Episode Of Variceal Bleeding Research Articles

Black esophagus complicating variceal bleeding

An 81-year-old frail Caucasian man experienced a first episode of acute variceal bleeding complicating portal hypertension. He had undergone right hepatectomy plus resection of hepatic segment 4 for a large, right-sided hepatoma 6 years previously. This had been followed by treatment with radioactive iodine (131I-Lipiodol), which had caused veno-occlusive disease in the remaining segments 2 and 3 leading to severe portal hypertension.

Obliterative Portal Venopathy: A Clinical and Histopathological Review

Non-cirrhotic portal hypertension (NCPH) is characterized by the elevation of the portal pressure in the absence of cirrhosis. Obliterative portal venopathy (OPV) as a cause of NCPH is being increasingly diagnosed, especially after recent reports of its occurrence in patients with HIV using didanosine. Patients usually present with episodes of variceal hemorrhage and other features of portal hypertension including jaundice, ascites, encephalopathy and hepatopulmonary syndrome. Hepatic synthetic function is typically well preserved and the laboratory evaluation in OPV patients typically reveals only mild nonspecific hematological abnormalities chiefly related to hypersplenism. Its diagnosis remains a challenge and patients are often mistakenly diagnosed as having cirrhosis. Despite the increasing recognition of OPV, its etiology and pathogenesis are still unclear. A number of etiologies have been proposed including genetic predisposition, recurrent bacterial infections, HIV infection and highly active antiretroviral therapy, an altered immune response, hypercoagulability, and exposure to chemicals and certain medications. Histopathological evaluation remains critical in excluding cirrhosis and other causes of portal hypertension, and is the only way of definitively establishing the diagnosis of OPV. Clinicians should have a high index of suspicion for OPV in patients who present with variceal bleeding and splenomegaly and who do not have other features of cirrhosis. The purpose of this review is to summarize the known etiologies for OPV and its associated clinical aspects and correlations, and to also provide ample histophotomicrographs of OPV to aid in the diagnosis. It will also help raise awareness of this entity amongst pathologists and clinicians alike.

The secondary prophylactic efficacy of beta-blocker after endoscopic gastric variceal obturation for first acute episode of gastric variceal bleeding

Background/AimsThe most appropriate treatment for acute gastric variceal bleeding (GVB) is currently endoscopic gastric variceal obturation (GVO) using Histoacryl®. However, the secondary prophylactic efficacy of beta-blocker (BB) after GVO for the first acute episode of GVB has not yet been established. The secondary prophylactic efficacy of BB after GVO for the first acute episode of GVB was evaluated in this study.MethodsNinety-three patients at Soonchunhyang University Hospital with acute GVB who received GVO using Histoacryl® were enrolled between June 2001 and March 2010. Among these, 42 patients underwent GVO alone (GVO group) and 51 patients underwent GVO with adjuvant BB therapy (GVO+BB group). This study was intended for patients in whom a desired heart rate was reached. The rates of rebleeding-free survival and overall survival were calculated for the two study groups using Kaplan-Meyer analysis and Cox's proportional-hazards model.ResultsThe follow-up period after the initial eradication of gastric varices was 18.14±25.22 months (mean±SD). During the follow-up period, rebleeding occurred in 10 (23.8%) and 21 (41.2%) GVO and GVO+BB patients, respectively, and 39 patients died [23 (54.8%) in the GVO group and 16 (31.4%) in the GVO+BB group]. The mean rebleeding-free survival time did not differ significantly between the GVO and GVO+BB groups (65.40 and 37.40 months, respectively; P=0.774), whereas the mean overall survival time did differ (52.54 and 72.65 months, respectively; P=0.036).Conclusions Adjuvant BB therapy after GVO using Histoacryl® for the first acute episode of GVB could decrease the mortality rate relative to GVO alone. However, adjuvant BB therapy afforded no benefit for the secondary prevention of rebleeding in GV.

