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Information on changes in splanchnic hemodynamics after liver transplantation is incomplete. In particular, data on long-term changes are lacking, and the relationship between changes in arterial and portal parameters is still under debate. The effect of liver transplantation on splanchnic hemodynamics was analyzed with echo-Doppler in 41 patients with cirrhosis who were followed for up to 4 years. Doppler parameters were also evaluated in 7 patients transplanted for acute liver failure and in 35 controls. In cirrhotics, portal blood velocity and flow increased immediately after transplantation (from 9.1 plus minus 3.7 cm/sec to 38.3 plus minus 14.6 and from 808 plus minus 479 mL/min to 2,817 plus minus 1,153, respectively, P

The association beta-blockers plus isosorbide-5-mononitrate (I5M) has been proposed for the treatment of portal hypertension in patients with insufficient response to beta-blockers alone, according to hemodynamic criteria. The mechanism of action in these patients is not clearly defined. Fifteen patients with cirrhosis and esophageal varices were evaluated by hepatic venous pressure gradient (HVPG) measurement and duplex-Doppler ultrasonography before and after 1 month of treatment with nadolol. Nine patients who did not exhibit a decrease in HVPG to 12 mm Hg or a percent decrease greater than 20% were classified as poor responders, and were studied again with the same methodology after 3 months of chronic administration of nadolol + I5M 20 mg twice per day. In poor responders, mean HVPG decrease after nadolol was 8.9% +/- 2.8%, and after the combination, it was 25.7% +/- 1.7% (P = .004). All patients except one became good responders to the association. Portal blood flow (PBF) decreased significantly after nadolol (P = .004), and remained unchanged after the addition of nitrates. Resistance to portal blood flow (RPBF) increased after nadolol (P = .02) and returned to baseline values during combined treatment (P = .03). In good responders, an adequate decrease in HVPG was associated with a decrease in PBF (P = .06) but no change in RPBF. A wide spectrum of combined changes in PBF and in RPBF after nadolol was observed in poor responders, ranging from no change in either parameter to a marked decrease in PBF counterbalanced by a marked increase in RPBF. The addition of I5M was followed in most cases by larger effects on resistance than on flow. Doppler parameters were not significantly correlated with the HVPG response to nadolol alone or associated with I5M. It is concluded that good hemodynamic responders to nadolol differ from poor responders in the lack of increase in RPBF after the drug. The addition of nitrates to nadolol is effective in decreasing portal pressure in most poor responders to nadolol alone. A decrease in outflow resistance is the main mechanism involved.

Doppler sonographic portal vein parameters are used for the noninvasive evaluation of portal hypertension in cirrhosis. The patency of a paraumbilical vein is a rather frequent finding in cirrhosis, which may affect hepatic hemodynamics and function. We evaluated portal and hepatic arterial parameters in 184 cirrhotic patients with and without a patent paraumbilical vein and the relationships with paraumbilical blood flow. A patent paraumbilical vein was found in 33.7% of patients. The prevalence was higher (56.8%) in Child C patients. Portal blood flow velocity (PBV) (10.8 ± 2.2 vs. 9.8 ± 2.4 cm/sec; P < .01) and volume (PBF) (995.0 ± 383.8 vs. 811.6 ± 318.7 mL/min; P < .001) were significantly higher, and effective portal liver perfusion (PLP) (portal blood flow-paraumbilical blood flow) (621.3 ± 420.8 vs. 811.6 ± 318.7 mL/min; P < .001) was significantly lower in patients with a patent paraumbilical vein than in those without. These differences were more evident in Child C patients (10.7 ± 2.0 vs. 8.3 ± 2.3 cm/sec; 935.7 ± 378.3 vs. 680.6 ± 239.4 mL/min; 369.0 ± 282.0 vs. 680.6 ± 239.4 mL/min). Portal vein diameter, the congestion index (CI) of the portal vein, hepatic arterial resistance indexes, and the severity of esophageal varices did not differ between the two groups. In patients with a patent paraumbilical vein, the Child-Pugh score and the prevalence of ascites were significantly higher than in those without. In conclusion, the evaluation of PBV and PBF in cirrhotic patients can provide misleading results if a paraumbilical vein is patent, underestimating the degree of portal hypertension. The CI and hepatic arterial resistance indexes are not influenced by the paraumbilical vein patency.

The aim of this study was to assess the interobserver, interequipment, and time-dependent variabilities of echo-Doppler measurements of portal blood flow velocity (PBV), portal vein diameters (PVDs) and their derived parameters, portal blood flow (PBF), and congestion index (CI) in cirrhotic patients. The influence of a cooperative training program of the operators on the reproductibility of the results was also investigated. The echo-Doppler parameters were independently measured in 15 patients by four skilled operators, using four echo-Doppler machines (Acuson, ATL, Hitachi-Esaote, Toshiba. Eight of the 15 patients were restudied after 15 days by the same operators using only one machine. Significantly different values of PBV, PBF, and CI were obtained. PBV variance was equipment-related (32%) and operator-related in a smaller portion (5%). No systematic effect related to the time of investigation was found. After training to define a precise protocol, new measurements were performed by four operators on 8 different patients. No significant differences were found among the operators for any of the parameters and the 95% confidence limits (CL) and coefficients of variation (CV) of PBV showed a marked decrease (CL from +/- 26.4% to +/- 15.6%). These results indicate that (1) a significant systematic variability exists between Doppler measurements with different equipment; (2) there is no significant time-dependent systematic variability of Doppler measurements; and (3) a cooperative training program reduces the interobserver variability for direct measurements, such as PBV.

It has been hypothesized that the magnitude of proximal sodium reabsorption affects the response to aldosterone antagonists in nonazotemic cirrhotic patients with ascites. To verify this hypothesis, we evaluated intrarenal sodium handling by lithium clearance in 51 nonazotemic ascitic cirrhotic patients and in 23 controls who were maintained on the same low-sodium diet (80 mmol/day). Seven of 51 cirrhotic patients underwent spontaneous diuresis, whereas 44 required diuretic treatment. Treatment was started with spironolactone at a dose of 150 mg once daily. The dose was increased to 300 mg and then to 500 mg once daily if no response ensued. Cirrhotic patients who did not experience ascites mobilization with 500 mg spironolactone were then treated with a combined diuretic regimen that included spironolactone at a fixed dose (500 mg once daily) and furosemide at an initial dose of 50 mg once daily. The dose was increased to 100, 150 and 200 mg once daily if no response was noticed. Response to diuretic treatment was defined as body weight loss greater than 700 gm every 3 days until ascites became clinically undetectable. Nonresponders (43%) to spironolactone showed lower sodium fractional excretion (0.34% ± 0.28% vs. 0.80% ± 0.50%; p < 0.001) because of a lower fractional sodium delivery to the distal tubule (18.2% ± 5.8% vs. 23.4% ± 7.2%; p < 0.025) than responders. Moreover, nonresponders showed lower distal sodium reabsorption, both in absolute terms (2,360 ± 723 μEq/min vs. 3,221 ± 960 μEq/min; p < 0.01) and as a percentage of filtered sodium load (17.5% ± 5.7% vs. 23.1% ± 7.6%; p < 0.01) despite higher values of plasma aldosterone (524 ± 542 pg/ml vs. 136 ± 213 pg/ml; p < 0.025). We conclude that unresponsiveness to adequate doses of spironolactone in nonazotemic ascitic cirrhotic patients is related to a pathophysiological condition in which the role of aldosterone in renal sodium retention is limited by markedly enhanced proximal sodium reabsorption. (HEPATOLOGY 1991;14:231–236.)