This is an abnormally increased amnionic fluid volume, and it complicates 1 to 2 percent of pregnancies (Biggio, 1999; Dashe, 2000; Magann, 2007; Pri-Paz, 2012). Also termed polyhydramnios, hydramnios may be suspected if the uterine size exceeds that expected for gestational age. The uterus may feel tense, and palpating fetal small parts or auscultating fetal heart tones may be difficult. An extreme example is shown in Figure 11-2.
Severe hydramnios—5500 mL of amnionic fluid was measured at delivery.
Hydramnios may be further categorized according to degree. Such categorization has been primarily used in research studies to stratify risks. Several groups have termed hydramnios as mild if the AFI is 25 to 29.9 cm, moderate if 30 to 34.9 cm, and severe if 35 cm or more (Dashe, 2002; Lazebnik, 1999; Pri-Paz, 2012). Mild hydramnios is the most common, comprising approximately two thirds of cases. Moderate hydramnios accounts for about 20 percent, and severe hydramnios approximately 15 percent. Using the single deepest pocket of amnionic fluid, criteria for mild is 8 to 9.9 cm, moderate is 10 to 11.9 cm, and severe hydramnios, ≥ 12 cm. An example of severe hydramnios seen sonographically is shown in Figure 11-3. These definitions fit the general rule that the AFI is approximately three times the measurement of the single deepest fluid pocket (Hill, 2003). In general, severe hydramnios is far more likely to have an underlying etiology and to have consequences for the pregnancy than mild hydramnios—which is frequently idiopathic and benign.
Sonogram of severe hydramnios at 35 weeks in a pregnancy complicated by fetal aqueductal stenosis. This pocket of amnionic fluid measures more than 15 cm, and the amnionic fluid index measured nearly 50 cm.
Common underlying causes of hydramnios include fetal congenital anomalies in approximately 15 percent and diabetes in 15 to 20 percent (Table 11-2). Congenital infection and red blood cell alloimmunization are less frequent reasons. Infections that may present with hydramnios include cytomegalovirus, toxoplasmosis, syphilis, and parvovirus (Chaps. 64 and 65). Hydramnios is often a component of hydrops fetalis, and several of the above etiologies—selected anomalies, infections, and alloimmunization—may result in a hydropic fetus and placenta. The underlying pathophysiology in such cases is complex but is frequently related to a high cardiac-output state. Severe fetal anemia is the classic example. Because the etiologies of hydramnios are so varied, hydramnios treatment also varies and is tailored in most cases to the underlying cause. These etiologies are discussed further in Chapter 15 (Hydrops Fetalis) and in other chapters covering specific topics.
TABLE 11-2Hydramnios: Prevalence and Associated Etiologies—Values in Percent ||Download (.pdf) TABLE 11-2 Hydramnios: Prevalence and Associated Etiologies—Values in Percent
The amnionic fluid glucose concentration is higher in diabetic women than in those without diabetes, and the amnionic fluid index may correlate with the amnionic fluid glucose concentration (Dashe, 2000; Spellacy, 1973; Weiss, 1985). Such findings support the hypothesis that maternal hyperglycemia causes fetal hyperglycemia, with resulting fetal osmotic diuresis into the amnionic fluid compartment.
Various anomalies may be found in the setting of hydramnios, and some are more characteristically linked with it than others. Because of this association, identification of hydramnios is an indication for targeted sonography. Many of the anomalies described next are displayed sonographically in Chapter 10 (Normal and Abnormal Fetal Anatomy).
Severe central nervous system abnormalities, such as anencephaly, hydranencephaly, or holoprosencephaly, can result in hydramnios due to impaired fetal swallowing. Fetal neuromuscular disorders such as myotonic dystrophy also may lead to excessive amnionic fluid. Obstruction of the fetal upper gastrointestinal tract—esophageal or duodenal atresia—is often associated with hydramnios. Other obstructive causes include clefts, micrognathia, congenital high-airway obstruction sequence, and fetal neck masses. Severe fetal thoracic abnormalities, such as diaphragmatic hernia, cystic adenomatoid malformation, and pulmonary sequestration, may be associated with hydramnios due to mediastinal shift and impaired swallowing, occasionally with development of hydrops. A common fetal renal anomaly, ureteropelvic junction obstruction, may at times result in paradoxical hydramnios. And although rare, tumors such as fetal sacrococcygeal teratoma, fetal mesoblastic nephroma, and large placental chorioangiomas are frequently accompanied by abnormally increased amnionic fluid volume.
The degree of hydramnios is associated with the likelihood of an anomalous infant (Many, 1995; Pri-Paz, 2012). For example, at Parkland Hospital, the prevalence of an anomalous infant was approximately 8 percent with mild hydramnios, 12 percent with moderate hydramnios, and more than 30 percent with severe hydramnios (Dashe, 2002). If no abnormality was detected with targeted sonography, the likelihood of a major anomaly identified at birth was 1 to 2 percent if the hydramnios was mild or moderate but exceeded 10 percent if hydramnios was severe. Dorleijn and associates (2009) have also reported an increased risk for abnormalities detected in the first year of life with apparent idiopathic hydramnios. The anomaly risk is particularly high with hydramnios coexistent with fetal-growth restriction (Lazebnik, 1999). If a fetal abnormality is encountered concurrent with hydramnios, amniocentesis should be considered, because the aneuploidy risk is significantly increased (Dashe, 2002; Pri-Paz, 2012).
