Portal Vein Thrombosis - a Tertiary Care Experience

Portal Vein Thrombosis - a Tertiary Care Experience

PORTAL VEIN THROMBOSIS - A TERTIARY CARE EXPERIENCE DR.N.RADHAKRISHNAN DM RESIDENT INSTITUTE OF MEDICAL GASTROENTEROLOGY MMC & RGGGH CHENNAI,TAMILNADU INDIA INTRODUCTION Portal vein thrombosis(PVT) is defined as a state of obstruction of blood flow in portal vein which can be

either partial or complete and associated with thrombus inside the vascular lumen(1). Portal vein thrombosis(PVT) has become an increasingly recognisable disorder during evaluation of cases of abdominal pain with usage of widespread imaging techniques. OVERLAY OF PORTAL VEIN The portal vein is formed by the confluence of the splenic and superior mesenteric veins. GRADES OF PORTAL VEIN THROMBOSIS

REVIEW OF LITERATURE First case of portal vein thrombosis was reported in a patient with ascites, splenomegaly and varices by Balfour and Steward in 1868(2). PVT in general is a rare clinical state with a low incidence of 0.7% and with a prevalence of 3.7% among general population(3). Higher incidence and prevalence rates are seen among cirrhotic patients with about 10% of PVT cases(4). Chronic liver disease-cirrhosis accounts for nearly 11.2 %(7)25.2%(8) of PVT patients. In patients with no chronic liver disease, hypercoagulable states and myeloproliferative disorders accounts for 40%-70%.

Local factors like intra abdominal surgeries,cancers and inflammatory conditions accounts for 10%--50% of PVT cases(8,9). Acute portal vein thrombosis(PVT) is diagnosed by the presence of thrombus in PV. Chronic PVT is made out by the presence of collaterals resulting due to long standing PVT(5,6). Patients with acute PVT present with nonspecific symptom making the diagnosis of PVT difficult. Diagnosis of PVT is done mostly using USG or CT imaging. Mortality due to PVT accounts for 23% in cases with no underlying liver disease or cancers(8,10).

Local factors Inflammatory Surgery related Cirrhosis Post liver transplant Sepsis Spleenectomy Pancreatitis Colectomy

Diverticulitis Portocaval Shunting Appenditicis Umblical vein catheterization Peptic ulcer disease Inflammatory bowel disease Abdominal trauma Hypercoagulable Etiologies Inherited disorders Acquired disorders

Factor V leiden mutation Myeloproliferative disorders Prothrombin Gene mutation Malignancies Antithrombin III deficiency Anti Phospholipid syndrome Protein C deficiency Anti Cardiolipin Antibody Protein S deficiency

Increased Homocysteine levels Oral contraceptive pills Pregnancy / post partum state COMPLICATIONS PORTAL VEIN THROMBOSIS EARLY/ACUTE DELAYED/CHRONIC 1.RECURRENT ABDOMINAL PAIN 2.PORTAL HYPERTENSION LEADING TO

A-ASCITES BSPLENOMEGALY C-VARICEAL FORMATION AND BLEED 1.YOUNG PATIENTS GROWTH RETARDATION 2.SPLENOMEGALYHYPERSPLENISM 3.PORTAL BILIOPATHY OBSTRUCTIVE JAUNDICE STUDY PROPER OBJECTIVE

The objective of this study ---is to observe the clinical presentation and to do the etiological work up of cases of PVT in a tertiary care centre. This study can help in increasing our knowledge and awareness about PVT thereby aiding in early diagnosis and expert intervention which can greatly reduce the morbidity in cases of PVT. STUDY METHODOLOGY The study is a cross- sectional observational study

done on patients found to have PVT,who presented to Institute of Medical Gastroenterology,MMC & RGGGH,during the period of Jan 2016July 2017. The clinical presentation of the above patients were observed and their etiological work up done. The clinical presentation includes patients age, sex, thrombus stagingacute or chronic. Acute cases identified as having thrombus in Portal vein and chronic cases identified as having established collaterals. PVT etiological work up includes, investigations like routine blood haemogram (leucocyte count, platelet count) blood chemistry like, C-reactive protein,

LDH, AST and ALT levels, alkaline phosphatase, serum amylase levels and procoagulant work up. Procoagulation screen includesMeasurement of Protein C and Protein S levels, homocystiene levels antithrombin levels, factor 5 Leiden mutation analysis, antiphospholipid antibodies detection. Imaging studies used---USG-Portal vein Doppler and Computed tomography. Patients diagnosed to have PVT by Portal vein Doppler were confirmed again by CT scan. RESULTS Totally 45 cases found to have PVT were taken into study. 27 were males and 18 were females. Clinical presentation-- 36 patients had acute portal vein

