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Amniotic fluid embolism is an uncommon but devastating obstetric emergency. We report hemodynamic data derived from pulmonary artery catheterization in four previously unpublished cases of amniotic fluid embolism syndrome. These findings confirm a recently published reinterpretation of the central hemodynamics of this condition.
The amniotic fluid (AF) was fractionated by dialysis, gel filtration and SDS/PAGE, and submitted to the assay of collagenous constituents. The collagenous character of peptides and proteins of amniotic fluid was confirmed by hydroxyproline (Hyp) assay and treatment with bacterial collagenase followed by electrophoresis and gel filtration of the digestion products. It was found that AF contains collagen degradation products but the classical method of Hyp determination described by Woessner (Arch. Biochem. Biophys., 1961, 93, 440-447) gives overestimated values due to the interference with other AF components. Fractionation of AF on Sephadex G-100 column allowed to remove the interfering material and to estimate the actual Hyp content which equals to approx. 6.2 microg/ml. About 70% of Hyp was found in low molecular dialyzable products and the rest (about 30%) appears to be a constituent of nondialyzable collagenous polypeptides of the molecular mass of about 7.9-26.3 kDa. It is suggested that such collagenous polypeptides may be the products of proteolytic conversion of collagen precursor (procollagen) into the monomeric form of this protein. No high molecular forms of collagen, corresponding to alpha-subunits, were found.
Amniotic fluid embolism is a rare cause of intrapartum maternal death. Some cases do not fit the typical picture of a multipara in her thirties at or near term. The case presented in this paper involves a 25-year-old gravida 3, para 0, abortion 2, who developed amniotic fluid embolism much earlier in gestation than is usually described.
Thirty amniotic fluid samples in late gestational age were analysed for HPL-values and the L/S-ratio. The pregnant women used in this study were healthy except three patients who developed a rh-incompatibility. The amniotic fluid was only obtained by abdominal amniocentesis. We found a decreasing tendency of the HPL-values in late pregnancy. The L/S-ratio increased. A significant correlation of both values could not be observed. In all three cases of rh-incompatibility the decrease of HPL and the increase of the L/S-ratio occurred obviously earlier and steeper. Further studies will prove the significance of these results.
Human amniotic fluid is rich in a binding protein for somatomedins. This binding protein competes with human placenta membranes for labelled somatomedin A. Consequently, the placenta radioreceptorassay for somatomedin can be used for detection of the binding protein. The protein was isolated from human amniotic fluid by a three-step procedure: First, stepwise ammonium sulphate precipitation; second, hydrophobic chromatography (phenyl-Sepharose); and third, anion-exchange chromatography (fast protein liquid chromatography). The total recovery of binding protein calculated with the placenta radioreceptorassay was 50%. Polyacrylamide gel electrophoresis under native and denaturating conditions of the isolated protein disclosed a single band. The relative molecular mass was 35000, determined by exclusion chromatography, and 32000 under denaturating conditions in sodium dodecyl sulphate/polyacrylamide gel electrophoresis. The isoelectric point was 4.3 according to chromatofocusing and the amino acid composition also disclosed a high content of acidic/amidated residues. The N-terminal amino acid sequence was Ala-Pro-Trp-Gln-Cys-Ala-Pro-Cys-Ser-Ala.
Amniotic fluid cells obtained by amnicentesis at 16-20 weeks' gestation were grown in culture until a confluent monolayer of cell had been formed. Radiolabeled pregnenolone, progesterone and 20 alpha-dihydroprogesterone were added to the cell cultures; steroid metabolites which formed after 24 and 48 hours of incubation were identified. Incubation of the cell cultures with pregnenolone-3H resulted in the formation of progesterone, 17alpha-progesterone and 20 alpha-dihydroprogesterone. A significant amount of progesterone was identified after incubating the cell cultures with 20 alpha-dihydroprogesterone. The results indicate that 3 beta-ol-dehydrogenase, 17 alpha-hydroxylase and 20 alpha-hydroxysteroid dehydrogenase enzymes are present in cultured amniotic fluid cells obtained at 16-20 weeks' gestation.
Amniotic fluid was analyzed for the presence of the 15,000 monomer molecular size glycoprotein found in human breast gross cystic disease fluid (GCDFP-15). From 24 weeks' gestation a log-linear increase in levels of GCDFP-15 was noted. The levels of GCDFP-15 doubled every 16 to 28 days, and the highest value recorded was 7,200 ng/ml. At delivery, levels of GCDFP-15 in cord blood plasma were in a background range (mean, 8 ng/ml). Maternal plasma levels of GCDFP-15 were one to tenfold higher in the third trimester of pregnancy when compared to those in nonpregnant women. Since saliva is known to contain high concentrations of GCDFP-15 (10 to 70 micrograms/ml), it is proposed that the levels in amniotic fluid originate from saliva and tracheobronchial secretions.