Although amnionic fluid volume abnormalities are associated with fetal malformations, the converse is not usually the case. In the Spanish Collaborative Study of Congenital Malformations that included more than 27,000 anomalous infants, only 4 percent were complicated by hydramnios, and another 3 percent with oligohydramnios (Martinez-Frias, 1999).
Hydramnios is generally defined in multifetal gestations as a single deepest amnionic fluid pocket measuring 8 cm or more. It may be further characterized as moderate if the single deepest pocket is at least 10 cm and severe if this pocket is at least 12 cm. In monochorionic pregnancies, hydramnios of one sac and oligohydramnios of the other are diagnostic criteria for twin-twin transfusion syndrome, which is discussed in Chapter 45 (Fetus-in-Fetu). In a review of nearly 2000 twin gestations, Hernandez and coworkers (2012) identified hydramnios in 18 percent of both monochorionic and dichorionic pregnancies. As in singletons, severe hydramnios was more strongly associated with fetal abnormalities. In the absence of an abnormality, pregnancy risks were not generally increased compared with twins with normal amnionic fluid volume.
When there is no obvious cause of hydramnios it is considered idiopathic. As shown in Table 11-2, this accounts for up to 70 percent of cases (Golan, 1993; Many, 1995; Panting-Kemp, 1999). Pregnancies with idiopathic hydramnios have been reported to have at least twice the likelihood of infant birthweight exceeding 4000 g (Lazebnik, 1999; Magann, 2010; Maymon, 1998). A rationale for this association is that larger infants have higher urine output, by virtue of their increased volume of distribution, and fetal urine is the largest contributor to amnionic fluid volume. Mild, idiopathic hydramnios is most commonly a benign finding, and associated pregnancy outcomes are usually good.
Unless hydramnios is severe or develops rapidly, maternal symptoms are infrequent. With chronic hydramnios, fluid accumulates gradually, and a woman may tolerate excessive abdominal distention with relatively little discomfort. Acute hydramnios, however, tends to develop earlier in pregnancy. It may result in preterm labor before 28 weeks or in symptoms that become so debilitating as to necessitate intervention.
Symptoms may arise from pressure exerted within the overdistended uterus and upon adjacent organs. When distention is excessive, the mother may suffer dyspnea and orthopnea to such a degree that she may be able to breathe comfortably only when upright (see Fig. 11-2). Edema may develop as a consequence of major venous system compression by the enlarged uterus, and it tends to be most pronounced in the lower extremities, vulva, and abdominal wall. Rarely, oliguria may result from ureteral obstruction by the enlarged uterus (Chap. 53, Lower Genital Tract Lesions). Maternal complications such as these are typically associated with severe hydramnios from an underlying etiology.
Maternal complications associated with hydramnios include placental abruption, uterine dysfunction, and postpartum hemorrhage. Placental abruption is fortunately infrequent. It may result from the rapid decompression of an overdistended uterus that follows fetal-membrane rupture or therapeutic amnioreduction. With prematurely ruptured membranes, a placental abruption occasionally occurs days or weeks after amniorrhexis. Uterine dysfunction consequent to overdistention may lead to postpartum atony and, in turn, postpartum hemorrhage.
Some outcomes that have been reported to be increased with hydramnios include cesarean delivery rate, birthweight > 4000 g, and importantly, perinatal mortality rate. The cesarean delivery rate is increased approximately threefold when hydramnios has been identified, and the perinatal mortality rate rises approximately fourfold (Biggio, 1999; Hill, 1987; Maymon, 1998). Pri-Paz and colleagues (2012) found that pregnancies with severe hydramnios were at particular risk, but reported no perinatal deaths with idiopathic hydramnios.
Risks appear to be compounded when a growth-restricted fetus is identified with hydramnios. Erez and associates (2005) reported that this combination was independently associated with a 20-fold increase in the perinatal mortality rate. The combination also has a recognized association with trisomy 18 (Sickler, 1997).
Considering that uterine distention from hydramnios may result in uterine size approaching that of a term gestation, preterm delivery is a logical concern. Somewhat surprisingly, studies of idiopathic hydramnios have generally found no association with preterm birth (Magann, 2010; Many, 1995; Panting-Kemp, 1999). Conversely, severe hydramnios and hydramnios concurrent with recognized fetal abnormalities have been linked with preterm birth (Many, 1995; Pri-Paz, 2012).
As noted previously, hydramnios etiologies are varied, and treatment is directed in most situations to the underlying cause. Occasionally, severe hydramnios may result in early preterm labor or the development of maternal respiratory compromise. In such cases, large-volume amniocentesis—termed amnioreduction—may be needed. The needle insertion technique is the same as for amniocentesis, described in Chapter 14 (Prenatal and Preimplantation Diagnostic Testing). However, either an evacuated container bottle or a larger syringe is connected to the needle via sterile intravenous tubing with a stopcock. In general, approximately 1000 to 1500 mL of fluid is slowly withdrawn during approximately 30 minutes, depending on the severity of hydramnios and gestational age. The goal is to restore amnionic fluid volume to upper normal range (Sonographic Assessment). Hydramnios severe enough to necessitate amnioreduction almost invariably has an underlying etiology, and subsequent amnioreduction procedures may be required as often as weekly or even semiweekly. Importantly, amnioreduction is typically performed later in gestation and carries additional risks of membrane rupture, preterm labor or its exacerbation, and placental abruption.