Amniotic Fluid Embolism (afe): Pathophysiology, Clinical Features, Diagnosis, Therapy
نویسندگان
چکیده
The occurrence of the amniotic fluid embolism syndrome is a rare and often fatal obstetric complication [1]. The amniotic fluid embolism (AFE) was described in 1926 by Meyer [2] as reported by Clark et al. [3] but is was not until 1941 before it became recognized as a clinical entity after the publication by Steiner and Lushbaugh [4]. Classically, AFE is a sudden event characterized by acute respiratory failure with severe maternal hypoxia, cardiovascular collapse, and coagulopathy [3]. AFE occurs when amniotic fluid and/or fetal elements (inclosing fetal squamous cells, mucin, meconium, vernix caseosa, and lanugo hairs) enter the maternal blood stream, and is confirmed by proving their existence in the maternal pulmonary vascularisation at autopsy [5,6]. Amniotic fluid embolism occur in 1/8000 to 1/80000 deliveries but with a maternal morbidity ranging from 26% in a recent report to 86% in earlier ones [7,8]. In the USA, this condition is the most common cause of peripartum maternal death and is responsible for
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Current Concepts of Immunology and Diagnosis in Amniotic Fluid Embolism
Amniotic fluid embolism (AFE) is one of the leading causes of maternal mortality and morbidity in developed countries. Current thinking about pathophysiology has shifted away from embolism toward a maternal immune response to the fetus. Two immunologic mechanisms have been studied to date. Anaphylaxis appears to be doubtful while the available evidence supports a role for complement activation....
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