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INTRODUCTION

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Sepsis is generally defined as a suspected or confirmed infection with evidence of systemic inflammation. Severe sepsis is sepsis with evidence of new organ dysfunction thought to be secondary to tissue hypoperfusion. Septic shock is present when cardiovascular failure occurs, reflected by persistent hypotension or the need for vasopressors despite adequate fluid resuscitation. 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, rickettsiae, and protozoa. The most likely microorganisms that cause sepsis varies based on possible patient exposure to drug-resistant microorganisms (e.g., due to recent hospitalization or other health care–associated exposure) and the specific anatomic site of suspected infection. Pneumonia, intraabdominal infection, urinary tract infection, and skin or soft tissue infections are the most common infections that precipitate sepsis.

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CLINICAL FEATURES

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The presence of sepsis may be apparent on the initial presentation of a critically ill patient. In some cases, however, sepsis can be challenging to identify early in a patient's evaluation. Abnormal vital signs such as hyperthermia or hypothermia, tachycardia, hypotension, and tachypnea may suggest sepsis as a diagnostic possibility in the right clinical circumstances. In particular, up to 40% of patients who present with undeifferentiated hypotension are later diagnosed with septic shock when a source of infection is identified through diagnostic testing.

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Traditionally sepsis has been categorized as a type of distributive shock associated with peripheral vasodilation, warm extremities, and a compensatory increase in cardiac output. However, this does not accurately reflect the presentation of all patients with sepsis. The combination of intravascular volume depletion and septic cardiomyopathy may also manifest as “cold shock,” with impaired peripheral perfusion and cool extremities,

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Many different abnormalities are possible with severe sepsis, reflecting different areas of end-organ damage. Severe sepsis is the leading cause of acute lung injury and acute respiratory distress syndrome (ARDS). Widespread inflammation secondary to sepsis commonly affects pulmonary function even in the absence of pneumonia. Refractory hypoxemia, decreased lung compliance, and a chest x-ray demonstrating bilateral pulmonary alveolar infiltrates are commonly found with ARDS. Renal manifestations of severe sepsis include acute renal failure with azotemia, oliguria, and anuria. The most frequent hepatic abnormality is cholestatic jaundice and is associated with elevation in transaminases, alkaline phosphatase, and/or bilirubin. The most frequent hematologic changes associated with sepsis are neutropenia or neutrophilia, thrombocytopenia, and disseminated intravascular coagulation (DIC). Hyperglycemia may develop, and uncontrolled hyperglycemia is a significant risk for adverse outcome. Cutaneous lesions that occur as a result of sepsis can be divided into five 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 ...

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