The portal hypertension is responsible for many of the manifestations of liver cirrhosis. Some of these complications are the direct consequences of portal hypertension, such as gastrointestinal bleeding from ruptured gastroesophageal varices and from portal hypertensive gastropathy and colopathy, ascites and hepatorenal syndrome, and hypersplenism. In other complications, portal hypertension plays a key role, although it is not the only pathophysiological factor in their development. These include spontaneous bacterial peritonitis, hepatic encephalopathy, cirrhotic cardiomyopathy, hepatopulmonary syndrome, and portopulmonary hypertension. 1. Introduction Portal hypertension (PH) is a common clinical syndrome defined as the elevation of hepatic venous pressure gradient (HVPG) above 5？mm？Hg. PH is caused by a combination of two simultaneous occurring hemodynamic processes: (1) increased intrahepatic resistance to passage of blood flow through the liver due to cirrhosis and (2) increased splanchnic blood flow secondary to vasodilatation within the splanchnic vascular bed. PH can be due to many different causes at prehepatic, intrahepatic, and posthepatic sites (Table 1). Cirrhosis of the liver accounts for approximately 90% of cases of PH in Western countries. Table 1: Causes of portal hypertension (PH). The importance of PH is defined by the frequency and severity of its complications including variceal bleeding, spontaneous bacterial peritonitis, and hepatorenal syndrome, which represent the leading causes of death and of liver transplantation in patients with cirrhosis. PH is considered to be clinically significant when HVPG exceeds 10 to 12？mm？Hg, since this is the threshold for the clinical complications of PH to appear [1]. Proper diagnosis and management of these complications are vital to improving quality of life and patients’ survival. This paper will review the multisystemic manifestations of PH in cirrhosis. 2. Gastrointestinal Manifestations 2.1. Gastroesophageal (GE) Varices Approximately 5–15% of cirrhotics per year develop varices, and it is estimated that the majority of patients with cirrhosis will develop GE varices over their lifetime. The presence of GE varices correlates with the severity of liver disease; while only 40% of child A patients have varices, they are present in 85% of child C patients (Table 2) [2]. Table 2: Child-Pugh-Turcotte (CPT) Classification of the Severity of Cirrhosis. Collaterals usually exist between the portal venous system and the systemic veins. The resistance in the portal vessels is normally lower than in
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