4.6 Delayed Emergence 

Delayed Emergence is a condition when the patient fails to regain consciousness 30 –60 min after general anesthesia.

4.6.1 Causes of delayed emergence:

• Over dose of anesthetics, narcotics and muscle relaxants
• The most frequent cause of delayed emergence is residual anesthetic, sedative, and analgesic drug effect. Delayed drug metabolism occurs in renal or hepatic failure, and smaller doses may be required.
• Potentiation by other drugs: sedative and analgesic premedication such as diazepam and morphine will potentiate the central nervous system depressant effects of anesthetic and analgesic drugs, and may delay emergence from anesthesia. Administration of naloxone (0.04 mg increments) and flumazenil (0.2 mg increments) readily reverses and can exclude the effects of an opioid and benzodiazepine, respectively.
• Effect of muscle relaxants: Inadequate spontaneous tidal volume may occur secondary to overdose or incomplete reversal of non-depolarizing muscle relaxants or in a patient with suxamethonium apnea. A nerve stimulator will assist the diagnosis. Alternatively inability to maintain head lift for 5 seconds in a patient who could normally comply with this request indicates residual block. Residual paralysis elicits agitation or uncoordinated motions that make a patient appear disoriented and combative.
• Intraoperative hyperventilation is a common cause of postoperative apnea. Because volatile agents raise the apneic threshold, the PaCO2 level at which spontaneous ventilation ceases, moderate postoperative hypoventilation may be required to stimulate the respiratory centers.
• Patients who do not breathe effectively during or after anesthesia may become hypercarbic (raised CO2) to a level that may produce sedation or even unconsciousness. Risk factors include underlying respiratory disease, particularly those with CO2 retention preoperatively, high dose opioids, obstructed airway and poor relaxant reversal.
• Metabolic disorders such as hypoglycemia, severe hyperglycemia and electrolyte disturbance may be responsible for delayed recovery after anesthesia.
• Severe hypothermia may lead to reduced conscious level. A core temperature of less than 33oC has a marked anesthetic effect itself and will potentiate the CNS depressant effects of anesthetic drugs. This will be discussed in post operative care session.

4.6.2 Care of delayed emergence

• Maintain a clear airway and give oxygen. Reintubate if indicated. Consider consultation with the surgeon and other specialty.
• Ensure adequate respiration. If indicated ventilate the patient effectively via an endotracheal tube. Monitor saturation of oxygen using pulse oximetry.
• Assess blood pressure, heart rate, ECG, peripheral perfusion, conscious level and urine output. Resuscitate as indicated.
• Review the history, investigations, and perioperative management, including the anesthetic chart and the timings of drug administration, looking for a possible cause of the delay in recovery.
• Assess for persisting neuromuscular blockade, using a nerve stimulator if available. Alternatively if the patient is awake enough to obey commands ask them to lift their head off the pillow for 5 seconds. If the patient is still paralyzed they should be sedated or kept anesthetized and ventilated until the block is fully reversed. A further dose of reversal agent eg; neostigmine 2.5mg plus glycopyrrolate 0.5mg or atropine 1mg may be tried. Where there is prolonged neuromuscular block in suxamethonium apnoea, prolonged ventilation (up to 12 - 36 hours) may be required.
• Look for signs of opioid narcosis - pin point pupils and slow respiratory rate. In this situation a test dose of naloxone may be given: IV increments of 100 to 200 micrograms are usually sufficient. (Child = 10 micrograms/kg, subsequent dose of 100 micrograms/kg if no response.). If too much is given the analgesic effect of the opioid will be antagonized and the patient will be in pain. The dose should therefore be titrated to effect. The duration of action of naloxone is approximately 20 minutes and this may be shorter than the effect of the opioid. Subsequent doses of naloxone may therefore be required, and these may be given intramuscularly.
• If delayed recovery is due to an excess of benzodiazepine (diazepam or midazolam) or other drugs, management is supportive, with maintenance of airway and ventilation until the drug has been metabolized. Where the specific benzodiazepine antagonist flumazenil is available it can be tried (iv increments of 0.1mg to a maximum adult dose of 1mg). However, Flumazenil is expensive, and may cause arrhythmias, hypertension and convulsions. Its use is generally not indicated.
• Measure the patient's temperature, and warm if necessary.
• Check blood glucose and plasma electrolytes and correct accordingly with consultation of the surgeon and other physician
• If no other cause can be found for delayed emergence from anesthesia, an intracerebral event may be suspected and a full neurological examination should be performed.