Delayed Emergence From Anaesthesia

Delayed emergence is failure to regain consciousness and respond to commands within about 30 to 60 minutes after the end of anaesthesia, when the expected drug effect should have worn off.

Epidemiology. Common and usually benign, but an unrecognised cause (hypoglycaemia, stroke, hypercapnia) can be serious.

Causes by frequency.

• Residual anaesthetic or sedative: overdose, slow elimination in obesity, hepatic or renal impairment, older age, hypothermia.
• Opioids and benzodiazepines, including premedication.
• Metabolic: hypoglycaemia, hyperglycaemia, hyponatraemia, hypercapnia, hypoxaemia, acidosis, uraemia, hepatic encephalopathy, myxoedema.
• Neurological: stroke, intracranial haemorrhage, raised intracranial pressure, non-convulsive seizures, cerebral gas embolism.
• Residual neuromuscular block (patient appears unresponsive).

Pathophysiology.

Delay reflects drug concentration, altered metabolism or direct brain dysfunction. Hypothermia slows hepatic metabolism and raises brain sensitivity to anaesthetic.

Unresponsiveness or poor response, slow breathing, small pupils (opioid), fixed or unequal pupils (structural), absent response to pain, shivering or hypothermia, and low saturation.

Red flags.

• Unequal or fixed pupils.
• Focal weakness, facial droop or posturing.
• Glucose under 3 mmol/L or over 20 mmol/L.
• Seizure activity.
• Respiratory rate under 8/min.
• Persisting unresponsiveness beyond 60 minutes after reversal.

Assess airway, breathing and circulation, then check pupils, glucose, temperature, train-of-four, saturation and end tidal carbon dioxide. Send blood gas, electrolytes, urea, creatinine and calcium. Obtain urgent CT of the head for focal signs, unequal pupils, anticoagulation or lack of response to reversal agents. Consider EEG and MRI.

Differential diagnosis.

• Drug effect.
• Residual neuromuscular block.
• Hypoglycaemia.
• Hypercapnic narcosis.
• Stroke or intracranial haemorrhage.
• Non-convulsive status epilepticus.
• Hypothermia.
• Hepatic encephalopathy.

Support ventilation and oxygenation, warm to 36 C, and treat reversible causes in order.

• Glucose 10%: 150 to 200 mL IV over 15 minutes when glucose is under 4 mmol/L, repeated every 10 to 15 minutes until over 4 mmol/L; maximum directed by repeat glucose, usually 400 mL in the first hour; monitor glucose every 10 to 15 minutes; caution in fluid overload and cerebral oedema.
• Naloxone (opioid effect, small pupils, slow breathing): 40 to 100 microgram IV every 2 to 3 minutes; maximum 400 microgram before reconsidering the diagnosis; monitor respiratory rate and pain; observe for 2 hours; use small increments in opioid dependence.
• Sugammadex (residual block, confirmed by train-of-four): 2 mg/kg IV if count is 2 or more, 4 mg/kg if post-tetanic count is 1 to 2; maximum 16 mg/kg; confirm ratio 0.9 or more; avoid if creatinine clearance is under 30 mL/min.
• Flumazenil (benzodiazepine effect): 200 microgram IV over 15 seconds, then 100 microgram every 60 seconds; maximum 1 mg in this setting; monitor for seizures and resedation (action is shorter than most benzodiazepines); avoid in epilepsy, benzodiazepine dependence and tricyclic overdose; reduce in hepatic impairment.

If there is no response after reversal and correction of metabolic causes, proceed to head CT and neurological assessment. Treat seizures with lorazepam 4 mg IV (children 0.1 mg/kg), repeated once after 10 minutes; maximum 8 mg; monitor respiration.

Monitoring. Level of consciousness (Glasgow Coma Scale), pupils, glucose, temperature, saturation and end tidal carbon dioxide every 5 to 15 minutes.

Referral and escalation. Critical care and neurology or neurosurgery for focal signs, raised intracranial pressure or a persisting depressed conscious level.

Special groups. Older adults, obese and hepatic or renal impairment patients clear drugs slowly. Children need weight based reversal and glucose checks.