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PubMed1985

Acute polyhydramnios complicating twin pregnancies.

Acute polyhydramnios in the second trimester is a typical complication in monozygous twin pregnancies. It is caused by a feto-fetal transfusion with anemia on the donor and polycythemia on the recipient twin. Contrary to the chronic hydramnios, there is no increase in malformations. In view of the high mortality rate (100%, according to most authors), the clinical management has to be reconsidered. During the years 1979 to 1983, 10 cases of acute polyhydramnios have been observed at the University Hospital in Zurich. This corresponds to an incidence of 9% in our twin population. All cases investigated were MZ twin pregnancies. With the exception of one patient, who underwent an abortion, all women were hospitalized, had bed rest and received recurrent removals of amniotic fluid and prophylactic tocolysis. The mean gestational age at the time of diagnosis was 23 4/7 weeks and at delivery 30 3/7 weeks. In two cases--one of which is presented in detail--with an unintentional puncture of a placental vessel, the recurrence of the hydramnios did not appear. Eight of 18 newborns survived. No malformations were found. Bed rest, tocolysis and recurrent amniocenteses seem to have a positive influence on the prolongation and outcome of the gestation in acute polyhydramnios.

Acute Disease↗
PubMed1997

Fetal hemoglobin changes in the twin oligohydramnios-polyhydramnios sequence.

Fetal hemoglobin concentration was measured in each twin from five monochorionic pregnancies complicated by twin-to-twin transfusion, diagnosed by growth discordance and coexistent oligohydramnios-polyhydramnios. In three cases the hemoglobin concentration of the smaller twin with oligohydramnios was lower than the normal mean for gestation, and the hemoglobin difference was more than 5 g/dl in two of these cases. In the other two cases, the hemoglobin concentration of the four fetuses with coexistent oligohydramnios-polyhydramnios was within the normal range. This suggests that twin-to-twin transfusion may occur without hemoglobin changes, or that alternatively coexistent oligohydramnios-polyhydramnios occurs in the absence of twin-to-twin transfusion.

Female↗
PubMed1996

[The polyhydramnios symptom: analysis of 56 cases].

Analysis of 56 CASES: 56 cases of polyhydramnios, which were diagnosed sonographically over a period of three years, were analysed retrospectively in this study. In 9334 births, the prevalence of this symptom was 0.6%. Malformations were the most common cause (26.7%) of polyhydramnios (p < 0.001). In comparison to our normal patient group gestational diabetes, twin pregnancies with elevated amniotic fluid of one twin, virus infections, fetal chromosome abnormalities were diagnosed at a significantly higher rate (p < 0.001). The perinatal mortality rate (28.5%) in comparison to our normal collective (1.6%) was also significantly higher. Because of the high mortality, polyhydramnios must be assessed precisely and treated if possible. Fetal karyotyping should be routinely performed in the second trimester.

Amniocentesis↗
PubMed1998

The effect of polyhydramnios and oligohydramnios on fetal lung maturity indexes.

The influence of amniotic fluid (AF) volume on common fetal lung maturity (FLM) indices was evaluated. Cases diagnosed with altered AF volume as estimated by ultrasound (n = 71; polyhydramnios = 33, oligohydramnios = 38) were matched to controls by: gestational age (GA) at amniocentesis, GA at delivery, neonatal weight, sex, and pregnancy complication. FLM was assessed on AF specimens obtained by transabdominal amniocentesis by planimetric and stechiometric L/S, phosphatidylglycerol (PG), and lamellar bodies counts (LB). In cases with polyhydramnios, L/S ratios (planimetric and stechiometric) were statistically lower in cases with respect to controls (2.1 +/- 0.9 vs. 2.8 +/- 1.0, p = 0.007, and 4.8 +/- 2.4 vs. 5.9 +/- 2.7, p < 0.04; respectively). Absence of PG was more frequent in (70.8% vs. 50%, p = 0.02). LB counts were lower in cases than in controls (15.5 +/- 12.1 x 10(3)/microL vs. 21.9 +/- 14.3 x 10(3)/microL, p < 0.05). In cases with oligohydramnios, no difference was found for planimetric and stechiometric L/S in comparison to controls (2.6 +/- 1.2 vs. 2.6 +/- 1.0, N.S. and 4.9 +/- 2.1 vs. 4.6 +/- 1.8, N.S.; respectively), absence of PG (62.5% vs. 50%, N.S.), and LB counts (27.2 x 10(3)/microL +/- 12.8 x 10(3)/microL vs. 28.6 x 10(3)/microL +/- 24.1 x 10(3)/microL, N.S.). In conclusion, oligohydramnios was not associated with altered FLM indices; in cases with polyhydramnios all FLM indices were significantly lower.

