Abstract and Introduction

Abstract
Hepatic hydrothorax is defined as a transudative pleural effusion, usually greater
than 500 mL, in patients with portal hypertension without any other underlying
primary cardiopulmonary cause. It develops most likely because of diaphragmatic
defects that allow for passage of fluid from the peritoneal space to the pleural
space. Because of the mechanical constraints of the thoracic cavity, this
complication of portal hypertension can be challenging to treat because patients
will become symptomatic when as little as 500 mL of fluid is present in the pleural
space. Treatments include salt restriction, diuretics, thoracentesis, transjugular
intrahepatic portosystemic shunt, video-assisted thoracoscopy, and pleurodesis.
It is important to note that a chest tube is not a potential treatment option; a
hepatic hydrothorax should not be treated with a chest tube unless there is frank
pus in the pleural fluid or a pneumothorax is present. The ultimate treatment is a
liver transplant; the development of a hepatic hydrothorax thus warrants a referral
to a liver transplant center.

Introduction
Patients with end-stage liver disease often suffer from complications of portal
hypertension. In these patients, 50% ultimately will develop ascites and 25% will
develop a variceal hemorrhage. Hepatic hydrothorax is a less common
complication of portal hypertension occurring in 5 to 10% of patients with
cirrhosis. Despite its infrequency, it remains a challenging problem for clinicians,
and its development warrants a liver transplant evaluation.
Hepatic hydrothorax is defined as a transudative pleural effusion, usually greater
than 500 mL in patients with portal hypertension without any other underlying
primary cardiopulmonary cause. The presence of portal hypertension and not
cirrhosis is the sine qua non for the development of hepatic hydrothorax; it should
be noted, however, that most patients (> 80%) with portal hypertension have
cirrhosis. Although patients with ascites can often tolerate 5 to 8 L of fluid in their
abdomen before becoming significantly symptomatic, a patient with a hepatic
hydrothorax will develop dyspnea, shortness of breath, and/or hypoxia when only
1 to 2 L of fluid accumulate in the pleural space. This is expected given the
structural characteristics of the thoracic cavity. As a result, this complication of
portal hypertension is challenging for both patients and clinicians.

Incidence
Four large series comprising 1155 cirrhotic patients with ascites cited an
incidence of hepatic hydrothorax of 6%.[14] In another series of 862 patients with
cirrhosis, 15% had a pleural effusion, but only 6.5% had enough fluid to require a
thoracentesis.[5]
As opposed to pleural effusions of cardiac origin that are typically bilateral, 79.5%
of pleural effusions in a patient with cirrhosis are right sided only, 17.5% are left
sided only, and 3% are bilateral.[6,7] This can be helpful in establishing the
diagnosis of hepatic hydrothorax versus cardiac

Pathophysiology
The etiology of hepatic hydrothorax is not completely understood. It is believed
that the underlying mechanisms leading to fluid retention in patients with hepatic
hydrothorax are similar to those leading to other forms of fluid accumulation in
patients with cirrhosis. Ascites formation involves the combination of portal
hypertension and splanchnic arterial vasodilation. These two events modify the
intestinal microcirculation and result in excess lymph formation relative to
absorptive capacity in the peritoneal cavity. Increased capillary pressure and
permeability secondary to splanchnic arterial vasodilation is the predominant
mechanism in this process.
Several observations indicate that the most likely cause of pleural effusions in
patients with cirrhosis is the passage of a large amount of ascites from the
peritoneal to the pleural cavity through diaphragmatic defects. [812] This
mechanism was first suggested following the observation of a pneumothorax
after injection of air into the peritoneal cavity; when air is infused intraperitoneally
in patients with hepatic hydrothorax, a chest x-ray performed within 48 hours can
detect air above the diaphragmatic surface in the right side of the chest.
[8]
Diaphragmatic defects can be demonstrated both grossly and microscopically
in patients with hepatic hydrothorax. Microscopic examination of these defects
reveals discontinuities in the collagen bundles that make up the tendinous portion
of the diaphragm.[8] Typically, the defects are smaller than 1 cm and tend to occur
on the right side. This right-sided predominance likely occurs due to the close
anatomical relationship of bare areas of the liver with the diaphragm as well as
the fact that the left side of the diaphragm is thicker and more muscular than the
right. Huang and colleagues[13] have classified the diaphragmatic defects into four
morphological types:

