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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since the introduction of the LeVeen modification of the peritoneovenous shunt (PVS) in 1974, these devices have been placed in a relatively large number of patients. The most common indication has been for medically intractable ascites in the setting of chronic liver disease. A review of a series of studies shows that we can expect approximately an 18% perioperative overall mortality rate, a 46% survival rate at 21 months, and loss of ascites in 59% of the survivors at 18 months. The PVS has not been shown by prospective trials to prolong survival significantly in patients with either intractable ascites or the hepatorenal syndrome (HRS), although it may shorten hospitalizations, compared with medical controls. A few well-documented cases of reversal of the HRS have been documented. The best results of PVS therapy have been evident in those patients with milder liver disease. The loss of ascites need not correlate with a functioning shunt. Alcohol abstinance is associated with hepatic functional recovery and may relate to the disappearance of renal sodium retention, resulting in shunt occlusion due to low flow. A number of serious complications with the PVS have been described. Nutritional repletion follows successful shunting, but might, in part, relate to simultaneous alcohol abstention. The more common complications of coagulopathy and fluid overload are preventable by total ascitic drainage at the time of surgery. Shunt patency remains a clinical problem. Only 18.6% of the total shunts placed functioned in the survivors at 2 yr. Perioperative infections with staphylococcal and Gram-negative organisms occur. Postoperative bacterial peritonitis or septicemia requires shunt removal for cure.
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PMID:The peritoneovenous shunt: expectations and reality. 219 58

In summary, the diagnosis of ascites should be considered in all patients presenting with abdominal distention. A careful history and physical examination should be performed to rule out conditions that mimic ascites. Ultrasonography should be performed in questionable cases of ascites since physical examination and radiographic signs of ascites are unreliable. Paracentesis can help determine the etiology. Ascitic fluid should be examined to rule out spontaneous bacterial peritonitis, one of the few curable complications of cirrhosis. An ascitic fluid PMN count of greater than 250 per mm3 proves a sensitive indicator of infection. Medical treatment of cirrhotic ascites includes dietary sodium restriction and diuretics++. Large-volume paracentesis, with or without the use of colloid infusions, may provide useful adjunctive therapy. In rare instances, intractable ascites may be treated with a peritoneovenous shunt, although the complications and mortality rate of this procedure are significant. Peritoneovenous shunting, however, has not been shown to improve survival.
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PMID:Ascites. 266 63

We studied the functional effects of intraperitoneal sepsis on systemic hemodynamics in general, and on renal function in particular, in sheep in whom bacterial peritonitis was induced by cecal perforation. In the first group of seven sheep (group 1) fluid was administered throughout the period of sepsis to maintain pulmonary capillary wedge pressure as close to presepsis values as possible. These sheep exhibited hemodynamic changes known to be associated with sepsis in man: increased cardiac output and decreased systemic vascular resistance. In a second group of seven sheep (group 2) fluid intake was restricted; compared with group 1, these sheep demonstrated a smaller increase in cardiac output that did not persist and that was associated with an increase in the systemic vascular resistance during the septic period. Plasma renin levels increased fivefold in group 2 but were unchanged in group 1. Serial renal biopsies during the septic period revealed that all sheep had evidence of tubular cell damage on electron microscopy: cell swelling, loss of the microvillous brush border, and cell necrosis. Both groups of sheep also demonstrated marked tubular proteinuria similar to that found in humans with generalized sepsis. Despite this, sheep in group 1 exhibited no functional renal changes: creatinine clearance levels rose slightly from control values, urine concentrating ability was unimpaired, and fractional excretion of sodium increased appropriately in response to a sodium load. In contrast, group 2 sheep exhibited a fall in creatinine clearance levels but fractional sodium excretion did not fall as would have been expected were renal function entirely normal. The results suggest that generalized "hyperdynamic" sepsis induces tubular cell damage and tubular proteinuria by an unknown mechanism. However, this does not necessarily produce renal impairment since the glomerular filtration rate does not fall unless volume contraction is also allowed to occur.
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PMID:Renal and cardiovascular response to nonhypotensive sepsis in a large animal model with peritonitis. 396 24

Although spontaneous bacterial peritonitis is considered a precipitating factor of renal impairment in cirrhosis, no study specifically addressing this problem has been reported. This study was aimed at assessing the incidence, clinical course, predictive factors and prognosis of renal impairment in cirrhotic patients with peritonitis. Therefore, 252 consecutive episodes of spontaneous bacterial peritonitis in 197 patients were analyzed. Clinical and laboratory data obtained before and after diagnosis of peritonitis were considered as possible predictors of renal impairment and hospital mortality. Renal impairment occurred in 83 (33%) episodes, and in every instance it fulfilled the criteria of functional kidney failure. Renal impairment was progressive in 35 episodes, steady in 27 and transient in 21. Blood urea nitrogen and serum sodium concentration before peritonitis and band neutrophils count in blood at diagnosis were independent predictors for the development of renal impairment. Renal impairment was the strongest independent predictor of mortality during hospitalization. Other independent prognostic factors were blood urea nitrogen level before peritonitis, age, positive ascitic fluid culture and serum bilirubin level during infection. These results indicate that renal impairment is a frequent event in cirrhotic patients with spontaneous bacterial peritonitis that occurs mainly in patients with kidney failure before infection. Renal impairment is the most important predictor of hospital mortality in cirrhotic patients with spontaneous bacterial peritonitis.
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PMID:Renal impairment after spontaneous bacterial peritonitis in cirrhosis: incidence, clinical course, predictive factors and prognosis. 798 50

