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228 Budd-chiari syndrome (BCS) and heparin induced thrombocytopenia (HIT)
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MANAGEMENT OF ECTOPIC VARICES: THE E D I N B U R G H EXPERIENCE
N. Kocharl, D. Tripathi 1, N.C. McAvoy 1, J. Leithead 1, H. Ireland2, D.N. Redhead 2, P.C. Hayes 1. 1Department of Hepatology, 2Department
of Radiology, Royal Infirmary of Edinburgh, Edinburgh, UK Introduction: Bleeding from ectopic varices is uncommon but can be difficult to manage. We report our experience of uncontrolled bleeding from ectopic varices managed by insertion of TIPSS. Methods: Patients in whom TIPSS was inserted for ectopic varices were selected from a TIPSS dedicated data-base. Results: Over 14 years, 732 TIPSS have been inserted. TIPSS was inserted for bleeding ectopic varices in 24 (males 11) patients. Mean age (SD) at TIPSS insertion was 56.6(10.6) years. Mean (SD) Child Pugh score was 7.6(1.84); A/B/C (%): 9/59/32. Aetiology of liver disease: alcoholic 15, cryptogenic 3, viral 2, others 4. Site of bleeding was rectal 11, stomal 7, duodenal 3, caput medusae 1, falciform ligament varix 1 and intraperitoneal varix 1. TIPSS was successful in 23/24 (96%). Complete data available on 20 patients. Portal pressure gradient (PPG) fell from 19(6.34) to 7.47(3.84)mmHg. Covered stents were used in 4 patients. Embolisation of varices was performed in 4 at the initial procedure. TIPSS insertion was initially effective in controlling bleeding in 18 (90%) patients. In four (covered stents 2, uncovered stents 2) of these patients bleeding recurred at 13 to 202 days after TIPSS insertion. This necessitated parallel shunt insertion for occluded shunts in 2, shunt extension for shunt insufficiency in 1, thrombin injection into the stomal varix in 2 patients and embolisation of varices in 1. These measures effectively controlled rebleeding in 3 patients and the fourth patient continues to have intermittent bleeding despite patent TIPSS. TIPSS was unsuccessful in controlling bleeding in 2 patients and one of these died due to liver failure 8 days post TIPSS. 14 patients died (7 liver related, 1 due to G.I. bleed) since the TIPSS insertion and 6 patients had liver transplant at a median duration of 248 (5 1869) days. Conclusions: TIPSS is effective in the management of bleeding ectopic varices. Variceal rebleeding is frequently related to shunt insufficiency. Additional therapies such as thrombin and embolisation may be effective in difficult cases and may have a role in index therapy as an adjunct to TIPSS.
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B U D D - C H I A R I S Y N D R O M E (BCS) AND HEPARIN INDUCED T H R O M B O C Y T O P E N I A (HIT)
A. Plessierl, Y. Consigny1, RE. Rautou 1, R. Boucari 1, A. Bezeaud 2, L. Boudaoud 2, J.J. Kiladjian 3, C. Brumpt2, V. Saada 2, B. Condat 1, D.C. Valla 1, M.H. Denninger2. 1Unit of Hepatology, 2Unit of Hematology,
Hdpital Beaujon, Clichy, France," 3Unit of Clinical Hematology, Hdpital Avicenne," AP-HP, Bobigny, France Background: HIT is an antibody-mediated and life-threatening adverse effect of heparin therapy frequently complicated by venous thrombosis. It occurs in 3.3% of surgical patients on prophylactic unfractionated heparin (UFH). Its incidence is low in medical patients. Early anticoagulation is recommended in patients with BCS. The aim of our study was to assess the incidence, the risk factors and the clinical events associated to HIT in consecutive BCS patients seen from 1996 to 2004. Methods: Fifty-nine consecutive patients received anticoagulation therapy. Platelets were monitored at least weekly. Diagnosis of HIT was based on the association of a drop in platelet counts >50% to a count <150• 109/1; and a positive HIT antibody test (PF4-dependent EIA). Patients with suspected HIT were immediately switched to danaparoid sulfate. Clinical events temporally related to HIT were recorded. Results: UFH was given to 9 patients, low-molecular weight heparin (LMWH) to 28, and UFH and LMWH to 17. Five received only vitamin K antagonists. Among 12 patients developing thrombocytopenia, HIT was
