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Case Reports

Ascites and Right


Pleural Effusion: Demonstration
of a Pentoneo-Pleural Communication
Jean Verreault, Serge Lepage, Guy Bisson, and Andre Plante
Departments ofNuc/ear Medicine and Internal Medicine,
University ofSherbrooke,
Sherbrooke, Qubec,Canada

Centre Hospitalier

Universitaire,

A 54-yr-oldfemale with known livercirrhosis presented with a right transudative pleural


effusion and ascites. To find the source of pleural fluid,[@TcJsuIfur
colloidwas injected
intraperitoneallyand a serial imaging study revealed its passage to the right pleural space on
2-hr and 24-hr images.

Mechanisms

proposed

in the formation of pleural effusion in liver

cirrhosis are (a) lymphatic drainage and (b) diaphragmatic defect. Radioisotope migration
speed may be a clue for differentiating these two mechanisms, being more rapid in the

presence of a diaphragmatic defect.


J NucIMed 27:17061709,
1986

leural effusions occur in 5% to 10% of patients with


cirrhosis

of the liver (1 ). In these

patients,

ascites

is

usually evident but a pleural effusion may develop in a


cirrhotic patient in the absence ofdetectable ascites (2).

The effusions are usually right-sided, but may be bilat


eral or left-sided. The precise mechanism
cumulation is not clear.

of fluid ac

We describe a case where a peritoneopleural com


munication

has been demonstrated

by radioisotopic

method. The possible mechanisms involved in the for


mation of pleural effusion in liver cirrhosis are dis
cussed.

CASE REPORT
A 54-yr-old white female was admitted for progressive
dyspnea of recent onset and signs of upper respiratory infec
tion. Her past history included a background

of considerable

alcohol ingestion, and a diagnosis of Laennec cirrhosis had


been previously made by liver biopsy.
On admission, the patient looked chronically ill. She was
afebrile with regular pulse rate of 120/mm and a blood pres
sure of 180/100. There were clinical signs of cirrhosis and
frank jaundice. Chest examination revealed evidence for a
massive right pleural effusion. Other physical findings in

cluded enlarged liver and evidence of free liquid in the pen


toneal cavity.
The chest x-ray demonstrated a large right pleural effusion.
Other laboratory tests were compatible with liver cirrhosis and
toxic effects ofalcohol. Thoracentesis revealed a fluid that had
the characteristics ofa transudate as did a sample of pentoneal
fluid. Forty-eight hours after the thoracentesis of 1,800 cc, the
right pleural space was completely refilled (Fig. 1).
To prove that right pleural effusion was related to ascites,
5 mCi of technetium-99m

(@mTc) sulfur colloid was injected

with aseptic technique into the right lower abdominal cavity.


A serial imaging study was done in anterior view at intervals
of 5 mm for 30 mm and at 2 and 24 hr postinjection (Fig. 2).
Images were obtained on a large field-of-view camera with an
all-purpose, parallel collimator. At 2 hr the radiocolloid ap
peared in the right hemithorax and at 24 hr activity was
further increased. It confirmed the presence of a peritoneo
pleural communication. The patient responded well to medi

cal therapy and pleural effusion resolved completely in 10


days.

DISCUSSION

The association ofhydrothorax with hepatic cirrhosis


has been recognized for many years but there has been
much speculation as to its origin.
In 1947, Higgins and his colleagues suggested that
pleural effusion was related to the fall in the concentra
Received Dec. 13, 1985;revision accepted Apr. 23, 1986.
For reprints contact: Jean Verreault, MD, Dept. of Nuclear tion of plasma proteins (3). In 1958, Morrow, Kantor
Medicine, Centre Hospitalier Universitaire, Sherbrooke, Qubec, and Armen suggested that the fluid might come from
the blood stream as a result of hypoalbuminemia or
Canada, J 1H-5N4.