A new method for ascites recirculation, consisting of a cellulose diacetate filter to remove substances with molecular weight > or = 300,000, cell debris and bacteria, followed by the concentration of ascitic fluid prior to i.v. infusion, was used 24 times in 19 patients with cirrhosis and massive or refractory ascites. The amount of ascites removed was 7.67 +/- 0.49 l, which was reduced to 407 +/- 37 ml. The procedure took 367 +/- 22 min to complete. No statistically significant changes in liver function tests, coagulative parameters, platelet count or natremia were found. The activity of coagulation and fibrinolytic systems was further assessed in six patients. No changes suggesting an activation of intravascular coagulation and/or primary fibrinolysis were disclosed. An asymptomatic fall in mean arterial pressure (from 88.6 +/- 2.6 to 80.3 +/- 3.0 mmHg; p = 0.02) occurred after paracentesis and was still present 48 h after ascites reinfusion. Plasma renin activity significantly decreased at the end of the procedure, but was not associated with a proportional reduction of plasma aldosterone concentrations. Both variables returned to baseline values 48 h later. A significant increase in the glomerular filtration rate occurred just after the end of the procedure (from 50.4 +/- 9.1 to 73.1 +/- 23.5 ml/min; p < 0.05) and subsided 48 h later. In contrast, no significant changes in diuresis and renal sodium excretion were found. Complications due to volume overload and sepsis did not occur; in one case, spontaneous bacterial peritonitis developed 3 days after the procedure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ascites apheresis, concentration and reinfusion for the treatment of massive or refractory ascites in cirrhosis. 800 9

Ascites is a manifestation of cirrhosis-induced portal hypertension. Pathogenesis is the result of a complex interaction of mechanical, humoral and neural events. Impaired excretion of sodium by the kidney is a hallmark of ascites, which is addressed by many of the available treatment options. Ascites contributes significantly to the morbidity and mortality rates of cirrhosis by increasing the likelihood of such fatal complications as variceal bleeding, hepatorenal syndrome and spontaneous bacterial peritonitis. Most ascitic patients respond to conservative or medical treatment. Five to 10 percent of the patients are refractory and may be candidates for surgical treatment. Peritoneovenous shunting is effective, and while safety is improved by following certain guidelines, its impact on survival is not clear. Portacaval shunting is also safe and effective. The use is accompanied by a prohibitively high morbidity rate because of encephalopathy, which limits its application despite what seems to be a significant impact on survival.
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PMID:Pathophysiologic factors and management of ascites. 842 10

The pathophysiology of ascites in patients with cirrhosis is complex and includes increases in hepatic sinusoidal pressure, the formation of hepatic and splanchnic lymph, renal sodium retention, and hypoalbuminemia. However, the role of hypoalbuminemia in ascites formation is controversial. Evaluating ascites in hypoalbuminemic patients with nephrotic syndrome could add to our understanding of the role of hypoalbuminemia in ascites development. We conducted a retrospective analysis of 52 adults and 21 children with nephrotic syndrome who were hospitalized in the Hadassah University Hospital on Mount Scopus during 1981-1994. There was a significant difference in the prevalence of ascites between pediatric (52%) and adult patients (23%) (p = 0.024). Pediatric patients had lower serum albumin levels than adults (1.70 +/- 0.08 g/dl vs. 2.10 +/- 0.07 g/dl, p = 0.001). Adult patients with ascites had lower serum albumin levels than adult patients without ascites (1.80 +/- 0.13 g/dl vs. 2.20 +/- 0.07 g/dl, p = 0.01). This difference was not found in pediatric patients. Temporary fluctuations in liver enzymes (up to four times the upper limit of normal for transaminases) were evident in five patients from the pediatric group with ascites, whereas all pediatric patients without ascites had completely normal liver enzymes (p = 0.035). Among the 12 adult patients with ascites, seven had liver disease (three with cirrhosis and four with amyloidosis), and two had right-sided congestive heart failure. Among the 40 adult patients without ascites, only four had liver disease (amyloidosis). The plasma albumin levels of the patients with amyloidosis without ascites were higher than patients with amyloidosis with ascites (1.90 +/- 0.10 g/dl vs. 1.50 +/- 0.07 g/dl, p = 0.03). Two patients with nephrotic syndrome and ascites (one without liver disease) had episodes of spontaneous bacterial peritonitis. Ascites in nephrotic syndrome is more common in children than in adults. Although in most pediatric patients ascites formation is probably a common manifestation of the general fluid retention, in most adult patients with nephrotic syndrome ascites can be attributed to both hypoalbuminemia and the presence of liver disease or congestive heart failure, with increased hepatic sinusoidal pressure.
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PMID:Ascites in Nephrotic syndrome. Incidence, patients' characteristics, and complications. 877 92

