In the last three posts, we have reviewed basic aspects of amniotic fluid production and measurement and common causes of decreased amniotic fluid, or oligohydramnios. Now let’s look at reasons decreased amniotic fluid increases the risk for fetal (and newborn) complications and death. Complications related to decreased amniotic fluid depend on the underlying cause, the degree of the decrease, the timing during pregnancy, and the longevity during fetal development. First, let’s look at the worst case scenario – the baby that has no fluid (anhydramnios) from very early in the pregnancy on…
As mentioned in our last post, the most common conditions that lead to anhydramnios include absence of the fetal kidneys (bilateral renal agenesis), nonfunctional kidneys secondary to bilateral renal dysplasia (polycystic and multicystic kidneys), and complete bladder outlet obstruction (posterior urethral valves, or other anomalies associated with maldevelopment of the fetal bladder or urethra). In rare circumstances, complete bilateral obstruction of the ureters (ureteropelvic or ureterovesical junction obstruction) can also be found. Under these conditions, where the baby has essentially no amniotic fluid from late first trimester on, the outcome is uniformly LETHAL.
Interestingly, it is not the absence of kidney function that kills these babies – it is the fact that in the absence of amniotic fluid, the fetal lungs do not develop sufficiently to support breathing once they are actually born! Any of these conditions associated with early and sustained anhydramnios result in the same outcome secondary to pulmonary hypoplasia and insufficiency, and this has been labeled ‘Potter’s syndrome (or sequence)’ after the physician who first described it. Although, it is not known why the absence of fluid results in Potter’s syndrome, it is thought that the constant compression of the thorax contributes, that the production of fluid by the fetal lungs is suppressed, and even that some movement of amniotic fluid (fetal urine) into the lungs is essential for normal development of functional alveoli. Most babies who are born with Potter’s syndrome cannot even make any kind of respiratory effort at birth, and those that do, cannot get sufficient oxygen into their bodies to allow survival.
If you notice, I did not include premature and prolonged rupture of membranes (PPROM) in this category of inevitable lethal outcome. It is true that if PPROM occurs prior to 20-22 weeks, the baby is at risk for the full consequences of Potter’s syndrome, and the earlier the PPROM and the more severe the oligohydramnios, the greater the likelihood is that this will occur. Indeed, during my training, we were taught simply to offer such women induction of labor, not only because the fetal outcome was expected to be dismal but also because the risk of infection to the mother was so high. (Of course, when I trained, it was the rare baby born before 27 weeks that had any chance of survival anyway). But, I must admit, many patients I have had over the years have proven that old teaching to be incorrect, or at least not a certain death sentence for their babies. Some of these women will carry their babies to a point where there is potential viability (today, 23 weeks and beyond) and, though they are at risk for pulmonary hypoplasia, the degree of this is very difficult to predict and it may not be lethal. However, these babies may also be at increased risk for fetal deformations (particularly of the skeleton, thorax, and head) secondary to compression during development and in its most severe form, a condition termed the fetal akinesia/hypokinesia deformation sequence in which there are not only compression malformations but poor development of muscle, tendons, and enervation secondary to the lack of fetal movement in utero.
Although the above conditions are very serious, they are also all the least common complications related to oligohydramnios. Indeed, most babies will not develop decreased amniotic fluid until beyond 24 weeks gestation, so the issues related to pulmonary hypoplasia and major deformations are, fortunately, rare. The most common reasons for oligohydramnios in the latter part of pregnancy are PROM and placental insufficiency. In the case of the former, this can lead to the acute (sudden) decrease in amniotic fluid and in the latter, a more gradual reduction. Leaving infection out of the equation (as a common cause of PROM and associated with its own morbidity and mortality), the primary cause of fetal complications under these circumstances are related to umbilical cord compromise, and in the case of placental insufficiency, decreased fetal oxygenation (ultimately the cause with its own consequences, not the effect, of decreased amniotic fluid).
Normally, I tell patients that the umbilical cord is a lot like a fire hose. It is a ‘closed system’ and the blood contained within it is under some pressure. In other words, just because it is wrapped around the baby’s neck, or other body parts, or even tied into a knot, does not mean the baby is going to necessarily die as the result – in fact most don’t. At least one-third of all babies are born with the cord looped around the neck (nuchal cord) and most do just fine. However, the blood in the umbilical cord vessels is under differential ‘pressures’ depending on whether it is the poorly oxygenated arterial blood (higher pressure) coming from the baby to the placenta or the well-oxygenated venous blood (low pressure) coming back to the baby from the placenta. Obviously, when there is compression on the umbilical cord, the venous blood flow is much more likely to be impeded than the arterial blood flow.
Even if the blood in the umbilical cord is under pressure, in the presence of decreased or absent amniotic fluid it is possible for the baby to trap the cord in a position where blood flow is significantly reduced and the baby can be damaged or even die as the result of too little oxygen. I always worry about this most when there is sudden rupture of the membranes, or if the cord falls (prolapses) through the cervix, and, particularly, in women who are very heavy. It is also one of the causes of fetal morbidity and mortality in placental insufficiency sequences (accompanied by intrauterine growth restriction) because oftentimes in these circumstances, not only is the placenta poorly developed (and has less ‘reserve’), but the cord is often thinner and smaller and not endowed with adequate cushioning due to a reduction in the amount of Wharton’s jelly surrounding the blood vessels (normally two arteries and one vein) in the umbilical cord and, therefore, more likely to be significantly compromised when compressed.
Intermittent (and incomplete) umbilical cord compression can often be identified by distinct abnormalities of the fetal heart rate (FHR) tracing (most commonly, ‘variable decelerations’). These are quite common in labor, particularly after the membranes have ruptured either spontaneously or as the result of the provider’s intervention (artificial rupture of membranes, or AROM). FHR monitoring is, therefore, one means of identifying the baby ‘at risk’ for umbilical cord compromise. Most babies that have decreased fluid and normal placental function tolerate this type of FHR deceleration quite well, although they are still at increased risk for cesarean delivery if the FHR tracing begins to develop signs of ‘nonreassurance’ and spontaneous vaginal delivery is still remote. Since we seem to have spent a fair amount of time on this topic today, I will reserve further discussion on the evaluation and management of pregnancies with oligohydramnios to our next post…