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The majority of sepsis cases are caused by gram-negative and gram-positive bacteria; however, sepsis is a heterogeneous clinical syndrome that can be caused by any class of microorganism including fungi, mycobacteria, viruses, ricketsiae, and protozoa. Predisposing factors for gram negative bacterial sepsis include diabetes mellitus, lymphoproliferative diseases, cirrhosis, burns, invasive procedures, and chemotherapy. Risk factors for gram positive sepsis include vascular catheters, burns, indwelling mechanical devices, and injection drug use. Nonbacterial sepsis is more commonly seen in immunocompromised individuals

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Vital signs often reveal hyperthermia or hypothermia, tachycardia, and tachypnea. Early clinical features of sepsis include obtundation; hyperventilation; hot, flushed skin; and a widened pulse pressure. In elderly, very young, or immunocompromised patients, the clinical presentation may be atypical, with no fever or localized source of infection.

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In the early stages of septic shock, vasodilation is common. Myocardial depression occurs; however, cardiac output and stroke volume are usually maintained. Sepsis is the most common condition associated with acute lung injury and acute respiratory distress syndrome (ARDS). Clinically, severe refractory hypoxemia, noncompliant “heavy” lungs, and a CXR showing bilateral pulmonary alveolar infiltrates are present.

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Renal manifestations of septic shock include acute renal failure with azotemia, oliguria, and active urinary sediment. The most frequent hepatic abnormality is cholestatic jaundice. Concentrations of transaminase, alkaline phosphatase (1 to 3 times the normal level), and bilirubin (usually not >10 milligrams/dL) increase.

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The most frequent hematologic changes of septic shock are neutropenia or neutrophilia, thrombocytopenia, and disseminated intravascular coagulation (DIC). Neutrophilic leukocytosis with a “left shift” results from demargination and release of less mature granulocytes from the marrow. Gram-negative infections precipitate DIC more readily than do gram-positive infections. Hyperglycemia can develop, even without a history of diabetes. Uncontrolled hyperglycemia is a significant risk for adverse outcome. Adrenal insufficiency may also be seen.

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Blood gas analysis performed early in the course of septic shock usually demonstrates respiratory alkalosis. As perfusion worsens and continues, tissue hypoxia generates more lactic acid and metabolic acidosis worsens.

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Cutaneous lesions that occur as a result of sepsis can be divided into 5 categories: direct bacterial involvement of the skin and underlying soft tissues (cellulitis, erysipelas, and fasciitis); lesions from hematogenous seeding of the skin or the underlying tissue (petechiae, pustules, cellulitis, ecthyma gangrenosum); lesions resulting from hypotension and/or DIC (acrocyanosis and necrosis of peripheral tissues); lesions secondary to intravascular infections (microemboli and/or immune complex vasculitis); and lesions caused by toxins (toxic shock syndrome).

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Septic shock should be suspected in any patient with a temperature of > 38.3°C (> 100.9°F) [>38.5°C (101.3°F) in children] or < 36°C (< 96.8°F) and a systolic blood pressure of < 90 mm Hg (or 2 SD below normal for age in children) with evidence of inadequate organ perfusion. The hypotension of septic shock does not typically reverse with rapid volume replacement of at least 1 L of isotonic crystalloid (or 20 mL/kg in children). History and physical examination findings combined with some basic laboratory or radiologic investigations usually identify a presumptive source for sepsis. Focus particular attention on the central nervous system, pulmonary system, intraabdominal structures, urinary tract, skin, and soft tissues. See Table 89-1 for diagnostic criteria, use of the qualifier “some” in the table acknowledges the fact that clinicians use judgement when making the diagnosis of “sepsis” in an individual patient.

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Table 89-1 Diagnostic Criteria for Sepsis in Adults and Children

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