Toxic: Alcohol abuse and overdose with drugs, for example opiates.

Metabolic/endocrine: Hypoglycaemia, hyperosmolar non-ketotic coma and diabetic ketoacidosis in diabetes; electrolyte disturbances, including hyponatraemia or hypernatraemia and hypercalcaemia; renal failure leading to uraemia; hepatic failure causing encephalopathy and raised ammonia; and myxoedema coma.

Vascular: SAH, hypertensive encephalopathy and vasculitis.

Ischaemia: Anoxic encephalopathy (post-CPR) and carbon monoxide poisoning.

Infection: Meningitis, encephalitis and generalised sepsis.

Posttraumatic following severe head injury.

Epilepsy: Postictal state and status epilepticus.

Others: Carbon dioxide narcosis and Wernicke’s encephalopathy.

• Focal (can be supratentorial or infratentorial):

Infarction.

Neoplasm: Primary or secondary.

Infection: Intraparenchymal abscess, subdural empyema and herpes simplex encephalitis.

Haematoma (subdural or extradural) and traumatic contusions.

Associations/Risk Factors

See under aetiology.

Pathology/Pathogenesis

Maintenance of consciousness relies upon an intact reticular activating system (RAS). Fibres for RAS start in the pons and ascend through mid-brain to terminate in thalamus and hypothalamus. An infratentorial lesion may directly affect the RAS while a supratentorial lesion may cause cortical dysfunction and transtentorial herniation leading to brainstem distortion and coma. Diffuse or metabolic causes result in coma by impairing cerebral metabolism.

History

It is important to obtain any relevant history from witnesses, ambulance staff, police, relatives or friends.

Examination

A sequential examination can proceed as follows:

• Airway (risk of compromised airway, therefore check need for airways adjunct or formal intubation and ventilation: inform on-call anaesthetist).
  
• Breathing (respiratory rate, rhythm and character, for example Cheyne–Stokes, hyperventilation, apneustic or ataxic pattern due to progressive herniation).
  
• Circulation (pulse rate, BP, rhythm—check for evidence of Cushing’s triad (↑BP, ↓PR and irregular respiratory pattern).
  
• GCS (see Appendix 2).
  
• Temperature and glucose (fingerstick).
  
• Appearance and inspection on exposure: Meningococcal purpuric rash, alcoholic fetor, jaundice, otorrhoea or blood from ear.
  
• Eyes: Pupils (size, symmetry and reaction), extraocular movements (spontaneous; internuclear opthalmoplegia; vestibulo-ocular reflex or caloric test; oculocephalic reflex or doll’s head manoeuvre) and fundoscopy (papilloedema).
  
• Brainstem function: Corneal reflex and gag reflex.
  
• Motor: Check tone, reflexes and plantar response and note any asymmetry. Response to pain as decorticate posturing (implying lesion at cortical or subcortical level) or decerebrate posturing (brainstem pathology) should be noted.
  
• Full general examination.