Warren shunt combined with partial splenectomy for children with extrahepatic portal hypertension, massive splenomegaly, and severe hypersplenism

To establish the importance of shunt surgery combined with partial resection of the spleen for selected pediatric patients with extra-hepatic portal vein obstruction (EHPVO), enormous splenomegaly and severe hypersplenism. Severe hypersplenism is often refractory to treatment with endoscopic sclerotherapy or band ligation and shunt surgery; however, to our knowledge, this is the first such study to be published. Distal splenorenal shunt with partial resection of the spleen was performed in 16 of 60 children treated for EHPVO in the Gastroenterology Department of our hospital. Upper gastrointestinal endoscopy had shown esophageal varices of varying grade in all patients and band ligation or endoscopic sclerotherapy had been done for children with a history of bleeding. The indications for surgery were pain and discomfort caused by a large spleen (5-15 cm below the costal margin) and symptomatic hypersplenism with leucopenia, thrombocytopenia, and anemia. Partial resection of the spleen was performed, starting with ligation of the branches and tributaries of the caudal two-thirds. When an ischemic line demarcated the splenic parenchyma, it was transected using electrocautery or LigaSure, leaving 20-30 % of splenic tissue. After the spleen resection, a Warren shunt was performed. Platelet and white blood cell counts and liver function tests were performed before and after the operation. Growth was assessed using SD scores (z scores) for height, weight, and body mass index at the time of surgery and 1 year later. Postoperative recovery was uneventful and the leukocyte and platelet counts normalized. The shunt patency rate was 100 %. Two cases of shunt stenosis were treated successfully with percutaneous angioplasty. There was no postoperative mortality. During the follow-up period, from 1 to 7 years, all 16 children were asymptomatic, with improved quality of life, growth, and nutrition. No episodes of variceal bleeding, sepsis or encephalopathy occurred. Our results demonstrate that shunt surgery with partial resection of the spleen is effective and safe for pediatric patients with massive splenomegaly and severe hypersplenism secondary to EHPVO.

Management of an acute variceal bleeding episode.

Thus, it should be suspected in any patient withcirrhosis and GI bleeding. The diagnosis is established byemergency endoscopy when one of the following is observed:active variceal bleeding (blood spurting or oozing from avarix), a white nipple or clot adherent to a varix, or the pres-ence of blood in stomach and varices without other potentialsources of bleeding.Mortality resulting from AVB has greatly decreased in thelast 3 decades to the current rate of 15% to 20%. This isprobably because of effective treatments [endoscopy, vasoac-tive drugs, and transjugular intrahepatic portosystemic shunt(TIPS)] as well as improved general medical care (antibioticprophylaxis, careful replacement of volemia, etc.).

Proposing a Gastroenterologistʼs “Secondary Survey”: When to Consider Factitious Disorder in the Differential Diagnosis

Purpose: We are regularly consulted to evaluate GI bleeding. Occasionally, the clinical history and endoscopic findings do not correlate. This case report highlights the need to consider factitious disorder in the differential diagnosis of GI bleeding. Case Report: A 35-year-old man presented to the Emergency Department with 2 episodes of hematemesis on the day of admission, one witnessed by hospital staff. He reported a history of hepatitis C cirrhosis with multiple episodes of variceal bleeding, undergoing endoscopic banding on his last episode 3 weeks prior. Vital signs were stable. Laboratory data revealed Hemoglobin 9.8, PT 17.5, AST 107, ALT 81, & AKP 51. He refused NG tube placement. Esophagogastroduodenoscopy revealed normal mucosa. He was managed with octreotide, PPI, and antibiotics. On hospital day 2, he had witnessed gross hematochezia. A nuclear medicine bleeding scan revealed no active bleeding, and hemoglobin remained at 9.5. A colonoscopy revealed 2 linear ulcers in the rectum, explaining his hematochezia, and 2 sharp metallic objects in the cecum, found to be straight edge razor blades. The patient denied foreign body ingestion. The Psychiatry team was consulted, & a diagnosis of factitious disorder was made. Discussion: Factitious disorder is a psychiatric condition in which a patient intentionally feigns symptoms or produces physical harm to assume the role of the sick, without motivation for secondary gain. Presentation can vary, from reporting symptoms that do not exist to self-inflicting physical harm: 1) toxic ingestions (esophagitis/gastritis from corrosive agents); and 2) foreign body ingestions (presentation and symptoms depend on object ingested, from abdominal pain to GI bleeding to obstruction). Subacute presentations may have vague complaints that mimic other disorders. In the inpatient setting, careful evaluation of the patient's history, physical exam, and diagnostic results must be the first step. When the pieces of the puzzle do not fit - in this case acute upper followed by acute lower GI bleeding - we propose a Gastroenterologist's “Secondary Survey” be performed, as is done in Trauma Surgery to evaluate for initially missed injuries, expanding the differential diagnosis to include potentially inorganic causes, i.e., factitious disorder. Conclusion: Careful performance of the secondary survey combined with adherence to physician practice guidelines for procedural diagnosis of GI bleeding established a diagnostic and therapeutic outcome, minimizing further harm. A gastroenterologist's “Secondary Survey” should be performed in patients whom the clinical presentation does not fit, to include Factitious Disorder as part of an expanded differential diagnosis of gastrointestinal disorders.

