Assessment of Amniotic Fluid Volume

in Pregnancy
Priyanka Jha, MBBS • Preethi Raghu, MD • Anne M. Kennedy, MB, BCh • Mark Sugi, MD • Tara A. Morgan, MD • Vickie Feldstein, MD
Liina Pōder, MD • Rubal Penna, DO
Author affiliations, funding, and conflicts of interest are listed at the end of this article.

Amniotic fluid (AF) is an integral part of the fetal environment and is essen-
tial for fetal growth and development. Pathways of AF recirculation include
the fetal lungs, swallowing, absorption through the fetal gastrointestinal
tract, excretion through fetal urine production, and movement. In addi-
tion to being a marker for fetal health, adequate AF is necessary for fetal
lung development, growth, and movement. The role of diagnostic imag-
ing is to provide a detailed fetal survey, placental evaluation, and clini-
cal correlation with maternal conditions to help identify causes of AF
abnormalities and thereby enable specific therapy. Oligohydramnios
prompts evaluation for fetal growth restriction as well as genito-
urinary issues, including renal agenesis, multicystic dysplastic
kidneys, ureteropelvic junction obstruction, and bladder outlet
obstruction. Premature preterm rupture of membranes should
also be clinically excluded as a cause of oligohydramnios.
Clinical trials evaluating amnioinfusion are underway as a
potential intervention for renal causes of oligohydramnios.
Most cases of polyhydramnios are idiopathic, with maternal
diabetes being a common cause. Polyhydramnios prompts
evaluation for fetal gastrointestinal obstruction and oro-
pharyngeal or thoracic masses, as well as neurologic or
musculoskeletal anomalies. Amnioreduction is per-
formed only for maternal indications such as symp-
tomatic polyhydramnios causing maternal respiratory
distress. Polyhydramnios with fetal growth restric-
tion is paradoxical and can occur with maternal
diabetes and hypertension. When these maternal
conditions are absent, this raises concern for an-
euploidy. The authors describe the pathways of
AF production and circulation, US and MRI as-
sessment of AF, disease-specific disruption of
AF pathways, and an algorithmic approach
to AF abnormalities.
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RSNA, 2023 • radiographics.rsna.org

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Supplemental RadioGraphics 2023; 43(6):e220146
https://doi.org/10.1148/rg.220146
Material
Content Codes: OB, US
Quiz questions Abbreviations: AF = amniotic fluid, AFI = AF index,
for this article are AFV = AF volume, ARPCKD = autosomal recessive
available through
polycystic kidney disease, DVP = deepest vertical
the Online Learning pocket, FGR = fetal growth restriction, MCDK =
Center. multicystic dysplastic kidney, PART = polyhydram-
nios affecting recipient-like twin, PPROM = preterm
premature rupture of membranes, PUV = posterior
urethral valve, TTTS = twin-twin transfusion syn-
drome, UPJ = ureteropelvic junction
TEACHING POINTS
„ Before 16 weeks of gestation, AF is primarily produced and maintained
through intramembranous flow across the amnion, chorion, and placental sur-
face. As the fetal kidneys develop after 16 weeks gestational age, fetal urine
production is the largest contributor to AF volume (AFV).
„ Guidelines recommend using DVP for diagnosing oligohydramnios and AFI
for polyhydramnios.
„ Severe oligohydramnios or anhydramnios is fatal due to the high incidence of
pulmonary hypoplasia.
„ Fetal gastrointestinal tract obstruction usually manifests with late polyhydram-
nios (after 24 weeks of gestation). Obstruction may be intrinsic or extrinsic
and leads to polyhydramnios due to a decreased amount of AF swallowed
by the fetus.
„ Polyhydramnios with FGR, in the absence of maternal diabetes or hyperten-
sion, is highly associated with an increased risk for aneuploidy (most common-
ly trisomy 18) .
Introduction
During pregnancy, the fetus is surrounded by the amniotic
fluid (AF) within the gestational sac. AF ensures a sterile
environment for the developing fetus and provides tempera-
ture regulation and shock absorption (1). AF allows adequate
space for fetal movement and the growth of organs, partic-
ularly the lungs (1). AF regulation occurs at three primary
levels: placental control of water and solute transfer; regula-
tion of fetal inflows and outflows; and maternal effect on fetal
fluid balance (1,2). Decreased AF production can be due to
fetal genitourinary abnormalities, placental insufficiency, or
fetal growth restriction (FGR) (1–3). Preterm premature rup-
ture of membranes (PPROM) can lead to AF leak and oligohy-
dramnios (4). Polyhydramnios develops from inadequate re-
sorption from gastrointestinal obstruction or from infrequent
or absent fetal swallowing caused by neurologic and muscu-
loskeletal disorders (1,3). Maternal causes of polyhydramnios
include diabetes and hypertension. Hence, AF monitoring is a
critical component of all obstetric US examinations (5).
In this article, we describe an algorithmic approach to AF
abnormalities based on AF production and circulation path-
ways and their disease-specific disruption (Fig 1, Table 1).
Diagnostic criteria and causes of polyhydramnios and oligo-
hydramnios (including those pertaining to twin pregnancies),
relevant interventions, and their indications are discussed.
AF Production and Circulation
Before 16 weeks of gestation, AF is primarily produced and
maintained through intramembranous flow across the am-
nion, chorion, and placental surface (1–3). As the fetal kid-
neys develop after 16 weeks gestational age, fetal urine pro-
Volume 43 Number 6 2 radiographics.rsna.org
duction is the largest contributor to AF volume (AFV) (1–3).
This urinary contribution plateaus around 34 weeks and
reaches a steady state for the rest of the gestation (1). Path-
ways of AF recirculation include swallowing and absorption
through the fetal gastrointestinal tract and lungs, excretion
through fetal urine, and movement (Fig 2) (1–3). Intact neu-
romuscular development is mandatory for swallowing. The
swallowed AF is absorbed in the gut and lungs or regurgitated
orally. Swallowing is critical for lung maturity. Fluid entering
the lungs causes branching of the distal alveolar buds (1–3).
Oligohydramnios leads to poor branching and fewer alveoli,
resulting in pulmonary immaturity. The absorbed fluid from
the gut is excreted from the fetal urinary tract into the am-
niotic cavity. When the fetus moves, the motion causes fluid
redistribution. Maternal and placental factors such as serum
osmolality, blood pressure, and changes in placental vascu-
larity affect the degree of intra­membranous flow and induce
changes in overall AFV (1).
Imaging Techniques
Ultrasonography
A complete obstetric US examination includes evaluation of
the uterus, cervix and adnexa, and placenta; complete fetal
anatomic survey; and AF assessment (5). Qualitative AFV as-
sessment is performed by visually comparing AF pockets to
the volume occupied by the fetus and placenta (1). The vol-
ume of intrauterine communicating pockets surrounding the
fetus should be equal to or slightly greater than that of the
volume occupied by the fetal parts and placenta in the first
and second trimesters. This method is particularly helpful in
the first trimester when semiquantitative measurements are
inapplicable or later in gestation for visual global assessment
of the pregnancy (1).
There are two semiquantitative measurements for evalu-
ating AFV: AF index (AFI) and deepest vertical pocket (DVP)
(5–7). After 20 weeks of gestation, either AFI or DVP can be
used to assess AFV (8). A proper AFI measurement technique
includes first imaging the entire uterus and then visually di-
viding the uterus into four equal quadrants. While keeping
the US probe perpendicular to the floor, the operator mea-
sures the longest anterior-posterior dimension of the largest
fluid pocket (in centimeters) in each quadrant while exclud-
ing any fetal parts, vessels, or the umbilical cord (Fig 3) (1).
The measurement starts at the superficial edge of the fluid
pocket and extends up to the deeper uterus or fetal parts (Figs
3B, 4A) (1). The fluid pocket must measure at least 1 cm wide
to be included in the AFI or DVP (Fig 4C) (1). The sum of all
four measurements equals the AFI (1,3). To assess the DVP,
the single largest pocket any where in the uterus is identified
and measured. Notably, this differs from the AFI because the
single largest pocket may not be in one of the outer quadrants
and can be more central. When none of the fluid pockets are 1
cm wide, this may be reported as severe oligohydramnios with
a few nonmeasurable pockets of fluid.
Per the American Institute of Ultrasound in Medicine
(AIUM) and Society for Maternal-Fetal Medicine (SMFM)
practice guidelines for singleton pregnancies, studies have
June 2023 Jha et al

