Management of varices and variceal hemorrhage in cirrhosis.

Variceal hemorrhage is a lethal complication of cirrhosis, particularly in patients in whom clinical decompensation (i.e., ascites, encephalopathy, a previous episode of hemorrhage, or jaundice) has already developed. Practice guidelines for the management of varices and variceal hemorrhage1 in cirrhosis are mostly based on evidence in the literature that has been summarized and prioritized at consensus conferences...

Non-invasive diagnostic and prognostic evaluation of liver cirrhosis and portal hypertension.

Cirrhosis is the final stage of most of chronic liver diseases, and is almost invariably complicated by portal hypertension, which is the most important cause of morbidity and mortality in these patients. This review will focus on the non-invasive methods currently used in clinical practice for diagnosing liver cirrhosis and portal hypertension. The first-line techniques include physical examination, laboratory parameters, transient elastography and Doppler-US. More sophisticated imaging methods which are less commonly employed are CT scan and MRI, and new technologies which are currently under evaluation are MR elastography and acoustic radiation force imaging (ARFI). Even if none of them can replace the invasive measurement of hepatic venous pressure gradient and the endoscopic screening of gastroesophageal varices, they notably facilitate the clinical management of patients with cirrhosis and portal hypertension, and provide valuable prognostic information.

Self-expandable metal stents in the treatment of acute esophageal variceal bleeding.

Acute variceal bleeding (AVB) is a life-threatening complication in patients with cirrhosis. Hemostatic therapy of AVB includes early administration of vasoactive drugs that should be combined with endoscopic therapy, preferably banding ligation. However, failure to control bleeding or early rebleed within 5 days still occurs in 15-20% of patients with AVB. In these cases, a second endoscopic therapy may be attempted (mild bleeding in a hemodynamically stable patient) or we can use a balloon tamponade as a bridge to definitive derivative treatment (i.e., a transjugular intrahepatic portosystemic shunt). Esophageal balloon tamponade provides initial control in up to 80% of AVB, but it carries a high risk of major complications, especially in cases of long duration of tamponade (>24 h) and when tubes are inserted by inexperienced staff. Preliminary reports suggest that self-expandable covered esophageal metallic stents effectively control refractory AVB (i.e., ongoing bleeding despite pharmacological and endoscopic therapy or massive bleeding precluding endoscopic therapy) with a low incidence of complications. Thus, covered self-expanding metal stents may represent an alternative to the Sengstaken-Blakemore balloon for the temporary control of bleeding in treatment failures. Further studies are required to determine the role of this new device in AVB.

Estudio del estado bucodental del paciente trasplantado hepático

Desde que se realizó en España el primer trasplante hepático en el año 1984 los avances en la técnica quirúrgica y en los fármacos inmunosupresores empleados han producido un aumento en el número de pacientes trasplantados. El objetivo del presente estudio fue valorar el estado bucodental de los pacientes trasplantados hepáticos. Se realizó un estudio descriptivo transversal de una muestra de pacientes que habían sido sometidos a un trasplante hepático en el Hospital Príncipes de España de la Ciudad Sanitaria y Universitaria de Bellvitge (L Hospitalet de Llobregat - Barcelona). Los datos recogidos fueron los de filiación, los de la historia médica general, los de la historia bucodental y los de la exploración intrabucal. En total fueron examinados 53 individuos, 28 hombres y 25 mujeres, con una edad media de 57,6 años. El tiempo medio del trasplante fue de 3 años y 9 meses. La causa más frecuente del trasplante hepático fue la cirrosis hepática por el virus de la hepatitis C (49,1%). Los inmunosupresores más utilizados fueron la ciclosporina y el tacrolimus. El índice CAOD de la muestra fue de 11,2. En cuanto a la patología periodontal, el 22% de los pacientes dentados presentaban agrandamiento gingival, la mitad de los dentados tenían recesiones gingivales y el 34% presentaban algún tipo de movilidad dentaria. A la exploración de la mucosa bucal, la patología más prevalente fue la lengua fisurada (39,6%), la lengua saburral (28,3%) y la xerostomía (18,9%). La patología bucodental de estos pacientes está relacionada con el uso de fármacos inmunosupresores y de otros factores tales como la falta de medidas preventivas. Los datos de este estudio demuestran que sería necesario instaurar tratamientos preventivos en este grupo de población

Revisión de la insuficiencia venosa de las extremidades inferiores. Estudio de un caso

La misión principal de la circulación venosa es el drenaje hacia el corazón del CO2 y demás catabolitos originados por el metabolismo celular para su posterior depuración pulmonar, hepática o renal.

Terutroban, A TP-receptor antagonist, reduces portal pressure in cirrhotic rats.

