Fever and Hypothermia

Published on 22/03/2015 by admin

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Last modified 22/03/2015

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4 Fever and Hypothermia

Mitchell P. Fink

Fever is defined as an increase in body temperature. Normal body temperature is 36.8°C ± 0.4°C. Normally body temperature varies in a circadian fashion by about 0.6°C, being lowest in the morning and highest in the late afternoon or early evening. In 1998, the Society of Critical Care Medicine and Infectious Disease Society of America suggested that is “reasonable in many ICUs to consider all patients with temperatures ≥ 38.3°C to be febrile, warranting special attention to determine if infection is present.”¹

Fever is triggered by the release of various cytokines—notably, interleukin 1-beta (IL-1β), tumor necrosis factor (TNF), and interleukin 6 (IL-6)—that are capable of up-regulating expression of the enzyme cyclooxygenase (COX)-2 and thereby causing secretion of prostaglandin E₂ (PGE₂) in the hypothalamus.² PGE₂ binds to prostaglandin receptors located on a cluster of neurons in the preoptic region of the hypothalamus. Although there are four subtypes of PGE₂ receptors, only one, PGE₂ receptor 3 (EPR3), is required for the development of fever in response to IL-1β, lipopolysaccharide (LPS), or PGE₂.² Activation of EPR3 triggers a number of neurohumoral and physiologic changes that lead to increased body temperature. The antipyretic effects of various nonsteroidal antiinflammatory drugs (NSAIDs) such as aspirin and ibuprofen is due to inhibition of COX-2-dependent PGE₂ biosynthesis in the central nervous system (CNS). The mechanism whereby acetaminophen reduces fever is probably independent of COX-2 inhibition and remains controversial and poorly understood.^3,⁴

Body temperature can be measured using an oral, axillary, or rectal mercury-filled glass thermometer. These traditional approaches, however, have been largely replaced by a variety of safer and more environmentally friendly methods that use thermistors located on catheters or probes situated in the pulmonary artery, distal esophagus, urinary bladder, or external ear canal.³ Infrared detectors can also be used to measure tympanic membrane temperature. Forehead skin temperature can be measured using a temperature-sensitive patch.

Fever is a cardinal sign of infection. Accordingly, the new onset of fever should trigger a careful diagnostic evaluation, looking for a source of infection. The diagnostic evaluation should be thorough and tailored to the recent history of the patient. For example, the possibility of a CNS infection should receive greater attention in a patient with recent or ongoing CNS instrumentation. By the same token, if a patient recently underwent a gastrointestinal surgical procedure, the clinician should have a high index of suspicion for an intraabdominal source of infection. Key elements in the assessment of new-onset fever in the intensive care unit (ICU) are listed in Box 4-1. Common sources of infection in ICU patients are listed in Box 4-2.

Box 4-1

Key Elements in the Evaluation of New-Onset Fever in ICU Patients

• Be familiar with the patient’s history. Pay particular attention to possible predisposing causes of fever.

• Perform a careful physical examination. Pay particular attention to surgical wounds and vascular access sites. Look for evidence of pressure-induced skin ulceration. In patients with recent median sternotomy, evaluate the stability of the chest closure. Perform a careful abdominal examination.

• Obtain or review a recent chest x-ray, looking for evidence of new infiltrates or effusions.

• Obtain appropriate laboratory studies. At a minimum, these studies should include a peripheral white blood cell count and cultures of blood and urine. If the patient is endotracheally intubated or has a tracheotomy, obtain a sample of sputum for Gram stain. In some centers, sputum is routinely cultured. In other centers, bronchoalveolar lavage or bronchial brushing for quantitative microbiology is performed using blind or bronchoscopic methods.

• Central venous catheters that have been in place for longer than 96 hours should be removed. The tip should be submitted for semiquantitative microbiology.

• In patients receiving antibiotics for more than 3 days, a stool sample should be analyzed for the presence of Clostridium difficile toxin.

• More extensive diagnostic evaluation should be considered in a graded fashion based on history, physical examination findings, laboratory results, persistence of fever despite presumably appropriate antimicrobial chemotherapy, or clinical instability. These additional tests and procedures include diagnostic thoracentesis, paracentesis, and lumbar puncture. Imaging studies should be considered, including abdominal or cardiac ultrasonography and head, chest, or abdominal computed tomography.

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