Figure 1. Proposed algorithm for identifying causes of AF disturbances. Diagram shows a multifactorial basis of oligohydramnios and polyhydramnios and
serves as a guide for focused anatomic evaluation for potential underlying structural abnormalities. ARPCKD = autosomal recessive polycystic kidney disease,
CNS = central nervous system, GI = gastrointestinal, GU = genitourinary, MCDK = multicystic dysplastic kidney, UPJ = ureteropelvic junction.

Table 1: Common and Uncommon Causes of Oligohydramnios and Polyhydramnios

Cause Oligohydramnios Polyhydramnios

Maternal Preterm premature rupture of mem-
branes (PPROM)
Maternal hypertension
Fetal Fetal growth restriction (FGR)
Genitourinary causes: renal agene-
sis, multicystic dysplastic kidney
(MCDK), autosomal recessive poly-
cystic kidney disease (ARPCKD),
bilateral UPJ obstruction, posterior
urethral valves (PUV), prune belly
syndrome
Placental Placental insufficiency (usually associ- Placental masses (eg, chorioangioma)
ated with growth restriction)
Diabetes
Obesity
Maternal hypertension
Fetal macrosomia
Hydrops
Gastrointestinal causes: esophageal atresia, duodenal atresia, jejunal or ileal
atresia
Extrinsic compression: cervical mass, mediastinal mass
Central nervous system anomalies with impaired swallowing
Skeletal causes: arthrogryposis akinesia sequence, skeletal dysplasia
Pulmonary causes: congenital pulmonary airway malformation
Genitourinary issues: unilateral UPJ obstruction, mesoblastic nephroma

shown that using DVP could overdiagnose polyhydramnios
and using AFI could overdiagnose oligohydramnios (6–10).
Therefore, guidelines recommend using DVP for diagnosing
oligohydramnios and AFI for polyhydramnios (9). For AF as-
sessment in twin pregnancies, DVP for each amniotic sac is
used (11).
AF nomograms varying with gestational age have been
published. The current standard of care uses DVP and AFI for
AF assessment (7,12–14). Nomograms are not widely used in
clinical practice yet (5,15).
Magnetic Resonance Imaging
Fetal MRI is being used for anatomic evaluation at many cen-
ters, especially when US is technically inadequate due to over-
lying soft tissue or oligohydramnios or when MRI has the po-
tential to add additional diagnostic or prognostic information
(16). Unlike US, semiquantitative measures for AF evaluation
have not been established for MRI. Hence, subjective assess-
ment becomes necessary. Artificial intelligence techniques
that may help with quantitative AF assessment at MRI are
currently under investigation (1,17,18).

Volume 43 Number 6 3 radiographics.rsna.org

June 2023 Jha et al
Figure 2. AF production and circulation. Illustration shows various mech-
anisms of AF production, including intramembranous flow and urine pro-
duction. AF circulates through fetal swallowing and is necessary for lung
development.
Technical Pitfalls.—The entire uterus should be analyzed for
AF pockets before measurements for AFI and DVP are per-
formed. All pockets should be identified, including any cen-
tral pockets (1). Manual US probe pressure should be eased
because too much pressure, or a far lateral approach, can lead
to underestimation of AFV. Additionally, color Doppler US
should be used to exclude the presence of cord in the pocket
(Fig 5). A thorough search is performed before zooming in on
the image for measurements. Images should be wide enough
to include adjacent fetal, placental, or uterine structures. The
fetal bladder should be identified, as a distended urinary blad-
der can mimic a fluid pocket (Fig 6) with severe oligohydram-
nios. Other potential AF mimics include cystic masses such as
cystic hygroma (Fig 7, Movie 1). Another potential pitfall is re-
verberation artifact superficially being incorrectly interpreted
as myometrium and hence excluded from measurement,
thereby leading to underestimation of AFV. DVP assessment
in multiple gestations can be challenging due to difficulty in
visualizing the intertwin membrane (1,11).
Oligohydramnios
Oligohydramnios is defined as a DVP measurement less
than 2 cm and an AFI of less than 5 cm (1,2,10). Current
guidelines recommend using DVP measurements to diag-
nose oligohydramnios (6–10). Nonvisualization of any AF is
anhydramnios. Severe oligohydramnios or anhydramnios is
fatal due to the high incidence of pulmonary hypoplasia.
There are two incidence peaks of oligohydramnios, the
first occurring between 13 and 21 weeks gestation and usu-
ally secondary to fetal genitourinary causes (1). The later
peak between 34 and 42 weeks gestation tends to be due to
placental or maternal causes (1). Genitourinary issues need
to be assessed with all cases of oligohydramnios. The timing
Volume 43 Number 6 4 radiographics.rsna.org
Figure 3. US technique for AF assessment. (A) The
probe should be held perpendicular to the long axis
of the maternal body, and the entire uterus should be
scanned before measurement to identify the deepest
pockets, as shown on the illustration. (B) Transabdom-
inal color Doppler US image at 24 weeks gestation
shows this technique. The fluid pocket must be mea-
sured in the maximum anterior-posterior distance in
each quadrant (calipers), excluding the cord and fetal
parts. The anterior measurement begins at the amniotic
or placental surface and continues to the deeper amni-
otic surface, fetal parts, or placenta.
of onset of oligohydramnios guides US assessment, although
detailed evaluation of all fetal organs and the placenta is al-
ways performed (1). Notably, AFV may remain normal up to
16 weeks gestation even in the presence of fetal renal abnor-
malities because of the initial contribution from membra-
nous AF production (1,2,10).
Maternal Causes of Oligohydramnios
Maternal hypertension can lead to vasoconstriction and af-
fect the placental exchange of fluid, resulting in placental
insufficiency and oligohydramnios (1). PPROM causes oli-
gohydramnios from AF leakage (19,20). Although a clinical
diagnosis, slow and prolonged leaks may be first diagnosed
during US. PPROM can be either spontaneous (usually from
infection) or iatrogenic (eg, after amniocentesis) (19,20).
PPROM portends a worse prognosis if oligohydramnios
June 2023 Jha et al

Figure 4. Technical pitfall of AF measurement at US: improper caliper placement. (A) Transabdominal color Doppler US image in a fetus at 33 weeks ges-
tation with hydrops shows that the AF pocket is incorrectly measured in the center (calipers). The largest anteroposterior dimension is located more laterally
(double-headed arrow) and represents the correct technique for measuring this fluid pocket. (B) Transabdominal AFI measurement in a different fetus at 29
weeks gestation. On these US images, none of the pockets are 1 cm wide (calipers) and should not be used for measurement, which could lead to errone-
ously overestimating the AFI. (C) Transabdominal color Doppler US image shows the correct technique for measurement (calipers). A fluid pocket should be
at least 1 cm wide to be measured for AF estimation, and the largest anteroposterior measurement is included between the calipers.