Increased production of vasoconstrictive prostanoids, such as thromboxane A2 (TXA2 ), contributes to endothelial dysfunction and increased hepatic vascular tone in cirrhosis. TXA2 induces vasoconstriction by way of activation of the thromboxane-A2 /prostaglandin-endoperoxide (TP) receptor. This study investigated whether terutroban, a specific TP receptor blocker, decreases hepatic vascular tone and portal pressure in rats with cirrhosis due to carbon tetrachloride (CCl4 ) or bile duct ligation (BDL). Hepatic and systemic hemodynamics, endothelial dysfunction, liver fibrosis, hepatic Rho-kinase activity (a marker of hepatic stellate cell contraction), and the endothelial nitric oxide synthase (eNOS) signaling pathway were measured in CCl4 and BDL cirrhotic rats treated with terutroban (30 mg/kg/day) or its vehicle for 2 weeks. Terutroban reduced portal pressure in both models without producing significant changes in portal blood flow, suggesting a reduction in hepatic vascular resistance. Terutroban did not significantly change arterial pressure in CCl4 -cirrhotic rats but decreased it significantly in BDL-cirrhotic rats. In livers from CCl4 and BDL-cirrhotic terutroban-treated rats, endothelial dysfunction was improved and Rho-kinase activity was significantly reduced. In CCl4 -cirrhotic rats, terutroban reduced liver fibrosis and decreased alpha smooth muscle actin (α-SMA), collagen-I, and transforming growth factor beta messenger RNA (mRNA) expression without significant changes in the eNOS pathway. In contrast, no change in liver fibrosis was observed in BDL-cirrhotic rats but an increase in the eNOS pathway. CONCLUSION: Our data indicate that TP-receptor blockade with terutroban decreases portal pressure in cirrhosis. This effect is due to decreased hepatic resistance, which in CCl4 -cirrhotic rats was linked to decreased hepatic fibrosis, but not in BDL rats, in which the main mediator appeared to be an enhanced eNOS-dependent vasodilatation, which was not liver-selective, as it was associated with decreased arterial pressure. The potential use of terutroban for portal hypertension requires further investigation.

Effect of meal ingestion on liver stiffness in patients with cirrhosis and portal hypertension.

BACKGROUND AND AIMS: Liver stiffness is increasingly used in the non-invasive evaluation of chronic liver diseases. Liver stiffness correlates with hepatic venous pressure gradient (HVPG) in patients with cirrhosis and holds prognostic value in this population. Hence, accuracy in its measurement is needed. Several factors independent of fibrosis influence liver stiffness, but there is insufficient information on whether meal ingestion modifies liver stiffness in cirrhosis. We investigated the changes in liver stiffness occurring after the ingestion of a liquid standard test meal in this population. METHODS: In 19 patients with cirrhosis and esophageal varices (9 alcoholic, 9 HCV-related, 1 NASH; Child score 6.9±1.8), liver stiffness (transient elastography), portal blood flow (PBF) and hepatic artery blood flow (HABF) (Doppler-Ultrasound) were measured before and 30 minutes after receiving a standard mixed liquid meal. In 10 the HVPG changes were also measured. RESULTS: Post-prandial hyperemia was accompanied by a marked increase in liver stiffness (+27±33%; p<0.0001). Changes in liver stiffness did not correlate with PBF changes, but directly correlated with HABF changes (r = 0.658; p = 0.002). After the meal, those patients showing a decrease in HABF (n = 13) had a less marked increase of liver stiffness as compared to patients in whom HABF increased (n = 6; +12±21% vs. +62±29%,p<0.0001). As expected, post-prandial hyperemia was associated with an increase in HVPG (n = 10; +26±13%, p = 0.003), but changes in liver stiffness did not correlate with HVPG changes. CONCLUSIONS: Liver stiffness increases markedly after a liquid test meal in patients with cirrhosis, suggesting that its measurement should be performed in standardized fasting conditions. The hepatic artery buffer response appears an important factor modulating postprandial changes of liver stiffness. The post-prandial increase in HVPG cannot be predicted by changes in liver stiffness.

Resultados del tratamiento de la hemorragia digestiva alta por varices esofagogástricas

Introducción: el tratamiento de la hemorragia digestiva alta por rotura de varices esofágicas y/o gástricas en pacientes con cirrosis hepática debe estar dirigido al control inicial de la hemorragia sin alterar más una función hepática ya deteriorada , y a la prevención de la recidiva hemorrágica precoz. Métodos endoscópicos, farmacológicos y quirúrgicos forman el conjunto de alternativas terapéuticas. Material y métodos: estudio prospectivo de los resultados obtenidos tras el seguimiento de 90 episodios hemorrágicos de un total de 54 pacientes, 35 hombres y 19 mujeres, con una edad media de 58 años (32-77), sobre los que se aplicó un protocolo terapéutico de la hemorragia aguda secundaria a la hipertensión portal, durante un periodo de 22 meses. La clasificación según Child-Pugh al ingreso fue 57% Child A, 34% Child B y 9% Child C. Resultados: la estancia media hospitalaria fue de 9 días (2-50). De los 90 episodios hemorrágicos, se registraron 15 recidivas hemorrágicas precoces (16,7%). Murieron 12 pacientes (mortalidad del 22,2% por pacientes y del 13,4% por episodios hemorrágicos). Se realizaron 12 intervenciones de urgencias por persistencia de la hemorragia. El 41% de los pacientes reingresaron por recidiva de la hemorragia al menos una vez durante el periodo de seguimiento. Conclusiones: el tratamiento de la hemorragia digestiva alta por varices esófago-gástricas con cirrosis hepática, requiere un conjunto de diferentes tratamientos para obtener la máxima eficacia en el episodio hemorrágico agudo y poder abarcar todas las posibles repercusiones a posteriori; dicho tratamiento debería ser realizado en un centro hospitalario que disponga de material y personal especializado en esta patología. En nuestra experiencia, la cirugía de urgencias, como tratamiento de rescate de la hemorragia persistente o recidivante a corto plazo, sólo tendría lugar en algunos pacientes con una buena función hepática dada su alta morbi/mortalidad