structural / Metabolic / Toxic / Infectious)
        │
        ▼
   ICU ADMISSION + ONGOING MONITORING

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KEY EXAM POINTS (High-Yield)

1. GCS ≤ 8 = intubate; always document GCS before sedation/paralysis
2. The most common cause of coma is metabolic/toxic — not structural
3. Preserved pupillary reflexes strongly suggest metabolic coma (structural causes typically impair pupils)
4. Never withhold glucose + thiamine in undifferentiated coma
5. Always exclude and treat hypoglycaemia first — it is the most easily reversible cause
6. Herniation: ipsilateral blown pupil → uncal herniation; treat as emergency
7. Succinylcholine is the fastest-onset paralytic for RSI but check K⁺ and contraindications in trauma
8. Hyperventilation is only a temporising measure for raised ICP (lasts <30 min)
9. Brain death apnoea test: PaCO₂ must exceed 60 mmHg — not simply "high"
10. Normal CT does not exclude encephalitis, axonal injury, posterior fossa infarction, isodense subdural

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