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The febrile patient represents a problem of daily importance for intensivists and consultants in the critical care unit (CCU). Fever is a cardinal sign of inflammation or infection. The main differential diagnostic difficulty in the CCU is to distinguish between fevers of infectious and noninfectious origin. The commonest noninfectious diseases presenting with fever in the intensive care setting include acute myocardial infarction, acute pulmonary embolism/infarction, acute pancreatitis, gastrointestinal hemorrhage, phlebitis, hematomas, attacks of acute gout, fevers owing to malignancies, and drug hypersensitivity reactions (i.e., drug fevers). These clinical entities must be differentiated from the infectious causes of fever. The commonest infections seen in the critical care setting include severe community-acquired and nosocomial pneumonias, intravenous line infections, septic pulmonary emboli, viral hepatitis, antibiotic-associated diarrhea/colitis, infected decubitus ulcers, and intra-abdominal or pelvic infection due to perforation, trauma, or surgery. Patients may be admitted to the CCU with urosepsis, but urosepsis rarely develops in the CCU except in nonleukopenic compromised hosts with catheter-associated bacteria (i.e., diabetics, patients with lupus, and patients receiving corticosteroids) 1,5 (Table 1) Sepsis is perhaps the most frequently misdiagnosed and overdiagnosed condition in the CCU. Sepsis is an imprecise term that implies the patient is ill from a sustained systemic bacteremia or fungemia. If sepsis is associated with hypotension, it is termed septic shock . It is essential to remember that sepsis does not occur spontaneously without an underlying cause. Many conditions mimic sepsis clinically, hemodynamically, and in terms of laboratory abnormalities. Before the clinician labels the patient as "septic" because of fever, leukocytosis, and a left shift with or without hypotension, a concerted effort must be made to eliminate the mimics of sepsis (i.e., pseudosepsis). 10,12 After the causes of pseudosepsis have been eliminated from diagnostic consideration by history, physical examination, and appropriate laboratory tests, a septic etiology may be pursued. It is also critical to remember that sepsis occurs in only a few well-defined situations and does not just happen. The organisms responsible for prolonged, sustained bacteremia with systemic manifestations (i.e., sepsis), either bypass or overcome the patient's host defenses. Such virulent organisms reside in high concentration in the distal gastrointestinal tract and pelvis. Virulent, aerobic gram-negative bacilli may originate from the urinary tract. A ruptured intra-abdominal viscus releases an overwhelming number of organisms that will overcome normal host defenses and present with bacteremia, peritonitis, or abscess. A smaller inoculum bypassing host defenses, as is the case with intravenous line sepsis, produces the same clinical manifestations as a ruptured intra-abdominal viscus. Equally as important conceptually, some clinical conditions virtually never result in sepsis; these include uncomplicated wound infections, superficial phlebitis, catheter-associated bacteria in normal hosts, community-acquired pneumonia in normal hosts, bacterial meningitis without concomitant bloodstream invasion, decubitus ulcers, osteomyelitis, and subacute bacterial endocarditis. 12,18 Some infections are regularly accompanied by bacteremia that is part of their clinical presentation. These include acute pyelonephritis, acute bacterial endocarditis, meningococcemia, overwhelming infection in asplenic patients, and intravascular infections. It is vital to remember the fundamental operative infectious disease principle in the diagnosis of sepsis. This key principle, simply stated, is, if you cannot identify one of the usual conditions in the proper location (i.e., a condition known to be associated with sepsis) then the patient probably does not have sepsis at all. A diligent search should be made for other causes for conditions mimicking sepsis, such as, pseudosepsis. 7,10
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Burke A. Cunha (1998) studied this question.
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