Virtually all burn patients have elevated core body temperatures and even a leukocytosis. Thus, fever after burn patients is not a reliable indicator of infection.
One study in children found that fever had no predictive value for the presence of infection and physical examination was a more reliable source of information about wound infection and sepsis. Furthermore, routine blood cultures have been shown to be of little value in working up a fever after burn patients.
Mild hyperthermia in the first 24 hours following injury is almost always the result of pyrogen release. The three endogenous pyrogens that mediate fever after burn are interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α, cachetin), and interferon-γ. In addition to inducing fever, these pyrogens also modulate a large number of host defense responses.
After 72 hours, burn patients develop systemic inflammatory response syndrome (SIRS), characterized by tachycardia, relative hypotension, and hyperthermia, which are the classic signs of sepsis that can occur without an infectious source.
In fact, body temperature may be as high as 39°C (102.2°F) and the leukocyte count may be as high as 20,000 cells/mL during satisfactory recovery. Thus, elevation of body temperature above normal, leukocytosis, and other signs of inflammation are common among burn patients and should be expected.
The hypermetabolic response elicited by a burn injury is marked by increased energy expenditure and muscle protein catabolism. Fever further increases energy expenditure and loss in burn patients. Thus, there is a theoretical metabolic benefit in attenuating fever after burn in such patients.
Mild elevation of body temperature is usually well tolerated and does not require specific treatment. However, body temperature higher than 39C may be treated with common antipyretics (e.g., acetaminophen, aspirin, indomethacin, or ibuprofen).
Burn patients also prefer warmer ambient temperature (26°C to 33°C) than do normal individuals because the fever after burn is an upward adjustment of the thermoregulatory center in the brain. This temperature range promotes patient comfort and reduces the physiologic demands of cold stress.
Treating fever after burn patients by surface cooling (ice packs, alcohol rubs, cooling blankets) is not uncommon but should be avoided because surface cooling creates a cold stress on an already critically ill patient.
Nonetheless, infection is a relatively common serious complication in patients with major thermal injuries. It is estimated that up to 75% of deaths following burn injury are related to infection. Immunosuppression is a universal feature of major thermal injury and burn patients are more susceptible to microbial colonization and infection.
Special attention to technique during bedside procedures and the use of universal precautions are a must. In one study, up to 100% of burn patients developed an infection from one or more sources during their hospital stay.
One might assume that prophylactic antibiotics, particularly against gram-positive organisms, are indicated; however, this practice has been shown to lead to the development of multidrug-resistant, gram-negative bacterial infections and fungal infections. In fact, studies have now verified that prophylactic antibiotics are not only unnecessary, but are also contraindicated in patients with thermal injuries. Exceptions to this statement are tetanus prophylaxis and perioperative antibiotics in patients who undergo excision and grafting. Otherwise, daily wound care and the
application of a topical, broad-spectrum antimicrobial agent are the mainstays for the initial prevention of wound infection. Ultimately, excision and grafting is the most efficacious means of reducing the incidence of burn wound sepsis.