CHAPTER 20 Approach to the Febrile Patient
Obtaining a body temperature measurement is important in the evaluation of all patients, especially the critical care patient. A rectal temperature higher than 102.5° F (39° C) is considered elevated in the unstressed dog or cat. The method of measurement must also be taken into account because ear, axillary, or toe web measurements will be lower than rectal temperature.
Too frequently the veterinarian associates any elevation in body temperature with true fever. The assumption often is made that the fever is caused by an infectious agent, even if there is no obvious cause. If the patient’s fever resolves after antibiotics are given, the assumption is made that it was caused by a bacterial infection. A normal body temperature often is assumed to mean the absence of disease. This approach to fever, hyperthermia, or normothermia can be misleading and may result in improper diagnoses and therapy (or the lack thereof).
The thermoregulatory center for the body is located in the central nervous system (CNS) in the region of the anterior hypothalamus (AH). Changes in ambient and core body temperatures are sensed by the peripheral and central thermoreceptors, and the information is conveyed to the AH via the nervous system. Thermoreceptors sensing that the body is below or above its normal temperature (normal “set point”) will stimulate the AH to cause the body to increase heat production and reduce heat loss through conservation if the body is too cold or dissipate heat if the body is too warm (Figure 20-1). Through these mechanisms, dogs and cats can maintain a narrow core body temperature range in a wide variety of environmental conditions. With normal ambient temperatures, most body heat is produced by muscular activity, even while at rest. Patients with severe neurologic impairment or cachexia and those under anesthesia may not be able to maintain a normal set point or generate a normal febrile response.
Figure 20-1 Normal thermoregulation.
(From Miller JB: Hyperthermia and fever of unknown origin. In Ettinger SJ, Feldman EC (eds): Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders/Elsevier.)
After birth, there is rapid heat loss in the puppy and kitten as a result of decreased environmental temperature and evaporative heat loss. Because the neonate has poorly developed muscles there is little to no ability to generate heat through shivering, and heat production must occur through nonshivering thermogenesis. Heat generation is primarily via the lipolysis of brown adipose tissue. Brown adipose tissue contains numerous mitochondria. Heat is produced when adenosine-5′-triphosphate synthesis is uncoupled from the oxidative process by a protein in the mitochondria. In the neonatal dog or cat, brown adipose tissue is used within the first 2 to 3 weeks of life. This process is only partially able to maintain body temperature, and an environmental temperature of approximately 85° F (30° C) is needed to maintain normal body temperature. Neonatal puppies and kittens cannot generate a true fever in response to pyrogens for the first few weeks of life until shivering thermoregulation can take place and there are increased stores of glycogen in the muscles and liver.
Hyperthermia is the term used to describe any elevation in core body temperature above the accepted normal for that species. Hyperthermia is a result of the loss of equilibrium in the heat balance equation such that heat is produced or stored in the body at a rate in excess of heat lost through radiation, convection, or evaporation. The term fever is reserved for those hyperthermic animals in which the set point in the AH has been “reset” to a higher temperature. In hyperthermic states other than fever, the hyperthermia is not a result of the body attempting to increase its temperature but is caused by the physiologic, pathologic, or pharmacologic intervention in which heat gain exceeds heat loss. Box 20-1 outlines the various forms of hyperthermia.
BOX 20-1 Classification of hyperthermia
True fever is a normal response of the body to invasion or injury and is part of the “acute phase response.” Other parts of the acute phase response include increased neutrophil numbers and phagocytic ability, enhanced T and B lymphocyte activity, increased acute phase protein production by the liver, increased fibroblast activity, and increased sleep. Fever and the other parts of the acute phase response are initiated by exogenous pyrogens that lead to the release of endogenous pyrogens.
True fever may be initiated by a variety of substances, including infectious agents or their products, immune complexes, tissue inflammation or necrosis, and several pharmacologic agents including many antibiotics. Collectively, these substances are called exogenous pyrogens. Their ability to directly affect the thermoregulatory center is probably minimal, and their action is to cause the release of endogenous pyrogens by the host. Box 20-2 lists some of the more important known exogenous pyrogens.
BOX 20-2 Exogenous pyrogens
In response to stimuli by an exogenous pyrogen, proteins (cytokines) released from cells of the immune system trigger the febrile response. Macrophages are the primary immune cell involved, although T and B lymphocytes and other leukocytes may play significant roles. The proteins produced are called endogenous pyrogens or fever-producing cytokines. Although interleukin-1 (IL-1) is considered the most important cytokine, at least 11 cytokines capable of initiating febrile responses have been identified (Table 20-1). Some neoplastic cells are also capable of producing cytokines that lead to a febrile response. The cytokines travel via the blood stream to the AH, where they bind to the vascular endothelial cells within the AH and stimulate release of prostaglandins (PGs), primarily prostaglandin E2 (PGE2) and possibly prostaglandin E2α(PGE2α). The set point is raised, and the core body temperature increases through increased heat production and conservation (Figure 20-2).
|Endogenous pyrogen||Principal source|
|Cachectin/tumor necrosis factor (TNF-α)||Macrophages|
|Lymphotoxin/tumor necrosis||Lymphocytes (T and B) factor-β (TNF-β; LT)|
Only gold members can continue reading. Log In or Register to continue
Premium Wordpress Themes by UFO Themes
You may also need
WordPress theme by UFO themes