Volume 43 Number 6 5 radiographics.rsna.org

June 2023 Jha et al

Figure 5. Technical pitfall of AF measure-

ment at US: hypoechoic cord mimicking AF.
(A) Transabdominal gray-scale US image
shows apparent hypoechoic “fluid” sur-
rounding the fetus (arrow). (B) Transabdomi-
nal color Doppler US image shows color sig-
nal filling the entire hypoechoic area (arrow),
consistent with umbilical cord and not AF.

Figure 6. Technical pitfall of AF measurement at US: distended fetal bladder mimicking a fluid
pocket in a patient with anhydramnios. (A) Focused transabdominal color Doppler US image in a fe-
tus at 23 weeks gestation shows a “fluid pocket” being measured (calipers). (B) Large-field-of-view
US image shows anhydramnios with a markedly distended urinary bladder, which was erroneously
measured as a fluid pocket (arrow). This shows the importance of imaging the entire uterus before
performing measurements.

which improve with increasing gestational age at diagnosis,

as the fetal lungs have a longer duration of normal develop-
ment (1).

Fetal Causes of Oligohydramnios

Fetal Growth Restriction.—FGR includes an estimated fetal

Figure 7. Technical pitfall of AF measurement at US: cystic
hygroma mimicking an AF pocket in a 28-year-old patient with
a fetus with Turner syndrome. Transabdominal color Doppler
US image shows a hypoechoic structure (arrow) in the fetal
nuchal region, which was initially measured as AF. This was
appropriately identified as a cystic hygroma after better visual-
ization of the overlying skin on cine clips (Movie 1).
manifests early (less than 25 weeks of gestation) or is pro-
longed (lasting for more than 14 days). Later onset after 25
weeks of gestation is associated with better survival rates,
Volume 43 Number 6 6 radiographics.rsna.org
weight or abdominal circumference measuring less than the
10th percentile for gestational age (21). Sometimes oligohy-
dramnios can manifest before FGR, common causes being
placental insufficiency and fetal aneuploidy (21). Further
Doppler US evaluation is indicated. With FGR, increased um-
bilical artery resistance (decreased or absent diastolic flow)
and decreased middle cerebral artery resistance (brain spar-
ing) are visualized (21,22). Increased uterine artery resistance
at uterine artery Doppler US can occur, although this this is
not universally performed (21,22). Assessment of placental
morphology should include placental thickness, placental
shape, and placental cord insertion site (21,22).
Renal Agenesis.—Nondevelopment of renal tissue constitutes
renal agenesis. US findings are anhydramnios, absent kidneys,
and empty urinary bladder (Fig 8) (21,22). “Lying down” adre-
nal gland may be seen with a flattened appearance of the ad-
renal glands. The normal Y-shape created by impression from
embryonic ascent of the kidneys is lost (Fig 8C, 8D) (1,21).
June 2023 Jha et al
Occasionally, structures such as the bowel can mimic the kid-
neys, and bladder secretions can mimic urine (1). In such cir-
cumstances, the absence of renal arteries arising from the aorta
confirms the diagnosis (Fig 8B). Oligohydramnios may not
develop until 16 weeks of gestation due to early membranous
AF production. This should not preclude the diagnosis of renal
agenesis when normal kidneys are not identified (2,23,24).
Ureteropelvic Junction Obstruction.—Ureteropelvic junction
(UPJ) obstruction is obstruction at the level of the renal pelvis.
A multidisciplinary consensus on the classification of urinary
tract dilatation summarizes the gestational age-based measure-
ments used to diagnose and risk-stratify urinary tract dilata-
tion antenatally (Table 2) (1,12,25–27). Measurement should
be in the axial plane of the kidneys, with the anteroposterior
dimension of the renal pelvis measured (Fig 9A) (1,25). UPJ
obstruction is suspected when the renal pelvis measures 5 mm
or more in the first and second trimesters up to 32 weeks, and
7 mm or more after 32 weeks of gestation. Peripheral calyceal
dilatation occurs with increasing severity of obstruction (Fig 9,
Movie 2) (1,25–27). Bilateral disease leads to oligohydramnios.
Persistent obstruction leads to postobstructive renal cystic dys-
plasia (1,25–27). Careful evaluation of the contralateral kidney
is indicated because there is a 10%–30% incidence of bilateral
UPJ obstruction and a 25% incidence of an additional contra-
lateral renal anomaly (1,25–27).
Unilateral UPJ obstruction is usually associated with nor-
mal AFV, since the other kidney can produce adequate urine
Volume 43 Number 6 7 radiographics.rsna.org
Figure 8. Fetal bilateral renal agenesis in a patient who
presented at 19 weeks gestation for a routine anatomy
scan. (A) Transabdominal US image acquired trans-
versely through the fetal abdomen shows absence of
both kidneys and minimal surrounding AF (oligohydram-
nios), consistent with bilateral renal agenesis. (B) Coronal
transabdominal color Doppler US image through the
fetal abdomen indicates absence of both renal arteries,
which confirms the diagnosis. In real-time evaluation,
other small aortic branches are seen that do not follow
the expected course of renal arteries. These branches,
such as the adrenal, lumbar, and celiac arteries, can
mimic renal arteries at color Doppler US. (C, D) Sagittal
transabdominal gray-scale US images through the renal
fossae show the associated “lying down” adrenal glands
(arrows), which is a sign of renal agenesis. This is thought
to be related to the absence of renal impression, which
would normally result in a Y-shape of the adrenal glands.
(25,26). Approximately one-third of these cases are paradox-
ically associated with polyhydramnios, which is thought to
be related to impaired renal concentrating ability and subse-
quently increased urine output (25,26).
Posterior Urethral Valves.—Bladder outlet obstruction from
posterior urethral valves (PUVs) in male fetuses can result in
oligohydramnios (25–27). Posteriorly oriented PUVs result in
partial or complete obstruction of the urethra and bladder and
eventually result in hydroureteronephrosis (25–27). US shows
a distended urinary bladder and dilated posterior urethra, to-
gether forming a “keyhole” appearance, and bilateral hydro-
ureteronephrosis (Fig 10) (25–27). Postobstructive renal cystic
dysplasia portends a poor prognosis, as it reflects renal paren-
chymal damage (1,25–27). Spontaneous decompression via the
bladder leads to urinary ascites, or urinomas can develop after
renal calyceal rupture (1,25–27).
Fetal intervention is considered for prevention of pulmo-
nary hypoplasia (23,24,28). Specifically, serial bladder drainage
is done to relieve the obstruction and obtain diagnostic evalu-
ation of fetal urine (29). A vesicoamniotic shunt can be placed
with the goal of decompression and AF reconstitution to allow
pulmonary development (29).
Multicystic Dysplastic Kidney.—Multicystic dysplastic kidneys
(MCDKs) are nonfunctioning kidneys caused by replacement
of renal tissue with noncommunicating cysts (1,30,31). US
images show multiple variably sized cysts, which can be focal
June 2023 Jha et al

Table 2: Multidisciplinary Consensus on Classification of Antenatal UTD (UTD Classification System) and US Findings

Parameter UTD A1 (Low Risk) UTD A2–A3 (Increased Risk)

Measurement by gestational age 16–27 weeks: APRPD 4 mm to <7 mm
Calyceal dilatation
Parenchymal thickness
Parenchymal appearance
Ureters
Bladder
Oligohydramnios
16–27 weeks: APRPD ≥7 mm
>28 weeks: APRPD ≥10 mm
>28 weeks: APRPD 7 mm to <10 mm
Central calyceal dilatation or no calyceal dilatation Peripheral calyceal dilatation
Normal Abnormal/thinned
Normal Abnormal (eg, increased echogenicity, cystic change)
Normal Abnormal
Normal Abnormal
No unexplained oligohydramnios Oligohydramnios attributable to genitourinary
causes (and not explainable by other anomalies)

Sources.—References 26 and 27.

