Membranous Obstruction of the Inferior Vena Cava in the United States

Rector, William G.; Xu, Yu; Goldstein, Leonard I.; Peters, Robert L.; Reynolds, Telfer B.

doi:10.1097/00005792-198503000-00005

Cited by 91 publications

(59 citation statements)

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“…Reports of hepatocellular carcinoma developing in MOVC are rare in Indian literature [7,[12][13][14][15] . However, such an association is commonly described in most other countries [5,49,50,53,[61][62][63][64] .…”

Section: Discussionmentioning

confidence: 99%

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Amarapurkar¹,

Punamiya²,

Patel³

2008

WJG

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AIM:To evaluate patterns of obstruction, etiological spectrum and non-surgical treatment in patients with Budd-Chiari syndrome in India. METHODS:Forty-nine consecutive cases of BuddChiari syndrome (BCS) were prospectively evaluated. All patients with refractory ascites or deteriorating liver function were, depending on morphology of inferior vena cava (IVC) and/or hepatic vein (HV) obstruction, triaged for radiological intervention, in addition to anticoagulation therapy. Asymptomatic patients, patients with diuretic-responsive ascites and stable liver function, and patients unwilling for surgical intervention were treated symptomatically with anticoagulation. RESULTS:Mean duration of symptoms was 41.5 ± 11.2 (range = 1-240) mo. HV thrombosis (HVT) was present in 29 (59.1%), IVC thrombosis in eight (16.3%), membranous obstruction of IVC in two (4%) and both IVC-HV thrombosis in 10 (20.4%) cases. Of 35 cases tested for hypercoagulability, 27 (77.1%) were positive for one or more hypercoagulable states. Radiological intervention was technically successful in 37/38 (97.3%): IVC stenting in seven (18.9%), IVC balloon angioplasty in two (5.4%), combined IVC-HV stenting in two (5.4%), HV stenting in 11 (29.7%), transjugular intrahepatic portosystemic shunt (TIPS) in 13 (35.1%) and combined TIPS-IVC stenting in two (5.4%). Complications encountered in follow-up: death in five, re-stenosis of the stent in five (17.1%), hepatic encephalopathy in two and hepatocellular carcinoma in one patient. Of nine patients treated medically, two showed complete resolution of HVT. CONCLUSION:In our series, HVT was the predominant cause of BCS. In the last five years with the availability of sophisticated tests for hypercoagulability, etiologies were defined in 85.7% of cases. Non-surgical management was successful in most cases.

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Section: Discussionmentioning

confidence: 99%

Changing spectrum of Budd-Chiari syndrome in India with special reference to non-surgical treatment

Amarapurkar¹,

Punamiya²,

Patel³

2008

WJG

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“…This lesion usually affects the inferior vena length hepatic vein stenosis among 86 patients with hecava and is commonly encountered in the absence of an obvipatic venous outflow block who were seen between 1970 ous thrombogenic condition. 5,6 Short-length inferior vena caand 1992. There were 25 patients with short-length heval stenosis has long been thought to be of congenital origin, 5 patic vein stenosis.…”

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confidence: 99%

Hepatic venous outflow block caused by short-length hepatic vein stenoses

et al. 1997

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venous lesions have been recognized. The first is thrombosis In contrast with the well-recognized membranous obfollowed by diffuse fibrous obliteration. This lesion affects struction of the inferior vena cava, short-length hepatic the hepatic veins more commonly than the inferior vena cava, vein stenoses are not well-recognized causes of hepatic and, when systematically investigated, an associated hypervenous outflow block. The aim of this study was to ascercoagulable state is usually identified. [2][3][4] The second type of tain the prevalence, causes, manifestations, and outvenous lesion is represented by a short-length stenosis, often come of short-length hepatic vein stenoses. We described as a web or a membrane, located at the terminal performed a retrospective study of patients with shortpart of a vein. This lesion usually affects the inferior vena length hepatic vein stenosis among 86 patients with hecava and is commonly encountered in the absence of an obvipatic venous outflow block who were seen between 1970 ous thrombogenic condition. 5,6 Short-length inferior vena caand 1992. There were 25 patients with short-length heval stenosis has long been thought to be of congenital origin, 5 patic vein stenosis. A thrombogenic condition was idenbut recent evidence suggested that it can be the sequela of a tified in 14 patients (56%). The lesions of the accompaprevious caval thrombosis.6 nying hepatic veins in these patients were variable Short-length hepatic vein stenoses has received little atten-(short-length stenoses, thromboses, or nonspecific tion. The purpose of this report is to describe the prevalence, changes) and similar to that seen in patients without causes, manifestations, and outcome of hepatic venous outshort-length hepatic vein stenosis. In 3 necropsied cases, flow block caused by short-length hepatic vein stenoses. the venous lesions were suggestive of fibrous sequela of prior thromboses. In patients with short-length hepatic PATIENTS AND METHODS vein stenosis, splenomegaly (28% vs. 55%, P õ .05) and hypersplenism were significantly less common; serum From January 1970 to December 1992, 147 patients with hepatictransaminase (P õ .001) and creatinine levels (P õ .02) venous outflow block were admitted to the Liver Units or Surgery were lower, prothrombin was higher (P õ .001), and 5-Departments at Hôpital Beaujon, Hôpital Louis Mourier, and Hôpital de la Salpêtrière. The diagnoses of hepatic venous outflow block were year survival was significantly better (Kaplan-Meier esmade when obstructions of the hepatic veins or inferior vena cava timates: 80% vs. 50%, P õ .05). In patients with hepatic were shown by imaging investigations or when centrilobular distenvenous outflow block, short-length hepatic vein stenosis sion was seen at liver biopsy in the absence of cardiac failure or is a common lesion that appears to be the sequela of pericarditis. 7 Imaging studies of the hepatic veins were reviewed.localized thrombosis. Long-term anticoagulation and Thirty-six cases (24.5%) were excluded because ...

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“…Some others have put forth the theory that it is an acquired condition. [1][2][3] Okuda et al 4 proposed the theory that the membrane or cord obstructing the inferior vena cava is the outcome of recurrent thrombosis and suggested the term "obliterative hepatocavopathy" to denote the condition. They also suggested that obliterative hepatocavopathy and primary hepatic vein thrombosis are different epidemiologically, pathologically, and clinically.…”

Section: Discussionmentioning

confidence: 99%