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CDHB

Stupor and Coma

Coma or stupor should be regarded as a potentially life-threatening emergency until:

1. Vital functions are stabilized.
2. The cause of coma/stupor is diagnosed.
3. Reversible causes are corrected.

This section is concerned with the diagnosis and management of the patient with stupor or coma of uncertain cause.

Emergency Management / Resuscitation

Refer to Emergency Management/Resuscitation.

Causes

There are 5 main causes of coma:

• Drug overdose
• Head injury
• Intracranial lesions (haemorrhage, infarction, tumour)
• Toxic/metabolic
• Infection

Distinguish between anatomic and metabolic causes. "Metabolic" implies any disorder which has a diffuse effect on cerebral metabolic pathways.

• Structural
  • Supratentorial
    • Extradural or subdural haematoma
    • Cerebral - haemorrhage, infarction, cyst or tumour, hydrocephalus.
  • Subtentorial
    • Brainstem / cerebellar - infarction, haemorrhage, tumour, abscess or cyst.
• Metabolic
  • Drugs - alcohol, hypnotics, psychotropics.
  • Hypoglycaemia / hyperglycaemia.
  • Hypoxia - shock, cardiac arrest, carbon monoxide.
  • Electrolyte or acid / base disturbance - acidosis, alkalosis, hyponatraemia, hypernatraemia, hypercapnia, hyperosmolar coma.
  • Encephalopathies - toxic, hepatic or renal failure.
  • Endocrine - hypopituitarism, hypothyroidism, hypoadrenalism.
  • Thiamine deficiency.
  • Hypothermia/hyperthermia.
• Other
  • Head injury.
  • Epilepsy / post-ictal.
  • Hysteria / hypnosis.
  • Infection - encephalitis, meningitis, septicaemia.

    Note: Obtaining an accurate history is vital - this may have to wait until general supportive care has been commenced - contact relatives, GP, friends.

Examination

General

• Look for evidence of head injury, IV drug abuse, signs of chronic illness.
• Temperature. Remember hypothermia/ hyperthermia. Use high (up to 42°C) or low (down to 25°C) reading thermometers if necessary.

Neurological

The neurological examination is directed at:

• Detecting meningeal irritation.
• Defining the level of consciousness.
• Assessing brainstem function.
• Looking for focal/lateralizing features.

Meningism

In all but the deepest coma, meningeal irritation (from meningitis or subarachnoid haemorrhage) will cause resistance to passive neck flexion (but not neck extension or rotation). Kernig's sign (resistance to hip flexion) is usually positive in association with neck stiffness in diffuse meningeal irritation from meningitis or subarachnoid haemorrhage.

The Level of Consciousness

The Glasgow Coma Scale is the best hierarchical assessment of the level of consciousness. The response to commands, calling the patient's first name and painful stimuli are recorded for eye opening, limb movement and vocalization. Suitable painful stimuli include supraorbital pressure (applied with the thumb) for central stimulation and nailbed pressure (applied with the shaft of a pen) for peripheral stimulation. All four limbs are tested individually for movement and the best response scored, but note should be made of any asymmetry. Assessment of the level of coma should be made serially. If there is deterioration, urgent action is required.

Brainstem Function

The brainstem reflexes are important in identifying lesions which may be affecting the reticular activating system (a region important in maintaining consciousness), explaining the reason for coma and determining the viability of the patient. The reflexes used relate to the pupils, corneal reflex, ocular movement and respiratory pattern.

• Pupil size and reactivity

  If the pupils are of normal size and reaction then the midbrain is intact and the cause of coma is more likely to be metabolic rather than structural. Note:

  • Opiates can produce pinpoint pupils with constriction to light too small to see.
  • Atropine and tricyclic poisoning can produce dilated and fixed pupils.
  • Enlarged (>5 mm) and unreactive pupil(s) suggest : a tectal midbrain lesion (intrinsic or secondary to compression), or unilateral or bilateral III nerve lesions, or mydriatic eye drops, or anticholinergic drugs, or orbital trauma.
  • Bilateral pinpoint pupils (<1 mm) suggest: bilateral pontine lesions, or opiate overdose, or miotic eyedrops for glaucoma.
  • Midposition fixed pupils suggest midbrain lesion.
  • Small reactive pupils suggest: diencephalic lesion, or metabolic cause.

