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Chronic intravenous infusion of angiotensin 1 [182 micrograms/(kg.day)] into fetal lambs caused gross polyhydramnios. Infusions of comparable volumes of vehicle or lower concentrations of angiotensin 1 [48 micrograms/(kg.day)] did not cause gross polyhydramnios.
In human fetuses with hemolytic diseases such as erythroblastosis fetalis, hydrops fetalis or polyhydramnios often develops. The mechanism(s) that produces these fluid imbalances is unknown, although lactate concentrations have been reported to be elevated in hydropic human fetuses with erythroblastosis. In this study we explored the role of lactate in producing fetal fluid imbalances. In seven near-term fetal sheep, we infused 5 mol/L sodium lactate at a rate of 10 mmol/hr for 3 days. Fetal plasma lactate rose by 6.0 +/- 1.0 (mean +/- SE) mmol/L above control. Fetal plasma osmolality and Na+ increased slightly, Cl- decreased, and bicarbonate rose in proportion to the Cl- decrease. Fetal renal lactate excretion was 1.1 +/- 0.3 mmol/hr while Na+ excretion was 10.6 +/- 1.9 mEq/hr. Fetal urine flow increased by 1.9 +/- 0.4 L/day and the urine remained hypotonic relative to fetal plasma throughout the infusion. Amniotic fluid lactate and Na+ rose during the infusion period and remained elevated during a 24-hour recovery period. Amniotic plus allantoic fluid volume at autopsy was 5.3 +/- 0.8 L compared with a normal of 0.5 to 1.0 L. There was little evidence of fetal edema. In summary, a moderate sustained elevation in fetal plasma lactate concentration appears to be a powerful osmotic agent for fetal accumulation of fluid from the maternal compartment over a period of days. This may be the primary mechanism whereby hydrops fetalis or polyhydramnios develops in severely anemic human fetuses.
This paper presents a case of chorioangioma associated with polyhydramnios and premature delivery in which the placental tumour was diagnosed before delivery using ultrasound. In cases of polyhydramnios careful ultrasonic examination not only of the fetus, but also of the placenta, is recommended.
Fifteen consecutive cases of polyhydramnios (PH) out of a total number of 8806 deliveries performed between the 28th and the 41st week of pregnancy were investigated during the period from 1979 to 1985. Three cases of acute PH and 12 cases of chronic PH of which 10 were idiopathic were distinguished. From the time the clinical diagnosis was established until delivery, maternal serum and amniotic fluid alpha-fetoprotein (AFP) and prolactin (PRL), as well as maternal serum oestrogens (OT), placental lactogen (HPL), chorionic gonadotropin (hCG) and pregnancy-specific beta 1-glycoprotein (SP1), were studied. A very high increase of maternal serum AFP in all the cases of PH was observed (p less than 0.001) and was associated with the high degree of risk for obstetrical complications, while, on the other hand, amniotic fluid AFP was increased only in PH associated with congenital abnormalities of the fetus. Maternal serum PRL was not different from normal values (p greater than 0.2), while amniotic fluid PRL was lower in all the cases of chronic idiopathic polyhydramnios studied. The protein hormones and the oestrogens showed a discrepancy in their elevation, according to the kind of PH, the outcome of pregnancy, and the condition of the infant at birth.
Forty-one congenital malformations were found in 28 newborns in a group of 197 cases of chronic polyhydramnios in singleton pregnancies. Of these, a total of 61% (17/28) was antenatally diagnosed ultrasonically. Nine newborns (4.5%) had malformations of the central nervous system (CNS), 9 (4.5%) cardiovascular malformations, 8 (4.1%) musculoskeletal anomalies, 7 (3.6%) malformations of the urinary and reproductive system, 4 (2%) respiratory system anomalies and 3 (1.6%) anomalies of the gastrointestinal system. Chromosomal abnormalities were found in three cases. As the association of polyhydramnios with fetal congenital anomalies is quite high (14.2% in our series), it is imperative to make a major effort to antenatally detect as many cases as possible. This means that in the case of hydramnios the following are required: ultrasound examination by an expert, echo ultrasonography when no other abnormalities are detected, and maybe even a chromosomal analysis.