Amniotic fluid embolism is the most unpredictable and catastrophic complication of pregnancy, accounting for 10% to 20% of maternal deaths. The pulmonary edema commonly seen in this syndrome is probably due primarily to alveolar capillary leakage and may be potentiated by high maternal extracellular volume, low colloid osmotic pressure, and, in some patients, by depressed myocardial function. In patients in whom resuscitation is successful, diuresis leads to rapid resolution of pulmonary edema. Amniotic fluid does not ordinarily enter the maternal circulation, and the identification of large numbers of fetal squames in the postpartum pulmonary microvasculature is probably of clinical significance.
Amniotic fluid from 72 pregnancies at risk for mucopolysaccharidosis have been analysed for glycosaminoglycans (GAG) by means of two-dimensional electrophoresis. Definite results were obtained in all cases and required only 3 days to report. Of the 66 cases for which GAG analysis was accompanied by enzyme assays on cultured amniotic fluid cells, there was agreement of results in 65. In the one case of disagreement the result of GAG analysis proved to be correct. Fourteen pregnancies were predicted to be affected and the predictions were confirmed by studies on fetal tissues and/or cultured cells, or in one case the birth of an affected infant. Of the 58 pregnancies predicted to be unaffected, 48 have so far gone to term and produced healthy infants. There have been no false negative predictions. The analytical method is simple, rapid, and, in this study, has been found completely reliable to prenatal diagnosis.
Amniotic fluid embolus, also known as anaphylactoid syndrome of pregnancy is a rare complication of pregnancy. When it occurs, the maternal mortality rate may be as high as 86%, and in survivors, the morbidity rate may be just as high. Hallmark clinical features include maternal cardiovascular collapse with disseminated intravascular coagulation, and fetal distress. Management centers on strategies to improve oxygenation, support circulation, and correct the coagulopathy. We report the case of a patient who developed amniotic fluid embolus and was effectively managed with aprotinin to control the coagulopathy associated with this devastating complication of pregnancy.
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Amniotic fluid infections manifested by an inflammatory response in the extraplacental membranes and subchorionic plate of the placenta are a common phenomenon thought to be due in most cases to ascending bacterial infections via intact membranes. Fatal spread to the fetus is much less common and more likely to occur in underprivileged communities. The probable reasons are nutritional deprivation in the mother or both, leading to production of a liquor with diminished ability to suppress bacterial growth. Zinc is one component of the antibacterial system but liquor levels of zinc vary widely and inconsistently with antibacterial activity. Dietary supplementation with zinc did not improve antibacterial activity of liquors in a population with diminished liquor antibacterial activity and large number of fatal infections. Other factors in the genesis of amniotic fluid infections may be interference with normal defence mechanisms as a result of coitus in late pregnancy and vaginal infections with Trichomonas vaginalis. Socioeconomic factors may play a role apart from their association with maternal nutrition, through diminished hygiene associated with insufficient use of water and insufficient availability and use of medical facilities.
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OBJECTIVE: The present study tested the hypothesis that an intra-amniotic infusion of amniotic fluid (AF) would produce a more sustained increase in AF volume than an infusion of lactated Ringer's solution. METHODS: Five chronically catheterized, late-gestation fetal sheep were studied over two 5-day periods with AF volume measured daily. After baseline measurements on day 1, 1 L of either warmed, previously frozen AF or warmed lactated Ringer's solution was infused intra-amniotically over 60 minutes. Two days later, the other fluid was infused. During the second week, fluids were infused in the opposite order. Analysis of variance (ANOVA) was used for statistical testing. RESULTS: Following intra-amniotic infusion (n = 20) of 1007 +/- 7 (SE) mL of either AF or Ringer's solution, intra-amniotic retention of the infused fluid was only moderate after 1 day (37.2% +/- 7.9%, P <.001) and was not significantly different from zero after 2 days (16.5% +/- 9.5%, P =.1). There were no significant differences in AF volume following infusion of AF versus lactated Ringer's solution or the order in which they were infused. AF compositional changes were similar except that pH and bicarbonate concentration were reduced as expected immediately after lactated Ringer's solution with a return to normal values after 1 day. AF lactate increased after lactated Ringer's solution infusion, declining to baseline values after 2 days. Fetal urine flow rate increased by 75% +/- 24% at 1 day postinfusion and there was no difference between infusates. CONCLUSIONS: The expansion of AF volume over 2 days following amnio-infusion does not appear to depend on minor compositional differences or the presence of microconstituents such as hormones, cytokines, or growth factors that are normally present in AF.
A radiometric bioassay based on the continuous monitoring of 14CO2 released from labeled glucose in the presence of amniotic fluid or amniotic fluid with added phosphate has been employed to detect the presence of a phosphate-sensitive bacterial inhibitor in amniotic fluid near term. The time required for detection of the inhibitory activity is approximately 12 hours, in contrast to approximately 36 hours required for a previously reported technique. Application of this radiometric bioassay to demonstrate bacterial growth inhibition by amniotic fluid and physicochemical properties of the inhibitory activity yielded results comparable to those obtained with the older method of plate counts of viable bacteria. By the new technique it was possible to demonstrate that the inhibitory activity was phosephate sensitive, heat stable, inactivated by metal chelation, removed by bentonite, and present in a low-molecular-weight fraction of amniotic fluid.