Fever is a nearly universal phenomenon; it is safe to say that practically everyone has had a fever at one time or another. It has been recognized for millennia as “a cardinal sign of disease” (Thompson, 2005, p. 484). Records show that Alexander the Great was treated by his physician for fever, and other ancient civilizations were known to use herbals for antipyresis (Griesman & Mackowiak, 2002). During the medieval period, fever (pyrexia) was seen as beneficial and was deliberately induced (Woodrow, 2003). By the mid-19th century, fever was known to be related to metabolic processes (Gregson & Mackowiak, 2004). Recent studies have shown that fever can be found in all higher vertebrates (Roberts, 1979), as well as in lower animals, from lizards to grasshoppers to goldfish. Even the single-celled paramecium exhibits a febrile response, a response that appears to have evolved millions of years ago (Kluger, Kozak, Conn, Leon, & Soszynski, 1991).
Despite this long history and commonality of experience, there is considerable disagreement regarding identification and management of fever, due in part to the inability to ethically conduct controlled studies in human beings. Much of our knowledge about this condition is based on animal studies, which may or may not be generalizable. Nonetheless, the results of these studies, together with an increased understanding of human physiology, have led to an improved appreciation of the nature of fever and increased awareness of its beneficial effects (Henker & Carlson, 2007).
There have been few changes to the nursing approach to fever in the past century, despite this increased understanding (Sund-Levander, Wahren, & Hamrin, 1998). Information related to the beneficial (or at least benign) nature of fever is not often transmitted to bedside caregivers; studies show lack of consistency among nurses regarding fever management (Thompson, 2005). According to Sund-Levander et al. (1998), “Nurses with more experience stressed the risk of complications and physiological consequences [of fever]...[while] the tendency among nurses with less experience were [sic] to stress the patient’s experience of the illness and their desires concerning what was pleasant” (p. 23). Nurses correctly regarded fever as a symptom of disease, rather than a disease itself, but did not consider its immunological role. Thus, “there is a risk that fever is considered the origin rather than the response to illness, which can lead to the belief that lowering the temperature improves the treatment” (Sund-Levander et al., 1998, p. 24).
Many nursing textbooks still give little room to discussion of fever, beyond including it as one of many symptoms of a variety of conditions. Available research references are also limited. A review of National Guideline Clearinghouse yielded considerable information on management of disease states that may cause fever, but few or no suggestions regarding fever itself. The Cochrane Library and the PubMed database likewise had little to offer.
Identifying and responding to fever in the geriatric population can be especially problematic because of functional status alterations, pharmacological stressors, and age-related physiological changes. The purpose of this review was to determine the appropriate management of fever in older adults using the information currently available.
Definition of Fever
Norman and Yoshikawa (1996) indicated “there is a paucity of literature that clearly establishes a range of normal temperatures and criterion for fever in elderly persons” (p. 93). The classic “normal” temperature of 98.6°F (37°C) was derived from a 19th-century study, using thermometers that were less accurate than current instruments and were calibrated 2.6°F to 2.4°F (1.4°C to 2.2°C) higher (Gregson & Mackowiak, 2004). Recent studies have reported a wide range of mean temperatures, ranging from 96°F to 100.7°F (35.6°C to 38.2°C), affected by age, gender, time of day, ambient temperature, and other factors (Auwaerter, 2007; Gregson & Mackowiak, 2004). Among older adults, Bauler (2001) found a mean oral temperature of 36.6°C (97.9°F), whereas Gomolin, Aung, Wolf-Klein, and Auerbach (2005) found mean temperatures ranging from 97.3°F to 97.8°F (36.3°C to 36.6°C) in a diurnal pattern.
