Ann Thorac Surg 1998;66:1803-1804
© 1998 The Society of Thoracic Surgeons
Case Reports
Hepatoatrial anastomosis and tricuspid valve replacement in Budd-Chiari syndrome 8.
Cynthia K. Chiu, MDa,
David M. Nagorney, MDa,
Hartzell V. Schaff, MDa
a Department of Surgery, Mayo Clinic and Mayo Foundation, Rochester, Minnesota, USA
Accepted for publication May 11, 1998.
Address reprint requests to Dr Schaff, Department of Surgery, Mayo Clinic, 200 First St SW, Rochester, MN 55905
e-mail: (schaff{at}mayo.edu)
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Abstract
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The rare complication of tricuspid valve stenosis due to displacement of a peritoneovenous shunt catheter developed in a patient with Budd-Chiari syndrome. Surgical management included shunt removal and tricuspid valve replacement combined with hepatoatrial anastomosis. The tricuspid valve was replaced with a bioprosthesis, and liver resection opened the stenotic confluence of the hepatic veins. The right atrium was sutured to the liver capsule, thereby restoring physiologic hepatic venous blood flow.
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Introduction
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The natural history of untreated Budd-Chiari syndrome often leads to progressive portal venous hypertension, producing ascites, esophageal variceal hemorrhage, and hepatic failure. Surgical management has been directed toward portosystemic shunting procedures, liver transplantation, or palliative peritoneovenous shunting of ascites [1]. However, peritoneovenous shunts also have intrinsic risks, including infection, bleeding, occlusion, and organ failure, that may require reoperation. The following case history describes the management of a complication of peritoneovenous shunting that necessitated tricuspid valve replacement. During the same operation, dorsocranial hepatic resection with hepatoatrial anastomosis was performed to manage the Budd-Chiari syndrome.
A 65-year-old woman with idiopathic hepatic veno-occlusive disease was hospitalized because of progressive ascites, peripheral edema, and exertional dyspnea. A peritoneovenous shunt had been placed 13 years earlier for treatment of ascites that was refractory to medical therapy. On admission (December 1992), blood pressure was 130/70 mm Hg, heart rate was 85 beats per minute, and temperature was 36.2°C. Physical examination demonstrated periorbital edema, conjunctival hemorrhages, perioral cyanosis, and a suffused face. Jugular veins were distended bilaterally. Prominent veins on the distal upper extremities drained only when the extremities were raised above her head.
On examination of the heart, a 2/6 pandiastolic murmur was heard at the left lower sternal border. Tense ascites and peripheral edema extending to the proximal lower extremities were present.
Ultrasonography of the liver confirmed the presence of a large amount of ascitic fluid and cirrhosis of the liver. The portal vein, splenic vein, hepatic veins, and inferior vena cava were patent. The subclavian and jugular veins were normal on magnetic resonance imaging. However, magnetic resonance imaging of the liver showed atretic hepatic veins. Nonfunction of the peritoneovenous shunt was demonstrated by radionuclide scanning.
Echocardiography demonstrated a markedly enlarged right atrium. The intravascular limb of the peritoneovenous catheter extended across the tricuspid valve, which was stenotic. Subsequent cardiac catheterization revealed a gradient of 17 to 22 mm Hg across the tricuspid valve and normal coronary arteries.
Hypothermic cardiopulmonary bypass was established; the superior vena cava was cannulated directly, and venous return from the inferior vena cava was obtained through a long cannula inserted through the right femoral vein. During extracorporeal perfusion, an oblique right atriotomy was made and the peritoneovenous shunt, which crossed the tricuspid valve, was removed. The stenotic tricuspid valve was excised and replaced with a 27-mm Carpentier-Edwards bioprosthesis in the small annulus. Histologic examination of the native valve leaflets demonstrated thickening as the result of fibrosis, granulation tissue, and organizing thrombus, consistent with chronic mechanical trauma.
After rewarming and release of the aortic cross-clamp, an abdominal incision was made and the diaphragm was divided to expose the inferior vena cava. The liver was enlarged and fibrotic. Obstruction of the ostia of the hepatic veins was visible through the venotomy in the inferior vena cava. After aspiration of ascites, the dorsocranial liver, including the confluence of the stenotic hepatic veins, was resected nonanatomically until hepatic blood flow through the transection surface was profuse. The atrial incision was extended through the cavoatrial junction. The vena cava and right atrium were then sutured to the liver capsule, allowing the intrahepatic veins to drain directly into the atrium (Fig 1). Atrioventricular pacing was commenced because of third-degree heart block.