Type 1: No obvious defect

Type 2: Blebs lying in the diaphragm

Type 3: Broken defects (fenestrations) in the diaphragm

Type 4: Multiple gaps in the diaphragm

Diaphragmatic defects occur in up to 20% of the noncirrhotic population;

interestingly, despite the prevalence of these defects, a pneumothorax only rarely
develops following laparoscopic procedures.[1416] Obviously the presence of
ascites alters the pressure gradient between the intrathoracic and intraabdominal
regions. In patients with ascites, the increasing abdominal pressure and the
diaphragmatic thinning secondary to malnutrition in some cirrhotic patients
enlarge these defects. When intraabdominal pressure increases, gaps can
develop between the muscle fibers of the diaphragm and lead to small
herniations of the peritoneum into the pleural space. These herniations, called
pleuroperitoneal blebs, may rupture and therefore facilitate passage of fluid. The
negative intrathoracic pressure favors the one-way transfer of fluid across these
defects, possibly with a valvular mechanism.[6,17,18] Interestingly, up to 20% of
patients with hepatic hydrothorax have no clinically significant ascites. [1924] Ascites
develops in patients with hepatic hydrothorax when the formation of ascitic fluid
exceeds its absorption by the peritoneal lymphatics and transfers into the pleural
space.
The valvular mechanism of hepatic hydrothorax development has been
corroborated with nuclear medicine studies using 99mTc-human albumin or 99mTcsulfur colloid and dye studies that show a unidirectional passage of these
markers from the abdominal to the pleural cavity in the first 24 hours after
administration.[23,2527] Also, radioactive isotope scans confirm communication
between the peritoneal cavity and the pleural space, even in the absence of
sonographic evidence of ascites.[25]Fluid can also leak directly from the liver into
the pleural space when bare areas of the liver are in contact with the defects in
the diaphragm.Continue Reading

Clinical Presentation
The clinical presentation of hepatic hydrothorax is typically dominated by signs
and symptoms of cirrhosis and ascites. A hepatic hydrothorax should be
suspected in a patient with cirrhosis who develops a unilateral (typically rightsided) pleural effusion. Hepatic hydrothorax can present asymptomatically or with

cough, dyspnea, hypoxia, or respiratory failure depending on various factors.

These include the volume of fluid in the pleural space, the rapidity of the
accumulation of the pleural fluid and the presence of coexistent cardiopulmonary
diseases. Most of these effusions tend to be small to moderate in size, with only
6% of patients having effusions that occupy greater than half of a hemithorax. [28]

Diagnosis
The diagnosis is based on the presence of cirrhosis with portal hypertension and
the exclusion of cardiopulmonary disease. The majority of effusions can be seen
on a frontal chest x-ray, although sometimes a lateral chest x-ray is needed as
well.
A thoracentesis should be performed to exclude a primary cardiopulmonary
process. In a study of 60 cirrhotic patients admitted to the hospital with pleural
effusions,[21] 70% (42 patients) were found to have an uncomplicated hepatic
hydrothorax (without infection, blood or pus). Of the other 18 patients, nine had
spontaneous bacterial empyema, two had pleural tuberculosis, two had
adenocarcinoma, two had parapneumonic effusion, and three were undiagnosed
exudates. When the effusion was right sided, 80% were an uncomplicated
hepatic hydrothorax; but when the effusion was left-sided only 35% were an
uncomplicated hepatic hydrothorax. Hence the presence of a left-sided pleural
effusion in a cirrhotic patient should not be assumed to be an uncomplicated
hepatic hydrothorax. Pleural fluid analysis is mandatory.
Diagnostic tests to be ordered on the pleural fluid include cell count, Gram stain
and culture in blood culture bottles, and serum and fluid protein, albumin, and
lactate dehydrogenase (LDH).[6,17] The composition of hepatic hydrothorax is
transudative in nature and therefore similar to the ascitic fluid; it will also have a
serum to pleural fluid albumin gradient greater than 1.1 as is found in ascites
secondary to portal hypertension. Other tests from the pleural fluid that would be
appropriate depending on the clinical circumstances include triglycerides, pH,
adenosine deaminase and polymerase chain reaction (PCR) for mycobacteria,
amylase, and cytology to exclude chylothorax, empyema, tuberculosis,
pancreatitis, and malignancy, respectively. These additional tests should be
considered when the fluid is an exudate or when the pleural effusion is left sided.
The characteristics and the interpretation of pleural fluid in hepatic hydrothorax
are described in Table 1. In uncomplicated hepatic hydrothorax the
polymorphonuclear cell count is less than 500 cells/mm 3, and the total protein
concentration is less than 2.5 g/dL.[17,29] LDH levels are also low consistent with a

