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Fetal Diagn Ther 2007;22:81–84
DOI: 10.1159/000097101
Voluminous Fetal Chylous Ascites:
A Case of Complete Spontaneous
Prenatal Regression
Elisabeth Chéreau Véronique Lejeune Marie Gonzales Bruno Carbonne
Department of Obstetrics and Gynecology, Hôpital Saint Antoine, Paris , France
ference (AC) of 230 mm, a measurement normal at 32 weeks)
( fig. 1 ). No other anomalies were observed, in particular, no oth-
er thoracic or pericardiac effusion and no hydramnios. Placental
thickness was normal. Peak systolic velocity in the middle cere-
bral artery was in the normal range for gestational age. Fetal car-
diac ultrasound was normal.
A work-up then began to determine the cause of this isolated
voluminous ascites. It included maternal blood tests for cytomeg-
alovirus and parvovirus B19 infection, amniocentesis to deter-
mine karyotype, perform a dosage of digestive enzymes, a testing
for cytomegalovirus and parvovirus B19, for cystic fibrosis muta-
tions and for metabolic storage disease (determinations of oligo-
sacchar ides, free sialic acid , acid hydrolases, and acid lipa ses). The
patient’s blood group was O RhD+, and no immune antibodies
were found.
In view of a substa ntial en largement of abdominal volume (AC
increased from 230 mm at 22 weeks to 283 mm at 25 weeks), a
needle aspiration was performed, at the same time as amniocen-
tesis, to partially evacuate the ascites: 150 ml fluid were aspirated.
The sample was then assessed for diagnostic purposes (cytologic,
biochemical, and bacteriological testing).
These examinations showed yellow exudate made up of 84%
lymphocy tes (hypoproteinemia and low serum albumin). The as-
pirated f luid was sterile and contained none of the viruses sought
(cytomegalovirus and parvovirus B 19). Digestive enzymes (i.e.
intestinal alkaline phosphatase [iAP]), were absent in ascitic flu-
id. Gamma-glutamyl transpeptidase was in the normal range
(31 IU/l). The normal glycosaminoglycans, tended to rule out
metabolic disease. Amniocentesis revealed a normal karyotype
(46 chromosomes), no standard cystic fibrosis mutations, and no
indications of any metabolic storage disease (normal levels of oli-
gosaccharides, free sialic acid, acid hydrolases, and acid lipases).
Digestive enzymes in amniotic fluid (iAP) and gamma-glutamyl
transpeptidase, were in the normal range for gestational age.
Key Words
Fetus Ascites Chylous Prenatal diagnosis
Abstract
We report a case of isolated voluminous fetal ascites discov-
ered during a routine fetal ultrasound at 22 weeks’ gesta-
tion. Analysis of the fluid showed it to be chyliform and ruled
out other causes of fetal ascites. Regular bimonthly ultra-
sound scans monitored its progressive diminution and then
its disappearance. Examination showed the child to be nor-
mal at birth. Though the literature indicates that prognosis
is usually favorable for infants with isolated fetal chylous as-
cites, spontaneous regression during pregnancy is an un-
common finding. Copyr ight © 2007 S. Karger AG, Base l
Case
Mrs. C. was referred to the Center for prenatal diagnosis at
Saint Antoine Hospital at 22 weeks’ gestation after discovery of
fetal ascites at a routine ultrasound examination. This was her
second pregnancy; 4 years before, she gave birth to a 3,300-g boy
in good health after an unremarkable pregnancy and normal de-
livery. The beginning of this pregnancy was also unremarkable.
The ultrasound at 11.5 weeks was normal, with nuchal translu-
cency of 1.2 mm and a crown-rump length of 56 mm.
