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Cirrhosis peritonitis

Cirrhosis Peritoneal Cefotaxime Regimen based on organism isolated 1. Add clindamycin or metronidazole if anaerobes are suspected 2. Other third-generation cephalosporins, extended-spectrum penicillins, aztreonam, and imipenem as alternatives 3. Aminoglycoside with antipseudomonal penicillin... [Pg.1135]

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. [Pg.213]

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. [Pg.323]

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... [Pg.323]

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... [Pg.326]

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. [Pg.331]

Primary peritonitis generally is caused by a single organism (.Staphylococcus aureus in patients undergoing continuous ambulatory peritoneal dialysis (CAPD) and Escherichia coli in patients with cirrhosis). [Pg.1129]

O Primary peritonitis develops in up to 25% of patients with alcoholic cirrhosis.3 Patients undergoing continuous ambulatory peritoneal dialysis (CAPD) average one episode of peritonitis every 2 years.4 Secondary peritonitis may be caused by perforation of a peptic ulcer traumatic perforation of the stomach, small or large bowel, uterus, or urinary bladder appendicitis pancreatitis diverticulitis bowel infarction inflammatory bowel disease cholecystitis operative contamination of the peritoneum or diseases of the female genital tract such as septic abortion, postoperative uterine infection, endometritis, or salpingitis. Appendicitis is one of the most common causes of intraabdominal infection. In 1998, 278,000 appendectomies were performed in the United States for suspected appendicitis.5... [Pg.1130]

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. [Pg.64]

Runyon BA, Squier SU, Borzio M Transloca-tion of gut bacteria in rats with cirrhosis to mesenteric lymph nodes partially explains the pathogenesis of spontaneous bacterial peritonitis. J Hepatol 1994 21 792-796. [Pg.65]

Runyon BA, Borzio M, Young S, Squier SU, Guarner C, Runyon MA Effect of selective intestinal decontamination with norfloxacin on spontaneous bacterial peritonitis, translocation, and survival in an animal model of cirrhosis. Hepatology 1995,21 1719-1724. [Pg.65]

Ascites is the pathologic accumulation of lymph fluid within the peritoneal cavity. It is one of the earliest and most common presentations of cirrhosis. [Pg.252]

Peritoneal dialysis Cirrhosis with ascites Nephrotic syndrome Secondary bacterial peritonitis... [Pg.470]

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). [Pg.402]

In compensated cirrhosis, sodium retention can occur in the absence of vasodilatation and effective hypovolaemia. Sinusoidal portal hypertension can reduce renal blood flow even in the absence of haemodynamic changes in the systemic circulation, suggesting the existence of a hepatorenal reflex. Portal hypertension increases the hydrostatic pressure within the hepatic sinusoids and favours transudation of fluid into the peritoneal cavity. [Pg.351]

The use of lUDs in patients with CLD has complicating factors. Owing to reduced hepatic complement synthesis and reticuloendothelial system dysfunction, patients with cirrhosis and ascites are prone to develop repeated episodes of spontaneous bacterial peritonitis (SBP). Historically, the risk of pelvic inflammatory disease (PID) was considered to be increased in lUD users during the first year after insertion, therefore it was thought that the presence of an lUD in approximation with the peritoneal surface in a patient with cirrhotic ascites might lead to SBP... [Pg.287]

Spontaneous bacterial empyema is found in 1-2% of patients with cirrhosis and ascites. The diagnosis is based on a positive bacterial test in the pleural fluid and a WBC count in excess of 250/mm (or a negative bacterial culture with a cell count exceeding 500/mm ) - which is analogous to spontaneous bacterial peritonitis. (105) (s. p. 302)... [Pg.299]

Spontaneous bacterial peritonitis (SBP) (H.O. Conn, 1964, 1971) is the term used to describe bacterially infected ascitic fluid in liver cirrhosis where the exact source of infection or path of infection is not known. [Pg.302]

Arroyo, V., Navasa, M., Rimola, A. Spontaneous bacterial peritonitis in liver cirrhosis. Treatment and prophylaxis. Infection 1994 22 (Suppl. 31) 167-175... [Pg.318]