Ascites formation in cirrhosis results from the interaction of "local" and "systemic" pathogenetic factors. Among local factors, post-sinusoidal portal hypertension plays the most important role, while the main systemic event is renal sodium retention. The latter precedes ascites formation and leads to plasma volume expansion. Many factors are responsible for renal sodium retention, but secondary hyperaldosteronism and reduced renal perfusion prevail. The events promoting the onset of sodium retention are far from being clarified. However, there is evidence that the main afferent mechanism is represented by the "effective" hypovolemia secondary to splanchnic venous vasodilation, due to portal hypertension, and reduced peripheral vascular resistance, which becomes evident in the advanced stage of the disease. Systemic hemodynamic abnormalities are responsible for the progressive reduction of renal perfusion, which ends in the hepatorenal syndrome. The appearance of ascites is a crucial event in the natural history of cirrhosis and has a negative prognostic meaning. In fact, ascites appears when pathogenetic factors, such as liver function abnormalities, portal and systemic hemodynamics, and renal function, have reached a critical threshold severity. Second, ascites itself induces additional complications, closely linked to its presence, such as spontaneous bacterial peritonitis, restrictive respiratory failure, or rupture of abdominal hernias. Finally, ascites implies pharmacological or invasive treatment which can lead to further morbidity or even to death.
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PMID:[Natural course and physiopathology of ascites in the cirrhotic patient]. 900 18

Ultrasonography detects ascites easily even in trace amounts. 80% of the cases are caused by hepatic disease, in the remaining 20% cancer, inflammation, pancreatic, renal, or cardiac disease can be found. The underlying disease should be investigated by few inexpensive laboratory test from serum, urine and ascites and by abdominal sonography. Hepatic ascites is caused by portal hypertension and disturbances of humoral factors. Sodium retention, peripheral, vasodilation, hyperdynamic circulation and progressive renal vasoconstriction lead to a stepwise deterioration of patients condition. Treatment with diuretics (furosemide, torsemide, or xipamide and spironolactone) and sodium-restriction (< 60 mval per day) control 85-90% of the cases with hepatic ascites. If this regimen fails, non-compliance, spontaneous bacterial peritonitis, hyponatremia or additional complications such as renal failure, Budd-Chiari syndrome or tumor should be considered. Ten to 15% of the patients develop refractory ascites and finally hepatorenal syndrome and have a poor prognosis. Early liver transplantation should be considered. Large volume paracentesis with albumin substitution is a therapeutic option in these patients. The transjugular intrahepatic portosystemic stent-shunt (TIPS) may be superior for patients with concurrent esophageal varices or hepatorenal syndrome. If TIPS is considered the patient should be referred to an experienced center. The peritoneo-venous shunt is restricted to rare indications. In the future, new drugs such as antagonists of endothelins or of the antidiuretic hormone may offer new therapeutic options.
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PMID:[Current ascites therapy]. 906 26

51 CAPD patients (age 55.5 +/- 14.5 yrs, 35 male, 16 female) on CAPD using 'O' set were studied retrospectively during the period January 1993 to April 1995. Etiology of ESRD was Diabetic nephropathy-25(49%) and the other causes-26(51%). The total duration of observation on 'O' set was 553 patient months, the mean duration was 10.8 +/- 6.1 months. 24 patients (47%) developed total of 30 episodes of peritonitis. The incidence of peritonitis was 18.4 patient months per episode of peritonitis. The organisms responsible for peritonitis were Gram positive-6(20%), Gram negative-3(10%), Fungal-1(3.3%), Mycobacterial-1(3.3%), Eosinophilic-1(3.3%), Sterile-12(40%) and unknown-6(20%) 2 patients of bacterial peritonitis and a patient with tuberculous peritonitis died while rest of the patients responded favourably to antibiotics. 13(52%) diabetic patients and 11(42%) non-diabetic patients had peritonitis (p-NS) and the peritonitis rates in diabetics and non diabetics were 18.3 and 18.6 patient months per episode respectively (p-NS). Exit site infection was seen in 5 patients (10%) (Staph aureus-4, Enterococci-1) and all responded to antibiotic therapy. 7 patients had total of 10 episodes of symptomatic accidental intraperitoneal sodium hypochlorite instillation, none had any long term adverse effects. The 'O' set procedure was done by self in 10(20%) and by others in 41(80%) cases. The peritonitis rates when performed by self and others were 18.5 and 18.4 patient months per episode respectively (p-NS). The cost of being on CAPD using 'O' set, Y-bag and twin bag were Rs. 1,50,000, 2,10,000 and 3,72,000 per annum respectively and cost of maintenance haemodialysis was 1,36,800 per annum. The cost of CAPD using 'O' set was comparable to that of maintenance haemodialysis. The 'O' set connector system in CAPD is found to be safe, cost effective and efficient.
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PMID:'O' set connector system in CAPD. 925 69


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