Perhaps the most important aspect of pyrexia in the critical care setting is its 'indicator' function to alert the clinician to an underlying problem or new complication. Therefore fever should always be seen as a warning sign rather than a problem to be solved. However, fever is such a common phenomenon that it may not always have sinister significance, and a single elevated temperature reading should not be overinvestigated.
Clearly, the strategy of choice in managing fever is to treat the underlying disease, but direct measures to reduce body temperature may also be necessary. Antipyretics reduce fever by reducing the thermoregulatory set-point. Acetaminophen (paracetamol) is generally the drug of choice. Although a poor inhibitor of prostaglandin synthesis in peripheral tissues, and thus a poor anti-inflammatory agent when compared with salicylates or non-steroidal anti-inflammatory drugs, it appears to be a more potent inhibitor of prostaglandin synthesis in the central nervous system. It acts by reducing prostaglandin levels in the hypothalamus, thus blocking the effects of endogenous pyrogens. It may be given by the oral, nasal, or rectal route. Aspirin and non-steroidal anti-inflammatory drugs have a similar antipyretic effect via prostaglandin synthesis but are generally avoided because of potential effects on the gastrointestinal tract. Salicylates should be avoided in children because of the risk of Reye's syndrome.
Glucocorticoids reduce pyrexia but are only indicated when other considerations demand their use or in the context of allergic-type febrile transfusion or drug reactions. The antipyretic action of glucocorticoids is mediated by several different mechanisms. Although it is clear that cytokines are the primary mediators of fever, cytokine blockade does not appear to have a role to play in the management of fever per se, although such therapy may be of value in the sepsis syndrome.
Heat loss may be promoted by the use of tepid sponging (not cold sponging which would cause cutaneous vasoconstriction) or cooling blankets. Such measures are often very effective, but it should be remembered that, if the set-point is still elevated, one may end up 'competing' with the thermoregulatory effector mechanisms which may be attempting to retain heat. For example, cooling a patient to 38 °C when the set-point is still at 39 °C may result in shivering and vasoconstriction, with increased energy expenditure and discomfort, if the patient is conscious (,M..a.n.t.h..o.u.s..e?,§/ 1995). Therefore, where possible, taking over the effector mechanisms for regulation of heat loss should be combined with an attempt to reduce the set-point.
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