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Antipyretic drugs in patients with fever and infection: literature review

23 May 2019
Volume 28 · Issue 10

Abstract

Background:

antipyretic drugs are routinely administered to febrile patients with infection in secondary care. However, the use of antipyretics to suppress fever during infection remains a controversial topic within the literature. It is argued that fever suppression may interfere with the body's natural defence mechanisms, and may worsen patient outcomes.

Method:

a literature review was undertaken to determine whether the administration of antipyretic drugs to adult patients with infection and fever, in secondary care, improves or worsens patient outcomes.

Results:

contrasting results were reported; two studies demonstrated improved patient outcomes following antipyretic administration, while several studies demonstrated increased mortality risk associated with antipyretics and/or demonstrated fever's benefits during infection. Results also demonstrated that health professionals continue to view fever as deleterious.

Conclusion:

the evidence does not currently support routine antipyretic administration. Considering patients' comorbidities and symptoms of their underlying illness will promote safe, evidence-based and appropriate administration of antipyretics.

Fever is frequently observed in secondary care, occurring in up to 36% of patients in general medical wards, and up to 50% in critical care (Niven et al, 2012; Kiekkas et al, 2013). Fever is a symptom, not an illness in itself, and it is defined as the ‘controlled’ rise in body temperature, triggered by infectious or non-infectious mechanisms (Suzuki et al, 2015).

It is a complex, physiological, adaptive response to infection, which gives hosts survival advantages during illness (Carey, 2010). Fever inhibits microbial reproduction and viral replication, as well as accelerating the rate of phagocytosis (Dai et al, 2015). This is achieved by regulated phagocytic responses to pathogenic presence and the stimulation of cytokines, which react with arachidonic acid, altering the hypothalamus' thermoregulation system (Drewry et al, 2017).

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