Hyperthermia is
characterized by an unchanged (normothermic) setting of the
thermoregulatory center in conjunction with an uncontrolled increase in body temperature that
exceeds the body’s ability to lose heat. Exogenous heat exposure and endogenous
heat production are two mechanisms by which hyperthermia can result in dangerously
high internal temperatures. Excessive heat production can easily cause
hyperthermia despite physiologic and behavioral control of body temperature.
For example, work or exercise in hot environments can produce heat faster than
peripheral mechanisms can lose it.
Although most patients
with elevated body temperature have fever, there are a few circumstances in
which elevated temperature represents not fever but hyperthermia. Heat
stroke, caused by
thermoregulatory failure in association with a warm environment, may be categorized
as exertional or nonexertional. Exertional heat stroke typically occurs in younger
individuals exercising at ambient temperatures and/or humidities that are
higher than normal. In a dry environment and at maximal efficiency, sweating
can dissipate ±600
kcal/h, requiring the production of>1 L of sweat. Even in normal
individuals, dehydration or the use of common medications (e.g.,
over-the-counter antihistamines with anticholinergic side effects) may help to
precipitate exertional heat stroke. Nonexertional or classic heat stroke typically occurs in either very young
or elderly individuals, particularly during heat waves. According to the
Centers for Disease Control and Prevention (CDC), there were 7000 deaths
attributed to heat injury in the United States from 1979 to 1997. The elderly,
the bedridden, persons taking anticholinergic or antiparkinsonian drugs or
diuretics, and individuals confined to poorly ventilated and
non-air-conditioned environments are most susceptible.
Drug-induced hyperthermia has become increasingly common as a result of the increased
use of prescription psychotropic drugs and illicit drugs. Drug-induced
hyperthermia may be caused by monoamine oxidase inhibitors (MAOIs), tricyclic
antidepressants, and amphetamines and by the illicit use of phencyclidine
(PCP), lysergic acid diethylamide (LSD), methylenedioxymethamphetamine (MDMA, “ecstasy”),
or cocaine.
Malignant hyperthermia occurs in individuals with an inherited abnormality of
skeletal-muscle sarcoplasmic reticulum that causes a rapid increase in
intracellular calcium levels in response to halothane and other inhalational
anesthetics or to succinylcholine. Elevated temperature, increased muscle
metabolism, muscle rigidity, rhabdomyolysis, acidosis, and cardiovascular
instability develop rapidly. This condition is often fatal. The neuroleptic
malignant syndrome (NMS)
occurs in the setting of neuroleptic agent use (antipsychotic phenothiazines, haloperidol,
prochlorperazine, metoclopramide) or the withdrawal of dopaminergic drugs and
is characterized by “lead-pipe” muscle rigidity, extrapyramidal side effects,
autonomic dysregulation, and hyperthermia. This disorder appears to be caused
by the inhibition of central dopamine receptors in the hypothalamus, which
results in increased heat generation and decreased heat dissipation. The serotonin
syndrome, seen with
selective serotonin uptake inhibitors (SSRIs), MAOIs, and other serotonergic
medications, has many overlapping features, including hyperthermia, but may be
distinguished by the presence of diarrhea, tremor, and myoclonus rather than
the leadpipe rigidity of NMS. Thyrotoxicosis and pheochromocytoma can also cause
increased thermogenesis.
It
is important to distinguish between fever and hyperthermia since hyperthermia
can be rapidly fatal and characteristically does not respond to antipyretics.
However, there is no rapid way to make this distinction. Hyperthermia is often
diagnosed on the basis of the events immediately preceding the elevation of
core temperature—e.g., heat exposure or treatment with drugs that interfere
with thermoregulation. However, in addition to the clinical history of the patient,
the physical aspects of some forms of hyperthermia may alert the clinician. For
example, in patients with heat stroke syndromes and in those taking drugs that
block sweating, the skin is hot but dry. Moreover, antipyretics do not reduce
the elevated temperature in hyperthermia, whereas in fever—and even in
hyperpyrexia—adequate doses of either aspirin or acetaminophen usually result
in some decrease in body temperature.
Source: Harrison_s_Principles_of_Internal_Medicine_16th_Edition
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