Just as the fetal outcome depends on the degree, underlying cause, timing during development and longevity of decreased amniotic fluid, to some extent, so do the management options. When the baby has complete absence of both kidneys (bilateral renal agenesis), or absence of functional kidneys (bilateral multicystic or polycystic renal dysplasia), and no amniotic fluid, then as we pointed out yesterday, the fetal outcome is clear – the condition (Potter’s sequence) is lethal. Since this outcome is inevitable, regardless of the gestational age at delivery, interruption of the pregnancy is a reasonable option if the patient wishes to proceed with that. When I trained, that was considered to be a reasonable option at any gestational age as well (whenever the patient was ready to proceed) and, in my mind, it still should be, however, there are many individuals and state regulations that consider this a ‘pregnancy termination’ and practitioners are reluctant to perform labor inductions in such women beyond the gestational age at which the state limits such procedures. Unfortunately, this might require a woman to carry her nonviable baby for 4-5 months after she has been given the diagnosis.
Another option under these circumstances is to offer the patient a program of ‘fetal hospice care.’ The goal of such programs is to allow women and their families the opportunity to spend as much time with the baby, before and after birth, as possible. We structure this with frequent office and ultrasound visits (for those who prefer) and ongoing counseling before and after delivery. In addition, we try to identify other families who have been through the same or a similar situation as a means of additional support. We will often identify one physician to lead the care of the pregnancy, avoid unnecessary testing and interventions, try to create a sensitive birth experience without fetal monitoring and with experienced nursing staff, have a neonatologist available to rapidly confirm the baby’s status following delivery, and allow the patient and any family members she welcomes to be present at the delivery to spend as much time with the baby as possible after birth. Although this approach is not for everyone, those that go through with it are almost always rewarded by the experience.
Less clear is the management of the ‘obstructive uropathies’ that are accompanied by reduced amniotic fluid and, indeed, discussion is beyond the scope of what we need to present herein. In brief, management and outcome depends on when in pregnancy the obstruction is detected and the extent of residual kidney function. As an example, if one is fortunate enough to detect an over-distended bladder and oligohydramnios as the result of posterior urethral valves (bladder out let obstruction) very early in pregnancy, there is the option to place a bladder shunt, diverting urine from the bladder into the space around the baby. Theoretically, this might help reduce the risk of pulmonary hypoplasia. However, the fetal outcome under these circumstances is highly variable. Sometimes the kidneys and the bladder have been too damaged by the obstruction to recover, sometimes the shunts have to be replaced repeatedly, and sometimes the babies still develop abdomens that remain distended and poorly muscularized as the result of the over-distention during critical stages of development – a condition called ‘prune belly syndrome' – and/or respiratory insufficiency. Complete, bilateral ureteral obstructions (between the kidneys and the bladder) are even more of a challenge, but fortunately these are very rare.
Management of premature rupture of membranes (PROM) also depends to a large extent on the timing in pregnancy. If this occurs prior to 20 (or even 22) weeks, the risk of fetal complications related to pulmonary hypoplasia and fetal deformations and the risks of maternal complications secondary to infection are so high that many practitioners will simply advise their patients to undergo pregnancy termination. Unfortunately, for counseling purposes, the outcome under these circumstances can be difficult to predict, particularly if the baby is able to maintain, even intermittently, a small amount of fluid within the uterine cavity. But it is likely that less than 5% of babies with PROM before 20 weeks have any chance at all of intact survivial.
For the patient who is reluctant to undergo pregnancy termination, an option is to simply counsel regarding risks and signs of infection (and the absolute necessity of proceeding with delivery once infection is suspected) and to follow the pregnancy over time. After initial stabilization and evaluation in the hospital, we offer most of these women outpatient management. Other than counseling there is no more that can be offered except perhaps antibiotics. There is no standard of care in the use of antibiotics under these circumstances (in fact some would decry it) but after several unexpectedly good outcomes under these circumstances, I have gotten into the routine of beginning, empirically, a broad spectrum IV cephalosporin antibiotic or penicillin to cover Group B Streptococcus, pending results of cervical-vaginal and urine cultures, as well as a 5-day course of azithromycin, and prolonged prophylactic therapy with metronidazole (the latter being given orally until delivery). Once the baby reaches the point of potential viability, hospitalization can be considered, if the patient desires more aggressive fetal surveillance.
