HISTORY
In 1971, Conn and Fessel described a syndrome of infected ascitic fluid in patients with hepatic cirrhosis, which they named SBP.
SBP is by definition an infection of previously sterile ascitic fluid, without any apparent intra-abdominal source of infection. The infecting organisms are usually those found among the normal intestinal flora.
CLEVELAND JOURNAL OF MEDICINE VOL 71.NUMBER 7.JULY2004
Incidence
Patients with cirrhosis are very suspectible to infection of ascitic fluid as apart of their general suspectibility to infection.
Approx 20-30% of cirrhotic patients with ascites develop spontaneous bacterial peritionitis.1
1970
5-10%
1987-1993
10-30%
Factors Mortality
SBP is deadly
Development of Renal Failure Hepatic encephalopathy High levels of serum Bilirubin Upper GI bleeding
Factors Mortality
SBP is deadly
Development of renal impairment after the diagnosis of SBP is probably the strongest independent predictor of death
Damage to the intestinal barrier leads to bacterial translocation and endotoxaemia and thus to impairment of liver function and increase in portal pressure, possibly causing further damage to the gut: a vicious circle.
A vicious circle
Microbiology
The pathogens responsible for the spontaneous bacterial peritionitis are Enteric gram-negative bacteria E.coli, Klebsiella pneumonia, Enterococcus species, Gram-positive bacteria Streptococcus pneumonia, Virdans streptococci
MANAGEMENT
The presentation depends on the stage at which the infection is diagnosed In the early stages , most patients are asymptomatic As the disease progresses, patients show signs and symptoms of peritoneal infection
DIAGNOSIS
The diagnosis relies on laboratory and microbiological tests. Currently, paracentesis with laboratory testing the ascitic fluid is the only way to confirm and rule out SBP in patients with cirrhosis.
Diagnosis
If SBP is suspected in a patient with clinically undetectable ascites, ultrasonography is indicated to identify the ascites and to perform guided paracentesis.
I nternational Journal of Gastroenterology and Hepatology 2005;54:1523-1526
Diagnosis
A polymorphonuclear cell count of more than 250 / mm3 in ascitic fluid is currently considered diagnostic of SBP and warrants the prompt start of antibiotic treatment
PROGNOSIS
The mortality rate of SBP exceeds > 30%, but if the disease is recognized and treated earlier, the rate is < 10%. Majority of patients have underlying severe liver disease, and may die of liver failure, hepato-renal syndrome, or bleeding complications from portal hypertension.
Treatment
Antibiotic Regimens In Evolution
Initially, the regimen most often used to treat SBP was a beta-lactam such as ampicillin or cephalotin, and an amninoglycoside such as gentamycin or tobrarmycin. However, in the first randomized comparative study of two different regimens for SBP, cefotaxime was superior to ampicillin plus tobramycin for resolving SBP. In that study, ampicillin plus tobramycin was also associated with nephrotoxicity or superinfections in approximately 10% of patients.
Several studies have since confirmed the effectiveness of cefotaxime in patients with SBP
Cleveland journal of medicine vol 71 number 7 july 2004.
Treatment
Starting empiric antibiotic therapy immediately improves survival in SBP, although mortality rate is still about 10% - 30% and those who survive are at high risk of a recurrence
Treatment
Empiric antibiotic treatment should be started once the polymorphonuclear cell count in ascitic fluid exceeds 250 / mm 3
Duration of Therapy
TREATMENT
At present, third-generation cephalosporins are considered the gold standard in the treatment of SBP in cirrhosis. Cefotaxime is considered to be one of the first-choice antibiotic therapies in the empirical treatment of SBP in patients with cirrhosis.
PROPHYLAXIS
At present, third-generation cephalosporins are considered the gold standard in the treatment of SBP in cirrhosis. Cefotaxime is considered to be one of the first-choice antibiotic therapies in the empirical treatment of SBP in patients with cirrhosis.
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