Prospective evaluation of anticoagulation and transjugular intrahepatic portosistemic shunt for the management of portal vein thrombosis in cirrhosis

There is no established management algorithm for portal vein thrombosis (PVT) in cirrhotic patients. The aim of our study was to prospectively evaluate anticoagulation and transjugular intrahepatic portosystemic shunt (TIPS) to treat PVT. Cirrhotics with non-malignant PVT were included. Low weight molecular heparin anticoagulation was considered in all; TIPS was indicated if thrombosis progressed or anticoagulation was contraindicated. Patients who were not anticoagulated nor received TIPS served as controls. Fifty-six patients (of whom 21 controls) were included. PVT was occlusive in 11/35, with extension to the superior mesenteric or splenic vein in 13/35. In the study group 33 patients were anticoagulated, with a recanalization rate of 36% (12/33) compared with 1/21 among controls. A time interval between appearance of thrombosis and anticoagulation < 6 months predicted chance of repermeation. Thrombus progression occurred in 15/21 non anticoagulated patients and in 5/33 anticoagulated patients (P < 0.001). TIPS was placed in six patients. There were five variceal bleedings and two intestinal venous ischaemia episodes in the control group, compared with one variceal bleeding episode in the study group. In cirrhotics with PVT, a treatment algorithm using anticoagulation and TIPS achieves a good chance of complete repermeation, reduces portal hypertensive complications, and decreases the rate of thrombosis progression.

Patients Whose First Episode of Bleeding Occurs While Taking a β-Blocker Have High Long-term Risks of Rebleeding and Death

Patients who have their first episode of variceal bleeding despite primary prophylaxis with a nonselective β-adrenergic receptor antagonist (also called a nonselective β-blocker [NSBB]) receive additional treatment by endoscopic band ligation to prevent further bleeding. However, little is known about their long-term outcomes. We collected data on 89 consecutive patients with cirrhosis who were admitted to the Liver Unit of Hospital Clínic, Barcelona, with acute esophageal variceal bleeding between June 2007 and February 2011. Thirty-four patients were receiving primary prophylaxis with NSBBs when they had their first episode of variceal bleeding, whereas 55 were not receiving NSBBs (controls). All patients were subsequently treated with a combination of endoscopic band ligation and NSBBs. Patients were examined after 1, 3, and 6 months and every 6 months thereafter until 2 years. After 2 years, a greater proportion of patients who had their first episode of bleeding while on NSBBs had further bleeding, compared with controls (48% vs 24%; P = .01). Primary prophylaxis with NSBBs and serum levels of bilirubin were independent predictors of rebleeding. Overall, 11 patients died, and 5 underwent liver transplantation. Liver transplantation-free survival was lower among patients who had their first episode of bleeding while taking NSBBs (66% vs 88% for controls; P = .02). Primary prophylaxis with NSBBs and Child-Pugh class were independently associated with liver transplantation-free survival. Patients who have their first episode of variceal bleeding while on primary prophylaxis with a β-blocking agent have an increased risk of further bleeding and death, despite adding endoscopic band ligation. These patients possibly require alternative treatment approaches.

