Incidence of large oesophageal varices in patients with cirrhosis: application to prophylaxis of first bleeding.

Calès, Paul; Desmorat, Hervé; Vinel, Jean–Pierre; Caucanas, J. P.; Ravaud, Alain; P, Gerin; Brouet, P; Pascal, Jean‐Pierre

doi:10.1136/gut.31.11.1298

Cited by 192 publications

(81 citation statements)

References 18 publications

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“…Variceal size is identified to be one of the most important factors responsible for first variceal hemorrhage [17] . 10% to 20% of small varices progress in size during one year [18] which is close to 20% to 30% risk of bleeding in first 2-year after first detection [19] . It seems that recognizing patients with elevated risk of bleeding for on time interventions will reduce morbidity and cost in initial diagnosis or periodic intervals thereafter.…”

Section: Discussionmentioning

confidence: 99%

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

Tarzamni¹,

Somi²,

Farhang³

et al. 2008

WJG

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AIM:To evaluate portal hypertension parameters in liver cirrhosis patients with and without esophageal varices (EV). METHODS:A cohort of patients with biopsy confirmed liver cirrhosis was investigated endoscopically and with color Doppler ultrasonography as a possible noninvasive predictive tool. The relationship between portal hemodynamics and the presence and size of EV was evaluated using uni-and multivariate approaches. RESULTS:Eighty five consecutive cirrhotic patients (43 men and 42 women) were enrolled. Mean age (± SD) was 47.5 (± 15.9). Portal vein diameter (13.88 ± 2.42 vs 12.00 ± 1.69, P < 0.0005) and liver vascular index (8.31 ± 2.72 vs 17.8 ± 6.28, P < 0.0005) were found to be significantly higher in patients with EV irrespective of size and in patients with large varices (14.54 ± 1.48 vs 13.24 ± 2.55, P < 0.05 and 6.45 ± 2.78 vs 10.96 ± 5.05, P < 0.0005, respectively), while portal vein flow velocity (13.25 ± 3.66 vs 20.25 ± 5.05, P < 0.0005), congestion index (CI) (0.11 ± 0.03 vs 0.06 ± 0.03, P < 0.0005), portal hypertensive index (2.62 ± 0.79 vs 1.33 ± 0.53, P < 0.0005), and hepatic (0.73 ± 0.07 vs 0.66 ± 0.07, P < 0.001) and splenic artery resistance index (RI) (0.73 ± 0.06 vs 0.62 ± 0.08, P < 0.0005) were significantly lower. A logistic regression model confirmed spleen size (P = 0.002, AUC 0.72) and portal hypertensive index (P = 0.040, AUC 0.79) as independent predictors for the occurrence of large esophageal varices (LEV). CONCLUSION:Our data suggest two independent situations for beginning endoscopic evaluation of compensated cirrhotic patients: Portal hypertensive index > 2.08 and spleen size > 15.05 cm. These factors may help identifying patients with a low probability of LEV who may not need upper gastrointestinal endoscopy.

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Section: Discussionmentioning

confidence: 99%

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

Tarzamni¹,

Somi²,

Farhang³

et al. 2008

WJG

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“…Aunque el riesgo de hemorragia es bajo en pacientes sin varices (1-2% al año) o con varices pequeñas (5% al año), las varices pequeñas tienen una tasa de crecimiento a varices medianas o grandes del 10 al 15% al año, siendo el ritmo mayor en los pacientes con cirrosis de etiología etílica o avanzada (Child-Pugh B-C). Por su parte, las varices grandes tienen un riesgo anual de sangrado del 15% (55)(56)(57). El riesgo medio de presentar al menos un episodio de sangrado en los enfermos con cirrosis y ascitis es del 30%, con el mayor riesgo para aquellos con varices grandes y enfermedad descompensada.…”

Section: Profilaxis Preprimaria De Las Varices Esofágicasunclassified

Profilaxis preprimaria de la hemorragia por varices

González-Alonso

Gómez

Martínez

2007

Rev. esp. enferm. dig.

