See discussions, stats, and author profiles for this publication at: https://www.researchgate.

net/publication/239322409

Polyhydramnios: Etiology, Diagnosis, and Treatment

Article  in  NeoReviews · June 2006

DOI: 10.1542/neo.7-6-e300

CITATION READS

1 1,596

1 author:

John Yeast
Saint Luke's Health System (KS, USA)
54 PUBLICATIONS   1,450 CITATIONS   

SEE PROFILE

All content following this page was uploaded by John Yeast on 06 May 2015.

The user has requested enhancement of the downloaded file.

 Polyhydramnios: Etiology, Diagnosis, and Treatment
John D. Yeast
NeoReviews 2006;7;e300-e304
DOI: 10.1542/neo.7-6-e300

The online version of this article, along with updated information and services, is
located on the World Wide Web at:
http://neoreviews.aappublications.org/cgi/content/full/neoreviews;7/6/e300

NeoReviews is the official journal of the American Academy of Pediatrics. A monthly publication,
it has been published continuously since 2000. NeoReviews is owned, published, and trademarked
by the American Academy of Pediatrics, 141 Northwest Point Boulevard, Elk Grove Village,
Illinois, 60007. Copyright © 2006 by the American Academy of Pediatrics. All rights reserved.
Online ISSN: 1526-9906.

Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010

Article neonatology

Polyhydramnios: Etiology, Diagnosis,

and Treatment
John D. Yeast, MD*
Objectives After completing this article, readers should be able to:

1. Understand the various causes of polyhydramnios.

Author Disclosure 2. Describe the pathways of amniotic fluid production and removal.
Dr Yeast did not 3. Appreciate the reason for preterm delivery following the diagnosis of polyhydramnios.
disclose any financial 4. Recognize the treatment methods for polyhydramnios.
relationships relevant 5. Explain the importance of sudden changes in fundal size during pregnancy.
to this article.

Introduction
Polyhydramnios, 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 Frequency

The 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.

Diagnosis
The 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.

e300 NeoReviews Vol.7 No.6 June 2006

Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010

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 in
most 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.
Causes
The 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 varies
by 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 almost 50 mL/h at
Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010
neonatology polyhydramnios
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 fetal
gastrointestinal 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 fetal
origin (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-
NeoReviews Vol.7 No.6 June 2006 e301
neonatology polyhydramnios

proves as the volume of fluid increases. With severe

Table 1. Causes of Polyhydramnios polyhydramnios, more than 30% of fetal studies result in
identification of a structural defect. Experienced perina-
Fetal Disorders tal consultation should be obtained to aid in overall
● Structural malformations management.
—Central nervous system structural defects Amniocentesis for fetal karyotype is strongly recom-
—Obstruction or atresia of portions of the mended, especially in the presence of a structural defect.
gastrointestinal tract
—Abdominal wall defects In addition, maternal screening for evidence of fetal-
● Aneuploidies maternal bleeding, congenital infection, and possibly
● Neuromuscular disorders hereditary anemias may be considered. Routine prenatal
Maternal Disorders laboratory results should be reviewed, especially glucose
screening, isoimmunization, and maternal serum
● Diabetes mellitus
screens. If no cause can be determined prior to delivery,
Combined Disorders the pediatric staff must evaluate the newborn carefully,
● Isoimmunization paying close attention to neuromuscular development
● Congenital infections and function as well as ruling out structural defects not
● Congenital anemias always seen during obstetric ultrasonography (certain
Idiopathic 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
tion or interruption of swallowing and gastrointestinal degree of excess amniotic fluid, the pregnancy may be at
absorption (Table 2). Neurologic inhibition of the swal- risk for PPROM, PTL, or maternal respiratory restric-
lowing mechanism, and perhaps inhibition of the regu- tion. Also, there is an increased risk of fetal death, prob-
latory mechanism of amniotic fluid homeostasis, can ably related to the underlying cause of the fluid disorder.
result from congenital disorders such as some aneu- The pregnancy in which amniotic fluid volume is
ploidies or neuromuscular disorders or acquired condi- increased should be followed carefully, with screening for
tions such as in utero viral infections that have central signs and symptoms of PTL, maternal compromise, or
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 Findings in
Table 2.

