Focus on fluids. Examining maternal hydration and amniotic fluid volume.
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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.
Meconium-stained amniotic fluid might signify underlying acute or chronic fetal hypoxia with adverse perinatal outcome, especially if associated with cardiotocographic abnormality. Management requires awareness of this potential risk, appropriate intrapartum care and a combined obstetricneonatal approach. Amnioinfusion can be an effective preventative measure.
Fibrinolytic activity (FA) was assessed by the fibrin plate technique in 47 amniotic fluid samples obtained at 35 to 39 weeks' gestation. In amniotic fluid the FA (63.1 +/- 2.5 mm2) was considerably elevated when compared with previously reported serum levels of pregnant women. After centrifugation of the amniotic fluid samples a highly significant reduction of FA in the supernatant was recorded (42.9 +/- 1.3 mm2), suggesting that the cells of fetal origin are the main source of the high plasminogen activator activity demonstrated in amniotic fluid. A significant rise in amniotic fluid FA was demonstrated beyond the 37th gestational week. Furthermore, significantly greater FA was recorded in amniotic fluid samples from women with spontaneous onset of labor within a week. However, a single FA determination in amniotic fluid obtained by routine amniocentesis was found to be of little value for prediction of the time interval to delivery.
OBJECTIVE: To measure acute and chronic changes in the placenta and amniotic fluid associated with performance of decompression amniocentesis in pregnancies with the twin oligohydramnios-polyhydramnios sequence (TOPS). METHODS: Amniotic fluid pressures, placental thickness, placental perfusion, and amniotic fluid volumes were measured in each sac of a monochorionic diamniotic twin gestation before and after decompression amniocentesis. Indigo carmine was injected into the polyhydramnic sac after decompression, and fluid from the oligohydramnic sac was sampled after equilibration. Spectrophotometric analysis of amniotic fluid specimens was performed for dye detection. Amniotic fluid volume and placental perfusion studies were repeated 1 week later. RESULTS: Three patients with TOPS were enrolled, and decompression amniocentesis was performed in the midtrimester. After decompression, amniotic fluid volume decreased in the polyhydramnic sac, amniotic fluid pressures decreased in both sacs, placental thickness increased, and umbilical artery Doppler velocimetry was unaffected. The amniotic fluid volume increased acutely in only one oligohydramnic sac after decompression, and ultrasonographic examination, amniotic fluid spectrophotometric analysis, and placental pathologic examination all identified interfetal membrane disruption as the etiology. CONCLUSIONS: Decompression amniocentesis as a treatment for TOPS does not result in acute or chronic changes in the amniotic fluid volume of the oligohydramnic sac in the absence of interfetal membrane disruption.
Serial samples of amniotic fluid were taken from 48 patients during labour. The lecithin/sphingomyelin (L/S) ratio was estimated and found to rise in 52 per cent, remain almost unchanged in 33 per cent and fall in 15 per cent. The rate of rise in the L/S ratio seemed inversely related to the length of labour.
BACKGROUND: The relationship between reduced amniotic fluid volume and increased risk of fetal distress in small-for-gestational age fetuses is not yet clear. Furthermore, the criteria used for the diagnosis of 'oligohydramnios' are different between the single deepest pocket method and amniotic fluid index. We investigated the relationship between the single deepest pocket and amniotic fluid index and their ability in predicting fetal distress in small-for-gestational age fetuses. METHOD: We examined 69 pregnant women with singleton pregnancy, intact membranes, birth weight below the 50% percentile - 1.5 s.d., in whom delivery occurred within seven days of the last estimation of amniotic fluid volume. Amniotic fluid volume was measured in each woman simultaneously by single deepest pocket and amniotic fluid index. Fetal distress was determined by intrapartum monitoring of fetal heart rate. RESULTS: Estimates of amniotic fluid volume measured by the two methods showed a significant correlation at 24 to 41 weeks of gestation. A cut-off value for single deepest pocket of 3.0 cm was associated with the highest accuracy in predicting fetal distress in small-for-gestational age fetuses. The rate of cesarean section among patients with single deepest pocket <3.0 cm was higher than that in amniotic fluid index <8.0 cm. CONCLUSION: Our results demonstrated that a single deepest pocket measurement of <3 cm is the most useful criterion for 'oligohydramnios' in the prediction of fetal distress.
In order to study the antimicrobial activity of amniotic fluid, attempts were made to evaluate the in vivo growth of bacteria in amniotic fluid and the role of transferrin in antibacterial activity. The bacteria chosen for these experiments were Escherichia coli, Staphylococcus aureus, Pseudomonas aeruginosa and Streptococcus faecalis, respectively. The results obtained were as follows: Amniotic fluid was shown have an antibacterial effect on Escherichia coli and Staphylococcus aureus, while Pseudomonas aeruginosa and Streptococcus faecalis proliferated readily in amniotic fluid. Individual difference in each sample appeared to be responsible for the inconsistent potency of the inhibitory effect observed. When amniotic fluid was heated at 100 degrees C for 5 minutes, the antibacterial activity was lost. The level of transferrin in amniotic fluid obtained at term was determined to be 29.1 +/- 17.6mg/dl (N = 90). The value correlated with neither those measured in cord sera nor maternal sera. The antimicrobial activity was restored by adding transferrin into heat-treated amniotic fluid at a concentration of 250mg/dl or higher. Simultaneous addition of transferrin and a sufficient concentration of iron made it possible to form a transferrin-iron complex. A subsequent decrease in unbound transferrin resulted in the loss of antibacterial properties.
