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At least 145 records · Page 8Linked to original sources
PubMed1984

Amniotic fluid activates complement. A role in amniotic fluid embolism syndrome?

A 30-year-old woman died with massive pulmonary microvascular leukostasis immediately after cesarean hysterectomy. We postulated that this might have resulted from amniotic fluid embolization and, therefore, tested amniotic fluids as activators of granulocytes and the plasma complement system. Normal human amniotic fluid failed to aggregate granulocytes, provoke a respiratory burst, or attract the cells chemotactically. However, amniotic fluid activated complement when incubated with normal plasma. The ability to activate complement resided in lipid-rich particulate material in the fluid, and activation proceeded mainly (but probably not exclusively) via the alternative complement pathway. Amniotic fluids varied widely in their ability to activate complement, with the most potent samples derived from women with distressed pregnancies. Plasma samples from donors also varied widely in their ability to be activated by amniotic fluid, and many of the most activatable plasma samples derived from gravid women. We propose that amniotic fluid embolization can, like "shock lung" syndrome, have a leukostatic early phase, and that complement and granulocyte activation on embolization of amniotic fluid can contribute to the pulmonary collapse characteristic of that syndrome, especially when a potently activating fluid is combined with a potently activatable plasma.

Adult↗
PubMed1975

[A case of amniotic fluid embolism (author's transl)].

A case of lethal amniotic fluid embolism is reported. The microscopic findings are documented and the patho-physiologic course of events is reconstructed. The unsuccessful treatment is compared with recommendations in the literature and critically evaluated.

Adult↗
PubMedDate not supplied

[Clinical aspects and therapy of amniotic fluid embolism. Illustration based on a case report].

A case of amniotic fluid embolism during the delivery of an at term pregnancy is reported. The 34-year old primipara with an unremarkable medical history suddenly suffered from a seizure in the second stage of labor. Shortly prior to this event, a prolonged fetal bradycardia was recorded. After forceps delivery a massive postpartum haemorrhage as the result of a consumption coagulopathy occurred. Immediate resuscitation with artificial ventilation improved the condition of mother and child. The substitution of packed red cells and platelets, fresh frozen plasma and other blood derivates was necessary. Mother and child survived without any physical damage or neurological deficit. Because of the clinical pattern we diagnosed an amniotic fluid embolism.

Adult↗
PubMed1997

[Amniotic fluid embolism in trial of labor. A case report].

Amniotic fluid embolism is a rare complication of pregnancy, which accounts for about 10% of all maternal deaths. A case of acute embolic episode occurred during labor in a 36-year-old patient with spontaneous rupture of membranes is described. Caesarean section was performed immediately, followed by hysterectomy; the baby survived but the mother died because of DIC and cardiorespiratory arrest.

Adult↗
PubMed1995

Amniotic fluid embolism: analysis of the national registry.

OBJECTIVE: We analyzed the clinical course and investigated possible pathophysiologic mechanisms of amniotic fluid embolism. STUDY DESIGN: We carried out a retrospective review of medical records. Forty-six charts were analyzed for 121 separate clinical variables. RESULTS: Amniotic fluid embolism occurred during labor in 70% of the women, after vaginal delivery in 11%, and during cesarean section after delivery of the infant in 19%. No correlation was seen with prolonged labor or oxytocin use. A significant relation was seen between amniotic fluid embolism and male fetal sex. Forty-one percent of patients gave a history of allergy or atopy. Maternal mortality was 61%, with neurologically intact survival seen in 15% of women. Of fetuses in utero at the time of the event, only 39% survived. Clinical and hemodynamic manifestations were similar to those manifest in anaphylaxis and septic shock. CONCLUSIONS: Intact maternal or fetal survival with amniotic fluid embolism is rare. The striking similarities between clinical and hemodynamic findings in amniotic fluid embolism and both anaphylaxis and septic shock suggest a common pathophysiologic mechanism for all these conditions. Thus the term amniotic fluid embolism appears to be a misnomer.

Adolescent↗
PubMed2007

Delayed presentation of amniotic fluid embolism: lessons from a case diagnosed at autopsy.

Amniotic fluid embolism (AFE) syndrome, a catastrophic cause of respiratory failure typically occurs during labour, or soon after delivery. Systemic hypotension is the most prominent haemodynamic alteration documented in patients with AFE, a consequence principally of severe left-sided heart failure. A 22-year-old female was admitted to the respiratory intensive care unit with severe eclampsia and acute respiratory failure 4 h following delivery. Her blood pressure was elevated (systolic 150-180 mm Hg, diastolic 90-110 mm Hg) throughout the admission. She succumbed in spite of therapy for eclampsia and mechanical ventilation. Autopsy revealed large numbers of polygonal, anucleate foetal squames and mucin in the pulmonary vasculature typical of AFE while changes of eclampsia were found in the liver and kidneys. It appears that AFE syndrome can have a delayed presentation, as late as 4 h after delivery and haemodynamic collapse may not be mandatory if the patient has coexisting systemic hypertension secondary to severe eclampsia.

Acute Disease↗
PubMed2000

[The clinical analysis of 38 cases with amniotic fluid embolism].

OBJECTIVE: To analyze the clinical course of amniotic fluid embolism (AFE) and identify the high risk factors. METHODS: Thirty-eight cases diagnosed as AFE in Suzhou region during period of past 15 years were analyzed retrospectively. Fifteen years were divided into 5 stages with 3 years each. RESULTS: Of 38 cases, 30 (78.9%) were primigravida and one twins. There were 34 maternal deaths. Among them, 31 died in the first four stages and 3 died in the last stage. There were 4 cases survived from AFE in the last stage. AFE accounted for 15% of total maternal deaths in the past 15 years, which is the second cause of maternal death. Of 38 cases, 2 (5.2%) occurred before 28 gestational weeks. 20 (52.6%) suffered from AFE during labour, 13 (34.2%) after delivery, and 3 (7.8%) before labour. All cases presented respiratory distress, cyanosis, chest discomfort and/or shock, cardiopulmonary collapse. Sixteen cases had postpartum hemorrhage and/or laboratory evidence of DIC. Of 38 cases, 15 (39.5%) died within one hour after onset of AFE. The predisposing factors for AFE included strong uterine contractions due to oxytocin or PEG augmented 17 cases (44.7%), pregnancy induced hypertension 11 cases (28.9%), multigravida and/or elder gravida 9 cases (23.7%) and cesarean section 8 cases (21.1%). CONCLUSIONS: AFE must be suspected in maternal cases with sudden collapse, especially the clinical symptoms of allergic reaction. Prevention of hypertonic uterine contraction and prompt resuscitation, and emergency surgical delivery can improve the prognosis of AFE.

Adult↗