Adult↗
PubMed1990

Doppler umbilical artery velocimetry in fetuses with polyhydramnios.

Polyhydramnios is a condition of multiple etiologies, many of a benign nature, but some of which are incompatible with life. To evaluate Doppler velocimetry results as a prognostic parameter in these fetuses, we reviewed all of our cases of polyhydramnios that underwent Doppler analysis in the third trimester. Fifty-four fetuses were studied. Eleven (20.4%) had abnormal waveforms and 43 (79.6%) had normal waveforms. An abnormal waveform was associated with a significantly higher incidence of congenital anomalies, perinatal mortality and intrauterine growth retardation. Six of the 11 fetuses had abnormal karyotypes. Macrosomia was present in 37.2% of fetuses with normal waveforms and in no fetus with an abnormal waveform. Doppler analysis may aid in the counseling and management of patients with polyhydramnios. In cases with an abnormal ratio, the physician and patients should be prepared for a poor outcome and third trimester genetic analysis should be strongly considered.

Chi-Square Distribution↗
PubMed1986

[Sonographic evaluation of the amount of amniotic fluid. I. Polyhydramnios--significance for the course of pregnancy and labor].

In this study, 3,274 pregnant patients were sonographically examined. Special attention was paid to the classification of the quantity of amniotic fluid according to sonographic criteria. An increase in amniotic fluid was observed in 6% of the patients examined. Cases in which the largest sonographically demonstrable amniotic fluid was significantly larger than the transverse thoracoabdominal diameter were classified as polyhydramnios. An amniotic fluid depot that was either as large as or up to 10% larger than the transverse thoracoabdominal diameter of the fetus was regarded as the upper normal range for the amount of amniotic fluid. These cases were compared with a randomly chosen control group with normal quantities of amniotic fluid with regard to the occurrence of complications during pregnancy and birth and to the incidence of fetal malformation. Patients with increased quantities of amniotic fluid more frequently had symptoms of toxemia (p less than 0.01). In patients with manifest diabetes mellitus the quantity of amniotic fluid was frequently in the upper normal range (p less than 0.01), while women with gestation diabetes frequently suffered from polyhydramnios (p less than 0.001). Fifteen percent of women with quantities of amniotic fluid in the upper normal range beared macrosomatic children (p less than 0.001). Twenty-seven percent of cases with polyhydramnios (p less than 0.001) and 8% of cases with a quantity of amniotic fluid in the upper normal range (p less than 0.01) were associated with serious fetal malformation.

Adult↗
PubMed2001

Polyhydramnios and arterio-arterial placental anastomoses may beneficially affect monochorionic twin pregnancies.

Our objective was to appraise whether an increased amniotic fluid pressure by polyhydramnios can beneficially affect monochorionic twins that are haemodynamically connected by arterio-venous plus arterio-arterial placental anastomoses. We assessed the effects of polyhydramnios in monochorionic twin placentas, combining (a) data from previous in vitro placental perfusion experiments in singleton term placentas under simulated normal and increased amniotic fluid pressures with (b) logical deduction from observations made in monochorionic twins. Our hypothesis is that in monochorionic placentas, an increased amniotic fluid pressure increases the placental microvascular resistance but not the resistance of placental chorionic plate arteries. Hence, an increased amniotic fluid pressure increases the microvascular resistance of the joint cotyledon, the arterio-venous resistance, but not the arterioarterial resistance. This proposed mechanism reduces arterio-venous but not oppositely directed arterio-arterial transfusion. Therefore, reversal of the normal direction of net foeto-foetal transfusion may develop, which will reduce the circulatory imbalance that evolved between the monochorionic foetal twins. In contrast, in monochorionic twins connected by unidirectional or bidirectional arterio-venous anastomoses reversal of the normal direction of net foeto-foetal transfusion will not occur. In conclusion, reversal of the normal direction of net foeto-foetal transfusion, induced by polyhydramnios, is protective against the onset and severity of twin-twin transfusion syndrome in monochorionic twins connected by arterio-venous plus arterio-arterial anastomoses, but not by unidirectional or bidirectional arterio-venous anastomoses.

Amniotic Fluid↗
PubMed1990

Polyhydramnios and associated maternal and fetal complications in singleton pregnancies.

