When excessive amniotic fluid (polyhydramnios or, simply, hydramnios) is present, there are increased risks of complications for both mother and baby. Some of the risks to the baby are obvious if there is an identifiable etiology for the hydramnios, such as maternal diabetes, multiple gestation, congenital malformation, chromosomal abnormality, severe fetal anemia secondary to isoimmunization or Parvovirus B19, neuromuscular disorders, or congenital infection. Indeed, past reviews confirm the risk for poor outcomes when an etiology is found. For example, Stoll and colleagues (Community Genet 1999;2:36-42) identified 290 cases of polyhydramnios in 225,669 consecutive pregnancies and diagnosed congenital malformations prenatally in 44.5% of the cases. Among these, 10.3% of the infants were stillborn, 41% had more than one malformation, 14.5% had a chromosomal abnormality.
Similarly, Biggio and colleagues (Obstet Gynecol 1999;94:773-7) compared 370 women with singleton pregnancies beyond 20 weeks' gestation and hydramnios with 36,426 controls who had normal amniotic fluid volumes. “The perinatal mortality rate in all women with hydramnios was 49 per 1000 births, compared with 14 per 1000 births in the control group (P < .001). Women with hydramnios had 25 times more anomalies than controls (8.4% versus 0.3%; P < .001)…the cesarean rate was three times higher in women with hydramnios compared with controls (47.0% versus 16.4%; P < .001).” Interestingly, in their study, the increased risks were concentrated in the nondiabetic women with hydramnios.
However, as we mentioned previously, 50-60% of hydramnios is idiopathic (without an identifiable cause). So the question remains, are there increased risks to the baby if no identifiable etiology for the hydramnios is found? In other words, does the excessive fluid alone seem to contribute to or be associated with poor perinatal outcome. The scientific literature would indicate that it does. For example, Magann and colleagues (Obstet Gynecol Surv 2007;62:795-802) recently presented an extensive review dating back more than 50 years and found that idiopathic hydramnios was linked “to fetal macrosomia (in the absence of diagnosed maternal diabetes), an increase in the risk of adverse pregnancy outcomes, and a 2- to 5-fold increase in the risk of perinatal mortality.” So, what are some of the pregnancy risks, irrespective of the cause of the excessive amniotic fluid.
Common risks secondary to overdistention of the uterus include abdominal pain, premature labor and delivery, and premature rupture of membranes. There is also an increased risk of uterine rupture, although this is rare in the absence of a previous cesarean delivery or other operative uterine procedure. In the presence of severe hydramnios, especially in a woman of small stature, overdistention of the uterus can put so much pressure on the mother’s diaphragm that she has difficulty breathing in ANY position and maternal cardiorespiratory decompensation may occur under these circumstances.
Often under these circumstances, placental perfusion is also reduced, the baby develops relative placental insufficiency, and as a consequence of the baby’s (and probably the placenta’s) unhappiness, the mother develops preeclampsia. Doppler flow studies have shown a greater incidence of fetal blood flow ‘redistribution’ (an indirect indicator of ‘placental insufficiency’) in the presence of hydramnios and this is most likely due to the excessive pressure on the umbilical vessels and the placenta itself resulting in decreased fetal perfusion. Indeed, any fetal condition associated with hydramnios that places the baby in a ‘distressed’ situation, particularly, severe fetal anemia and other causes of hydrops fetalis, increases the risk for maternal preeclampsia.
Indeed, the very first obstetrical patient I ever saw die (30 years ago) had a baby with hydrops secondary to severe maternal Rh-isoimmunization and polyhydramnios. An attempt was made to transfuse the baby in utero and afterwards she was sent to the antepartum unit for monitoring. I noticed her blood pressure was elevated and checked her urine to also find 4+ proteinuria. I remember notifying her attending physician ( I was a second year resident at the time) that she appeared to be developing severe preeclampsia and was brushed off that this was simply the ‘stress of the procedure that she had just been through.’ When I came in to round on her the next morning, she was not in her bed and when I asked if she had been discharged, I was told that she had had a hypertensive crisis in the middle of the night, a cerebrovascular accident, and could not be resuscitated. The occurrence of severe maternal preeclampsia in the presence of fetal hydrops has come to be known as “mirror syndrome” in which the mother’s condition reflects (and is probably driven by) the dire fetal condition (Vidaeff, et al. J Reprod Med 2002;47:770-4). Needless to say, there are some things one NEVER forgets!
Hydramnios can also cause several complications related to the onset and course of labor. Too much fluid often leads to lack of ‘engagement’ of the fetal head in the pelvis and/or an unstable fetal lie (breech or transverse). This can be a special problem when the membranes rupture (spontaneously or artificially) because if there is no ‘presenting part’ obstructing the cervix, the umbilical cord can suddenly prolapse with the gush of fluid through the cervix into the vagina turning a relatively uncomplicated situation into an emergency. Acute release of the fluid and decompression of the uterus can also cause sudden separation of the placenta (placental abruption) from the uterine wall. Stretching of the uterine muscle (myometrium) can also result in abnormal labor patterns secondary to poor contractility (myometrial dysfunction) and at times can result in poor contraction (involution) of the uterus following delivery, a situation that is usually accompanied by post-partum hemorrhage. All of these complications contribute to the increased rate of cesarean deliveries in pregnancies with hydramnios and the increased rate of maternal and fetal complications.
One other complication which occurs frequently (and is often not thought about) in the presence of hydramnios, particularly if this is associated with diabetes or simply, with fetal macrosomia, is immaturity of fetal lung development. As we have pointed out in earlier posts, late preterm (near-term) elective delivery of a baby just because it is “too big” can have tragic consequences. It is not unusual for macrosomic babies to have a 2-3 week lag in the functional ability of their lungs at birth because excessive insulin production (hyperinsulinemia) that often accompanies macrosomia can delay the production of the lung surfactants that reduce surface tension in the alveoli and are necessary for expansion of these so that oxygen exchange can occur normally. There is nothing sadder than seeing a 10 lb baby of a diabetic mother laying in the neonatal intensive care unit struggling to survive with severe respiratory distress syndrome and persistent fetal circulation as a consequence of an elective (often cesarean) delivery.
Having discussed some of the more common complications of polyhydramnios, in our next (and final!?!) post on the topic of amniotic fluid, we will address the evaluation and management of the pregnancy with too much amniotic fluid…