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Polyhydramnios: Etiology, Diagnosis,and TreatmentJohn D. Yeast, MD*

Author Disclosure

Dr Yeast did not

disclose any financial

relationships relevant

to this article.

Objectives After completing this article, readers should be able to:1. Understand the various causes of polyhydramnios.

2. Describe the pathways of amniotic fluid production and removal.

3. Appreciate the reason for preterm delivery following the diagnosis of polyhydramnios.

4. Recognize the treatment methods for polyhydramnios.

5. Explain the importance of sudden changes in fundal size during pregnancy.

IntroductionPolyhydramnios, sometimes referred to as hydramnios, is a relatively uncommon compli-

cation affecting pregnancy that refers to the presence of an excessive amount of amniotic

fluid relative to gestational age. Onset may be gradual or sudden, based on the cause.

Gradual onset may be largely asymptomatic. In this situation, the diagnosis is suspected

when fundal height exceeds that expected for gestational age. In contrast, sudden onset of

polyhydramnios often is symptomatic, characterized by contractions and significant ab-

dominal discomfort. Polyhydramnios has potential serious consequences, primarily related

to the cause, but also due to the increased risk of adverse pregnancy outcome, such as

preterm labor (PTL) or preterm premature rupture of the membranes (PPROM).

Incidence and FrequencyThe exact incidence of polyhydramnios is unknown because mild, asymptomatic cases may

be discovered only at the time of delivery and are underreported. Several series have

suggested that the incidence may range up to 1.6% in a low-risk population. Most cases are

mild and often not associated with any significant sequelae. Approximately 35% of cases

could be classified as moderate or severe, requiring further diagnostic or therapeutic

measures.

Prior to the routine use of diagnostic ultrasonography, the incidence of polyhydramnios

seemed much lower. Today, though, ultrasonography studies may reveal an abnormal

increase in amniotic fluid volume earlier in pregnancy, resulting in more cases being

reported. Intuitively, it seems that earlier diagnosis via ultrasonography could improve

outcome, but that has not yet been proven conclusively.

DiagnosisThe clinical suspicion of abnormally large fundal size remains critical to the diagnosis of

polyhydramnios. Serial measurements of uterine height at the time of prenatal visits can

stimulate the clinician to consider possible causes of abnormal fundal size. Subsequently,obstetric ultrasonography can confirm the presence of abnormally increased amniotic fluid

volume and allow a thorough study of the fetus for possible anatomic causes.

Over the past 25 years, a number of investigators have created models to standardize the

measurement of amniotic fluid volume. In some instances, they have compared and

contrasted formulas for measuring amniotic fluid volume with precise, objective invasive

methods, such as dye dilution studies. Others have compared subjective assessment of

amniotic fluid volume with various formula models. Subjective measurements, however,

do not allow comparisons of values between different observers.

An experienced sonographer can assess the amniotic fluid volume subjectively and have

*Professor and Vice Chairman, Department of Obstetrics and Gynecology, University of Missouri-Kansas City School of

Medicine; Director of Medical Affairs, Saint Luke’s Hospital of Kansas City, Kansas City, Mo.

Article neonatology

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a high index of suspicion that the amount is increased. In

addition, a sonographer can use one of the objective

methods to diagnose polyhydramnios. However, when

intraobserver results are compared, there is a poor corre-

lation unless the fluid volume is very abnormal.

The amniotic fluid index (AFI) has been the most

studied objective measure of amniotic fluid volume. The

sonographer divides the uterus into four quadrants and

measures the greatest vertical depth of fluid without fetal

parts present in each quadrant. The sum of these mea-

surements is the AFI. This method is not used prior to

20 weeks’ gestation. The upper limit of normal for the

AFI is 20 cm, with values of 20 to 24 cm considered

borderline.

Normal AFI values generally are well supported inmost studies. However, diagnosing polyhydramnios by

AFI compared with dye studies showed a sensitivity of

only 30% and a positive predictive value of 57%. As

expected, specificity was good at 98%. Other methods of

objectively measuring amniotic fluid volume, such as

measuring the greatest two diameters of the largest

pocket of amniotic fluid noted (50 cm being the crite-

rion for polyhydramnios) or measuring the single deep-

est pocket of fluid noted (8 cm indicating polyhydram-

nios) also have poor sensitivity, at 38% and 29%,

respectively.

Despite the poor correlation of objective measure-ments of fluid volume with precise dye-dilution studies, a

subjective suspicion of polyhydramnios should be fol-

lowed by ultrasonography using one of the objective

measures of amniotic fluid noted. Serial studies subse-

quently can be employed to evaluate for changes in fluid

volume.