transudate. Total protein and albumin may be slightly higher in hepatic

hydrothorax compared with levels in the ascitic fluid. [11,30] Diuresis can also
increase the total protein levels in the fluid that is sampled. When uncertainty
exists regarding the etiology of the pleural effusion, the finding of an elevated
serum soluble Fas ligand may help distinguish a hepatic hydrothorax from one
resulting from heart failure in patients with viral hepatitis. [31]
In addition to pleural fluid analysis, other tests may also be important and
informative. Pertinent laboratory tests such as a basic metabolic panel, hepatic
panel, prothrombin time, and brain natriuretic peptide (BNP) should be obtained
in the proper clinical setting. In addition, a computed tomographic (CT) scan of
the chest will exclude mediastinal, pulmonary, or pleural lesions or malignancies.
Echocardiography should be performed to evaluate cardiac function.Continue
Reading

Spontaneous Bacterial Empyema

A spontaneous bacterial empyema (SBEM) is an infection of a preexisting
hydrothorax in which pneumonia has been excluded. However, this term may be
confusing because there is typically no evidence of pus or abscess in the thoracic
cavity; for this reason, some authors have proposed that it be called spontaneous
bacterial pleuritis.[32] However, this name has not gained acceptance, and most
published studies referring to infections of the pleural fluid in cirrhotics use the
term SBEM.
Infection of the pleural fluid must be considered in any patient with hydrothorax
who develops fever, pleuritic pain, encephalopathy, or unexplained deterioration
in renal function. Therefore a high index of suspicion is essential for its diagnosis.
In the evaluation of a hepatic hydrothorax, a thoracentesis should be performed,
and a cell count from that fluid should always be sent. The diagnostic criteria for
SBEM are as follows:

Positive pleural fluid culture and a polymorphonuclear count greater than 250 cells/mm 3

Negative pleural fluid culture and a polymorphonuclear count greater than 500 cells/mm 3

No evidence of pneumonia on a chest x-ray

Fluid should be inoculated at the bedside directly into a blood culture bottle. This
increases the sensitivity for the diagnosis of SBEM from 33 to 77%. [33]

The incidence of SBEM is similar to the reported incidence of spontaneous

bacterial peritonitis (SBP); 15 to 20% of hospitalized patients with cirrhosis will
have SBP, and in a prospective study Xiol and colleagues found a 13% incidence
of SBEM.[3336] Interestingly up to 40% of cases of SBEM are not associated with
SBP.[33] Some patients will not have ascites, supporting the hypothesis that enteric
microorganisms reach the pleural space through bacteremia as has been
reported in SBP.[37] This is in addition to direct spread of the infection from the
peritoneal space through the diaphragmatic defects. Because SBEM can develop
without simultaneous SBP, a thoracentesis should be performed in a patient with
a clinical suspicion for an infection even if a paracentesis has not revealed an
infection. The most frequent bacteria involved are Enterobacteriaceae
(Escherichia coli and Klebsiella pneumonia), Streptococcus species and
Enterococcus species. Not surprisingly, these are also the most common
bacterial causes of SBP.
Treatment for SBEM typically involves the use of a third-generation
cephalosporin. The use of albumin in preventing hepatorenal syndrome is the
standard of care in patients with SBP but it has not been studied in patients with
SBEM.[38] These patients should be placed on life-long (or until a liver transplant)
prophylaxis for the prevention of SBEM or SBP with norfloxacin, ciprofloxacin, or
bactrim.
Chest tube insertion is not indicated in the management of SBEM unless frank
pus is present. Chest tube insertion can lead to renal insufficiency, prolonged
drainage through the insertion site following removal, increased risk of secondary
infection, and further protein loss.[39,40] This will be further discussed in the
treatment section of this article.
A few studies have evaluated the risk factors for developing SBEM. Sese and
colleagues found that a low pleural fluid total protein (less than 1.0 mg/dL) and
low C3 levels as well as a higher Child-Pugh Score were associated with the
development of an SBEM.[30] Simultaneous SBP is also a risk factor.[5]Mortality is
as high as 20% in patients with SBEM.[33,41] Just as the development of SBP is an
indication for a liver transplant evaluation, the development of SBEM should
prompt a referral to a liver transplant center.Continue Reading

