Ascites treatment

The usual duration of therapy for peritonitis associated with CAPD is 10 to 14 days, but up to 3 weeks of therapy may be required. Antimicrobial therapy should be continued until dialysate fluid is clear, cultures are negative for 2 to 3 days, and the patient is asymptomatic. When parenteral agents are administered, the initial dose would be the same as that for patients with normal renal function, whereas subsequent doses should be much less or given less frequently for renally excreted agents and should account for possible loss through peritoneal dialysis. Serum concentrations should be performed for aminoglycosides and vancomycin. Some studies have demonstrated that for patients with spontaneous bacterial peritonitis associated with cirrhotic ascites, treatment duration may be as short as 5 days when ascitic fluid polymorphonuclear cell counts are used to guide treatment. 

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. 

While all species lost body weight following treatment with 2,3,7,8-TCDD, other signs of toxicity were species dependent. Ascites was seen in mice. Anorexia, dehydration, depression, emaciation, intestinal hemorrhage, and alopecia were seen in dogs. Certain rabbits treated intra-peritoneally with 2,3,7,8-TCDD developed skin lesions typical of those associated with acnegens. 

The goals of treating ascites are to minimize acute discomfort, re-equilibrate ascitic fluid, and prevent SBP. Treatment should modify the underlying disease pathology without directed therapy, fluid will rapidly reaccumulate. 

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

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. 

The patient should be evaluated for clinical signs of ascites and managed with pharmacologic treatment (e.g., diuretics) and paracentesis. Careful... 

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. 

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. 

Pleural effusions or ascites In patients with significant third space accumulations, evacuate the fluid before treatment and monitor plasma methotrexate levels. Psoriasis lesions Lesions of psoriasis may be aggravated by concomitant exposure to ultraviolet radiation. Radiation dermatitis and sunburn may be recalled by the use of methotrexate. 

Beside this dermatoxic activity pederin (147) has various biological activities (92). When administered in appropriate doses to partially hepatectomized rats, this compound stimulates development of hepatic tissues. The inhibitory effect at the cellular level has been found in chicken heart fibroblast cultures, and mice embryo, dog kidney, HeLa, and KB cell lines. In plants, root growth of Lupinus albus is inhibited and mitosis in Allium cepa blocked at the metaphasic stage. Also, pederin (147) inhibits protein synthesis and growth of yeast cells. In addition, the treatment of rat ascites sarcoma with purified extracts of P. fuscipes produces almost complete regression. 

OKT-3 was first approved for general medical use in the USA in 1986. Its indication was the treatment of acute kidney transplant rejection (Table 10.4). OKT-3 is produced via ascites grown in mice. The intact antibody is subsequently purified by a combination of ammonium sulphate fractionation and anion exchange chromatography. Despite its therapeutic effectiveness, the product does display some limitations. Its antigenicity in humans (the HAMA response) is one obvious factor which limits its prolonged use. 

This can be divided into treatment for the complications ascites, neuropsychiatric disease and variceal bleeding and specific treatments for, in particular, copper and iron retention, and for biliary and autoimmune disease. 

Diuretics, typically spironolactone, form the main therapy, combined with restricted salt intake. Sodium restriction is usually unnecessary where fluid retention is mild, and if marked limitation (less than 40 mmol per day intake) is imposed, may lead to impaired nutrition and is poorly accepted. Diuretic treatment often requires reinforcement with loop diuretics. Treatment can be maintained if urinary sodium excretion is at least 30 mmol per day. Removal of ascites through diuresis requires fluid transfer through the intravascular fluid compartment. If diuresis is too intense the intravascular fluid volume is reduced and hypotension causes hepatorenal failure to follow. The aim should be, through monitoring weight loss, to restrict fluid removal to 0.5 kg per day. In this way the risks of hyponatraemia, renal and hepatic impairment should be reduced. 

Hepato-renal syndrome rapid progressive (type I) with rising serum creatinine levels, or non-progressive and less severe (type II) impairment of renal function, often consequent on bacterial peritonitis, with persistent ascites responds to vasoconstrictor treatment, typically with terlipressin through constriction of splanchnic vessels and improved renal perfusion. Withdrawal of treatment does not seem to lead inevitably to recurrence. Haemodialysis may also stabilise patients. 

Peritonitis infection of ascitic fluid, characteristically by gram negative organisms without an obvious cause, is common in patients with increasing ascites, and is diagnosed by raised ascitic polymorphonuclear cell counts. Treatment with third generation cephalosporins, or amoxicillin and clavulanic acid is effective. Concurrent albumin supplementation helps prevent renal failure. 

Azizov KhA (1998) Surgical treatment of the patients with a liver cirrhosis in conditions portal hypertension decompensation with ascite syndrome. MD Thesis (in Russian) Tashkent, Uzbekistan, p 45... 

In animals, the first in vivo experiments were performed with bacterial extracts in a guinea pig sarcoma model by Gratia and Linz [88], and with LPS in mouse primary subcutaneous tumors by Shear and Turner [4], The antitumoral effect of LPS on the growth of subcutaneous or intramuscular tumors has been extensively investigated [61,147-153], On ascitic tumors, treatment with LPS was shown to be efficient in some cases [153-155] while failing in others [61,156],... 

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