Toward a Comprehensive New Classification of Portal Vein Thrombosis in Patients With Cirrhosis
2016; Elsevier BV; Volume: 151; Issue: 4 Linguagem: Inglês
10.1053/j.gastro.2016.08.033
ISSN1528-0012
AutoresShiv Kumar Sarin, Cyriac Abby Philips, Patrick S. Kamath, Ashok Choudhury, Hitoshi Maruyama, Filipe Nery, Dominique Valla,
Tópico(s)Venous Thromboembolism Diagnosis and Management
ResumoPortal vein thrombosis (PVT) generally refers to a complete or partial obstruction of portal venous blood flow due to the presence of a thrombus in the lumen of the vein. A cavernoma that develops as a consequence of a demonstrated thrombus is evidence of a chronic thrombosis. Extrahepatic portal vein obstruction encompasses thrombotic and nonthrombotic occlusions of the portal vein as well as cavernoma formation with or without features of portal hypertension.1Tsochatzis E.A. Senzolo M. Germani G. et al.Systematic review: portal vein thrombosis in cirrhosis.Aliment Pharmacol Ther. 2010; 31: 366-374Crossref PubMed Scopus (247) Google Scholar The designation "malignant" or "tumor" thrombosis for obstruction by neoplastic tissue growing into the portal venous lumen is misleading. Therefore, it is better termed tumorous invasion of the portal vein and described as a distinct clinical entity because the genesis, treatment, outcome, and prognosis are distinct. The prevalence of nontumorous portal vein obstruction in the general population at necropsy is nearly 1% in Malmö, Sweden.2Scalabre A. Gorincour G. Hery G. et al.Evolution of congenital malformations of the umbilical-portal-hepatic venous system.J Pediatr Surg. 2012; 47: 1490-1495Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar In patients with cirrhosis, cross-sectional estimates have ranged between 0.6 and 26%.1Tsochatzis E.A. Senzolo M. Germani G. et al.Systematic review: portal vein thrombosis in cirrhosis.Aliment Pharmacol Ther. 2010; 31: 366-374Crossref PubMed Scopus (247) Google Scholar However, the prevalence could vary with age, presence and origin of underlying hepatic and nonhepatic diseases, velocity of portal venous blood flow, the procoagulant status and liver transplantation (LT) status of the patients. The prognosis and treatment of PVT depends on the nature, site, extent, and rapidity of development, duration of thrombosis, risk factors for thrombosis, stage of liver disease and the acute and chronic precipitating event(s) (Figure 1). Because of the large number of variables and protean presentations of PVT, there is lack of clarity in the literature and a need for early detection, a comprehensive classification, and an algorithmic approach to management. The present commentary addresses these issues in PVT in the context of cirrhosis and provides a potentially universally acceptable classification for structural and functional assessment of PVT and assess response to therapies. In the recent Clinical Practice Guidelines of The European Association for the Study of the Liver, acute PVT has been defined as a recent formation of a thrombus within the portal vein and/or right or left branches. In the absence of recanalization, the portal venous lumen is obliterated while portoportal collaterals develop resulting in the cavernomatous transformation of the portal vein.3García-Pagán J.C. Busacarini E. Janssen H.L.A. et al.EASL clinical practical guidelines: vascular diseases of the liver.J Hepatol. 2016; 64: 179-202Abstract Full Text Full Text PDF PubMed Scopus (545) Google Scholar The American Association for Study of Liver Diseases defines acute PVT as sudden formation of thrombus within the portal vein lumen, and chronic, when the obstructed portion is replaced by a network of hepatopetal collaterals bypassing the thrombosed portion of portal vein.4DeLeve L.D. Valla D.C. Garcia-Tsao G. et al.Vascular disorders of the liver.Hepatology. 