*From the Departments of Internal Medicine (Drs. Buchholz and Kaplan) and Medical Radiology (Dr. Hauser), University Hospital Zurich, Switzerland.
Correspondence to: Vladimir Kaplan, MD, Department of Internal Medicine, Zurich University Hospital, Raemistrasse 100, CH-8091 Zurich, Switzerland; e-mail: firstname.lastname@example.org
-year-old white woman presented with progressive dyspnea, orthopnea, and
a weight gain of 10 lb over a period of 2 weeks. The patient’s history
was remarkable for coronary heart disease for which she underwent
percutaneous transluminal coronary angioplasty of a filiform circumflex
artery stenosis 1 year before admission, and for a chronic hepatitis C
evolving to cirrhosis with recurrent variceal hemorrhage requiring
On admission, the patient had tachypnea with a respiratory rate of 30
breaths/min. The heart rate was 100 beats/min with a regular rhythm.
The BP was 110/70 mm Hg. There were no murmurs, nor was there a third
heart sound. The jugular veins were not distended. A right-sided
dullness on thoracic percussion was noted. A chest radiograph revealed
a large right-sided pleural effusion but no evident cardiomegaly (Fig 1
). Thoracentesis was performed, and 2,000 mL of clear fluid with a
protein level of 1 g/dL and a lactate dehydrogenase of 180 U/L were
removed. The WBC count was 200/μL. Results of fluid cultures
and cytologic studies remained negative. An ultrasound of the abdomen
showed minimal perihepatic ascites. Echocardiography revealed a normal
left ventricular function. The patient was started on furosemide, 80 mg
qd, and spironolactone, 200 mg qd. Over the next week, the
pleural effusion and dyspnea recurred. With repeated thoracentesis, an
additional 2,000 mL of fluid were aspirated. Diuretics were
discontinued because symptomatic arterial hypotension developed. A
therapeutic procedure was performed (Fig 2
The procedure consisted of the placement of a 10-mm diameter
transjugular intrahepatic portosystemic shunt (TIPS), as seen on the
radiograph in projection on the right upper abdomen (Fig 2). The
portosystemic pressure gradient dropped from 20 to 11 mm Hg. The
pleural effusion resolved within days (Fig 2), and dyspnea did not
recur. Shunt patency was documented by Doppler ultrasound.
Unfortunately, portosystemic encephalopathy evolved over the following
days, which could be adequately controlled with enteral lactulose
What is the diagnosis?
Diagnosis: Hepatic hydrothorax
Hepatic hydrothorax is defined as pleural effusion in a cirrhotic
patient without primary pulmonary or cardiac disease.1The
frequency of hepatic hydrothorax in cirrhotic patients is reported to
be around 5%.2The pleural effusion is predominantly
right sided (85% of cases) but may be bilateral.3–
Although most often accompanied by significant ascites, it can occur in
its absence.4 Hepatic hydrothorax originates secondary to
ascitic fluid movement from the abdominal cavity to the pleural space
via defects in the diaphragm.3 These defects include holes
and blebs on the central tendinous portion of the
diaphragm.5 The cyclic negative intrathoracic pressure
during breathing and the positive intra-abdominal pressure create an
unidirectional flow of ascites across the diaphragm.
Signs and symptoms are primarily those of liver cirrhosis and
ascites. Rarely, pulmonary symptoms such as cough and dyspnea
predominate. In a patient with right-sided pleural effusion and known
liver cirrhosis with ascites, and no concomitant pleural or cardiac
disease, a hepatic hydrothorax is most likely. At thoracentesis,
protein levels are low (< 2.5 g/dL) and similar to what can be found
in cirrhotic ascites. The polymorphonuclear leukocyte count should not
exceed 500/μL; otherwise, a concomitant spontaneous bacterial
empyema exists.6 Radiolabeled colloid injected into the
peritoneal cavity can be used to demonstrate the communication between
the peritoneal and pleural space.4
The principles of management are the same as for treatment of
cirrhotic ascites. In most patients, symptoms are controlled
effectively with sodium restriction and diuretics (distal-acting agents
plus loop diuretics). Thoracentesis is the most effective method for
rapid relief of symptoms. If repeated thoracentesis is required for
symptom control, placement of a TIPS is the treatment of choice. In
patients with refractory hepatic hydrothorax, relief of symptoms can be
achieved in 60 to 80% of patients following TIPS
placement.7 Major complications are shunt occlusion,
portosystemic encephalopathy, and postprocedure sepsis.7
However, the prognosis for patients with hepatic hydrothorax remains
poor despite symptom control following TIPS placement, and liver
transplantation as a definitive treatment modality should be
Become a CHEST member and receive a FREE subscription as a benefit of membership.
Individuals can purchase this article on ScienceDirect.
Individuals can purchase a subscription to the journal.
Individuals can purchase a subscription to the journal or buy individual articles.
Learn more about membership or Purchase a Full Subscription.
Institutional access is now available through ScienceDirect and can be purchased at myelsevier.com.
Some tools below are only available to our subscribers or users with an online account.
Download citation file:
Web of Science® Times Cited: 6
Customize your page view by dragging & repositioning the boxes below.
Enter your username and email address. We'll send you a reminder to the email address on record.
Athens and Shibboleth are access management services that provide single sign-on to protected resources. They replace the multiple user names and passwords necessary to access subscription-based content with a single user name and password that can be entered once per session. It operates independently of a user's location or IP address. If your institution uses Athens or Shibboleth authentication, please contact your site administrator to receive your user name and password.