Occurrence of hepatopulmonary syndrome in Budd–Chiari syndrome and the role of venous decompression

De, Binay K; Sen, Sambit; Biswas, Pranab Kumar; Mandal, S. K.; Das, Debasish; Das, Uttam Kumar; Guru, Supriya; Bandyopadhyay, Kausik

doi:10.1053/gast.2002.32419

Cited by 79 publications

(36 citation statements)

References 32 publications

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“…In two recent Indian studies, MOVC was present in 0% and 17.2%, while IVC involvement was seen in 56.2% and 62% cases, respectively [24,40] . In our series, IVC involvement in the majority of cases was due to IVC thrombosis.…”

Section: Discussionmentioning

confidence: 88%

“…All previous Indian series, except two [29,32] , describe the predominance of IVC up to 79.2% [7,9,[11][12][13]15,30,39,40,42] or IVC-HV obstruction up to 57.7% [14,24,25,35] ; HV involvement was described in 0%-32% of cases in these series [7,9,[11][12][13][14][15]24,25,30,35,39,40,42] . Of the two distinct previous series, one (total 53 cases) showed similar frequency of HV (35.8%), IVC (33.9%) and combined IVC-HV involvement (30.1%) [29] ; whereas the other series involving only chronic BCS showed predominance of HV (45.9%) followed by combined IVC-HV (29.7%) and IVC involvement (24.3%) [32] .…”

Section: Discussionmentioning

confidence: 90%

“…In our series, radiological intervention protocols according to morphology of the obstruction yielded good results. Previous Indian series have shown the efficacy of balloon angioplasty of IVC with or without stent placement [11][12][13]37,39,40,[43][44][45] , with a re-stenosis rate ranging from 16.6% to 28.5% [11,39] . Balloon angioplasty of HV thrombosis has shown variable results throughout the world, restricting its use to short-segment HV thrombosis only [4,77] .…”

Section: Discussionmentioning

confidence: 99%

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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: 88%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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

Amarapurkar¹,

Punamiya²,

Patel³

2008

WJG

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“…82 On the other hand, cavoplasty, which is cited as a treatment option for patients with Budd-Chiari syndrome, has resulted in complete reversion of HPS. 85 Embolization of possible arteriovenous communications has also been reported to have been successful. 86 Oxygen therapy is indicated to improve the clinical condition of patients with severe hypoxemia who are known to be responsive to O 2 supplementation.…”

Section: Hps Treatment and Prognosismentioning

confidence: 99%

Hepatopulmonary syndrome: an update

Macedo

Lopes

2009

Sao Paulo Med. J.

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Hepatopulmonary syndrome (HPS) is a clinical threesome composed of liver disease, intrapulmonary vascular dilatation (IPVD) and arterial gas abnormalities. Its occurrence has been described in up to 32% of cirrhotic candidates for liver transplantation. It also affects non-cirrhotic patients with portal hypertension. Its pathogenesis is not well defined, but an association of factors such as imbalance in the endothelin receptor response, pulmonary microvascular remodeling and genetic predisposition is thought to lead to IPVD. Diagnosis is based on imaging methods that identify these dilatations, such as contrast echocardiography or perfusion scintigraphy with RESUMOA síndrome hepatopulmonar (SHP) é considerada uma tríade clínica composta de doença hepática, dilatações vasculares intrapulmonares (IPVD) e alterações de gases arteriais. Há descrição de sua ocorrência em até 32% dos cirróticos candidatos ao transplante de fígado, acometendo também não cirróticos com hipertensão portal. Sua etiopatogenia não está bem definida, mas se especula que a associação de fatores como o desequilíbrio na resposta dos receptores vasculares de endotelina, o remodelamento microvascular pulmonar e a predisposição genética propiciem as IPVD. O diagnóstico baseia-se em métodos de imagem que identifiquem essas dilatações, como a ecocardiografia com contraste ou a cintilografia de perfusão com 99m Tc, além da análise de gases arteriais, para identificar elevação da diferença alvéolo-arterial de O 2 ou hipoxemia. Não existe tratamento medicamentoso eficaz e sua resolução completa ocorre apenas com o transplante de fígado. A importância do diagnóstico da SHP está em priorizar os candidatos ao transplante, uma vez que sua presença está associada ao pior prognóstico. O objetivo deste artigo é fazer revisão das teorias de etiopatogenia da

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“…Как правило, ГПС встречается при циррозе печени, однако имеются описания случаев дан-ного осложнения у пациентов с предпеченочной формой портальной гипертензии при отсутствии хронического заболевания печени, с синдромом Бадда-Киари и даже с острыми или хрониче-скими воспалительными заболеваниями печени без цирроза или портальной гипертензии [3][4][5][6][7].…”

Section: Introductionunclassified

Hepatopulmonary syndrome and liver transplantation: the review and a case report

Малиновская¹,

Джинер²,

Остроумов³

et al. 2017

Transplantologiâ (Mosk.)

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Occurrence of hepatopulmonary syndrome in Budd–Chiari syndrome and the role of venous decompression

Cited by 79 publications

References 32 publications

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

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

Hepatopulmonary syndrome: an update

Hepatopulmonary syndrome and liver transplantation: the review and a case report

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