1706

Verreault,
Lepage,
Bisson
etal

The Journal of Nuclear Medicine

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bumin from the peritoneal to pleural spaces in a patient

with right hepatic hydrothorax. The autopsy showed no


gross defect in the right diaphragm.
Since lymphatics are more abundant in the right than

in

the

left

diaphragm

(10),

this

mechanism

might

ex

plain that hepatic hydrothorax are more frequently right


sided. In addition to this, Leak (11) used electron
microscopy

to show that pores of 41


2 @z
in diameter

exist between mesothelial cells and diaphragmatic lym


phatics. They provide a system of open channels
through which fluids and cells may rapidly be removed
from the serous cavities. What remains unclear is how
and why the fluid leaves the lymphatic system and
enters the pleural space instead ofbeing expelled toward

I
FIGURE 1
Chest x-ray showing large right pleural effusion
hypertension

in the azygous and hemiazygous

systems

or be secondary to ascites either by direct passage of


fluid through a diaphragmatic

defect or by its transport

the larger collecting vessels. It may result from lym


phatic system overload (12).
There is strong evidence to support the two mech
anisms. We think that each of these can explain the
formation of hydrothorax from ascites depending on
the case. Lymphatic drainage is probably the first mech
anism to occur in reaction to the presence of ascites. It
can be the way by which hydrothorax will be formed if
there is an overload of the lymphatic system. If it is
insufficient, the abdominal

pressure increases and may

cause subsequent rupture ofthe diaphragm. One objec


tion to this assumption may be that pleural effusions
can be present in liver cirrhosis without ascites. In these
cases, the alternative explanation is that there is con
genital diaphragmatic weakness caused by an insuffi
dent deposition of muscle and tendon bundles. We

through the diaphragmatic lymphatics (4).

proposed that the clue to distinguish between these two

Hypoproteinemia
as a sole cause can be eliminated
for there are many patients, cirrhotic or not, who have
low serum protein levels but never develop hydrothorax
(5). Ifazygous hypertension is present due to collaterals
between this system and the portal system, transudation

mechanisms

jected intrapentoneally
is mixed with ascites fluid and
consider that its migration from peritoneal to pleural

of fluid into the chest might appear. However, this


cannot explain hydrothorax occurring in Meigs' syn

space was right sided as was the pleural effusion, we


can presume that there is a relationship between ascites

drome where there is no portal hypertension. The most


probable explanation is that hydrothorax is derived
directly from the peritoneal fluid either through a defect
in the diaphragm or through the lymphatic channels

extends to the time required to show accumulation of


the agent in the pleural space. If it happens within a

that penetrate it.


At least three studies (68)have provided evidence
that hydrothorax

complicating

cirrhosis

is generated

from ascites through a diaphragmatic defect acquired


as a result of increased intra-abdominal pressure. This
has been demonstrated either by rapid passage of dye
from the ascites into the pleural effusion, induction of
a hydropneumothorax by the intra-abdominal instilla
tion of oxygen, thoracoscopy,

or by necropsy findings.

The other mechanism proposed in literature is that


peritoneal fluid passes to the pleural space through the

may be the use of radioisotope

injected

intraperitoneally as we did.
Indeed, when we assume that the radiocolloid in

fluid and pleural effusion. Furthermore,

our proposal

few minutes, as it was reported by Faiyaz and Goyal


(13), a diaphragmatic defect is probably present partic

ularly when the accumulation is as intense as peritoneal


activity. If it takes a longer period of time as was seen

for our patient, the peritoneopleural communication


may be attributed to diaphragmatic lymphatics partic
ularly when that accumulation is less intense than per
itoneal activity.
Such a study can be done either by the use of[@mTc1
sulfur colloid or [99mTc]macroaW@ted albumin. The
radiopharmaceutical

can be injected intraperitoneally

diaphragmatic lymphatics. Johnston and Rodolfo (9)


