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Rationale:
- Perioperative hypothermia >2°C below normal core temperature is common.
- Neonates and infants are especially vulnerable to perioperative hypothermia.
- Hypothermia is causally related to exposure to the cold wet antiseptic scrub, the infusion of cold intravenous fluids, surgical
exposure of body cavities, and the anesthetic-induced impairment of thermoregulation and sympathetic vascular tone affecting
heat distribution during the perioperative period.
- Hypothermia during the postoperative period can be exacerbated by various drugs (β-blockers, vasodilators, analgesics, tranquilizers)
and the sympathectomy produced by spinal or epidural analgesia.
- Examine the patient who is shivering for hypothermia. Shivering, a normal protective mechanism of thermogenesis, should be
differentiated from the shaking rigors of sepsis and the autonomic discharge associated with recovery from anesthesia. Because
shivering is uncomfortable to the patient and recognized to increase oxygen consumption and the risk for cardiac ischemia,
many postoperative patients are administered such drugs as meperidine during the postoperative period that decrease shivering.
Such therapy should be reconsidered in the case of hypothermia.
- The presence of perioperative hypothermia predisposes the patient to increased surgical bleeding, infection, myocardial ischemia,
and increased oxygen consumption from shivering.
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Evidence:
- Two studies found that the rate of hypothermia is greatest during the first hour after the induction of general anesthesia.
The decrease in the level of muscle activity decreases heat production. Impairment of peripheral vasoconstriction permits
accelerated heat loss at the periphery. The impairment of shivering, another homeostatic mechanism, decreases the generation
of heat. Decreased vasomotor tone permits the redistribution of cold peripheral blood to the warm body core, lowering the
core temperature (32; 33).
- In one study done in the intensive care unit, hypothermia was seen in up to 58% of postoperative admissions (34).
- The type of surgery (major or minor) and the temperature of the operating room have been shown to be the principal factors
responsible for decreases in core temperature in neonates and infants. In one case series, all neonates experienced a decline
in core temperature following the induction of anesthesia, regardless of the type of surgery. In contrast, infants experienced
decreases in core temperature only with major surgery (35).
- Studies determined that passive insulation for heat conservation and conservative management strategies improve outcome by
reducing cutaneous heat loss by ~30% (33; 36). Implementation of appropriate management strategies significantly improved the outcome for a hypothermic patient (37).
- In two studies, perioperative hypothermia was greatest in neonates and burned patients, under conditions of decreased ambient
operating-room temperature, and in general anesthesia with epidural or spinal anesthesia (38; 39).
- Two studies, one a randomized, controlled trial, associated perioperative hypothermia (>1.3°C) with an increased risk for
myocardial ischemia related to increasing peripheral vasoconstriction and cold-induced arterial hypertension (40; 41).
- A randomized, controlled trial showed that maintenance of normothermia during the perioperative period in patients having
cardiac risk factors is associated with decreased cardiac morbidity (40).
- Studies have found that prolonged perioperative hypothermia is associated with an increased morbidity related to immunosuppression
(42; 43), cardiac ischemia (44), coagulopathy (45; 46), impaired wound healing (47), and cardiac arrhythmias (40; 41).
- One study in which swine were cooled to 0°C (32°F) resulted in a 54% reduction in the rate of fibrinogen synthesis but had
no effect on fibrinogen breakdown (48). In another study done with human volunteers, cooling of the volar forearm from 0°C (32°F) to 2.2°C (28°F) while maintaining
a normal core volume resulted in the doubling of the bleeding time (49).
- One study showed that hypothermia independently predicted mortality in critically ill patients with systemic inflammatory
response syndrome (50).
- In rats undergoing laparotomy with installation of human fecal matter to induce sepsis, postoperative mild hypothermia (32°C
[89.6°F]) reduced survival at 120 hours to 10% compared with 50% for normothermic rats (51). In another experiment, rats were randomized to be cooled to 32°C (89.6°F) just before this procedure and rewarmed to 38°C
(100.4°F) immediately after or kept constantly at 38°C (100.4°F). The mild pre- and intraoperative hypothermia reduced short-term
survival by 22% in this sepsis model (52). In septic mice with anesthesia-induced hypothermia, survival was 42% in the group kept at room temperature postoperatively
compared with 60% among those immediately rewarmed for 1 hour (53).
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Comments:
- In vitro studies of human monocytes have shown that mild hypothermia (32°C [89.6°F]) delays activation but prolongs production
of TNF-α and IL-1β (54).
- Cultured human monocytes exposed in vitro to lipopolysaccharide under conditions of mild hypothermia increased the production
of cytokines compared with those in normothermic conditions. During hypothermia, the ratios of proinflammatory IL-12 and TNF-α
to anti-inflammatory IL-10 increased, suggesting that hypothermia-related cytokine production has a net proinflammatory effect
(55).
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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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