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.

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.

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 and increased lactate production. Even in the setting of adequate organ perfusion, septic patients may still be unable to shunt pyruvate to the Krebs cycle due to cytokine induced mitochondrial dysfunction. Parallel with activation of the inflammatory cascade goes activation of the clotting cascade. Activation of monocytes, macrophages, and endothelial cells leads to surface expression of tissue factor in these cells. Tissue factor will bind to factor VII activating the extrinsic pathway of the clotting cascade. The latter leads to diffuse microvascular clotting (disseminated intravascular coagulation) that worsens distal organ ischemia and dysfunction. This activation explains the common finding of thrombocytopenia and prolonged bleeding times in septic individuals. Cytokines may also suppress secretion of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and cortisol with adrenal failure. This condition renders the septic patient resistant to the vasoconstrictive action of catecholamines since cortisol allows up regulation of catecholamine receptors within blood vessels.

The diagnosis of sepsis in pregnancy may not be as apparent as in non-pregnant individuals as signs and symptoms of sepsis may be less pronounced. Some of the findings may overlap with those in normal pregnancy, such as tachycardia, hyperventilation, and leukocytosis. Mild elevations in serum creatinine, otherwise not significant in non-pregnant patients, may be worrisome during gestation. Other signs and symptoms to keep in mind include vomiting, diarrhea, maculopapular rash, and mental changes. Early identification and treatment requires a high index of suspicion. Sepsis should be considered in any patient suspected to have an infection who develops evidence of end organ dysfunction including confusion, hypoxia, hypotension, coagulopathy, oliguria, ileus, hyperglycemia, and elevation in liver function tests, among others. Once suspected, cultures should be obtained and antibiotics started. Initial fluid resuscitation and administration of broad-spectrum antibiotics should not be delayed.

The general management guidelines for a patient with sepsis are outlined in Table 9-2. The following discussion will concentrate on the overall principles for the management of sepsis, mostly septic shock.