Note.—APRPD = anteroposterior renal pelvis diameter, UTD = urinary tract dilatation.

Figure 9. Fetal bilateral UPJ obstruction in a 25-year-old patient who presented with fetal size measuring less than that expected at 32 weeks gestation.
(A) Axial transabdominal gray-scale US image through the mid abdomen shows bilateral dilated renal pelves (calipers) measuring greater than 10 mm an-
teroposteriorly, corresponding to antenatal urinary tract dilatation (UTD) A2–A3 classification. Oligohydramnios was present, with the DVP measuring 1.5 cm.
(B) Coronal transabdominal US image shows fluid distention of the bilateral renal pelves (hydronephrosis) (arrows) with tapering at the UPJ and no ureteral
dilatation, consistent with bilateral UPJ obstruction. (C) Sagittal gray-scale US image shows right hydronephrosis (arrow) with fluid visualized in the urinary
bladder (arrowhead), which can be seen with partial obstruction.

Figure 10. Fetal PUV in a 28-year-old patient at 22 weeks gestation with

anhydramnios at the time of second-trimester anatomy scan. Coronal
gray-scale US image through the fetus shows a keyhole appearance of the
distended urinary bladder (∗). The dilated posterior urethra (solid arrow) is
depicted, which leads to the keyhole appearance. Note the severity of blad-
der distention when compared with the fetal calvarium (dotted arrow). No
identifiable fluid pockets are consistent with anhydramnios. P = placenta.

the time of diagnosis (1,30,31). Bilateral cases develop severe

oligohydramnios. Additionally, 40% of patients with unilateral
MCDK have a contralateral renal anomaly, which is associ-
ated with a worse prognosis (1,30,31). Unilateral or focal cys-
tic MCDK can be associated with normal AFV as long as some
normal functioning renal tissue is present.

Autosomal Recessive Polycystic Kidney Disease.—Autosomal

recessive polycystic kidney disease (ARPCKD) is a single gene
or involve the entire kidney (Fig 11) (1,30,31). Enlarged renal disorder that causes nonfunctioning kidneys due to dilata-
size is initially seen, but renal atrophy can be observed in later tion of the distal tubules of the renal collecting system, which
stages (1,30,31). MCDK is postulated to represent a sequela of causes the microcystic appearance (32). US findings include
obstruction leading to cystic replacement of the renal paren- progressively enlarging echogenic kidneys (Fig 12, Movie 3)
chyma. However, images usually do not show obstruction at (1,32,33). Increased echogenicity is secondary to microcystic
Volume 43 Number 6 8 radiographics.rsna.org
June 2023 Jha et al

Figure 11. Fetal MCDK in a 23-year-old patient at 23 weeks gestation with anhydramnios noted at a
routine second-trimester anatomy scan. (A, B) Coronal gray-scale (A) and color Doppler (B) US images
show enlarged bilateral kidneys replaced with numerous variably sized cysts (arrows). Although some
intervening parenchymal tissue can be identified, this is usually nonfunctional and fibrotic. Visible
renal cysts in utero portend a poor prognosis for postnatal renal function. MRI was performed because anhydramnios precluded evaluation of multiple fetal
anatomic structures. (C) Correlative sagittal T2-weighted fetal MR image through the fetus shows one of the enlarged bilateral MCDKs (arrow). Note the com-
plete absence of AF due to associated anhydramnios.

and a large thin-walled urinary bladder. The degree of oligohy-

dramnios is variable, and it can manifest in the late first or early
second trimester (1,34).
Although a rare entity, prune belly syndrome should be con-
sidered as a differential diagnosis for PUV when atypical imag-
ing features are seen (1,34). Prune belly syndrome is more likely
if the entire urethra is dilated. The bladder is thin walled, and
anterior abdominal wall bulging can be seen due to muscular
laxity. Conversely, the keyhole bladder appearance and bladder
trabeculations are seen with PUV (1,34).

Dysplastic Kidneys.—Occasionally with oligohydramnios or

Figure 12. Fetal ARPCKD at 25 weeks gestation in a 19-year-
old patient with anhydramnios at second-trimester anatomy
scan. Coronal transabdominal color Doppler US image
through the fetal abdomen shows bilateral enlarged kidneys
with echogenic parenchyma (arrows), which is a hallmark of
ARPCKD. Note that renal enlargement may not occur until the
mid second trimester, and oligohydramnios may not develop
until later in pregnancy, depending on the severity of disease.
change, which is below the resolution limits of US. Hence, indi-
vidual cysts are not separately identified. Macrocysts are rarely
seen (1,32,33).
The timing of oligohydramnios onset is variable, and it may
not develop until later in pregnancy. Most cases are detected at
or after 24 weeks with severe oligohydramnios or anhydram-
nios (1,32,33). ARPCKD is also associated with hepatic fibrosis,
which is the most common cause of mortality in patients who
reach adulthood (1,32,33).
Prune Belly Syndrome.—Prune belly syndrome is the triad of de-
ficient abdominal musculature, renal collecting system dilata-
tion, and cryptorchidism. Almost all cases occur in male fetuses
(34). US images show marked bilateral hydroureteronephrosis
Volume 43 Number 6 9 radiographics.rsna.org
anhydramnios, US images show unilateral or bilateral renal tis-
sue but no fluid is depicted in the urinary bladder (1). A critical
search for any cause of urinary obstruction is indicated. When
no obstructive cause is detected, dysplastic nonfunctioning kid-
neys can be diagnosed on the basis of exclusion of other causes.
The kidneys can appear echogenic at US (1). Donor twins in
monochorionic twin pairs with twin-twin transfusion syndrome
(TTTS) may have such findings, when no urine-filled bladder
or restoration of AF in the donor sac occurs, even after therapy
with fetoscopic laser ablation. Prolonged hypoperfusion is the
cause of irreversible renal injury in the donor twin (1,11).
Placental Causes of Oligohydramnios
Placental causes of oligohydramnios are often diagnoses of ex-
clusion, are frequently accompanied by FGR, and closely over-
lap with maternal diabetes and hypertension (21,22). Placental
morphology assessment includes nonspecific imaging features
such as thickening or placental calcifications, usually not sig-
nificantly contributing to identifying the cause of oligohydram-
nios (21,22).
Imaging Considerations
When evaluating a case of oligohydramnios, a thorough eval-
uation of the fetal kidneys, ureters, and bladder is necessary.
June 2023 Jha et al

Figure 13. Amnioinfusion performed for severe oligohydramnios in an fetus at 22 weeks gestation with blad-
der outlet obstruction caused by PUVs (not shown). (A) Preinfusion transverse gray-scale US image shows
near-complete absence of AF, in keeping with oligohydramnios. The catheter tip (arrow) can be seen within the
amniotic sac with increasing fluid during amnioinfusion. (B) Postinfusion US image shows reconstitution of the
AF volume surrounding the fetal thorax.