2009; 49: 1729-1764Crossref PubMed Scopus (727) Google Scholar Although simple and useful, these definitions are predominantly anatomic and have limitations of only considering occlusion as a defining point. The consequence of thrombotic occlusion of the portal vein such as ascites or portal hypertension are not part of the definition. Development of acute PVT can have different functional consequences depending on whether the liver is diseased or healthy. Furthermore, chronic thrombosis may not always be followed by cavernoma formation; moreover, cavernoma formation may be a result of congenital malformations in the absence of thrombosis.2Scalabre A. Gorincour G. Hery G. et al.Evolution of congenital malformations of the umbilical-portal-hepatic venous system.J Pediatr Surg. 2012; 47: 1490-1495Abstract Full Text Full Text PDF PubMed Scopus (17) Google Scholar Important "functional and hemodynamic aspects" and underlying pathogenic aspects, are currently not included in the definition of PVT. In fact, PVT may be best defined as a syndrome in which the presence of a thrombus in the portal vein or its branches presents either as an incidental finding on abdominal imaging; or with a myriad of abdominal signs and symptoms that represent complications of portal hypertension; or a composite of both acute abdominal and portal hypertensive manifestations in the presence or absence of cirrhosis and/or malignancy. In the present commentary, we focus only on PVT in cirrhosis. The modality and context of assessment of PVT may influence the prevalence rate of PVT in patients with cirrhosis, being 0.6% when evaluated by percutaneous angiographic studies, 4.4% when evaluated by ultrasound Doppler, and 10% to 12% when evaluated by computed tomography and MRI.5Nery F. Chevret S. Condat B. et al.Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.Hepatology. 2015; 61: 660-667Crossref PubMed Scopus (352) Google Scholar, 6Saad W.E. Portosystemic shunt syndrome and endovascular management of hepatic encephalopathy.Semin Interv Radiol. 2014; 31: 262-265Crossref PubMed Scopus (35) Google Scholar, 7Violi F. Ferro D. Basili S. et al.Ongoing prothrombotic state in the portal circulation of cirrhotic patients.Thromb Haemost. 1997; 77: 44-47Crossref PubMed Scopus (72) Google Scholar Whereas initial studies have indicated a high prevalence of ≤26%, and annual yearly incidence of new PVT of 7.4% to 16% in patients with cirrhosis, however, larger studies have shown these figures to be lower.8Violi F. Corazza R.G. Caldwell S.H. et al.Portal vein thrombosis relevance on liver cirrhosis: Italian Venous Thrombotic Events Registry.Intern Emerg Med. 2016 Mar 30; ([Epub ahead of print])Google Scholar, 9Harding D.J. Perera M.T.P. Chen F. et al.Portal vein thrombosis in cirrhosis: Controversies and latest developments.World J Gastroenterol. 2015; 21: 6769-6784Crossref PubMed Scopus (75) Google Scholar In a prospective study of 1243 patients with Child's A and B cirrhosis, the cumulative incidence of new PVT after 1 and 5 years were 4.6% and 10.7%, respectively.5Nery F. Chevret S. Condat B. et al.Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.Hepatology. 2015; 61: 660-667Crossref PubMed Scopus (352) Google Scholar In a large study of 33,368 patients being evaluated for LT, 2096 (6.3%) were found to have PVT, more so in cirrhosis related to nonalcoholic steatohepatitis.10Stine J.G. Shah N.L. Argo C.K. et al.Increased risk of portal vein thrombosis in patients with cirrhosis due to nonalcoholic steatohepatitis.Liver Transpl. 2015; 21: 1016-1021Crossref PubMed Scopus (111) Google Scholar In patients with advanced cirrhosis and those undergoing LT, the prevalence is higher and has been reported to be from 5% to 16%.9Harding D.J. Perera M.T.P. Chen F. et al.Portal vein thrombosis in cirrhosis: Controversies and latest developments.World J Gastroenterol. 