Management

Patients with hepatic hydrothorax tend to have advanced liver disease with
significant complications related to portal hypertension. They should be referred
for a liver transplant evaluation as definitive treatment for hepatic hydrothorax. In
patients awaiting liver transplant and in those who are not transplant candidates,
the aims of therapy for hepatic hydrothorax are twofold: (1) to relieve symptoms
and (2) to prevent pulmonary complications (see Table 2 ). An algorithm for the
management of hepatic hydrothorax is outlined in [Fig. 1].

Figure 1.

Treatment algorithm for hepatic hydrothorax. *Diuretics should be started with

furosemide 40 mg/day and spironolactone 100 mg/day. If there is no response,
diuretics may be increased in a stepwise fashion every 5 days by doubling doses
(ratio of 40:100 mg), furosemide up to 160 mg/day and spironolactone up to 400
mg/day. TIPS, transjugular intrahepatic shunt.

Diuretics
The first step in the management of a hepatic hydrothorax is a simple and
inexpensive treatmentto create a negative sodium balance by restricting

sodium intake and administering diuretics. Patients should be on a 2000 mg/day

sodium-restricted diet. Diuretics (typically furosemide and spironolactone) should
be coadministered as well to produce a renal excretion of sodium of at least 120
mEq of sodium/day. The best initial regimen is the combination of furosemide 40
mg/day and spironolactone 100 mg/day.[42] If there is no response, compliance
with diet and medications should be addressed, and then diuretics may be
increased in a stepwise fashion every 5 days by doubling the doses;
spironolactone up to 400 mg/day and furosemide up to 160 mg/day. The goal is
to achieve an average weight loss of 0.5 kg/day in patients without edema and 1
kg/day in those with peripheral edema.[43,44]Patients should also be instructed to
avoid nonsteroidal antiinflammatory drugs (NSAIDs), which can cause sodium
retention and renal failure.
Unfortunately some patients are unable to tolerate the appropriate amount of
diuretics without increasing their creatinine or developing hyponatremia. In a
retrospective study of 405 cirrhotic patients admitted over a 5-year period with
ascites, seven of 27 patients (25.9%) were refractory to medical treatment. [3] In a
prospective study of 60 cirrhotic patients with hepatic hydrothorax, 13 (21.7%)
were considered refractory.[30] In these patients other treatment modalities are
required and will be discussed later in this article.

Thoracentesis and Paracentesis

In patients who are symptomatic, a thoracentesis needs to be performed to
relieve the dyspnea, respiratory distress, or hypoxia. There are well-documented
risks associated with a thoracentesis, including a pneumothorax and hemothorax,
but it is usually safe and well tolerated. However, when a thoracentesis is
required more than once every 2 to 3 weeks in patients on maximal sodium
restriction and optimal diuretics, alternative treatments must be considered
because the complication rate increases as more procedures are needed.
As a general rule, no more than 2 L of fluid should be removed because of the
risk of pulmonary edema and hypotension.[45] However, this "2 liter rule" was
developed in patients with causes of the pleural effusion other than cirrhosis;
patients with cirrhosis may be able to tolerate the removal of larger volumes of
fluid. Given the relatively small volume of fluid removed at thoracentesis we do
not administer intravenous albumin to avoid circulatory dysfunction unlike its
routine use with large-volume paracentesis.
Coagulopathy is not considered a contraindication to therapeutic thoracentesis.
One study demonstrated no increased risk of bleeding in patients with

prothrombin times up to twice the midpoint of the normal range, or platelet counts
of more than 50,000/L; the authors concluded that prophylactic transfusions are
not necessary.[21,46] Patients with a serum creatinine more than 6 mg/dL had
greater blood loss compared with those with lower values.
A large-volume paracentesis can also offer similar rapid relief of respiratory
distress in those with ascites and hepatic hydrothorax and should be attempted
prior to a thoracentesis. Angueira and Kadakia [47] found a significant increase in
total lung capacity and symptomatic improvement within 2 hours after an average
of 3.5 L of ascitic fluid was removed by a paracentesis.

