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.