Amniotic fluid dynamics.

Amniotic fluid was once considered to be a stagnant pool, approximately circulating with a turnover time of one day. Adequate amniotic fluid volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Even though different hypotheses have been advanced on the mechanisms regulating this turnover, the inflow and outflow mechanism that keeps amniotic fluid volume within the normal range is not entirely clear. Regulatory mechanisms act at three levels: placental control of water and solute transfer; regulation of inflows and outflows from the fetus; and, maternal effect on fetal fluid balance. Amniotic fluid is 98-99% water. The chemical composition of its substances varies with gestational age. When fetal urine begins to enter the amniotic sac, amniotic osmolarity decreases slightly compared with fetal blood. After keratinization of the fetal skin, amniotic fluid osmolarity decreases further with advancing gestational age. The low amniotic fluid osmolarity, which is produced by the inflow of markedly hypotonic fetal urine, provides a large potential osmotic force for the outward flow of water across the intramembranous and transmembranous pathways. Within certain limits, amniotic fluid mirrors the metabolic status of the fetoplacental unit; for that reason, a study of its components and their respective variations in the different weeks of pregnancy provides useful indications, both for a correct assessment of fetal maturation and for an evaluation of kidney function parameters and placental insufficiency.

Increased urinary flow without development of polyhydramnios in response to prolonged hypoxia in the ovine fetus.

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.

Indomethacin therapy and fetal urine production in twins with polyhydramnios.

Indomethacin has been used in twins with polyhydramnios to decrease amniotic fluid volume. Under therapy, a marked reduction of both fetuses' urine production has been demonstrated within 24 hours concomitant with maternal symptomatic relief. Discontinuation of therapy was associated with a rapid increase in fetal urine production. The clinical observation indicates that the benefit of indomethacin in prolonging such pregnancies is most probably the result of relief of polyhydramnios through decreased fetal urine production.

Fetal urine production in normal twins and in twins with acute polyhydramnios.

In twelve twin pregnancies with normal amniotic fluid volume, the urine output of each twin was lower than in fetuses from singleton pregnancies, and the combined urine output of both twins was between the 50th and 95th centile for singletons. In three twin pregnancies at 21-24 weeks of gestation with acute polyhydramnios, presumed to be due to the twin-twin transfusion syndrome, the urine output of the smaller fetus was zero and that of the larger was above the 95th centile for normal singleton pregnancies. These three pregnancies were managed by repeated amniocenteses and rapid drainage of large volumes of amniotic fluid. With advancing gestation, there was a tendency for normalization of urine output in the twins.

Amniotic fluid glucose values in normal and abnormal pregnancies.

Glucose values were determined in 102 urine samples of newborn infants and in 2295 amniotic fluid (AF) samples of women between the 14th and 42nd week of pregnancy. One thousand, six hundred fifty-five of the AF samples derived from normal pregnancies, 50 from pregnancies with fetal malformations, 115 from cases of hydramnios, 246 from pregnant women with an abnormal oral glucose tolerance test, and 230 from insulin-dependent diabetics. Mean AF glucose concentration rises slightly between the 14th and 17th week of pregnancy, decreasing from 46 to about 16 mg% at the end of pregnancy. In cases of fetal malformations, 68% of the glucose levels was below the tenth percentile of normal values. Hydramnios showed no deviation from normal values. In patients with abnormal glucose tolerance, AF glucose increased by a total of 42% and by 67% in fetal hyperinsulinism. Insulin-dependent diabetics had glucose values elevated by a total of 77% and by 106% in fetal hyperinsulinism. The AF glucose profile reflects the level of maternal blood glucose that is transported to the fetus and excreted in the fetal urine as a major source of glucose in AF.