Coma
Occurs when pathways between cerebral cortex and reticular activating system in pons interrupted.
Causes
Vascular
Haemorrhage
Infarction
ICP
Blood
Oedema
SOL (tumour, abscess)
CSF (hydrocephalus)
Infection
Meningitis
Encephalitis
Abscess
Neuronal metabolism
Glucose
Hypoxia
Hypercapnia
Acid-base
Temperature
Endocrine
Thiamine
Seizures
Drugs/Poisons
GCS
Severity and progression.
Motor response most reliable component.
Decerebrate - upper limb extension.
Decorticate - the upper limb flexion (corticate cuddle).
Pupils
Unilateral dilation of a pupil suggests raised ICP and uncal herniation of the temporal lobe compressing the third nerve.
Midbrain lesions typically result in loss of light reflex with mid-positioned pupils.
Pontine damage causes reactive miotic pupils (pontine = pinpoint).
Fixed–dilated pupils indicate severe brainstem damage.
Drugs - opioids, sympathomimetics, antimuscarinics.
CT
Urgent unless cause clear and no evidence raised ICP.
LP should not be undertaken until CT has confirmed patent basal cisterns.
PCR allows confirmation of infective causes even after ABX.
Management
Treat cause
Secondary injury protection
Cerebral ischaemia
Initiates a cascade of intracellular events that result in cell death.
Level of hypoxia at which neurones become clinically ‘silent’ is different from the level causing cell death.
Clinical picture may therefore be reversible.
Areas of cell death (trauma, infarction) will be surrounded by an area of tissue with reversible hypoxia.
Infarction
Aspirin if confirmed ischaemia.
Thrombolysis within 3h if systemic or 6h if directly into affected artery.