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[Roles of prostaglandins and leukotrienes in the pathogenesis of amniotic fluid embolism].
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[Amniotic fluid embolism].
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Does amniotic fluid embolism recur?
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Immunologic studies in presumed amniotic fluid embolism.
OBJECTIVE: To evaluate the potential role of immunologic mechanisms that involve mast cell degranulation (anaphylaxis) or complement activation in the mechanism of amniotic fluid embolism. METHODS: This study was a case series of nine women with presumed amniotic fluid embolism and a control group of 22 women who had normal labor. Women were from community and tertiary referral hospitals in Japan and the United States. Main outcome measures were maternal peripartum complement levels (C3 and C4), serum levels of tryptase, urinary histamine concentrations, and serum levels of a fetal antigen (sialyl Tn). RESULTS: Serum tryptase and urinary histamine measurements were negative in women with amniotic fluid embolism; seven of nine had elevated levels of fetal antigen. All eight who had serum available for testing had abnormally low levels of complement. Mean C3 level of 44.0 mg/dL and C4 level of 10.7 mg/dL were significantly lower than corresponding postpartum control values of 117.3 mg/dL and 29.4 mg/dL (P =.018 for C3, P =.012 for C4). Postpartum C3 and C4 levels decreased by 8% and 5%, respectively, compared with intrapartum values (P =.003 for C3, P =.021 for C4) but were still within normal range. CONCLUSION: Serologic findings suggest a role for complement activation in the mechanism of amniotic fluid embolism. Laboratory data from this series did not implicate mast cell degranulation (anaphylaxis) in the pathophysiology of the disease.
A simple, noninvasive, sensitive method for diagnosis of amniotic fluid embolism by monoclonal antibody TKH-2 that recognizes NeuAc alpha 2-6GalNAc.
OBJECTIVE: The sialyl Tn structure (NeuAc alpha 2-6GalNAc alpha 1-O-Ser/Thr) recognized by monoclonal antibody TKH-2 is a characteristic component in meconium and amniotic fluid. The purpose of this study was to determine whether amniotic fluid embolism could be detected by quantification of this antigen in maternal serum by means of an assay using antimucin monoclonal antibody TKH-2. STUDY DESIGN: Sialyl Tn antigen was measured in the serum of women with meconium-stained amniotic fluid and compared with the level in those with clear amniotic fluid, as well as that in women with a clinical picture suggesting amniotic fluid embolism. The concentration of sialyl Tn antigen was determined by an immunoradiometric competitive inhibition assay. RESULTS: Serum sialyl Tn antigen levels in women with meconium-stained amniotic fluid (20.3 +/- 15.4 U/ml) at delivery were slightly higher than those in women with clear amniotic fluid (11.8 +/- 5.6 U/ml). A significantly elevated level of sialyl Tn antigen was observed in serum of patients with amniotic fluid embolism and amniotic fluid embolism-like symptoms (105.6 +/- 59.0 U/ml, p < 0.01). CONCLUSION: The method for detecting sialyl Tn antigen in the serum of patients with amniotic fluid embolism is a direct way to demonstrate the release of meconium- or amniotic fluid-derived mucin into the maternal circulation and is a simple, noninvasive, sensitive method for diagnosis of amniotic fluid embolism.
Amniotic fluid embolism.
A critical review of animal and human data leads to a reassessment of traditional concepts of amniotic fluid embolism. Left ventricular failure, rather than pulmonary hypertension, is the major hemodynamic derangement consistently seen in humans. The detection of squamous cells in the pulmonary artery blood of pregnant women is not pathognomonic for amniotic fluid embolism.
A fatal case of amniotic fluid embolism.
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Amniotic fluid embolism with haemostasis complications: primary fibrinogenolysis or disseminated intravascular coagulation?
Amniotic fluid embolism (AFE) is characterized by the passage of amniotic fluid (AF) into the maternal circulation during or just after childbirth. AFE is a rare disorder occurring in 1/8,000 to 1/80,000 deliveries but with a maternal morbidity ranging from 26% in a recent report to 86% in earlier ones. In patients who survive, AFE may affect coagulation resulting in severe bleeding. While disseminated intravascular coagulation (DIC) is usually seen in such cases, we reported a case of AFE in which the hemostatic abnormalities were compatible with primary fibrinogenolysis rather than with DIC.