Insulin concentrations in amniotic fluid were correlated with fetal age and with fetal weight in order to test the hypothesis that fetal insulin regulates fetal growth. No significant correlation could be detected. Insulin levels in amniotic fluid in diabetics, however, were significantly higher than in nondiabetics. In the same samples of amniotic fluid C-peptide proved to be very unstable during long term storage.
The amniotic and chorionic membranes obtained at term and term amniotic fluid contain a soluble protease activity which cleaves [14C]-labeled globin at acid pH. In contrast, a salt extract of the pellet fraction obtained from the fetal membranes displays only negligible protease activities at the pH range of 4-8. Specific activities of the proteases in the soluble and salt-extractable fractions of fetal membranes which were intact before onset of labor were not significantly different from the respective activities in cases of premature rupture of fetal membranes (PROM). However, the protease activity of the amniotic fluid was found to increase with advancing gestational age and to reach maximal activity at term. A heat-sensitive and nondializable protease inhibitory activity was found in term amniotic fluid. This inhibitory activity acted on the cytosolic protease of amniotic membranes from control and PROM cases, but not on the soluble protease of chorionic membranes, and had a similar potency in fluids from PROM cases or fluids collected at term. These results do not support a role for fetal membrane proteases, amniotic fluid proteases, or amniotic fluid protease inhibitory activities in the etiology of PROM. However, the observed changes in amniotic fluid protease activity with fetal age suggest a physiological role for the enzyme in normal fetal development.
This study examined whether cortisol, present in amniotic fluid (AF), could reach the fetal blood, and might be available to various fetal organs and to the fetal membranes and placenta. [3H]Cortisol ([3H]F) was injected into the AF of five sheep at 130--143 days gestation. Samples of AF and fetal blood were collected for 120 min, at which time the fetuses were delivered and fetal organs and fluid were collected for measurement of the [3H]F content. [3H]F disappeared from AF with an initial half-life of about 40 min and was detected in fetal blood by 30 min after intraamniotic injection. At 120 min after injection, [3H]F was widely distributed within the pregnant uterus, and the highest concentrations of radioactivity were found in allantoic fluid, fetal membranes, and placental tissue. The concentration of [3H]F in the umbilical vein was higher than in umbilical arterial blood in four of five sheep. [3H]F and [3H]cortisone were found in several fetal tissues, including adrenal, kidney, pancreas, lung, and liver. [3H]F in tracheal and stomach fluid was generally less than in fetal blood. We conclude that 1) cortisol can reach the fetus from AF, 2) a major route of entry may be via the vasculature of the fetal membranes, 3) a considerable proportion of [3H]F is retained by the fetal membranes, and 4) interconversion of [3H]F and [3H]cortisone may occur in some fetal tissues.
Insulin, prolactin, and lecithin phosphorus levels were measured in 97, 62, and 44 amniotic fluid samples from third trimester normal, gestational diabetic, and insulin-dependent diabetic patients, respectively. There was no difference in lecithin phosphorus concentration (index of fetal lung maturity) among the three groups. The amniotic fluid insulin level was significantly higher in insulin-dependent diabetic patients, whereas there was no difference in amniotic fluid prolactin levels among the groups. Correlations of amniotic fluid prolactin levels with both lecithin phosphorus and insulin levels were not statistically significant in any of the groups. This is probably because amniotic fluid prolactin is decidual, rather than fetal, in origin. Even though amniotic fluid insulin levels, which reflect fetal levels, were significantly higher in insulin-dependent diabetic patients, there was no difference in the amniotic fluid lecithin phosphorus concentration in diabetic pregnancies compared with that in normal pregnancies. Moreover, there was a positive, and not a negative, correlation between amniotic fluid insulin and amniotic fluid lecithin phosphorus levels in diabetic pregnancies. These results do not support the theory that fetal hyperinsulinemia results in delayed pulmonic maturation in diabetic pregnancies.
Prolactin (PRL) levels and Na+, K+, Cl-, Ca++ concentrations in maternal serum and amniotic fluid from 64 women in normal term pregnancy were measured by immunoenzymetric assay and flame photometry. The mean amniotic fluid PRL concentration was 597.7 (SE 31.5) ng/ml and the mean amniotic fluid Na+, K+, Cl- and Ca++ levels were 125.6 (SE 0.9) mmol/l, 4.5 (SE 0.1) mmol/l, 109.3 (SE 1.3) mmol/l and 2.0 (SE 7.5 E-02) mmol/l, respectively. There was no correlation between PRL levels in maternal serum and amniotic fluid, and the electrolyte concentrations in amniotic fluid. A close correlation was found between the concentrations of Na+ and Cl- in maternal serum and amniotic fluid. Thus, even though PRL may participate in the regulation of electrolytes in the amniotic fluid compartments, our findings provide indirect evidence for the existence of other regulatory mechanisms.
