Infective peritonitis

Posted by e-Medical PPT
Primary--->the peritoneal infection is not directly related to other intra-abdominal abnormalities.
Secondary --->an intra-abdominal process, such as a ruptured appendix or a perforated peptic ulcer, is evident.
Tertiary ---> a later stage of the disease, when clinical peritonitis and signs of sepsis persist after treatment for secondary peritonitis, and no pathogens or only low-grade pathogens are isolated from the peritoneal exudate.

Primary peritonitis, sometimes referred to as spontaneous bacterial peritonitis (SBP): infection of the peritoneal cavity without an evident source.

Primary peritonitis may occur in children without predisposing disease
particularly in children with cirrhosis and in 2% of children with NS, (some reported in UTI)

Among 63 consecutive adult patients with cirrhosis and ascites studied prospectively using optimal aerobic and anaerobic bacteriologic techniques, primary peritonitis was found in 5.

Bacteriologic Characteristics
Several decades ago, the organisms reported to cause primary peritonitis in children were Streptococcus pneumoniae and group A streptococci.
By the 1970s the number of nephrotic children with streptococcal peritonitis had declined.
The relative frequency of peritonitis caused by gram-negative enteric bacilli had increased.
In cirrhotic patients, microorganisms presumably of enteric origin account for up to 69% of the pathogens.
E coli is the most frequently recovered pathogen, followed by Klebsiella pneumoniae, S. pneumoniae, and other streptococcal species, including enterococci.
Anaerobes and microaerophilic organisms are infrequently reported. 
In one series, sterile cultures occurred in 35% of patients with clinical findings consistent with primary peritonitis.

The WBC in peritoneal fluid usually is greater than 300 cells/mm3 (in 85% of cases, >1000/mm3), with PMN predominating in > 80% of cases.

Ascitic fluid pH < 7.35 and a lactate > 25 mg/dl were more specific but less sensitive than a WBC> 500 cells/mm3
using all three parameters together increased the diagnostic accuracy.
Gram staining of the sediment, when positive, is diagnostic, but it is negative in 60 to 80% of patients with cirrhosis and ascites.

One of exclusion of a primary intra-abdominal source of infection.
Oral and intravenous contrast with CT scanning has greatly enhanced detection of intra-abdominal sources of peritonitis.
Patients with primary peritonitis usually respond within 48 to 72 hours to appropriate antimicrobial therapy.
An exponential rate of decline in the number of ascitic fluid leukocytes after the initiation of antimicrobial therapy for primary peritonitis  differentiate primary from secondary bacterial peritonitis.
Paracentesis for smear and culture is indicated in all cirrhotic patients with ascites and in children with gross proteinuria and abdominal pain.
However, paracentesis is not without hazard.
Major complications include perforation of the bowel with generalized peritonitis or abdominal wall abscess and serious hemorrhage.

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