Chapter 017. Fever and Hyperthermia (Part 6) doc

Chapter 017. Fever and Hyperthermia
(Part 6)

Regimens for the Treatment of Fever
The objectives in treating fever are first to reduce the elevated
hypothalamic set point and second to facilitate heat loss. Reducing fever with
antipyretics also reduces systemic symptoms of headache, myalgias, and
arthralgias.
Oral aspirin and NSAIDs effectively reduce fever but can adversely affect
platelets and the gastrointestinal tract. Therefore, acetaminophen is preferred to all
of these agents as an antipyretic. In children, acetaminophen must be used because
aspirin increases the risk of Reye's syndrome. If the patient cannot take oral
antipyretics, parenteral preparations of NSAIDs and rectal suppository
preparations of various antipyretics can be used.Treatment of fever in some
patients is highly recommended. Fever increases the demand for oxygen (i.e., for
every increase of 1°C over 37°C, there is a 13% increase in oxygen consumption)
and can aggravate preexisting cardiac, cerebrovascular, or pulmonary
insufficiency. Elevated temperature can induce mental changes in patients with
organic brain disease. Children with a history of febrile or nonfebrile seizure
should be aggressively treated to reduce fever, although it is unclear what triggers
the febrile seizure and there is no correlation between absolute temperature
elevation and onset of a febrile seizure in susceptible children.In hyperpyrexia, the
use of cooling blankets facilitates the reduction of temperature; however, cooling
blankets should not be used without oral antipyretics. In hyperpyretic patients with
CNS disease or trauma, reducing core temperature mitigates the ill effects of high
temperature on the brain.
Treating Hyperthermia
A high core temperature in a patient with an appropriate history (e.g.,
environmental heat exposure or treatment with anticholinergic or neuroleptic
drugs, tricyclic antidepressants, succinylcholine, or halothane) along with
appropriate clinical findings (dry skin, hallucinations, delirium, pupil dilation,

muscle rigidity, and/or elevated levels of creatine phosphokinase) suggests
hyperthermia. Attempts to lower the already normal hypothalamic set point are of
little use. Physical cooling with sponging, fans, cooling blankets, and even ice
baths should be initiated immediately in conjunction with the administration of IV
fluids and appropriate pharmacologic agents (see below). If insufficient cooling is
achieved by external means, internal cooling can be achieved by gastric or
peritoneal lavage with iced saline. In extreme circumstances, hemodialysis or even
cardiopulmonary bypass with cooling of blood may be performed.Malignant
hyperthermia should be treated immediately with cessation of anesthesia and IV
administration of dantrolene sodium. The recommended dose of dantrolene is 1–
2.5 mg/kg given intravenously every 6 h for at least 24–48 h—until oral
dantrolene can be administered, if needed. Procainamide should also be
administered to patients with malignant hyperthermia because of the likelihood of
ventricular fibrillation in this syndrome. Dantrolene at similar doses is indicated in
the neuroleptic malignant syndrome and in drug-induced hyperthermia and may
even be useful in the hyperthermia of the serotonin syndrome and thyrotoxicosis.
The neuroleptic malignant syndrome may also be treated with bromocriptine,
levodopa, amantadine, or nifedipine or by induction of muscle paralysis with
curare and pancuronium. Tricyclic antidepressant overdose may be treated with
physostigmine.
Acknowledgment
The substantial contributions of Jeffrey A. Gelfand to this chapter in
previous editions are gratefully acknowledged.
FURTHER READINGS
De Koning HD et al: Beneficial response to anakinra and thalidomide in
Schnitzler's syndrome. Ann Rheum Dis 65:542, 2006
Dinarello CA: Infection, fever, and exogenous and endogenous pyrogens:
Some concepts have changed. J Endotoxin Res 10:202, 2004
Hawkins PN et al: Spectrum of clinical features in Muckle-Wells syndrome
and response to anakinra. Arthritis Rheum 50:607, 2004 [PMID: 14872505]

Hoffman HM et al: Prevention of cold-associated acute inflammation in
familial cold autoinflammatory syndrome by interleukin-1 receptor antagonist.
Lancet 364:1779, 2004 [PMID: 15541451]
Keane J et al: Tuberculosis associated with infliximab, a tumor necrosis
factor-α-neutralizing agent. N Engl J Med 345:1098, 2001 [PMID: 11596589]
Pascual V et al: Role of interleukin-1 (IL-1) in the pathogenesis of systemic
onset juvenile idiopathic arthritis and clinical response to IL-1 blockade. J Exp
Med 201:1479, 2005 [PMID: 15851489]
Simon A, van der Meer JW: Pathogenesis of familial periodic fever
syndromes or hereditary autoinflammatory syndromes. Am J Physiol Regul Integr
Comp Physiol 292:R86, 2007
——— et al: Beneficial response to interleukin-1 receptor antagonist in
TRAPS. Am J Med 117:208, 2004
Wallis RS et al: Differential effects of TNF blockers on TB immunity. Ann
Rheum Dis 64(Suppl3):132, 2005
——— et al: Granulomatous infectious diseases associated with tumor
necrosis factor antagonists. Clin Infect Dis 38:1261, 2004
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