The maternal syndrome of preeclampsia : A forme fruste of the systemic inflammatory response syndrome

Abstract

Preeclampsia is a pregnancy-specific condition, and can be considered to have two component syndromes: maternal, characterized by hypertension and proteinuria, and fetal, manifested by intrauterine growth restriction (IUGR). Maternal deaths due to severe preeclampsia most commonly follow the onset of neutrophil-mediated complications, hepatocellular necrosis and the acute respiratory distress syndrome (ARDS). Hepatocellular necrosis and ARDS are both features of the systemic inflammatory response syndrome (SIRS). Preeclampsia may persist, often deteriorating transiently, following the delivery of the placenta, much as SIRS persists following the resolution of trauma, burns or sepsis. In both conditions there is a systemic response with inflammatory mediator release, endothelial cell dysfunction, a hyperdynamic state, end organ hypoperfusion, and neutrophil activation, resulting in the clinical syndromes. Both preeclampsia and SIRS result from differential responses to initiating factors. Preeclampsia results from incomplete placentation, which also underlies the development of intrauterine growth restriction in isolation (without preeclampsia). Similarly, sepsis, trauma and burns also occur in patients who have unremarkable recoveries rather than developing SIRS. Is preeclampsia a form of SIRS?