Fetal megavesica is a rare syndrome caused by morphological or functional obstruction of the fetal urethra. It is the textbook example of a single cause producing a sequence of changes in fetal development.
Fig.1. Horizontal section through the fetal abdomen at 16+5 weeks pregnancy, showing fetal megavesica and bilateral dilatation of the renal pelvis.
Fetal megavesica is a rare syndrome caused by morphological or functional obstruction of the fetal urethra. It is the textbook example of a single cause producing a sequence of changes in fetal development. In this case dilatation of the lower and upper urinary tract, oligohydramnios and pulmonary hypoplasia may result and lead to the prune belly sequence (PBS), defined by the triad of absent or hypoplastic abdominal musculature, urinary tract anomalies and cryptorchidism (1)
Clinical severity depends on the time of intrauterine diagnosis (2,3). The earlier the diagnosis the higher the embryofetal mortality rate.
Fetal renal function has been monitored by fetal urinanalysis in the second half of pregnancy: in addition to electrolytes and osmolarity (4,5,6) the parameters identifying fetuses likely to benefit from intrauterine therapy include urine and amniotic fluid microprotein (7,8,9). The only report which showed gestational age dependence of fetal urine electrolytes and osmolarity assessed only four fetuses at 17–20 weeks (5). Recently, successful treatment of fetal megavesica in the first half of pregnancy has been published (10).
A 32-year-old Gravida 4, Para 3 was referred for fetal sonography at 16+4 weeks post menstrual age (16+4 wks p.m.). Family history and patient history were uneventful. She was sure of her dates, and a vaginal ultrasound at 10+3 weeks was consistent with these dates. The patient denied having any regular medication or problems during the ongoing pregnancy.
Prenatal diagnostic findings
Fetal ultrasound at 16+5 wks p.m. gave the following results:
Active fetus with head and limb measurements according to dates (BPD 40mm, femur 21mm). Amniotic fluid was normal. The fetal abdomen was markedly distended by a cystic mass measuring 35x36x39mm, which led to dilatation of the fetal upper urinary tract. Therefore, fetal megavesica was diagnosed (Fig. 1).
The fetal urinary bladder was emptied by transabdominal intrauterine vesicocentesis and 25ml clear urine was collected.
Urinanalysis gave the following results:
Sodium: 77 mmol/lChloride: 75 mmol/lOsmolarity: 169 mosm/lÃ2-Microglobulin: 4.9 mg/l
Fetal karyotyping performed with fetal urine gave a numerically and structurally normal male result.
Six days after vesicocentesis, the urinary bladder was of normal size but showed marked muscular thickening (Fig.2). Surprisingly, there was no further overdistension of the fetal bladder and amniotic fluid remained normal throughout the further course of pregnancy. The only sign suggestive of an urinary tract problem was bilateral dilatation of fetal renal calices measuring 8mm at 36 wks. p.m. (Fig. 3).