2015; 21: 6769-6784Crossref PubMed Scopus (75) Google Scholar Multiple studies have shown that progression of PVT in cirrhosis is quite variable. The most common aspect in natural history is spontaneous resolution or an unchanged appearance. Nonprogression or resolution has been reported from 33% to 75% in many other studies. Maruyama et al showed that, in patients without PVT at baseline, the cumulative incidence of PVT was 12.8%, 20% and 38.7% at 1, 5, and 8 to 10 years, respectively. The natural course of PVT was improvement or regression in 47.6% of patients and stabile course in 45.2%. In another study, the cumulative rate of PVT was 4.6% at 1 year and 8.2% and 10.7% at 3 and 5 years, suggesting that the risk factors of PVT are already present at baseline.11Ghabril M. Agarwal S. Lacerda M. et al.Portal vein thrombosis is a risk factor for poor early outcomes after liver transplantation: analysis of risk factors and outcomes for portal vein thrombosis in waitlisted patients.Transplantation. 2016; 100: 126-133Crossref PubMed Scopus (106) Google Scholar Nonprogression or resolution has been reported from 33% t o 75% in many other studies,5Nery F. Chevret S. Condat B. et al.Causes and consequences of portal vein thrombosis in 1,243 patients with cirrhosis: results of a longitudinal study.Hepatology. 2015; 61: 660-667Crossref PubMed Scopus (352) Google Scholar, 9Harding D.J. Perera M.T.P. Chen F. et al.Portal vein thrombosis in cirrhosis: Controversies and latest developments.World J Gastroenterol. 2015; 21: 6769-6784Crossref PubMed Scopus (75) Google Scholar and PVT with cirrhosis has been shown to have little influence on prognosis.9Harding D.J. Perera M.T.P. Chen F. et al.Portal vein thrombosis in cirrhosis: Controversies and latest developments.World J Gastroenterol. 2015; 21: 6769-6784Crossref PubMed Scopus (75) Google Scholar PVT in patients on wait list at the time of LT and PVT posttransplant pose different challenges and the data are equivocal. In 1 study, patients with PVT at transplant have been reported to have higher 90-day mortality and graft failure than those without PVT at the time of surgery.12Englesbe M.J. Schaubel D.E. Cai S. et al.Portal vein thrombosis and liver transplant survival benefit.Liver Transpl. 2010; 16: 999-1005Crossref PubMed Scopus (180) Google Scholar However, in another study only older age predicted development of PVT in LT recipients awaiting LT. Ninety-day patient and graft survival rates were similar at 6 months, even though survival was significantly lower at 1 year in patients with PVT.13Hauch A. Winkler C. Katz E. et al.Portal vein thrombosis in liver transplantation: radiologic evaluation, risk factors, and occult diagnosis.Hepatoma Res. 2016; 2: 36-41Google Scholar PVT diagnosed during LT did not lead to inferior outcomes but transfusion rates were greater in presence of PVT, whereas duration of stay and morbidity were not.14Chen H. Turon F. Hernández-Gea V. et al.Nontumoral portal vein thrombosis in patients awaiting liver transplantation.Liver Transpl. 2016; 22: 352-365Crossref PubMed Scopus (91) Google Scholar Occurrence of PVT in post-LT recipients can also significantly reduce both graft and patient survival.15Wells P.S. Anderson D.R. Bormanis J. et al.Value of assessment of pretest probability of deep-vein thrombosis in clinical management.Lancet. 1997; 350: 1795-1798Abstract Full Text Full Text PDF PubMed Scopus (1030) Google Scholar The pretest probability of developing thrombosis in deep vein thrombosis patients includes predisposing factors, risk factors, and clinical symptoms and signs.10Stine J.G. Shah N.L. Argo C.K. et al.Increased risk of portal vein thrombosis in patients with cirrhosis due to nonalcoholic steatohepatitis.Liver Transpl. 2015; 21: 1016-1021Crossref PubMed Scopus (111) Google Scholar Deep vein thrombosis is likely to be present when there is a high pretest probability in a given patient such as recent bed confinement in an elderly patient in last 3 days, major surgery within last 12 weeks, previous history of deep vein thrombosis, or leg swelling. A pretest probability assessment for PVT based on currently suspected or established predisposing and risk factors is presented (Supplementary Table 1). The presence of one or more of these factors could suggest a high probability of development/presence of PVT. We propose that presence of 2 major, or 1 major and 2 minor, or 4 minor criteria can give a high probability for the development or pretest probability of the presence of PVT in a cirrhotic patient. This pretest scoring system would need to be assessed in prospective clinical studies. To develop a new classification, a review of all the available classification systems of PVT (Supplementary Table 2)16Stieber A.C. Zetti G. Todo S. et al.The spectrum of portal vein thrombosis in liver transplantation.Ann Surg. 1991; 213: 199-206Crossref PubMed Scopus (201) Google Scholar, 17Nonami T. Yokoyama I. Iwatsuki S. et al.The incidence of portal vein thrombosis at liver transplantation.Hepatology. 