Portal hypertension is defined as elevation of the hepatic venous pressure gradient to >5 mmHg, which occurs as a consequence of cirrhosis (Chap. 157). It is caused by increased intrahepatic resistance to the passage of blood flow through the liver due to cirrhosis together with increased splanchnic blood flow due to vasodilatation within the splanchnic vascular bed.
TABLE 158-1Classification of Portal Hypertension ||Download (.pdf) TABLE 158-1 Classification of Portal Hypertension
Portal vein thrombosis
Splenic vein thrombosis
Massive splenomegaly (Banti’s syndrome)
Congenital hepatic fibrosis
Hepatic sinusoidal obstruction (venoocclusive syndrome)
Inferior vena caval webs
Severe congestive heart failure
The primary complications of portal hypertension are gastroesophageal varices with hemorrhage, ascites (Chap. 45), hypersplenism, hepatic encephalopathy, spontaneous bacterial peritonitis (Chap. 45), hepatorenal syndrome (Chap. 45), hepatocellular carcinoma (Chap. 72).
About one-third of pts with cirrhosis have varices, and one-third of pts with varices will develop bleeding. Bleeding is a life-threatening complication; risk of bleeding correlates with variceal size and location, the degree of portal hypertension (portal venous pressure >12 mmHg), and the severity of cirrhosis, e.g., Child-Pugh classification (see Table 157-3).
Esophagogastroscopy: procedure of choice for evaluation of upper GI hemorrhage in pts with known or suspected portal hypertension. Celiac and mesenteric arteriography are alternatives when massive bleeding prevents endoscopy and to evaluate portal vein patency (portal vein may also be studied by ultrasound with Doppler and MRI).
TREATMENT Esophagogastric Varices
See Chap. 43 for general measures to treat GI bleeding. CONTROL OF ACUTE BLEEDING
Choice of approach depends on clinical setting and availability.
PREVENTION OF RECURRENT BLEEDING
Endoscopic intervention is employed as first-line treatment to control bleeding acutely. Endoscopic variceal ligation (EVL) is used to control acute bleeding in >90% of cases. EVL is less successful when varices extend into proximal stomach. Some endoscopists will use variceal injection (sclerotherapy) as initial therapy, particularly when bleeding is vigorous.
Vasoconstricting agents: somatostatin or octreotide (50–100 µg/h by continuous infusion).
Balloon tamponade (Sengstaken-Blakemore- or Minnesota tube). Can be used when endoscopic therapy is not immediately available or in pts who need stabilization prior to endoscopic therapy. Complications—obstruction of pharynx, asphyxiation, aspiration, esophageal ulceration. Generally reserved for massive bleeding, failure of vasopressin and/or endoscopic therapy.
Transjugular intrahepatic portosystemic shunt (TIPS)—portacaval shunt placed by interventional radiologic technique, reserved for failure of other approaches; risk of hepatic encephalopathy (20–30%), shunt stenosis or occlusion, infection.
EVL should be repeated until obliteration of all varices is accomplished.
Propranolol or nadolol—nonselective ...