Ann Thorac Surg 2000;69:609-611
© 2000 The Society of Thoracic Surgeons
Case Reports
Transjugular intrahepatic portosystemic shunt for recurrent hepatic hydrothorax
Lori D. Conklin, MDa,
Anthony L. Estrera, MDb,
Morris A. Weiner, MDc,
Patrick R. Reardon, MDd,
Michael J. Reardon, MDe
a Division of General Surgery, Department of Surgery, Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA
b Division of Cardiothoracic Surgery, Department of Surgery, Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA
c Division of Cardiovascular Radiology, Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA
d Department of Surgery, Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA
e Baylor College of Medicine, The Methodist Hospital, Houston, Texas, USA
Address reprint requests to Dr Reardon, Department of Surgery, Baylor College of Medicine, 6550 Fannin, Suite 1619, Houston, TX 77030
e-mail: reardonm{at}bcm.tmc.edu
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Abstract
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For many years, pleural effusions have been recognized as a complication of cirrhosis, occurring in approximately 5.5% of patients. Recent studies have confirmed that small defects in the diaphragm allow for passage of ascitic fluid into the pleural space. Successful management of these patients is challenging, as many of the treatment options can be associated with increased morbidity. The initial treatment should focus on eliminating and preventing the recurrence of ascites with diuretics and water and salt restriction. For those patients who do not respond medically, more invasive techniques have been used including serial thoracentesis, chest tube placement, chemical pleurodesis, and peritoneovenous shunts. We present a patient with recurrent pleural effusions secondary to hepatic cirrhosis who was unsuccessfully treated medically, and subsequently treated with thoracentesis, chest tube drainage and pleurodesis, with ultimate resolution after transjugular intrahepatic portosystemic shunt placement.
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Introduction
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Hepatic hydrothorax is defined as the accumulation of a significant amount of ascitic fluid in the pleural space of a cirrhotic patient without primary pulmonary or cardiac disease [1]. It occurs in approximately 5.5% of patients with cirrhosis (range, 0.4% to 12.2%), and recent studies have confirmed that small defects in the diaphragm allow for passage of ascitic fluid into the pleural space [2, 3]. Successful management of these patients is challenging, as many of the treatment options can be associated with increased morbidity [4, 5]. The initial treatment should focus on eliminating and preventing the recurrence of ascites with diuretics and water and salt restriction [6]. For those patients who do not respond medically, more invasive techniques have been used, including serial thoracentesis, chemical pleurodesis, chest tube thoracostomy, thoracotomy, and peritoneovenous shunts. We present a patient with recurrent pleural effusions secondary to hepatic cirrhosis unsuccessfully treated with thoracentesis, then thoracotomy and talc pleurodesis at another institution, with resolution after transjugular intrahepatic portosystemic shunt (TIPS) placement.
A 49-year-old man with a long history of alcohol abuse and chronic hepatitis B and C was transferred to Baylor College of Medicine and The Methodist Hospital for further evaluation and treatment of a recurrent hepatic hydrothorax. The patient had been treated in the past for smaller pleural effusions by successfully managing his underlying cirrhosis; however, over the past several months, the effusions were enlarging and becoming more difficult to control. He presented to an outside hospital with shortness of breath, and a chest roentgenogram taken on admission revealed a large right-sided pleural effusion (Fig 1). A computed tomographic scan of the chest revealed no evidence of tumor or lympadenopathy. A computed tomographic scan of the abdomen revealed a hydrothorax, cirrhosis of the liver, mild splenomegaly, and ascites. An upper endoscopy was also performed that was positive for varicies. A thoracentesis was performed and approximately 1,500 mL of fluid was evacuated. A second thoracentesis was done the next day for recurrence of the effusion, and an additional 1,200 mL of fluid was removed. A mini-thoracotomy was performed with talc pleurodesis and placement of two chest tubes for recurrence of a large effusion 2 days later. Over the next 7 days, his condition continued to deteriorate with the chest tubes draining approximately 2 L per day, and cultures taken of the fluid were positive for Pseudomonas and Staphylococcus aureus. He also developed a large left-sided pulmonary infiltrate, and became febrile with a white blood cell count in the 30,000 to 40,000 K/ul range. At that time, he was treated with intravenous antibiotics for pneumonia and transferred to our institution where he continued to drain more than 2 L per day of straw-colored fluid from his chest tubes. For the next 2 weeks, the effusion was treated medically with salt and water restriction as well as large doses of diuretics. In addition, he was given intravenous antibiotics to treat the pneumonia. However, the chest tube output remained high. Because thoracentesis and pleurodesis failed, and the chest tube output remained very large, a TIPS procedure was performed. The patient was taken to interventional radiology where two overlapping 12 by 60 mm Wallstents (Boston Scientific, Boston, MA) were placed between the right hepatic vein and the right portal vein (Fig 2). The portosystemic gradient decreased from 23 mm Hg before TIPS to 8 mm Hg after TIPS. Within 3 days, the chest tube drainage had resolved, allowing the chest tubes to be removed. The patient was discharged home the following day without incident. A 1-month follow-up examination revealed no evidence of a recurrent hydrothorax. The patient is currently doing well 8 months after TIPS placement with no evidence of recurrence of the hydrothorax (Fig 3).