1992; 16: 1195-1198Crossref PubMed Scopus (230) Google Scholar, 18Yerdel M.A. Gunson B. Mirza D. et al.Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome.Transplantation. 2000; 69: 1873-1881Crossref PubMed Scopus (556) Google Scholar, 19Ma J. Yan Z. Luo J. et al.Rational classification of portal vein thrombosis and its clinical significance.PLoS One. 2014; 9: e112501Crossref PubMed Scopus (28) Google Scholar, 20Jamieson N.V. Changing perspectives in portal vein thrombosis and liver transplantation.Transplantation. 2000; 69: 1772-1774Crossref PubMed Scopus (77) Google Scholar, 21Bauer J. Johnson S. Durham J. et al.The role of TIPS for portal vein patency in liver transplant patients with portal vein thrombosis.Liver Transpl. 2006; 12: 1544-1551Crossref PubMed Scopus (83) Google Scholar, 22Shi J. Lai E.C. Li N. et al.A new classification for hepatocellular carcinoma with portal vein tumor thrombus.J Hepatobiliary Pancreat Sci. 2011; 18: 74-80Crossref PubMed Scopus (149) Google Scholar, 23deFranchis R. Expanding consensus in portal hypertension report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.J Hepatol. 2015; 63: 743-752Abstract Full Text Full Text PDF PubMed Scopus (19) Google Scholar would be worthwhile. The proposed new classification covers different variables and situations to describe the anatomic and functional aspects of PVT (Table 1 and Supplementary Figure 1). It is simple to use and helps to describe a patient with PVT precisely, including the site, degree, presentation, and functional relevance of the thrombosis. For example, a patient with cirrhosis is incidentally found to have a new and complete occlusion of the main portal vein trunk, with no evidence of bowel ischemia, would be designated as PVT type 1, occlusive, recent, and asymptomatic. The first section describes anatomic and the later 3, the functional aspects of PVT. One may depict these by using letters as well: PVT-I, ORAs. Another example is a cirrhotic patient who presents with features of acute abdominal pain, and on contrast-enhanced computed tomography examination has total occlusion of both the branches of the portal vein with the thrombus extending into the mesenteric vein along with bowel ischemia. The diagnosis is PVT type IIb, occlusive, recent, symptomatic with acute with bowel ischemia or PVT type IIb, ORSAbi with possible mesenteric extension. The other variables such as the extent and the nature of underlying liver disease could be added to the classification, if necessary. Although this classification has been developed for a population with cirrhosis, it could also be evaluated for non-cirrhotic patients. It can be argued why 2 terms, recent and acute have been used. A careful look at the 2 cases presented would show that both the clinical scenarios presented had recent onset PVT; one was an asymptomatic presentation whereas the other was a symptomatic presentation—acute with features of bowel ischemia. Thus, the term recent is broad and signifies the chronology, whereas asymptomatic and symptomatic describe resultant clinical scenarios. The term acute in clinical medicine is most often understood as a symptomatic presentation of a disease, as is also adopted in this classification for cirrhotic patients with PVT.Table 1Anatomico-Functional Classification of PVT in CirrhosisSite of PVT – (Type 1, 2a, 2b, 3) Type 1: Only trunk Type 2: Only branch: 2a, one branch; 2b, both branches Type 3: Trunk and branchesDegree of portal venous system occlusion (O, NO) O: Occlusive: No flow visible in PV lumen on imaging/Doppler study NO: Nonocclusive: Flow visible in PV lumen through imaging/Doppler studyDuration and Presentation (R, C) R: Recent (first time detected in previously patent PV, presence of hyperdense thrombus on imaging, absent or limited collateral circulation, dilated PV at the site of occlusion) Asymptomatic: (As) Symptomatic: (S), Acute PVT features (with or without ABI) Ch: Chronic (no hyperdense thrombus; previously diagnosed PVT on follow-up, portal cavernoma and clinical features of PHT) Asymptomatic Symptomatic: features of portal hypertension (with or without PHT)Extent of PV system occlusion (S, M, SM) Splenic vein, mesenteric vein or bothType and presence of underlying liver disease: Cirrhotic, noncirrhotic liver disease, post-liver transplant, HCC, local malignancies, and associated conditionsABI, acute bowel ischemia; HCC, hepatocellular carcinoma; IMV, inferior mesenteric vein; PHT, portal hypertension; PVT, portal vein thrombosis; PV, portal vein; SV, splenic vein. Open table in a new tab ABI, acute bowel ischemia; HCC, hepatocellular carcinoma; IMV, inferior mesenteric vein; PHT, portal hypertension; PVT, portal vein thrombosis; PV, portal vein; SV, splenic vein. In a patient with cirrhosis who develops acute PVT, there could be 2 baseline clinical scenarios: presence of preexisting significant portal hypertension with varices or absence of clinically significant portal hypertension. The clinical outcome and management issues in the first situation could be challenging, with rapid development of ascites, variceal bleed and early bowel ischemia.24Harki J. Plompen E.P. van Noord D. et al.Gastrointestinal ischaemia in patients with acute and chronic portal vein thrombosis.J Hepatol. 2014; 60: S239-S240Abstract Full Text PDF PubMed Google Scholar Early prevention (with beta-blockers) and endoscopic management of variceal bleed is required and needs to be tailored on a case to case basis against the need for initiating anticoagulant therapy. The role of transjugular intrahepatic portosystemic shunting to unblock the occluded portal venous system is still unclear.25Senzolo M. Burra P. Patch D. et al.TIPS for portal vein thrombosis (PVT) in cirrhosis: not only unblocking a pipe.J Hepatol. 2011; 55 (author reply 947-948): 945-946Abstract Full Text Full Text PDF PubMed Scopus (22) Google Scholar The outcome in such patients is largely determined by the Child's status, available collateral network and the degree and rapidity of increase in hepatic venous pressure gradient. Use and choice of anticoagulants, although indicated, should be weighed in the presence of a deranged international normalized ratio and coagulation anomalies. In patients with no clinically significant PHT, close observation for development of ascites and varices needs to be monitored and low-molecular-weight heparin can be considered, although studies demonstrating its efficacy are lacking. Some issues that are not easy to include in the classification have been excluded. An asymptomatic PVT patient can become symptomatic if the thrombus later extends into the mesenteric system, whereby a diagnosis of acute PVT would be erroneously made. Moreover, acute PVT may be reported in such situations as developing a cavernoma in as short a duration as 0 to 2 days. Defining and diagnosing "acute-on-chronic PVT" is a challenge and requires careful longitudinal studies as this entity may have a different disease course.19Ma J. Yan Z. Luo J. et al.Rational classification of portal vein thrombosis and its clinical significance.PLoS One. 2014; 9: e112501Crossref PubMed Scopus (28) Google Scholar PVT in pre-transplant and posttransplant settings has distinct presentations and outcomes. PVT in the posttransplant state should probably be included in a separate designation because the liver is no longer cirrhotic. As data become available, the classification may be improvised to include the etiology and comorbid conditions associated with PVT. PVT is indeed a heterogeneous group of diseases that may be placed into a syndrome based on clinical presentations. The present commentary highlights the clinical presentation as that of greatest relevance in a patient with cirrhosis, and the entity of PVT should