Polyhydramnios and premature labor at twenty-seven weeks secondary to an intrafetal renal cyst are described. Antenatal fetal cyst decompression successfully reversed the polyhydramnios and prevented premature delivery, resulting in a full-term healthy infant delivered vaginally at thirty-nine weeks. Urologic investigation postpartum revealed a probable congenital ureteropelvic junction obstruction.
OBJECTIVE: To test the hypothesis that amniotic fluid volume is increased in aquaporin 1 knockout mice. STUDY DESIGN: Transgenic mice deficient in aquaporin 1 protein were generated by targeted gene disruption, as described previously. After a cesarean section was performed, intact, individual gestational sacs were removed from the uterus and weighed. Amniotic fluid volume, osmolality, and fetal and placental weights were determined. Data were analyzed by a 1-way analysis of variance for ranks; Dunn's post hoc test was used to analyze significant trends. RESULTS: Analysis of 16 litters showed 35 wild-type, 52 heterozygote, and 33 aquaporin 1 knockout mice. The knockout mice had a greater volume of amniotic fluid and lower amniotic fluid osmolality than their wild-type and heterozygote counterparts. There were no significant differences in fetal or placental weights among the groups. CONCLUSIONS: Aquaporin 1 null fetuses produce a greater volume of more dilute amniotic fluid. Our findings show that aquaporin 1 water channels in fetal membranes may contribute to amniotic fluid volume regulation. We speculate that idiopathic polyhydramnios may be associated with a deficiency of aquaporin 1 channels in human fetal membranes. Transgenic aquaporin 1 knockout mice provide a unique animal of polyhydramnios.
Described is a pregnancy complicated by pregnancy-induced hypertension, polyhydramnios, and obstructive renal failure due to an overdistended uterus. A review of the literature disclosed that only five such cases have been reported previously. Fetal outcome was generally related to the duration of gestation at the onset of polyhydramnios.
We describe a case of congenital cystic adenomatoid malformation treated by thoracoamniotic shunting using a double-flower catheter. An ultrasound examination at 25 weeks' gestation revealed a cystic mass within the fetal thoracic cavity, hydrops and polyhydramnios. Thoracoamniotic shunting under ultrasound guidance using a double-flower catheter was performed at 27 weeks. The procedure not only decompressed the lung cyst but also improved the secondary physiological changes, i.e. mediastinal shift, hydrops and polyhydramnios. A 2438-g male neonate was delivered at 37 weeks with no respiratory problems and resection of the right lower pulmonary lobe was successfully performed 24 h after birth.
We present two cases of twin reversed arterial perfusion (TRAP) sequence complicated by severe polyhydramnios during the second trimester. Both cases were successfully managed at 27 and 26 weeks with ultrasound-guided intrafetal alcohol ablation of the acardiac twin and amniodrainage. The pump twins were delivered at 35 and 37 weeks, respectively, and both had uneventful postnatal courses. These cases suggest that, in the setting of severe polyhydramnios, prenatal intervention in TRAP sequence could certainly improve the otherwise poor prognosis of the pump twin. Targeting the main intra-abdominal vessel of the acardiac twin rather than its umbilical cord seems to be a good alternative in the prenatal treatment of these cases. The option of percutaneous intrafetal alcohol injection is widely available and less invasive, simpler and easier to perform than recently advocated endoscopic techniques.
Polyhydramnios and oligohydramnios in twin gestation is most often caused by twin-twin transfusion syndrome. Presented is a monozygotic twin pair with polyhydramnios and oligohydramnios, in which both twins had glomerulocystic kidney disease of differing severity. The more severely affected donor twin died of renal failure in the neonatal period. The surviving twin is well following unilateral nephrectomy. This case illustrates the varied spectrum of pathology in glomerulocystic kidney disease.