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Fig 3. Chest roentgenogram 8 months after transjugular intrahepatic portosystemic. The wall stent can be clearly seen in the right upper quadrant of the abdomen.
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Comment
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Pleural effusions have been recognized as a complication of cirrhosis for many years. The pleural fluid usually accumulates on the right side, it is frequently sudden in onset, and accompanied by severe respiratory distress. Almost all reported cases of hepatic hydrothorax have been described in patients with ascites; however, they occasionally appear in the absence of clinical ascites. They tend to be recalcitrant to repeated thoracentesis or prolonged chest tube drainage secondary to a rapid voluminous recurrence. The pleural fluid is chemically described as a transudate, and is generally similar to that found in the peritoneal cavity [6].
Proposed mechanisms for the accumulation of a hepatic hydrothorax have included such theories as azygos vein hypertension and hypoproteinemia [7]. Recently it has been confirmed that the hydrothorax is formed when ascitic fluid is delivered directly into the chest through transdiaphragmatic migration of the fluid into the pleural space, either by lymphatics or defects in the diaphragm [1, 5]. These defects have been described as 1 mm in diameter and located in the tendinous part of the right hemidiaphragm. They are covered with pleuroperitoneum and are raised into blebs or blisters as the pressure of the ascitic fluid impacts on the diaphragm. Eventually this blister ruptures and a one-way valve is formed from the peritoneal cavity into the thorax, allowing large amounts of fluid to enter [2, 3].
The pathogenesis for the development of a hepatic hydrothorax makes it difficult to treat as the pressure difference between the abdominal and pleural cavities is intensified by inspiration. Standard initial treatment focuses on dimunition and elimination of ascites by controlling the underlying cirrhosis and improving liver function. This may be accomplished medically by placing the patient on salt and fluid restriction with diuretic therapy, or surgically with a liver transplantation [5, 7]. Medical treatment has been known to fail secondary to patient noncompliance, electrolyte abnormalities, and hypovolemia, resulting in hepatic encephalopathy, azotemia, and end-organ hypoperfusion [5].
When the hydrothorax becomes refractory to diuretic therapy resulting in an increase in symptoms, repeated thoracentesis may be required for temporary relief [6]. Although this intervention is useful in resolving respiratory symptoms quickly, it is not viewed as a permanent solution, as ascites production is not affected. Repeated thoracentesis results in large fluid shifts, protein loss, and depletion of body albumin stores. In addition, the risks associated with the procedure itself such as pneumothorax, infection, and bleeding become more significant each time the procedure is performed.
In patients who fail to improve after diuretics, dietary modifications, and occasional thoracentesis, the pleural space can be drained with chest tube thoracostomy followed by chemical pleurodesis. This treatment option is used primarily in an effort to overcome the restrictive effects a large pleural effusion has on lung compliance. This approach has been associated with several complications including pain, a prolonged intensive care unit stay, and the inability to remove the required chest tube secondary to fluid reaccumulation [8].
The surgical approach to a hepatic hydrothorax involves reducing the pressure in both the hepatic and splanchnic vascular beds. This can be accomplished by performing an open side-to-side portal systemic shunt. However, patients with refractory ascites are generally poor operative candidates with higher operative mortality rates [8]. In our critically ill patient, an adequate vascular shunt within the liver was created with the placement of a TIPS, resulting in the resolution of the hepatic hydrothorax and enabling the indwelling chest tubes to be removed. In conclusion, patients with recalcitrant hepatic hydrothorax can be treated with a TIPS procedure if medical therapy and drainage procedures have failed.
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References
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Accepted for publication June 12, 1999.
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Abstract
Introduction
