Treatment of a right-sided pleural effusion in a patient with liver cirrhosis.

A 72-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 endoscopic sclerotherapy. 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/mL. 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 administration. What is the diagnosis? *From the Departments of Internal Medicine (Drs. Buchholz and Kaplan) and Medical Radiology (Dr. Hauser), University Hospital Zurich, Switzerland. Manuscript received March 30, 1999; revision accepted May 26, 1999. Correspondence to: Vladimir Kaplan, MD, Department of Internal Medicine, Zurich University Hospital, Raemistrasse 100, CH-8091 Zurich, Switzerland; e-mail: vladimir.kaplan@dim. usz.ch roentgenogram of the month