Polyhydramnios refers to an excess of amniotic fluid during pregnancy and manifests as a uterus that is larger than expected for the given gestational age. This condition arises from either reduced swallowing of amniotic fluid by the fetus or increased fetal urination. GI obstructions such as duodenal atresia and tracheoesophageal fistula, as well as neural tube defects like anencephaly, which affects the swallowing center of the brain, can impair fetal swallowing and cause polyhydramnios.
Polyhydramnios associated with increased fetal urination can result due to either a fetal high-output state or maternal hyperglycemia. For example, fetal anemia can elevate cardiac output and enhance renal blood flow, thereby promoting greater urination. Similarly, maternal hyperglycemia can lead to an excess transfer of glucose to the fetus and fetal hyperglycemia, which induces osmotic diuresis and increases renal blood flow, also increasing fetal urination.
Oligohydramnios is characterized by insufficient amniotic fluid volume, and manifests as a uterus smaller than expected for the gestational age. Decreased fetal urination is a common cause and can be due to either inadequate urine production by the kidneys or a lower urinary tract obstruction.
Conditions like bilateral renal agenesis or autosomal recessive polycystic kidney disease can lead to insufficient urine production and can cause oligohydramnios. Medications like ACE inhibitors or ARBs may lead to reduced levels of angiotensin II, which in turn can adversely affect kidney development and contribute to decreased urine output. In males, posterior urethral valves can obstruct urine flow at the proximal urethra near the bladder outlet, resulting in oligohydramnios.
Oligohydramnios poses significant risks to fetal development, most notably manifesting as Potter sequence. Potter sequence is associated with features like clubbed feet due to a lack of cushioning for the fetus and pulmonary hypoplasia due to insufficient amniotic fluid for swallowing.
Polyhydramnios refers to the presence of excessive amniotic fluid in the uterus, leading to a uterus size larger than expected for the gestational age. It arises from two main mechanisms: decreased swallowing of amniotic fluid by the fetus or increased fetal urination. Decreased swallowing can be due to GI obstructions like duodenal atresia or tracheoesophageal fistula, or neural defects like anencephaly that affect the swallowing center in the brain. Increased fetal urination can result from conditions like fetal anemia or maternal hyperglycemia, as seen in maternal diabetes.
Oligohydramnios is characterized by insufficient amniotic fluid volume, causing the uterus to appear smaller than expected for the gestational age. This condition can adversely affect fetal development, movement, and cushioning. It can lead to a series of complications collectively known as Potter sequence, which includes manifestations like clubbed feet and pulmonary hypoplasia. The latter occurs because insufficient amniotic fluid limits the amount available for the fetus to swallow, affecting lung development.
Oligohydramnios is typically caused by decreased fetal urination, which can occur due to insufficient urine production by the kidneys or obstruction in the lower urinary tract. Conditions like bilateral renal agenesis or autosomal recessive polycystic kidney disease can lead to decreased urine production. In males, a congenital defect called posterior urethral valves can obstruct urination. Additionally, in utero exposure to ACE inhibitors or ARBs can lead to decreased angiotensin II levels, affecting fetal kidney development and ultimately causing oligohydramnios.
Maternal diabetes can be a contributing factor to polyhydramnios. Excessive glucose from the mother crosses the placenta, leading to fetal hyperglycemia. This leads to fetal polyuria, resulting in an accumulation of excessive amniotic fluid in the uterus.
Anencephaly, a neural tube defect, can cause polyhydramnios due to a defect in the swallowing center in the brain, leading to decreased swallowing of amniotic fluid by the fetus. This results in an accumulation of excessive amniotic fluid in the uterus, manifesting as polyhydramnios.