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Research

Delayed Awakening in the Pacu
Presented by - Douglas Hartnett, MD
Department of Anestheiology
Tacoma Anesthesia Associates/Tacoma General Hospital
(extracted from article in Spring 2005 issue of "Off the Cuff" Newsletter)

Emergence from general anesthesia

Following an inhalational-based anesthetic, the speed of emergence is directly proportional to alveolar ventilation and inversely proportional to the agent’s blood solubility. As the duration of anesthesia increases, emergence also becomes increasingly dependent on total tissue uptake of the anesthetic, which is a function of agent solubility, the average concentration used and the duration of exposure. Therefore, recovery from nitrous and sevoflurane is much slower than halothane and isoflurane. Emergence from an intravenous anesthetic is a function of its pharmacokinetics. Recovery from most IV agents is dependent chiefly on redistribution rather than elimination half-life. This changes once the total administered dose increases and the tissue becomes saturated. Once this occurs, the termination of action becomes increasingly dependent on the elimination or metabolic half-life. Under these conditions, advanced age or renal or hepatic disease can prolong emergence.

Preoperative medications can also influence the speed of emergence. Premedication with agents which outlast the procedure may prolong emergence. Midazolam is a suitable premed as it is short acting. Pentobarbital, hydroxyzine, promethazine, droperidol, lorazepam and scopolamine can all contribute to postoperative somnolence. The effects of preoperative sleep deprivation, alcohol or sedative ingestion can also be additive to those of anesthetic agents and prolong awakening.

Delayed awakening

Delayed awakening or emergence may be said to occur when the patient fails to regain consciousness 60-90 minutes following general anesthesia. However, a response to stimulus should ideally be obtainable within 30-45 minutes after a reasonably conducted anesthesia.

The most frequent cause of delayed awakening following general anesthesia is residual anesthetics, sedative and analgesic drug effects. The most common cause of delayed emergence from inhalational anesthesia is hypoventilation.

Assessment

The evaluation of prolonged unconsciousness after anesthesia requires an organized analysis.

Level of preoperative responsiveness
Is there unrecognized intoxication with drugs and alcohol, was their pre-existing mental dysfunction

Preoperative and intraoperative medications
The time and amount of all medications given should be noted and any unusual intraoperative events should be reviewed.

Stimulus
Firm tactile stimulus which is often more effective than verbal stimulation should be used to elicit arousal

Ventilation
The rate and character of spontaneous ventilation can help indicate residual anesthesia depth.

Autonomic Tone
Heart rate, rhythm and systemic blood pressure can indicate the adequacy of cerebral perfusion and the level of autonomic tone.

Differential Diagnosis

Drugs (opoids, benzodiazepines, residual anesthesia, etc)

Skeletal muscle weakness (hypothyroid, incomplete neuromuscular reversal)

CNS event (stroke, increased ICP)

Hypoxia/Hypercarbia

Electrolyte disturbance (hypoglycemia, hyponatremia, hypocalcemia)

Metabolic (hepatic/renal encephalopathy, hyperosmolar coma, DKA)

Pulmonary edema/embolus

Treatment

Initial management should include pharmacologic agents aimed at the most likely sedative drug.

Naloxone in small dosed (0.04mg increments every 2 minutes up to 0.2mg)

Flumazenil a competitive benzodiazepine antagonist in a dose up to 1mg will reverse sedation from Midazolam and diazepam. It should be remembered that Flumazenil has a short duration of action so repeat doses may be needed.

Physostigmine (1.25mg) will counteract sedation caused by inhalational anesthetics and other sedative medications.

Profound neuromuscular blockade can mimic unconscious in the PACU by preventing a motor response to stimuli. This could occur after gross over dosage, if reversal agents are omitted, in patients with Phase II blockade caused by excessive succinycholine administration or pseudocholi nesterace deficiency. Observation of purposeful movements, spontaneous ventilation or reflex activity eliminates residual paralysis as an explanation.

Once pharmacologic causes are ruled out, metabolic and structural origins must be investigated.

Hypothermia below 33 degrees C can produce unconsciousness and increase the duration of depressant medications. At core temperatures below 30 degrees C, fixed dilation of pupils, absence of reflexes and evolution of coma can occur.

Hypoglycemia can impair consciousness and can be ruled out by evaluation of serum glucose. It can also eliminate hyperosmolar coma caused secondary to hyperglycemia.

Hyperosmolar states such as hypernatremia should be ruled out with evaluation of serum electrolyte concentrations and osmolarity.

Arterial blood gas analysis will reveal severe hypercarbia and CO2 narcosis or unrecognized hypoxemia underlie responsiveness.

If a diagnosis remains elusive, a thorough neurologic evaluation should be performed with a neurologist. Occasionally unresponsiveness in the PACU is caused by grand mal seizures secondary to delirium tremens or an underlying seizure disorder. CNS depression secondary to IV local anesthetic toxicity can mimic postoperative coma. Intraoperative hypotension, dysrythmias or hypoxemia must be considered in trauma patients and following neurosurgery. Cerebral thromboembolism is another possibility especially after cardiac, proximal major vascular, invasive neck surgery and in patients who have undergone internal jugular, subclavian or intre-arterial cannulation. Patients with atrial fibrillation, carotid bruits or hypercoagulation states are also at increased risk of thromboembolism.