ASGE Guideline: the role of endoscopy in the management of variceal hemorrhage, updated July 2005

Qureshi, Waqar; Adler, Douglas G.; Davila, Raquel E.; Egan, James; Hirota, William K.; Leighton, Jonathan A.; Rajan, Elizabeth; Fanelli, Robert D.; Wheeler-Harbaugh, Jo; Baron, Todd H.; Faigel, Douglas O.

doi:10.1016/j.gie.2005.07.031

Cited by 123 publications

(70 citation statements)

References 58 publications

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“…2 Because there is an effective treatment to prevent variceal hemorrhage, practice guidelines have recommended screening patients with cirrhosis for varices with EGD. [4][5][6][7] However, the adherence of practicing gastroenterologists to these guidelines is unsatisfactory, as shown by two recent studies. 20,21 There has been considerable interest in developing noninvasive markers of GEV to decrease the burden of EGD and provide a diagnostic indicator for clinicians with respect to the selection and timing for screening EGD.…”

Section: Discussionmentioning

confidence: 99%

“…1 Current guidelines recommend screening for gastroesophageal varices (GEV) with esophagogastroduodenoscopy (EGD) in all patients with cirrhosis and starting prophylactic therapy in those with medium to large varices. [4][5][6][7] In patients without varices, EGD is repeated in 2-3 years, whereas in patients with small varices, the recommendation is to repeat EGD in 1-2 years. 2 Because of the cost and invasive nature of endoscopic screening, there is interest in developing a noninvasive predictor of the presence and development of GEV that would decrease the number of EGDs performed.…”

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confidence: 99%

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Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

et al. 2007

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Current guidelines recommend esophagogastroduodenoscopy (EGD) in patients with cirrhosis to screen for gastroesophageal varices (GEV). Thrombocytopenia has been proposed as a noninvasive test to predict the presence of GEV. There is no agreement regarding a specific platelet count (PLT) that can reliably predict GEV. The present longitudinal study aims to (1) further investigate the relationship between varices and PLT at the time of endoscopy, (2) investigate whether changes in PLT from the baseline over time can predict the development of GEV, and (3) investigate whether changes in PLT correlate with the hepatic venous pressure gradient (HVPG). A secondary analysis was conducted for 213 subjects with compensated cirrhosis with portal hypertension but without GEV enrolled in a randomized, placebo-controlled, double-blind trial of a nonselective beta-blocker used to prevent GEV. PLTs were obtained every 3 months, and HVPG measurements and EGD were done annually. The PLTs were compared between subjects who did and did not develop GEV. In a median follow-up of 54.9 months, 84 patients developed GEV. PLT was greater than 150,000 in 15% of patients at the development of GEV. A receiver operating curve did not show any PLT with high sensitivity or specificity for the presence of GEV. Subjects with clinically insignificant portal hypertension (HVPG < 10 mm Hg) whose PLT remained greater than 100,000 had a 2-fold reduction in the occurrence of GEV (P ‫؍‬ 0.0374). A significant correlation was found between HVPG and PLT at the baseline, year 1, and year 5 (P < V ariceal hemorrhage is a leading cause of morbidity and mortality in cirrhosis. 1-3 Primary prophylaxis with nonselective beta-blockers and endoscopic therapy with band ligation are effective in preventing variceal hemorrhage in patients with large varices. 1 Current guidelines recommend screening for gastroesophageal varices (GEV) with esophagogastroduodenoscopy (EGD) in all patients with cirrhosis and starting prophylactic therapy in those with medium to large varices. [4][5][6][7] In patients without varices, EGD is repeated in 2-3 years, whereas in patients with small varices, the recommendation is to repeat EGD in 1-2 years. 2 Because of the cost and invasive nature of endoscopic screening, there is interest in developing a noninvasive predictor of the presence and development of GEV that would decrease the number of EGDs performed. The ideal noninvasive marker should be widely available at a reasonable cost, require minimal expertise, be reproducible, and be relatively unaffected by any other factors. A number of clinical, laboratory, and ultrasonographic variables have been considered. 8 However, the accuracy of these variables in predicting varices is currently inadequate to be recommended for clinical practice. 2 As varices are a direct consequence of portal hypertension, it is not surprising that the degree of portal hypertension determined by the hepatic venous pressure gradient (HVPG) has been found to be predictive of the

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

et al. 2007

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“…The upper gastrointestinal endoscopy is safe in pregnancy with a small risk of fetal hypoxia from sedation and patient positioning. The mainstay of treatment remains endoscopic variceal ligation (EVL), [17][18][19] the first case during pregnancy was reported by Starkel et al 20 Endoscopic sclerotherapy has also been reported by a few, [21][22][23][24] however EVL remains the preferred choice as it avoids any potential risk of sclerosant injection. Medical therapy with vasopressors for acute variceal bleeding have a role.…”

