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• W2113162578 abstract "Stage of portal vein thrombosisJournal of HepatologyVol. 54Issue 5PreviewSimilar to previous recommendations [1–3], a stage-dependent therapeutic strategy of non-malignant and non-cirrhotic portal vein thrombosis (PVT) is advocated in the recent Baveno V consensus [4]. At recent or acute stage of PVT, the predominant goals of treatment are to maximize the rate of portal vein recanalization and to prevent thrombus extension upstream into the superior mesenteric vein and its possible secondary intestinal infarction. At the old or chronic stage, the primary therapeutic objectives are shifted to the prevention and treatment of variceal bleeding and management of portal biliopathy. Full-Text PDF Open Access We read with great interest the letter by Dr. Qi et al. [[1]Xingshun Qi Guohong Han Ming Bai Daiming Fan Stage of portal vein thrombosis.J Hepatol. 2011; 54: 874Google Scholar]. We do agree with them that, at times, it is difficult to make a precise diagnosis of acute and chronic portal vein thrombosis on the basis of contrast enhanced CT alone, especially if it is in the transition period and the disease is evolving. In making a proper diagnosis, one needs to take into account the natural history, including the rapidity of development of the thrombus, the appearance of symptoms, the extent of the thrombosis, and the development of complications. Previous and present attempts by the same group of workers [1Xingshun Qi Guohong Han Ming Bai Daiming Fan Stage of portal vein thrombosis.J Hepatol. 2011; 54: 874Google Scholar, 2Qi X. Han G. Wang J. Wu K. Fan D. Degree of portal vein thrombosis.Hepatology. 2010; 51: 1089-1090Crossref PubMed Scopus (26) Google Scholar] and by others [[3]Stieber A.C. Zetti G. Todo S. Tzakis A.G. Fung J.J. Marino I. et al.The spectrum of portal vein thrombosis in liver transplantation.Ann Surg. 1991; 213: 199-206Crossref PubMed Scopus (191) Google Scholar] have only looked at the degree and duration of the development of PVT. The figures enclosed with the present communication [[1]Xingshun Qi Guohong Han Ming Bai Daiming Fan Stage of portal vein thrombosis.J Hepatol. 2011; 54: 874Google Scholar] clearly show opening-up of various porto–porto collateral channels and development of a cavernoma. Of course, it is not easy to hypothesize the age of the cavernoma, in the absence of full clinical details. A Doppler flow image would have been quite helpful to determine the nature of the thrombosis and the degree of involvement of splanchnic circulation. A second look at the consensus statements of the Baveno V [[4]de Franchis R. Revising consensus in portal hypertension: report of the Baveno V consensus workshop on methodology of diagnosis and therapy in portal hypertension.J Hepatol. 2010; 53: 762-768Abstract Full Text Full Text PDF PubMed Scopus (1097) Google Scholar] may help clarify the situation in the patient under consideration. A recent thrombosis is defined as non-enhancing material within the portal vein (PV) with increased hepatic enhancement in the arterial phase. It is important to note that the recommendations are that a CT/MR angiography is more helpful to determine the nature of the thrombosis. In the given case, the collaterals are already enhanced in the CT images after the contrast injection. There is, however, a non-enhanced material also seen inside the PV, suggestive of a possible recent thrombosis. It is well known that in patients with EHPVO, thrombosis could be an ongoing process, and both clinical situations could co-exist. However, once the cavernoma forms, there remains no doubt about the process being chronic. Because of these reasons, the proposed nomenclature by Dr. Qi et al. of partial and complete in both acute and chronic stages seems a bit empirical. All these issues were discussed in the Baveno meeting. Further, the Baveno statement clearly mentions the role of both Color Doppler ultrasound and the contrast enhanced US to confirm the recent thrombosis and differentiate it from the chronic thrombosis; a yard-stick, which was not followed by the authors [[1]Xingshun Qi Guohong Han Ming Bai Daiming Fan Stage of portal vein thrombosis.J Hepatol. 2011; 54: 874Google Scholar]. In the Baveno V conference, a detailed discussion on different clinical scenarios of EHPVO was presented by us and was then deliberated at length by global experts. A comprehensive consensus classification was finally approved (manuscript under preparation). The consensus statement reads “Baveno classification of EHPVO: This classification utilizes five main characteristics of portal vein obstruction, namely: the site of obstruction (trunk or branches), the clinical presentation (recent or chronic), nature of underlying liver disease, the degree of occlusion and the extent of involvement”. Such a classification is needed and once published would hopefully be found useful for new studies, as it will bring uniformity in reporting the results and comparing the outcome. We are delighted that Dr. Han and colleagues have looked into the various complications of chronic EHPVO. In fact, several large series have reported the long-term outcome of portal vein occlusion. Development of portal biliopathy, progressive hepatic dysfunction as a result of chronic deprivation of blood flow and growth factors, and growth retardation (if the portal vein occlusion has occurred in pre-pubertal age) are well known complications of chronic EHPVO [[5]Sarin S.K. Agarwal S.R. Extrahepatic portal vein obstruction.Semin Liver Dis. 2002; 22: 43-58Crossref PubMed Scopus (178) Google Scholar]. These complications highlight the need for early detection and intervention in such patients. It is well accepted that the outcome of long standing portal biliopathy, an entity identified nearly 20 years ago, remains dismal. Endoscopic interventions and even surgical shunts do not fully reverse the process [6Sarin S.K. Kumar A. Noncirrhotic portal hypertension.Clin Liver Dis. 2006; 10: 627-651Abstract Full Text Full Text PDF PubMed Scopus (52) Google Scholar, 7Chaudhary A. Dhar P. Sarin S.K. Sachdev A. Agarwal A.K. Vij J.C. et al.Bile duct obstruction due to portal biliopathy in extrahepatic portal hypertension: surgical management.Br J Surg. 1998; 85: 326-329Crossref PubMed Scopus (122) Google Scholar]. It is associated with high morbidity and mortality. Similarly, growth retardation is commonly seen in nearly 30–50% of the subjects [[8]Sarin S.K. Bansal A. Sessan S. Nigam A. Portal vein obstruction in children leads to growth retardation.Hepatology. 1992; 15: 229Crossref PubMed Scopus (87) Google Scholar]. At the Baveno V meeting, management of these complications was discussed. It was proposed that Rex bypass (mesenterico-left portal bypass) in children with EHPVO [[9]Mack C.L. Superina R.A. Whitington P.F. Surgical restoration of portal flow corrects pro-coagulant and anticoagulant deficiencies associated with extrahepatic portal vein thrombosis.J Pediatr. 2003; 142: 197-199Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar] has been shown to reverse complications associated with EHPVO including retardation of growth and development, minimal encephalopathy, coagulopathy, and hypersplenism. It prevents portal hypertensive bleeding and may prevent development of biliopathy. Of course, proper patient selection and expertise would be required for optimal outcome. Placement of TIPS stents and liver transplantation could also be occasionally helpful. EHPVO remains a challenge for hepatologists and we do hope that with a better understanding of the pathophysiology and mechanisms of PV thrombosis, we may be able to prevent development of such thrombosis and/or detect them early enough for proper repermeation. The authors who have taken part in this study declared that they do not have anything to disclose regarding funding or conflict of interest with respect to this manuscript." @default.
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