thrombosis and 9 patients had a chronic presentation .The main symptoms were,abdominal distension in 18 patients(51%),abdominal pain in 10 patients(27%) pain associated with diarrhoea and vomiting in 5 patients(14%) and pain with nausea and anorexia in 3 patients(8%). Blood examination results showed elevated leucocyte count in 20(55%)increased C-reactive protein in 28(77%)increased LDH levels in 14(22 tested,64%) of the 36 acute cases tested. D-dimer levels were detected in all 18 patients(100%) tested. Patients with increased serum amylase levels

were taken in as pancreatitis being a cause and thrombocytosis were seen in patients with myeloproliferative disorder. Detection of PVT were done mostly by Portal vein Doppler in 32 patients(72%) computed tomography in 12 patients(27%) and MRI abdomen in 1(1%). Etiological work up-24(54%) patients had chronic liver disease, some with cirrhosis. 9(20%) patients had prothrombotic conditions, out of which 6(13%) patients had myeloproliferative disorders diagnosed using bone marrow biopsy and 3(7%) patients had procoagulant states,2-Antiphospholipid antibodies(APLA)positives and 1Protien c and protrien

S deficiency. Prothrombtic risks were seen in 4(9%) patients out of which,2 had increased homocystiene levels and 2 patients were taking OCPs. Local factors were leading to PVT in6(13%) of cases due to factors like,post surgical complication in 2(post subtotal gastrectomy and splenectomy), septic cholangitis in 1, chronic pancreatitis in 2 and crohns disease in 1 patient. The cause for PVT could not be identified in 2(4%) cases. Total Sample N=45 100%

Median Age (Years) 45 Males 27 60% Acute 14 32% Chronic

9 20% Chronic Plus Acute 22 48% Abdominal Distension 18 51% Abdominal Pain

10 27% Vomiting and Diarrhoea 5 14% Nausea and Anorexia 3 8% WBC

20 55% 22 Patient Tested CRP LDH 28 14 77% 64% 18 Patients Tested

D-Dimers 18 100% Ultrasound- PV Doppler 32 72% Computed Tomography 13 26%

Magnetic Resonance Imaging 1 2% Chronic Liver Disease 24 54% Prothrombotic Disorder 9 20%

Myeloproliferative Disease 6 13% Coagulation Disorder 3 7% Local Factor 6 13%

Prothrombin Risk 4 9% Idiopathic 2 4% Thrombosis Staging Presentation of Acute Thrombosis Laboratory: Elevated parameters

Diagnostic Method (primary Diagnosis) Causal Factors of PVT DISCUSSION The analysis on 45 patients with PVT-median age was 45,ranging from 18 to 72. Clinical presentation of PVT in acute state were abdominal distension(ascites),abdominal pain which could not be explained by clinical examination or laboratory findings. Some patients with abdominal pain had associated vomiting, diarrhoea and anorexia symptoms as well. The blood investigation results were non specific,still

some patients had elevated leucocyte count, C-reactive protein and LDH levels. Patients who underwent D-dimer testing showed elevated levels thereby aiding in suspecting PVT in cases of abdominal pain and elevated D- dimer levels, though it is sensitive but not specific. Imaging studies mostly used to establish PVT was USG- Portal vein Doppler and Computed tomography. Patients diagnosed to have PVT by Portal vein Doppler were confirmed again by CT scan. CT scan used to picture thrombus in portal and mesenteric circulation also provided a clear picture of abdominal organ examination and aided in detecting local

precipitating factors for PVT,eg.,Pancreatitis. The etiological workup of patients with PVT showed that more than one causative factor were seen in many cases which showed that their occurrence were similar to some previous studies done to find the cause of PVT(8,9,10). The causes identified falls under three major categories, Chronic liver disease, prothrombotic states and local factors with a prevalence of 54%,29% and 13% respectively in our study. In two cases cause could not be identified. Prothrombotic states includes, myeloproliferative disorder, procoagulant states like APLA positivity and

protein C and S deficiency and patients with prothrombotic risks with a contribution of 13%,7% and 9% respectively. Prothrombotic risks included patients on Oral contraceptive pills(12) and patients with elevated homocystiene levels(13,14). The local factors leading to PVT consists of inflammatory conditions like cholangitis(15), pancreatitis(5), inflammatory bowel disease(16), abdominal trauma(17), intra abdominal surgeries esp. Post splenectomy(18) and carcinomas of stomach,Liver and pancreas encroaching the portal vein. CONCLUSION Higher incidence of PVT were seen among patients with

chronic liver disease. Prothrombotic states like myeloproliferative disorders and coagulation defects were the next common causes detected. PVT presenting as plain abdominal pain, pain associated with nausea, vomiting and diarrhoea were seen in patients as well,thereby suggesting that PVT is an important differential diagnosis in patients presenting as abdominal pain with a negative work up for common causes. With the help of widespread and improved Imaging techniques,earlier diagnosis of PVT can be achieved and

early intervention can greatly reduce the morbidity of patients. TREATMENT The goals of treatment are the same in acute and chronic PVT which are(1) to correct the cause(2)to prevent the thrombus from extending and(3) to maintain portal vein patency. Anti coagulants are the best options to recanalise portal vein. Till date No clear literature or controlled trails are available for anti coagulants use in PVT(19).

