Objective To characterize amniotic pressure (AP) in pregnancies with normal amniotic fluid volume. Design Observational study, mainly cross‐sectional. Setting Fetal medicine unit within a tertiary referral hospital. Subjects Patients undergoing transamniotic invasive procedures in whom amniotic fluid volume was subjectively assessed as normal on ultrasound. Those beyond 16 weeks with a deepest vertical pool on ultrasound <3.0 or >8.0 cm were excluded. Overall 194 pregnancies were studied on 232 occasions between 7 and 38 weeks gestation. Interventions Manometry readings referenced to the top of the maternal abdomen were obtained via a fluid‐filled line from the needle hub and either connected to a pressure transducer (n= 190) or held vertically against a ruler (n−42). Main outcome measures AP in mm Hg, AP corrected for gestational age (z scores), semi‐quantitative ultrasonic indices of amniotic fluid volume, clinical variables. Results AP in singleton pregnancies increased with advancing gestation (P<0.001), and the sigmoid‐shaped regression curve plateaued in the mid‐trimester. AP z scores were not influenced by volume‐related phenomena such as twin gestation, the deepest vertical pool, or amniotic fluid index, nor by maternal age, parity, gravidity, fetal sex, or subsequent spontaneous preterm delivery. Conclusions These findings suggest that AP is not principally determined by intrauterine volume. We speculate that AP, which reflects change in uterine tension as a function of radius, may instead be determined by gestation‐specific anatomical and hormonal influences on gravid uterine musculature. A reference range for AP has been constructed for use in amnioinfusion and amnioreduction procedures.

Thirteen fetuses (five twin, one triplet) were compromised by fetofetal transfusion syndrome in six pregnancies, five in the mid trimester, and one in the third trimester. This diagnosis, which was suspected because of ultrasound findings of discordant growth, discordant amniotic fluid volumes, concordant external genitalia, and monochorial placentation, was confirmed postnatally in each. Nine fetuses underwent blood sampling to aid diagnosis and assessment of fetal welibeing. In contrast to fetofetal transfusion syndrome investigated postnatalHy, a difference in haemoglobin concentration of 50 g/l or more in utero was found in only one pregnancy, which was near term, although ali had fetal erythroblastaemia and a difference in weight of 20% or more. In vivo confirmation of shared circulation was achieved in two pregnancies by transfusing adult Rh negative red celis into the smaller fetus and then detecting them by Kleihauer testing in blood aspirated from the larger. Invasive procedures also yielded information on fetal blood gas measurements (acidaemia in four and hypoxaemia in six) and amniotic pressure (raised in two). We suggest that comparison of haemoglobin concentrations is inaccurate in fetofetal transfusion syndrome in utero, the diagnosis of which may necessitate detection of a shared circulation using a marker such as adult red celHs.

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Urine was aspirated on two consecutive days from the dilated bladder of nine fetuses with lower urinary tract obstruction. Gestational age ranged from 17 to 35 weeks. Renal dysplasia was diagnosed histologically in four fetuses, whereas the other five had normal renal histology or only partial dysplasia. Urinary sodium (Na+) and osmolality (Osm) decreased significantly in the second urine sample 1 day after bladder emptying (median decrease: Na+ = -11.3 per cent; Osm = -13.3 per cent). Although there were no significant differences between fetuses with or without renal dysplasia, normalization of an initially raised urine Na+ concentration occurred at the second sample in a fetus with partially normal renal histology, thus correcting a false-positive diagnosis of dysplasia. Bladder pressure was measured at the time of the first urine sampling in seven fetuses and in a further eight with bladder outlet obstruction undergoing a single urine aspiration at 18-28 weeks. Bladder pressure was increased above the reference range in 8 of 15 fetuses with urinary obstruction, but there was no correlation between pressure and the degree of impairment of renal function. Although no conclusive clinical guidelines can be drawn from this study for the evaluation of fetal renal function, these findings suggest that, in lower urinary tract obstruction, tubular reabsorption is impeded by the standing pressure in the urinary tract and that improvement of renal function may occur following relief of obstruction.