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Follow-up
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Postoperatively, the patient’s condition improved gradually, with decreased ascites (14.1-kg weight loss) and resolution of dyspnea and peripheral edema. A permanent ventricular pacemaker was inserted 2 weeks postoperatively. Anticoagulation with warfarin was established, and she was dismissed 31 days postoperatively. Two months postoperatively, a sternal wound infection was debrided and treated successfully with antibiotic therapy over a 6-month period. At 4 years postoperatively, the patient demonstrated no signs or symptoms of hepatic venous congestion. Liver function tests were normal (aspartate aminotransferase, 32 U/L), except for bilirubin (total, 5.5 mg/dL; direct, 0.19 mg/dL), and she had no exercise limitation (New York Heart Association functional class I). She has required no additional medical therapy.
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Comment
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Peritoneovenous shunts in debilitated patients can lead to postoperative respiratory compromise, pneumonia, myocardial infarction, pulmonary embolus, and cardiac arrest [2]. Placement of peritoneovenous shunts for the treatment of Budd-Chiari syndrome carries specific risks, including disturbances in wound healing, bleeding, occlusion, and systemic complications (hepatic, renal, and cardiac failure) [3]. The present case was unusual in that the peritoneovenous shunt was displaced across the tricuspid valve, and we postulated that repetitive trauma caused leaflet fibrosis with subsequent valvular stenosis, which is a rare complication of peritoneovenous shunts. The diagnosis was made by echocardiography [4].
The tricuspid valve is susceptible to trauma by right-sided venous catheters. Injury to the valvular endothelium promotes an intense fibrous reaction, leading to the development of valvular stenosis [4]. The resultant tricuspid stenosis in this case was treated successfully with tricuspid valve replacement.
Because operation for tricuspid valve was necessary for our patient, we believed that concomitant dorsocranial hepatic resection and hepatoatrial anastomosis should be performed for management of hepatic venoocclusive disease. This method was developed originally by Senning [5] in an effort to relieve the symptoms of Budd-Chiari syndrome while reestablishing hepatic venous outflow to the inferior vena cava and the right side of the heart. He postulated that resection of part of the liver, including the stenosed or occluded veins, could restore unobstructed hepatic venous blood flow to the inferior vena cava and the right side of the heart [5]. Reestablishing blood flow from the occluded hepatic veins in the physiologic direction obviates the risk of hepatic encephalopathy inherent to portosystemic shunting procedures [6]. The risks of portosystemic shunt malfunction due to thrombosis or compression are also eliminated [6]. Transcaval liver resection with hepatoatrial anastomosis leads to rapid decompression of the portal system without exposing patients to the risks of infection and rejection associated with liver transplantation [7].
The long-term results of Senning’s procedure are excellent. Pasic and colleagues [7] reported the late results of 17 patients in whom transcaval liver resection with hepatoatrial anastomosis was performed between 1980 and 1990. Actuarial 1-, 5-, and 10-year survival rates after the operation were calculated to be 82%, 76%, and 57%, respectively, compared with 68.8%, 44.4%, and 44.4% after liver transplantation, as reported by Halff and colleagues [8].
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Acknowledgments
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The authors thank Mr John V. Hagen for the illustration.
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References
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- Wang Z.G., Jones R.S. Budd-Chiari syndrome. Curr Probl Surg 1996;33:83-211.[Medline]
- Schumacher D.L., Saclarides T.J., Staren E.D. Peritoneovenous shunts for palliation of the patient with malignant ascites. Ann Surg Oncol 1994;1:378-381.[Medline]
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- Foster-Smith K., Edwards W.D., O’Murchu B., Tajik A.J., Schaff H.V., Schwartz R.S. Severe tricuspid stenosis: an unusual and unique cause. Am Heart J 1995;130:621-624.[Medline]
- Senning A. Transcaval posterocranial resection of the liver as treatment of the Budd-Chiari syndrome. World J Surg 1983;7:632-640.[Medline]
- Bansky G., Ernest C., Jenni R., Zollikofer C., Burger H.R., Senning A. Treatment of Budd-Chiari syndrome by dorsocranial liver resection and direct hepatoatrial anastomosis. J Hepatol 1986;2:101-112.[Medline]
- Pasic M., Senning A., von Segesser L., Carrel T., Turina M. Transcaval liver resection with hepatoatrial anastomosis for treatment of patients with the Budd-Chiari syndrome. J Thorac Cardiovasc Surg 1993;106:275-282.[Abstract]
- Halff G., Todo S., Tzakis A.G., Gordon R.D., Starzl T.E. Liver transplantation for the Budd-Chiari syndrome. Ann Surg 1990;211:43-49.[Medline]
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Abstract
Introduction
