Elevation of core body temperature above normal.
Fever defined as a single oral temperature of at least 38.3C or 101F.
Febrile state referred to a temperature of at least 38C (100.4F) for at least one hour.
Estimated that fever is the primary complaint for 30% of patients seen by pediatricians.
In response to infections occurs in more than one third of patients.
Preoptic area and the anterior hypothalamus play key roles in thermal homeostasis.
Cytokine induction of temperature such as interleukin-1 ,and interleukin-6 by pathogens or inflammatory stimuli triggers prostaglandin E2 production by brain endothelial cells, which resets the thermoregulatory setpoint in the preoptic area, eliciting a febrile response.
The preoptic area also controls cutaneous vasoconstriction, non-shivering thermogenesis in brown adipose tissue and shivering thermogenesis in skeletal muscles.
Thermal receptors that are present in the skin, spinal cord and abdomen send impulses to the hypothalamus via the spinal cord.
Fever related anorexia is mediated by prostaglandin.
Counterregulatory cytokines such as interleukin 10 and other anti-pyretic mediators function as inhibitors of fever and prevent detrimental elevations of temperature.
Body temperature >41C treatment is indicated.
Each 1degree C increase in body temperature is accompanied by a 13% increase in oxygen consumption.
The overwhelming majority of nontoxic but febrile infants and young children have a viral infection.
The risk of poor functional outcome is increased with even mild temperature elevation after ischemic stroke or intracerebral hemorrhage.
Sustained fevers associated with poor outcome after aneurysmal subarachnoid hemorrhage.
Frequency of fever among hospitalized patients is about 29%.
Pulmonary infections are the predominant causes of infectious fever in patients with stroke.
Occurs in about 25% of patients in neurologic intensive care units and is associated with depressed level of consciousness.
Subarachnoid hemorrhage associated with increased risk of developing fever.
About 53% of fevers in critically ill medical and surgical patients have infection as the cause of fever.
One component of the response to a complex body reaction involving cytokine mediated increase in body temperature, increase in acute phase reactants, and activation of endocrine and immunologic mechanisms.
Treatment of fever is based on the rationale that it places additional physiologic stress on patients.
Fever may enhance immune cell function, inhibit growth of pathogens, increase the activity of antimicrobial drugs, induces heat sensitive shock proteins that activate host defenses, enhances T cell responses, and studies have shown the hiigher early fever is associated with a lower risk of death among patients in the ICU admitted for infection.
Fever generates hepatic iron sequestering compounds that bind the free iron necessary for microbial replication.
In a randomized study of 700 patients with fever treated with intravenous acetaminophen or placebo did not affect the number of ICU free days open (Young P et al).
Temperatures up to 39.5°C in critically ill patients have no adverse effects and may even be associated with favorable outcomes.