Cirrhosis ascites

In 110 patients with cirrhosis, ascites, and hyponatremia in a multicenter, double-blind, randomized, placebo-con-trolled study of three fixed doses of satavaptan (5,12.5, or 25 mg/day) for 14 days plus spironolactone 100 mg/day, satavaptan was associated with improved control of ascites. Thirst was the main adverse effect (4). 

Gines et al. (45) monitored 234 patients with cirrhosis, ascites, and a glomerular filtration rate (GFR) of more than 50 mL/min. These authors found that the hepatorenal syndrome developed within 1 year in 18%, and within 5 years in 39%, of these... 

HPI AH is a 57-year-old man who just received an orthotopic liver transplant for hepatitis C cirrhosis. PMH includes hepatitis C cirrhosis, ascites, and hepatic encephalopathy. 

Bone marrow depression, anemia, leukopenia, and basophilic stippling are associated with chronic arsenic exposure. Arsine (AsHj) poisoning can produce widespread hemolysis. Cirrhosis, ascites, and destruction of renal tissues have been reported. Arsine exposure may also cause renal failure (Forth et al. 1996). 

If the patient with kidney failure also has cirrhosis or some other form of hver failure, this additional ammonia load may present a stress that cannot be adequately handled by the diseased liver. The result may be increased blood and central nervous system ammonia levels with development of encephalopathy (Fraser Arieff, 1985). Thus, patients with cirrhosis and end-stage kidney disease are at particular risk for developing encephalopathy since both conditions act synergistically to increase both blood and central nervous system ammonia. It should also be noted that plasma urea and serum creatinine do not always adequately reflect renal function in patients with severe liver disease. Recent studies suggest that many patients who have cirrhosis, ascites, and normal plasma urea and creatinine may in fact have severe renal functional impairment (Gines et al., 1988 Papadakis Arieff, 1987 Takabatake et al., 1988). In such individuals, differentiation of hepatic from uremic encephalopathy on clinical grounds may be difficult. 

Diuretics are one of the dmg categories most frequendy prescribed. The principal uses of diuretics are for the treatment of hypertension, congestive heart failure, and mobilization of edema fluid in renal failure, fiver cirrhosis, and ascites. Other applications include the treatment of glaucoma and hypercalcemia, as well as the alkafinization of urine to prevent cystine and uric acid kidney stones. 

Ascites. Patients with cirrhosis, especially fiver cirrhosis, very often develop ascites, ie, accumulation of fluid in the peritoneal cavity. This is the final event resulting from the hemodynamic disturbances in the systemic and splanchnic circulations that lead to sodium and water retention. When therapy with a low sodium diet fails, the dmg of choice for the treatment of ascites is furosemide, a high ceiling (loop) diuretic, or spironolactone, an aldosterone receptor antagonist/potassium-sparing diuretic. 

Loop diuretics are used in the treatment of edema associated with CHF, cirrhosis of the liver, and renal disease, including the nephrotic syndrome. These drug s are particularly useful when a greater diuretic effect is desired. Furosemide is the drug of choice when a rapid diuresis is needed or if the patient has renal insufficiency. Furosemide and torsemide are also used to treat hypertension. Ethacrynic acid is also used for the short-term management of ascites caused by a malignancy, idiopathic edema, or lymphedema. 

Antimicrobial prophylaxis if ascites/cirrhosis present preferably before endoscopy... 

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 a high aldosterone state spironolactone is a direct aldosterone antagonist and a primary treatment for ascites. 

Ascites is the accumulation of fluid in the peritoneal space and is often one of the first signs of decompensated liver disease. Ascites is the most common complication of cirrhosis and portends a dire prognosis.14... 

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... 

FIGURE 19-3. Factors involved in the development of ascites. NO, nitric oxide. (From Chung RT, Podolsky DK. Cirrhosis and its complications. In Kasper DL, Braunwald E, Fauci AS, et al, (eds.) Harrison s Principles of Internal Medicine. 16th ed. New York McGraw-Hill, 2005 1858-1869, with permission.)... 

Signs and symptoms of SBP in a patient with cirrhosis and ascites should prompt a diagnostic paracentesis (Fig. 19-4). In SBP, there is decreased total serum protein, elevated white blood cell count (with left shift), and the ascitic fluid contains at least 0.250 x 103/mm3 (0.250 x 109/L) neutrophils. Bacterial culture of ascitic fluid may be positive, but lack of growth does not exclude the diagnosis. 