Dlnis-Rlbeiro, M., Cortez-Pinto, H., Marlnho, R., Valente, A., Ral-mundo, M., Salgado, M.J., Ramalho, F., Alexandrlno, P., Carnelro-de-Moura, M. Spontaneous bacterial peritonitis in patients with hepatic cirrhosis evaluation of a treatment protocol at specialized units. Rev. Espan. Enferm. Dig. 2002 94 478-481... [Pg.318]

Llovet, JJM., Rodrignez-Igleslas, R, Moltlnho, E., Planas, R, Bataller, R., Navasa, M., Menacho, M., Pardo, A., Castells, A., Cabre, E., Arroyo, V., GassnU, MA., Rodes, J. Spontaneous bacterial peritonitis in patients with cirrhosis undergoing selective intestinal decontamination. X Hepatol. 1997 26 88-95... [Pg.318]

Mlhas, A.A., Tonssaint, J., Sh Hsu, H., Dotherow, R, Achord, J.L. Spontaneous bacterial peritonitis in cirrhosis clinical and laboratory features, survival and prognostic indicators. Hepato-Gastroenterol. 1992 39 520- 522... [Pg.318]

Sort, R, Navasa, M., Arroyo, V., Aldeguer, X., Planas, R., Lulz-del-Arbol, L., Castells, L., Vargas, V., Soriano, G., Guevara, M., Gines, R, Rodes, J. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. New Engl. J. Med. 1999 341 403-409... [Pg.318]

Nair, S., Kumar, K.S., Sachan, P., Corpuz, M. Spontaneous fungal peritonitis (Candida glabrata) in a patient with cirrhosis. J. Clin. Gastroenterol. 2001 32 362-364... [Pg.509]

Complications such as variceal bleeding, hepatic encephalopathy, ascites and infections as well as reduced renal function also influence the mortality rate of liver cirrhosis (in Germany some 25,000/year). The main causes of death are hepatic coma or liver failure (25-40%), bleeding (20-30%), infections (about 10%) and HCC (about 5%). Spontaneous bacterial peritonitis is fatal in 50-70%, and with liver dysfunction even in 90% of cases. Occurrence of the hepatorenal syndrome is almost invariably fatal. [Pg.740]

Fig. 37.1 Grey-coloured, medium-coarse tubercular cirrhosis in haemochromatosis with hepatocellular carcinoma in the foreground, white, flat tumour granuloma of the right hepatic lobe with vascularization at the tumour margin and small cancer umbilicus in the background, two additional tumour granulomas. Carcinomas infiltrating the peritoneal serosa in the right upper abdomen... Fig. 37.1 Grey-coloured, medium-coarse tubercular cirrhosis in haemochromatosis with hepatocellular carcinoma in the foreground, white, flat tumour granuloma of the right hepatic lobe with vascularization at the tumour margin and small cancer umbilicus in the background, two additional tumour granulomas. Carcinomas infiltrating the peritoneal serosa in the right upper abdomen...
The penetration of routinely used fluoroquinolones into ascitic fluid after intravenous administration has been studied in patients with uncompensated hepatic cirrhosis (125). Three patients received three doses of ciprofloxacin 200 mg, six received three doses of ciprofloxacin 300 mg, seven received three doses of pefloxacin 400 mg, and six received three doses of ofloxacin 400 mg. Pefloxacin and ofloxacin produced serum and ascitic fluid concentrations above the MICs of the common pathogens that cause spontaneous bacterial peritonitis, and the authors concluded that... [Pg.1402]

Eosinophilia occurred in a 35-year-old man with alcoholic cirrhosis taking norfloxacin 400 mg bd for prophylaxis of spontaneous bacterial peritonitis (5). [Pg.2583]

Trauma (and other causes of acute blood loss), C third-spacmg of fluid (e.g., burns, pancreatitis, peritonitis), vomiting, diarrhea, diuretics, renal or adrenal (i.e., sodium wasting) disease v Heart failure, hepatic cirrhosis, nephrotic syndrome, iatrogenic (intravenous fluid overload) ... [Pg.1748]


See other pages where Cirrhosis peritonitis is mentioned: [Pg.235]    [Pg.235]    [Pg.202]    [Pg.330]    [Pg.1130]    [Pg.36]    [Pg.55]    [Pg.505]    [Pg.155]    [Pg.508]    [Pg.532]    [Pg.731]    [Pg.733]    [Pg.736]    [Pg.857]    [Pg.1379]   


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