During the 10-year period 1 January 1979 to 31 December 1988, polyhydramnios occurred in 537 patients with singleton pregnancies delivered at the Mercy Maternity Hospital. Associated maternal and fetal complications and the perinatal outcome of these pregnancies with polyhydramnios were analysed. In 248 of the 537 pregnancies (46%) in this group there were no maternal complications or fetal malformations and the perinatal mortality (PNM) rate was 2.4%. The PNM rate increased significantly to 13.1% when there was associated pre-eclampsia, 10% with gestational diabetes, and to 7.6% with miscellaneous complications. When polyhydramnios was associated with a fetal or placental malformation the PNM rate was 61.4%. The commonest malformations were central nervous system (31%), musculoskeletal (12%) and gastrointestinal system anomalies (10%). Placental chorioangioma occurred in two patients (0.4%) and both babies died. In women with low oestriol excretion (18% of the 455 tested) the PNM rate increased five times to 22.7%.

Congenital Abnormalities↗
PubMed1990

Acute polyhydramnios in twin pregnancies.

This paper reports the experience with acute polyhydramnios complicating twin pregnancies at the Mercy Maternity Hospital for the 10-year and 2-month period from January, 1979 to February, 1989 during which time there were 13 such cases, an incidence of 1 in 4,044 pregnancies. Acute polyhydramnios complicated 1.7% of all twin pregnancies. The perinatal mortality rate was 88.5% and accounted for 16.7% of the perinatal deaths in twins. No major fetal malformations were found. One case of acute polyhydramnios was successfully managed with ultrasonographically guided serial amniocenteses. The management of this rare condition is considered.

Acute Disease↗
PubMed1993

The significance of recurrent polyhydramnios.

A study of 30 women who had polyhydramnios in more than 1 pregnancy revealed that 8 of the 36 resultant pregnancies (22.2%) were associated with diabetes mellitus, 14 (37.8%) with fetal macrosomia, and the perinatal mortality was 16.2% (6 of 37). The incidence of major fetal malformations or abnormalities was 18.9% (7 of 37); 4 of the 6 deaths resulted from malformations (anencephalus (2), hydrocephalus (1), nonimmune hydrops (1)), and the other 2 deaths were from hyaline membrane disease associated with prematurity. Recurrent polyhydramnios occurred in 1 in 1,720 pregnancies. The onset was acute in 3, subacute in 2 and chronic in 31, the perinatal deaths in these categories being 2, 1 and 3 respectively. The risk of recurrent polyhydramnios is the risk of fetal malformation and premature delivery. The latter may be preventable by prompt therapy with indomethacin, and serial amniocentesis if this therapy fails.

Congenital Abnormalities↗
PubMed2007

Acute recurrent polyhydramnios: a combination of amniocenteses and NSAID may be curative rather than palliative.

Acute recurrent polyhydramnios is a rare occurrence characterized by a poor fetal outcome. This is a case report describing a 34-year-old woman presenting with acute recurrent polyhydramnios. Treatment with non-steroidal anti-inflammatory drugs (NSAID) and therapeutic amniocenteses was initiated immediately and resulted in a decreased amniotic fluid production from 30 weeks' gestation. Even after the discontinuation of NSAID treatment, the amniotic fluid production normalized, and the woman delivered a healthy boy at 39 weeks 2 days' gestation. Amniotic prolactin was measured at three occasions using an enzyme-linked immunosorbent assay. As in normal pregnancies, amniotic prolactin levels decreased by 80% from highest to lowest value in this case of resolving acute recurrent polyhydramnios.

Acute Disease↗
PubMed1983

Chronic idiopathic polyhydramnios: evidence for a defect in the chorion laeve receptor for lactogenic hormones.

Binding of human GH (hGH) to the lactogenic receptor of human chorion laeve has been compared in membrane preparations from normal pregnancies and those complicated by chronic idiopathic polyhydramnios. Specific binding of [125I]hGH was significantly lower (mean +/- SE, 1.64 +/- 0.28%; n = 5) in chronic idiopathic polyhydramnios than in normal pregnancies (2.93 +/- 0.4%; n = 16). Scatchard analysis data were consistent with a reduced lactogenic hormone receptor concentration being the explanation for this reduced hGH binding. By contrast, the specific binding of [125I]insulin to its receptor was unchanged when chorion laeve from hydramniotic pregnancies (7.29 +/- 1.98%; n = 4) was compared with that from normal pregnancies (8.63 +/- 1.35%; n = 7). We conclude that a lactogenic hormone receptor defect exists in the chorion laeve of pregnancies complicated by chronic idiopathic polyhydramnios. Such impaired binding for PRL may explain the development of excessive amniotic fluid volumes, which is characteristic of this complication of pregnancy.