Case report: a fatal case of amniotic fluid embolism.
A primigravida was induced for PET, the liquor was meconium stained; she was put on oxytocin in-fussion and developed hypertonic uterine action. She then had an amniotic fluid embolism which presented clinically as profound shock, dyspnoea, tachycardia, cyanosis, hypotension and pyrexia. The patient was delivered by vacuum extraction. The picture was further complicated by pulmonary oedema intravascular microcoagulation and anuria. She deteriorated rapidly and died despite treatment with double strength plasma (in the absence of fibrinogen), massive hydrocortiosone therapy, blood transfusion amd sub-total hysterectomy. Post mortem findings in the lungs confirmed amniotic fluid embolism.
[Amniotic fluid embolism in multiple pregnancy in the second trimester of gestation].
A rare case of amniotic fluid embolism in the 26-th week of pregnancy is presented. After the McDonald operation for the repair of the incompetent cervix, a premature rupture of the membranes occurred. After a five-day period of amniorrhea an elevation of the body temperature over 39 degrees C was observed, as well as respiratory distress, cyanosis, and coma. It ended with the patient's death. The pathomorphological finding demonstrated the amniotic fluid embolism of the lung and brain arterioles.
[Experimental studies on amniotic fluid embolism].
The circulatory state of the so-called experimental amniotic fluid embolism (AFE) was studied in 39 dogs. The repeated infusion of a large quantity of human amniotic fluid had not produced the symptoms of AFE. But the infusion of human meconium-stained amniotic fluid, meconium suspension, its supernatant or boiled meconium suspension, or canine bile had produced the various typical shock symptoms of AFE. In these cases the shock effects were especially strong in the infusion of meconium suspension and the meconium-stained amniotic fluid. In these shock symptoms, arterial pressure decreased quickly after the infusion. When sudden death was fortunately avoided, right ventricular pressure increased and increases in pulmonary arterial pressure and pulmonary vascular resistance were indicated. In most cases cardiac output decreased. Central venous pressure increased suddenly before death. These experiments suggested that the pulmonary vasoconstriction was produced by the chemical factors in the amniotic fluid and by vasoactive substances released from the embolized lung. It also seemed that this pulmonary vasoconstriction rather than mechanical obstruction of pulmonary arterioles was probably the major cause of the shock symptoms of AFE.
Gastric fluid aspiration fatally complicating amniotic fluid embolism; (case report).
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[Sudden death during delivery due to pulmonary amniotic-fluid embolism].
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[Case of amniotic fluid embolism treated with ypsilon-amino-caproic acid].
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Cardiopulmonary distress during obstetrical anaesthesia: attempts to diagnose amniotic fluid embolism in a case series of suspected allergic anaphylaxis.
BACKGROUND: Cardiopulmonary distress during obstetrical anaesthesia may result from a drug-induced allergic reaction, but, in the obstetrical setting, allergic anaphylaxis may be inseparable from amniotic fluid embolism in terms of the clinical presentation. Further investigations, using allergy tests and other laboratory analyses, are then needed to pursue a diagnostic clarification. METHODS: Twelve women suspected of having developed anaphylaxis during obstetrical anaesthesia underwent allergy follow-up investigations and further serological tests with the amniotic fluid embolism marker sialyl Tn and complement factors (C3 and C4) in an attempt to differentiate amniotic fluid embolism from drug-induced allergic anaphylaxis. RESULTS: The diagnostic programme revealed one case of probable amniotic fluid embolism and four cases of probable drug-induced allergic anaphylaxis. Of the remaining seven cases, there were two cases that, by diagnostic exclusion, could be classified as possible cases of amniotic fluid embolism. The cause of the reactions remained unresolved in five cases. CONCLUSIONS: It can be difficult to differentiate between anaphylaxis and amniotic fluid embolism, especially amongst survivors. Diagnostic markers that can be applied on peripheral blood samples are promising, but larger studies are needed to validate their use in the diagnosis of causes of cardiopulmonary distress during obstetrical anaesthesia.