Oligohydramnios should prompt an evaluation of bladder
morphology and hydroureteronephrosis. When normal gen-
itourinary anatomy is ascertained, fetal growth and maternal
and placental causes are assessed. FGR can be accompanied by
oligohydramnios (21,22). Lung development can be assessed by
using the thoracic circumference measurement as a surrogate
and comparing it with the measurement on gestational age–
based nomograms. When oligohydramnios is extreme, early
(less than 22–24 weeks of gestation), and persistent, there is a
nearly 80% mortality rate from pulmonary hypoplasia because
the canalicular phase of lung development occurs at 16–28
weeks (overlapping with the timing of oligohydramnios) and is
vulnerable to the effects of low AF (23,24,29).
Potter sequence should be included in the fetal evaluation
and includes distinctive facial features including a recessed
chin, a flattened depressed bridge of the nose, hypertelorism,
low-set ears that lack cartilage, prominent epicanthal folds, and
a crease beneath the lower lip. This collection of facial features
is sometimes called Potter facies (1). Extremity and joint con-
tractures and clubfoot deformity can also occur (1).
US evaluation of fetal anatomy may be markedly limited in
severe oligohydramnios, in which case MRI can be helpful for
better visualization (35). MRI can also play a role lung volume-
try (Fig S1) (35–37).
Interventions
Worsening oligohydramnios may require early delivery or
fetal intervention. In addition to specific genitourinary inter-
ventions such as vesicoamniotic shunt placement, major fetal
interventions performed for oligohydramnios include amnio-
infusion and amniopatch (23,24,29,38). These procedures are
usually performed by maternal fetal medicine (MFM) special-
ists. Sometimes radiologists may be involved based on insti-
tutional practices to provide sonographic guidance for needle
placement.
Amnioinfusion.—Amnioinfusion aims to restore normal AFV
around the fetus by using sterile saline or ringer lactate infu-
sion to primarily allow pulmonary development. Additionally,
it can have a diagnostic role by achieving better visualization of
fetal anomalies (Fig 13) (23,24,39,40).
Volume 43 Number 6 10 radiographics.rsna.org
The Renal Anhydramnios Fetal Therapy (RAFT) trial is cur-
rently underway to assess the benefit of serial amnioinfusion in
patients with anhydramnios of renal origin such as agenesis or
renal failure from renal anomaly (23,24). Nine fetal treatment
centers have collaborated to participate in this trial to deter-
mine whether repeated amnioinfusions can reverse the effects
of early pregnancy renal anhydramnios to allow sufficient lung
development and therefore fetal survival to successful neonatal
dialysis. Assessment of lung development is done via baseline
and postamnioinfusion fetal MRI with lung volume quantifica-
tion (Fig S1) (23). The trial is underway and results are pending.
Per this protocol, after antibiotic prophylaxis, amnioinfusion of
normal saline or lactated Ringer solution is performed. The
fluid volume infused at each amnioinfusion ranges from 300 to
800 mL of warmed isotonic fluid, following general guidelines
of 10–20 mL of isotonic fluid for each week of pregnancy. The
aim is DVP of 4–5 cm and low-normal AFI for gestational age.
If PPROM occurs, amnioinfusions are stopped (23).
Although uncommon, complications of amnioinfusion in-
clude uterine overdistension, chorioamnionitis, cord prolapse,
fetal bradycardia, and rarely AF embolism (23,38–40).
Amniopatch.—Amniopatch is a low-risk intervention used to
create an artificial membrane seal in the event of iatrogenic
PPROM. It is performed by infusing a combination of saline,
cross-matched allogeneic platelets, and cryoprecipitate into the
amniotic sac (38). Doubling of fetal survival rates has been re-
ported (38).
Polyhydramnios
Polyhydramnios is defined as a DVP of 8 cm or more or an AFI
of 24 cm or more (8). The reported incidence is approximately
1%–2% of singleton pregnancies by using these thresholds (41).
Per American Institute of Ultrasound in Medicine (AIUM) and
Society for Maternal-Fetal Medicine (SMFM) guidelines, AFI is
preferred over DVP for diagnosing polyhydramnios (5,8).
Of all fetuses with polyhydramnios, approximately two-
thirds are male, and 28% have associated macrosomia (1). Fetal
macrosomia is diagnosed when the estimated fetal weight ex-
ceeds the 90th percentile. The characteristic finding is a large
abdominal circumference with increased truncal echogenic fat.
June 2023 Jha et al
Mild polyhydramnios is most commonly idiopathic (50%–70%
of cases) (1). This diagnosis of exclusion is made when no ma-
ternal or structural fetal abnormalities are identified (1).
Maternal Causes of Polyhydramnios
Diabetes is the most common maternal cause of polyhydram-
nios (42,43). It is hypothesized that maternal hyperglycemia
leads to fetal hyperglycemia resulting in increased AFV due
to osmotic diuresis (42,43). Hence, polyhydramnios and fetal
macrosomia may be the first indicator of poor glucose control
in pregnancy. Diabetes may also be associated with caudal re-
gression syndrome (Fig S2).
Maternal obesity is common among pregnant women with
pregestational diabetes. Although causation has not been es-
tablished, obesity increases the risk of developing gestational
diabetes and fetal macrosomia, which are both associated with
polyhydramnios (44).
Fetal Causes of Polyhydramnios
Fetal Hydrops
Fetal hydrops is defined as excessive fluid accumulation in two
or more fetal compartments, including skin edema, ascites,
and pleural or pericardial effusion (Fig 14) (1). Assessment for
skin thickening in hydrops is a subjective assessment, where
the skin and subcutaneous tissues appear stratified with hy-
poechoic areas from edema. No specific measurements exist
for identifying integumentary edema and thickening, which
remains a subjective assessment.
Fetal hydrops can be categorized into two types: immune
and nonimmune (1,45,46). Nonimmune is the most common
Volume 43 Number 6 11 radiographics.rsna.org
Figure 14. Polyhydramnios and fetal hydrops in a fetus at
21 weeks gestation with a history of anti-Kell isoimmuniza-
tion. (A–C) Transabdominal gray-scale US images of the
fetus show unilateral pleural effusion (arrow in A), ascites
(dotted arrow in B), and scalp edema (arrowhead in C),
consistent with fetal hydrops. No anatomic explanation for
hydrops was identified. Note the excess fluid around the
fetus in B. (D) Spectral Doppler US image of the fetal mid-
dle cerebral artery (MCA) shows elevated peak systolic ve-
locity (PSV), indicating fetal anemia. MCA PSV of 40.4 cm/
sec corresponds to 1.51 multiples of median (MoM), which
is greater than 1.5 MoM and consistent with fetal anemia as
the cause for hydrops.
type, accounting for over 90% of all hydrops cases (46). Fetal
volume overload from multiple causes such as infection, ane-
mia, heart failure, and lymphatic obstruction can lead to hy-
drops (46).
Additionally, nonimmune fetal hydrops (NIFH) can also oc-
cur with chromosomal anomalies such as Turner syndrome, tri-
somy 21, and trisomy 18. In these cases, hydrops can be present
without any additional anatomic abnormalities. Genetic test-
ing for NIFH ranges from standard chromosomal microarray or
karyotype to gene panels and broad approaches such as whole
exome sequencing (46). Some genetic disorders can manifest
with characteristic phenotypic features that can be assessed
at prenatal US, such as hepatomegaly with lysosomal storage
disorders, hyperechoic kidneys with congenital nephrosis, or
pulmonary valve stenosis with RASopathies (46). However, a
comprehensive evaluation includes prenatal US and genetic
testing and considers many other factors such as patient and
family history.
Immune hydrops accounts for 10% of hydrops cases. This
type of fetal hydrops is related to hemolytic disease and fetal
anemia, with rhesus (Rh) antigen incompatibility being the
most common cause (45). When Rh-incompatibility occurs
in Rh-negative mothers who are sensitized by Rh-positive
blood, usually from the first Rh-positive pregnancy, they de-
velop antibodies against Rh-positive red blood cells. These
antibodies attack the red blood cells of subsequent Rh-pos-
itive fetuses in utero, leading to hemolytic anemia. These
high-risk pregnancies undergo serial sonographic surveil-
lance with Doppler US evaluation of middle cerebral ar-
tery peak systolic velocity to assess fetal anemia (Fig 14D)
(45,47–49).
June 2023 Jha et al