T he ultrasound at 22 week s showed feta l ascites: the inf ant had
a thin ned abdominal wal l and a very enlarged ab domina l circum-
Received: November 4, 2005
Accepted a fter revision: March 28 , 2006
Published o nline: November 27, 2006
Pr. Bruno Carbon ne
Depar tment of Obstetrics and Gy necology, Hôpital Sa int Antoine
184, rue du Faubou rg Saint Antoine
FR–75012 Paris (France)
Tel. +33 1 49 28 27 45, Fax +33 1 49 28 27 56, E-Ma il bruno.carbonne@sat.aphp.fr
© 200 7 S. Karger AG, Basel
1015–3837/07/0222–0081$23.50/0
Accessible online at:
www.karger.com/fdt
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Fetal Diagn Ther 2007;22 :81–84
82
This work-up thus ruled out the usual causes of fetal ascites:
digestive or renal causes, chromosomal anomalies, metabolic
storage diseases, cystic fibrosis or infection.
Accordingly, we monitored this isolated chylous ascites of un-
determined cause by ultrasound.
The AC remained enlarged ( 1 97th percentile) for the ultra-
sounds at 25, 27 and 28 weeks; as volume tended to stabilize, we
decided against a possible peritoneal-amniotic shunt.
Ultrasound at 30 and 32 weeks found progressive diminution
of the ascites with AC remaining at the 97th percentile. No other
anomalies were detected and fetal growth was normal.
The 35-week ultrasound showed that the ascites had disap-
peared almost entirely; only a thin strip of effusion below the di-
aphragm remained ( fig. 2 ). The AC then was at only the 50th per-
centile. The ascites had disappeared completely at 36.5 weeks
( fig. 3 ).
Fig. 1. U ltr asoun d sc an of t he fe tal a bdom en at 22 we eks . Volu mi-
nous transonic ascites with thinned abdominal wall ‘floating’ in
amniotic fluid. a Axial view. b Coronal view.
Fig. 2. Ultrasound scan of the fetus at 35 weeks: persistence of a
strip of effusion.
Fig. 3. Ultrasound scan of the fetus at 36.5 weeks: disappearance
of ascites.
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Fetal Chylous Ascites Fetal Diagn Ther 2007;22 :81–84
83
The patient went into spontaneous labor at 39 weeks and gave
birth vagina lly to a 3230-g boy. Clinical examination and abdom-
inal ultrasound showed neither ascites nor any other anomaly.
Neonatal course was normal with enteral feeding (exclusive
breast-feeding) from the onset. The child had no gastrointestinal
disorders. No other supplementary examinations were conduct-
ed. After 36 months follow-up, growth and development are con-
sidered normal.
Discussion
Antenatal discovery of chylous ascites is rare. Most in-
formation in the literature concerns chylous ascites dis-
covered at birth, probably corresponding to fetal ascites
that did not regress antenatally, especially in countries
where obstetrical ultrasound is not widespread. Alter-
nately, ascitis could also occur or increase sharply after
birth once the neonate is fed. The diagnosis of chylous as-
citis requires paracentesis for cy tologic examination. Dos-
age of digestive enzymes in amniotic and ascitic fluids
allows to rule out other causes of peritoneal effusion such
as meconial peritonitis and/or bowel obstruction. An ex-
haustive literature review (search of Pubmed from 1979 to
April 2004 with the following key words: fetus; ascites;
chyl * ; neonatal) identified 17 cases of chylous ascites dis-
covered before birth [1–9] . Fourteen other cases of chy-
lous ascites involved their discovery at birth [10–18] .
Chylous ascites is rare among the ascites discovered
either before or after birth. A recent series [3] found only
three cases of chylous ascites among 79 cases of fetal as-
cites identified by ultrasound. The diagnosis of the chy-
loform nature of the ascites is based on cytologic and bio-
che mic a l a na ly si s o f t he f lu id . O th er ca us es of fe ta l a sc it es
(e.g. chromosomal, metabolic, infectious) should be
sought systematically [19] . Chylous ascites in a fetus or
newborn may be caused by an obstruction or compres-
sion of lymphatic vessels, a wound, fistula, exudative en-
teropathy or exudate from the wall of the retroperitoneal
lymphatics [1] . These different causes explain the possi-
bility of spontaneous regression of chylous ascites, either
spontaneously by the closing of a gap or after a diet ex-
cluding long-chain triglycerides, which reduces the
lymph flow, or by surgical treatment of a wound or fis-
tula. They therefore require such a diet, or even exclusive
parenteral feeding if the ascites enlarge or simply do not
regress in the neonatal period. Even rarer are wounds,
fistula or compression; any of these requires consider-
ation of surgery in the neonatal period in the absence of
improvement.
