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J Thorac Cardiovasc Surg 2008;136:1367-1369
© 2008 The American Association for Thoracic Surgery
Brief Communication |
Division of Chest Medicine, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan
Received for publication October 15, 2007; accepted for publication December 2, 2007. * Address for reprints: Ping-Hung Kuo, MD, Division of Chest Medicine, Department of Internal Medicine, National Taiwan University Hospital No. 7, Chung-Shan S Rd, Taipei 100, Taiwan. (Email: Kph712{at}ntuh.gov.tw).
Hepatic hydrothorax, a manifestation of end-stage liver disease, is defined as the presence of more than 500 mL of pleural effusion in patients with liver cirrhosis who do not have cardiopulmonary diseases or malignancies that could explain this effusion.1
Strauss and Boyer2 have reported incidences of 85.4 right-sided, 12.5% left-sided, and 2% bilateral hepatic hydrothoraces. The most likely cause is fluid transfer from the abdomen to the pleural space through diaphragmatic defects.1 Optimal management remains unclear, and thoracocentesis is frequently required for immediate symptom relief. Alternative treatments, including pleurodesis by tube thoracostomy or video-assisted thoracoscopic surgery (VATS), diaphragm repair, transjugular intrahepatic portosystemic shunt, peritoneovenous shunts, or liver transplantation, should be considered when frequent therapeutic thoracocentesis is needed.1 We report here the first case of refractory hepatic hydrothorax in which a 5-year remission was achieved by nonsurgical OK-432 pleurodesis.
A 78-year-old woman with hepatitis C–related Child–Pugh class C liver cirrhosis came to our hospital with new-onset dyspnea and bilateral lower leg pitting edema. There was a history of refractory right-sided hepatic hydrothorax 5 years previously that was managed with OK-432 pleurodesis through a pigtail after failure of repeated minocycline pleurodesis. Surgical intervention was refused by the patient at that time because of older age and poor liver reserve. The patient had a 5-year symptom-free period with a regimen of oral diuretics and sodium restriction.
The physical examination revealed icteric sclera, right lower lung field dullness with decreased breath sound, and bilateral lower extremity pitting edema. The oxygen saturation was 82% on room air. Results of the neurologic examination were unremarkable. The hemogram was normal, whereas blood biochemistry studies revealed hyponatremia (130 mmol/L), hypoalbuminemia (2.8 g/dL), and abnormal liver function (total bilirubin 3.5 mg/dL, direct bilirubin 1.42 mg/dL, aspartate aminotransferase 58 units/L, alanine aminotransferase 24 U/L).
Chest radiography showed a large amount of right pleural effusion (Figure 1, A ). Echocardiography revealed a good left ventricular ejection fraction. Chest computed tomographic scan disclosed right-sided pleural effusion with right lower lobe atelectasis, marked liver cirrhosis, esophageal varices, and minimal ascites. Cytologic studies of the pleural effusion and ascites were both negative.
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No further thoracocentesis was required for symptom relief. Follow-up chest radiographs (Figure 1, B) 6 months later showed a right loculated pleural effusion. Chest ultrasonography (Figure 2 ) revealed thickened pleura of up to 5 mm over the right hemidiaphragm. The patient has remained free of symptoms and is leading an uneventful life.
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Medical treatments of salt restriction and diuretics are mainstays of therapy for hepatic hydrothorax but have only a temporary effect in a third of cases.2 Although peritoneovenous shunt and transjugular intrahepatic portosystemic shunt have been reported to be useful, frequently encountered complications, such as hepatic encephalopathy and infection, limit their clinical applications. These procedures are thus better reserved as a bridge to liver transplantation.1
Successful pleurodesis with tetracycline through a tube thoracostomy for hepatic hydrothorax was first reported in 1977.2 Repair of diaphragmatic defects with sutures and biologic glue by VATS was successfully applied for this condition in 1996. Since then, VATS pleurodesis with or without diaphragmatic repair has been considered the technique of choice.3 The chemical agents used included tetracycline, talc, minocycline, and OK-432.2,4,5
OK-432 is an immune modulator purified from the SU strain of Streptococcus pyogenes A3 that has been proved effective in controlling malignant ascites and pleural effusion.6 In Japan, it is also used in pleurodesis for pneumothorax and chylothorax.7-8 The experience of OK-432 pleurodesis for hepatic hydrothorax through a tube thoracostomy is limited to a small number of Japanese patients.9
Previous reports on hepatic hydrothorax have used different definitions of successful pleurodesis. Radiologic evidence of recurrence is frequently observed within 2 months, even after VATS pleurodesis.3,5 Our patient is the first reported to undergo OK-432 pleurodesis that resulted in a 5-year remission. The second pleurodesis with OK-432 was once again successful in terms of dramatic resolution of the recurrent hepatic hydrothorax after failure of repeated minocycline pleurodesis.
In conclusion, patients with end-stage liver cirrhosis and refractory hepatic hydrothorax have few therapeutic options. Our case demonstrates that OK-432 pleurodesis through a pigtail catheter is safe and can provide an effective alternative for patients for whom surgical intervention is not suitable.
References
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