Fever is a cardinal symptom in critically ill patients. It develops in response to various infectious or non-infectious stimuli. A febrile response is just one component of a complex array of host defense responses, collectively termed as acute phase response (APR), which occurs during the time-course of the systemic inflammation. The APR is a pronounced systemic reaction to disturbances of homeostasis, which is caused by infections, tissue injury, neoplastic growth, or immunological disorders; fever is one of the most prominent components of the APR, a hallmark of disease [1, 2]. During systemic inflammation, phases of fever and phases of hypothermia can alternate, depending on the severity of a given inflammatory insult or on environmental conditions [3, 4]. It is a matter of debate, whether the strength of the fever or the degree of hypothermia is of prognostic value for the final outcome (i.e. survival) in critically ill patients .According to the classical view, fever develops in several steps starting with the appearance of a given pathogenic agent, the “exogenous pyrogen”, in the afflicted host. This exogenous pyrogen, in turn, causes the release of fever-producing substances by the host’s polymorphonuclear leukocytes and by other cells. These substances are, therefore, called
Journal of Basic and Clinical Physiology and Pharmacology – de Gruyter
Published: Nov 27, 2017
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