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Rationale:
- Cutaneous vasodilatation caused by alcohol promotes convective and radiant heat loss.
- Alcohol and other drugs (e.g., meperidine and phenothiazines) interfere with the body's capacity to generate heat by shivering
and impair heat conservation by altering vascular tone.
- The sedation caused by benzodiazepines may impair appropriate adaptive responses to cool temperatures.
- The muscle relaxant baclofen and cannabinoids induce hypothermia by acting centrally on the hypothalamus.
- Ingestion of alcohol sedatives and analgesics will indirectly decrease heat production by inducing sedation, thus decreasing
the level of physical exercise.
- Compromised mental faculties resulting from drug or alcohol ingestion can cloud judgment and increase the risk for prolonged
exposure.
- NSAIDS may block reacting peripheral vasodilation during mild hypothermia.
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Evidence:
- Several studies confirm that alcohol intoxication is a significant risk factor for accidental hypothermia and death. Alcohol
impairs judgment and facilitates heat loss by overexposure and cutaneous vasodilatation (1; 2; 3; 4). Furthermore, a high blood-alcohol level inhibits lipolysis and the formation of ketone bodies during mild hypothermia,
robbing the body of energy substrate needed to sustain the work of shivering and an increased cardiac output (5). Urocortinergic projections from the Edinger-Westphal nucleus to the dorsal raphé nucleus in the midbrain may mediate the
hypothermic response to ethanol (6).
- Two studies—one a single-blind, crossover study and the other a randomized, controlled trial—have shown that benzodiazepines
have a small, direct effect on thermoregulation, reducing core body temperature by less than 1°C at therapeutic doses. Older
patients experience a more prolonged decrease in temperature for a given dose (7; 8).
- A case study found that baclofen, commonly used to prevent muscle spasms in patients with spinal-cord injury or stroke, induces
mild hypothermia in a dose-dependent fashion (9). Such patients are already at increased risk for hypothermia because of immobility and impaired shivering. Experimental
data from rats suggest that the hypothermic effect of baclofen is mediated centrally by γ-aminobutyric acid type-A receptors
(10; 11), which also appear to modulate the mild hypothermia induced by activation of the cannabinoid-1 receptor by marijuana (11).
- In one study, in vitro preparations of canine femoral and renal arteries showed increasing relaxation with progressive hypothermia
down to 20°C (68°F). The addition of indomethacin attenuated the vasodilation (12). Although there are no published case reports of hypothermia after NSAID use in adults, ibuprofen has been linked to hypothermia
after a therapeutic dose in a child and an overdose in a teenager (13; 14). Although an effect on CNS thermoregulatory mechanisms cannot be ruled out, the loss of the normal vasodilatory response
to body cooling could have contributed to the hypothermia in these patients.
- Studies found that hypothalamic lesions associated with Wernicke's encephalopathy can lead to thermal dysregulation and hypothermia
(15).
- According to one study, age may increase susceptibility to the hypothermic effects of ethanol (16).
- Several studies of mentally impaired patients found that the severity of hypothermia is often related to the severity of impaired
judgment and the type of antipsychotic drug administered (17; 18; 19; 20; 21; 22; 23; 24; 25).
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Comments:
- Patients with a history of chronic alcohol abuse often have some degree of malnutrition, which further limits heat production.
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Albert Cheung, MD has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Dmitri Guvakov, MD, PhD has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Stuart Weiss, MD, PhD has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Wenjun Martini, PhD, editorial consultant, has no financial relationships with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
Deborah Korenstein, MD, FACP, Co-Editor, PIER, has no financial relationships with pharmaceutical companies, biomedical device
manufacturers, or health-care related organizations. Richard B. Lynn, MD, FACP, Co-Editor, PIER, has no financial relationships
with pharmaceutical companies, biomedical device manufacturers, or health-care related organizations.
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