Embolism during pregnancy: thrombus, air, and amniotic fluid

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Presentation transcript:

Embolism during pregnancy: thrombus, air, and amniotic fluid Alfredo F Gei, MD, Rakesh B Vadhera, MD, FRCA, FFARCS, Gary D.V Hankins, MD Anesthesiology Clinics of North America Volume 21, Issue 1, Pages 165-182 (March 2003) DOI: 10.1016/S0889-8537(02)00052-4

Fig. 1 Components of amniotic fluid and their role in pathophysiology of AFE. Surfactant enhances production of leukotrienes C4 and D4. Endothelin and Prostaglandins E2 and F2α cause coronary vasoconstriction and negative inotropic effect. Leukotrienes induce hypertension followed by hypotension, pronounced negative inotropic effects and bronchoconstriction. IL-1 and TNF-α induce production of endothelin. Thromboxane A2 causes increases in coronary and pulmonary vascular resistance. Collagen and thromboplastin induce platelet activation. Anesthesiology Clinics of North America 2003 21, 165-182DOI: (10.1016/S0889-8537(02)00052-4)

Fig. 2 Chronology and incidence of signs and symptoms of AFE. Amniotic fluid embolism seems to have a logarithmic presentation with a decreasing intensity, frequency and mortality as time elapses since the onset of symptoms. The majority of seriously affected patients will die within the first 30 to 60 minutes after the onset of symptoms (Incidence data modified from Morgan M. Amniotic fluid embolism. Anaesthesia 1979;34:20–32). Anesthesiology Clinics of North America 2003 21, 165-182DOI: (10.1016/S0889-8537(02)00052-4)