Amniotic Fluid - 3 - Oligohydramnios: Causes of Too Little Amniotic Fluid | Fruit of the Womb
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Amniotic Fluid - 3 - Oligohydramnios: Causes of Too Little Amniotic Fluid

Having discussed where amniotic fluid comes from and how we assess amniotic fluid volume, let’s address the most common amniotic fluid abnormality – too little fluid or oligohydramnios. There are 3 primary reasons why there is too little amniotic fluid: 1) rupture of membranes; 2) fetal abnormalities; 3) placental abnormalities.

Spontaneous rupture of membranes (SROM) can occur at any time in pregnancy. Most of the time, the membranes remain intact until the onset of labor, or just before labor, after the cervix has begun to change (efface and dilate). If membranes rupture prior to the onset of uterine contractions, it is called premature rupture of membranes or PROM, and if they are ruptured for more than 24 hours, prolonged premature rupture of membranes or PPROM. There are lots of things that can lead to rupture of membranes, but the ones we worry about most are infection, fetal anomalies that result in too much fluid (polyhydramnios or hydrammnios) and uterine overdistention, and cervical incompetence. The earlier in pregnancy that the membranes rupture, the greater the likelihood that it is associated with infection (with or without cervical incompetence) and this is usually infection with organisms that the mother carries in her body that get inside the uterus by ascending vaginal, blood-borne, or lymphatic transmission. However, the focus of this discussion is not to discuss SROM, but to remind readers that it is a very common cause of decreased amniotic fluid and when it occurs, the baby and the mother need to be evaluated carefully to look for causes. Since infection is often associated with PROM, that is usually what constitutes the greatest risk to the baby.

The least common, but often most serious, causes of decreased amniotic fluid are fetal abnormalities. If you recall in our first post on this subject, most of the amniotic fluid from early midtrimester on is fetal urine. Abnormalities of the fetal kidneys and urinary tract can lead to decreased urine output or the complete absence of amniotic fluid (anhydramnios) in the most severe cases. Babies can have the complete absence of both kidneys (bilateral renal agenesis), nonfunctioning kidneys associated with polycystic or multicystic renal dysplasia, or obstructive uropathies where there is blockage of urine at the urethra (usually the result of ‘posterior urethral valves’ in male children), or blockage of the ureters at various levels between the kidneys and the bladder (e.g., ureteropelvic junction (UPJ) or ureterovesical junction (UVJ)obstructions). An important point to note here is that if the baby only has ONE nonfunctioning kidney, or a blockage that affects only ONE side, the amniotic fluid is usually normal and the consequences of too little fluid for too long do not develop. However, if both kidneys are affected, this can lead to the complete absence of amniotic fluid and a condition that has been named “Potter’s sequence” which will be detailed in our next post on this subject.

Other causes of decreased fluid that may be transient (and therefore less serious) and/or reversible are congenital viral infections, such as cytomegalovirus (CMV) which has a predilection for the fetal kidneys, or conditions that affect maternal hydration. With regard to the latter, as we pointed out previously, if the mother becomes very dehydrated, or if she has a condition that severely decreases her plasma volume, the fluid around the baby, which depends so much on passive distribution from the mother across the placenta, can acutely decrease. Common conditions in which this is seen include: hyperemesis (too much vomiting), diarrhea, maternal sepsis, hemorrhage, placental abruption or previa, diabetic ketoacidosis, excessive fluid loss during fever or heat exposure, and severe preeclampsia. Oligohydramnios resulting from many of these conditions can be reversed or improved with expansion of the maternal plasma volume.

The last conditions I would like to discuss that lead to decreased amniotic fluid are those that result in decreased perfusion (blood flow) to the fetal kidneys. When it comes right down to it, the kidneys are ‘nonessential organs’ with regard to survival of the baby while it is inside its mother. For example, babies that have bilateral renal agenesis (no kidneys at all) can go all the way to term because the placenta and the mother serve as the means of removing ‘waste products’ from the baby. (They cannot survive after delivery for the reasons I will detail in my next post). Production of urine by the baby requires blood flow through the kidneys. When babies become dehydrated, or when they have to, preferentially, send blood to ‘essential organs’ such as the brain and the heart because they are not receiving enough oxygen and nutrients to support their whole bodies’ needs, their regulatory mechanisms of survival shut down blood flow to the kidneys, thereby, curtailing the production of urine.

This can occur as the result of primary fetal problems such as severe anemia associated with isoimmunization or parvovirus infections, or cardiac malformations or dysfunction from a variety of different causes. More commonly, however, this occurs as the result of abnormalities of placentation (small placentas and/or placentas that have not had normal invasion of the maternal spiral arterioles in the placental bed), wherein the babies have outgrown the capacity of the placenta to provide sufficient oxygen and/or nutrients. When ‘placental insufficiency’ occurs it is usually accompanied by intrauterine fetal growth restriction (IUGR). This usually means the baby is small for its gestational age, but there are occasions when this can occur in large babies, such as those seen in uncontrolled diabetic mothers, whose size also exceeds the capacity of the placenta to maintain their metabolic demands. When the amniotic fluid starts to go down in circumstances of placental insufficiency, this is also usually the result of ‘fetal blood flow redistribution’ away from the kidneys and to the essential organs necessary for survival.

Having discussed some of the more common causes of oligohydramnios, in our next installment of this series, we will address the evaluation, management, and consequences decreased amniotic fluid in pregnancy ….
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