Amniotic Fluid - 6 - Polyhydramnios: Causes of Too Much Amniotic Fluid

Polyhydramnios (excessive amniotic fluid), also termed hydramnios, is usually defined by vertical pockets of amniotic fluid > 8 cm or as a 4-quadrant amniotic fluid index (AFI) > 95th percentile for the gestational age. Polyhydramnios has a multitude of causes and associations but is seen in only about 1-2% of all pregnancies. It can occur gradually or rapidly depending on the underlying etiology. About 50-60% of polyhydramnios is ‘idiopathic’ which means we haven’t been smart enough to figure out why there is too much fluid. It is not necessarily associated with increased urine production by the baby, but it may have a genetic basis because it can recur in sequential pregnancies, even without an etiology being identified. In some instances there is just excessive fluid and it doesn’t necessarily increase significantly over time and in other cases, it gets progressively worse and may cause both fetal and maternal complications.

There are some specific conditions in which polyhydramnios is frequently associated. The easiest to understand are the fetal anomalies that inhibit or prevent fetal swallowing or block the passage of fluid through the fetal bowel. (Recall, much of the amniotic fluid around the baby is urine and the baby must be able to swallow that and move it through the bowel to the colon where it can be reabsorbed). Common structural gastrointestinal abnormalities that are accompanied by polyhydramnios include esophageal atresia (incomplete development of the esophagus), tracheoesophageal fistulas (aberrant connections, sometimes ending in ‘blind pouches’, between the trachea and the esophagus), duodenal atresia with the classic “double bubble” seen by ultrasound in the upper abdomen (and at least 30% of these associated with Down syndrome – trisomy 21), other small bowel atresias and obstructions (the lower in the small bowel the obstruction, the greater the number of fluid-filled loops of bowel), gastroschisis (a condition in which much of the small bowel is outside the abdomen through a small defect adjacent to the fetal umbilical cord insertion site), gastrointestinal ‘malrotations’ and ‘midgut volvulus’.

Other fetal anomalies associated with polyhydramnios probably have different reasons for contributing to the excessive fluid. Large neural tube defects and certain neuromuscular disorders (such as myotonic dystrophy), for example, probably exert their effects by impairing the ability of the baby to actually swallow fluid, even if the esophagus and gastrointestinal tract are patent. Certain cardiac defects and fetal arrhythmias may contribute by virtually putting the baby into congestive heart failure. Heart failure is also likely to be a major contributing factor when the baby has severe anemia secondary to maternal isoimmunization, a fetal hemoglobinopathy, or bone marrow suppression of red blood cell synthesis as is seen with congenital Parvovirus B19 infections.

Other congenital infections (e.g., syphilis, toxoplasmosis, cytomegalovirus) may also result in excessive amniotic fluid although the actual causes of this may be different depending on the organism involved. Indeed, any condition that results in immune or nonimmune fetal hydrops, including chromosomal abnormalities and inborn errors associated with severe metabolic or cardiac dysfunction, may be accompanied by polyhydramnios. One of the more unusual conditions that is associated with polyhydramnios and fetal hydrops is the so-called “mirror syndrome” that occurs in some cases of severe maternal preeclampsia. Lithium toxicity appears to cause polyhydramnios by causing the baby to have a condition called diabetes insipidus which results from inadequate vasopressin (antidiuretic hormone – ADH) secretion by the posterior pituitary gland and, subsequently, massive production of very dilute (unconcentrated) urine.

The most common clinical condition that is often accompanied by polyhydramnios is diabetes, particularly, gestational diabetes and type 2 diabetes. It is much less likely to be found in long-standing diabetics, particularly, if they have significant kidney, cardiac, or vascular disease. In diabetics, polyhydramnios is more common if the diabetes is poorly-controlled and/or the baby is macrosomic. At times, even improving the diabetic control will not reduce the increased amniotic fluid. The etiology of the increased fluid in certain diabetics is unclear, but when present, it increases the risk for a poor fetal outcome.

In the next post, we will continue with a discussion of polyhydramnios – pregnancy complications, evaluation, and management….

Labels: fetal hydrops, fetal macrosomia, isoimmunization, polyhydramnios

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