support it by the demonstration of unidirectional trans

at the end of the usual diagnostic or therapeutic peri


toneal puncture. It can show the source of pleural
effusions in liver cirrhosis and also in patients with

port of carbon particles and radioiodinated serum al

peritoneal

Volume27
Number 11
November1986

dialysis

(14). We postulate

that the speed at

1707

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FIGURE 2
Serial anterior imagingstudy of abdomen and thorax. A: 5 mm, B: 30 mm, C: 2 hr. D: 24 hr after intraperitoneal injection
of [@TcJsuffur
colloid.Migrationof radioisotope is seen on 2 hr (C)and 24 hr (D)images
which the radioisotope migrates from peritoneal to
pleural space may be a clue for differentiation between
the two pathophysiological mechanisms proposed in
the literature. Such a differentiation may influence the
patient's treatment. If transit time is rapid, a macro
scopic diaphragmatic defect could be sought. If transit
is slow, only medical treatment has to be contemplated.

ACKNOWLEDGMENT
The authors thank Mrs. LiseCt
for her excellentsecre
tanal assistance.
REFERENCES
1. Brody iS: Diseases of the pleura, mediastinum,

dia

phragm and chest wall. In Cecil Textbook ofMedicine,


Vol. 1, Wyngaarden and Smith, Philadelphia, Saun
ders,1982,p 423
2. Singer JA, Kaplan MM, Katz RL: Cirrhotic pleural

FOOTNOTE
.

Picker

1708

International,

effusion
Highland

Heights,

OH.

Verreauft,
Lepage,Bissonet al

in the absence

of ascites.

Gastroenterology

73:575577,
1977

The Journal of Nudear Medicine

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9.
3. Higgins G, Kelsall AR, O'Brien JR. et al: Ascites in
chronic diseases of the liver. QJ Med 16:263274,
1947
4. Morrow CS, Kantor M, Armen RN: Hepatic hydro
10.

Johnston RF, Loo RV: Hepatic hydrothorax: Studies


to determine the source offluid and report of thirteen

thorax. Ann Internal Med 49: 193202,1958


5. McKay DG, Sparling Hi, Robbins SL: Cirrhosis of
the liver with massive hydrothorax. Arch Internal Med

ed., London,

79:501509,
1947
6. Williams MH: Pleural effusion produced by abdom

mo-pleural communication in a patient with Laen


nec's cirrhosis ofthe liver and ascites.Ann Intern Med
33:216221,
1950
7. Emerson

PA, Davies JH: Hydrothorax

complicating

ascites. Lancet 1:487488,


1955
8. Lieberman FL, Hidemura R, Peters RL, et al: Patho
genesis and treatment of hydrothorax complicating
cirrhosis with ascites. Ann Intern Med 64:341351,
1966

Volume 27
Number 11
November1986

cases.
Ann Intern
Med 61:385401
,I964

Brash JC: Cunningham s


Textbook ofAnatomy, 9th
Oxford University

Press, 1951, p 1423

11. Leak L: Gross and ultrastructural

morphologic fea

tures of the diaphragm. Am Rev Resp Dis 119:321,


1979
12. Dumont AE, Mulholland JH: Flow rate and compo
sition ofthoracic duct lymph in patients with cirrhosis.
N EnglJ Med 263:47 1474,1960
13. Faiyaz U, Goyal PC: Unilateral pleural effusion with

out ascites in liver cirrhosis. Postgrad Med 74:309


315,1983
14. Spadaro JJ, Thakur V. Nolph KD: Technetium-99m-

labelled macroaggregated albumin in demonstration


of trans-diaphragmatic leakage of dialysate in perito
neal dialysis. Am J Nephrol 2:3638,1982

1709

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Ascites and Right Pleural Effusion: Demonstration of a Peritoneo-Pleural


Communication
Jean Verreault, Serge Lepage, Guy Bisson and Andre Plante
J Nucl Med. 1986;27:1706-1709.

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http://jnm.snmjournals.org/content/27/11/1706

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