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Coma

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Non-traumatic coma

Aetiology

Likely causes of nontraumatic coma based on neurological findings

No focal or lateralising signs

With meningism

Without meningism

  • anoxic-ischaemic conditions
  • metabolic disturbance
  • intoxication
  • systemic infections
  • hyper/hypothermia
  • epilepsy

Focal brainstem or lateralising cerebral signs

History

Examination

CNS

  • position, posture and spontaneous movement of patient
  • GCS
  • meningism: important to distinguish neck stiffness due to meningeal irritation from neck stiffness due to coning. Former associated with positive Kernig's and Brudzinski's (flexing of one hip causes flexion of the other) signs
  • fundi: ? papilloedema, haemorrhage, emboli, retinopathy
  • brainstem reflexes:
    • pupils: midbrain lesions cause loss of light reflex with mid-point pupils; pontine lesions cause miosis but normal light response; pin-point pupils following pontine haemorrhage; central diencephalic herniation causes fixed dilated pupils: can be distinguished from fixed dilatation due to atropine-like drugs by pilocarpine induced miosis; Horner's associated with anhydrosis of ipsilateral side of body may be due to an ipsilateral lesion in the hypothalamus, thalamus or brainstem; Horner's with ipsilateral anhydrosis of face only may be due to disease affecting the wall of the ipsilateral carotid artery; metabolic coma may make light reflexes unduly brisk and therefore pupils relatively small; most drug intoxications cause small and sluggishly reactive pupils
    • corneals: usually retained until coma is very deep except in drug induced coma. Loss of corneal reflex sign of poor prognosis if not due to drugs
    • spontaneous eye movements:
      • conjugate deviation of eyes suggests ipsilateral hemisphere or contralateral brainstem lesion
      • depression of eyes below meridian seen with damage at level of midbrain tectum and in metabolic coma
      • disconjugate resting position of eyes suggests damage to IV or VI fascicles or nerves
      • roving eye movements: cannot be mimicked and exclude pyschogenic causes
      • periodic alternating gaze ("ping-pong" gaze) is repetitive conjugate horizontal ocular deviation. Aetiology uncertain
      • spontaneous nystagmus reflects interaction between the oculovestibular system and the cerebral cortex and thus is rare in coma
      • retractory nystagmus may be seen with midbrain lesions
      • ocular bobbing associated with destructive lesions in low pons and with cerebellar haematoma or hydrocephalus
    • reflex eye movements:
      • oculocephalic reflex. Lost in patients with pontine depression.
      • oculovestibular reflex more useful and accurate. Normal response is nystagmus with quick phase to contralateral side. Tonic response with conjugate movement of eye towards stimulated side indicates an intact pons suggesting a supratentorial cause for coma. Dysconjugate or no response indicates BS damage/depression. Vertical movement of eye suggests drug OD because many drugs affect lateral eye movement. Definitive way of identifying patients in psychogenic coma who will show normal nystagmus and frequently be distressed by the procedure
    • gag
  • motor function: tone, response to pain and reflexes. ? asymmetry

  • tremors: most often seen in early hypoglycaemic encephalopathy, TTX, acute uraemia, hypercapnia, drug intoxication (especially with sympathomimetics)
  • myoclonus: multifocal asynchronous myoclonus seen in hypoxic-ischaemic encephalopathy, chronic hepatic failure, uraemia, respiratory failure, intoxication with methaqualone and psychedelic agents
  • flap: hepatic failure, respiratory failure, subacute uraemia
  • rigidity: end-stage hepatic failure, hypoglycaemia, acute renal failure, hyperthermia, hypothermia. Rigidity with dystonic posturing suggests amphetamine or phenothiazine poisoning
  • fits: occur in metabolic encephalopathy due to uraemia, hypoglycaemia, various types of metabolic disturbance (eg ethylene glycol, salicylates)

