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INTRODUCTION

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Sepsis is the leading cause of mortality in intensive care units and accounts for 10% of direct maternal deaths in North America.* Most deaths in sepsis are due to multiple organ dysfunction. The obstetric patient is particularly vulnerable to sepsis because of the association between pregnancy and infectious complications such as pyelonephritis, chorioamnionitis, endometritis, wound infection, necrotizing fasciitis, and cholecystitis. Septic shock occurs in up to 4% of bacteremic patients, and 40% to 60% of patients in septic shock have bacteremia. The relationship between bacteremia and sepsis also depends on other contributing factors, such as immune suppression, and associated medical conditions. In obstetrical care, sepsis may be secondary to infections from viruses, fungi, gram-positive bacteria, gram-negative bacteria, and anaerobes. Importantly, positive cultures are not required to establish the diagnosis of sepsis.

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Authors of previous edition.

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DEFINITIONS

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The definition of sepsis has recently been changed. Sepsis is now defined as life threatening organ dysfunction caused by an abnormal host response to an infection. Organ dysfunction may be identified by an acute increase in two or more points in the Sequential Organ Failure Assessment Score (SOFA)(Table. 9-1). The term severe sepsis is not used anymore. Septic shock is defined as sepsis with hypotension requiring vasopressor therapy and a serum lactate above 2 mmol/L.

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Table Graphic Jump Location
TABLE 9-1Sequential Organ Failure Assessment (SOFA) Score
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PATHOGENESIS

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Sepsis occurs secondary to an abnormal host response to infection. A massive inflammatory response results in end organ damage (brain, lungs, heart, liver, gut, kidney, and hematological). Cytokines induce production of nitric oxide with resultant vasodilation and hypotension (distributive shock). Diffuse endothelial injury leads to increased vascular permeability with third spacing of fluid and hypovolemia. The decrease in systemic vascular resistances allows for a “high cardiac output” state. The latter does not mean that the heart is spared in sepsis; on the contrary, the heart is significantly affected during sepsis. Many cytokines are cardio depressant resulting in decreased systolic function. Diastolic dysfunction may also occur secondary to edema in the ventricular wall with resultant decrease in compliance. The ventricle then is unable to accommodate preload resulting in pulmonary edema in the setting of excessive fluid resuscitation. Severe hypotension (from both vasodilation and hypovolemia from third spacing) leads to end organ ischemia ...

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