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SN10 SHORT NOTE 5M

Write a short note on the clinical approach to coma, including the Glasgow Coma Scale.

General Medicine · Final Professional

Definitions

Consciousness has two components: arousal (wakefulness), maintained by the ascending reticular activating system (ARAS) of the brainstem and thalamus, and awareness (content), requiring the cerebral cortex. Coma results from damage to either.

StateDescription
ComaUnrousable unresponsiveness — eyes closed, no response to vigorous stimulation, no sleep-wake cycles
StuporRousable only by vigorous, repeated stimulation
Vegetative stateWakefulness without awareness — eyes open with sleep-wake cycles, but no purposeful response
Minimally conscious stateInconsistent but reproducible evidence of awareness
Locked-in syndromeFully conscious and aware, but quadriplegic and anarthric from ventral pontine lesion; communicates only by vertical eye movements and blinking. Frequently misdiagnosed as coma — a devastating error
Brain deathIrreversible loss of all brainstem function

Mechanism — WHY the Patient Is Comatose

Coma requires one of three lesions:

1. Diffuse bilateral cortical dysfunction — metabolic, toxic, hypoxic, infective.

2. Brainstem lesion damaging the ARAS — pontine haemorrhage, basilar occlusion.

3. Mass lesion causing herniation and secondary brainstem compression.

A unilateral hemispheric lesion does not cause coma unless it is large enough to shift and compress the brainstem — a point that guides the whole assessment.

Causes

Causes of coma

Structural — stroke (infarct or haemorrhage), subarachnoid haemorrhage, subdural or extradural haematoma, tumour, abscess, trauma, hydrocephalus

Infective — meningitis, encephalitis, cerebral malaria, sepsis, tuberculoma

Metabolic — hypoglycaemia, hyperglycaemia (DKA, HHS), hyponatraemia, hypercalcaemia, uraemia, hepatic encephalopathy, hypothyroidism (myxoedema coma), adrenal crisis, hypoxia and hypercapnia

Toxic — alcohol, opioids, benzodiazepines, tricyclics, carbon monoxide, organophosphates, heavy metals

Others — post-ictal state and non-convulsive status epilepticus, hypothermia and hyperthermia, Wernicke's encephalopathy, hypertensive encephalopathy, psychogenic unresponsiveness

The Glasgow Coma Scale

ResponseScoreCriteria
Eye opening (E)4Spontaneous
3To speech
2To pain
1None
Verbal (V)5Oriented
4Confused conversation
3Inappropriate words
2Incomprehensible sounds
1None
Motor (M)6Obeys commands
5Localises to pain
4Withdraws from pain
3Abnormal flexion (decorticate)
2Extension (decerebrate)
1None

Total 3–15. Severity: severe ≤ 8, moderate 9–12, mild 13–15. A GCS of 8 or less indicates inability to protect the airway and is the conventional threshold for intubation.

Reporting rules: always record the three components separately (E, V, M) rather than only the total, since the same total can reflect very different states; the motor score carries the most prognostic weight; and record the best response. Note limitations — intubation (record V as "T"), sedation, periorbital swelling, aphasia, and deafness all confound the score.

Clinical Assessment

1. Resuscitate first — ABC, and check glucose immediately.

2. History from relatives, paramedics and any witness: speed of onset (abrupt suggests vascular or seizure; gradual suggests metabolic, infective or mass lesion), preceding headache, fever, trauma, seizure; past medical history (diabetes, epilepsy, liver or renal disease, psychiatric illness); drug and alcohol history, and access to medicines and poisons; and the environment in which the patient was found.

3. General examination: vital signs including temperature; breath odour (ketones, alcohol, uraemia, hepatic fetor); skin — needle marks, rash (meningococcal purpura), jaundice, cyanosis, cherry-red discoloration (carbon monoxide), signs of trauma including Battle's sign and raccoon eyes; check for a medical alert bracelet; examine for neck stiffness (avoid if cervical spine injury is possible).

4. Neurological examination — the localising core:

  • Pupils: pinpoint and reactive → opioids or pontine lesion; fixed mid-dilated unilateral → third nerve compression from uncal herniation (an emergency); fixed dilated bilateral → severe hypoxia, brain death, atropine, or massive herniation; normal reactive pupils in a deeply comatose patient strongly suggest a metabolic or toxic cause.
  • Fundoscopy — papilloedema, subhyaloid haemorrhage (subarachnoid haemorrhage).
  • Eye movements: spontaneous roving movements imply an intact brainstem; oculocephalic (doll's eye) reflex and oculovestibular (cold caloric) testing assess brainstem integrity (never perform doll's eye testing with a suspected cervical injury).
  • Corneal reflex, gag and cough reflexes.
  • Motor response — asymmetry indicates a structural lesion; decorticate posturing localises above the red nucleus, decerebrate posturing below it and is more ominous.
  • Respiratory pattern: Cheyne–Stokes (bihemispheric or metabolic), central neurogenic hyperventilation (midbrain), apneustic (pons), ataxic (medulla — pre-terminal).
  • Reflexes and plantars; fundal and meningeal signs.
CLINICAL PEARL

Pupils are the most valuable single sign in coma, because the pathways controlling them are anatomically adjacent to the ARAS and are relatively resistant to metabolic insult. Preserved, symmetrical, reactive pupils in a deeply unconscious patient point strongly to a metabolic or toxic cause rather than a structural one — and metabolic causes are the reversible ones.

Investigations

  • Capillary glucose immediately, then electrolytes, calcium, renal and liver function, ammonia, CBC, coagulation, arterial blood gas, blood cultures, thyroid function and cortisol where indicated.
  • Toxicology — blood alcohol, urine drug screen, paracetamol and salicylate levels, carboxyhaemoglobin.
  • CT brain — urgently for structural causes; MRI for posterior fossa and early ischaemia.
  • Lumbar puncture after imaging, for suspected meningitis, encephalitis or subarachnoid haemorrhage with a negative CT.
  • EEG — essential to detect non-convulsive status epilepticus, an important reversible cause of unexplained coma.
  • ECG, chest X-ray, and cervical spine imaging in trauma.

Management

1. Airway, breathing, circulation — intubate if GCS ≤ 8 or the airway is unprotected; oxygen, ventilation, fluids and vasopressors as required. Immobilise the cervical spine if trauma is possible.

2. The "coma cocktail" — give immediately where indicated: glucose (after or with thiamine in the malnourished or alcoholic, to avoid precipitating Wernicke's), naloxone for suspected opioid toxicity, and consider empirical antibiotics and aciclovir where CNS infection is possible.

3. Treat the identified cause — surgical evacuation of haematoma, antibiotics, antiepileptics, correction of electrolytes, antidotes, dialysis.

4. Manage raised intracranial pressure — head-up positioning, normocapnia, avoidance of hypotonic fluids, mannitol or hypertonic saline, and neurosurgical referral.

5. General care: eye protection, pressure area care, DVT prophylaxis, nutrition, bladder and bowel care, and glycaemic control.

6. Prognostication and communication with the family, and, where recovery is impossible, discussion of ceilings of care and organ donation in accordance with local law.

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