- Ron Beloosesky, MD
Ron Beloosesky, MD
- Assistant Professor, Obstetrics and Gynecology Department
- Rambam Medical Center at the Technion Faculty of Medicine, Haifa, Israel
- Michael G Ross, MD, MPH
Michael G Ross, MD, MPH
- Distinguished Professor of Obstetrics and Gynecology
- David Geffen School of Medicine at UCLA
- Section Editors
- Charles J Lockwood, MD, MHCM
Charles J Lockwood, MD, MHCM
- Section Editor — Obstetrics
- Senior Vice President, USF Health
- Dean, Morsani College of Medicine
- Professor, Obstetrics and Gynecology
- University of South Florida
- Deborah Levine, MD
Deborah Levine, MD
- Section Editor — Imaging
- Professor of Radiology
- Director of Ob/Gyn Ultrasound
- Department of Radiology
- Beth Israel Deaconess Medical Center
Polyhydramnios (also known as hydramnios) refers to an excessive volume of amniotic fluid. It has been associated with an increased risk of various adverse pregnancy outcomes, including preterm birth, placental abruption, and fetal anomalies [1-3]. Polyhydramnios should be suspected clinically when uterine size is large for gestational age. The diagnosis is made prenatally by ultrasound examination using a noninvasive qualitative or quantitative approach. (See "Assessment of amniotic fluid volume".)
The incidence of polyhydramnios in a general obstetric population generally ranges from 1 to 2 percent [4-8]. Reported rates are influenced by variations in diagnostic criteria, the population studied (low or high risk), the subjective volume of fluid where polyhydramnios is diagnosed (eg, mild, moderate, or severe), and the gestational age (preterm, term, or postterm) at examination. In one series of 93,332 singleton pregnancies delivering at a single hospital from 1991 to 1997, polyhydramnios was diagnosed during antepartum sonography in 708 pregnancies (0.7 percent of deliveries); mild, moderate, and severe disease occurred in 66, 22, and 12 percent of cases, respectively .
The volume of amniotic fluid reflects the balance between fluid production and movement of fluid out of the amniotic sac; the regulation of this process is incompletely understood. (See "Physiology of amniotic fluid volume regulation".) In late gestation, the primary sources of amniotic fluid production are fetal urination and secretion of lung fluid; oral and nasal secretions make minimal contributions. The main routes of amniotic fluid removal are fetal swallowing and absorption via the intramembranous pathway. Even a relatively minor increase in daily fetal urine production or decrease in fetal swallowing can result in a marked increase in amniotic fluid volume (AFV) [9-11].
The most common cause of severe polyhydramnios are fetal anomalies (often associated with an underlying genetic diagnosis), while maternal diabetes, multiple gestation, and idiopathic factors are more often associated with milder cases. In one series of 272 singleton pregnancies with polyhydramnios, approximately one-third were associated with a congenital anomaly and one-quarter were associated with maternal diabetes; the remaining 40 percent were considered idiopathic . After birth, an abnormality is diagnosed in up to 25 percent of cases considered idiopathic prenatally [12-15]. Fetal infection, Bartter syndrome, anemia, and neuromuscular disorders account for some of these cases and should be considered in the differential diagnosis if a structural abnormality and maternal diabetes are excluded, although Bartter syndrome and neuromuscular diseases are quite rare.
Polyhydramnios has been associated with fetal anomalies in most organ systems. The most common structural anomalies associated with polyhydramnios are those that interfere with fetal swallowing and/or absorption of fluid [16,17]. Decreased swallowing may be due to a primary gastrointestinal obstruction (eg, duodenal, esophageal, or intestinal atresia), neuromuscular disorders (eg, anencephaly), or to secondary obstruction of the gastrointestinal tract (eg, massive unilateral dysplastic kidneys).
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- Leung WC, Jouannic JM, Hyett J, et al. Procedure-related complications of rapid amniodrainage in the treatment of polyhydramnios. Ultrasound Obstet Gynecol 2004; 23:154.
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- Kramer WB, Saade GR, Belfort M, et al. A randomized double-blind study comparing the fetal effects of sulindac to terbutaline during the management of preterm labor. Am J Obstet Gynecol 1999; 180:396.
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- Gilbert WM, Cheung CY, Brace RA. Rapid intramembranous absorption into the fetal circulation of arginine vasopressin injected intraamniotically. Am J Obstet Gynecol 1991; 164:1013.
- Kullama LK, Nijland MJ, Ervin MG, Ross MG. Intraamniotic deamino(D-Arg8)-vasopressin: prolonged effects on ovine fetal urine flow and swallowing. Am J Obstet Gynecol 1996; 174:78.
- Mann SE, Dvorak N, Gilbert H, Taylor RN. Steady-state levels of aquaporin 1 mRNA expression are increased in idiopathic polyhydramnios. Am J Obstet Gynecol 2006; 194:884.
- Zhu X, Jiang S, Hu Y, et al. The expression of aquaporin 8 and aquaporin 9 in fetal membranes and placenta in term pregnancies complicated by idiopathic polyhydramnios. Early Hum Dev 2010; 86:657.
- Aviram A, Salzer L, Hiersch L, et al. Association of isolated polyhydramnios at or beyond 34 weeks of gestation and pregnancy outcome. Obstet Gynecol 2015; 125:825.
- Kramer MS, Rouleau J, Baskett TF, et al. Amniotic-fluid embolism and medical induction of labour: a retrospective, population-based cohort study. Lancet 2006; 368:1444.
- CLINICAL MANIFESTATIONS
- CLINICAL SIGNIFICANCE
- POST-DIAGNOSTIC EVALUATION
- MANAGEMENT OF POLYHYDRAMNIOS
- Antepartum fetal monitoring
- Indications for intervention
- - Gestational age based approach
- Pregnancies under 32 weeks
- Pregnancies over 32 weeks
- - Amnioreduction
- - Prostaglandin synthetase inhibitors
- - Investigational approaches
- Management of labor
- Timing of delivery
- SUMMARY AND RECOMMENDATIONS