scholarly journals AMNIOTIC FLUID EMBOLISM- PRESENTING AS GENERALISED ERYTHEMA AND RASHES (POSSIBILITY OF ANAPHYLACTOID REACTION SECONDARY TO AMNIOTIC FLUID EMBOLISM)

2017 ◽  
Vol 6 (13) ◽  
pp. 1059-1060
Author(s):  
Priya Veluthakunju
2019 ◽  
Vol 220 (1) ◽  
pp. S404
Author(s):  
Tomoaki Oda ◽  
Naoaki Tamura ◽  
Yukiko Kohmura-Kobayashi ◽  
Naomi Furuta-Isomura ◽  
Chizuko Yaguchi ◽  
...  

2013 ◽  
Vol 7 (1) ◽  
pp. 17-21 ◽  
Author(s):  
Michael D Benson

Amniotic fluid embolism was first recognized in 1926, in a Brazilian journal case report, on the basis of large amounts of fetal material in the maternal pulmonary vasculature at autopsy. The first English language description appeared in 1941 and consisted of eight parturients dying suddenly in which, once again, fetal material was seen in the pulmonary vasculature. A control group of 34 pregnant women dying of other recognized causes did not have fetal material in their lungs. The incidence of recognized, serious illness is on the order of two to eight per 100,000, with a mortality rate ranging from 13% to 35%. The diagnosis rests largely on one or more of four clinical signs: circulatory collapse, respiratory distress, coagulopathy, and seizures/ coma. The only confirmatory laboratory test remains autopsy findings although serum tests for fetal antigen, insulin-like growth factor binding protein-1, and complement are currently being investigated. One of the paradoxes of diagnosis is that fetal material in the pulmonary circulation at autopsy is specific for amniotic fluid embolism, while the same finding in the living is not. The mechanism of disease remains uncertain although the best available evidence suggests that complement activation might have a role. In contrast, mast cell degranulation probably is not a mechanism, so amniotic fluid embolism is not an anaphylaxis or anaphylactoid reaction as has been occasionally suggested. Perhaps the greatest unknown is not why 1 in 50,000 pregnant women develop what appears to be an immune response to their fetus, but rather why the other 49,999 do not?


2020 ◽  
Vol 1 (1) ◽  
pp. 54-71
Author(s):  
Ratih kumala fajar apsari ◽  
Bambang Suryono Suwondo

Emboli cairan amnion (EAK) adalah komplikasi kehamilan yang jarang namun membawa angka mortalitas yang tinggi. Patogenesis yang tepat dari kondisi ini masih belum diketahui. Emboli air ketuban (EAK) atau amniotic fluid embolism (AFE) atau anaphylactoid syndrome of pregnancy adalah salah satu komplikasi kehamilan yang paling membahayakan. Cairan ketuban, debris fetal diduga menyebabkan kolaps kardiovaskular dengan cara memicu reaksi imun/anafilaktoid maternal. Patofisiologi EAK hingga kini masih belum jelas tetapi diduga melibatkan kaskade immunologis. Kematian maternal bisa terjadi karena cardiac arrest mendadak, perdarahan karena koagulopati, dan kegagalan organ multipel dengan acute respiratory distess syndrome (ARDS). Gejala dan tanda EAK antara lain dispnea akut, batuk, hipotensi, sianosis, bradikardia fetal, ensefalopati, hipertensi pulmoner akut, koagulopati, dan sebagainya. Diagnosis EAK adalah bersifat klinis dan ditegakkan setelah menyingkirkan kemungkinan penyebab lain. Penatalaksanaan bersifat suportif dan memerlukan persalinan janin jika diperlukan, support respiratorik, dan support hemodinamik. Prognosis maternal setelah EAK masih sangat buruk meski tingkat survival janin sekitar 70%. Pasien dengan EAK paling baik dikelola di unit perawatan kritis oleh tim multidisiplin dan dengan manajemen supportif.   Amniotic Fluid Embolism Abstract Amniotic fluid embolism (AFE) is a rare complication of pregnancy carrying a high mortality rate. The exact pathogenesis of the condition is still not known. Amniotic fluid embolism (AFE) or anaphylactoid syndrome of pregnancy is one of the most dangerous pregnancy complications. Amniotic fluid, fetal debris is thought to cause cardiovascular collapse by triggering a maternal immune / maternal anaphylactoid reaction. The pathophysiology of AFE remains unclear but is thought to involve an immunological cascade. Maternal deaths may occur due to sudden cardiac arrest, bleeding due to coagulopathy, and multiple organ failure with ARDS. AFE symptoms and signs include acute dyspnea, cough, hypotension, cyanosis, fetal bradycardia, encephalopathy, acute pulmonary hypertension, coagulopathy. Management is supportive, respiratory support, and haemodynamic support. The maternal prognosis is very poor even though the survival rate of the fetus is about 70%. Patients with AFE are best managed in a critical care unit by a multidisciplinary team and management is largely supportive


1977 ◽  
Vol 38 (03) ◽  
pp. 0724-0727 ◽  
Author(s):  
H Graeff ◽  
R Hafter ◽  
R von Hugo

1991 ◽  
Vol 7 (4) ◽  
pp. 877-882 ◽  
Author(s):  
Steven L. Clark

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