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INTRODUCTION

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Sepsis, severe sepsis, and septic shock are a continuum in the systemic response to infection. 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 syndrome (MODS), the final stage in the sepsis spectrum. 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 fascitis, 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. Overall, gram-negative aerobic bacilli used to be the predominant organisms associated with sepsis. However, the incidence of infection with gram-positive organisms in patients with sepsis has increased and may now equal that of gram-negative infections.

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DEFINITIONS

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Sepsis is the development of systemic inflammatory response syndrome (SIRS, Table 9-1) in response to infection. Sepsis is called severe when there is evidence of end-organ damage. Septic shock is defined as sepsis-induced hypotension (systolic blood pressure <90 mm Hg, a mean arterial pressure <70 mm Hg, or a reduction in systolic blood pressure of >40 mm Hg from baseline) despite volume replacement (or requirement for vasopressors). Sepsis-induced tissue hypoperfusion is defined as infection-induced hypotension, elevated lactate (≥4 mmol/L), or oliguria (urine output <0.5 mL/kg/h for at least 2 hours despite adequate fluid resuscitation).

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TABLE 9-1.Definition of Systemic Inflammatory Response Syndrome
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PATHOGENESIS

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Sepsis has been viewed as an uncontrolled inflammatory response to infection. This hypothesis was based on animal studies as well as measures of immune response in humans, including cytokine levels. This view has been recently challenged by the failure to decrease mortality in clinical trials of anti-inflammatory agents, and by evidence of a severely compromised immune system that is unable to eradicate the infection. The immunological response in patients with sepsis may even be biphasic, with an anti-inflammatory phase following an initial overwhelming response. The cardiovascular manifestations of sepsis are the results of alterations in peripheral vascular tone and cardiac function. The decrease in vascular tone affects both the arterial and venous systems, and is believed to be due to an increase in smooth muscle relaxants such as nitric oxide. Microvascular changes such as endothelial cell swelling, fibrin deposition, and aggregation of circulating cells also contribute to the abnormal blood flow seen in patients with sepsis. Cardiac output depends on the intravascular volume status of the patient. In the early stages of septic shock, cardiac output may be decreased because of hypovolemia and low cardiac filling. Cardiac output increases after fluid replacement. ...

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