The course during pregnancy was stable in half the
antenatally-discovered cases and marked by increased
ascites in the others. With the exception of one case dis-
covered at 16 weeks [6] , all were discovered at a gesta-
tional age above 22 weeks and in 8 cases after 30 weeks.
None of these, however, observed the disappearance of
the ascites during pregnancy, as we did. The absence of
spontaneous regression in previous reports may be due to
a later diagnosis or to the fact that peritoneal effusions
had been aspirated. In one case, a peritoneal-amniotic
shunt, placed when the ascites increased massively [8] ,
enabled the pregnancy to continue through 36 weeks. All
but one case (discovered very late, [1] ) of ascites identified
antenatally were aspirated during pregnancy. Three ar-
ticles specified that labor was induced. One infant was
delivered by cesarean at 34 weeks [7] . Mean term at de-
livery was 36–37 weeks, with most newborns healthy and
of normal size, with transient respiratory distress in some
cases, due to the abdominal volume. No reports describe
aspiration immediately before delivery to avoid abdomi-
nal dystocia.
Contrary to pleural chylous effusions, chylous ascites
do not cause compression of other organs because of the
distensibility of the abdominal wall. Large chylothorax
may cause pulmonary hypoplasia, cardiac insufficiency
and hydrops. Pleuro-amniotic shunting is thus often re-
quired. In our case, peritoneal-amniotic shunting – ini-
tially considered because of the wide distension of the
abdominal wall – was finally not deemed necessary since
a spontaneous regression of the ascites was observed after
partial aspiration.
Postnatal course was favorable in all cases except one
in the literature. That infant died after several days of life:
he was born with gastrointestinal malrotation, and py-
loric stenosis, and had acute renal failure and dissemi-
nated intravascular coagulation after surgery [1] . In 12
cases, medical treatment, including a diet excluding long-
chain triglycerides and/or enteral nutrition sufficed for
the ascites to disappear completely in 15–30 days. Spon-
taneous disappearance without any treatment was noted
in less than 2 weeks in two of the newborns [6] . In the
remaining two cases, persistence of the ascites made sur-
gery necessary, despite appropriate medical treatment
that included a diet excluding first long-chain triglycer-
ides and then enteral nutrition [7] . 99-Technetium albu-
min scintigraphy revealed lymphatic fluid diffusion into
the peritoneal cavity from the right suprarenal region. In
both cases, laparoscopy showed the area of lymphatic
leaking, stained red by indigo carmine administered pre-
operatively by subcutaneous and oral routes. Laparotomy
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Fetal Diagn Ther 2007;22 :81–84
84
was performed to ligate and occlude the lymphatic vessels
with biological glue. The postoperative course was satis-
factory and the ascites disappeared totally in both new-
borns.
In 11 of the 14 cases discovered at birth, medical treat-
ment alone was sufficient to resolve the ascites. Surgical
treatment was necessary for the other three. In one case,
a peritoneovenous shunt led to a favorable outcome [13] .
A voluminous inguinal hernia required surgical treat-
ment for another [15] . For the third, a laparotomy found
a lymphatic leakage and occluded it with fibrin glue [10] .
After the disappearance of the primary ascites one infant
had a recurrence at 8 months, followed by a rapid degra-
dation of his general condition. He died of chylothorax,
pericarditis and lung disease. No anatomical anomalies
were found [17] .
Overall, there were only two deaths after birth among
these rare cases of isolated chylous ascites. The death did
not seem directly related to the ascites in either case, but
rather to a gastroi ntestinal ma lformation in one case and
pulmonary and pericardiac effusion in the other. The
long-term prognosis seems therefore favorable: ascites
disappears in most cases, with or without medical or sur-
gical intervention.
Fetal chylous ascites is thus a rare disease. Its progno-
sis is generally good when it is an isolated disorder. Most
often, chylous ascites is idiopathic and outcome is favor-
able, that is, it disappears entirely, either spontaneously
or by dietary treatment (no long-chain triglycerides and/
or enteral nutrition).
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