Peritonitis

     It occurs in patients with ascites in the absence of recognized, secondary causes
such as bowel perforation or intra-abdominal abscess; it’s noted in patients with 
cirrhosis and poor hepatic synthetic function.

     The bacteria isolated from the ascitic fluid are those of the normal 
intestinal flora; 92% 
are monomicrobial (G negatives in 2/3; E. coli 50%,followed by Klebsiella and other Gram negatives; 
G + [25%, with streptococcal sp the most common]; anaerobic is rare).  
    Impaired activity of the RES, decreased serum and ascitic C levels, and a low ascitic protein 
level are some of the mechanisms responsible for the entrance of enteral organisms into the 
ascitic fluid.  Portal hypertension increases bacterial translocation to the lymphatic system and 
portal vein; the mechanisms responsible for this action are bacterial overgrowth due to 
impaired gastrintestinal transit, impaired host defense, or, most likely, morphologic and 
functional damage to the bowel mucosa.
     Impaired peripheral clearance of bacteria has also been demonstrated in patients with 
cirrhosis; in these ones, bacteria persist longer in the circulation and eventually 
gain access to the ascitic fluid as a result of decreased opsonic activity in serum
and other neutrophil defects including chemotaxis.
     Thus, primary bacteremia in conjunction with secondary seeding of the ascitic fluid 
is the most likely explanation for the development of this disease.

     An ultrasound should be done for detection and diagnostic aspiration of ascitic
fluid.  Fever and abdominal pain are common; onset or worsening of hepatic encephalopathy,
rebound tenderness, and decreased bowel sounds have a varied frequency; subtle
clinical findings 
such as mild hepatic encephalopathy, diarrhea, back pain, hypothermia, and refractoriness to 
diuretics are observed.  
     It may be entirely asymptomatic (10%). But this disease should be considered in patients with 
ascites in whom there’s clinical deterioration, either in the presence or in the absence of 
peritoneal signs.
     Gram staining of ascitic fluid may help identify peritonitis due to gut 
perforation, but it 
infrequently detects bacteria in SBP.  Special smears and cultures for TB are reserved for specific 
clinical situations, such as those in which a high fluid cell count has a predominance of lymphocytes.
     The PMN count in ascitic fluid is the best predictor of SBP; count > 500/mm3
has a sensitivity of 80% and a specificity of 98%, and you can consider SBP even
in the absence of clinical 
signs and symptoms of peritonitis; a cell count < 250/mm3, in the setting of sterile fluid, 
rules out SBP.  
     For bacterial cultures, 10 ml of ascitic fluid should be inoculated at the
bedside in blood-culture 
bottles.

     In an initial specimen of ascitic fluid, a leukocyte count greater than 10.000/mm3,
a protein concentration > 1 g/dl, and the finding of polymicrobials, particularly
in the setting of anaerobic bacteria or fungi, raise suspicion of secondary rather 
than primary peritonitis. 
     If, after 48 hours of antibiotic, a diagnostic paracentesis shows an increase 
in PMN, Rx, TC, or water-soluble contrast studies of the upper and lower GIT must
be performed to exclude bowel perforation or intra-abdominal abscess; it’s 
important because secondary 
one is best treated surgically.

     Mortality (35%); factors associated with a poor outcome: BT > 8 mg/dl, albumin
< 2,5 g/dl, creatinine > 2,1 mg/dl, hepatic encephalopathy, hepatorenal syndrome
and upper GI bleeding 
(all indicators of poor liver function).  
     After an initial episode of SBP, the probability of a recurrence
at 1 year is of 70%, but 
in most patients the severity of the liver disease dictate the prognosis; thus, in general, they’re 
candidates for liver transplantation.

     Cefotaxima, 2 g, EV, 8/8 hours, for 5 days, is the drug of choice, and have
a cure of at least 85%; 
repeat paracentesis 48 hours after therapy has been initiated to confirm that cell counts have 
decreased.