confirmed in 8 (14% of all patients) within a median delay of 7 days from initiation of heparin therapy (range 5 13 days). Three patients had a radiological procedure immediately preceding HIT. UFH had been given to 87% of the patients who developed HIT vs 40% of those who did not (p 0.033). A myeloproliferative disease was present in 8/8 (100%) patients who developed HIT vs 22/48 (46%) of those who did not (p 0.027). In relation to HIT, venous thrombosis developed in 5 patients (involving the portal vein in 3, IVC and hepatic veins in 1, pulmonary embolism in 1); liver failure in 2; and haematoma in 2. Median Clichy score before HIT was 5.3 (range 3.1 7.1) vs 7.4 (range 5.7 8.7) after HIT (p 0.012). The 3-yr survival rate was 90%, IC (48 97) in patients who developed HIT, (4 later liver transplantation and 2 deaths). Conclusion: HIT is an extremely frequent and severe complication of UFH therapy for BCS. Myeloproliferative diseases constitute a major risk factor for HIT in BCS patients. LMWH should be preferred to UFH for short term anticoagulation in BCS patients.
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SOLUBLE VASCULAR CELL ADHESION MOLECULE HAS A POTENTIAL PROGNOSTIC ROLE IN A L C O H O L I C OR VIRAL CIRRHOTIC PATIENTS
D. Rincon, O. Lo Iacono, A. Hernando, C. Ripoll, M.V. Catalina, R. Lorente, G. Clemente, A. Matilla, R. Bafiares. Liver and Tranplant
Unit/Hospital General Universitario GregorioMara~on, Madrid, Spain Background and Aims: The role of soluble vascular cell adhesion molecule (sVCAM) in the natural history of cirrhosis has not been reported. Aims of this study were: to investigate whether sVCAM are associated with hemodynamic systemic and splanchinic abnormalities and to evaluate their prognostic value in cirrhotic patients who underwent a hemodynamic study. Methods: We studied, using immunoassays, the serum levels of sVCAM in peripheral and hepatic vein in 120 consecutive patients, with chronic liver disease, who underwent a hemodynamic study. Results: We excluded patients with OLT (n 12), HIV infected (n 2), evaluated for acute liver failure (n 5) or with cryptogenic or cholestasic or non-cirrhotic liver disease (n 15). The aims was evaluated in 86 patients [61M/25F; age 51.1(8.3) years] with alcoholic (31) or viral (HBV: 6, HCV: 49) cirrhosis, 11 of them with HCC (Milan criteria). The mean values of HVPG [18.2(4.6) vs 17.5(7.0)], MELD [16.1(6.1) vs 13.4(6.3)] and sVCAM [2525(1215) vs 2930(1412)] were similar (p us) in alcoholic vs viral patients. Mean follow-up was 312(170) days; 19 patients died or were transplanted and 4 were dropped-out during follow-up. A strong correlation in serum levels of sVCAM was observed between peripheral and hepatic vein (r 0.867; p 0.0001). At univariate analysis, sVCAM was inversely related with mean arterial pressure (r 0.272; p 0.003), systemic vascular resistance (r 0.296; p 0.025), serum Na (r 0.302; p 0.005). A close correlation was observed with MELD and Child Pugh scores (r 0.45; p 0.0001 and r 0.46; p 0.0001, respectively). A relationship between sVCAM with HVPG (r 0.48; p 0.006) and with cardiac output (r 0.48; p 0.04) was observed only in alcoholic cirrhosis. Cumulative survival was significantly lower in patients with sVCAM levels below the median value (0.67, 0.52, 0.45 vs. 0.94, 0.83, 0.77 at 6, 12 and 18 months respectively; log-rank 7.61; p 0.006). In a multivariate model including MELD score, Child score, Serum sodium, HVPG and sVCAM, only sVCAM levels (HR 2.6; 95%CI 1 6.8) was retained in the model. Conclusions: sVCAM, as marker of endothelial dysfunction, is associated with circulatory alterations in cirrhotic patients and could be evaluated as useful non-invasive prognostic survival marker.
