Anesthesia and surgery predispose patients to hypothermia, usually defined as a body temperature less than 36°C.

Unintentional perioperative hypothermia is more common in patients at the extremes of age, and in those undergoing abdominal surgery or procedures of long duration, especially with cold ambient operating room temperatures.

Hypothermia (in the absence of shivering) reduces metabolic oxygen requirements and can be protective during cerebral or cardiac ischemia.

 Nevertheless, hypothermia has multiple deleterious physiological effects In fact, unintended perioperative hypothermia has been associated with an increased mortality rate.



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TABLE 52–1Deleterious effects of hypothermia.

Cardiac arrhythmias and ischemia

Increased peripheral vascular resistance

“Left shift” of the hemoglobin–oxygen saturation curve

Reversible coagulopathy (platelet dysfunction)

Increased postoperative protein catabolism and stress response

Altered mental status

Impaired renal function

Delayed drug metabolism

Impaired wound healing

Increased risk of infection

Body temperature may fall as a result of heat loss by radiation, evaporation, conduction, and convection. [1]

Radiation causes 55-65% of the body's heat loss.

Evaporation occurs via the skin and airway and accounts for 30% of the heat loss.

Normally, in a dry environment, only 15% of the body's heat loss results from conduction. However, the thermal conductivity of water is approximately 30 times that of air, so the body loses heat rapidly when immersed in water or covered in wet clothing, leading to a rapid decline in body temperature. Convection accounts for a minor amount of heat loss, but it becomes more significant in a windy environment. The amount of heat dissipated by any of these mechanisms is proportional to the temperature difference between the body and environment.

Opposing the loss of body heat are the mechanisms of heat conservation and gain. In general, a thermostat in the preoptic region of the hypothalamus controls these mechanisms.

This human thermostat is set to a precise reference temperature, usually very close to 37°C (98.6°F). It responds to thermoregulatory mechanisms, the temperature of blood, and temperature receptors deep within the body and in the skin.

When the preoptic area of the hypothalamus is stimulated, various heat conservation and production mechanisms become activated. When the sympathetic nerves are excited, they cause the blood vessels in the skin to markedly constrict. The flow of warm blood from the core of the skin is depressed, thereby reducing the transfer of heat to the body surface. This reduction of blood flow in the skin is the prime physiologic regulator of heat loss from the body. The temperature of the skin decreases to approach the temperature of surrounding air, which lowers the temperature gradient and further decreases heat loss.

Stimulation of the sympathetic nerves also causes secretion of epinephrine and norepinephrine by the adrenal medullae. These hormones increase the metabolic rate of all cells, thereby enhancing heat production. Impulses from the preoptic hypothalamus also activate the primary motor center for shivering, which, in turn, increases the tone of muscles. The resulting enhancement of muscle metabolism can increase heat production by as much as 500%.


Unintentional perioperative hypothermia is more common in patients at the extremes of age, and in those undergoing abdominal surgery or procedures of long duration, especially with cold ambient operating room temperatures.




Complications of Injecting Drug Use

  • Local problems—Abscess (Figures 240-2 
    Image not available.

    A 32-year-old woman with type 1 diabetes developed large abscesses all over her body secondary to injection of cocaine and heroin. Her back shows the large scars remaining after the healing of these abscesses. (Courtesy of ­Richard P. Usatine, MD.)

    and 240-3; Abscess), cellulitis, septic thrombophlebitis, local induration, necrotizing fasciitis, gas gangrene, pyomyositis, mycotic aneurysm, compartmental syndromes, and foreign bodies (e.g., broken needle parts) in local areas.2
    • IDUs are at higher risk of getting methicillin-resistant Staphylococcus aureus(MRSA) skin infections that the patient may think are spider bites (Figure 240-4).
    • Some IDUs give up trying to inject into their veins and put the cocaine directly into the skin. This causes local skin necrosis that produces round atrophic scars (Figure 240-5).
  • IDUs are at risk for contracting systemic infections, including HIV and hepatitis B or hepatitis C.
    • Injecting drug users are at risk of endocarditis, osteomyelitis (Figures 240-6and 240-7), and an abscess of the epidural region. These infections can lead to long hospitalizations for intravenous antibiotics. The endocarditis that occurs in IDUs involves the right-sided heart valves (see Chapter 50, Bacterial Endocarditis).2 They are also at risk of septic emboli to the lungs, group A β-hemolytic streptococcal septicemia, septic arthritis, and candidal and other fungal infections.


