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Surgical resection of hepatocellular carcinoma in cirrhotic patients: prognostic value of preoperative portal pressure.

BACKGROUND & AIMS Although resection of hepatocellular carcinoma complicating cirrhosis is restricted to patients with preserved liver function, postoperative hepatic decompensation develops in some patients. The aim of this study was to determine the value of increased portal pressure in the development of postoperative hepatic decompensation. METHODS Twenty-nine cirrhotic patients with Child-Pughs class A disease and hepatocellular carcinoma (all except one < 5 cm) scheduled to undergo resection were evaluated by conventional criteria and by a systemic and hepatic hemodynamic study. Predictors of decompensation were assessed among a series of 44 clinical, analytical, tumoral, and hemodynamic parameters. RESULTS Eleven patients had unresolved decompensation 3 months after surgery. Bilirubin and blood ureic nitrogen levels, platelet count, wedged hepatic venous pressure, hepatic venous pressure gradient, and indocyanine green intrinsic clearance were significantly associated with unresolved decompensation, but only hepatic venous pressure gradient was significant, in the multivariate analysis (P = 0.0001; odds ratio, 1.90; 95% confidence interval, 1.12-3.22). The preoperative gradient of patients with unresolved decompensation was higher than that of patients without it (13.9 +/- 2.4 and 7.4 +/- 3.5 mm Hg, respectively; P < 0.001). CONCLUSIONS Cirrhotics with increased portal pressure are at high risk of hepatic decompensation after resection of hepatocellular carcinoma. Surgical resection should therefore be restricted to patients without portal hypertension.

Relation between portal pressure response to pharmacotherapy and risk of recurrent variceal haemorrhage in patients with cirrhosis

In patients with variceal bleeding as a complication of hepatic cirrhosis, propranolol therapy reduces the risk of recurrent variceal haemorrhage. However, the relation between portal pressure response to pharmacological treatment and clinical events has not been well defined. This relation was prospectively investigated in 69 cirrhotic patients receiving continued propranolol therapy after an episode of variceal bleeding. Hepatic venous pressure gradient (HVPG) was measured before and at 3 months of continued drug therapy. At 3 months HVPG had fallen by 20% or more in 25 patients. During follow-up of 28 (SD 17) months rebleeding occurred in 2 of these 25 patients compared with 23 of 44 who had lesser reductions in HVPG. Cumulative probability of rebleeding at 1, 2, and 3 years was 4%, 9%, and 9% in patients with a decrease in HVPG > or = 20%, and 28%, 39%, and 66% in patients with a decrease in HVPG < 20% (p < 0.001, log-rank test). On multivariate analysis, a decrease in HVPG > or = 20% was the only independent predictor of rebleeding (relative risk 0.09, 95% CI 0.02-0.41. Of the 8 patients in whom the HVPG fell to 12 mm Hg or less, none rebled. This study suggests that measurement of the HVPG response to pharmacotherapy will provide useful prognostic information on the long-term risk of variceal rebleeding.

Hemodynamic Effects of Acute Changes in Intra-abdominal Pressure in Patients With Cirrhosis

BACKGROUND Changes in intra-abdominal pressure (IAP) have significant circulatory effects. However, whether this may influence the gastroesophageal collateral blood flow in patients with cirrhosis has not been studied. METHODS In 14 portal hypertensive cirrhotics, serial hemodynamic measurements were obtained in baseline conditions 30 minutes after the mechanical increase of IAP by 10 mm Hg and 30 minutes after returning IAP to baseline levels. RESULTS Increasing IAP caused similar increases in free and wedged hepatic venous pressures (+10.3 mm Hg and +11.0 mm Hg, respectively; P < 0.005), without changing the hepatic venous pressure gradient (HVPG). However, there were significant decreases in cardiac output (-18%; P < 0.005) and hepatic blood flow (-20%; P < 0.05), whereas azygos blood flow, an index of gastroesophageal collateral blood flow, increased markedly (+23%; P < 0.005). The opposite occurred after releasing the high IAP. CONCLUSION In portal hypertensive cirrhotics, acute changes in IAP did not change HVPG but markedly modified splanchnic and systemic hemodynamics. Brief elevations of IAP may have deletereous effects, as shown by the increase in azygos blood flow and the decrease in cardiac output and hepatic blood flow, whereas reduction of a high IAP causes the opposite changes and may be beneficial.

Effects of Ethanol Consumption on Hepatic Hemodynamics in Patients With Alcoholic Cirrhosis

