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INTRODUCTION

DEFINITIONS

  • Systemic inflammatory response syndrome (SIRS)—Two or more of the following:

    • – Fever (oral temperature >38°C) or hypothermia (oral temperature <36°C)

    • – Tachypnea (>24 breaths/min)

    • – Tachycardia (>90 beats/min)

    • – Leukocytosis (>12,000/μL), leukopenia (<4000/μL), or >10% bands; may have a noninfectious etiology

  • Sepsis—SIRS with a proven or suspected microbial etiology

  • Severe sepsis—Sepsis with one or more signs of organ dysfunction

  • Septic shock—Sepsis with hypotension (arterial blood pressure <90 mmHg or 40 mmHg below pt's normal blood pressure for at least 1 h despite fluid resuscitation) or need for vasopressors to maintain systolic blood pressure ≥90 mmHg or mean arterial pressure ≥70 mmHg

ETIOLOGY

  • Blood cultures are positive in 20–40% of sepsis cases and in 40–70% of septic shock cases.

  • A single bacterial species accounts for ∼70% of isolates in positive blood cultures; the remainder are fungal or polymicrobial.

EPIDEMIOLOGY

  • The incidence of severe sepsis and septic shock in the United States continues to increase, with >700,000 cases each year contributing to >200,000 deaths.

  • Invasive bacterial infections are a prominent cause of death around the world, especially among young children.

  • Sepsis-related incidence and mortality rates increase with age and preexisting comorbidity, with two-thirds of cases occurring in pts with significant underlying disease.

  • The increasing incidence of sepsis is attributable to the aging of the population, longer survival of pts with chronic diseases, a relatively high frequency of sepsis among AIDS pts, and medical treatments that circumvent host defenses (e.g., immunosuppressive agents, indwelling catheters, and mechanical devices).

PATHOPHYSIOLOGY

Local and Systemic Host Responses

  • Hosts have numerous receptors that recognize highly conserved microbial molecules (e.g., lipopolysaccharide, lipoproteins, double-stranded RNA), triggering the release of cytokines and other host molecules that increase blood flow and neutrophil migration to the infected site, enhance local vascular permeability, and elicit pain.

  • Many local and systemic control mechanisms diminish cellular responses to microbial molecules, including intravascular thrombosis (which prevents spread of infection and inflammation) and an increase in anti-inflammatory cytokines (e.g., IL-4 and IL-10).

Organ Dysfunction and Shock

  • Widespread vascular endothelial injury is believed to be the major mechanism for multiorgan dysfunction.

  • Septic shock is characterized by compromised oxygen delivery to tissues followed by a vasodilatory phase (a decrease in peripheral vascular resistance despite increased levels of vasopressor catecholamines).

CLINICAL FEATURES

  • Hyperventilation

  • Encephalopathy (disorientation, confusion)

  • Acrocyanosis and ischemic necrosis of peripheral tissues (e.g., digits) due to hypotension and DIC

  • Skin: hemorrhagic lesions, bullae, cellulitis, pustules. Skin lesions may suggest specific pathogens—e.g., petechiae and purpura suggest Neisseria meningitidis, and ecthyma gangrenosum suggests Pseudomonas aeruginosa.

  • Gastrointestinal: nausea, vomiting, diarrhea, ileus, cholestatic jaundice

Major Complications

  • Cardiopulmonary manifestations

    • – Ventilation-perfusion mismatch, increased alveolar capillary permeability, increased pulmonary water content, and decreased pulmonary compliance impede oxygen exchange and lead to acute respiratory distress syndrome (progressive diffuse pulmonary infiltrates and arterial hypoxemia) in ∼50% of pts.

    • – Hypotension: Normal or increased cardiac output and decreased systemic vascular resistance ...

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