Chest Tube Placement

Various authors have cautioned against the placement of a chest tube in patients
with cirrhosis because they are fraught with multiple complications:
pneumothorax, hemothorax, empyema, electrolyte abnormalities, and
hepatorenal syndrome.[39,48,49] Despite this plea, many patients still have chest
tubes placed when they present with respiratory distress and a hydrothorax.
Orman and Lok[40] reviewed the records of 17 patients admitted to a tertiary care
center with a chest tube placed for hepatic hydrothorax. Sixteen out of 17
patients had at least one complication, and 12 patients had more than one
complication. These included 11 patients with acute kidney injury, seven patients
with a pneumothorax, and five patients with an empyema. Liu and
colleagues[48] reviewed the outcomes of 59 patients with cirrhosis undergoing
chest tube placement and found a complication rate of 80% and a 27% mortality;
a caveat of this study is that it included patients who had a chest tube placed for
a pneumothorax or empyema, which are indications that require a chest tube to
be placed.
The drainage of large volumes of protein-rich pleural fluid may lead to renal
failure and electrolyte disturbances in this patient population. It can also be
difficult to remove the chest tube because there is often a rapid reaccumulation of
fluid once the chest tube is clamped.
In lieu of placing a chest tube other modalities must be considered in the
treatment of patients with an uncomplicated hepatic hydrothorax. It should also
be noted that the presence of SBEM is not an indication for a chest tube
placement unless frank pus is noted on the thoracentesis.

Transjugular Intrahepatic Portosystemic Shunt

Transjugular intrahepatic portosystemic shunt (TIPS) is a procedure that creates

an anastomosis between the portal and hepatic veins, decompressing the hepatic
and splanchnic vascular bed and resulting in a reduction in portal pressure. It is
now the standard of care in patients with refractory hepatic hydrothorax.
Contraindications to placing a TIPS are age > 70, significant hepatic
encephalopathy, large portal vein thrombosis, right-sided heart failure, elevated
pulmonary arterial pressures, and an elevated model for end-stage liver disease
(MELD) score (typically greater than 18). This elevated MELD score is a marker
for more severe hepatic dysfunction. Because TIPS shunts blood away from the
liver and reduces the effective portal perfusion to the liver, it can precipitate liver
failure in patients with already significant hepatic dysfunction. In a carefully
selected population though, TIPS can lead to significant improvements in the
complications related to portal hypertension.
Several groups have reported a beneficial effect of TIPS in patients with hepatic
hydrothorax. Unfortunately, few of the studies described the rigor with which the
refractoriness of the hydrothorax to medical therapy was determined. Despite this
shortcoming, most series have demonstrated response rates in the range of 70 to
80%.[20,5056]
The most recently published and largest series to date was reported by
Dhanasekaran and colleagues in 2010.[55] In their study 73 patients with refractory
hepatic hydrothorax had a TIPS placed. Fifty-nine percent of patients had a
complete response, 20% had a partial response, and 21% had no response to
TIPS placement. The short-term survival rates at 30, 60, and 90 days were 81,
78, and 72%, respectively. The long-term survival rates at 1, 3, and 5 years were
48, 26, and 15%, respectively. These survival rates are equivalent to other
previously published rates; Wilputte and colleagues [56]found that the 30-, 90-, and
150-day mortality was 14, 25, and 53%, respectively, after TIPS placement.
Encephalopathy developed in 15% of patients.[55]
Risk factors for mortality after TIPS placement for hepatic hydrothorax have been
described. These include a Child-Pugh score 10, a pre-TIPS MELD score > 15,
and an elevated pre-TIPS creatinine.[55,56] In addition, a lack of response in the
hydrothorax after TIPS placement is associated with an increased mortality rate.

Surgical Repair of Diaphragm Defects

Evaluation for defects in the diaphragm by open thoracotomy and by
videothoracoscopy has been used to identify diaphragmatic defects. If the defect
can be identified, biologic glue or sutures can be used to close and seal these

defects.[10,23,57] In small, uncontrolled reports, good results have been seen in

patients in whom the fenestrations can be localized and closed. Milanez de
Campos and colleagues[58]performed 21 thoracoscopies in 18 patients with
hepatic hydrothorax with an overall success rate of 48%. In the five patients
where diaphragmatic defects were identified and closed, four had resolution of
the hepatic hydrothorax, and the fifth patient developed empyema and died
secondary to pneumonia and liver failure. Morbidity (57.1%) and mortality
(38.9%) were high in this study during a follow-up period of 3 months, raising
questions about the utility of such an approach. Although there are no head-tohead comparison studies, the mortality rate in this thoracoscopic study can be
placed in the context of the lower 90-day mortality (25%) reported with TIPS.
Often the surgical techniques are combined with pleurodesis, which is described
below.