Figure 15. Fetal duodenal atresia in a 36-year-old pa-

tient with noninvasive prenatal test results consistent
with trisomy 21 (Down syndrome). (A) Transabdominal
gray-scale US image obtained transversely through
the fetal abdomen shows a “double bubble” configu-
ration from a dilated stomach and duodenum (arrows),
consistent with duodenal obstruction. The AFV was
increased but not apparent at the level of this image.
The duodenum should never be fluid filled in a fetus. When a fluid-filled duodenum is present, along with a
fluid-distended stomach, this creates the double bubble appearance, which is seen with duodenal obstruc-
tion. (B) Postnatal babygram shows a similar double bubble appearance (circle) corresponding to the dilated
obstructed stomach and proximal duodenum. No air-filled small bowel loops were seen, and duodenal atresia
was confirmed at postnatal evaluation.

Fetal Gastrointestinal Tract Obstruction
Fetal gastrointestinal tract obstruction usually manifests with
late polyhydramnios (after 24 weeks of gestation). Obstruc-
tion may be intrinsic or extrinsic and leads to polyhydram-
nios due to a decreased amount of AF swallowed by the fetus
(50). Causes of obstruction include gastrointestinal atresias
and oral, cervical, or intrathoracic masses. Gut atresias can be
associated with other VACTERL anomalies (vertebral defects,
anal atresia, cardiac defects, tracheoesophageal fistula, renal
anomalies, and limb abnormalities) (50,51).
Esophageal, Duodenal, and Jejunal Atresia.—Esophageal
atresia manifests with an absent or small stomach at US.
Sometimes, a small fluid-filled pouch can be seen in the neck
representing the atretic proximal esophagus (1). Approxi-
mately one-third of cases of esophageal atresia are associated
with tracheoesophageal fistulas and trisomy 18 or 21 (51,52).
Duodenal atresia manifests with a fluid-distended stom-
ach and proximal duodenum in a “double bubble” appearance
(Fig 15, Movie 4). Persistent fluid in the duodenum is always
abnormal (1). One-third of duodenal atresia cases are associ-
ated with trisomy 21 (51). Jejunal atresia manifests with sau-
sage-shaped distended proximal bowel loops. Variable gastric
and esophageal distention may be present (1,53).
Extrinsic Obstruction.—Extrinsic obstruction from masses
such as oropharyngeal teratoma (Fig S3, Movie 5) or medias-
tinal masses can impair swallowing and lead to polyhydram-
nios (1). With cervical masses, the fetus may be in a “stargaz-
ing” position due to the mass causing neck hyperextension
(1,54). The severity of polyhydramnios depends on the size
of the mass and degree of obstruction. MRI may be indicated
to help evaluate the anatomic extent and mass effect on the
airways. However, MRI sequences may be degraded due to
Volume 43 Number 6 12 radiographics.rsna.org
dielectric artifact if there is severe polyhydramnios (Fig S3)
(55). Close interval follow-up is required as masses may rap-
idly enlarge, and hemodynamic changes can lead to fetal hy-
drops. Since spontaneous breathing at birth could be jeopar-
dized, delivery should be performed at a tertiary care facility
with the ability to perform ex utero intrapartum treatment
procedures (56).
Central Nervous System Anomalies
Multiple central nervous system anomalies lead to polyhy-
dramnios due to impaired swallowing (1). Absent swallowing
and inadequate absorption interrupt an important AF recircu-
lation pathway (1). This can be seen with numerous primary
neurologic anomalies such as anencephaly and Dandy-Walker
syndrome, to name a few (Fig 16) (57).
Arthrogryposis, Akinesia Sequence
Arthrogryposis, akinesia sequence is a heterogeneous group of
disorders with a common sequela of limited or absent extrem-
ity motion leading to decreased fetal movement and swallow-
ing, impaired fluid circulation, and resultant polyhydramnios
(58).
Severe Skeletal Dysplasia
Common skeletal dysplasias include thanatophoric dysplasia,
achondroplasia, achondrogenesis, and osteogenesis imper-
fecta and are characterized by skeletal findings such as short
limbs, poor ossification, bowed or broken bones, and cranio-
synostosis (59). These result in late (third trimester) polyhy-
dramnios due to decreased fetal movement (Fig 17) (59).
Congenital Pulmonary Airway Malformation
Congenital pulmonary airway malformation is the abnormal
bronchial proliferation of a lung segment, which can cause
June 2023 Jha et al

Figure 16. Polyhydramnios and multiple fetal central nervous

system anomalies in a 35-year-old pregnant patient with a
known history of fetal neurologic abnormality who presented
with worsening abdominal distention at 33 weeks gestation.
Axial transabdominal gray-scale US image of the fetal head
shows an enlarged posterior fossa with vermian hypoplasia
(solid arrow), consistent with Dandy-Walker malformation
and bilateral ventriculomegaly (dotted arrows). Impaired fetal
swallowing secondary to neurologic abnormalities can lead
to polyhydramnios. Additional central nervous system anom-
alies, including holoprosencephaly and gray matter heteroto-
pia, were confirmed at MRI (not shown).

