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Sepsis occurs as the result of a systemic maladaptive inflammatory response to an infectious insult. It is the leading cause of mortality in intensive care units (ICUs) in developed countries and the incidence is increasing worldwide.1 The literature regarding management of sepsis in the pregnant patient is limited and pregnant women have typically been excluded from landmark trials that have guided the management of sepsis over the last decades. Most cases of severe sepsis/septic shock are managed in ICUs and, therefore, obstetricians and maternal fetal medicine specialists are unfamiliar with management principles.


The pathophysiology of sepsis is not completely understood. After exposure to a microorganism (bacteria, virus, parasite, fungi), the inflammatory cascade is activated. Massive production of inflammatory and anti-inflammatory cytokines together with endothelial derived factors like nitric oxide and other mediators like prostaglandins, leukotrienes, and complement lead to loss of vasomotor tone with profound vasodilation and increased vascular permeability (secondary to cytokine-induced endothelial injury) with subsequent third spacing. Edema in the extravascular compartment (interstitium, pleural and pericardial spaces, lung, brain, abdomen, heart walls) leads to increased total body water but decreased intravascular effective volume. Septic patients commonly appear edematous despite suffering from severe hypovolemia (especially during and immediately after aggressive fluid resuscitation). The profound decrease in systemic vascular resistances facilitates the so-called “increased cardiac output” seen in septic patients. However, the myocardium function in sepsis is also altered by the action of substances like nitric oxide, interleukin-1, oxygen-derived free radicals, and tumor necrosis factor α. The latter substances inhibit myocardial contractility leading to biventricular systolic dysfunction (up to 60% of patients with sepsis have an ejection fraction <45%). Both systolic and diastolic dysfunction may occur. Edema within the wall of the left ventricle leads to a “stiff” ventricle that will not expand adequately during diastole impending proper ventricular filling leading to congestive heart failure (diastolic dysfunction). Not infrequently, myocyte injury from proinflammatory cytokines may lead to leakage of troponins. Typically, patients with systolic dysfunction tend to present with biventricular dilation. The latter appears to be an adaptive response, as dilation will allow for more intracavitary filling leading to an increased stroke volume despite a decrease in ejection fraction (preload recruitment). These cardiac changes tend to resolve spontaneously among survivors of sepsis. Patients with isolated diastolic dysfunction usually have worse outcomes.

Almost all patients with severe sepsis have clotting abnormalities ranging from silent biochemical changes to full blown disseminated intravascular coagulopathy (DIC). Activation of the clotting cascade in sepsis results from tissue factor expression in mococytes, neutrophils, and the endothelium as part of the inflammatory response. Once tissue factor is expressed in the surface of these cells, it binds factor VII activating the clotting cascade through the extrinsic pathway. Development of DIC contributes to organ hypoperfusion (secondary to microvascular occlusion) and multiorgan failure. Platelet and clotting factor consumption leads to thrombocytopenia and prolongation of clotting times. ...

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