How fever works
How does fever happen?
Once endogenous pyrogens have been produced by the primary immune response, they must travel to the brain to actually induce fever. After their increased production by activated immune cells, cytokines such as IL-1, IL-6, and TNF are distributed throughout the body through the blood, as they are all soluble proteins. Now, then, these cytokines must have a target to signal and cause a reaction.
As it plays a central role in thermal regulation, it is unsurprising that destruction of the hypothalamus would result in a lack of febrile response; however, experimental evidence shows that direct stimulation of the hypothalamus by IL-1 does not induce fever (6). This potentially contradicting data suggested that although both the hypothalamus and IL-1 appear to be essential to induce fever, as the response will not occur when one of these factors is missing, there must be another link connecting the two, as they do not seem to directly interact. After searching for potential mediators that would convey the signal, the most likely current candidate appears to be prostaglandin E (PGE). This hypothesis is strongly supported by a study in which protein production of a specific PGE receptor was knocked out in mice, resulting in the impairment of febrile response (7). Since the complete signal was eliminated by recombination of the gene for PGE receptor, this appears to confirm that PGE is necessary to transduce the signal responsible for inducing fever to the brain. The use of PGE also appears to be conserved in the febrile response of ectotherms, as it has been shown to play an essential role in signaling fever in toads and salamanders (8).
Set point regulation
To learn more about specifically where in the brain controls for the mechanism of feverish response lie, researchers microinjected rats with PGE (9). They observed distinct responses in the three regions tested (the preoptic anterior hypothalamic area (POA), the organumn vasculosum laminae terminalis (OVLT), and the rostral third ventricle), noting that the OVLT was far more responsive to PGE exposure, even at a fraction of the dose. It appears that within these essential regions, prostaglandin might be affecting the firing rates of thermally sensitive neurons which are responsible for sensing and maintaining the thermal set point through their signals to heat loss and production responses (6). An in vitro study showed that incubation of these thermally sensitive neurons (cultured from mice) both increased synaptic firing rates and decreased postsynaptic inhibitory signals, which in vivo should result in a differential response to temperatures sensed within the body (10). This neurologic response both connects the immune response to the physiological increase in temperature as well as explaining the mechanism behind the host’s change in thermal set point.
Monitor client temperature—degree and pattern. Note shaking, chills or profuse diaphoresis.
Monitor environmental temperature. Limit or add bed linens, as indicated.
Provide tepid sponge baths. Avoid use of alcohol.
Administer antipyretics, such as acetylsalicylic acid (ASA) (aspirin) or acetaminophen (Tylenol).
Provide cooling blanket, or hypothermia therapy, as indicated.
Temperature of 102_F to106_F (38.9_C–41.1_C) suggests acute infectious disease process. Fever pattern may aid in diagnosis: sustained or continuous fever curves lasting more than 24 hours suggest pneumococcal pneumonia, scarlet or typhoid fever; remittent fever varying only a few degrees in either direction reflects pulmonary infections; and intermittent curves or fever that returns to normal once in 24-hour period suggests septic episode, septic endocarditis, or tuberculosis (TB). Chills often precede temperature spikes. Note: Use of antipyretics alters fever patterns and may be restricted until diagnosis is...
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