Acute Variceal Bleeding

Bleeding from gastroesophageal varices is a frequent complication of cirrhosis. Mortality from a variceal bleeding episode has decreased in the last 2 decades from 40% to 15 to 20% due to the implementation of effective treatments and improvement in the general medical care. Initial treatment should include adequate fluid resuscitation and transfusion to maintain hemoglobin around 7 to 8 g/dL, and prophylactic antibiotics (norfloxacin or ceftriaxone). It is currently recommended that a vasoactive drug be started as soon as variceal bleeding is suspected. Vasoactive therapy should be maintained for up to 5 days to prevent early rebleeding. Where available, terlipressin, a vasopressin derivative, is the preferred agent because of its safety profile; it represents the only drug with proven efficacy in improving survival. Somatostatin and octreotide are used and are as effective as terlipressin in control of bleeding but have not been shown to reduce mortality. Endoscopic therapy must be performed within the first 12 hours after admission when the patient is stable. Variceal band ligation is the recommended endoscopic treatment, but injection sclerotherapy is an alternative if band ligation is technically difficult. Despite this standard of care, 10 to 20% of patients may still exhibit initial failure to control bleeding or early rebleeding within the first 5 days. In failures to control bleeding the use of rescue transjugular intrahepatic portosystemic shunt (TIPS) using covered stents is the best alternative. In mild early rebleeding a second course of endoscopic therapy may be attempted. If rebleeding is severe, placement of TIPS using covered stents is the first-choice rescue treatment. In refractory variceal bleeding episodes, balloon tamponade may be used as a temporary bridge to TIPS. Identification of patients that are at high risk of treatment failure may guide new strategies to improve outcomes. Indeed, a recent trial has shown that placement of TIPS, using covered stents, within 72 hours of admission in patients at high risk of treatment failure (i.e., those Child B with active bleeding or Child C less than 14 points) markedly decreased rebleeding and improved survival.

Gastric variceal bleeding caused by an intrahepatic arterioportal fistula that formed after liver biopsy: a case report and review of the literature

An intrahepatic arterioportal fistula is a rare cause of portal hypertension and variceal bleeding. We report on a patient with an intrahepatic arterioportal fistula following liver biopsy who was successfully treated by hepatectomy after unsuccessful arterial embolization. We also review the literature on symptomatic intrahepatic arterioportal fistulas after liver biopsy. A 48-year-old male with bleeding gastric varices and hepatitis B virus-associated liver cirrhosis was transferred to our hospital; this patient previously underwent percutaneous liver biopsies 3 and 6 years ago. Abdominal examination revealed a bruit over the liver, tenderness in the right upper quadrant, and splenomegaly. Ultrasonographic examination, computed tomography, and angiography confirmed an arterioportal fistula between the right hepatic artery and the right portal vein with portal hypertension. After admission, the patient suffered a large hematemesis and developed shock. He was treated with emergency transarterial embolization using microcoils. Since some collateral vessels bypassed the obstructive coils and still fed the fistulous area, embolization was performed again. Despite the second embolization, the collateral vessels could not be completely controlled. Radical treatment involving resection of his right hepatic lobe was performed. For nearly 6 years postoperatively, this patient has had no further episodes of variceal bleeding.