$92
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MANAGEMENT OF ECTOPIC VARICES: THE E D I N B U R G H EXPERIENCE
N. Kocharl, D. Tripathi 1, N.C. McAvoy 1, J. Leithead 1, H. Ireland2, D.N. Redhead 2, P.C. Hayes 1. 1Department of Hepatology, 2Department
of Radiology, Royal Infirmary of Edinburgh, Edinburgh, UK Introduction: Bleeding from ectopic varices is uncommon but can be difficult to manage. We report our experience of uncontrolled bleeding from ectopic varices managed by insertion of TIPSS. Methods: Patients in whom TIPSS was inserted for ectopic varices were selected from a TIPSS dedicated data-base. Results: Over 14 years, 732 TIPSS have been inserted. TIPSS was inserted for bleeding ectopic varices in 24 (males 11) patients. Mean age (SD) at TIPSS insertion was 56.6(10.6) years. Mean (SD) Child Pugh score was 7.6(1.84); A/B/C (%): 9/59/32. Aetiology of liver disease: alcoholic 15, cryptogenic 3, viral 2, others 4. Site of bleeding was rectal 11, stomal 7, duodenal 3, caput medusae 1, falciform ligament varix 1 and intraperitoneal varix 1. TIPSS was successful in 23/24 (96%). Complete data available on 20 patients. Portal pressure gradient (PPG) fell from 19(6.34) to 7.47(3.84)mmHg. Covered stents were used in 4 patients. Embolisation of varices was performed in 4 at the initial procedure. TIPSS insertion was initially effective in controlling bleeding in 18 (90%) patients. In four (covered stents 2, uncovered stents 2) of these patients bleeding recurred at 13 to 202 days after TIPSS insertion. This necessitated parallel shunt insertion for occluded shunts in 2, shunt extension for shunt insufficiency in 1, thrombin injection into the stomal varix in 2 patients and embolisation of varices in 1. These measures effectively controlled rebleeding in 3 patients and the fourth patient continues to have intermittent bleeding despite patent TIPSS. TIPSS was unsuccessful in controlling bleeding in 2 patients and one of these died due to liver failure 8 days post TIPSS. 14 patients died (7 liver related, 1 due to G.I. bleed) since the TIPSS insertion and 6 patients had liver transplant at a median duration of 248 (5 1869) days. Conclusions: TIPSS is effective in the management of bleeding ectopic varices. Variceal rebleeding is frequently related to shunt insufficiency. Additional therapies such as thrombin and embolisation may be effective in difficult cases and may have a role in index therapy as an adjunct to TIPSS.
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B U D D - C H I A R I S Y N D R O M E (BCS) AND HEPARIN INDUCED T H R O M B O C Y T O P E N I A (HIT)
A. Plessierl, Y. Consigny1, RE. Rautou 1, R. Boucari 1, A. Bezeaud 2, L. Boudaoud 2, J.J. Kiladjian 3, C. Brumpt2, V. Saada 2, B. Condat 1, D.C. Valla 1, M.H. Denninger2. 1Unit of Hepatology, 2Unit of Hematology,
Hdpital Beaujon, Clichy, France," 3Unit of Clinical Hematology, Hdpital Avicenne," AP-HP, Bobigny, France Background: HIT is an antibody-mediated and life-threatening adverse effect of heparin therapy frequently complicated by venous thrombosis. It occurs in 3.3% of surgical patients on prophylactic unfractionated heparin (UFH). Its incidence is low in medical patients. Early anticoagulation is recommended in patients with BCS. The aim of our study was to assess the incidence, the risk factors and the clinical events associated to HIT in consecutive BCS patients seen from 1996 to 2004. Methods: Fifty-nine consecutive patients received anticoagulation therapy. Platelets were monitored at least weekly. Diagnosis of HIT was based on the association of a drop in platelet counts >50% to a count <150• 109/1; and a positive HIT antibody test (PF4-dependent EIA). Patients with suspected HIT were immediately switched to danaparoid sulfate. Clinical events temporally related to HIT were recorded. Results: UFH was given to 9 patients, low-molecular weight heparin (LMWH) to 28, and UFH and LMWH to 17. Five received only vitamin K antagonists. Among 12 patients developing thrombocytopenia, HIT was
confirmed in 8 (14% of all patients) within a median delay of 7 days from initiation of heparin therapy (range 5 13 days). Three patients had a radiological procedure immediately preceding HIT. UFH had been given to 87% of the patients who developed HIT vs 40% of those who did not (p 0.033). A myeloproliferative disease was present in 8/8 (100%) patients who developed HIT vs 22/48 (46%) of those who did not (p 0.027). In relation to HIT, venous thrombosis developed in 5 patients (involving the portal vein in 3, IVC and hepatic veins in 1, pulmonary embolism in 1); liver failure in 2; and haematoma in 2. Median Clichy score before HIT was 5.3 (range 3.1 7.1) vs 7.4 (range 5.7 8.7) after HIT (p 0.012). The 3-yr survival rate was 90%, IC (48 97) in patients who developed HIT, (4 later liver transplantation and 2 deaths). Conclusion: HIT is an extremely frequent and severe complication of UFH therapy for BCS. Myeloproliferative diseases constitute a major risk factor for HIT in BCS patients. LMWH should be preferred to UFH for short term anticoagulation in BCS patients.
