Portal hypertension ascites and

Lieberman, F.L., Denison, E.K., Reynolds, T.B. The relationship of plasma volume, portal hypertension, ascites, and renal sodium retention in cirrhosis the overflow theory of ascites formation. Ann. N. Y Acad. Sci. 1970 170 202-206... 

Ascites is the effusion and accumulation of fluid in the abdominal cavity. Ascites is the most common chnical finding in patients with portal hypertension. Ascites itself is not life threatening, but is uncomfortable and may compromise respiration (from upward displacement of the diaphragm and compression of the lungs). It also predisposes individuals to spontaneous bacterial peritonitis, which is life threatening. 

Hepatic cirrhosis may be associated with portal hypertension, ascites, encephalopathy, spontaneous bacterial peritonitis, and hepatocellular carcinoma. Portal hypertension is directly responsible for the formation of esophageal varices, which may give rise to massive upper gastrointestinal bleeding. Therapy is aimed at correcting hypovolemic shock and at achieving hemostasis at the bleeding site. 

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. 

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... 

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... 

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. 

Garcia-Tsao G Current management of the complications of cirrhosis and portal hypertension Variceal hemorrhage, ascites, and spontaneous bacterial peritonitis. Gastroenterology 2001 120 726-748. 

The resulting resistance to blood flow results in portal hypertension and the development of varices and ascites. Hepatocyte loss and intrahepatic shunting of blood results in diminished metabolic and synthetic function, which leads to hepatic encephalopathy (HE) and coagulopathy. 

Cirrhosis results in elevation of portal blood pressure because of fibrotic changes within the hepatic sinusoids, changes in the levels of vasodilatory and vasoconstrictor mediators, and an increase in blood flow to the splanchnic vasculature. The pathophysiologic abnormalities that cause it result in the commonly encountered problems of ascites, portal hypertension and esophageal varices, HE, and coagulation disorders. 

The treatment of ascites secondary to portal hypertension includes abstinence from alcohol, sodium restriction, and diuretics. Sodium chloride should be restricted to 2 g/day. 

Portal hypertension most commonly occurs as a consequence of chronic liver disease. Portal hypertension Is caused by Increased blood flow within the portal venous system and increased resistance to portal flow within the liver. Splanchnic blood flow is increased in patients with cirrhosis due to low arteriolar resistance that is mediated by increased circulating vasodilators and decreased vascular sensitivity to vasoconstrictors. Intrahepatic vascular resistance is increased in cirrhosis due to fixed fibrosis within the spaces of Disse and hepatic veins as well as reversible vasoconstriction of hepatic sinusoids and venules. Among the consequences of portal hypertension are ascites, hepatic encephalopathy, and the development of portosystemic collaterals—especially gastric or esophageal varices. Varices can rupture, leading to massive upper gastrointestinal bleeding. 

Alcoholics with chronic liver disease may have disorders of fluid and electrolyte balance, including ascites, edema, and effusions. These factors may be related to decreased protein synthesis and portal hypertension. Alterations of whole body potassium induced by vomiting and diarrhea, as well as severe secondary aldosteronism, may contribute to muscle weakness and can be worsened by diuretic therapy. Some alcoholic patients develop hypoglycemia, probably as a result of impaired hepatic gluconeogenesis. Some alcoholics also develop ketosis, caused by excessive lipolytic factors, especially increased cortisol and growth hormone. 

This patient illustrates a complicated clinical course of oq-antitrypsin deficiency. Our patient had liver disease that presented during infancy and developed into hepatic cirrhosis. He exhibited most of the complications of cirrhosis, including portal hypertension with ascites, hyperammonemia, malnutrition, and variceal hemorrhage. These complications of cirrhosis are not unique to a,-antitrypsin deficiency, but it is important to note the potential severity of the liver disease associated with this condition. 

Mrs MW presented with a swollen abdomen, swollen ankles, pitting oedema and breathlessness. There are two key factors involved in the pathogenesis of ascites formation, namely, sodium and water retention and portal hypertension. 

A 31-year-old white man with depression, hepatitis C, and cirrhosis of the liver was hospitalized for alcohol detoxification. He had taken methadone 50 mg bd for opium dependence for 6 months. He developed bilateral pedal edema and 27 kg weight gain. There was no ascites, portal hypertension, or congestive heart failure. Most of his laboratory tests were within the reference ranges, except for reduced prothrombin time and platelet count. After stopping alcohol, his methadone dose was reduced to 60 mg/day his edema resolved 15 days later. When the dose of methadone was increased to 70 mg/day there was a progressive increase in the edema. When methadone was withdrawn his edema completely resolved and he lost 8 kg in 2 weeks. 

This is the presence of excess fluid in the peritoneal cavity, leading to a swollen abdomen (Figure 4.3). The accumulation of ascitic fluid represents a state of sodimn excess in the body. Patients often present with hyponatraemia, but this is thought to be due to the dilutional effect of excess water rather than to low sodium. There are three theories of the cause of ascites formation. The underfill theory suggests that there is a reduction in circulating plasma volume as a result of accumulation in the splanchnic area due to vascular dilatation in portal hypertension. This activates the plasma renin, aldosterone and sympathetic nervous systems, which leads to sodium and water retention by the kidneys. 

Both drugs are gastric irritants and should probably be avoided in patients with varices or a history of variceal bleeding or coagulopathy, or a risk thereof. Niacin can also cause thrombocytopenia. This patient has a varix and would be at risk of a variceal bleed if decompensation occurred. Niacin and acipimox also commonly cause pruritus. They are also vasodilators and may potentiate the effect of drugs that lower blood pressure (spironolactone, propranolol, furosemide), which are used to treat ascites and portal hypertension. 

BUSULFAN TIOGUANINE t risk of nodular regenerative hyperplasia of the liver, oesophageal varices and portal hypertension Mechanism uncertain Monitor liver function and for clinical and biochemical indices of liver toxicity (e.g. ascites, splenomegaly). Ask patients to report any symptoms suggestive of oesophageal bleeding... 

Ascites and oedema are due to portal venous hypertension together with decreased plasma colloid osmotic pressure causing hyperalodosteronism as with nephrotic oedema (above). Furthermore, diversion of renal blood flow from the cortex to the... 

Jalan R, Hayes P C 1997 Hepatic encephalopathy and ascites. Lancet 350 1309-1315 Krige J E J, Beckingham IJ 2001 Portal hypertension — 1 varices. British Medical Journal 322 348-351 also Portal hypertension — 2 ascites, encephalopathy, and other conditions. 322 416—418 Koff R S 1998 Hepatitis A. Lancet 351 1643-1649 Lauer G M, Walker B D 2001 Hepatitis C virus infection. 

The most frequent cause of posthepatic portal hypertension is right ventricular insufficiency. The central venous pressure is transferred to the hepatic veins and the sinusoids. Constrictive pericarditis leads to a state of pronounced posthepatic portal hypertension with the early development of ascites. Severe tricuspid valve incompetence also culminates in this condition. A membranous obstruction of the inferior vena cava was likewise described in 1968 as a genetically determined cause of posthepatic portal hypertension (S. Yamamoto et al.). Three variants can be distinguished by angiography, depending on the different ways in which the hepatic veins are involved or whether they are affected at all. Thrombosis of the inferior vena cava can develop either from thrombosis of the pelvic veins or independently in the presence of predisposing factors. 

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