be characterized in both functional and anatomic terms and not only the latter. We believe that the proposed definition and classification of PVT provides clinicians and investigators a more uniform reporting system. The new classification should be of immense help in recruitment of a homogenous group of patients and define clear endpoints in trials of natural history of the disease and the efficacy of anticoagulant therapies in cirrhotic patients with PVT. In addition, we advocate validation and use of preset variables for segregating "high-risk" cirrhotic patients for early detection of PVT and introduction of preventive strategies. Supplementary Table 1Proposed Parameters for Predicting Pretest Probability of PVT in CirrhosisMajor CharacteristicMinor CharacteristicChild's class B or C cirrhosisEvidence of a largacte portosystemic shunt, large IGV1Prior history of resolved PVTActive hepatocellular malignancyAssociated prothrombotic risk factors – factor V LM, prothrombin gene mutation, MTHFR mutation.History of/or active systemic venous thrombotic events or abortionsClinical symptoms and signs of acute abdomenNew onset or worsening portal hypertension complicationsRecent abdominal interventions – endoscopic, radiological or surgicalPortal flow velocity < 15 cm per second at any time during prior Doppler evaluationsPVT, portal vein thrombosis. Open table in a new tab Supplementary Table 2Classification Systems of PVTStieber Classification (1991)16Stieber A.C. Zetti G. Todo S. et al.The spectrum of portal vein thrombosis in liver transplantation.Ann Surg. 1991; 213: 199-206Crossref PubMed Scopus (201) Google ScholarNonami Classification (1992)17Nonami T. Yokoyama I. Iwatsuki S. et al.The incidence of portal vein thrombosis at liver transplantation.Hepatology. 1992; 16: 1195-1198Crossref PubMed Scopus (230) Google ScholarType A: segmental main PV involvedType B: main PV and SMVType C: main PV and SV, main PV, SMV, SV, and IMV without considering PV branch involvement.Grade 1: thrombosis of Intrahepatic portal vein branches onlyGrade 2: thrombosis of first branches of portal vein or at bifurcationGrade 3: partial obstruction of PVGrade 4: complete obstruction of PV trunkImportanceFirst classification attemptInvolves whole of portal venous systemLimitationsOnly anatomicNo clear delineation between acute or chronic, No reference to the amount of vessel occlusion. No clinical implicationsImportancePure consideration for portal veinLimitationsOnly anatomic, Does not involve complete portal venous systemNo delineation between acute or chronic, No clinical implicationsYerdel Classification (2000)18Yerdel M.A. Gunson B. Mirza D. et al.Portal vein thrombosis in adults undergoing liver transplantation: risk factors, screening, management, and outcome.Transplantation. 2000; 69: 1873-1881Crossref PubMed Scopus (556) Google ScholarJingqin Ma et al (2014)19Ma J. Yan Z. Luo J. et al.Rational classification of portal vein thrombosis and its clinical significance.PLoS One. 2014; 9: e112501Crossref PubMed Scopus (28) Google ScholarGrade 1: minimally or partially thrombosed PV where in thrombus is mild or confined to 50% occlusion including total occlusion with or without minimal extension into SMVGrade 3: complete thrombosis of both PV and proximal SMVGrade 4: complete thrombosis of PV and both proximal and distal SMVComplete PVT (with or without cavernoma)Partial PVT (with or without cavernoma)Type I: partial PVT without cavernomaType II: partial PVT with cavernomaType III: complete PVT without cavernomaType IV: complete PVT with cavernomaImportanceConsideration of portal venous system involvementManagement decisions in surgical procedures, including liver transplantationLimitationsOnly anatomicNo clear delineation between acute or chronicNo clinical therapeutic decisivenessImportanceConsiders acute and chronic formsClinically relevant, can assess progression of PVTand help therapeutic decisionsLimitationsPurely anatomic, No functional relevanceNo etiology assessmentJaimeson Classification (2000)20Jamieson N.V. Changing perspectives in portal vein thrombosis and liver transplantation.Transplantation. 