Porth's Essentials of Pathophysiology, 4e

67

Inflammation, the Inflammatory Response, and Fever

C h a p t e r 3

Manifestations of Fever The physiologic behaviors that occur during the develop- ment of fever can be divided into four successive stages: a prodrome; a chill, during which the temperature rises; a flush; and defervescence (see Fig. 3-9). During the first or prodromal period, there are nonspecific complaints, such as mild headache and fatigue, general malaise, and fleeting aches and pains. During the second stage or chill, there is the uncomfortable sensation of being cold and the onset of generalized shaking, although the temperature is rising. Vasoconstriction and piloerection usually precede the onset of shivering. At this point the skin is pale and covered with goose flesh. There is an urge to put on more clothing or covering and to curl up in a position that conserves body heat. When the shiver- ing has caused the body temperature to reach the new set point of the temperature control center, the shiver- ing ceases, and a sensation of warmth develops. At this point, the third stage or flush begins, during which cuta- neous vasodilatation occurs and the skin becomes warm and reddened. The fourth, or defervescence, stage of the febrile response is marked by the initiation of sweat- ing. Not all persons proceed through all four stages of fever development. Sweating may be absent, and fever may develop gradually, with no indication of a chill or shivering. Common manifestations of fever are anorexia, myal- gia, arthralgia, and fatigue. These discomforts are worse when the temperature rises rapidly or exceeds 39.5°C (103.1°F). Respiration is increased, and the heart rate usually is elevated. Dehydration occurs because of sweating and the increased vapor losses caused by the rapid respiratory rate. The occurrence of chills com- monly coincides with the introduction of pyrogen into the circulation. This is one of the reasons that blood cultures to identify the organism causing the fever are usually drawn during the first signs of a chill. Many of the manifestations of fever are related to the increases in the metabolic rate, increased need for oxygen, and use of body proteins as an energy source. During fever, the body switches from using glucose (an excellent medium for bacterial growth) to metabolism based on protein and fat breakdown. With prolonged fever, there is increased breakdown of endogenous fat stores. If fat breakdown is rapid, metabolic acidosis may result (see Chapter 8). Headache is a common accompaniment of fever and is thought to result from the vasodilatation of cerebral vessels occurring with fever. Delirium is possible when the temperature exceeds 40°C (104°F). In the elderly, confusion and delirium may follow moderate elevations in temperature. Because of the increasingly poor oxy- gen uptake by the aging lung, pulmonary function may prove to be a limiting factor in the hypermetabolism that accompanies fever in older persons. Confusion, incoordination, and agitation commonly reflect cere- bral hypoxemia. Febrile seizures can occur in some children. 39 They usually occur with rapidly rising tem- peratures and/or at a threshold temperature that differs with each child.

Herpetic lesions, or fever blisters, develop in some persons during fever. They are caused by a separate infection by the type 1 herpes simplex virus that estab- lished latency in the regional ganglia and is reactivated by a rise in body temperature. Management of Fever Fever usually is a manifestation of a disease state, and as such, determining the cause of a fever is an impor- tant aspect of its treatment. Sometimes it is difficult to establish the cause. A prolonged fever for which the cause is difficult to ascertain is often referred to as fever of unknown origin (FUO). Fever of unknown origin is defined as a temperature of 38.3°C (101°F) or higher that is present for 3 weeks or longer. 40,41 Among the causes of FUO are malignancies (i.e., lymphomas, metastases to the liver or central nervous system); infections such as human immunodeficiency virus or tuberculosis, or abscessed infections; and drug fever. Malignancies, par- ticularly non-Hodgkin lymphoma, are important causes of FUO in the elderly. Cirrhosis of the liver is another cause of FUO. The methods of fever treatment focus on modifica- tions of the external environment intended to increase heat transfer from the internal to the external environ- ment, support of the hypermetabolic state that accom- panies fever, protection of vulnerable body organs and systems, and treatment of the infection or condition causing the fever. Because fever is a disease symptom, its manifestation suggests the need for treatment of the primary cause. Modification of the environment ensures that the environmental temperature facilitates heat transfer away from the body. Sponge baths with cool water or an alcohol solution can be used to increase evaporative heat losses. More profound cooling can be accomplished through the use of a cooling blanket or mattress, which facilitates the conduction of heat from the body into the coolant solution that circulates through the mattress. Care must be taken so that cooling methods do not pro- duce vasoconstriction and shivering that decrease heat loss and increase heat production. Adequate fluids and sufficient amounts of simple carbohydrates are needed to support the hypermeta- bolic state and prevent the tissue breakdown that is characteristic of fever. Additional fluids are needed for sweating and to balance the insensible water losses from the lungs that accompany an increase in respira- tory rate. Fluids also are needed to maintain an ade- quate vascular volume for heat transport to the skin surface. Antipyretic drugs, such as aspirin, ibuprofen, and acetaminophen, often are used to alleviate the discom- forts of fever and protect vulnerable organs, such as the brain, from extreme elevations in body temperature. These drugs act by resetting the hypothalamic tem- perature control center to a lower level, presumably by blocking the activity of cyclooxygenase, an enzyme that is required for the conversion of arachidonic acid to prostaglandin E 2 .