CausesThe production of amniotic fluid and the maintenance of

normal amniotic fluid volume are critical to the develop-

ment of a normal fetus. (See the article by Gilbert in this

issue of NeoReviews .) Production of amniotic fluid variesby gestational age. Early in the pregnancy, fluid primarily

results from transmembranous secretion via the amnion

and the body surface of the embryo. By the early second

trimester, the fetus begins to produce urine, and fluid

also is secreted from the fetal lungs, egressing into the

amniotic cavity. By 20 to 22 weeks’ gestation, the fetal

skin surfaces keratinize and no longer are a source of

amniotic fluid. Thus, most of the fluid in the latter half of

gestation comes from the fetal kidneys and, to a lesser

extent, fetal lungs.

Fetal urine production is estimated at 2 to 5 mL/h

around 22 to 24 weeks’ gestation and almost50 mL/h at

term. These estimates are based on ultrasonography-

derived measures of fetal bladder volume changes in

pregnancy. Lung fluid production has been estimated to

be 150 to 170 mL/d, with most of the fluid excreted into

the amniotic fluid compartment. Lung fluid production

appears to be critical to maintaining growth and devel-

opment of the alveoli. In addition, some studies suggest

that the excess amount of fluid produced creates a pres-

sure differential in the terminal bronchioles that further

expands the developing alveolar buds.

Fluid leaves the amniotic cavity in the second half of

pregnancy largely via two routes. First, fetal swallowing

normally accounts for the vast amount of fluid leaving

the amniotic compartment. It is estimated that the late-

term fetus swallows about 500 to 1,000 mL/d. The fetalgastrointestinal tract absorbs fluid and solutes and re-

turns them to the maternal compartment via the pla-

centa. Less well understood is the egress of fluid via the

intramembranous process. It is well documented in fetal

lambs and other animal models that a moderate amount

of fluid can be absorbed via the placental surface. Inter-

estingly, in fetal sheep models, occlusion of fetal swallow-

ing results in a marked increase of intramembranous fluid

flow. One estimate of normal flow via the transmembra-

nous route is approximately 300 to 400 mL/d.

Regulation of normal amniotic fluid volume, that is,

the balance of fluid production and removal, is poorly understood. Animal models that artificially increase fluid

production or restrict fluid removal by one mechanism

show that alternate mechanisms can readily adapt and

adjust their role in homeostasis of fluid volume. How-

ever, the “sensors” that control such mechanisms are

unknown. Possibly, fluid volume, osmolality, and elec-

trolyte concentrations all contribute to amniotic fluid

homeostasis in the healthy fetus.

From a clinical perspective, polyhydramnios results

from an overproduction of amniotic fluid or an interrup-

tion in the removal of fluid from the amniotic cavity.

Causes can be subdivided further into maternal or fetalorigin (Table 1). The primary maternal cause of polyhy-

dramnios is diabetes mellitus, which may contribute up

to 25% of the cases recognized. However, such cases of

polyhydramnios usually are in the mild-to-moderate

range and seldom are associated with significant morbid-

ity. The precise cause in maternal diabetes seems to be

the increase in fetal urine production, probably related to

increased osmotic gradients in fetal blood flow from the

placenta due to hyperglycemia.

Fetal causes of polyhydramnios can be divided primar-

ily into two general categories: neurologic inhibition of

the fetal swallowing mechanism and mechanical obstruc-

neonatology polyhydramnios

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tion or interruption of swallowing and gastrointestinal

absorption (Table 2). Neurologic inhibition of the swal-

lowing mechanism, and perhaps inhibition of the regu-

latory mechanism of amniotic fluid homeostasis, can

result from congenital disorders such as some aneu-

ploidies or neuromuscular disorders or acquired condi-tions such as in utero viral infections that have central

nervous system manifestations. More common causes are

mechanical obstruction of swallowing, such as atresia of

the esophagus or bowel or obstruction of the gastroin-

testinal tract by intra-abdominal masses. Less common

causes of polyhydramnios are severe fetal anemia with

associated hydrops, usually due to isoimmunization or

fetal-maternal hemorrhage. In these latter diagnoses, the

increased amniotic fluid volume may result from high-

output cardiac perfusion of the kidneys, with resultant

increased urine production, or from cardiac failure and

reduced swallowing mechanisms.Based on some series, 40% to 60% of cases of polyhy-

dramnios do not have an apparent cause during preg-

nancy. So-called “idiopathic” polyhydramnios can occur

with a healthy fetus, although careful neonatal evaluation

still is indicated.

Evaluation and TreatmentEvaluation of the fetus by thorough, targeted anatomic

ultrasonography is the cornerstone of determining a

diagnosis and cause when polyhydramnios is suspected.