Amniotic fluid from 19 patients with preeclampsia was compared with samples from normotensive control subjects with respect to the levels of prostaglandin 6-keto prostaglandin F1 alpha, thromboxane B2, and the ratio of 6-keto prostaglandin F1 alpha to thromboxane B2. The study found no significant differences in the levels of these prostanoids or the ratio of 6-keto prostaglandin F1 alpha to thromboxane B2 (study patients, 2.7 +/- 2.1; control patients, 2.8 +/- 1.9) between groups.
Cytospin preparations of amniotic fluid samples from 200 pregnancies, taken between 16 and 20 weeks' gestation, were examined without knowledge of the fluid alpha-fetoprotein (AFP) level. The specimens were taken because of the possibility of neural tube closure defect. All but eight cases showed predominantly squamous cells, amnion cells, macrophages and blood cells. AFP levels in these fluids were within the normal range in 178 cases, unequivocal in 11, undetectable in 2 and raised in 1; none of the babies in these cases had a neural tube closure defect. In eight cases a large population of small cells with dark nuclei and a population of large, foamy macrophages were present in addition to the other cell types; all of these babies had a neural tube closure defect (five anencephaly and three anencephaly with spina bifida). This technique may provide a useful additional method of diagnosis of neural tube closure defects.
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.
Lung surfactant in amniotic fluid, and hence the maturity of the fetal lungs, can be assessed by observation of stable microbubbles (less than 15 micron diameter). Bubbles are formed by agitation with a Pasteur pipette and examined in hanging drops under the 10 x power of a microscope. Either after a count of bubbles, or after a general survey of hanging drops, the fluid is given a stable microbubble rating. A 'strong' rating indicates that the idiopathic respiratory distress syndrome will not occur after delivery, and that the lecithin/sphingomyelin ratio will indicate maturity. Complete absence of stable microbubbles suggests a high risk of respiratory trouble for the newborn infant, as does a weak or lower rating in the 30 to 37 week gestational age group. The test takes 5 to 10 minutes to perform, is cheap and easy, is not affected by blood, but may be affected by meconium. If a 'strong' rating is found, measurement of the L/S ratio can safely be omitted.
The objective of this study was to evaluate the predictive values of the amniotic fluid index for measures of perinatal morbidity and for clinical observations consistent with oligohydramnios. We evaluated positive and negative predictive value of the amniotic fluid index for measures of perinatal morbidity and for clinical observations consistent with oligohydramnios at various cutoff values for amniotic fluid index in a cohort of 449 consecutive postdates patients who had a clinician's observation of amniotic fluid quantity and quality recorded at the time of rupture of membranes. Newborn morbidity was a rare event. Clinical observations consistent with oligohydramnios had significant positive and negative predictive values for some measures of newborn morbidity. The last amniotic fluid index performed during antepartum testing had 95% confidence intervals for relative risks for these measures of newborn morbidity that included unity and therefore were not significant. At a cutoff value of 5.0 cm, the positive predictive value of the amniotic fluid index for clinical observations consistent with oligohydramnios was 50%; the negative predictive value was 85%, with a prevalence of clinical observations consistent with oligohydramnios of 19%. The presence of fetal heart rate decelerations did not significantly improve the positive predictive value of the amniotic fluid index. Higher positive predictive values were obtained at cutoff values of 4 cm and 3 cm with minimal loss in negative predictive value. The amniotic fluid index did not possess significant predictive value for measures of newborn morbidity. Clinical observations consistent with oligohydramnios at the time of rupture of membranes did have predictive value for some of these measures and thus probably are a reflection of the actual amount of fluid present inside the uterus prior to rupture of membranes. The amniotic fluid index is only a fair predictor of clinical observations consistent with oligohydramnios. Thus, a positive test correctly predicted these observations 50% of the time, with 50% false-positive results. Undertaking delivery in the 50% of patients without clinical observations consistent with oligohydramnios may lead to a higher cesarean section rate since these patients do not require induction and are subject to the risk of a failed induction of labor. A negative test correctly predicted observations consistent with normal fluid 85% of the time, with a false-negative rate of 15%. Thus, a negative test was no guarantee that observations consistent with oligohydramnios, and thus newborn morbidity, would not subsequently appear. Frequent testing with multiple modalities and induction of labor when the Bishop score is favorable remain sensible options. Induction of labor in postdates patients with a low amniotic fluid index needs to be evaluated in a yet-to-be-performed prospective randomized control trial before a low amniotic fluid index is assumed to be the sole indicator for induction of labor. More stringent cutoff values for amniotic fluid index may be justified.