In recent years, there has been increasing recognition of the clinical importance of amniotic fluid disorders, both as a reflection of underlying fetal anomalies and as independent risk factors for adverse pregnancy outcomes. Yet, despite decades of investigation, the regulation of amniotic fluid volume and composition remains incompletely understood. This results in part from the complexities inherent in amniotic fluid dynamics: an enigmatic interaction of several sites of fetal fluid excretion and acquisition. As detailed in the article by Brace, throughout the second half of gestation the fetus excretes significant volumes of urine to the amniotic cavity as well as proportionately smaller volumes of lung fluid. Fetal resorption of amniotic fluid occurs primarily by fetal swallowing of amniotic fluid, and in sheep and perhaps in humans, to a lesser degree by intramembranous absorption. Therefore, fetal swallowing represents the major route of amniotic fluid resorption during intrauterine life.
Of all the known major sites of human fetal-amniotic fluid exchange (urine, lung, swallowing), the measurement and regulation of swallowing is the least well understood. Animal models have long been available to quantify fetal urine and lung liquid production, and human fetal urine flow has been quantified by ultrasound (US) methods. Until recently, both human and animal fetal swallowing have been assessed only indirectly via disappearance of labeled tracers from amniotic fluid, methods that do not permit accurate determinations of swallowed volume or any means to assess short term regulatory mechanisms. The development of an ovine fetal model combining computer analysis of esophageal electromyograms and ultrasonic flow probe recording has yielded important information regarding the regulation of fetal swallowing activity and volume swallowed. By combining animal and human data, this article will present an overview of the authors' current knowledge of fetal swallowing and the interaction of swallowing and amniotic fluid volume homeostasis.
University of California Los Angeles, School of Medicine, Department of Obstetrics and Gynecology Harbor-UCLA Medical Center, Torrance, California
Correspondence: Michael G. Ross, MD, MPH, University of California Los Angeles, School of Medicine, Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, 1000 West Carson Street, Torrance, CA 90502.
Supported in part by March of Dimes Birth Defects Foundation Grants and National Institutes of Health Awards HL 40899 and DK 43311.