Norman and Yoshikawa (1996) also suggested that “fever should be considered to be present under the following circumstances: Persistent elevation of body temperature of at least 2°F [(1.1°C)] over baseline values; oral temperatures of 99°F (37.2°C) or greater on repeated measurements; rectal temperatures of 99.5°F (37.5°C) on repeated measurements” (p. 95). This definition is widely cited and has become the standard of care. A single oral temperature of 100°F (37.8°C) is adequate to define a fever, and repeated measurements should be taken within 15 to 30 minutes to guard against errors in recording (T. Yoshikawa, personal communication, October 9, 2008). Norman (personal communication, October 8, 2008) suggested two measurements 1 hour apart on a stable patient, with a shorter interval on an unstable patient. Yoshikawa and colleagues anticipate publishing updated guidelines soon.
The guidelines discussed above assume the use of oral or rectal temperature measurements as approximations of core body temperature. However, these methods are falling into relative disuse in daily practice. Infrared thermometry is now being used in many clinical situations, and tympanic thermometry is the method of choice in most long-term care facilities. There has been little research to verify the validity or reliability of either of these new methods. Gregson and Mackowiak (2004) cited a study showing tympanic thermometry to be poorly correlated to rectal or oral measurements. Further study is needed to verify the validity of these increasingly common methods of temperature measurement.
Fever Versus Hyperthermia
Understanding the difference between fever and hyperthermia is important; many health care providers (both medical and nursing) fail to make this distinction. Roberts (1979), for example, used the terms interchangeably, even while admitting they are not exactly the same thing. Woodrow (2003) considered only the level of temperature elevation, regardless of underlying etiology. Sund-Levander et al. (1998) found that nurses in general were unaware of the difference between fever and hyperthermia. This distinction has important implications with regards to nursing management of patients with elevated body temperature.
As discussed in more detail below, fever is one aspect of the complex febrile response involving multiple physiological systems (Griesman & Mackowiak, 2002), resulting in a change in the hypothalamic temperature setpoint. It is “a regulated rise in core temperature in response to a physiological threat to the host” (Gregson & Mackowiak, 2004, Fever versus Hyperthermia, ¶1, italics added). In short, it is a symptom, a controlled and adaptive response to pathological stress.
Hyperthermia, on the other hand, is unregulated—a “significant elevation in body temperature without an associated pathological process” (Thompson, 2005, p. 486) and without change in the setpoint (Henker & Carlson, 2007). The most common etiology in older adults is the inability to regulate heat (Gregson & Mackowiak, 2004) and/or shed excessive heat (Henker & Carlson, 2007). This inability to shed heat is usually related to extremely high ambient temperatures, mediated by a variety of disease states and medications, as well as physiological changes (Collins, 2001; Douglas & Morris, 2006; High, 1999; Millsap, 2007).
Because there is no change in the hypothalamic setpoint, antipyretic agents are ineffective in treating this condition (Gregson & Mackowiak, 2004; Griesman & Mackowiak, 2002; Henker & Carlson, 2007). Body temperature in hyperthermia is usually at least 105°F (40°C) (Collins, 2001; Millsap, 2007) and has been reported as high as 114°F (45.6°C) (Gregson & Mackowiak, 2004)—temperatures that can cause neurological symptoms (Henker & Carlson, 2007). Hyperthermia is a medical emergency of extreme temperature elevations that requires immediate treatment to prevent excessive morbidity and mortality, whereas fever is a usually benign condition marked by modest body temperature elevation.
Pathophysiology of Fever
Although the precise mechanisms are not entirely understood, it is clear that the interplay of multiple physiological systems produces a complex febrile response, of which fever is one aspect (Griesman & Mackowiak, 2002; Holtzclaw, 2001). There is no single organ of control; the febrile response is mediated by the hypothalamus, limbic system, brain stem, reticular formation, spinal cord, and sympathetic ganglia (Gregson & Mackowiak, 2004). This response is “characterized by a cytokine-mediated rise in core temperature...and a host of other immunologic, neurologic, endocrinologic, and physiologic changes” (Gregson & Mackowiak, 2004, Fever versus Hyperthermia, ¶1). Despite this complexity, it seems that core body temperature is primarily directed by changes in the hypothalamic temperature setpoint.
