Physiology of Amniotic Fluid Volume Regulation

Amniotic fluid surrounds the fetus during intrauterine development. This fluid provides several important benefits to the fetus in that it cushions the fetus against trauma, has antibacterial properties to lessen infections, and functions as a reservoir that may provide a short-term source of fluid and nutrients to the fetus. In addition, at least moderate amounts of amniotic fluid are required for the fetal musculoskeletal system to develop normally, for gastrointestinal system development, and for the fetal lungs to develop and mature as needed in preparation for the breathing of air that must commence abruptly at birth. Hence, it is not surprising to find that oligohydramnios (too little amniotic fluid) and polyhydramnios (too much amniotic fluid) are associated with increased rates of perinatal morbidity and mortality.1,2 Although fetal congenital anomalies and a variety of disease states such as fetal infection or anemia are often associated with oligohydramnios or polyhydramnios, many times the fetus is normal except for the aberration in amniotic fluid volume (AFV). Even with a normal fetus, abnormal amniotic fluid volumes are associated with increased perinatal morbidity and mortality. Hence, it is important to understand the physiological regulation of AFV so that appropriate therapies can be developed to restore AFV to its normal range and thereby, reduce the rates of fetal and neonatal compromise caused by oligohydramnios or polyhydramnios. This article reviews the changes in AFV that normally occur across gestation, the multiple pathways that allow water and solutes to enter and leave the amniotic compartment, and what is known about the flow rates through each of these pathways. These flows are then discussed relative to the regulation of AFV. The discussion is limited to the latter half of gestation because little is known about amniotic flows during early gestation. Finally, the widely accepted concept that chronic fetal hypoxia causes oligohydramnios is reviewed with the result that chronic fetal hypoxia appears to cause polyhydramnios rather than oligohydramnios.