Figure 17. Fetal skeletal dysplasia in a

25-year-old patient with severe polyhy-
dramnios and fetal size greater than that ex-
pected for 34 weeks gestation. Severe poly-
hydramnios was noted with an AFI greater
than 35 cm. (A) Coronal transabdominal
gray-scale US image of the foot shows post­
axial polydactyly with supernumerary digits
(arrows). Bilateral postaxial polydactyly of
the hands and feet was present (not shown).
(B) Transabdominal gray-scale image of the
femur shows shortening of the long bones,
with the femur measuring 5.1 cm, which is 7
weeks behind the gestational age and less
than the 3rd percentile for gestational age.
(C) Gray-scale US image shows that the foot
length is normal for gestational age, with
the femur measuring smaller than the foot,
which is highly suggestive of skeletal dysplasia. Based on this combination of findings, chondroectodermal dysplasia
was suggested at the time of diagnosis and confirmed postnatally.

mass effect on mediastinal structures such as the esophagus
and obstruct swallowing (1). Additionally, the mass creates
transudative fluid, which contributes to polyhydramnios (1).
These appear as echogenic lung masses and can occur as hy-
brid lesions along with bronchopulmonary sequestrations (60).
Mesoblastic Nephroma
Mesoblastic nephroma is a benign solid mesenchymal tumor
of the fetal kidney. Seventy percent of cases are associated with
polyhydramnios and are frequently progressive and severe.
There are various proposed mechanisms for polyhydramnios,
the most common of which include hypercalcemia leading to
polyuria, renal hyperemia causing increased urinary output,
and bowel obstruction if the mass is large (Fig 18) (61).
Placental Causes of Polyhydramnios
Placental Chorioangioma.—Chorioangioma is a benign vas-
cular tumor of the placenta (Fig 19) typically manifesting as
a heterogeneous vascular mass protruding into the amniotic
sac adjacent to the cord insertion (62). Internal spectral Dop-
pler US will demonstrate arterial flow contiguous with the
fetal circulation and matching the fetal heart rate (62–64).
Large masses (>5 cm) can cause leakage of transudate from
vessels and result in polyhydramnios. Nonimmune fetal hy-
drops (NIFH) can occur secondary to arteriovenous shunt-
ing in the mass, which also increases the risk of developing
high-output heart failure (63). Additionally, hemolysis can
lead to fetal anemia (63).

Volume 43 Number 6 13 radiographics.rsna.org

June 2023 Jha et al
Imaging Considerations
The role of US at the time of diagnosis is to evaluate for fetal
structural causes of polyhydramnios, including fetal gastro-
intestinal obstruction and neurologic and muscular disorders
that can prevent swallowing and decrease movement. Poly-
hydramnios with FGR, in the absence of maternal diabetes or
hypertension, is highly associated with an increased risk for
aneuploidy (most commonly trisomy 18) (65). When polyhy-
dramnios is detected in later gestation, all fetal organs and the
placenta should be reassessed for a latent diagnosis of potential
abnormalities that were undetectable earlier in pregnancy.
At follow-up imaging, the AFI should be measured, along
with cervix length for risk of cervical incompetence and
preterm labor. Patients with polyhydramnios have the pro-
Volume 43 Number 6 14 radiographics.rsna.org
Figure 18. Fetal mesoblastic nephroma in a
22-year-old pregnant patient at 28 weeks ges-
tation with a fetal abdominal mass. (A) Trans-
abdominal gray-scale US image shows a large
mass (calipers and arrow) in the abdomen
without an identifiable right kidney, consistent
with a mass of renal origin. (B) Gray-scale
US image obtained more superiorly than A
shows that the mass (arrow) compresses and
displaces the stomach (arrowhead), which
results in impaired transit and associated
polyhydramnios.
Figure 19. Placental chorioangioma with poly-
hydramnios. (A) Transabdominal gray-scale US
image shows a heterogeneous placental mass
(arrow), protruding into the amniotic sac, consis-
tent with a chorioangioma. P = placenta. (B) Color
Doppler US image shows the mass (arrow) to be
highly vascular. (C) Coronal T2-weighted fetal
MR image similarly shows a heterogeneous mass
(arrow) arising from the placenta (P) and protrud-
ing into the amniotic cavity. (D) Due to the large
amount of mucin produced by the chorioangioma,
chorioamniotic separation (arrow) can occur, with
mucin present in the potential space between the
chorion and amnion (∗), as depicted on the coronal
T2-weighted fetal MR image.
pensity for gradual cervical shortening with advancing ges-
tation because of to uterine distention and pressure on the
cervix. However, this is not always directly proportional to
the severity of polyhydramnios (66,67). Other complications
include placental abruption, cord prolapse (Fig 20, Movie 6),
premature labor, and PPROM (1).
Interventions
There are no fetal indications for intervention in cases of mild
idiopathic polyhydramnios. Reduction amniocentesis (also
known as amnioreduction) is considered for severe maternal
discomfort or dyspnea and respiratory distress, which happen
from diaphragmatic pressure resulting from uterine distention
(Fig S4) (68,69). Amnioreduction can relieve diaphragmatic
June 2023 Jha et al

Figure 20. Cord prolapse complicating PPROM in a

30-year-old pregnant patient with a history of clear fluid
leakage. Transabdominal color Doppler US image of
the cervix shows color Doppler signal in the region of
the cervix (arrow) with the fetus still in utero, consistent
with cord prolapse. Anhydramnios is present, compati-
ble with the history of PPROM.

pressure and ease maternal breathing. In severe cases, serial

amnioreductions may be necessary based on maternal symp-
toms. A case report of amnioreduction along with emergent
cervical cerclage for polyhydramnios causing cervix shortening
has been described (70).
An AF sample from amniocentesis can be sent for chromo-
somal testing (68). Complications of amniocentesis include
chorioamniotic separation, chorioamnionitis, PPROM, fetal
injury, and miscarriage (68,69).
AF Disturbances in Multiple Gestations
In twin pregnancies affected by AF disturbances, determi-
nation of chorionicity and amnionicity is essential (11). Di-
chorionic twins affected by AF disturbances are approached
similar to singleton pregnancies. However, in monochorionic
pregnancies, AF disturbances prompt a search for conditions
such as TTTS, polyhydramnios affecting recipient-like twin
(PART), and unequal sharing of placental vasculature (11).
Figure 21. Monochorionic twin pregnancy complicated
by stage 3 TTTS in a 29-year-old patient. (A) Transab-
dominal gray-scale US image shows anhydramnios of
the smaller donor twin with a “shrink-wrapped” appear-
ance and stuck position against the uterine wall (arrow).
The larger recipient twin (R) demonstrated polyhydram-
nios. Note the difference in twin sizes, which often
accompanies TTTS. (B) Spectral Doppler US image for
evaluation of the umbilical artery of the smaller donor
twin shows absent end-diastolic flow (arrows). Polyhy-
dramnios was demonstrated in the larger twin’s amni-
otic sac (∗). This is compatible with stage 3 TTTS.

AF and Monochorionic Multiple Gestations

Twin-Twin Transfusion Syndrome
TTTS is thought to be caused by abnormal and unbalanced
placental vascular connections, where one twin (donor)
partly perfuses the other twin (recipient) through an artery-
to-vein anastomosis (Figs 21, 22; Movie 7) (11). This unidi-
rectional flow can lead to severe oligohydramnios in the do-
nor twin, with an inability to visualize the urinary bladder.
When low fluid progresses to anhydramnios, the donor twin
can appear “stuck” to the uterine wall (Figs 21, S4) (11). The
donor twin may be growth restricted and demonstrate in-
creased umbilical artery resistive flow at Doppler US evalu-
ation (Fig 21B) (11). On the other hand, the recipient twin
shows polyhydramnios and signs of volume overload and
may be larger than the donor twin (although the growth dis-
cordance is not a diagnostic criterion) (Figs 21, 22) (11).
The severity of TTTS is staged on the basis of imaging
findings, with the Quintero staging system used most widely
(Table 3) (11,71). In monoamniotic twins, polyhydramnios
may be the only early finding, highlighting the importance
of bladder assessment and cord Doppler US evaluation
(11,71). Close US surveillance with serial Doppler evalua-
tion is indicated for surveillance and to evaluate for poten-
tial intervention.
Polyhydramnios Affecting Recipient-like Twin
In a monochorionic twin pair, PART manifests with normal
fluid in one amniotic sac and polyhydramnios in the other

