abortion) or blunt abdominal trauma ( 6). In rare cases, it also occurs during pregnancy following intrauterine surgery (e.g. Pathophysiology and clinical manifestationĪFE occurs during labor and delivery/Cesarean section (55% to 76% antenatally) or up to 48 hours postpartum ( 3, 4, 11). Why some women tolerate the transfer of amniotic fluid or its components with no problems or clinical symptoms and others do not can currently only be the subject of speculation ( 13) it is also unclear whether allergic diatheses or previous sensitization to specific fetal antigens are disposing factors for AFE ( 11, 21). Another pathophysiological mechanism may be complement activation triggering AFE ( 18, 19). These and other immunological and clinical similarities to anaphylactic shock have led to the anaphylactoid reaction hypothesis (anaphylactoid syndrome of pregnancy ). squames) amniotic fluid also contains numerous vasoactive substances (bradykinin, histamine, and others) and procoagulant substances that can lead to endothelial activation and a massive inflammatory reaction ( 18, 20). This is because in addition to insoluble fetal components (e.g. Amniotic fluid can enter the maternal circulation via endocervical veins, lesions of the uterus, or the site of placental attachment ( 16).Īlthough previously proposed explanations of the development of AFE envisaged a purely mechanical obstruction of the pulmonary vessels by amniotic fluid components ( 17), today humoral and immunological factors are considered to be responsible ( 18, 19). The pathogenesis of AFE is not yet fully clear. To our knowledge, the present article is the first to discuss AFE from the point of view of an obstetrician, an intensive care physician, and a forensic pathologist. Varying clinical symptoms, difficult diagnosis (including differential diagnosis), and uncertainty regarding post-mortem evidence mean that AFE poses an interdisciplinary challenge. Rapid diagnosis and immediate obstetric and intensive care play a decisive role in maternal prognosis and survival ( 14, 15). Between 24% and 50% of surviving children manifest persistent neurological deficits ( 11, 14, e5). In industrialized countries case-related maternal mortality is between 13.5% and 44% ( 3– 7, 10), and perinatal mortality between 7% and 38% ( 11– 13). There are no figures on the incidence of AFE in Germany. In 2011 AFE was the leading cause of death resulting directly from childbirth in Germany, accounting for 8 out of 12 cases, but an autopsy was performed in only one case ( 9). However, only deaths among inpatients are recorded. They are then evaluated annually by a panel of experts (the Maternal Death Working Group of the AQUA Institute). In Germany, cases of maternal death in childbirth are reported by hospitals voluntarily and in anonymized form to the quality assurance agency for the state in question. et al.: BMC Pregnancy & Childbirth 2012 12: 7 *2Case-related validation from prospective studies The histological or immunohistochemical demonstration of formed amniotic fluid components in the pulmonary bloodflow establishes the diagnosis of AFE. The sudden, unexplained death of a pregnant woman necessitates a forensic autopsy. Low-level evidence favors treating women suffering from AFE by securing the airway, adequate oxygenation, circulatory support, and correction of hemostatic disturbances. Its treatment requires immediate, optimal interdisciplinary cooperation. Its main clinical features are severe hypotension, arrhythmia, cardiac arrest, pulmonary and neurological manifestations, and profuse bleeding because of disseminated intravascular coagulation and/or hyperfibrinolysis. AFE is diagnosed on clinical grounds after the exclusion of other causes of acute cardiovascular decompensation during delivery, such as pulmonary thromboembolism or myocardial infarction. The identified risk factors for AFE are maternal age 35 and above (odds ratio 1.86), Cesarean section (OR 12.4), placenta previa (OR 10.5), and multiple pregnancy (OR 8.5).
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