  Reminder: Pupillary pathways are relatively resistant to metabolic insults with the exception of drugs and anoxia.

• Corneal Reflex

  Gently touch the cornea with a wisp of cotton wool. Intact blink reflex confirms integrity of cranial nerves V (afferent) and VII (efferent) plus pontine connections. Brushing the eyelashes is an alternative but less potent stimulus.

• Eye Movements

  The oculomotor examination comprises observation of eye deviation, spontaneous eye movements, caloric testing, and oculocephalic reflex (Doll's eye response):

  • Eye deviation.
    • Except for mild ocular divergence, dysconjugate ocular deviation suggests structural brainstem lesion if pre-existing strabismus excluded. Eyes that are directed straight ahead have no localizing value.
    • Conjugate horizontal (lateral) eye deviation is due to either a large ipsilateral hemisphere lesion or contralateral pontine lesion.
    • Conjugate downwards deviation is usually due to brainstem lesions (mostly from tectal compression), but may be seen in hepatic coma.
    • Downwards and converged eyes are seen in thalamic and subthalamic lesions.
    • Conjugate upwards deviation is poorly localizing.
  • Spontaneous eye movements.
    • Spontaneous, conjugate, roving movements suggest midbrain and pons intact and favours bilateral hemisphere dysfunction or metabolic/toxic cause.
    • Nystagmus in a comatose patient suggests an irritative or epileptic supratentorial focus.
  • Oculocephalic reflex (Doll's eye response):
    • This reflex is tested by sudden passive rotation of the head laterally whilst observing the movement of the eyes. In coma with an intact brainstem the eyes will move conjugately and in a direction opposite to head movement. The types of possible response parallel the ocular responses in caloric testing.
    • Oculocephalic (and caloric) responses are generally normal in hemisphere lesions.

      Note: Do not attempt the oculocephalic manoeuvre if neck injury is suspected.

  • Consider performing caloric testing - seek advice.

Respiratory Pattern

• The pattern of respiration has less localizing value than the neuro-ophthalmic changes detailed above but may give useful additional information.
  • Cheyne-Stokes respiration (slow oscillation between hyperventilation and hypoventilation) suggests bilateral cerebral hemisphere dysfunction and if stable, usually implies a relatively good prognosis.
  • Apneustic breathing (prolonged inspiratory gasp with end-inspiratory pause) generally accompanies lower pontine lesions.

Motor Function

• Observe responses to noxious stimuli applied to nailbeds, sternum or supraorbital ridges. Normal responses include withdrawal of limb ± grimace/groan, and implies intact sensory and motor pathways to and from cortex. Note that adduction/flexion of a limb can occur at spinal reflex level.
• Abnormal Responses include several stereotyped postures of limbs:
  • Decorticate posturing /rigidity (flexion of elbows and wrists, leg extension). Decorticate posturing generally carries a less serious prognosis and is associated with more rostral supratentorial lesions.
  • Decerebrate posturing/rigidity (extension of arms and legs).
    Decerebrate posturing is often associated with brainstem or diencephalic injury. Note that these patterns are often incomplete, variable and can interchange. Both may accompany hypoxic or hypoglycaemic coma.
• Look for any asymmetry of limb movement or reflexes which would favour an anatomic lesion. (Hypoglycaemia is however a well described metabolic cause of focal neurologic signs).
• The presence of partial (focal) seizures generally indicates a focal cause of coma, though some metabolic causes, especially hypoglycaemia, can produce focal seizures.
• The presence of multifocal myoclonus or generalized seizures raises possibility of metabolic or ischaemic-hypoxic aetiology.

Investigations

• CBC + diff.
• Glucose, Na, K, osmolality, Ca, AST, ALT, GGT, ALP, bili.
• Arterial blood gases.
• Blood cultures - 2 sets.
• Drug screen.
• CT brain unless metabolic cause definitely identified. MRI if CT inconclusive.
• If meningitis a possibility give antibiotics, do CT, then lumbar puncture if safe to do so.
• EEG may be considered to identify psychogenic unresponsiveness or partial complex status epilepticus.

Topic Code: 1541