Postanesthetic Shivering

The incidence of postoperative shivering-like tremor is reportedly approximately 40%, but it now appears to be less as more patients are kept normothermic and opioids are administered more frequently and in larger doses than in the past. It is a potentially serious complication, with oxygen consumption increased roughly 100% in proportion to intraoperative heat loss.^[132] Interestingly, though, myocardial ischemia is poorly correlated with shivering, thus suggesting that an increased metabolic rate is not the primary etiology of this complication.^[122] In addition to increasing intraocular and intracranial pressure, postoperative shivering probably aggravates wound pain by stretching incisions.

Over the years, postanesthetic tremor has been attributed to uninhibited spinal reflexes, pain, decreased sympathetic activity, pyrogen release, adrenal suppression, respiratory alkalosis, and most commonly, simple thermoregulatory shivering in response to intraoperative hypothermia. Unfortunately, the etiology of postanesthetic shivering-like tremor remains unclear. Certainly, much postoperative tremor is simply normal shivering. As early as 1972, however, investigators recognized the existence of at least two distinct tremor patterns.^[133] That perceptive observation was subsequently confirmed in a study that used electromyography to demonstrate that postoperative tremor has (1) a tonic pattern resembling normal shivering, typically with a 4- to 8-cycle/min waxing-and-waning component, and (2) a phasic, 5- to 7-Hz bursting pattern resembling pathologic clonus.^[134] The clonic pattern was consistent with the previous observation that pathologic spinal cord responses, including clonus, nystagmus, and exaggerated deep tendon reflexes, were common during recovery from general anesthesia.^[135]

It was not until 1991 that a triple crossover study in volunteers established that the tonic and clonic patterns were both thermoregulatory, that is, always preceded by core hypothermia and arteriovenous shunt vasoconstriction.^[136] The tonic pattern consistently demonstrated the 4- to 8-cycle/min waxing-and-waning pattern of normal shivering^[16] and is apparently a simple thermoregulatory response to intraoperative hypothermia. In contrast, the clonic pattern is not a normal component of thermoregulatory shivering and appears to be specific to recovery

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Postanesthetic shivering can be treated by skin surface warming ^[86] because the regulatory system tolerates more core hypothermia when cutaneous warm input is augmented.^[5] However, the skin surface contributes only 20% to control of shivering,^[5] and the available skin surface warmers increase mean skin temperature just a few degrees centigrade.^[139] Consequently, cutaneous warming compensates for only small amounts of core hypothermia and will not usually prove effective in most patients with core temperatures much below 35°C.^[140] Postanesthetic shivering can also be treated with a variety of drugs, including clonidine (75 µg IV),^{[88] [141]} ketanserin (10 mg IV),^[88] tramadol,^{[142] [143]} physostigmine (0.04 mg/kg IV),^[144] and magnesium sulfate (30 mg/kg IV).^[89] The specific mechanisms by which ketanserin, tramadol, physostigmine, and magnesium sulfate stop shivering remain unknown. Similarly, how clonidine arrests shivering also remains unknown, but clonidine^[32] and dexmedetomidine^[23] comparably reduce the vasoconstriction and shivering thresholds, thus suggesting that they act on the central thermoregulatory system rather than preventing shivering peripherally. Postoperative shivering has recently been reviewed in detail.^[145]

Alfentanil, a pure μ-receptor agonist, significantly impairs thermoregulatory control.^[22] However, meperidine is reportedly considerably more effective in treating shivering than equianalgesic doses of other μ-agonists are.^[146] Clinically, this efficacy is manifested as a shivering threshold that is reduced twice as much as the vasoconstriction threshold^[28] without a decrease in the gain or maximum intensity of shivering.^[47] The efficacy of meperidine is, at least partially, preserved during the administration of moderate doses of naloxone (0.5 µg/kg/min) but virtually obliterated by enormous doses (5.0 µg/kg/min).^[147] These data suggest that the action of this drug is, in part, mediated by non-μ-opioid receptors. Meperidine possesses considerable κ activity^[148] and also has central anticholinergic activity. However, neither mechanism appears to mediate meperidine's special antishivering activity.^[149] Instead, it may result from agonist activity at central α-adrenoceptors.^[150] Whatever the mechanism, meperidine appears to be considerably more effective in the treatment of postoperative shivering than other opioids are.