OBJECTIVE: In the ovine fetus subjected to 24 hours of hypoxia, urinary flow is normal within a few hours from the onset of hypoxia and there is a maintained inhibition of swallowing. We hypothesized that 4 days of fetal hypoxia would lead to polyhydramnios. STUDY DESIGN: Five late-gestation fetal sheep were subjected to hypoxia for 4 days and 7 other late-gestation fetal sheep served as time control animals. Fetal hypoxia was produced on postsurgical days 5 through 9 by continuous intratracheal nitrogen insufflation to the ewe. On days 3, 5, 7, and 9 after surgery, amniotic fluid volume, fetal urinary flow rate, and the compositions of maternal and fetal blood, amniotic fluid, and fetal urine were measured. A 3-factor analysis of variance was used for statistical analysis. RESULTS: During the period of experimental hypoxia the mean (+/-SE) fetal PaO(2) was 16.0 +/- 0.6 mm Hg, versus 21.2 +/- 0.7 mm Hg in control sheep (P <.001). Fetal hypoxia was associated with increased urinary flow on days 7 and 9, averaging 1410 +/- 310 and 2101 +/- 345 mL/d, respectively, versus 585 +/- 92 and 699 +/- 78 mL/d, respectively, in control animals (P <.001). Amniotic fluid volume was unchanged with time and averaged 960 +/- 159 mL in hypoxic fetuses on postsurgical days 7 through 9 and 851 +/- 130 mL in control animals (P =.60). Fetal blood lactate increased in the hypoxic animals, averaging 3.4 +/- 2.1 mmol/L versus 1.6 +/- 0.3 mmol/L in control animals (P =.02). Fetal urinary excretions of sodium, potassium, chloride, and lactate increased significantly during hypoxia, by 170% to 400%. CONCLUSION: Four days of nitrogen-induced hypoxia in the ovine fetus resulted in excess fetal urinary flow approximating 1000 mL/d greater than normal without the development of polyhydramnios. Because amniotic fluid volume did not change and hypoxia is a known inhibitor of fetal swallowing, we speculate that intramembranous absorption of amniotic water, electrolytes, and lactate increased.
The phenotypical characteristics in 20 children with achondroplasia were examined in relation to the occurrence of polyhydramnios. A history of polyhydramnios (9 of 20 cases) was associated with a lower height (SD) (P <.05), more severe shortening of the lower segment and upper limbs (P =.0001), and higher frequency of left-handedness (P =.0081).
Neu-Laxova syndrome is a rare group of congenital malformations including intrauterine growth retardation (IUGR), microcephaly, central nervous system alterations, facial abnormalities, ichthyosis, limb abnormalities, generalized edema, polyhydramnios, and perinatal death. Thirty cases have been identified since the publication of the first two cases and only five of them had a prenatal diagnosis. The earliest diagnosis in a published case was at week 32 of gestation. This study illustrates that the detection of the syndrome during the second trimester of gestation is possible, with emphasis on the detection of the early appearance of polyhydramnios and the association of the syndrome with the Arabic ethnic group.
The appearances of the amnion from two patients with polyhydramnios and two patients with oligohydramnios are described. In polyhydramnios the amnion showed a normal incidence of all the four patterns found in normal amnion at term and no abnormal features were noted. In oligohydramnios, two of four normal patterns predominated and intercellular canals were sparse.
Eight patients with acute polyhydramnios were encountered in 31 103 pregnancies, an incidence of 1 in 3888. All patients with acute polyhydramnios had monozygous twin pregnancies and 14 of the 16 infants were normal. The condition occurred in the second trimester and usually ended in premature delivery within a few days. The perinatal mortality was 100 per cent and accounted for 14.9 per cent of the perinatal mortality in twins.
Prenatal administration of indomethacin for the treatment of polyhydramnios at 27 weeks' gestation resulted in the rapid restoration of normal amniotic fluid volume. However, after 16 days therapy, fetal echocardiography revealed constriction of the fetal ductus arteriosus which did not reverse during the 17 days after the therapy was discontinued. The constriction resulted in right heart failure but no long-term effects on the infant after birth. Indomethacin is a powerful treatment for polyhydramnios but its use requires close monitoring of the fetal heart.
OBJECTIVE: Our aim was to evaluate the consequences of polyhydramnios on maternal plasma volume and maternal serum aldosterone and atrial natriuretic peptide (ANP) concentrations in monochorionic twin pregnancies complicated by twin-to-twin transfusion syndrome (TTTS). METHODS: The maternal plasma volume, ionograms as well as plasma ANP and aldosterone concentrations were compared in normal monochorionic diamniotic twin pregnancies and in TTTS. RESULTS: The maternal plasma volume was normal in TTTS despite severe polyhydramnios. The plasma aldosterone concentration was higher in pregnancies complicated by TTTS. CONCLUSION: The high plasma aldosterone concentration is likely to maintain normal plasma volume despite progressive extravascular volume enhancement. This suggests that TTTS is present early in pregnancy as a chronic phenomenon starting before its clinical expression and may trigger compensatory maternal hyperaldosteronism.