Medical Management of Chronic Liver Diseases (CLD) in Children (Part II)

Treatment of the causes of many chronic liver diseases (CLDs) may not be possible. In this case, complications must be anticipated, prevented or at least controlled by the best available therapeutic modalities. There are three main goals for the management of portal hypertension: (i) prevention of the first episode of variceal bleeding largely by non-selective β-adrenoceptor antagonists, which is not generally recommended in children; (ii) control of bleeding by using a stepwise approach from the least to most invasive strategies; (iii) and prevention of re-bleeding using bypass operations, with particular enthusiasm for the use of meso-Rex bypass in the pediatric population. Hepatic encephalopathy management also consists of three main aspects: (i) ruling out other causes of encephalopathy; (ii) identifying and treating precipitating factors; and (iii) starting empiric treatment with drugs such as lactulose, rifaximin, sodium benzoate, and flumazenil. Treatment of mild ascites and peripheral edema should begin with the restriction of sodium and water, followed by careful diuresis, then large-volume paracentesis associated with colloid volume expansion in severe cases. Empiric broad spectrum antimicrobial therapy should be used for the treatment of spontaneous bacterial peritonitis, bacterial and fungal sepsis, and cholangitis, after taking appropriate cultures, with appropriate changes in therapy after sensitivity testing. Empirical therapies continue to be the standard practice for pruritus; these consist of bile acid binding agents, phenobarbital (phenobarbitone), ursodeoxycholic acid, antihistamines, rifampin (rifampicin), and carbamazepine. Partial external biliary diversion can be used in refractory cases. Once hepatorenal syndrome is suspected, treatment should be initiated early in order to prevent the progression of renal failure; approaches consist of general supportive measures, management of concomitant complications, screening for sepsis, treatment with antibiotics, use of vasopressin analogs (terlipressin), and renal replacement therapy if needed. Hepatopulmonary syndrome and portopulmonary hypertension are best managed by liver transplantation. Provision of an adequate caloric supply, nutrition, and vitamin/mineral supplements for the management of growth failure, required vaccinations, and special care for ensuring psychologic well-being should be ensured. Anticoagulation might be attempted in acute portal vein thrombosis. Some CLDs, such as extrahepatic biliary atresia (EHBA), Crigler-Najjar syndrome, and Indian childhood cirrhosis, require special considerations. For EHBA, Kasai hepatoportoenterostomy is the current standard surgical approach in combination with nutritional therapy and supplemental fat and water soluble vitamins, minerals, and trace elements. In type 1 Crigler-Najjar syndrome, extensive phototherapy is the mainstay of treatment, in association with adjuvant therapy to bind photobilirubin such as calcium phosphate, cholestyramine, or agar, until liver transplantation can be carried out. Treating Indian childhood cirrhosis with penicillamine early in the course of the disease and at doses similar to those used to treat Wilson disease decreases the mortality rate by half. New hopes for the future include extracorporeal liver support devices (the molecular adsorbent recirculating system [MARS®] and Prometheus®), hepatocyte transplantation, liver-directed gene therapy, genetically engineered enzymes, and therapeutic modalities targeting fibrogenesis. Hepapoietin, a naturally occurring cytokine that promotes hepatocyte growth, is under extensive research.

P36 Morbidity and mortality associated with varices in patients with primary biliary cirrhosis

IntroductionSeveral studies have shown that gastro-oesophageal varices (GOV) are relatively common in patients with PBC, and can occur in pre-cirrhotic and asymptomatic patients as well as in patients with advanced...

Recurrent bleeding of parastomal varices: Case report

Bleeding of parastomal varices is an unusual complication of portal hypertension. We report a case with recurrent parastomal variceal bleeding who had chronic liver disease secondary to autoimmune hepatitis and who had undergone abdominoperineal resection for rectal cancer. She presented four episodes of parastomal variceal bleeding in one month and was successfully treated with combined polidocanol and cyanoacrylate glue.

