Portal hypertension (PHTN) can occur in cirrhotic and noncirrhotic patients and can be classified as presinusoidal or prehepatic (extrahepatic or intrahepatic), sinusoidal or hepatic, or post-sinusoidal or post-hepatic (Fig. 61-1). Portal pressure can be measured directly, or more commonly indirectly, by calculating the hepatic vein pressure gradient (HVPG) by subtracting the measured free hepatic vein pressure (FHVP) from the wedged hepatic vein pressure (WHVP). Portal pressure is normally <6 mm Hg and clinically significant PHTN is defined as an HVPG greater than 10 to 12 mm Hg (Table 61-1).
Portal hypertension and sites of obstruction.
TABLE 61-1PORTAL HYPERTENSION |Favorite Table|Download (.pdf) TABLE 61-1 PORTAL HYPERTENSION
Hepatic vein pressure gradient (HVPG) = Wedged hepatic vein pressure (WHVP) – Free hepatic vein pressure (FHVP)
Normal: HVPG <6 mm Hg
Clinically significant portal hypertension: HVPG >10-12 mm Hg
The most common complications of PHTN include gastroesophageal varices, portal hypertensive gastropathy, splenomegaly and hypersplenism, ascites, hepatic hydrothorax, hepatic encephalopathy, hepatorenal syndrome, hepatopulmonary syndrome, portopulmonary hypertension, and cirrhotic cardiomyopathy (Table 61-2). The management of PHTN has changed dramatically over the past two decades and has been the subject of several clinical practice guideline publications.1 Medical, endoscopic, and radiologic management strategies have largely replaced many surgical procedures such as selective and nonselective shunts, devascularization procedures, and peritoneovenous shunts. This chapter emphasizes the role of current therapies in the management of patients with PHTN and its complications.
TABLE 61-2COMPLICATIONS OF PORTAL HYPERTENSION |Favorite Table|Download (.pdf) TABLE 61-2 COMPLICATIONS OF PORTAL HYPERTENSION
|Gastric varices ||Hepatic encephalopathy |
|Esophageal varices ||Hepatorenal syndrome |
|Portal hypertensive gastropathy ||Hepatopulmonary syndrome |
|Splenomegaly and hypersplenism ||Portopulmonary hypertension |
|Ascites ||Cirrhotic cardiomyopathy |
|Hepatic hydrothorax || |
Although descriptions of PHTN and its complications go back over four centuries, surgical therapy was pioneered by Nicolai Eck, who first performed an end-to-side portacaval shunt in an animal model in 1883.2 Pavlov described hepatic encephalopathy, referred to as meat intoxication at the time, as a consequence of diverting portal flow, which he believed was due to nitrogenous compounds that were not being cleared by the liver. The first portosystemic shunt in a human was performed by Vidal in 1903, but Whipple and colleagues pioneered the era of surgical decompression of portal hypertension in the 1940s. In the 1960s and 1970s, Drapanas developed the mesocaval shunt, Warren and Inokuchi developed selective variceal bed decompression with the distal splenorenal and coronary vein-caval shunts, respectively, Sarfeh studied and popularized small diameter H-grafts, and Sugiura pioneered gastroesophageal devascularization and splenectomy. In the 1980s, endoscopic sclerotherapy and band ligation were introduced for control of variceal hemorrhage. The subsequent development of pharmacologic therapy, transjugular intrahepatic portosystemic shunts (TIPS), and the pioneering work of Starzl and Calne in the 1960s and 1970s, making liver transplantation a viable alternative for patients with end-stage liver ...