Urinary tract anomalies and dysfunctional voiding: a spectrum dictated by the influence of amniotic pressure upon fetal urodynamics.

The etiologic basis of urinary tract anomalies and dysfunctional voiding largely remain unknown. However, the travel of urine from renal pelvis into the amniotic cavity under the pressures exerted by amniotic fluid satisfactorily explains the etiologic basis. Amniotic pressure is affected by the changes in maternal intraabdominal pressure. The intraabdominal pressure of the fetus is also dictated by the amniotic pressure. Amniotic pressure compresses the urethra throughout the length, and may increase both bladder leak point pressure and urethral resistance. Furthermore, the urine is propelled against amniotic pressure. These factors closely simulate outflow obstruction. Since the pressure within the bladder with minimal urine content reflects the intraabdominal pressure, intravesical pressure is also elevated during fetal life. Additionally, elevated intravesical pressures impair ureteral drainage. The compressive effect exerted by fetal intraabdominal pressure upon ureters, further elevate the pressure within the renal pelvis. While forwarding the urine against these pressures may result in anomalies of the urinary tract, the increased work load of the detrusor may act as a state of injury that forms the basis of dysfunctional voiding.