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OBJECTIVE: Our purpose was to determine the acute-phase central hemodynamic and respiratory effects of raw, filtered, filtered and boiled, and meconium-containing amniotic fluid. STUDY DESIGN: Pregnant goats (Capra hircus) in the last one third of pregnancy were given freshly collected autologous amniotic fluid in a volume of 2.5 ml/kg of body weight. Observations were then made at 10, 30, 60, 120, and 180 minutes after amniotic fluid embolism. Pulmonary artery catheters and femoral artery lung water catheters were placed for specimen and data collection. RESULTS: Marked pressor responses were observed in both the pulmonary and systemic circulations with all amniotic fluid infusions. The pressor response was similar with raw, filtered, and filtered and boiled amniotic fluid. The pressor response seen with amniotic fluid containing meconium was significantly greater than that seen with the other forms. No significant effects were observed on cardiac or respiratory function except in the meconium group, where transient left ventricular dysfunction was accompanied by an acute increase in extravascular lung water and dysoxia. CONCLUSIONS: The Capra hircus model is appropriate for the further study of amniotic fluid embolism. The acute pressor effects are transient and involve both the systemic and pulmonary circulations. Left ventricular dysfunction and dysoxia were observed only with embolism of amniotic fluid containing meconium.
Pulmonary embolism is the leading cause of maternal death in the United States. Amniotic fluid embolism (AFE) represents the least preventable and most lethal of complications with a reported mortality of 86% and an associated fetal demise of 50%. Although it is widely accepted as a clinical entity, AFE is incompletely understood. A combination of clinical presentation, laboratory findings, and exclusion of other pathologies leads to the diagnosis of AFE. The mainstays of treatment are oxygenation, maintenance of cardiac output, and correction of coagulopathy. The prognosis for the patient experiencing AFE remains bleak because it is largely unpredictable and, except for supportive measures, cannot be corrected.
Pulmonary embolism is the leading cause of maternal death in the United States. Amniotic fluid embolism (AFE) represents the least preventable and most lethal of complications. AFE has a reported mortality of 86% and an associated fetal demise of 50%. AFE is widely accepted as a clinical entity but is not completely understood. A combination of clinical presentation, laboratory findings, and exclusion of other abnormalities leads to the diagnosis of AFE. The mainstays of treatment are oxygenation, maintenance of cardiac output, and correction of coagulopathy. The prognosis for the patient experiencing AFE remains bleak because the course of the disorder is largely unpredictable, and AFE cannot be corrected. Only supportive measures can be given.
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UNLABELLED: Tissue factor (TF) is known to be present in a high concentration in amniotic fluid. The main question of this study is whether tissue factor pathway inhibitor (TFPI), a natural inhibitor of TF, is present in amniotic fluid. The study group consisted of 28 women with normal pregnancy course, and at the first stage of termed labour. Fifteen non-pregnant women were the control group. TF and TFPI were studied by an immunoenzymatic method (ELISA). The level of TFPI in amniotic fluid was 38.7% of that in blood plasma (16.81+/-5.34ng/ml versus 43.41+/-18.70ng/ml, P<0.001), while the level of TF in amniotic fluid was 44.8 times higher than in blood plasma (9995.93+/-8533.11pg/ml versus 252.66+/-28.84pg/ml, P<0.001). CONCLUSIONS: (i) It was found, for the first time, that amniotic fluid contains TFPI (ii) It is reasonable to assume that the intrusion of amniotic fluid into the blood-stream may influence the plasmatic TFPI-TF equilibrium resulting in intravascular blood coagulation.
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A case of severe ARDS following amniotic fluid embolism is described. During the 15 month period of I.C.U. treatment a number of respiratory complications had to be overcome. Chronic hypercapnia led to changes of bone and soft tissue composition. The patient was discharged home with a marked restriction of pulmonary function. Respiratory infections continue to occur.