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Home | Articles | Neurology | Coma

Coma

Last updated 20th May 2022

Always exclude hypoglycaemia in coma as it can clinically mimic most causes of coma!

Causes

  1. These are best considered as structural or metabolic
  2. A useful way to remember the causes is as follows
    Causes
    A=Apoplexy (the old name for stroke) this should include SAH, SDH, & non-vascular causes including tumour
    E=Epilepsy, electrolyte imbalance eg hypo or hypernatraemia, hypercalcaemia
    I=Injury, infection including meningitis and encephalitis
    O=Overdose
    U=Uraemia
    3Ds=Drink, Drugs, Diabetes
    5Hs=Hypoglycaemia, hypothermia, hepatic failure, hypothyroidism, hysterical

 

Clinical Scenarios

  1. Coma with focal brain stem or lateralising signs – consider stroke, abscess, tumour. Occasionally hypoglycaemia. Needs CT scan
  2. Coma with no focal or lateralising signs – consider overdose, epilepsy, metabolic causes. Also likely to need CT scan.
  3. Coma with neck stiffness – must exclude meningitis and subarachnoid haemorrhage. Again likely to need CT scan.

Neurological Evaluation

  1. The most important element in the evaluation of a comatose patient is the witness account, if available.
  2. This is followed by the coma examination which has 5 important components.

General Examination

  1. Bruising around eyes (racoon eyes) or mastoid process (Battle’s sign ) suggest intracranial trauma
  2. Petechial rash suggests meningococcal septicaemia
  3. Neck stiffness suggests meningitis/SAH but can be subtle or absent if deeply comatose
  4. Cherry red lips suggest carbon monoxide poisoning

Respiratory Patterns

  1. Cheyne-Stokes or periodic breathing is common and does not distinguish structural from metabolic causes
  2. Hyperventilation suggests acidosis eg DKA, aspiration or pulmonary oedema

Pupil Responses

  1. Unilateral unreactive dilated pupil suggests either herniation of uncus (part of temporal lobe) or an expanding PCA aneurysm
  2. Bilateral fixed dilated pupils suggests coning, anoxic encephalopathy from cardiac arrest or tricyclic poisoning (usually large but with some reaction)
  3. Pinpoint pupils which are reactive to light (though this may be difficult to see) suggest pontine haemorrhage or infarction, or opiate overdose

Eye Movements

  1. Conjugate deviation of both eyes means ipsilateral hemisphere lesion, usually a large stroke – patient looks away from the hemiparesis
  2. Bilateral fixed mid position (absent dolls eye movements) indicates severe brain stem dysfunction but do not rotate neck if there is suspicion of cervical spine injury
  3. Random roving conjugate eye movements (windshield wiper eye) are non-localising

Motor Responses

  1. Hemiparesis likely to represent a structural cerebral hemisphere or brain stem lesion
  2. Decorticate posture (arms flexed, legs extended) means disorder above the brain stem ie large cortical or subcortical lesion
  3. Decerebrate (arms and legs extended) carries a worse prognosis & usually means brain stem compression, but can occasionally occur with metabolic causes eg hypoglycaemia

Immediate Management

  • Airway
  • Breathing – high flow oxygen
  • Circulation – heart rate, BP, capillary return
  • Disability – ie neurological dysfunction including capillary blood glucose
  1. If GCS <8 call Anaesthetist as will be unable to protect airway during CT head scan
  2. Altered consciousness (AVPU = V or less) without a clear diagnosis should warrant senior review

Investigations

  1. Consider all of the following tests: BG, U&E, LFT, CRP, FBC, blood culture, blood gases, blood and urine for drug screen, CXR, ECG
  2. Plus urgent CT scan followed by LP in selected cases

Consider and Correct Reversible Causes

  1. Glucose – consider 50ml 50% glucose in all patients especially diabetic NB rapid reagent tests have false negative rate 6-8% for hypoglycaemia so pre-treatment blood sample for laboratory analysis is useful retrospectively
  2. Thiamine – consider if ophthalmoplegia or signs of alcohol abuse (Wernickes). If in doubt give IV pabrinex paired ampoules – see Alcohol Withdrawal Section
  3. Naloxone – consider in any unconscious patient in whom cause unclear, especially if pinpoint pupils or needle marks.  A bolus of 0.4mg will cause convulsions in opiate dependent patients. Suggest 0.1mg boluses repeated to 0.4mg whilst supporting airway/breathing. Always important to oxygenate and ventilate patient before giving Naloxone as it can cause a surge in catecholamines which can precipitate VF in the presence of raised CO2. Consider using a bag-valve mask with augmented ventilations before giving Naolxone in hypoventilating patients.
  4. Flumazenil – consider if benzodiazepine overdose likely, but note can be pro-convulsant or pro-arrhythmic if tricyclic overdose. Give 0.2mg IV initially see page on Benzodiazepines.

Coma Following Cardiac Arrest

  1. Indicators of poor prognosis include delay >10 min before CPR, CPR duration >30 min, coma >72 hours post arrest
  2. Consider ventilation on ICU for up to 24 hours for stable patients with reasonable prior functional status, then stop sedation and muscle relaxants and re-assess neuro function.  Selected patients will be suitable for therapeutic hypothermia for first 24 hours in ICU
  3. Absence of roving eye movements on day 1, absence of motor or pupil responses/dilated pupils on day 3, predicts death or persistant vegetative state.

Content Updated by Dr Ondrej Dolezal