In some cases, cirrhosis is diagnosed incidentally before the patient develops symptoms or acute complications. Other patients may have decompensated cirrhosis at initial presentation they may present with variceal bleeding, ascites, SBP, or HE. Patients may also have some of the laboratory abnormalities and/or signs and symptoms listed above that are associated with cirrhosis.28... 

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. 

The target in treating ascites is to effect a fluid loss of approximately 0.5 L per day.22 Because ascites equilibrates with vascular fluid at a much slower rate than does peripheral edema, aggressive diuresis is associated with intravascular volume depletion and should be avoided unless patients have concomitant peripheral edema. Patients with peripheral edema in addition to ascites may require increasing furosemide doses until euvolemia is achieved intravenous diuretics are often necessary.22 Diuretic therapy in cirrhosis is typically lifelong. 

Blei AT, Cordoba J, and the Practice Parameters Committee of the American College of Gastroenterology. Hepatic encephalopathy practice guidelines. Am J Gastroenterol 2001 96 1968-1976. Gines P, Cardena A, Arroyo V, Rodes J. Management of cirrhosis and ascites. N Engl J Med 2004 350 1646-1654. 

Runyon BA. American Association for the Study of Liver Diseases (AASLD) Practice Guideline Management of adult patients with ascites due to cirrhosis. Hepatology 2004 39 841-856. 

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

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. 

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. 

Ascites is the pathologic accumulation of lymph fluid within the peritoneal cavity. It is one of the earliest and most common presentations of cirrhosis. 

An elevation of prothrombin time was the single most reliable manifestation of cirrhosis. The combination of thrombocytopenia, encephalopathy, and ascites had the highest predictive value. 

Malabsorption of protein and fat occurs when the capacity for enzyme secretion is reduced by 90%. A minority of patients develop complications including pancreatic pseudocyst, abscess, and ascites or common bile duct obstruction leading to cholangitis or secondary biliary cirrhosis. 

Peritoneal dialysis Cirrhosis with ascites Nephrotic syndrome Secondary bacterial peritonitis... 

Decompensated liver disease is complicated by jaundice, refractory ascites, bacterial peritonitis, coagulopathy, and variceal bleeding and may require liver transplantation. The number of liver transplants for decompensated cirrhosis doubled from 1990 to 2004, when 5845 cadaveric (orthotopic) liver transplants were performed (65). 

Other Systemic Effects. No studies were located regarding other effects in humans following inhalation exposure to 1,4-dichlorobenzene. Ascites, esophageal varices, hemorrhoids, and tarry stools are all secondary effects of subacute, yellow atrophy and cirrhosis of the liver (Cotter 1953). 

The diuretic effect of spironolactone develops fully only with continuous administration for several days. Two possible explanations are (1) the conversion of spironolactone into and accumulation of the more slowly eliminated metabolite canrenone (2) an inhibition of aldosterone-stimulated protein synthesis would become noticeable only if existing proteins had become nonfunctional and needed to be replaced by de novo synthesis. A particular adverse effect results from interference with gonadal hormones, as evidenced by the development of gynecomastia (enlargement of male breast). Clinical uses include conditions of increased aldosterone secretion, e.g., liver cirrhosis with ascites. 

Prevention of potassium depletion when dietary intake is inadequate in the following conditions Patients receiving digitalis and diuretics for CHF significant cardiac arrhythmias hepatic cirrhosis with ascites states of aldosterone excess with normal renal function potassium-losing nephropathy certain diarrheal states. 

Dexamethasone Testing of adrenal cortical hyperfunction cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Tnamc/no/one Treatment of pulmonary emphysema where bronchospasm or bronchial edema plays a significant role, and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome) in conjunction with diuretic agents to induce a diuresis in refractory CHF and in cirrhosis of the liver with refractory ascites and for postoperative dental inflammatory reactions. 

Hepatic cirrhosis and ascites In these patients, sudden alterations of electrolyte balance may precipitate hepatic encephalopathy and coma. Do not institute therapy until the basic condition is improved. 

Electrolyte imbalance and BUN increases Hyponatremia and hypochloremia may occur when amiloride is used with other diuretics. Increases in BUN levels usually accompany vigorous fluid elimination, especially when diuretic therapy is used in seriously ill patients, such as those who have hepatic cirrhosis with ascites and metabolic alkalosis, or those with resistant edema. 

Cirrhosis of the liver accompanied by edema or ascites - For maintenance therapy in conjunction with bed rest and the restriction of fluid and sodium. 

Chronic hepatic impairment (cirrhosis) The excretion of ofloxacin may be reduced in patients with severe liver function disorders (eg, cirrhosis with or without ascites). Do not exceed a maximum dose of 400 mg/day. 

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