![]() Each quadrant should be examined systematically. The uterus should be divided into four quadrants to assess amniotic fluid index. Many cases of polyhydramnios are idiopathic, meaning no definite cause is identified. In these cases, it may be associated with fetal macrosomia. Increased amniotic fluid production occurs as a result of fetal polyuria, such as in uncontrolled maternal diabetes with persistently elevated maternal blood sugars. This can occur due to gastrointestinal malformations, fetal neurologic problems such as anencephaly, or mechanical obstruction of the esophagus by other intrathoracic processes. If the fetus is unable to swallow the typical amounts of amniotic fluid, this can lead to polyhydramnios. The normal fetus is constantly swallowing amniotic fluid and urinating to create more fluid. Oligohydramnios can also occur because the patient's amniotic membrane has ruptured and amniotic fluid is leaking out of the uterus. Therefore, decreased amniotic fluid volume due to decreased urine production by the fetal kidney is a reflection of chronic hypoperfusion of the fetus. When the fetus receives inadequate nutrients and oxygen from the placenta, blood is shunted away from the fetal kidney, glomerular filtration rate decreases, and urinary output decreases. It is the same mechanism that causes oliguria in critically ill adults. Decreased urine production by the fetal kidney typically reflects inadequate blood flow to the fetal kidney, caused by shunting of fetal blood flow away from the kidney to the heart and brain. ![]() Urinary tract obstruction can occur anywhere along the fetal urinary tract and can be catastrophic for the fetus. Decreased fetal urine output can have a number of causes, which fall into two general categories: fetal urinary tract obstruction and decreased urine production by the fetal kidney.
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