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Maternal Death Following Cardiopulmonary Collapse After Delivery: Amniotic Fluid Embolism or Septic Shock Due to Intrauterine Infection?
Author(s) -
Romero Roberto,
Kadar Nicholas,
Vaisbuch Edi,
Hassan Sonia S.
Publication year - 2010
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2010.00823.x
Subject(s) - amniotic fluid embolism , septic shock , medicine , amniotic fluid , shock (circulatory) , obstetrics , maternal death , pregnancy , sepsis , surgery , fetus , biology , population , genetics , environmental health
Citation Romero R, Kadar N, Vaisbuch E, Hassan SS. Maternal death following cardiopulmonary collapse after delivery: amniotic fluid embolism or septic shock due to intrauterine infection? Am J Reprod Immunol 2010; 64: 113–125 Problem  The amniotic fluid embolism (AFE) syndrome is a catastrophic complication of pregnancy frequently associated with maternal death. The causes and mechanisms of disease responsible for this syndrome remain elusive. Method of study  We report two cases of maternal deaths attributed to AFE: (1) one woman presented with spontaneous labor at term, developed intrapartum fever, and after delivery had sudden cardiovascular collapse and disseminated intravascular coagulation (DIC), leading to death; (2) another woman presented with preterm labor and foul‐smelling amniotic fluid, underwent a Cesarean section for fetal distress, and also had postpartum cardiovascular collapse and DIC, leading to death. Results  Of major importance is that in both cases, the maternal plasma concentration of tumor necrosis factor‐α at the time of admission to the hospital and when patients had no clinical evidence of infection was in the lethal range (a lethal range is considered to be above 0.1 ng/mL). Conclusion  We propose that subclinical intraamniotic infection may be a cause of postpartum cardiovascular collapse and DIC and resemble AFE. Thus, some patients with the clinical diagnosis of AFE may have infection/systemic inflammation as a mechanism of disease. These observations have implications for the understanding of the mechanisms of disease of patients who develop cardiovascular collapse and DIC, frequently attributed to AFE. It may be possible to identify a subset of patients who have biochemical and immunological evidence of systemic inflammation at the time of admission, and before a catastrophic event occurs.

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