Management of PPROM after viability has been obtained usually involves hospitalization from the outset, careful assessment for infection (even to the extent of including amniocentesis to evaluate the fluid around the baby for evidence of infection and inflammatory markers) and ongoing fetal monitoring to try to balance the risks and benefits of continuing intrauterine management versus delivery. Again, this topic is best suited for another entire post alone.
One of the more challenging, and more common, situations involving the management of pregnancies with reduced amniotic fluid is in the setting of ‘placental insufficiency’ that usually is the late culmination of abnormalities of placentation that occurred very early in pregnancy. As we discussed in our last post, when babies are not getting enough across the placenta to meet metabolic demands and to maintain normal patterns of symmetrical growth, they are able to ‘redistribute’ blood flow to essential organs such as the brain and heart. One sign that this is occurring is progressive growth of the fetal head out of proportion to that of the abdomen – asymmetrical fetal growth restriction. Eventually a critical stage is reached at which point so much blood flow is diverted away from the nonessential organs such as the kidneys, that fetal urine production drops and subsequently the amniotic fluid volume, placing the baby at risk for both cord compromise and too little oxygen. When babies truly start to become unhappy in these situations, it is not uncommon for their mothers to develop hypertensive complications of pregnancy (preeclampsia) and these frequently accompany intrauterine growth restriction.
One of the most effective means we have of ascertaining that these blood flow changes are occurring, sometimes even before significant growth abnormalities have taken place, is Doppler flow velocimetry. This is a noninvasive ultrasound-based technique that allows us to measure resistance to flow (and at times velocity of the flow) in blood vessels. In normal pregnancies, resistance to blood flow from the baby to the placenta as measured in the umbilical arteries is usually very low – indeed, blood normally continues to flow to the placenta even between beats (end diastole) of the fetal heart. At the same time, under normal conditions, resistance to blood flow to the fetal brain (usually measured in the middle cerebral artery, or MCA) is usually high. Though this resistance often decreases as pregnancy progresses, resistance to intracranial blood flow should always exceed resistance indices found in the umbilical arteries. In contrast, when there is decreased resistance in the MCA, this suggests fetal blood flow redistribution and it is often accompanied by increased resistance in the umbilical arteries reflecting the abnormalities in placentation (invasion of the maternal spiral arterioles) that led the pregnancy to this point. When the resistance in the MCA actually falls below that found in the umbilical arteries, the baby may well be at a critical stage requiring delivery, regardless of the gestational age.
When we follow the pregnancy with reduced amniotic fluid, there is not necessarily going to be a single test that tells us the baby is better off out than in. It is one of those situations where we may have to use several of the antepartum testing modalities – nonstress test (NST), contraction stress test (CST), biophysical profile (BPP), and Doppler flow velocimetry - we have at our disposal to aid in the decision-making process. This is especially important when there are complications related to oligohydramnios in the very premature baby. There are many times when the maternal condition must be factored into the decisions as well, particularly, when there is evidence of preeclampsia accompanying intrauterine fetal growth restriction associated with placental insufficiency. One must also be very cautious in the pregnancy with placental insufficiency because the baby often has had time to adapt to the chronic stress of its environment and can often appear better off than it really is even just before decompensating completely.
This concludes an overview of the pregnancy with decreased amniotic fluid. I apologize if I over-simplified some aspects of this discussion, but I wanted to present the information in a way that most of our readers could grasp the basic concepts. In the next post we will begin a discussion of increased amniotic fluid – polyhydramnios (or, simply hydramnios)...