Histological subclassification of cirrhosis using the Laennec fibrosis scoring system correlates with clinical stage and grade of portal hypertension

Further histological subclassification of cirrhosis may be useful because of heterogeneity of severity within cirrhosis. We aimed to determine the relationship between histological subclassification and clinical stage of cirrhosis as well as grade of portal hypertension. One hundred-twenty-three biopsy-proven cirrhosis patients, whose clinical stage of cirrhosis and hepatic venous pressure gradient (HVPG) could be estimated, were included in this prospective study. Histology of cirrhosis was blindly subclassified using the Laennec fibrosis scoring system semi-quantitatively without knowledge of the clinical stage or the HVPG results. The Laennec system subclassifies cirrhosis as mild - thin septa, moderate - at least two broad septa, and severe - at least one very broad septum or many minute nodules. Clinical stages were determined by the presence or absence of varices, ascites, and variceal hemorrhage. Biological and laboratory data were also collected. Alcohol intake was the most common cause of cirrhosis in this cohort (87, 70.7%). Histology of cirrhosis subclassified using the Laennec scoring system significantly correlated with both the clinical stage of cirrhosis (p < 0.001) and HVPG (mild: 8.1 ± 2.6 mm Hg, moderate: 12.4 ± 3.3mm Hg, severe: 16.3 ± 4.0 mm Hg, p < 0.001). With higher grades of histological subclassification of cirrhosis, increased frequency in both severe portal hypertension (HVPG ≥ 12 mm Hg) and episodes of variceal hemorrhage were observed (p < 0.001). Histological subclassification of cirrhosis by the Laennec fibrosis scoring system is tightly correlated with both the clinical stage of cirrhosis and grade of portal hypertension. This suggests that cirrhosis should be subclassified into different stages according to its histological severity.

Noncirrhotic portal hypertension in HIV infection

Liver disease in the HAART era is one of the leading causes of morbidity and mortality in HIV-infected individuals in Western countries. Even if the majority of cases rely on identifiable causes (viral hepatitis, steatohepatitis, alcohol abuse, drug toxicity, etc.), the cause of liver abnormalities remains unknown for a subset of patients, some of whom present with noncirrhotic portal hypertension (NCPH). In 2006, the first reports of NCPH in HIV-infected patients attracted special attention. Typically, individuals unaware of any underlying liver illness presented with variceal bleeding, occasionally fatal. Interestingly, severe portal hypertension occurred in the absence of liver function impairment in most cases. Liver biopsy revealed a distinctive histological feature characterized by massive absence of portal veins along with focal obliteration of small portal veins. After extensive ruling out of other causes, the role of antiretroviral toxicity (particularly didanosine exposure) emerged as the major contributor to this condition. Other potential factors could be an enhanced microbial translocation from the gut and prothrombotic conditions. NCPH is an uncommon condition, although increasingly being reported in HIV-infected individuals. It generally presents as a clinical episode of decompensated portal hypertension, generally with gastrointestinal bleeding. Long-lasting HIV infection and prolonged antiretroviral exposure are universally recognized in these patients. The involvement of didanosine has been highlighted in most series. Removal of this drug and prevention of variceal bleeding episodes are currently the most effective prophylactic and therapeutic interventions.

Prognostic markers in patients who have recovered from an acute variceal bleeding: role of HVPG measurement.

Variceal bleeding is one of the most severe complications of cirrhosis which despite recent advances in its management, still carries a high mortality. This situation is especially important in those patients surviving a first episode of variceal bleeding who are at higher risk of recurrent bleeding with an estimated 60% risk within one year after the first bleeding episode. Therefore, prevention of rebleeding remains a very important issue in the management of variceal bleeding. However, the risk of rebleeding is not homogeneous through the overall spectrum of bleeding patients, suggesting the need to stratify the rebleeding risk and to adjust the intensity of therapy according to this risk. In this manuscript we will review the utility of HVPG measurement in variceal rebleeding and its potential impact in tailoring therapy.

