Hypothermia, or subnormal body temperature, may be classified as primary or secondary. Primary hypothermia typically results from environmental exposure despite normal heat production by the body. Secondary hypothermia results from alterations in heat production because of illness, injury, or drugs. Understandably secondary hypothermia may frequently influence morbidity and mortality in critically ill animals.

There are four basic mechanisms of heat loss:

 Convection transfers heat from the body surface to air or water moving past the animal.

 Conduction transfers heat from the body surface to colder objects in contact with the skin.

 Radiation is the exchange of heat between the body and objects in the environment that are not in contact with the skin, independent of the temperature of the surrounding air.

 Evaporation occurs when moisture in contact with skin or the respiratory tract dissipates into the air.

Thermoregulation

Receptors for cold and warm are distributed throughout the body. Cold signals traverse A-delta fibers, and signals from warmth receptors are relayed through C fibers.

Processing thermoregulatory information occurs through three pathways:

1.  Afferent thermal sensing from the periphery

2.  Central regulation in the hypothalamus

3.  Efferent responses

Given these three pathways, peripheral body temperatures are constantly fluctuating while the posterior hypothalamic thermoregulatory center maintains a relatively constant core temperature. Cellular metabolism results in heat production by the body, and heat is lost from the body when core heat is transferred through variably conductive tissues to the skin and is subsequently lost to the environment. Specifically, heat is transferred from the body's core to the skin through a multitude of blood vessels, including venous plexuses and capillaries with arteriovenous connections that are under the control of the autonomic nervous system. The rate of blood flow through these arteriovenous anastomoses varies depending on the degree of vasoconstriction or vasodilation desired. Increased blood flow leads to increased heat loss, whereas decreased blood flow results in core heat conservation.

Heat production due to the body's various metabolic processes is directly proportionate to body mass, and, thus cutaneous heat loss is a function of body surface area. Small companion animals have higher surface- area-to-body-mass ratios that make them uniquely susceptible to heat loss. Additionally, cachectic, debilitated, immobile, and critically ill patients have impaired thermoregulatory capabilities and may not be able to retain or seek heat.

Hypothermic Spiral

As core body temperature dips below 94°F (34.4°C), thermoregulation is impaired, and animals characteristically cease to shiver or seek heat. Peripheral vasodilation rather than vasoconstriction predominates, leading to continued core heat loss. Additionally, heat production decreases because of the decreased metabolic rate. Concurrently severe hypothermia depresses the central nervous system, ultimately resulting in a hypothalamus that is less responsive to hypothermia. Indeed, when the body core temperature drops below 88°F (31.1°C), thermoregulation ceases.

Potential Complications

There are many potential complications associated with primary and secondary hypothermia, including:

 Cardiac: sinus bradycardia, prolonged P-R interval increased Q-T interval, J/Osborn wave, atrial fibrillation, ventricular fibrillation

 Vasculature: initial hypersensitivity and subsequent hyposensitivity of both alpha- and beta-receptors

 Pulmonary: bradypnea, reduced tidal volume, hypoventilation

 Clinical pathology: hypoglycemia, hypokalemia, thrombocytopathia, secondary coagulopathy, azotemia, relative polycythemia

 Neurologic: depression, coma

 Immunologic: impair oxidative killing by neutrophils, reduce phagocytosis, impaired chemotaxis, pancytopenia, decreased cytokine and antibody production, poor wound healing

Anesthesia/Surgery

General anesthesia and surgery result in both primary and secondary hypothermia. Intubated patients inspire cold, dry air delivered directly to the lungs. Routine aseptic preparation of surgical sites promotes evaporative heat loss, and cold table surfaces and open body cavities will exacerbate heat loss through conduction and radiation, respectively. Anesthetic agents affect the hypothalamic thermoregulatory center in such a way that thermogenic responses are not triggered until low temperatures are reached. Centrally mediated thermoregulatory vasoconstriction is directly inhibited to cause peripheral vasodilation. Anesthesia decreases the metabolic rate by 15% to 40% and inhibits muscular activity to cause decreased heat production. Coagulopathy and platelet dysfunction logically represent serious complications in surgical or posttraumatic patients at risk for hemorrhage. Hypothermia delays anesthetic recovery and can lead to surgical complications such as dysrhythmias, hypotension, respiratory depression, bradycardia, coagulopathy, altered blood viscosity, and anesthetic drug overdose. Minimizing the duration of anesthetic and surgical procedures may reduce the incidence of secondary hypothermia.

Rewarming Interventions

Therapeutic efforts are aimed at rapidly rewarming patients during fluid resuscitation as well as reducing additional heat loss. Resuscitative efforts should not contribute to the hypothermia. Rewarming hypothermic animals can be accomplished by several different methods, including:

 Passive surface (e.g., room temperature blankets)

 Active surface (e.g., heated blankets, Bair hugger, circulating heated water bed)

 Active core rewarming (e.g., peritoneal/gastric/ pleural/urinary bladder lavage, warm water enemas, warmed IV fluids)

It has been recommended to warm the animal by at least 1–2°C per hour; however, faster rates may be necessary. Moderate intravascular volume support is recommended during active rewarming in hypovolemic shock; this will support mean arterial blood pressure (MAP) and resolve most cases of hypothermia-induced hypotension, bradycardia, hypoventilation, and coagulopathy while avoiding volume overload.

Electrolytes and acid-base status should be monitored and alterations addressed. Electrocardiography, MAP, and blood gases should be monitored closely in severely hypothermic patients. Surface rewarming should always accompany active core rewarming to reduce core-to-peripheral temperature gradients. During external heating, care must always be taken to prevent skin burns by controlling the temperature of the external heating devices or placing a barrier between the heat source and the patients.

A patient's core body temperature may continue to drop for a period of time after the onset of rewarming. This condition, referred to as the "afterdrop", is caused by the return of cold peripheral blood to the body core and movement of blood from the warmer core to the periphery. A second important complication to anticipate is the development of rewarming shock. Rapid rewarming will cause a great metabolic burden on patients as well as significant vasodilation that may overwhelm an already compromised circulatory system.

References

1.  Byers CG. Cold critters: understanding hypothermia. Vet Med. 2012;107(2):82–87.

2.  Byers CG. Cold critters: assessing, preventing, and treating hypothermia. Vet Med. 2012;107(2):88–90.

3.  Oncken A, Kirby R, Rudloff E. Hypothermia in critically ill dogs and cats. Compend Contin Educ Pract Vet. 2001;23:506–521.