ABSTRACT
OBJECTIVE: To find association between fetal urine production rate (FUPR) and fetal inflammatory response syndrome (FIRS) in preterm premature rupture of membranes (PPROM). METHODS: A prospective cohort study of 70 pregnant women with PPROM at 28-34 weeks of pregnancy was conducted. FUPR was calculated by performing serial fetal bladder volume measurements ultrasonographically and was repeated weekly until delivery. After delivery, cord blood interleukin-6 (IL-6) levels were measured. Placental tissue histopathology was performed and neonatal outcomes were noted. RESULTS: Out of 70 recruited patients with PPROM, 44 had evidence of FIRS (62.86%). Mean FUPR at the time of delivery was significantly reduced in neonates with evidence of FIRS compared with the Non-FIRS group (13.89 ± 8.06 ml/h vs. 25.89 ± 4.94 ml/h). Out of 41 patients with reduced FUPR, 39 neonates had FIRS whereas only five out of 29 neonates with normal FUPR had FIRS (P < 0.001). Severe neonatal morbidity was found in 24 out of 41 (58.54%) neonates with reduced FUPR prenatally. The occurrence of respiratory distress syndrome, necrotizing enterocolitis, and sepsis was significantly high in neonates with reduced FUPR. CONCLUSION: Reduced FUPR is strongly associated with FIRS in cases of PPROM and hence can be used as an early predictor of adverse neonatal outcomes.
Subject(s)
Chorioamnionitis , Fetal Membranes, Premature Rupture , Biomarkers , Female , Fetal Diseases , Gestational Age , Humans , Infant, Newborn , Interleukin-6 , Placenta/pathology , Pregnancy , Prospective Studies , Systemic Inflammatory Response SyndromeABSTRACT
OBJECTIVES: To evaluate whether fetal urine production measurement is useful for predicting adverse outcomes in patients with uteroplacental insufficiency. METHODS: We enrolled patients with uteroplacental insufficiency at 24 to 40 weeks' gestation and normal pregnancies matched for gestational age and divided them into 3 groups according to perinatal outcomes: group 1 (n = 141), a control group of normal pregnancies; group 2 (n = 29), uteroplacental insufficiency without adverse outcomes; and group 3 (n = 18), uteroplacental insufficiency with adverse outcomes. An adverse outcome was defined as 1 or more of the following: (1) cesarean delivery because of fetal distress; (2) admission to the neonatal intensive care unit; (3) cord arterial pH less than 7.15 at birth; and (4) low 5-minute Apgar score (<7). The fetal urine production rate was obtained by serial bladder volume measurement using virtual organ computer-aided analysis. For bladder volume determination, we scanned the bladder in the 3-dimensional mode and defined the bladder surface contour in the reference plane, repeating the rotation of the reference plane with an angle of 30° and determining the surface contour on each plane. Statistical methods, including the Mann-Whitney U test, Fisher exact test, χ(2) test, and Kruskal-Wallis analysis of variance, were used. RESULTS: Group 3 had a lower mean fetal urine production rate than groups 1 and 2, whereas the urine production rate was not different between groups 1 and 2 (group 1, 49.0 mL/h; group 2, 59.4 mL/h; group 3, 20.7 mL/h; P < .001 between groups 1 and 3 and between groups 2 and 3). This difference between groups 2 and 3 remained significant after adjusting for the amniotic fluid index, umbilical artery Doppler pulsatility index, and presence of fetal growth restriction. CONCLUSIONS: Uteroplacental insufficiency cases with adverse perinatal outcomes had a lower fetal urine production rate than those without adverse outcomes. This difference might be used to predict adverse perinatal outcomes in uteroplacental insufficiency.