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Core temperature is normally the same as the central venous blood temperature (except during periods of relatively rapid temperature change as can occur during and after extracorporeal perfusion). image When there is no attempt to actively warm an anesthetized patient, core temperature usually decreases 1°C to 2°C during the first hour of general anesthesia (phase one), followed by a more gradual decline during the ensuing 3 to 4 h (phase two), eventually reaching a point of steady state (phase three). With general, epidural, or spinal anesthesia most of the initial decrease in temperature during phase one is explained by redistribution of heat from warm “central” compartments (eg, abdomen, thorax) to cooler peripheral tissues (eg, arms, legs) from anesthetic-induced vasodilation. Actual heat loss from the patient to the environment is a minor contributor. Continuous heat loss to the environment is the primary driver for the slower decline during phase two. At steady state, heat loss equals metabolic heat production (Figure 52–1).


Unintentional hypothermia during general anesthesia follows a typical pattern: a steep drop in core temperature during the first hour (phase one, redistribution), followed by a gradual decline during the next 3 to 4 h (phase two, heat loss), eventually reaching a steady state (phase three).

image In the normal unanesthetized patient the hypothalamus maintains core body temperature within very narrow tolerances, termed the interthreshold range, with the threshold for sweating and vasodilation at one extreme and the threshold for vasoconstriction and shivering at the other. Increasing core temperature a fraction of a degree induces sweating and vasodilation, whereas a minimally reduced core temperature triggers vasoconstriction and shivering. image Anesthetic agents inhibit central thermoregulation by interfering with these hypothalamic reflex responses. For example, isoflurane produces a dose-dependent decrease in the threshold temperature that triggers vasoconstriction (3°C decrease for each percent of inhaled isoflurane). Both general and neuraxial anesthetics increase the interthreshold range, albeit by different mechanisms. Spinal and epidural anesthetics, like general anesthetics, lead to hypothermia by causing vasodilation and internal redistribution of heat. The thermoregulatory impairment from conduction anesthesia that allows continued heat loss is likely also due to altered perception by the hypothalamus of temperature in the anesthetized dermatomes.

Intraoperative Considerations

A cold ambient temperature in the operating room, prolonged exposure of a large wound, and the use of large amounts of room-temperature intravenous fluids or high flows of unhumidified gases can contribute to hypothermia. Prewarming the patient for half an hour with convective forced-air warming blankets prevents phase one hypothermia by eliminating the central–peripheral temperature gradient. Methods to minimize phase two hypothermia from heat loss during anesthesia include use of forced-air warming blankets and warm-water blankets, heated humidification of inspired gases, warming of intravenous fluids, and increasing ambient operating room temperature. Passive insulators such as heated cotton blankets or so-called space blankets have limited utility unless virtually the entire body is covered.

Postoperative Considerations

Shivering can occur in postanesthesia care units (PACUs) or critical care units as a result of actual hypothermia or neurological aftereffects of general anesthetic agents. Shivering is also common immediately postpartum. Shivering in such instances represents the body’s effort to increase heat production and raise body temperature and may be associated with intense vasoconstriction. Emergence from even brief general anesthesia is sometimes also associated with shivering. Although shivering can be part of nonspecific neurological signs (posturing, clonus, or the Babinski sign) sometimes observed during emergence, shivering is typically associated with hypothermia and volatile anesthetics. Shivering appears to be more common after longer durations of surgery and the use of greater concentrations of a volatile agent. Occasionally, shivering is intense enough to cause hyperthermia (38–39°C) and metabolic acidosis, both of which promptly resolve when the shivering stops. Both spinal and epidural anesthesia lower the shivering threshold and vasoconstrictive response to hypothermia; shivering may also be encountered in the PACU following regional anesthesia. Other causes of shivering should be excluded, such as sepsis, drug allergy, or a transfusion reaction. Intense shivering may increase oxygen consumption, CO2 production, and cardiac output. These physiological effects are often poorly tolerated by patients with preexisting cardiac or pulmonary impairment.

Postoperative shivering may increase oxygen consumption as much as fivefold, may decrease arterial oxygen saturation, and may be associated with an increased risk of myocardial ischemia. Although postoperative shivering can be effectively treated with small intravenous doses of meperidine (12.5–25 mg) in adults, the better option is to reduce the likelihood of shivering by maintaining normothermia. Shivering in intubated and mechanically ventilated patients can also be controlled with sedation and a muscle relaxant pending normothermia and dissipation of all effects of anesthesia.

image Postoperative hypothermia should be treated with a forced-air warming device, if available; alternately (but less satisfactorily) warming lights or heating blankets can be used. In addition to an increased incidence of myocardial ischemia, hypothermia has been associated with arrhythmias, increased transfusion requirements, and increased duration of muscle relaxant effects, the latter of which can be especially harmful in the recently extubated patient.


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