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INTRODUCCIÓNLas varices esofágicas son una manifestación clínica de la hipertensión portal, cuya causa más frecuente en nuestro medio es la cirrosis. La hemorragia digestiva alta por rotura de varices esofágicas es su complicación más grave, con una mortalidad elevada y una reducción de la supervivencia del 50% al año (1). El tratamiento actual de la hipertensión portal consiste en identificar a los pacientes que presentan varices, para administrar fármacos que al reducir la presión portal, también disminuyan la presión y la tensión variceal y con ello el riesgo de rotura y hemorragia. Otra estrategia que se ha planteado es identificar a los enfermos con presión portal elevada, pero que aún no han desarrollado varices, con objeto de tratarlos con fármacos reductores de la presión portal y así evitar que las varices lleguen a formarse. Este artículo describe las bases fisiopatológicas en las que se fundamenta REV ESP ENFERM DIG (Madrid) Vol. 99. N.°12, pp. 714-721, 2007 Correspondencia: Agustín Albillos Martínez. Servicio de Gastroenterología. Hospital Universitario Ramón y Cajal. Ctra. de Colmenar km 9,600. 28034 Madrid: e-mail: aalbillosm@meditex.es 2007; 99: 714-721. González-Alonso R, Garrido Gómez E, Albillos Martínez A. Profilaxis preprimaria de la hemorragia por varices. Rev Esp Enferm Dig RESUMENLa formación de colaterales portosistémicas, en especial en la unión esofagogástrica, es una de las consecuencias más graves de la hipertensión portal. El aumento de la presión portal es la fuerza más importante que dirige la formación de varices esofagogástri-cas, siendo necesario para que esto ocurra que la presión portal (estimada por el gradiente de presión venosa hepática) alcance un valor mínimo de 10 mmHg. Posteriormente, la hiperemia esplác-nica también contribuye al desarrollo de las varices. Las colaterales portosistémicas se forman por repermeabilización de vasos preexistentes, remodelado vascular y angiogénesis. El objetivo de la profilaxis preprimaria es evitar o retrasar la formación de varices esofagogástricas. En modelos experimentales de hipertensión portal, la administración precoz de vasoconstrictores esplácnicos como los beta-bloqueantes, de inhibidores de la síntesis de óxido nítrico o de sustancias anti-angiogénicas, inhibe la formación de colaterales portosistémicas. Sin embargo, los ensayos clínicos con beta-bloqueantes realizados en pacientes con cirrosis sin varices con objeto de retrasar su formación no han alcanzado los resultados esperados.Palabras clave: Hipertensión portal. Varices esofágicas. Hemorragia digestiva alta. Profilaxis. Cirrosis hepática. ABSTRACTPortosystemic collateral formation, particularly at the gastroesophageal junction, is a most serious consequence of portal hypertension. Increased portal pressure is the most significant force underlying gastroesophageal variceal formation, to which end portal pressure (estimated from the hepatic venous pressure gradient) must reach at least 10 mmHg. Subsequently, splanchnic hyperemia also contributes to variceal development. ...

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“…However, we assumed that small varices progressed to moderate or to large varices at a rate of 10% per year. 4 This estimate was varied from 0% to 50% in our sensitivity analysis.…”

Section: Model Assumptionsmentioning

confidence: 99%

“…The prevalence of moderate or large varices among unstratified cirrhotic patients without a history of variceal hemorrhage has been reported in several trials and ranges from 9% to 50%. [4][5][6][7]17 The mean prevalence of moderate-to-large varices in the subgroup of patients with Child's class A or B cirrhosis is 40%, [4][5][6][7]17 and we adopted this as our base case estimate. Because the precision of this estimate is unlikely to be reproduced between different populations, we varied it from 0% to 100% in our sensitivity analysis.…”

Section: Clinical Inputs and Probability Estimates Derived From Systementioning

confidence: 99%

“…[1][2][3] The most advanced stage of chronic liver disease is cirrhosis, and up to half of patients with Child's class A or B cirrhosis have moderate or large underlying esophageal varices. [4][5][6][7] Once esophageal varices form, the risk of variceal bleeding within 2 years is 20% to 35%, 8,9 and the risk of dying from an initial variceal bleed is up to 50%. 10 In light of the substantial human and economic costs of variceal hemorrhage, several strategies have been developed for the primary prophylaxis against an initial bleed, including ␤-blocker (BB) therapy and endoscopic band ligation (EBL).…”

mentioning

confidence: 99%

See 1 more Smart Citation

Endoscopic screening for esophageal varices in cirrhosis: Is it ever cost effective?

Spiegel

Targownik²,

Dulai³

et al. 2003

Hepatology

142

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Current guidelines for the management of patients with compensated cirrhosis recommend universal screening endoscopy followed by prophylactic ␤-blocker therapy to prevent initial hemorrhage in those found to have esophageal varices. However, the cost-effectiveness of this recommendation has not been established. Our objective was to determine whether screening endoscopy is cost-effective compared with empiric medical management in patients with compensated cirrhosis. Decision analysis with Markov modeling was used to calculate the costeffectiveness of 6 competing strategies: (1) universal screening endoscopy (EGD) followed by ␤-blocker (BB) therapy (EGD3 BB) if varices are present, (2) EGD followed by endoscopic band ligation (EBL) (EGD3 EBL) if varices are present, (3) selective screening endoscopy (sEGD) in high risk patients followed by BB therapy if varices are present (sEGD3 BB), (4) selective screening endoscopy followed by EBL (sEGD3 EBL) if varices are present, (5) empiric ␤-blocker therapy in all patients, and (6) no prophylactic therapy ("Do Nothing"). Cost estimates were from a third-party payer perspective. The main outcome measure was the cost per initial variceal hemorrhage prevented. The "Do Nothing" strategy was the least expensive yet least effective approach. Compared with the "Do Nothing" strategy, the empiric ␤-blocker strategy cost an incremental $12,408 per additional variceal bleed prevented. Compared with the empiric ␤-blocker strategy, in turn, both the EGD3 BB and the EGD3 EBL strategies cost over $175,000 more per additional bleed prevented. The sEGD3 BB and sEGD3 EBL strategies were more expensive and less effective than the empiric ␤-blocker strategy. In conclusion, empiric ␤-blocker therapy for the primary prophylaxis of variceal hemorrhage is a cost-effective measure, as the use of screening endoscopy to guide therapy adds significant cost with only marginal increase in effectiveness. (HEPATOLOGY 2003;37:366-377.)

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Incidence of large oesophageal varices in patients with cirrhosis: application to prophylaxis of first bleeding.

Cited by 192 publications

References 18 publications

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

Portal hemodynamics as predictors of high risk esophageal varices in cirrhotic patients

Profilaxis preprimaria de la hemorragia por varices

Endoscopic screening for esophageal varices in cirrhosis: Is it ever cost effective?

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