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PubMed2005

The syndrome of amniotic fluid embolism: a potential contribution of bradykinin.

OBJECTIVE: Amniotic fluid embolism is a potentially fatal complication of pregnancy; although several hypotheses have been formulated, the pathophysiology of this condition is not well known. An exaggerated release of bradykinin, which is activated by products of the amniotic fluid that enter the maternal circulation, could explain the symptoms that are present in amniotic fluid embolism. The objective of this study was to assess whether bradykinin is involved in amniotic fluid embolism. STUDY DESIGN: The plasma bradykinin-generating capacity was measured serially in a patient who experienced amniotic fluid embolism. RESULTS: The plasma bradykinin-generating capacity was found to be very low at the time of the initial clinical manifestations, which were characterized by severe hypotension, cardiorespiratory arrest, and coagulopathy. CONCLUSION: This study suggests a potential role for bradykinin release in the pathophysiology of amniotic fluid embolism.

Adult↗
PubMed1976

[Pathogenesis of amniotic fluid embolism].

The reason for existant of amniotic fluid embolism is the disposition, which will be favoured by the overaction of the sympathic system, by age and the number of pregnancy. It happens especially by premature rupture of membrane, pathologic contents in the amniotic fluid, high pressure in the uterus, bad uterine muscel with laceration and with opened endymyometric veins. Pathophysiologic connection between the stages of amniotic fluid embolism are discussed in detail.

Elasticity↗
PubMed1992

Amniotic fluid embolism and leukotrienes--the role of amniotic fluid surfactant in leukotriene production.

Surfactant rich lipid (lipid) was extracted from cell free 10,000 x g pellets of amniotic fluid. White blood cells (WBC) were isolated from human donors. 36 x 10(7) WBC and 5 g rabbit lung were incubated with pretreated lipid or dipalmitoyl lecithin (lecithin). Leukotrienes (LTs) were identified by high performance liquid chromatography (HPLC) and bioassay, and quantified by radioimmunoassay. Peaks of LTC4 and LTD4 on HPLC and guinea-pig ileum contraction could be identified in lipid and lecithin groups, but not in the control group. LTC4 production by lipid and lecithin groups was significantly higher than that by the control group. An involvement of amniotic fluid surfactant in leukotriene production is suggested.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1996

Immunohistochemical identification of syncytiotrophoblastic cells and megakaryocytes in pulmonary vessels in a fatal case of amniotic fluid embolism.

The histological diagnosis of amniotic fluid embolism (AFE) is based on finding amniotic fluid components in the pulmonary microvasculature. In addition to the distinctive constituents of AFE, placental and decidual tissue fragments as well as isolated trophoblastic cells and megakaryocytes are potentially detectable within pulmonary vessels. The identification of single syncytiotrophoblastic cells (STC), and their differentiation from circulating megakaryocytes (MK) within the lumen of small and medium-sized pulmonary vessels is difficult by classical morphological methods. In a fatal case of AFE, we have successfully detected the simultaneous presence of STC and MK in the pulmonary microvasculature by means of a panel of specific monoclonal (CD61-GpIIIa, beta-hCG) and polyclonal (FVIII-vW, hPL) antibodies. The immunohistochemical analysis for identification of STC and MK should provide more precise data on their incidence and distribution in physiological and pathological conditions as well providing new insights into their physiopathological implications and their correlation with AFE and other gynaecological complications.

Adult↗
PubMed1986

Amniotic fluid embolism and leukotrienes.

Extracts of experimental amniotic fluid embolism from rabbit lungs showed the same biologic activities as leukotrienes and a peak on high-performance liquid chromatography at the same retention time as leukotriene D4. Acute death was prevented by administration of 5-lipoxygenase inhibitor. These results suggest the possibility that leukotrienes contribute to the clinical and pathophysiologic features of amniotic fluid embolism.

Animals↗
PubMed1997

Sudden maternal deaths from amniotic fluid embolism.

Sudden maternal death from amniotic fluid embolism is a rare but serious complication which usually occurs during late pregnancy, often during labour or shortly after, with more than 80% mortality. Such a death causes immense stress to both the relatives and the attending doctors as it is sudden and unexpected. Three such deaths are discussed here. Traditionally, it was believed that this complication usually occurred in prolonged and difficult labour, but there is evidence contrary to this, and it is not possible to predict when and where this fatal complication will occur. Current views and various pathophysiologic mechanisms leading to the fatal outcome are also discussed.

Adult↗
PubMedDate not supplied

Amniotic fluid embolism: historical perspectives & new possibilities.

Amniotic fluid embolism (AFE) is a rare obstetric catastrophe that occurs suddenly and without warning. AFE is a condition that is poorly understood and often difficult to diagnose, but has a high maternal and neonatal morbidity and mortality. Since it was first described in 1926, the underlying pathophysiology has eluded researchers and clinicians. While a new understanding of the syndrome has emerged with the advent of a national registry in the 1980s, recommendations for diagnostic methods and treatment in the acute phase of the event remain unclear. The purpose of this article is to provide the reader with a historical look at the phenomenon of AFE, a description of its suspected pathophysiology, and recommendations for nursing interventions. A review of data from the national registry and other classic studies are included.

Adult↗
PubMed1995

Endothelin has a role in early pathogenesis of amniotic fluid embolism.

The early pathogenesis of amniotic fluid embolism is not completely understood. The entrance of amniotic fluid (AF) into the systemic circulation leads to an initial phase of pulmonary vasospasm, pulmonary hypertension and cor pulmonale. We studied the effect of AF on endothelin (ET) production in vivo and in vitro. Injection of rabbits (pregnant and nonpregnant) with meconium-stained AF, raw AF and supernatant AF led to a significant increase in serum ET. This result was confirmed by using human umbilical vein endothelial cell cultures incubated with the same types of AFs. After infusion of rabbits with AFs, we observed that the lung, heart and kidney were positively stained for ET and von Willebrand factor. AF was found to have an injurious effect on endothelial cells measured by using fura-2. The maximal injurious effect of AFs was observed for the meconium-stained AF. We hypothesized that the early pathological changes in AF embolism may be mediated by ET.

Animals↗