Portal hypertension

Bruet, A., Flngerhut, A., Eugene, C., Fendler, J.P. Varices intestinales et hypertension portale. Gastroenterol. Clin. Biol. 1984 8 725-732... 

Drouhin, F., Fischer, D., Vadrot, J., Denis, J., Johanet, C., Abuaf, N., Feldmann, G., Labayle, D. Hypertension portale idiopathique associee a une collagfeose proche du lupus erythemateirx dissemine. Gastroenterol. Clin. Biol. 1989 13 829-833... 

Leger, L., Lemmgre, G., Premont, M., Salmon, R., Klioua, Z., Battesti, J.-R Hypertension portale au cours de la sarcoidose. Trois observations dont une avec foie fibreux et hepatome malin a stroma osseux. Nouv. Presse Med. 1980 9 1021-1024... 

It is not clearly understood why in some cases oedema without ascites and in other cases ascites without oedema as well as ascites together with oedema or even pleural effusion without ascites occur. Ascites develops most frequently during the course of liver disease (= hepatogenic ascites), in particular in chronic liver diseases with portal hypertension (= portal ascites), (s. tab. 16.7) Various mechanical, biochemical and neural disorders overlap in their effects and pathways, depending on the underlying liver disease. Only rarely is ascites found in diseases with presinusoidal localization of portal hypertension (such as portal vein thrombosis) or with minor restrictions in the synthesis of albumin (as in biliary cirrhosis). Formation of ascites occurs in about 50% of all cirrhotic patients within 10 years of... 

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

Describe the epidemiology and social impact of portal hypertension and cirrhosis. 

List the treatment goals for a patient with portal hypertension and its complications. 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

FIGURE 19-1. The portal venous system. (From Timm EJ, Stragand JJ. Portal hypertension and cirrhosis. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 694, with permission.)... 

Portal hypertension is a consequence of increased resistance to blood flow through the portal vein. Increased resistance is usually due to restructuring of intrahepatic tissue (sinusoidal damage) but may also be caused by presinusoidal damage such as portal vein occlusion from trauma, malignancy, or thrombosis. A third (and the least common) mechanism is outflow obstruction of the hepatic vein. This latter damage is posthepatic, and normal liver structure is maintained. This chapter will focus on portal hypertension caused by intrahepatic damage from cirrhosis. 

Sinusoidal damage from cirrhosis is the most common cause of portal hypertension. The sinusoids are porous vessels within the liver that surround radiating rows of hepatocytes, the basic functional cells of the liver (Fig. 19-2). Progressive destruction of hepatocytes and an increase in fibroblasts and connective tissue surrounding the hepatocytes culminate in cirrhosis. Fibrosis and regenerative nodules of scar tissue... 

Increased intrahepatic resistance to portal flow increases pressure on the entire splanchnic bed an enlarged spleen (splenomegaly) is a common finding in cirrhotic patient and can result in thrombocytopenia due to splenic sequestration of the platelets. Portal hypertension mediates systemic and splanchnic arterial vasodilation through production of nitric oxide and other vasodilators in an attempt to counteract the increased pressure gradient. Nitric oxide causes a fall in systemic arterial pressure unfortunately, this activates both the renin-angiotensin-aldosterone and sympathetic nervous systems and... 

The aim of pharmacologic treatment in portal hypertension is to decrease portal pressure and reduce the effects of sympathetic activation. 

The pathophysiologic mechanisms of portal hypertension and of cirrhosis itself are entwined with the mechanisms of ascites (Fig. 19-3). Cirrhotic changes and the subsequent decrease in synthetic function lead to a decrease in production of albumin (hypoalbuminemia). Albumin is the major intravascular protein involved in maintaining oncotic pressure in the vascular system low serum albumin levels and increased capillary permeability allow fluid to leak from the vascular space into body tissues. This can result in peripheral edema, ascites, and fluid in the pulmonary system. The obstruction of hepatic sinusoids and... 

The splanchnic system drains venous blood from the GI tract to the liver. In portal hypertension there is increased resistance to drainage from the originating organ so collateral vessels (varices) develop in the esophagus, stomach, and rectum to compensate for the increased blood volume. Varices divert blood meant for hepatic circulation back to the systemic circulation this has the unintended deleterious effect of decreasing clearance of medications and potential toxins through loss of first-pass metabolism. Varices are weak superficial vessels, and any additional increase in pressure can cause these vessels to rupture and bleed.15... 

Clinical Presentation of Cirrhosis and Complications of Portal Hypertension... 

The serum albumin-to-ascites gradient is greater than or equal to 1.1 g/dl (11 g/L) in association with portal hypertension. 

FIGURE 19-4. Treatment algorithm for active gastrointestinal bleeding resulting from portal hypertension. (From Schianotd, Bodenheimer HC. Complications of Chronic Liver Disease. In Friedman SL, McQuaid KR, Grendell JH (eds.)... 

Patients with ascites or known varices must be assumed to have portal hypertension and are treated as such, even if direct measurements of portal pressure have not been made.29... 

A value of greater than or equal to 1.1 g/dL (greater than or equal to 11 g/L) identifies portal hypertension as the cause of the ascites with 97% accuracy.22,30 In portal hypertension the ascitic fluid is low in albumin this balances the oncotic pressure gradient with the hydrostatic pressure gradient of... 

Drug therapy for portal hypertension and cirrhosis can alleviate symptoms and prevent complications but it cannot reverse cirrhosis. Drug therapy is available to treat the complications of ascites, varices, spontaneous bacterial peritonitis, hepatic encephalopathy, and coagulation abnormalities. 

Non-selective fi-blockers such as propranolol and nadolol are first-line treatments to reduce portal hypertension. This effect reduces bleeding and decreases mortality in patients with known varices. Use of (1-blockers to prevent variceal formation is controversial. 

Only non-selective p-blockers reduce bleeding complications in patients with known varices. Blockade of P, receptors reduces cardiac output and splanchnic blood flow. 02-Adrenergic blockade prevents p2-receptor-mediated splanchnic vasodilation while allowing unopposed a-adrenergic effects this enhances vasoconstriction of both the systemic and splanchnic vascular beds. The combination of P, and P2 effects makes the non-selective p-blockers preferable to car-dioselective agents in treating portal hypertension.1,36,41... 

Because p-blockers decrease blood pressure and heart rate, they should be started at low doses to increase tolerability. Propranolol is hepatically metabolized, and its half-life and pharmacologic effects are prolonged in portal hypertension. A reasonable starting dose of propranolol is 10 mg two to three times daily. 

Lubel JS, Angus PW. Modern management of portal hypertension. Int Med J 2005 35 45-49. 

Portal hypertension Increased blood pressure within the portal vein that supplies the liver. 

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