U. Dutta et al.: Hepatic Vein Block due to IVC Stent 521 Blocking of the Hepatic Vein Outflow by Neointima Covering a Wallstent Across a Membranous Stenosis of the Inferior Vena Cava Usha Dutta, 1 Pramod K. Garg, 1 Rajeev Agarwal, 2 S. Dutta Gupta, 3 G. A. Prasad, ~ Rakesh K. Tandon, ~ 'Department of Gastroenterology, All India Institute of Medical Sciences, New Delhi 110029, India 2Department of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India 3Department of Pathology, All India Institute of Medical Sciences, New Delhi 110029, India Upendra Kaul, 2 Abstract A 31-year-old man presented with idiopathic membranous obstruc- tion of the suprahepatic inferior vena cava (IVC) and was treated by balloon dilation and placement of a Wallstent. The patient im- proved markedly. However, he developed obstruction of the hepatic vein outflow secondary to neointima formation over the stent that covered the hepatic vein ostia. The patient died of liver failure and septicemia. We believe that this is the first report of such a serious complication. Key words: Inferior vena cava, obstruction--Stent--Hepatic vein obstruction Hepatic venous outflow tract obstruction (HVOTO) is caused by occlusion of hepatic veins (HV) and/or inferior vena cava (IVC). IVC obstruction is most commonly caused by either a membrane or a thrombus [1] and is relieved either by surgical bypass or percu- taneous balloon angioplasty [2-4]. Following balloon dilation, stent placement across the dilated segment of IVC has been pro- posed to prevent recurrent stenosis [5, 6]. The long-term results of such balloon angioplasty and stent placement are reported to be good [7]. We report here a young man who underwent balloon angioplasty followed by stent placement across the HV orifice for a membranous obstruction of the IVC and presented later with HV obstruction. Case Report A 3l-year-old man was hospitalized in April 1994 with bleeding from esophageal varices, hepatomegaly, abdominal wall collaterals, and ascites. On ultrasonography (US), the IVC was narrowed just proximal to the entry of the HVs with absence of a normal triphasic wave form on Doppler US. The HVs were patent. Upper gastrointestinal endoscopy showed large varices which were band ligated. A wedge biopsy of the liver obtained during laparoscopy was suggestive of HVOTO (dilated central veins and sinusoidal spaces). There was no clinical or laboratory evidence (including bone marrow examina- tion) of any myeloproliferative disorder, paroxysmal nocturnal hemoglo- binuria, occult malignant process, or radiation exposure. Protein C, protein S, and antithrombin III levels were normal. Lupus anticoagulant and anti- cardiolipin antibodies were absent. An inferior venacavagram (IVCgram) obtained 2 months later demon- strated membranous stenosis of the suprahepatic segment of the IVC with a residual lumen diameter of 5.4 mm and a pressure gradient of 12 mmHg (Fig. 1). The stenosis was dilated with an 18-mm balloon; a tight waist was seen on the balloon prior to dilation. To prevent recurrence of the stenosis, Correspondence to: R.K. Tandon, M.D. a 22-mm diameter, 10-cm-long Wallstent (Schneider AG Europe, Wsiter- land, Switzerland) was placed across the stenosis. The IVC diameter in- creased to 15.2 mm with no residual gradient (Fig. 2). Following this, the patient showed dramatic improvement, with decrease in ascites and hepatomegaly and disappearance of pedal edema and abdom- inal wall collaterals. The liver function tests also normalized. Esophageal varices were eradicated over five separate sessions of endoscopic variceal ligation. The patient had no subsequent variceal bleeding. A follow-up IVCgram 2 months later showed a patent stent with no pressure gradient. The patient remained well for the next 5 months until he developed recurrence of ascites and right subcostal pain. Clinical examination revealed hepatomegaly with ascites and pedal edema. A possibility of blockage of the IVC stent was considered. Ultrasonography revealed that the stent was patent but a high velocity flow jet from the HVs indicated a partial HV block. He was scheduled to undergo a side-to-side portocaval shunt for hepatic vein block. In the meantime, however, he developed septicemia, disseminated intravascular coagulation (DIC), and acute renal failure. At this stage, repeat US revealed obstructed, narrowed HVs with a thrombus in a collateral vessel. The stent was patent and the high velocity jet from the HV seen earlier had disappeared, possibly indicating further compromise of the HV ostia. He succumbed to liver failure and septicemia. Autopsy revealed hepatomegaly and old and fresh thrombi in the dilated HVs. The right hepatic vein (RHV) had an approximately 3-month-old thrombus and the left hepatic vein (LHV) a 3-week-old thrombus. The IVC was patent with the stent in position. A significant finding was that the stent was well embedded in the IVC wall and most of it was endothelialized, covering the HV ostia and thus obstructing them (Fig. 3). The right atrium had an organized thrombus at the opening of the IVC, which was partially obstructing the opening. Discussion HVOTO is an important cause of post-sinusoidal portal hyperten- sion. The most common cause of HVOTO in India is membranous obstruction of the IVC [8]. Balloon dilation has been regarded as the procedure of choice for treating IVC obstruction [2-4]. Because of its limitations in a subset of patients and potential for restenosis, several workers have implanted stents in the IVC [5-7]. The present case highlights the development of hepatic venous obstruction possibly as a consequence of IVC stent placement. The IVC stent had become endothelialized, covering the HV ostia and resulting in obstruction of the HV's outflow into the IVC, leading to stagnation of blood and subsequent thrombosis in the HV. The patient started having pain in the right hypochondrium and ascites about 2 months before he died. The thrombus in the RHV was about 3 months old and that in the LHV was 3 weeks old. Obstruction of only one HV is unlikely to cause clinically evident hepatic outflow obstruction. We believe that the RHV was blocked first and when the LHV also was blocked by the endothelialized IVC stent, the patient manifested with features of acute Budd-Chiari syndrome.