BACKGROUND & AIMS Increased portal blood flow represents a compensatory mechanism preventing hepatic hypoxia after ethanol consumption. In addition, alcohol increases hepatic vascular resistance. Thus, ethanol consumption, by increasing hepatic vascular resistance and portal flow, may worsen portal hypertension in patients with cirrhosis. The aim of this study was to investigate the effects of ethanol consumption on hepatic hemodynamics in patients with alcohol-induced cirrhosis. METHODS Measurements of hepatic venous pressure gradient (HVPG), azygos blood flow, hepatic blood flow, heart rate, and arterial pressure were obtained in 16 patients with alcohol-induced cirrhosis and portal hypertension before and after random administration of a noncaloric fruit drink (250 mL, n = 7) or of an identical beverage plus 0.5 g/kg of ethanol (n = 9). RESULTS Vehicle caused no effects. By contrast, ethanol increased HVPG (P < 0.0001). The increase in HVPG was maximum at 15 minutes and remained significant at 45 minutes (P < 0.05 vs. vehicle). Ethanol increased azygos blood flow (P < 0.05) without changes in hepatic blood flow. Heart rate and arterial pressure slightly increased. CONCLUSIONS Oral ethanol consumption increases portal pressure and portocollateral blood flow in patients with alcohol-induced cirrhosis. These findings suggest that even moderate alcohol consumption worsens the portal-hypertensive syndrome and, therefore, may increase the risk of variceal bleeding in patients with alcohol-induced cirrhosis.

Análisis del curso clínico de la pancreatitis aguda hipertrigliceridémica y su comparación con el de la litiásica

Fundamento y objetivo La hipertrigliceridemia es una causa aceptada de pancreatitis aguda, pero su curso clinico no esta bien definido. Ademas, la presencia de suero lipemico puede interferir en la determinacion de las enzimas pancreaticas y dificultar el diagnostico. El objetivo fue analizar el comportamiento clinico de las pancreatitis agudas por hipertrigliceridemia y el valor diagnostico de la determinacion serica de las enzimas pancreaticas en esta enfermedad. Pacientes y metodo Se analizaron retrospectivamente 31 datos demograficos, clinicos y analiticos de 19 pancreatitis agudas por hipertrigliceridemia y se compararon con los de 19 pancreatitis agudas de etiologia litiasica sin hipertrigliceridemia. El diagnostico de pancreatitis aguda se realizo cuando existian un cuadro clinico y datos radiologicos y/o laparotomicos compatibles. Se considero que habia pancreatitis aguda por hipertrigliceridemia cuando la cifra de trigliceridos era superior a 1.000 mg/dl y se excluian otras etiologias. Se considero que habia pancreatitis aguda litiasica cuando los calculos eran identificados por ultrasonografia, la cifra de trigliceridos era inferior a 200 mg/dl y no existia consumo de alcohol. Resultados Las pancreatitis agudas por hipertrigliceridemia presentaban, respecto a las pan creatitis agudas litiasicas, antecedentes familiares y personales de hipertrigliceridemia (9 frente a 0), mas episodios previos de pancreatitis (13 frente a 2), mayor numero de complicaciones (29 frente a 5) y de pancreatitis graves (13 frente a 5). No hubo mortalidad en ningun grupo. Las cifras de amilasa y lipasa apoyaron el diagnostico en el 26 y el 58% de las pancreatitis agudas por hipertrigliceridemia, frente al 58 y el 79% de las pancreatitis agudas litiasicas, respectivamente. Las pancreatitis agudas por hipertrigliceridemia precisaron de un mayor tiempo de hospitalizacion (24 [45] frente a 7,6 [3,1] dias; p = NS). No se han identificado factores demograficos ni analiticos que permitan predecir la gravedad de las pancreatitis agudas por hipertrigliceridemia. Conclusiones Las pancreatitis agudas por hipertrigliceridemia suelen ser recidivantes y su curso clinico es mas grave que el de las pancreatitis agudas litiasicas. Las cifras de amilasa y lipasa son menos utiles para el diagnostico de pancreatitis agudas hipertrigliceridemicas que en el de las litiasicas.

Nicardipine increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis

The present study investigated the hemodynamic effects of nicardipine, a new calcium channel blocker, and placebo in 14 patients with cirrhosis. Sixty minutes after nicardipine administration (20 mg orally; n = 8), there was a significant increase in hepatic blood flow (25 +/- 21%; p < 0.05) and azygos blood flow (33 +/- 40%; p < 0.05) but no significant change in the hepatic venous pressure gradient. As a result of the increase in hepatic blood flow and the lack of change in the hepatic venous pressure gradient, nicardipine significantly reduced hepatic sinusoidal resistance (-14 +/- 15%; p < 0.05). Enhanced liver perfusion was associated with a significant increase in the hepatic clearance of indocyanine green (from 241 +/- 81 to 265 +/- 92 ml/min, p < 0.05). A mild, well-tolerated decrease in mean arterial pressure (-10 +/- 6%, p < 0.05), without significant changes in cardiac output, systemic vascular resistance and heart rate, was also observed. Placebo administration (n = 6) did not cause significant changes in systemic or hepatic hemodynamics. The results of the present study show that nicardipine, unlike other calcium channel blockers, effectively increases hepatic blood flow and the hepatic clearance of indocyanine green in patients with cirrhosis. The acute beneficial effects of nicardipine should be confirmed in chronic studies.

Effects of end-to-side portacaval shunt and distal splenorenal shunt on systemic and pulmonary haemodynamics in patients with cirrhosis

Background : Patients with cirrhosis exhibit splanchnic, peripheral and pulmonary vasodilation, which are thought to play a role in increasing portal pressure, promoting sodium retention and determining arterial hypoxaemia. The present study investigated whether these abnormalities are influenced by portal hypertension or by portal systemic shunting.