Volume 43 Number 6 15 radiographics.rsna.org

June 2023 Jha et al
Table 3: Quintero Staging for Twin-Twin Transfusion
Syndrome
Stage US Findings
1 Oligohydramnios in donor twin and polyhydramnios
in recipient twin; visible fluid-filled bladder identi-
fied in donor twin
2 Nonvisualization of the urinary bladder in donor
twin, in addition to concomitant oligohydramnios
and polyhydramnios
3 Spectral Doppler US abnormalities in umbilical artery
and/or umbilical vein of either the recipient or
donor twin (ductus venosus abnormalities are not
considered in Quintero staging)
4 Hydrops in either fetus
5 In utero death of one or both fetuses
Note.—Reprinted, with permission, from reference 29.
(Fig 23) (11,72). Most of these cases do not progress to TTTS,
but increased surveillance is indicated to monitor fetal growth
and AF volume (11,72). The presence of an arterial-arterial
anastomosis is thought to be protective against progression to
TTTS (11,72).
Isolated Oligohydramnios
In monochorionic twins, isolated oligohydramnios is diag-
nosed when there is oligohydramnios in one twin and normal
AF volume in the other. This may be related to growth restric-
tion and should prompt evaluation for additional genitouri-
nary causes for oligohydramnios in the affected twin (11).
Special Diagnostic Considerations
Frequent US surveillance is indicated in all twin pregnan-
cies, particularly in monochorionic twin pregnancies because
of the higher rate of complications. It is recommended that
US surveillance be performed every 2 weeks beginning at 16
weeks of gestation in addition to a complete anatomic eval-
uation between 18 and 22 weeks (as is recommended in all
pregnancies) (11,73). Doppler US evaluation of different fetal
vessels, including the umbilical artery, ductus venosus, mid-
Volume 43 Number 6 16 radiographics.rsna.org
Figure 22. Reduction amniocentesis complicated
by chorioamniotic separation. (A) Transabdominal
gray-scale US image after amniocentesis shows
chorioamniotic separation (∗). The recipient (R) and
donor (D) amniotic sacs are also shown. Note the
increased echogenicity of the donor AF.
(B) Transabdominal gray-scale US image shows
that the chorioamniotic separation is accompanied
by a shredded appearance of the membranes
(arrows).
dle cerebral artery, and umbilical vein, is performed as needed
based on the suspected complication (11,22).
Interventions
In TTTS, fetoscopic laser ablation of abnormal vascular anas-
tomoses to achieve dichorionization may interrupt the abnor-
mal perfusion between twins (11,29,73). This is usually per-
formed for Quintero stage 2 or higher, with some institutions
performing interventions for stage 1 disease, on a case-by-case
basis (11,29,73). Additionally, selective feticide (usually with
radiofrequency ablation) can be performed in cases where
one of the twins has severe congenital anomalies potentially
incompatible with life, has severe growth restriction, or is
moribund. Complications include chorioamniotic separation
(Fig 22), placental abruption, and intra-abdominal leakage of
fluid. Premature rupture of membranes occurs in 18%–30%
of cases, more often with earlier gestational age at the time of
intervention (<17 weeks) (11,29,73).
Genetic Testing and AF Abnormalities
Genetic testing is becoming widely available for evaluating
fetal abnormalities. As early as the first trimester, noninva-
sive prenatal testing (NIPT) can be performed in which the
maternal blood can be sampled and fetal DNA separated
and analyzed for chromosomal abnormalities (74,75). This
analysis can be performed as two variants: one in which
karyotype abnormalities are identified, and a more detailed
second variant in which the whole genome sequencing can
be performed. When abnormal NIPT results are detected,
further evaluation with amniocentesis or chorionic venous
sampling could be performed (76–78). When oligohydram-
nios or polyhydramnios is detected, genetic testing can be
performed to test for karyotype abnormalities and single
gene disorders (79). In a study evaluating chromosomal ab-
normalities and polyhydramnios, roughly 13% of neonates
had a chromosomal or genetic abnormality with a prenatal
diagnosis of polyhydramnios. The severity of polyhydram-
nios and reduced fetal movements was independently as-
sociated with the presence of such genetic diseases (80).
Additionally, nonisolated polyhydramnios has been shown
to be associated with several microdeletion and/or microdu-
plication syndromes, regardless of whether the pregnancy is
June 2023 Jha et al

Figure 23. PART in a 31-year-old pregnant patient who

presented for routine surveillance of a monochorionic diam-
niotic twin gestation pregnancy at 19 weeks gestation.
(A) Transabdominal gray-scale US image shows polyhy-
dramnios for the first twin (deepest pocket of 9.5 cm, cali-
pers) and normal fluid for the cotwin. PART was diagnosed.
(B) Transabdominal gray-scale US image from follow-up
US 10 days later shows oligohydramnios and a stuck ap-
pearance against the uterine wall (arrow) for the cotwin,
representing evolution to TTTS. (C) Polyhydramnios for the
first twin was again seen (maximum vertical pocket, 9.2 cm).
Both urinary bladders were visualized (not shown), compati-
ble with progression to stage 1 TTTS.

singleton or multiple (81). At this time, there is insufficient
evidence to recommend chromosomal microarray analysis
in pregnancies with isolated polyhydramnios (81). Similarly,
there is insufficient evidence to support invasive prenatal
testing in pregnancies with isolated oligohydramnios with-
out identifiable phenotypic abnormalities (79). It is highly
recommended to pursue genetic analysis, when available,
for patient counseling and management, as it provides guid-
ance for current and future pregnancies.
Conclusion
AFV is a key indicator of fetal well-being. AF disturbances in-
dicate a fetal, placental, or maternal pathologic condition. The
degree and timing of AF disturbances and a thorough under-
standing of the underlying mechanisms of fluid homeostasis
can help make an accurate diagnosis. A detailed evaluation
of fetal anatomy and structural anomalies helps direct clini-
cal assessment and management toward potential maternal
or placental factors. Knowledge of the latest interventions for
AFV derangements and their indications can inform the per-
formance and reporting of follow-up US examinations.
Author affiliations.—From the University of California San Francisco, 505 Par-
nassus Ave, San Francisco, Calif (P.J., P.R., M.S., T.A.M., V.F., L.P.); University
of Utah Hospital, Salt Lake City, Utah (A.M.K.); and Inland Imaging, Seat-
tle, Wash (R.P.). Presented as an education exhibit at the 2022 RSNA Annual
Meeting. Received June 14, 2022; revision requested August 10 and received
November 8; accepted November 10. Address correspondence to P.J. (email:
jhap@stanford.edu).
Current address.—P.J. Stanford University, Department of Radiology, 300
Pasteur Drive Room S056, Stanford, CA 94305. T.A.M. Department of Radiol-
ogy, Mayo Clinic Hospital, Phoenix, Az.
Disclosures of conflicts of interest.—P.J. Royalties from Elsevier; Ana Lev
Toaff Award from the Society of Radiologists in Ultrasound; expert testimony
payment from and board member for Donahue, Durham, and Noonan, P.C.
A.M.K. Editorial board member of RadioGraphics; royalties from Elsevier;
speaker honoraria from World Class CME UC Davis. M.S. Royalties from El-
sevier; consultant for Nextrast Inc (oral contrast start-up; no fees received).
T.A.M. Royalties from Elsevier.
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