Section: Esophageal Varicesmentioning

confidence: 99%

Pregnancy with Portal Hypertension

Aggarwal

Negi

Aggarwal

et al. 2014

Journal of Clinical and Experimental Hepatology

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Even though pregnancy is rare with cirrhosis and advanced liver disease, but it may co-exist in the setting of noncirrhotic portal hypertension as liver function is preserved but whenever encountered together is a complex clinical dilemma. Pregnancy in a patient with portal hypertension presents a special challenge to the obstetrician as so-called physiological hemodynamic changes associated with pregnancy, needed for meeting demands of the growing fetus, worsen the portal hypertension thereby putting mother at risk of potentially life-threatening complications like variceal hemorrhage. Risks of variceal bleed and hepatic decompensation increase many fold during pregnancy. Optimal management revolves round managing the portal hypertension and its complications. Thus management of such cases requires multi-speciality approach involving obstetricians experienced in dealing with high risk cases, hepatologists, anesthetists and neonatologists. With advancement in medical field, pregnancy is not contra-indicated in these women, as was previously believed. This article focuses on the different aspects of pregnancy with portal hypertension with special emphasis on specific cause wise treatment options to decrease the variceal bleed and hepatic decompensation. Based on extensive review of literature, management from pre-conceptional period to postpartum is outlined in order to have optimal maternal and perinatal outcomes. ( J CLIN EXP HEPATOL 2014;4:163-171) P regnancy associated with liver diseases is an infrequent situation, but when seen together, presents a complicated clinical situation. Portal hypertension develops as a result of number of etiologies. In the west, cirrhosis is the commonest cause of portal hypertension. In the setting of cirrhotic portal hypertension, pregnancy is very rare due to hepatocellular damage leading to amenorrhea and infertility, the incidence of cirrhosis in pregnancy has been reported as 1 in 5950 pregnancies. 1 Cirrhosis may get exacerbated during pregnancy and has significant adverse effects on the mother and the baby. [2][3][4] In the developing countries, other causes like extrahepatic portal vein obstruction contribute significantly to noncirrhotic portal hypertension (NCPH). Mostly liver function is much better preserved in women with NCPH and pregnancy is spontaneous in these women. Portal hypertension associated with pregnancy is a high risk situation as both pregnancy and portal hypertension share some of the hemodynamic changes. The physiological changes, in adaptation to the pregnancy and fetal needs, worsen the portal hypertension resulting in potentially life-threatening variceal bleed and other complications. Pregnancy is a potential hazard for occurrence of recurrent variceal bleed due to its hyperdynamic state causing increase in flow to the collaterals. 5-7 Therefore management in pregnancy requires knowledge of both the effects of changes during pregnancy on portal hemodynamics and the effects of portal hypertension and its cause on both mother and fetus, hepatotoxic...

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“…The causes of UGIB have been classified into variceal bleeding (esophageal and gastric varices) and non-variceal bleeding (peptic ulcer, erosive gastroduodenitis, reflux esophagitis, tumor, vascular ectasia, etc). Currently, emergency esophagogastrodu odenoscopy (EGD) is the standard investigation of choice for active UGIB since it provides both diagnosis and treatment of UGIB [2][3][4][5][6][7][8][9][10][11] . However, in the real life situation, emergency EGD is seldom available in most hospitals due to the difficulty of setting up emergency services in non-official time, an insufficiency of well-trained endoscopists and medical teams and lack of equipment.…”

Section: Introductionmentioning

confidence: 99%

Upper gastrointestinal bleeding etiology score for predicting variceal and non-variceal bleeding

Pongprasobchai¹,

Nimitvilai²,

Chasawat³

et al. 2009

WJG

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AIM:To identify clinical parameters, and develop an Upper Gastrointesinal Bleeding (UGIB) Etiology Score for predicting the types of UGIB and validate the score. METHODS:Patients with UGIB who underwent endoscopy within 72 h were enrolled. Clinical and basic laboratory parameters were prospectively collected. Predictive factors for the types of UGIB were identified by univariate and multivariate analyses and were used to generate the UGIB Etiology Score. The best cutoff of the score was defined from the receiver operating curve and prospectively validated in another set of patients with UGIB. RESULTS:Among 261 patients with UGIB, 47 (18%) had variceal and 214 (82%) had non-variceal bleeding. Univariate analysis identified 27 distinct parameters significantly associated with the types of UGIB. Logistic regression analysis identified only 3 independent factors for predicting variceal bleeding; previous diagnosis of cirrhosis or signs of chronic liver disease (OR 22.4, 95% CI 8.3-60.4, P < 0.001), red vomitus (OR 4.6, 95% CI 1.8-11.9, P = 0.02), and red nasogastric (NG) aspirate (OR 3.3, 95% CI 1.3-8.3, P = 0.011).The UGIB Etiology Score was calculated from (3.1 × previous diagnosis of cirrhosis or signs of chronic liver disease) + (1.5 × red vomitus) + (1.2 × red NG aspirate), when 1 and 0 are used for the presence and absence of each factor, respectively. Using a cutoff ≥ 3.1, the sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) in predicting variceal bleeding were 85%, 81%, 82%, 50%, and 96%, respectively. The score was prospectively validated in another set of 195 UGIB cases (46 variceal and 149 non-variceal bleeding). The PPV and NPV of a score ≥ 3.1 for variceal bleeding were 79% and 97%, respectively. CONCLUSION:The UGIB Etiology Score, composed of 3 parameters, using a cutoff ≥ 3.1 accurately predicted variceal bleeding and may help to guide the choice of initial therapy for UGIB before endoscopy.

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ASGE Guideline: the role of endoscopy in the management of variceal hemorrhage, updated July 2005

Cited by 123 publications

References 58 publications

Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

Platelet count is not a predictor of the presence or development of gastroesophageal varices in cirrhosis

Pregnancy with Portal Hypertension

Upper gastrointestinal bleeding etiology score for predicting variceal and non-variceal bleeding

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