Amniotic Fluid Dynamics

Volume of Amniotic Fluid

In the first trimester of pregnancy the amnion does not contact the placenta or decidua, and the amniotic cavity is surrounded by the fluid-filled exocoelomic cavity. The exocoelomic fluid participates in the exchange of molecules between mother and fetus; the function of the AF at this early gestational period is uncertain. Importantly, coelomic fluid may contain antioxidants and proinflammatory cytokines and cytokine receptors that may influence placental function and fetal and placental development. ^, By the end of the first trimester of human gestation the exocoelomic cavity progressively obliterates, and the amniotic cavity is the only significant deposit of extrafetal fluid.

AF volumes have been directly measured in the first half of pregnancy, during which time the volume increases logarithmically. AF volumes were first estimated in the latter two-thirds of human pregnancies through the use of dye dilution techniques. ^, These original quantitative findings have been supported by semiquantitative measurements of AF volume performed with ultrasound ( Fig. 4.1 ).

Each of these methods demonstrates that AF volume increases progressively between 10 and 30 weeks of gestation. Typically, volume increases from less than 10 mL at 8 weeks to 630 mL at 22 weeks and 770 mL at 28 weeks of gestation. After 30 weeks the increase slows, and AF volume may remain unchanged until 36 to 38 weeks of gestation, when it tends to decrease. As a pregnancy proceeds past the due date, AF volume decreases sharply, averaging 515 mL at 41 weeks. Subsequently, there is a 33% decline in AF volume per week, consistent with the increased incidence of oligohydramnios in postterm gestations.

The rate of change of AF volume depends on the gestational age. Total AF volume increases at a rate of 10 mL/wk at the beginning of the fetal period, increasing to 50 to 60 mL/wk at 19 to 25 weeks’ gestation and then decreasing until the rate of change equals zero (i.e., volume is at maximum) at 34 weeks. Thereafter total AF volume falls, with the decrease averaging 60 to 70 mL/wk at 40 weeks’ gestation. Although the complete mechanisms that produce these alterations in AF volume throughout gestation are unclear, it is important to note that, when expressed as a percentage, the rate of change decreases consistently throughout the fetal period. Therefore the decrease in AF volume near term represents a natural progression rather than an aberration.

The volume of AF may be dramatically altered in pathologic states. Excessive AF volume (polyhydramnios) may total many liters, and the volume of AF in conditions of reduced fluid (oligohydramnios) may be near zero. Fetal anatomic abnormalities such as renal agenesis or esophageal atresia may affect the normal processes for production and resorption of AF, respectively, leading to abnormal AF volumes. In addition, transient changes such as maternal dehydration or fetal anemia may alter AF flow and therefore AF volume. AF volume abnormalities may also occur without apparent cause. Abnormalities of AF volume in general have been associated with poorer perinatal outcomes. Specific issues are discussed elsewhere in the text.

Production and Composition of Amniotic Fluid

The AF in the first trimester of pregnancy has rarely been the subject of study. It appears that human AF in the first trimester is isotonic with maternal or fetal plasma but contains minimal protein components. First-trimester AF also demonstrates an extremely low oxygen tension and an increased concentration of sugar alcohols, the product of anaerobic metabolism. In the second half of pregnancy the human fetus produces dilute urine, which is a major component of AF, causing the AF composition to diverge from that of serum. In particular, human AF osmolality decreases by 20 to 30 mOsm/kg with advancing gestation to levels approximately 85% to 90% of maternal serum osmolality. In the same period, AF urea, creatinine, and uric acid increase, resulting in AF concentrations of urinary byproducts two to three times higher than in fetal plasma.

It is thought that early AF arises as a transudate of plasma, either from the fetus through nonkeratinized fetal skin or from the mother across the uterine decidua or the placenta surface or both; however, the actual mechanism is unknown. Production and resorption of AF have been extensively studied in the latter half of pregnancy, most commonly in the sheep model, though recent ultrasound studies have provided insights into human fetal urine production and swallowed volumes. Evidence suggests that the entire volume of AF turns over on a daily basis, making this a highly dynamic system. The volume of AF is influenced by a complex interplay of productive and absorptive mechanisms ( Fig. 4.2 ). These mechanisms act to maintain AF volume, and there is some evidence that they may be regulated to normalize AF volume in pathologic conditions.

The major contributors to AF volume in the latter portion of pregnancy are fetal urine and fluid produced by the fetal lung. Minor contributors are transudation across the umbilical cord and skin and water produced as a result of fetal metabolism. Although some data on these processes in the human fetus are available, the bulk of the information about fetal AF circulation derives from animal models, primarily the sheep.