In early gestation, fluid is produced from the fetal surface of the placenta, from transfer across the amnion, and from embryonic surface secretions.

In mid to late gestation, fluid is produced by fetal urination and alveolar transudate. By 16 weeks, there is about 250 mL of fluid, increasing to approximately 800 mL by 34 to 36 weeks’ gestation.

Fluid is removed by fetal swallowing and absorption at the amnion-chorion interface.

The most accurate measurement of AFV is by dye dilution techniques or direct measurement at the time of hysterotomy. Ultrasound provides a standard noninvasive tool to estimate AFV (Table 8-1).

The incidence of polyhydramnios in the general population is about 1%.

Implications: Mildly increased AFV is usually clinically insignificant. Markedly increased AFV is associated with increased perinatal morbidity due to preterm labor, cord prolapse upon membrane rupture, underlying comorbidities, and congenital malformations. Abruptio placentae is associated with polyhydramnios and rupture of membranes due to rapid decompression of the overdistended uterus. Increased maternal morbidity also results from postpartum hemorrhage due to uterine overdistention leading to atony. If polyhydramnios is severe, uterine distention can cause venous and ureteral compression causing severe lower extremity edema and hydronephrosis.

The most common etiology of polyhydramnios is idiopathic (Fig. 8-1); however, in severe cases, a cause is more often apparent and likely to be associated with a detectable fetal anomaly. Specific causes include:

Ultrasound estimates AFV, identifies multiple gestations, and may detect fetal abnormalities. Amniocentesis for karyotype is offered if any anomalies are diagnosed.

Treatment is aimed at the underlying cause. Mild to moderate polyhydramnios can be managed expectantly until the onset of labor or spontaneous rupture of membranes. If the patient develops significant dyspnea, abdominal pain, or difficulty ambulating, treatment becomes necessary.

The etiology of oligohydramnios includes ruptured membranes, fetal urinary tract malformations, postterm pregnancy, placental insufficiency, and medications reducing fetal urine production. Rupture of membranes must be considered at any gestational age. Renal agenesis or urinary tract obstruction often becomes apparent during the second trimester of pregnancy, when fetal urine flow begins to contribute significantly to AFV. Placental insufficiency can cause both oligohydramnios and intrauterine growth restriction. The cause of oligohydramnios in postterm pregnancies may be deteriorating placental function (Fig. 8-2).

Ultrasound is used to diagnose oligohydramnios. Rupture of membranes should be evaluated, and in cases of preterm gestation with uncertain membrane status, a tampon dye test can be performed (see Chapter 9).

Treatment for oligohydramnios is limited. Maternal intravascular fluid status appears to be closely tied to that of the fetus; maternal hydration (intravenous or oral) may improve the AFV depending on the etiology of oligohydramnios. In cases of obstructive genitourinary defects, in utero surgical diversion has produced
some promising results. For optimal benefit, urinary diversion must be performed before renal dysplasia develops and early enough in gestation to permit normal lung development. Until near term, oligohydramnios is managed with frequent fetal surveillance. Indications for induction of labor include term gestation or nonreassuring fetal testing after 34 weeks. Oligohydramnios is not a contraindication to labor. There is no consensus as to which of the measurements of AFV is most recommended when deciding if induction for oligohydramnios is indicated. MVP may be a superior option to AFI, as AFI measurement has a higher rate of false positives for oligohydramnios and thus increases induction and cesarean section rates without evidence of improvement in neonatal outcomes.

Constitutionally small mothers and inadequate weight gain: Women who weigh <100 pounds at conception have double the risk for a small-for-gestational-age newborn. Inadequate or arrested weight gain after 28 weeks of pregnancy is also associated with IUGR. Underweight women should have a 28 to 40 pounds of weight gain during pregnancy.

Chronic maternal disease: Multiple medical conditions of the mother, including chronic hypertension, cyanotic heart disease, pregestational diabetes, malnutrition, and collagen vascular disease, can cause growth restriction. Preeclampsia and smoking are associated with IUGR.

Fetal infection: Viral causes including rubella, CMV, hepatitis A, parvovirus B19, varicella, and influenza are among the best known infectious antecedents of IUGR. In addition, bacterial (listeriosis), protozoal (toxoplasmosis), and spirochetal (syphilis) infections may be causative.