Pleurodesis
Pleurodesis is a technique that consists of the ablation of the space between the
parietal and visceral pleura with a sclerosing agent injected by tube
thoracostomy. Transudative pleural effusions are notoriously difficult to
pleurodese due to the absence of inflamed pleural surfaces that are required for
successful adhering of parietal and visceral surfaces together. In addition, the
rapid fluid reaccumulation prevents the visceral and parietal pleural surfaces from
approximating long enough for the inflammatory process to result in pleural
symphysis.[59,60]
Pleurodesis with tetracycline or talc has been used. The irritant is administered
through a chest tube or by thoracoscopy. In the study described earlier by
Milanez de Campos and colleagues,[58] aerosolized talc was effective in
preventing recurrence of the effusion in only 10 patients (47.6%). Effusions
recurred within 3 months in 43.7% of patients; in addition there were several
complications noted, including fever, chest pain, empyema, incomplete
reexpansion, pneumonia, and wound infection. A smaller study by Mouroux and
colleagues[10] utilized video-assisted thoracoscopy (VATS) to repair diaphragmatic
defects in addition to pleurodesis in eight patients with refractory hepatic
hydrothorax. Hydrothorax resolution occurred in the six patients where a defect
was found and repaired, with a follow-up of 7 to 36 months. In a similar study,
Ferrante and colleagues[61] performed VATS and talc pleurodesis in 15 patients
with refractory hepatic hydrothorax. No visual defect was found in any of these
patients. Control of symptoms and resolution of the effusion were achieved in 11

patients (73%) in the first 30 days after the procedure, with eight patients
remaining asymptomatic for a median follow-up of 5.5 months and three
experiencing recurrence of the effusion between 45 and 60 days after the VATS.
Unfortunately, complications included pain around the chest tube site, low-grade
fever with leukocytosis, pleurocutaneous fistula, and empyema. Takayama and
colleagues[62] reported on a technique of thoracoscopic pleurodesis using argon
beam coagulation, fibrin glue, and minocycline in nine patients with refractory
hydrothorax. In this small study all patients showed clinical improvement with two
recurrences.
Finally Northup and colleagues[63] described a technique of a thoracoscopically
guided mechanical pleurodesis followed by talc instillation combined with
simultaneous extended percutaneous peritoneal drainage tube placement to
allow complete adherence of the pleural space. In this small series of five
patients, no visual defects were found. The drains were left in place for a mean of
12.6 days. Patients were followed for up to 132 days without recurrence of the
effusion, although two patients received a liver transplant within 1 month of the
procedure. The authors state that the success of their procedure was based on
two aspects: (1) the meticulous mechanical abrasion (up to 30 minutes) of the
entire diaphragmatic surface and (2) the addition of the peritoneal catheter aided
in decreasing the hydrostatic pressure from the peritoneal cavity driving fluid into
the pleural space. There were no deaths attributable to the procedure, although
four patients required hospitalization for 3 or more weeks.
Continuous positive airway pressure in conjunction with pleurodesis may help to
facilitate pleural apposition by creating a positive intrathoracic pressure gradient,
which inhibits the flux of ascites into the pleural space. [63,64]
Although VATS with pleurodesis appears promising, most reports include small
numbers of patients and are uncontrolled. Therefore, medical management and
TIPS should be attempted first, and VATS with pleurodesis should be considered
only if these measures fail.Continue Reading

Summary
Hepatic hydrothorax occurs in 5 to 10% of patients with cirrhosis and portal
hypertension. The entrance of fluid into the pleural space occurs when defects
develop in the diaphragm. Medical management with salt restriction and diuretics
is first-line therapy. Other treatments include thoracentesis, TIPS, VATS, and

pleurodesis. Ultimately the only cure for hepatic hydrothorax is a liver transplant
(see [Fig. 1]).

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