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      Coil-Assisted Retrograde Transvenous Obliteration (CARTO) for the Treatment of Portal Hypertensive Variceal Bleeding: Preliminary Results

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          To describe the technical feasibility, safety, and clinical outcomes of coil-assisted retrograde transvenous obliteration (CARTO) in treating portal hypertensive non-esophageal variceal hemorrhage.


          From October 2012 to December 2013, 20 patients who received CARTO for the treatment of portal hypertensive non-esophageal variceal bleeding were retrospectively evaluated. All 20 patients had at least 6-month follow-up. All patients had detachable coils placed to occlude the efferent shunt and retrograde gelfoam embolization to achieve complete thrombosis/obliteration of varices. Technical success, clinical success, rebleeding, and complications were evaluated at follow-up.


          A 100% technical success rate (defined as achieving complete occlusion of efferent shunt with complete thrombosis/obliteration of bleeding varices and/or stopping variceal bleeding) was demonstrated in all 20 patients. Clinical success rate (defined as no variceal rebleeding) was 100%. Follow-up computed tomography after CARTO demonstrated decrease in size with complete thrombosis and disappearance of the varices in all 20 patients. Thirteen out of the 20 had endoscopic confirmation of resolution of varices. Minor post-CARTO complications, including worsening of esophageal varices (not bleeding) and worsening of ascites/hydrothorax, were noted in 5 patients (25%). One patient passed away at 24 days after the CARTO due to systemic and portal venous thrombosis and multi-organ failure. Otherwise, no major complication was noted. No variceal rebleeding was noted in all 20 patients during mean follow-up of 384±154 days.


          CARTO appears to be a technically feasible and safe alternative to traditional balloon-occluded retrograde transvenous obliteration or transjugular intrahepatic portosystemic shunt, with excellent clinical outcomes in treating portal hypertensive non-esophageal variceal bleeding.

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          Most cited references 34

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          Prevalence, classification and natural history of gastric varices: a long-term follow-up study in 568 portal hypertension patients.

          To determine the prevalence and natural history of gastric varices, we prospectively studied 568 patients (393 bleeders and 175 nonbleeders) with portal hypertension (cirrhosis in 301 patients, noncirrhotic portal fibrosis in 115 patients, extrahepatic portal vein obstruction in 117 patients and hepatic venous outflow obstruction in 35 patients). Primary (present at initial examination) gastric varices were seen in 114 (20%) patients; more were present in bleeders than in non-bleeders (27% vs. 4%, respectively; p < 0.001). Secondary (occurring after obliteration of esophageal varices) gastric varices developed in 33 (9%) patients during follow-up of 24.6 +/- 5.3 mo. Gastric varices (compared with esophageal varices) bled in significantly fewer patients (25% vs. 64%, respectively). Gastric varices had a lower bleeding risk factor than did esophageal varices (2.0 +/- 0.5 vs. 4.3 +/- 0.4, respectively) but bled more severely (4.8 +/- 0.6 vs. 2.9 +/- 0.3 transfusion units per patient, respectively). Once a varix bled, mortality was more likely (45%) in gastric varix patients. Gastric varices were classified as gastroesophageal or isolated gastric varices. Type 1 gastroesophageal varices (lesser curve varices) were the most common (75%). After obliteration of esophageal varices, type 1 gastroesophageal varices disappeared in 59% of patients and persisted in the remainder; bleeding from persistent gastroesophageal varices was more common than it was from gastroesophageal varices that were obliterated (28% vs. 2%, respectively; p < 0.001). Type 2 gastroesophageal varices, which extend to greater curvature, bled often (55%) and were associated with high mortality. Type 1 isolated gastric varices patients had only fundal varices, with a high (78%) incidence of bleeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Natural history of portal hypertension in patients with cirrhosis.

