16 Hyperthermia and pyrexia
The thermoregulatory centre is located in the hypothalamus and controls core body temperature closely around the thermoregulatory set point. This is achieved through a balance between heat loss and heat gain. Heat loss occurs via evaporation, conduction, convection and radiation. In people, evaporative cooling is mainly by perspiration. In dogs, evaporative cooling is mainly through panting that brings large amounts of air into contact with the nasal and oral mucosa. Minimal perspiration occurs through the footpads. Heat dissipation also occurs via radiation and convection through the skin. Heat gain can be classified as endogenous production (from metabolic processes and exercise) or exogenous gain (from the environment). Thermoregulatory mechanisms are summarized in Box 16.1.
Marked elevations in core body temperature may have severe consequences, with cellular injury possible above 41.5°C. Multiple organs and body systems may be affected, and disseminated intravascular coagulation (DIC) and multiple organ dysfunction syndrome (MODS) are possible sequlae.
In dogs and cats, normal core (rectal) temperature is approximately 38.0–39.0°C, although some normal fluctuation outside this range is likely during the day. This range reflects the normal thermoregulatory set point. Core temperature may become elevated due to hyperthermia and/or pyrexia. An important distinction exists between these two processes that has important implications in terms of appropriate management.
In hyperthermia the thermoregulatory set point is unchanged and the hypothalamus attempts to return core temperature to normal limits. Clinically significant consequences occur when physiological attempts to cool the body become overwhelmed and active cooling is therefore appropriate. The most common causes of hyperthermia are heat stress (see Ch. 38) and severe or sustained seizure activity (see Ch. 24). Other causes include malignant hyperthermia, primary brain lesions and drug reactions.
Hyperthermia is identified most commonly in dogs and is a rare presentation in cats. In most (but not all) hyperthermic animals, the history is suggestive of this being the cause of temperature elevation and the diagnosis is usually relatively straightforward.
Clinical Tip
Wetting the patient with cool water and then applying one or more fans is likely to be the most effective method of cooling. This will promote heat loss predominantly via evaporation, convection and conduction. Excessively cold water should be avoided (see below under ice baths) and although common practice, placing towels on the patient will impede maximum heat loss and should be avoided. Clipping of fur may be helpful in some cases although the author has not found this to be necessary and the time delay in clipping bigger dogs in particular must be borne in mind. Conduction may be further promoted by keeping the patient on a cool surface (e.g. steel worktop). The common practice of applying alcohol to footpads is unlikely to be very effective given the small surface area involved and poses risks with respect to the patient subsequently licking the alcohol.
It is very important to cease active cooling when rectal temperature is less than 39.5°C to prevent rebound hypothermia that may persist for a period of several hours or longer. Rebound hypothermia may occur as a result of hyperthermia-induced dysfunction of the thermoregulatory centre that is therefore unable to stimulate heat production as core temperature declines.
Other methods of active cooling reported include ice water baths, various forms of lavage and cold water enemas. Ice water may cause intense peripheral vasoconstriction, thereby impairing heat loss. Shivering may also occur that will increase heat production and ice water is likely to be uncomfortable to the patient. The use of ice water baths is not recommended. Gastric lavage, peritoneal lavage, bladder lavage and cold water enemas are labour intensive, carry risks and may affect monitoring of temperature in the case of enemas. In addition, their use makes it more difficult to avoid rebound hypothermia and they are only recommended in the most severe of cases where other measures fail to reduce core temperature satisfactorily. The author has thus far never needed to resort to one of these methods.
Intravenous isotonic crystalloid therapy should also be implemented in all hyperthermic patients with the rate and volume used being determined by each patient’s individual circumstances (see Ch. 4). Occasionally colloids may need to be employed. Intravenous fluids administered at room temperature will help to lower core temperature directly as well as increase peripheral blood flow, thereby encouraging heat dissipation. Intravenous fluids should not be cooled to lower than room temperature prior to administration. As the thermoregulatory set point is unchanged in hyperthermic animals, the use of antipyretic agents is contraindicated because these agents reduce the set point. Animals that have suffered heat-induced hypothalamic injury may temporarily lose the ability to compensate for changes in their thermoregulatory set point induced by exogenous factors such as antipyretic drugs.
Judicious sedation, using butorphanol and/or acepromazine, can prove useful in the treatment of hyperthermia, in particular in brachycephalic animals, by reducing heat production from breathing and by calming the patient.
Clinical Tip
Pyrexia occurs as a result of pyrogens acting on the hypothalamus, causing the thermoregulatory set point to be raised. The hypothalamus therefore stimulates heat production and heat conservation. Pyrogens may be exogenous or endogenous, although the majority of exogenous pyrogens cause pyrexia by stimulating the release of endogenous pyrogens. Exogenous pyrogens may be involved in infectious disorders (e.g. bacteria, bacterial endotoxins, viruses) as well as for example with intoxication or neoplasia, while endogenous pyrogens (e.g. cytokines, prostaglandins) may be generated for example in inflammation or with neoplasia.
Pyrexia is a physiological defensive mechanism and active cooling is inappropriate unless temperature elevation is severe enough to potentially cause tissue injury (>41.5°C). Cooling pyrexic animals may reduce body temperature but this will most likely cause the thermoregulatory centre to stimulate heat production and conservation further (i.e. to return body temperature to the raised set point) which is counterproductive. Treatment of pyrexia should therefore be aimed at identifying and addressing the underlying cause.
Antipyretic agents, typically nonsteroidal antiinflammatory agents (NSAIAs), have a role in the treatment of pyrexia and may contribute to improving patient morbidity. However, the potentially beneficial effect of pyrexia must not be discarded and the use of NSAIA therapy is not necessarily indicated in all cases. In those animals in which the primary underlying cause can be directly addressed (e.g. appropriate antibiosis for bacterial infection), or in which clinical signs are not too severe or prolonged, there is an argument for withholding NSAIA therapy to allow the beneficial effects of pyrexia to occur. In addition, withholding NSAIA therapy will allow resolution of pyrexia to be interpreted more reliably as a positive response to treatment of the primary disorder. In the author’s experience, pyrexia resolves satisfactorily in a large proportion of patients in which the primary disorder is addressed, often with temporary provision of intravenous fluid therapy. If NSAIA therapy is considered, due attention must be paid to other possible contraindications (especially hypovolaemia, hypoperfusion from other causes, dehydration, renal insufficiency and gastrointestinal abnormalities).