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Robillard, J., Gauvin, F., Molinaro, G., Leduc, L., Adam, A. and Rivard, G.E. (2005) The syndrome of amniotic fluid embolism: A potential contribution of bradykinin. American Journal of Obstetrics and Gynecology, 193, 1508-1512. doi:10.1016/j.ajog.2005.03.022
has been cited by the following article:
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TITLE:
Amniotic fluid embolism: literature review and an integrated concept of pathomechanism
AUTHORS:
Mieczysław Uszyński
KEYWORDS:
Amniotic Fluid Embolism; Amniotic Cells, Tissue Factor; Leukotriens; Disseminated Intravascular Coagulation; Pulmonary Vasoconstriction
JOURNAL NAME:
Open Journal of Obstetrics and Gynecology,
Vol.1 No.4,
November
21,
2011
ABSTRACT: Literature concerning procoagulant activity of the amniotic fluid and pathomechanism of amniotic fluid embolism (AFE) was surveyed and a new concept of its pathogenesis, called the integrated concept of AFE, was presented. According to this concept, two components of the amniotic fluid are involved: (i) apoptosis-affected amniotic cells showing a special role in the initiation of disseminated intravascular coagulation (DIC) and (ii) leukotrienes (formerly called slow-reacting substances), inducing bronchial and pulmonary vascular smooth muscle contraction. Although each of these components initiates a different pathogenic pathway, they both lead to the formation of a mechanical barrier on blood flow through the lungs (amniotic debris + microemboli) and/or functional barrier (pulmonary vasoconstriction). An old dilemma, concerning indications for heparin therapy in AFE was recalled in the light of the new concept.