2000; 69: 1772-1774Crossref PubMed Scopus (77) Google ScholarType 1: Thrombosis confined to the portal vein beyond the confluence of the SV and SMVType 2: Extension of thrombus into the SMV but with patent mesenteric vesselsType 3: Diffuse thrombosis of splanchnic venous system but with large collateralsType 4: Extensive splanchnic venous thrombosis but with only fine collateralsImportanceConsideration of portal venous system involvementConsidered portal hypertension evolution and implicationsLimitationsNo clinical, therapeutic decisivenessOnly anatomicDifficult to delineate acute versus chronicNo etiology descriptionBauer et al (2006)21Bauer J. Johnson S. Durham J. et al.The role of TIPS for portal vein patency in liver transplant patients with portal vein thrombosis.Liver Transpl. 2006; 12: 1544-1551Crossref PubMed Scopus (83) Google ScholarGrade 1: <25% occluded in PV, SMV, or SVGrade 2: 26%–50% occluded in PV, SMV, or SVGrade 3: 51%–75% occluded in PV, SMV or SVGrade 4: 76%–100% occluded in PV, SMV, or SVImportanceConsideration of portal venous system involvementGave a quantifiable grading systemCan be used for therapeutic monitoringLimitationsPurely anatomic, difficult to precisely determine degree of occlusionRelation of degree of occlusion to flow has not been explainedNo etiologic descriptionShie et al (2011) – for malignant PVT in cirrhosis22Shi J. Lai E.C. Li N. et al.A new classification for hepatocellular carcinoma with portal vein tumor thrombus.J Hepatobiliary Pancreat Sci. 2011; 18: 74-80Crossref PubMed Scopus (149) Google ScholarType I0: Tumor thrombus formation found under microscopyType I: Tumor thrombi involving segmental branches of portal vein or aboveType II: Tumor thrombi involving right/left portal veinType III: Tumor thrombi involving the main portal vein trunkType IV: Tumor thrombi involving the superior mesenteric veinImportanceConsideration of portal venous system involvementCan be utilized to see tumoral progressionLimitationsOnly for tumoral PVTNo clinical or therapeutic implicationsNo prognostic values between different gradesBaveno VI – Classification (2015)23deFranchis R. Expanding consensus in portal hypertension report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.J Hepatol. 2015; 63: 743-752Abstract Full Text Full Text PDF PubMed Scopus (19) Google ScholarSite of PVT – (Types 1, 2a, 2b, 3) Type 1: Only trunk Type 2: Only branch: 2a - One, 2b - Both branches Type 3: Trunk and branchesPresentation (R, Ch) R: Recent (clinical presentation and presence of hyperdense thrombus on imaging) Ch: Chronic (with portal cavernoma and clinical features of portal hypertension, no hyperdense thrombus)Type of underlying liver disease: (C, N, H, L, A) C: Cirrhotic N: Non-cirrhotic liver disease H: HCC and other local malignancies L: Post-liver transplant A: Absence of underlying liver diseaseDegree of portal venous system occlusion (I,T) I: Incomplete: Flow visible in PV lumen through Imaging T: Total: No flow visible in PV lumen on imagingExtent of PV system occlusion (S, M) Splenic vein (S), mesenteric (M) vein or both (SM)ImportanceDefined acute and chronic thrombosisEtiology and underlying disease includedDegree of occlusion and presence or absence of blood flow included; response to therapy can be monitoredUseful for treating clinicians, surgeons and radiologistsLimitationsFunctional consequences not includedIMV, inferior mesenteric vein; PVT, portal vein thrombosis; PV, portal vein; SV, splenic vein; SMV, superior mesenteric vein. Open table in a new tab PVT, portal vein thrombosis. IMV, inferior mesenteric vein; PVT, portal vein thrombosis; PV, portal vein; SV, splenic vein; SMV, superior mesenteric vein. Classification of Portal Vein Thrombosis in CirrhosisGastroenterologyVol. 152Issue 5PreviewI believe that further comments are appropriate about the need of a new classification of portal vein thrombosis (PVT) in patients with cirrhosis, as discussed in the interesting paper recently published in Gastroenterology.1 Full-Text PDF
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