The probability of diagnosing a fetal structural defect as

the cause of the increased amniotic fluid volume im-

proves as the volume of fluid increases. With severe

polyhydramnios, more than 30% of fetal studies result in

identification of a structural defect. Experienced perina-

tal consultation should be obtained to aid in overall

management.

Amniocentesis for fetal karyotype is strongly recom-

mended, especially in the presence of a structural defect.

In addition, maternal screening for evidence of fetal-

maternal bleeding, congenital infection, and possibly

hereditary anemias may be considered. Routine prenatal

laboratory results should be reviewed, especially glucose

screening, isoimmunization, and maternal serum

screens. If no cause can be determined prior to delivery,

the pediatric staff must evaluate the newborn carefully,

paying close attention to neuromuscular developmentand function as well as ruling out structural defects not

always seen during obstetric ultrasonography (certain

cardiac defects, midline cleft malformations, and tra-

cheoesophageal fistulas).

For most cases of polyhydramnios, no intervention or

aggressive therapy is indicated. However, based on the

degree of excess amniotic fluid, the pregnancy may be at

risk for PPROM, PTL, or maternal respiratory restric-

tion. Also, there is an increased risk of fetal death, prob-

ably related to the underlying cause of the fluid disorder.

The pregnancy in which amniotic fluid volume is

increased should be followed carefully, with screening forsigns and symptoms of PTL, maternal compromise, or

Table 2. Findings inPolyhydramnios

Increase in Fetal Urine Output

● Hydrops● Some central nervous system lesions associated with

decreased antidiuretic hormone output● Maternal diabetes

Decreased Fetal Swallowing

● Some central nervous system lesions● Aneuploidies● Neuromuscular disorders

Decreased Gastrointestinal Absorption of Fluid

● Gastrointestinal obstruction or atresia● Nongastrointestinal obstructive masses

Fetal Structural Disorders Associated With Large-volume Transudates

● Open neural tube defects● Abdominal wall defects

Table 1.

Causes of PolyhydramniosFetal Disorders

● Structural malformations—Central nervous system structural defects—Obstruction or atresia of portions of the

gastrointestinal tract—Abdominal wall defects

● Aneuploidies● Neuromuscular disorders

Maternal Disorders

● Diabetes mellitus

Combined Disorders

● Isoimmunization● Congenital infections● Congenital anemias

Idiopathic





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fetal jeopardy. Reduction in maternal activity and in-

creased bedrest may be prudent, although neither has

been shown conclusively to change outcome. In some

instances, polyhydramnios resolves spontaneously.

Maternal symptoms are the most common reason for

therapeutic intervention. If the patient becomes symp-

tomatic, either with uterine irritability, respiratory com-

promise, or discomfort, treatment may be necessary to

prolong the pregnancy. Based on gestational age, two

options are available: amnioreduction or the use of pros-

taglandin inhibitors to attempt a medical reduction of

fluid production.

Amnioreduction should be performed by personnel

familiar with the procedure. Using ultrasonography

guidance, a large-bore needle is placed in the amnioticcavity, and fluid is removed via a suction pump. The goal

is to remove fluid slowly, reducing fluid volume to a

near-normal AFI of less than 25 cm. Some patients

require mild sedation, analgesics, or tocolytics for the

procedure, although most tolerate the amnioreduction

without incident. The amniotic fluid volume should be

evaluated frequently (at least twice weekly) and the pro-

cedure repeated when symptoms recur or volumes begin

to increase significantly. Some patients may require serial

procedures to prolong pregnancy. Careful informed con-

sent must be obtained because the procedure may pre-

cipitate PTL or PPROM. Also, the risk/benefit balance versus gestational age must be considered carefully.

Some data suggest that prostaglandin inhibitors, such

as indomethacin or ibuprofen, may reduce fetal urine

production. Although no controlled, randomized stud-

ies have compared methods of therapy, medical therapy

may be considered, especially when polyhydramnios de-

velops at early gestational ages. Due to the concern over

fetal ductus arteriosus closure with prostaglandin treat-

ment, therapy should be conducted only in perinatal

centers that have the ability to follow fetal ductal blood

flow. In addition, it would seem prudent not to use such

therapy beyond 32 weeks gestational age.Treatment of significant polyhydramnios prior to

term may include corticosteroid therapy to enhance fetal

lung maturity. Antepartum surveillance with ultrasonog-

raphy and cardiotocography should be employed prior to

delivery. The goal of all therapy is to assure fetal and

maternal well-being and allow the fetus to reach matu-

rity. In some cases, however, delivery prior to fetal ma-

turity may result or be indicated. The method of delivery

depends on fetal well-being and standard obstetric indi-

cations. Increased amniotic fluid volume does increase

the chance of fetal malposition or funic (cord) presenta-

tion. Sudden uterine decompression with PPROM or

amniotomy can result in placental abruption. The fetus

should be monitored continuously at all times during

labor and delivery.