RS

- pattern of breathing gives important clues
- periodic breathing is common in patients with metabolic encephalopathy. Occasionally Cheyne-Stokes seen in this group
- long cycle periodic breathing suggests relatively high BS lesion
- central neurogenic hyperventilation implies a lesion at the level of the upper pons
- short cycle periodic breathing: lesion low in BS. Associated with poor prognosis
- smell of breath: ?ketones, alcohol, uraemic foetor

Autonomic response

- hypotension unresponsive to volume expansion in the context of metabolic/drug induced coma suggests intoxication with barbiturates or opiates, myxoedema, Addisonian crisis. Occult sepsis must be excluded

Investigation

  • EEG. Major use is in diagnosis of subclinical status epilepticus, particularly in patients with acute structural brain lesions, or complex partial seizures. May also be useful in diagnosis of feigned coma. Prognostic value probably not as great as that obtained from careful observation of clincal signs
  • evoked potentials: somatosensory and brainstem auditory evoked potentials may prove to be useful in determining likely prognosis. Considerable technical problems as a result of electrical interference in ICU

Prognosis

Prognosis in nontraumatic coma

Levy DE, Bates D, Caronna JJ et al

Annals of Internal Medicine 94: 293-301; 1981

- 500 patients
- serial neurological examinations
- followed up for 1 year
- early neurological signs related to best level of functional recovery
- 5 levels of recovery defined:

  • good: able to resume normal life
  • moderate disability: unable to regain their previous level of function but independent in daily living
  • severe disability: retain cognition but dependent on others for daily support
  • vegetative state: awake but unaware
  • no recovery: persistent coma to death

- the longer coma lasted the less the chances of regaining independent function. Only one patient who survived in coma for a week achieved a good recovery within a year. About 1/3 of patients who appeared vegetative at end of 1 day regained independent activity within 1 year; when vegetative state persisted for 1 wk or more the likelihood of achieving a mod disability or good recovery within 1 year declined to 7%
- no evident relation between outcome and presence of epilepsy or myoclonus
- patients with subarachnoid haemorrhage and other cerebrovascular disorders had worst outcome: 74% never recovered from coma, and only 9% achieved mod disability or good recovery.
- patients with hepatic encephalopathy and miscellaneous, largely metabolic causes of coma did best: only 47% remained in coma and 1/3 regained independent recovery
- patients with hypoxic-ischaemic disease had intermediate level of recovery with 58% failing to wake from coma and 12% recovering to mod disability or making a good recovery
- on admission to study (min of 6 hrs of coma) absence of 2 of corneal, pupillary or oculovestibular associated with 97% chance of persistent coma or vegetative state, 2% chance of severe disability and 1% chance of mod disability or good recovery
Time Sign Cohort No. False +ve 95% confid
with survivors interval sign
24h Absent 500 90 0 0-5%
corneals
24h Absent 210 52 0 0-5%
pupillary
response
3d Motor 210 70 0 0-5%
response
worse than
withdrawal
7d Absent 210 16 0 0-5%
roving
eye
movements

  • Other data suggest that prognostication should be delayed until day 3. 18% of patients with no pupillary response immediately after cardiac arrest have recovered pupillary responses by day 3
  • Absence of pupillary, corneal and doll’s eyes reflexes, GCS <5 and flexion response or worse ̃ severe disability, vegetative state, persistent coma or death
  • EEG and sensory evoked potentials allow detection of additional patients with poor prognosis. SEP probably more sensitive. Absence of cortical SEP ̃ poor prognosis.

  G Bryan Young

Neurologic Prognosis after Cardiac Arrest

NEJM 2009; 361: 605-611

If a patient is in comatosed state ≥ 24 hours after resuscitation or after hypothermic cerebral protection therapy, the guideline from American Academy of Neurology should be used to assess for poor prognosis. Assessment of motor response may be delayed until until 6 days or longer in patients given hypothermic cerebral protection therapy. If SSEP response is absent on day 1 , the study should be repeated at day 3 or later. If absent , it suggests poor prognosis.

 


© Charles Gomersall December 1999

Last update on 26th August 2009 by Thomas Li

 

©Charles Gomersall, February, 2015 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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