Gregson and Mackowiak (2004) described the complex, and only partially understood, role of pyrogens (fever-causing cytokines) in the febrile response. Pyrogens may be classified as endogenous or exogenous, although Gregson and Mackowiak considered this distinction to be artificial. Exogenous pyrogens include a variety of bacterial products and foreign antigens (Dinarello, 2004) that may interact directly with Toll-like receptors (TLRs) in the hypothalamus, elevating the setpoint. More commonly, they stimulate phagocytic cells, such as macrophages, neutrophils, monocytes, and natural killer cells, to release endogenous pyrogens, primarily the interleukins, interferons, and tumor necrosis factor (Dinarello, 1999; Gregson & Mackowiak, 2004; High, 1999; Kluger et al., 1991; Roberts, 1979). “It is noteworthy that cells that are demonstrated to produce endogenous pyrogens also have a major role in many other features of the immune response” (Roberts, 1979, p. 241). Monocytes produce pyrogens in response to infection, inflammation, antigen-antibody complexes, complement components, inflammatory bile acids, and androgenic steroid metabolites (Dinarello, 1999; Gregson & Mackowiak, 2004). Pyrogens are also released by lymphomas, for unknown reasons (Roberts, 1979).
Fever is mediated by endogenous pyrogens (a term rejected by Dinarello  in favor of pyrogenic cytokines) through elevation of the hypothalamic setpoint, although the precise mechanism by which this happens is unclear (Gregson & Mackowiak, 2004; Huether & Defriez, 2006). Dinarello proposed that the various pyrogens interact with TLRs or cytokine receptors on the anterior hypothalamus, triggering activation of cyclooxygenase-2 and production of prostaglandin E2 (PGE2) on the brain side of the blood-brain barrier. PGE2 then interacts directly with receptors in the brain, stimulating the biochemical changes that result in fever.
Pyrogens do not act unchecked; they are opposed by endogenous cryogens, cytokines that act to decrease the hypothalamic setpoint. The interplay of these two sets of chemical messengers creates a negative feedback loop that results in a protective thermal ceiling (Huether & Defriez, 2006, Kluger et al., 1991). Kluger et al. (1991) stated, “This highly-regulated nature of fever is one of many indirect pieces of evidence that fever is not simply a by-product of infection but has evolved as an important and carefully orchestrated host defense response” (p. 255).
The febrile response displays less vigor in older adults because of age-related decrease in the immune response and other physiological changes (Crew, 1995). Although there is little or no change in the overall numbers of white cells, T-cell proliferation in response to stimuli is depressed, as is production of interleukin (IL) by those cells. There is decreased proliferation and antibody production by Beta-cells, as well as diminished IL production by macrophages. The result is diminished host defense and febrile response; “The decline in immune function, largely due to diminished T-cell function... is the hallmark of biological aging” (Crew, 1995, p. 496).
Animal studies have shown that aging results in physiological changes in almost all components of the febrile response: immunologic, endocrinologic, metabolic, autonomic, and behavioral (Norman & Yoshikawa, 1996). Older adults are more likely to have diminished production and conservation of body heat (Collins, 2001; Emmett, 1998; Gomolin et al., 2005; Norman & Yoshikawa, 1996), resulting in a lower baseline core body temperature. Pharmacological attenuation of the febrile response is common, as is diminished hypothalamic sensitivity and response to pyrogens (Emmett, 1998). As many as 20% to 30% of older adults will have blunted or absent fever response to infection (Auwaerter, 2007; Emmett, 1998; Norman & Yoshikawa, 1996). For example, Bauler (2001) found no significant temperature difference between patients with signs of infection and those without. The lower baseline temperature renders it even more difficult to detect what limited febrile response may be present.