Low‐molecular‐weight heparin in patients with advanced cirrhosis

The use of low-molecular-weight heparins (LMWH) in patients with advanced liver diseases is frequently avoided because of the enhanced risk of bleeding complications. However, many patients with impaired liver function are at a high risk of thrombosis or have an indication for therapeutic anticoagulation. Therefore, the aim of this study was to evaluate the pharmacokinetics of LMWH in patients with cirrhosis. Eighty-four consecutive patients with cirrhosis and a clinical indication for prophylactic or therapeutic anticoagulation were included. The LMWH doses were chosen according to current guidelines. Antifactor Xa activity (anti-Xa) was assessed on two consecutive days, 4 h after drug administration. The severity of liver disease was quantified using Child-Turcotte-Pugh score, the MELD score and clinical features and was correlated with the anti-Xa value and the occurrence of complications. Antifactor Xa activity was negatively correlated with the severity of the liver disease, and a positive correlation was observed between antithrombin-III (AT) levels and anti-Xa value. AT itself was negatively correlated with the severity of liver disease. Seven patients had an episode of variceal bleeding. No patient died during the observation interval and no thromboembolic events occurred. Prophylactic use of LMWH in patients with cirrhosis appears to be safe. A decreased anti-Xa value in cirrhotic patients and a negative correlation with liver function challenge the unconditional use of anti-Xa assays in LMWH monitoring in cirrhotic patients and reveals a potential limitation of anti-Xa analysis in these patients. Low levels of AT, because of reduced hepatic synthesis, are the most likely cause of this phenomenon.

High doses of β-blockers and alcohol abstinence improve long-term rebleeding and mortality in cirrhotic patients after an acute variceal bleeding

We analysed prognostic indicators of long-term outcome in cirrhotic patients surviving the critical 6-week period after an episode of acute variceal bleeding. All patients with oesophageal variceal bleeding from 2001-2007 were prospectively registered. Follow-up extended from day 42 after index bleeding to last visit, death or liver transplantation (LT). Multivariate Cox regression analysis was performed. Two hundred and fifty variceal bleeding episodes were registered. Fifty-four patients (26%) died before day 42, and 123 patients were finally included. Median follow-up was 23.5 months. Nadolol+/-nitrates alone or combined with variceal ligation were used as prophylaxis in 93% of patients. During follow-up, 43 patients (35%) experienced rebleeding, 34 (27.5%) died and 10 (8%) were transplanted. Follow-up beta-blocker dose (HR 0.993, 95% CI 0.987-0.998, P=0.027) and alcohol abstinence (HR 0.324, 95% CI 0.152-0.691, P=0.004) were independent rebleeding predictors. The Cox analysis disclosed the Child-Pugh score (HR 1.24, 95% CI 1.08-1.43, P=0.002), creatinine (HR 1.82, 95% CI 1.17-2.82, P=0.008), beta-blocker dose (HR 0.992, 95% CI 0.987-0.997, P=0.003), viral cirrhosis (HR 2.72, 95% CI 1.31-5.67, P=0.008), hepatocellular carcinoma (HR 9.44, 95% CI 3.54-25.20, P<0.001) and alcohol abstinence (HR 0.29, 95% CI 0.13-0.62, P=0.002) to be independent prognostic markers for mortality/LT. High doses of beta-blockers and alcohol abstinence decrease rebleeding and mortality in cirrhotic patients surviving the 6-week period after acute variceal bleeding.

T1006 Poor Adherence to Guidelines for Prevention of Recurrent Variceal Bleeding Among Veterans

