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.
Methods: Sixty-one patients with cirrhosis who had haemodynamic measurements before and after end-to-side portacaval shunt (n = 30) or distal splenorenal shunt (n = 31) were evaluated.
Results: End-to-side portacaval shunts were more effective than distal splenorenal shunts in decompressing the portal system (portocaval pressure gradient 3.2 +/- 2.5 vs splenocaval gradient 6.5 +/- 3.2 mmHg, P < 0.0001), because of a greater shunt blood flow (33 +/- 12 vs 21 +/- 12 mL/min per kg, P < 0.005). Azygos blood flow and hepatic blood flow decreased significantly after both surgical shunts. However, end-to-side portacaval shunts caused a greater decrease in peripheral resistance than distal splenorenal shunts (-23 +/- 18 vs -11+/- 27%, P < 0.05). Mean arterial pressure and pulmonary vascular resistance were significantly reduced after an end-to-side portacaval shunt (-7 +/- 10%, P < 0.001 and -14 +/- 33%, P < 0.004, respectively), but not after splenorenal shunt.
Conclusions: These results show that end-to-side portacaval shunts, despite normalizing portal pressure, worsen the peripheral and pulmonary vasodilatation. The splenorenal shunt that maintained a higher portal pressure, caused less peripheral vasodilatation and did not enhance pulmonary vasodilatation. These findings suggest that portal systemic shunting is more important than increased portal pressure in determining peripheral vasodilatation in cirrhosis.