Etiology of Fever
When confronted with fever, most care providers immediately consider infection, and rightly so. It is important, however, to remember that any condition that stimulates the release of pyrogenic cytokines by monocytes will result in fever (Gregson & Mackowiak, 2004). Besides infection, these conditions include activity, inflammation, increased metabolism, injury, and exposure to toxins (Huether & Defriez, 2006; Woodrow, 2003). Fever was cited by Millsap (2007) as the clinical manifestation of numerous conditions, both infectious and noninfectious. Ferri (2008) listed 18 noninfectious causes of fever (not including parasitic diseases). He also noted that infection was the causative agent only 25% of the time in fever of unknown origin; collagen-vascular diseases accounted for almost as many (24%), with malignancy causing 15%, and a variety of other conditions accounting for another 8% (with the remaining cases undetermined). Other fever-producing conditions of note include drug fever, thromboembolic disease, and inflammatory bowel disease (Ferri, 2008; Zenone, 2006).
Lowdon (2005) found that an infective cause was found in only 25% to 37% of older adults with fever of unknown origin. Zenone (2006) found three primary causes of fever of unknown origin: infection, malignancy, and noninfectious inflammatory disease (NIID), an umbrella term covering a variety of connective tissue diseases, vasculotides, and granulomatous diseases. “NIID emerged as the most frequent cause of [fever of unknown origin], particularly in the elderly” (Zenone, 2006, p. 637). Although infection was more likely to be the causative agent of fever of unknown origin in younger adults, in older adults there was a greater preponderance of NIIDs such as giant cell arteritis and polymyalgia rheumatica. NIIDs were found in 36.1% of older adults with fever of unknown origin, with infection and malignancy in 14.8% each. Although small (n = 61 older adults), this study provided evidence that compels caregivers to consider both infectious and noninfectious causes for a demonstrated fever.
Infection rates in fever of unknown origin fail to include more easily identified infectious causes of fever, such as simple urinary tract or respiratory infections. Auwaerter (2007), Collins (2001), and Norman and Yoshikawa (1996) concluded that fever in older adults is typically associated with infection. Norman and Yoshikawa (1996) cited a study by Castle et al., which demonstrated a temperature of 100°F (37.8°C) to be 98.3% specific for infection. They indicated, “Clinicians should be highly suspicious of the presence of a serious bacterial infection in nursing home patients who experience a change in functional status and exhibit an increase in baseline temperature” (Norman & Yoshikawa, 1996, p. 97). Alteration in cognitive function, especially the development of delirium, is often present before (or in the absence of) fever in older adults with an infection. Keating, Klimek, Levine, and Kiernan (1984) found that in older patients, fever was significantly less likely to be related to a benign process and more likely to be infection related. Febrile older adults had increased rates of hospitalization and death. Life-threatening consequences or death occurred in almost 30% of those older than age 60 who had body temperatures of greater than 103°F (39.4°C).
The blunted febrile response has important ramifications for patients and caregivers. The lack of measurable fever may lead to delayed diagnosis and treatment, resulting in a poor prognosis with increased morbidity and mortality (High, 1999; Norman & Yoshikawa, 1996). In addition, “the absence of fever responses to infection and therefore the beneficial effects of fever production may explain the increase in morbidity and mortality rates seen in very elderly persons” (Huether & Defriez, 2006, p. 466). Infectious diseases in general in older adults are associated with higher morbidity and mortality. Regardless of whether the fever itself is treated, it is important to identify its etiology because it is often treatable, and failure to do so will likely have adverse consequences (Norman, Wong, & Yoshikawa, 2007).
Benefits of Fever
Animal studies have shown fever to have numerous physiological benefits for control of infection, with the actual temperature being less important than the degree of elevation above what is normal for the species (Roberts, 1979). It has been suggested that increased body temperature may create a “thermic shock” that disrupts the invader (Kluger et al., 1991, p. 264). Many, although not all, studies found increased migration of neutrophils and greater production of antimicrobial chemicals by those cells (Roberts, 1979). Even under normothermic conditions, T-cells showed increased responsiveness if initially sensitized while the subject was febrile (Kluger et al., 1991; Roberts, 1979). Lymphocyte response and total lymphocyte count are enhanced, as are antibody sensitization and response and stabilization of normal cell membranes (Kluger et al., 1991; Roberts, 1979).
