List the potential causes of delayed awakening in a patient after a prolonged stay in Intensive Care, and outline how you would determine what factors were contributory.
• Potential causes include: prolonged effects of sedative drugs, metabolic encephalopathy (especially renal or hepatic failure), endocrine problems (especially hypothyroidism), systemic sepsis, and a myriad of specific neurological problems (eg. status epilepticus, raised intracranial pressure, intracranial haemorrhages, severe Guillain Barre, critical illness polyneuropathy). Residual muscular paralysis must be excluded.
• Sedative drugs may have a prolonged effect because of altered kinetics (including context sensitive half-time, or decreased biotransformation or excretion eg. renal or hepatic failure) or altered dynamics (potentiation of effect by other drugs or organ failure, sensitivity to effect of usual dosage).
Assessment of contributory factors may be a complex process. Important steps include:
• Detailed history of neurological state, drugs administered, previous neurological problems
• Careful examination (in particular neurological, but also for signs of other chronic diseases).
Detailed neurological exam should include global CNS assessment (including ability to move eyes or poke out tongue if no other apparent motor responses: locked in syndrome, severe myoneuropathy), and search for focal signs (pupils, tone, movement, reflexes). Nerve stimulator should be used to assess residual paralysis.
• Biochemical investigations for severity of electrolyte imbalance, creatine kinase, renal and hepatic dysfunction (including ammonia), and to exclude treatable endocrine disorders (including T4/TSH).
• Consider use of specific reversal agents (eg. naloxone and flumazenil [may need multiple ampoules]).
• May require other specific investigations (but put into context, and not done as a routine).
Such investigations include CT scan of head, MRI, EEG, EMG and lumbar puncture.
List the potential causes of delayed awakening? There could be thousands.
A tabulated answer is called for.
|Vascular causes||Hypotension, cerebral hypoxia||Routine monitoring of BP and SaO2|
|Vasospasm post SAH||CTA, DSA|
|Septic encephalopathy||Diagnosis of exclusion|
|Neoplastic causes||CNS malignancy||Contrast CT|
|Drug-related causes||Sedative drugs||Drug levels, drug history|
|Impaired clearance of sedative drugs||Renal and hepatic function testing|
|Intrinisic neurological causes||Status epilepticus||EEG|
|Cerebral oedema (of whatever aetiology)||CT|
|Autoimmune causes||CNS vasculitis||Vasculitic screen, LP, CTA, MRA|
|Traumatic causes||Intracranial injury (eg. contusion)||CT|
|Concussion||Diagnosis of exclusion|
|Endocrine/metabolic causes||Electrolyte derangement, eg. hyponatremia||EUC / CMP|
|Uremic encephalopathy||Renal function tests|
|Hepatic encephalopathy||LFTs, ammonia level|
Thus, investigations should consist of:
- BSL, EUC, CMP, LFT, TFT and random cortisol
- Blood cultures
- CSF analysis
- CT brain pre and post-contrast
- MRI / MRA
- Functional studies:
- Routine monitoring obs of BP and SaO2
Management would obviously be directed at the possible causes.