Background: Variceal hemorrhage is the most lethal complication of cirrhosis, with 20% mortality rate within the first 6 weeks. When untreated, the risk of rebleeding is as high as 60% within 2 years. Guidelines have been proposed by the AASLD to prevent recurrence of variceal hemorrhage. We hypothesize that adherence to these guidelines is suboptimal at this Veterans Affairs Hospital. Aims: (1) To determine the proportion of patients who adhered to current AASLD guidelines for secondary prophylaxis of variceal bleeding, (2) to identify barriers to adherence and (3) to compare outcomes between patients who were compliant and those non-compliant with the guidelines. Methods: All cirrhotic patients presenting to the NF/SGVHS with an index episode of esophageal variceal bleeding between 1/1/2000 and 12/31/ 2008 were identified. Individual charts were reviewed. Primary endpoints were rebleeding or death. Statistical analyzes were performed as appropriate. Results: 67 male patients were included, mean age 59 years old (range 35-81), and followed for a mean of 18.7 months (range 0-85). Beta-blockers were initiated prior to discharge in 55 patients (82%). After index EVL, GI recommended repeat EGD in 46/67 (69%), EGD was ordered prior to discharge in 37/67 (55%), and performed within the guideline recommended 7-14 days in only 4/67 (6%). 18/67 (27%) had EVL within 30 days. Reasons for nonadherence were: MD did not order EGD in 16/32 (50%), patient cancelled in 13/32 (41%) and clinic cancelled in 3/32 (9%). Regardless of the interval between EGDs, 26 patients achieved eradication of varices, and only 9 (13.4%) had follow-up EGD for confirmation of eradication. In all, 26 patients (38.8%) suffered a rebleeding episode, and 51 (76%) were deceased by the end of the study period. Rebleeding rate was 25% of those re-scoped within 2 weeks, 35.7% of those re-scoped within 15-30 days, and 40% of the remaining patients (p=NS). There was also no difference in rebleeding rate according to eradication status. However, mortality was higher among patients who did not achieve eradication (55% vs. 21%, p= 0.0011). Conclusion: Only a negligible proportion of patients undergo appropriate secondary prophylaxis for esophageal variceal bleeding and this poor adherence is associated with increased mortality. Further efforts should be directed toward strategies to provide guideline concordant care should be targeted towards educating providers and identifying patient centered barriers to adherence. One strategy we are exploring is the creation of an order set for EGD scheduling prior to discharge.

T1007 Survey of Current Opinions and Practices in Hepatitis C

Background: Variceal hemorrhage is the most lethal complication of cirrhosis, with 20% mortality rate within the first 6 weeks. When untreated, the risk of rebleeding is as high as 60% within 2 years. Guidelines have been proposed by the AASLD to prevent recurrence of variceal hemorrhage. We hypothesize that adherence to these guidelines is suboptimal at this Veterans Affairs Hospital. Aims: (1) To determine the proportion of patients who adhered to current AASLD guidelines for secondary prophylaxis of variceal bleeding, (2) to identify barriers to adherence and (3) to compare outcomes between patients who were compliant and those non-compliant with the guidelines. Methods: All cirrhotic patients presenting to the NF/SGVHS with an index episode of esophageal variceal bleeding between 1/1/2000 and 12/31/ 2008 were identified. Individual charts were reviewed. Primary endpoints were rebleeding or death. Statistical analyzes were performed as appropriate. Results: 67 male patients were included, mean age 59 years old (range 35-81), and followed for a mean of 18.7 months (range 0-85). Beta-blockers were initiated prior to discharge in 55 patients (82%). After index EVL, GI recommended repeat EGD in 46/67 (69%), EGD was ordered prior to discharge in 37/67 (55%), and performed within the guideline recommended 7-14 days in only 4/67 (6%). 18/67 (27%) had EVL within 30 days. Reasons for nonadherence were: MD did not order EGD in 16/32 (50%), patient cancelled in 13/32 (41%) and clinic cancelled in 3/32 (9%). Regardless of the interval between EGDs, 26 patients achieved eradication of varices, and only 9 (13.4%) had follow-up EGD for confirmation of eradication. In all, 26 patients (38.8%) suffered a rebleeding episode, and 51 (76%) were deceased by the end of the study period. Rebleeding rate was 25% of those re-scoped within 2 weeks, 35.7% of those re-scoped within 15-30 days, and 40% of the remaining patients (p=NS). There was also no difference in rebleeding rate according to eradication status. However, mortality was higher among patients who did not achieve eradication (55% vs. 21%, p= 0.0011). Conclusion: Only a negligible proportion of patients undergo appropriate secondary prophylaxis for esophageal variceal bleeding and this poor adherence is associated with increased mortality. Further efforts should be directed toward strategies to provide guideline concordant care should be targeted towards educating providers and identifying patient centered barriers to adherence. One strategy we are exploring is the creation of an order set for EGD scheduling prior to discharge.