Although attempts to correlate fever with morbidity and mortality have had mixed results (Kluger et al., 1991), morbidity and mortality studies in animals have provided indirect evidence of fever’s beneficial effects. Lack of febrile response in animal studies often led to death (Roberts, 1979). Fever was correlated with diminished mortality in general, negative nasal washings, and increased survival of newborn lambs with induced viral infections. Decreased (normal) body temperature was correlated with increased morbidity and mortality and longer recovery periods after illness. Cold-blooded animals such as goldfish and lizards had improved survival rates when allowed to self-select areas of higher ambient temperature. It should be noted, however, that while survival increased when body temperatures rose, temperature elevations beyond a certain point resulted in decreased survival rates (Kluger et al., 1991).
There is little literature describing the physiological effects of fever in conditions other than infection. Fever has been shown to have adverse effects on neoplastic tissue and helps promote a positive nitrogen balance (Roberts, 1979). Fever was also associated with a significantly diminished mortality rate in patients with peritonitis (Roberts, 1979), although it is possible the survival rate resulted not from the fever itself, but from a strong immune response that resulted in elevated body temperature.
Management of Fever
Little or no evidence suggests that fever puts older adults at risk for long-term complications or neurological symptoms (Huether & Defriez, 2006; Poth & Belfer, 1998; Roberts, 1979), and there is little clear benefit seen in reducing body temperature (Auwaerter, 2007; Gregson & Mackowiak, 2004). Roberts (1979) stated, “There is minimal danger from relatively high temperatures in most patients, and the febrile response may benefit the host both by direct effects and by directing medical management of the illness” (p. 242). “Reaching a diagnosis is in-variably more difficult if empirical therapies obfuscate the cause of the fever” (Auwaerter, 2007, p. 463). Effective antipyresis may even be detrimental; the lower body temperature may limit the host defense response (Henker & Carlson, 2007). “Because fever is a beneficial response to infection, suppression of fever...should be reviewed carefully” (Huether & Defriez, 2006, p. 466).
Nonetheless, there is an exception to every rule, and there is a time to treat a fever, although there is no clear consensus as to when this is (Henker & Carlson, 2007). The one widely accepted indication for antipyretic therapy is the comorbidity of fever in a patient with severe coronary artery disease (CAD). Fever increases metabolic rate by 10% to 12% per degree C (1.8°F) (Henker & Carlson, 2007; Kluger et al., 1991; Roberts, 1979; Sund-Levander et al., 1998). There is a corresponding increase in both anabolic and catabolic rates, with catabolic rates predominating, thus creating a negative nitrogen balance (Kluger et al., 1991). Increased heart rate and changes in hemodynamic status “can contribute to a mismatch in oxygen delivery and myocardial oxygen consumption in elderly patients, particularly those with CAD” (Henker & Carlson, 2007, p. 79). Therefore, these patients should be treated at a lower threshold to minimize the deleterious effects of fever.
When treating fever, health care providers must take care to avoid exacerbating underlying problems or creating new ones. The defervescent stage, identified by falling temperature, diaphoresis, and shivering, is a time of particular concern. Diaphoresis increases heat dissipation but causes discomfort (Henker & Carlson, 2007). Shivering must be prevented, especially in those with CAD. Shivering is “a principle thermogenic mechanism” (Gregson & Mackowiak, 2004, Thermoregulation, ¶1) that not only counteracts attempts to decrease body temperature but also increases cellular oxygen consumption by as much as 400% (Henker & Carlson, 2007; Sund-Levander et al., 1998). According to Sund-Levander et al. (1998), “Shivering can be more strenuous for the heart and circulatory system than a few days of 39°C [(102.2°F)]” (p. 24).