Suggested ReadingCardwell MS. Polyhydramnios: a review. Obstet Gynecol Surv. 1987;

42:612–617Carlson D, Platt L, Medearis A, Horenstein J. Quantifiable poly-

hydramnios: diagnosis and management. Obstet Gynecol 1990;75:989–993

Chauhan SP, Magann EF, Morrison JC, Whitworth NS, HendrixNW, Devoe LD. Ultrasonographic assessment of amniotic fluiddoes not reflect actual amniotic fluid volume. Am J Obstet

Gynecol. 1997;177:291–296Dashe JS, McIntire DD, Ramus RM, Santos-Ramos R, TwicklerDM. Hydramnios: anomaly prevalence and sonographic detec-tion. Obstet Gynecol. 2002;100:134–139

Elliott JP, Sawyer AT, Radin TG, Strong RE. Large-volume thera-peutic amniocentesis in the treatment of hydramnios. Obstet Gynecol. 1994;84:1025–1027

Golan A, Wolman I, Sagi J, Yovel I, David MP. Persistence of

polyhydramnios and preterm delivery. Gynecol Obstet Invest.

1994;37:18–20Harding R, Bocking AD, SiggerJN, Wickham PJ. Composition and

volume of fluid swallowed by sheep. Q J Exp Physiol. 1984;69:487–495

Hill L, Breckle R, Thomas ML, Fries JK. Polyhydramnios: ultra-sonically detected prevalence and neonatal outcome. Obstet

Gynecol. 1987;69:21–25Kirshon B, Mari G, Moise KJ Jr. Indomethacin therapy in the

treatment of symptomatic polyhydramnios. Obstet Gynecol.

1990;75:202–205Magann EF, Chauhan SP, Barrilleaux PS, Whitworth NS, Martin

JN. Amniotic fluid index and single deepest pocket: weak indi-cators of abnormal amniotic fluid volumes. Obstet Gynecol.

2000;96:737–740Modena AB, Fieni S. Amniotic fluid dynamics. Acta Biomed Ateneo

Parmense. 2004;75(suppl):11–13Moise KJ Jr. Polyhydramnios. Clin Obstet Gynecol . 1997;40:

266–279Ott WJ. Reevaluation of the relationship between amniotic fluid

volume and perinatal outcome. Am J Obstet Gynecol. 2005;192:

1803–1809PhelanJP, ParkYW, Ahn MO,Rutherford SE.Polyhydramniosand

perinatal outcome. J Perinatol. 1990;10:347–350Piantelli G, Bedocchi L, Cavicchioni O, et al. Amnioreduction for

treatment of severe polyhydramnios. Acta Biomed Ateneo Par- mense. 2004;75:56–58

Pritchard JA. Fetal swallowing and amniotic fluid volume. Obstet Gynecol. 1966;28:606– 610

Quinlan RW, Amelia CC, Martin M. Hydramnios: ultrasounddiagnosis and its impact on perinatal management and preg-

nancy outcome. Am J Obstet Gynecol. 1983;145:306–311Smith C, Plambeck RD,Rayburn WF,Albaugh KJ.Relationof mild

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NeoReviews Quiz

4. Polyhydramnios is a complication of pregnancy whose estimated incidence is up to 1.6% of pregnancies ina low-risk population. Of the following, the most accurate statement regarding polyhydramnios is that:

A. Approximately 10% of cases have no identifiable cause.B. Cases that have a gradual onset are generally asymptomatic.C. Early diagnosis has been proven to improve perinatal outcome.D. Measurement of the amniotic fluid index is best performed before 20 weeks’ gestation.E. Most cases are moderate-to-severe and associated with sequelae.

5. Polyhydramnios results from an overproduction of amniotic fluid or an interruption in its removal from theamniotic cavity. The causes of polyhydramnios can be of maternal or fetal origin. Of the following, themost common fetal cause of polyhydramnios is:

A. Decreased absorption of amniotic fluid due to gastrointestinal atresia.B. Decreased fetal swallowing from neuromuscular disorder.C. Excessive transudation of fluid from an abdominal wall defect.D. Increased fetal lung fluid secretion associated with gestational diabetes.E. Increased fetal urine output from hydrops associated with anemia.

6. The treatment of polyhydramnios during pregnancy depends on several factors, including the degree of excess amniotic fluid, maternal symptoms, and gestational age of the fetus. Of the following, the most common obstetric intervention for polyhydramnios is:

A. Amnioreduction.B. Expectant observation.C. Reduction in maternal activity.D. Treatment with diuretics.

E. Treatment with prostaglandin inhibitors.





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DOI: 10.1542/neo.7-6-e3002006;7;e300 NeoReviews

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