INTRODUCTION
Preterm premature rupture of membranes (PPROM) is defined as spontaneous rupture of membranes before the onset of uterine contractions and before 37 weeks period of gestation. It complicates about 2-4.5% of all deliveries but is responsible for 40% of preterm deliveries and 10% of perinatal mortality1,2. Conservative management for PPROM less than 34 weeks of gestational age is currently the accepted modality of treatment in the absence of chorioamnionitis. The rationale of conservative management in PPROM focuses mainly on prolonging the period of gestation and fetal lung maturation versus the increasing risk of potentially severe complications from maternal and neonatal infections with longer latency period. The maternal complications associated with PPROM include subclinical and clinical chorioamnionitis, premature placental separation and postpartum endometritis. Fetal complications include premature birth, infection and fetal distress due to umbilical cord compression or placental abruption.
Numerous biomarkers have been studied to detect early maternal and fetal infection, but none have been proven to be accurate in predicting the same. Early infection is not reliably predicted by investigations such as erythrocyte sedimentation rate (ESR), total leukocyte count (TLC), neutrophil count or vaginal bacterial cultures. Clinical signs like fever, fetal or maternal tachycardia appear late. Amniotic fluid culture is the most reliable test but is of limited value because of its invasive nature. Hence alternative noninvasive tests for early identification of chorioamnionitis are needed for women with PPROM.
In PPROM, micro-organisms in amniotic cavity may reach fetus and stimulate the synthesis of pro-inflammatory cytokines3. This leads to development of acute phase response which is almost similar to systemic inflammatory response syndrome (SIRS) seen in adults. The fetal response to intrauterine infection is termed as fetal inflammatory response syndrome (FIRS). FIRS is characterized by multi-organ involvement including the hematopoietic system, thymus, adrenal glands, heart, lungs, brain, skin, and kidneys4. It is defined by elevated IL-6 levels in cord blood or presence of characteristic histologic features of placenta which includes funisitis and chorionic vasculitis.
SIRS is characterized by redistribution of blood flow to more vital organs like heart and brain and thereby decreasing the blood supply to kidneys and hence decreased urine production. Therefore, we hypothesise that there might be a redistribution of blood flow in fetuses with FIRS with reduced blood supply to fetal kidneys, similar to that seen in SIRS. We propose to study fetal urine production rate (FUPR) measured as an early marker of fetal inflammatory response syndrome (FIRS) in patients with PPROM, so that the cases of FIRS can be picked up antenatally and timely intervention in the form of delivery can be undertaken to optimise maternal and neonatal outcomes.