REFERENCES 1-Kocher G, Himmelmann A. Portal vein thrombosis (PVT):a study of 20 noncirrhotic cases. Swiss Med Wkly 2005; 135:372-376 [PMID: 16106327]. 2-Wang JT, Zhao HY, Liu YL. Portal vein thrombosis. Hepatobiliary Pancreat Dis Int 2005; 4: 515-518 [PMID: 16286254]. 3-Plessier A, Darwish-Murad S, Hernandez-Guerra M, Consigny Y, Fabris F, Trebicka J, Heller J, Morard I, Lasser L,Langlet P, Denninger MH, Vidaud D, Condat B, Hadengue A, Primignani M, Garcia-Pagan JC, Janssen HL, Valla D. Acute portal vein thrombosis unrelated to cirrhosis: a prospective multicenter follow-up study. Hepatology 2010; 51: 210-218 [PMID: 19821530 DOI: 10.1002/hep.23259]. 4-Ponziani FR, Zocco MA, Campanale C, Rinninella E, Tortora A, Di Maurizio L, Bombardieri G, De Cristofaro R, DeGaetano AM, Landolfi R, Gasbarrini A. Portal vein thrombosis: insight into physiopathology, diagnosis, and treatment. World J Gastroenterol 2010; 16: 143-155 [PMID: 20066733 DOI:10.3748/wjg.v16.i2.143]. 5-Valla DC, Condat B. Portal vein thrombosis in adults: pathophysiology,pathogenesis and management. J Hepatol 2000;32:86571. 6-Sheen CL, Lamparelli H, Milne A, Green I, Ramage JK. Clinical features,

diagnosis and outcome of acute portal vein thrombosis.Q J Med 2000;93:5314. 7-Amitrano L, Guardascione MA, Brancaccio V, Margaglione M,Manguso F, et al. Risk factors and clinical presentation of portal vein thrombosis in patients with liver cirrhosis. J Hepatol 2004;40:73641. 8-Janssen HLA, Wijnhoud A, Haagsma EB, van Uum M, van Nieuwkerk CMJ, Adang RP, et al. Extrahepatic portal vein thrombosis: aetiology and determinants of survival. Gut 2001; 49:7204. 9-Denninger MH, Chait Y, Casadevall N, Hillaire S, Guillin MC,Bezeaud A, et al. Cause of portal or hepatic venous thrombosisin adults: The role of multiple concurrent factors. Hepatology 2000;31:58791. 10-Condat B, Pessione F, Hillaire S, Denninger MH, Guillin MC,Poliquin M, et al. Current outcome of portal vein thrombosis in adults: Risk and benefit of anticoagulant therapy. Gastroenterology 2001;120:4907. 11-Bombeli T, Basic A, Fehr J. Prevalence of hereditary thrombophilia in patients with thrombosis in different venous systems.Am J Hematology 2002;70:12632. 12-Belicova M, Lukac B, Dvorsky J, Peter G, Mokan M, Kubisz

P.Thromboembolic disease and present oral contraception. Clin Appl Thromb Hemost 2003;9:4551. 13-Den Heijer M, Rosendaal, Blom HJ, Gerrits WBJ, Bos GMJ.Hyperhomocysteinemia and venous thrombosis: a meta-analysis.Thromb Haemost 1998;80:8747. 14-Hainaut P, Jaumotte C, Verhelst D, Wallemacq P, Gala JL, Zech F, et al. Hyperhomocysteinemia and venous thromboembolism: a risk factor more prevalent in the elderly and in idiopathic cases.Thromb Res 2002;106:1215. 15-Plemmons RM, Dooley DP, Longfield RN. Septic thrombophlebitis of the portal vein (pylephlebitis): diagnosis and management in the modern era. Clin Infect Dis 1995;21:111420. 16-Tsujikawa T, Ihara T, Sasaki M, Inoue H, Fujiyama Y, Bamba T. Effectiveness of combined anticoagulant therapy for extending portal vein thrombosis in Crohns disease. Dis Colon Rectum 1996;39:8235. 17-Duvoux C, Radier C, Gouault-Heilmann M, Texier JP, Le Cudonnec B, Dhumeaux D. Une cause rare de thrombose portale:le traumatisme ferm de labdomen. Gastroenterol Clin Biol 1994;18:1657. 18-Hassn AM, Al-Fallouji MA, Ouf TI, Saad R. Portal vein thrombosis following

splenectomy. Br J Surg 2000;87:36273. 19-Lee HK, Park SJ, Yi BH, Yeon EK, Kim JH, Hong HS. Portal vein thrombosis: CT features. Abdom Imaging 2008; 33: 72-79 [PMID: 17694406 DOI: 10.1007/s00261007-9200-x

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