Normal human body temperature displays a circadian rhythm. Body temperature is lowest in the predawn hours, at 36.1°C (97°F) or lower, and rises to 37.4°C (99.3°F) or higher in the afternoon. Normal body temperature is maintained by thermoregulatory mechanisms that balance heat loss with heat production.[1,2,3]
Radiation, chemotherapy, and biologic agents, both independently and in combination, increase the risk of cardiovascular disease in survivors of childhood cancer; in fact, cardiovascular death has been reported to account for 26% of the excess absolute risk of death by 45 or more years from diagnosis in adults who survived childhood cancers, and is the leading cause of noncancer mortality in select cancers such as Hodgkin lymphoma (HL).[1,2] During the 30 years after cancer treatment, survivors are...
Abnormal elevations of temperature result from either hyperthermia or pyrexia (fever). Hyperthermia results from failure of thermal control mechanisms. In fever, thermoregulatory mechanisms are intact, but the hypothalamic set-point is elevated above normal by exogenous or endogenous pyrogens. There are three phases to fever. In the initiation phase, cutaneous vasoconstriction promotes heat retention and shivering generates additional heat. When the new (elevated) set-point is reached, heat production balances heat loss and shivering stops. With lowering of the set-point to normal, cutaneous vasodilatation promotes heat loss to the environment in the form of sweating. These same mechanisms maintain normal core body temperature in afebrile individuals.[1,2,3,4]
Response to fever varies with age. In older people, inadequate thermoregulatory mechanisms may contribute to hyperthermia and result in arrhythmias, ischemia, mental status changes, or heart failure from increased metabolic demands. In children between the ages of 6 months and 6 years, febrile convulsions may occur.
In this summary, unless otherwise stated, evidence and practice issues as they relate to adults are discussed. The evidence and application to practice related to children may differ significantly from information related to adults. When specific information about the care of children is available, it is summarized under its own heading.
The major causes of fever in cancer patients include infection, tumor (also known as paraneoplastic fever), drugs (allergic or hypersensitivity reactions), blood product transfusion, and graft-versus-host disease (GVHD).[2,3,4,5,6,7,8] Infection is a particularly important cause in the neutropenic host, given its high frequency (almost two-thirds of patients) and potentially fatal outcome. Whereas gram-negative infections predominated as the cause of neutropenic fever in cancer patients in the 1970s and early 1980s, gram-positive infections, mainly streptococci and coagulase staphylococci, have predominated since. The increased incidence of staphylococcal and streptococcal infections relates to the use of intravascular devices, severe mucositis due to high-dose chemotherapy, and prophylactic antibiotic therapy with fluoroquinolones. Although fluoroquinolone use has not decreased the morbidity or mortality of neutropenic fever, it has resulted in increased incidence of resistant gram-negative bacteremia. Many consider paraneoplastic fever to be more common in primary tumors such as renal cell carcinomas and lymphomas, but available data suggest that it occurs in tumors of diverse primary sites. Hypersensitivity reactions, pyrogen production, primary cytokine production and tumor necrosis with secondary cytokine production are among the postulated causes of tumor fever. Drug causes of fever include a variety of cytotoxic chemotherapy agents, biologic response modifiers, vancomycin, amphotericin, and multiple other medications. Tumor-associated fevers may be cyclic, occur at a specific time of the day, or be intermittent, alternating with afebrile periods lasting days or weeks.[3,4] Fever pattern does not differentiate drug-associated fever from other causes of fever, except when the temporal relationship is unambiguous. For many drugs, a highly variable lag time between the initiation of the offending agent and the onset of fever masks the causative relationship.[4,6,7,10]