Chorion↗
PubMed1991

Acute polyhydramnios associated with chorioangioma. A case report.

A case of acute polyhydramnios occurred at 26 weeks' gestation. Prenatal sonography demonstrated a placental chorioangioma. Acute polyhydramnios is clinically distinct from nonacute polyhydramnios and carries a high perinatal mortality rate. As in our case, fetal death often results from complications of prematurity.

Acute Disease↗
PubMed1990

[Electron microscopic study of the amniotic epithelium in polyhydramnios and oligohydramnios].

Totally 25 cases without any fetal anomaly, 10 with polyhydramnios, 10 with oligohydramnios and 5 with normal volume of amniotic fluid were taken into consideration. Their amnion covering the placenta and umbilical cord were examined under electron microscope. In the group with polyhydramnios the microvilli facing the amniotic cavity were denser in certain regions. The intercellular space was widened and the terminal bars were opened. Within the cells the number of vesicles were increased and there were large cysternas within these vesicles. It was postulated that the large cysternas found in the basal and apical parts of the cell were composed of macropinocytotic vesicles of the basal membrane. In the group with oligohydramnios the microvilli on the apical side were diminished. The intercellular space of the lateral side was narrowed. The electron density of the basal lamina was increased. The cellular structures were apparently reduced having just a few vesicles and lipid granules. Both in polyhydramnios and oligohydramnios the amniotic epithelium cells covering the placenta and umbilical cord are responsible for the transfer of the fluid into the amniotic cavity. Possibly they control the amount of fluid by reducing or increasing its passage.

Amnion↗
PubMed1998

Polyhydramnios as a prenatal symptom of the digeorge/velo-cardio-facial syndrome.

Prenatal diagnosis of the DiGeorge/velo-cardio-facial syndrome has become possible since it was recognized that this syndrome is caused by a submicroscopic deletion in chromosome 22q11. In a sporadic patient presenting a conotruncal heart defect and polyhydramnios, the del 22q11 was made prenatally by fluorescence in situ hybridization (FISH) after amniocentesis. Seven additional patients with a del 22q11 were identified, who presented during pregnancy with polyhydramnios. In one of them, unilateral hydronephrosis was present. These findings further add to a growing list of clinical presentations of a del 22q11 and suggest that in patients with polyhydramnios and a conotruncal heart defect or uropathy, fetal karyotyping should be complemented by FISH for a del 22q11.

Amniocentesis↗
PubMed1977

Primary pulmonary hypoplasia: report of a case with polyhydramnios.

We describe a case of extreme primary pulmonary hypoplasia. No other congenital anomalies and none of the conditions known to be associated with pulmonary hypoplasia were present. Pregnancy had been complicated by substantial polyhydramnios. The hypoplasia was due to a marked deficiency of the respiratory parenchyma in the presence of normal upper airways and bronchi. Virtually no parenchymal development had occurred and there were very few bronchioles, alveolar ducts, and alveoli. The changes differ from those seen in pulmonary hypoplasia secondary to congenital diaphragmatic hernia, bilateral renal agenesis, anomalies of the urinary outflow tracts, and malformations of the thoracic cavity, in which the pulmonary hypoplasia appears to be compressive in nature. While neither the etiology or pathogenesis of the pulmonary hypoplasia are apparent in this case, the presence of substantial polyhydramnios during pregnancy suggests the possibility that the developing lungs may offer an important surface area for reabsorption and recycling of constituents of amniotic fluid.

Adult↗
PubMed2000

Acute recurrent polyhydramnios and amniotic prolactin.

A 25 year-old patient in her third pregnancy presented with acute polyhydramnios at 24 weeks' gestation, which was the same time as in the two previous pregnancies. In both she had preterm premature rupture of membranes, preterm delivery and neonatal deaths. In the third pregnancy, amnioreductions combined with medical treatment resulted in the birth by Caesarean section of a normally formed live male at 31 weeks of pregnancy. Acute recurrent polyhydramnios is an extremely rare condition of unknown aetiology. We hypothesized that amniotic prolactin plays a role in this pathology. It was measured serially in amniotic fluid and high levels were found.

Acute Disease↗