            All patients with cirrhosis will eventually develop portal hypertension and esophagogastric varices. Bleeding from ruptured esophagogastric varices is the most severe complication of cirrhosis and is the cause of death in about one third of patients. The rate of development and growth of esophageal varices is poorly defined but in general seem to be related to the degree of liver dysfunction. Once varices have formed, they tend to increase in size and eventually to bleed. In unselected patients, the incidence of variceal bleeding is about 20% to 30% at 2 years. Variceal size is the single most important predictor of a first variceal bleeding episode. Several prognostic indexes based on endoscopic and clinical parameters have been developed to predict the risk of bleeding; however, their degree of accuracy is unsatisfactory. Death caused by uncontrolled bleeding occurs in about 6% to 8% of patients; the 6-week mortality rate after a variceal hemorrhage is 25% to 30%. There are no good prognostic indicators of death caused by uncontrolled bleeding or death within 6 weeks. Untreated patients surviving a variceal hemorrhage have a 1- to 2-year risk of rebleeding of about 60% and a risk of death of about 40% to 50%. The risk of bleeding is greatest in the first days after a bleeding episode and slowly declines thereafter. All patients surviving a variceal hemorrhage must be treated to prevent rebleeding. Varices can also be found in the stomach of cirrhotic patients, alone or in association with esophageal varices. Gastric varices bleed less frequently but more severely than esophageal varices. Portal hypertensive gastropathy is a common feature of cirrhosis, and its prevalence parallels the severity of portal hypertension and liver dysfunction. Portal hypertensive gastropathy can progress from mild to severe and vice-versa or even disappear completely. Acute bleeding from portal hypertensive gastropathy seems to be relatively uncommon, and less severe than bleeding from varices.
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              Retrograde transvenous obliteration of gastric varices.

               S Hirota,  M Tomita,  M Sako (1999)
              To evaluate the clinical efficacy, techniques, and complications associated with balloon-occluded retrograde transvenous obliteration of gastric varices. Between December 1994 and November 1997, balloon-occluded retrograde transvenous obliteration was performed on 20 patients with gastric varices in danger of rupture and with gastrorenal shunts; three patients also had hepatic encephalopathy. The sclerosant was injected into the gastric varices during balloon occlusion. The degree of progression of the gastric varices and of collateral veins was classified into five grades, with grade 1 being least progression and grade 5 most progression; collateral veins that had developed were treated with embolization. Follow-up consisted of fiberoptic endoscopy and computed tomography. Technical success was achieved in all patients. Occlusion of collateral veins was essential for the occlusion of gastric varices with a grade greater than grade 2. The clinical symptoms of hepatic encephalopathy in the three patients improved remarkably. Follow-up endoscopy 3 months after the procedure revealed the disappearance of gastric varices in 15 patients and reduced variceal size in five. During the follow-up period, 19 patients had no recurrence of gastric varices; three patients had aggravation of the esophageal varices. Balloon-occluded retrograde transvenous obliteration is a feasible alternative to a transjugular intrahepatic portosystemic shunt for patients with large gastrorenal shunts or hepatic encephalopathy (or both).

                Author and article information

                Clin Transl Gastroenterol
                Clin Transl Gastroenterol
                Clinical and Translational Gastroenterology
                Nature Publishing Group
                October 2014
                02 October 2014
                1 October 2014
                : 5
                : 10
                : e61
                [1 ]Division of Interventional Radiology, Department of Radiology, UCLA Medical Center, David Geffen School of Medicine at UCLA , Los Angeles, California, USA
                [2 ]Division of Hepatology, Department of Medicine, Pfleger Liver Institute, University of California at Los Angeles , Los Angeles, California, USA
                [3 ]Dumont-UCLA Transplant Center, Pfleger Liver Institute, Division of Liver and Pancreas Transplantation, Department of Surgery, David Geffen School of Medicine at University of California , Los Angeles, California, USA
                Author notes
                [* ]Division of Interventional Radiology, Department of Radiology, Ronald Reagan Medical Center at UCLA, David Geffen School of Medicine at UCLA , 757 Westwood Plaza, Suite 2125, Los Angeles, California 90095-743730, USA. E-mail: EdwardLee@
                Copyright © 2014 American College of Gastroenterology

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit

                Original Contributions

                Gastroenterology & Hepatology


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