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  • Temperature: The hypothalamic thermoregulatory center balances excess heat production from metabolic activity in muscle and liver with heat dissipation from the skin and lungs to maintain a normal body temperature of 36.8° ± 0.4°C (98.2° ± 0.7°F), with diurnal variation (lower in a.m., higher in p.m.).

  • Fever: an elevation of body temperature (>37.2°C/98.9°F in the morning and >37.7°C/99.9°F in the evening) in conjunction with an increase in the hypothalamic set point

  • Fever of unknown origin (FUO): temperatures >38.3°C (>101°F) on two or more occasions and an illness duration of ≥3 weeks, with no known immunocompromised state and unrevealing laboratory and radiologic investigations into the cause

  • Hyperpyrexia: temperatures >41.5°C (>106.7°F) that can occur with severe infections but more commonly occur with CNS hemorrhages

  • Hyperthermia: an uncontrolled increase in body temperature that exceeds the body’s ability to lose heat without a change in the hypothalamic set point. Hyperthermia does not involve pyrogenic molecules.

  • Pyrogen: any fever-causing substance, including exogenous pyrogens (e.g., microbial toxins, lipopolysaccharide, superantigens) and pyrogenic cytokines (e.g., IL-1, IL-6, TNF)


  • Pathogenesis: The hypothalamic set point increases, causing peripheral vasoconstriction (i.e., heat conservation). The pt feels cold as a result of blood shunting to the internal organs. Mechanisms of heat production (e.g., shivering, increased hepatic thermogenesis) help to raise the body temperature to the new set point. Increases in peripheral prostaglandin E2 account for the nonspecific myalgias and arthralgias that often accompany fever. When the set point is lowered again by resolution or treatment of fever, processes of heat loss (e.g., peripheral vasodilation and sweating) commence.

  • Etiology: Most fevers are associated with self-limited infections (usually viral) and have causes that are easily identified.


  • History: A meticulous history is essential, with particular attention to the chronology of events (e.g., in the case of rash: the site of onset and the direction and rate of spread; see below) and the relation of symptoms to medications, pet exposure, sick contacts, sexual contacts, travel, trauma, and the presence of prosthetic materials.

  • Physical examination: A thorough physical examination should be performed. A consistent site for taking temperatures should be used. Temperature–pulse dissociations (relative bradycardia) should be noted if present (sometimes present, for example, with typhoid fever, brucellosis, leptospirosis, factitious fever). Close attention should be paid to any rash, with precise definition of its salient features.

    1. Lesion type (e.g., macule, papule, nodule, vesicle, pustule, purpura, ulcer; see Chap. 59 for details), configuration (e.g., annular or target), arrangement, distribution (e.g., central or peripheral)

    2. Classification of rash

      1. Centrally distributed maculopapular eruptions (e.g., viral exanthems, exanthematous drug-induced eruptions)

      2. Peripheral eruptions (e.g., Rocky Mountain spotted fever, secondary syphilis, bacterial endocarditis)

      3. Confluent desquamative erythemas (e.g., toxic shock syndrome)

      4. Vesiculobullous eruptions (e.g., varicella, primary HSV infection, ecthyma gangrenosum)

      5. Urticaria-like eruptions: in the presence of fever, usually due to urticarial vasculitis caused by serum ...

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