Other concerns focus primarily on the undesirable side effects of antipyretic medications. Acetylsalicylic acid (aspirin) and nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in reducing the hypothalamic setpoint, especially in prostaglandin-mediated fever (Buffum & Buffum, 2000) but have the well-known side effects of gastrointestinal upset or lesions and renal toxicity. Some NSAIDs, as well as external cooling measures, may cause vasospasm in patients with CAD (Gregson & Mackowiak, 2004; Griesman & Mackowiak, 2002). Age-related changes prolong elimination of NSAIDs, with a greater likelihood of side effects (Buffum & Buffum, 2000). Acetaminophen (Tylenol® and others) is generally effective and well tolerated but presents the slight risk of hepatotoxicity with long-term use, especially at higher dosages, and is less effective in opposing prostaglandins.
In light of these concerns, health care providers must consider carefully whether to use antipyretic agents, weighing the risks against the possible benefits (Gregson & Mackowiak, 2004). According to Thompson (2005), “Febrile patients not at risk or in discomfort should be monitored and educated about the beneficial effects of fever on the immune system” (p. 490). Although reducing fever does not improve morbidity and mortality, antipyretic agents may limit fever-related cognitive effects (Gregson & Mackowiak, 2004; Griesman & Mackowiak, 2002). “The role of antipyretic drugs in fever management is primarily to reduce symptoms of malaise and headache” (Holtzclaw, 2001, p. 213). Short courses of antipyretic therapy at approved dosages carry low risk of toxicity and may provide symptomatic relief, while decreasing metabolic demands (Gregson & Mackowiak, 2004). To prevent complications related to shivering, it is recommended that antipyretic agents be given on a regular schedule during the acute illness to minimize temperature fluctuations and recurrent defervescence (Gregson & Mackowiak, 2004).
Each institution should develop a protocol for identifying and managing fever in older adults in accordance with current evidence. Such a protocol should include a process for identifying the patient’s baseline temperature. In addition:
- “Standing orders” prescribing the use of antipyretic agents for fever should be avoided. Fever in an elderly patient should be reported to the health care provider to be investigated and managed on a case-by-case basis.
- It is important to identify a fever with a single oral reading of 100°F (37.8°C) or greater, or two temperature measurements of 99°F (37.2°C) orally or 99.5°F (37.5°C) rectally 1 hour apart, with a shorter interval for a patient who is unstable or deteriorating.
- Attempts to reduce body temperature should be avoided unless the patient has severe CAD or another medical condition that will be exacerbated by an increased metabolic rate.
- Conditions or treatments that promote shivering should also be avoided, especially in patients with CAD. If shivering occurs, the health care provider must take steps to ensure the patient is warm, dry, and comfortable, even at the cost of undermining antipyretic therapy or maintaining temperature elevation.
- The negative effects of defervescence can be limited by administering antipyretic agents (if used) regularly during the acute phase of the illness, rather than on an as-needed basis depending on a predetermined temperature.
- Prior to, or concomitant with, the use of antipyretic agents, the health care provider should educate the patient (and/or the patient’s family) about the beneficial effects of fever and the role of fever in identifying and guiding treatment of the disease process.
- If the patient does not respond to antipyretic agents or if the patient remains febrile in absence of evident infection, the etiology should be reconsidered.
Appropriate management of older adults with fever is contingent on a thorough understanding and appreciation of the nature of this condition. As Kluger et al. (1991) stated, “If fever had no adaptive function, it is unlikely, because of its high metabolic cost, that it would have persisted throughout millions of years of evolution in so many different animals” (p. 256). The role and benefits of fever in the normal physiological system and in disease, as well as the caution necessary in treating this symptom, are becoming increasingly evident. It is neither necessary nor sufficient to automatically use antipyretic agents to treat fever. The most effective antipyretic is a definite diagnosis and specific therapy (Auwaerter, 2007).
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