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SOLUBLE VASCULAR CELL ADHESION MOLECULE HAS A POTENTIAL PROGNOSTIC ROLE IN A L C O H O L I C OR VIRAL CIRRHOTIC PATIENTS
D. Rincon, O. Lo Iacono, A. Hernando, C. Ripoll, M.V. Catalina, R. Lorente, G. Clemente, A. Matilla, R. Bafiares. Liver and Tranplant
Unit/Hospital General Universitario GregorioMara~on, Madrid, Spain Background and Aims: The role of soluble vascular cell adhesion molecule (sVCAM) in the natural history of cirrhosis has not been reported. Aims of this study were: to investigate whether sVCAM are associated with hemodynamic systemic and splanchinic abnormalities and to evaluate their prognostic value in cirrhotic patients who underwent a hemodynamic study. Methods: We studied, using immunoassays, the serum levels of sVCAM in peripheral and hepatic vein in 120 consecutive patients, with chronic liver disease, who underwent a hemodynamic study. Results: We excluded patients with OLT (n 12), HIV infected (n 2), evaluated for acute liver failure (n 5) or with cryptogenic or cholestasic or non-cirrhotic liver disease (n 15). The aims was evaluated in 86 patients [61M/25F; age 51.1(8.3) years] with alcoholic (31) or viral (HBV: 6, HCV: 49) cirrhosis, 11 of them with HCC (Milan criteria). The mean values of HVPG [18.2(4.6) vs 17.5(7.0)], MELD [16.1(6.1) vs 13.4(6.3)] and sVCAM [2525(1215) vs 2930(1412)] were similar (p us) in alcoholic vs viral patients. Mean follow-up was 312(170) days; 19 patients died or were transplanted and 4 were dropped-out during follow-up. A strong correlation in serum levels of sVCAM was observed between peripheral and hepatic vein (r 0.867; p 0.0001). At univariate analysis, sVCAM was inversely related with mean arterial pressure (r 0.272; p 0.003), systemic vascular resistance (r 0.296; p 0.025), serum Na (r 0.302; p 0.005). A close correlation was observed with MELD and Child Pugh scores (r 0.45; p 0.0001 and r 0.46; p 0.0001, respectively). A relationship between sVCAM with HVPG (r 0.48; p 0.006) and with cardiac output (r 0.48; p 0.04) was observed only in alcoholic cirrhosis. Cumulative survival was significantly lower in patients with sVCAM levels below the median value (0.67, 0.52, 0.45 vs. 0.94, 0.83, 0.77 at 6, 12 and 18 months respectively; log-rank 7.61; p 0.006). In a multivariate model including MELD score, Child score, Serum sodium, HVPG and sVCAM, only sVCAM levels (HR 2.6; 95%CI 1 6.8) was retained in the model. Conclusions: sVCAM, as marker of endothelial dysfunction, is associated with circulatory alterations in cirrhotic patients and could be evaluated as useful non-invasive prognostic survival marker.