Retrograde Flow of Portal Vein Blood in Patients with Cirrhosis

Abstract

In 1907, Herrick demonstrated that hepatic arterial flow could reflux into the portal vein (1). Spontaneous reversal of portal vein flow in patients with cirrhosis can occur only when the hepatic outflow resistence exceeds the resistance through portal venous collaterals and probably represents an advanced stage of portal hypertension. This report confirms the occasional existence of hepatofugal flow of portal venous blood in patients with cirrhosis and describes the radiographic characteristics of umbilical vein portograms demonstrating this phenomenon. Angiograms obtained from 2 of 150 patients with cirrhosis of the liver who had umbilical vein portography form the basis of this communication. Method The technic of umbilical vein catheterization has been previously reported (2, 3). This approach to the portal venous system is used whenever splenic puncture fails to demonstrate a portal vein or cannot be carried out because of contraindications, technical difficulties, or prior splenectomy. Umbilical vein catheterization has also been performed in patients with bleeding esophageal varices who were too ill to withstand a major surgical procedure, in order to monitor the response of the portal pressure to conservative modalities, such as thoracic duct lymph drainage (4), vasopressin (5), and extracorporeal umbilicosystemic shunts (6). Results The injection of a radiopaque substance, under pressure, through an umbilical vein catheter results in dispersion of the agent throughout the intrahepatic portal venous system. In patients without cirrhosis, the contrast medium rarely refluxes caudad in the portal vein but progresses cephalad through the liver. In patients with cirrhosis and portal hypertension, the contrast material refluxes caudad in the portal vein and into splenic, mesenteric, and coronary collaterals (Fig. 1, A). Angiograms obtained several seconds after completion of the injection show opacification of the liver as the medium passes through hepatic sinusoids (Fig. 1, B). Figure 2 illustrates a portogram series obtained from a patient with cirrhosis of the liver and bleeding esophageal varices, who had an umbilical vein catheter inserted to monitor the response of the portal pressure to vasopressin. This patient had ascites, muscle wasting, encephalopathy, prothrombin time of twenty-one seconds, serum bilirubin of 16.4 mg/100 ml and serum albumin of 2.0 g/100 ml. The vasopressin reduced the portal pressure 10 cm and controlled the bleeding. The patient was eventually discharged from the hospital and is alive twelve months later. Figure 2, A demonstrates the beginning of the portogram as 40 ml of 75 per cent Hypaque is injected at a pressure of 125 p.s.i. The right branch of the portal vein is not visualized, and the contrast material has begun to reflux into the splenic, mesenteric, and coronary veins. Figure 2, B is the portogram obtained at one second.