causes of polyhydramnios are severe fetal anemia with Polyhydramnios

associated hydrops, usually due to isoimmunization or
fetal-maternal hemorrhage. In these latter diagnoses, the Increase in Fetal Urine Output
increased amniotic fluid volume may result from high- ● Hydrops
output cardiac perfusion of the kidneys, with resultant ● Some central nervous system lesions associated with
increased urine production, or from cardiac failure and decreased antidiuretic hormone output
● Maternal diabetes
reduced swallowing mechanisms.
Based on some series, 40% to 60% of cases of polyhy- Decreased Fetal Swallowing
dramnios do not have an apparent cause during preg- ● Some central nervous system lesions
nancy. So-called “idiopathic” polyhydramnios can occur ● Aneuploidies
● Neuromuscular disorders
with a healthy fetus, although careful neonatal evaluation
still is indicated. Decreased Gastrointestinal Absorption of Fluid
● Gastrointestinal obstruction or atresia
Evaluation and Treatment ● Nongastrointestinal obstructive masses
Evaluation of the fetus by thorough, targeted anatomic Fetal Structural Disorders Associated With Large-
ultrasonography is the cornerstone of determining a volume Transudates
diagnosis and cause when polyhydramnios is suspected.
● Open neural tube defects
The probability of diagnosing a fetal structural defect as ● Abdominal wall defects
the cause of the increased amniotic fluid volume im-

e302 NeoReviews Vol.7 No.6 June 2006

Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010

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 amniotic
cavity, 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
Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010
neonatology polyhydramnios
amniotomy can result in placental abruption. The fetus
should be monitored continuously at all times during
labor and delivery.
Suggested Reading
Cardwell MS. Polyhydramnios: a review. Obstet Gynecol Surv. 1987;
42:612– 617
Carlson 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, Hendrix
NW, Devoe LD. Ultrasonographic assessment of amniotic fluid
does not reflect actual amniotic fluid volume. Am J Obstet
Gynecol. 1997;177:291–296
Dashe JS, McIntire DD, Ramus RM, Santos-Ramos R, Twickler
DM. 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 –20
Harding R, Bocking AD, Sigger JN, 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;69:21–25
Kirshon B, Mari G, Moise KJ Jr. Indomethacin therapy in the
treatment of symptomatic polyhydramnios. Obstet Gynecol.
1990;75:202–205
Magann 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;96:737–740
Modena AB, Fieni S. Amniotic fluid dynamics. Acta Biomed Ateneo
Parmense. 2004;75(suppl):11–13
Moise KJ Jr. Polyhydramnios. Clin Obstet Gynecol. 1997;40:
266 –279
Ott WJ. Reevaluation of the relationship between amniotic fluid
volume and perinatal outcome. Am J Obstet Gynecol. 2005;192:
1803–1809
Phelan JP, Park YW, Ahn MO, Rutherford SE. Polyhydramnios and
perinatal outcome. J Perinatol. 1990;10:347–350
Piantelli 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: ultrasound
diagnosis and its impact on perinatal management and preg-
nancy outcome. Am J Obstet Gynecol. 1983;145:306 –311
Smith C, Plambeck RD, Rayburn WF, Albaugh KJ. Relation of mild
idiopathic polyhydramnios to perinatal outcome. Obstet Gy-
necol. 1992;79:387–389
Underwod MA, Gilbert WM, Sherman MP. Amniotic fluid: not just
fetal urine anymore. J Perinatol. 2005;25:341–348
NeoReviews Vol.7 No.6 June 2006 e303
neonatology polyhydramnios

NeoReviews Quiz
4. Polyhydramnios is a complication of pregnancy whose estimated incidence is up to 1.6% of pregnancies in
a 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 the
amniotic cavity. The causes of polyhydramnios can be of maternal or fetal origin. Of the following, the
most 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.

e304 NeoReviews Vol.7 No.6 June 2006

Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010
 Polyhydramnios: Etiology, Diagnosis, and Treatment
John D. Yeast
NeoReviews 2006;7;e300-e304
DOI: 10.1542/neo.7-6-e300

Updated Information including high-resolution figures, can be found at:

& Services http://neoreviews.aappublications.org/cgi/content/full/neoreview
s;7/6/e300
Permissions & Licensing Information about reproducing this article in parts (figures,
tables) or in its entirety can be found online at:
http://neoreviews.aappublications.org/misc/Permissions.shtml
Reprints Information about ordering reprints can be found online:
http://neoreviews.aappublications.org/misc/reprints.shtml

Downloaded from http://neoreviews.aappublications.org by J Michael Coleman on August 19, 2010

View publication stats