Infective peritonitis. 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. .
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1. Infective peritonitis Warunee Punpanich
Infectious Disease Division
Queen Sirikit National Institute of Child Health
Grand Round 14 June 2006
2. Infective peritonitis 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.
3. Primary peritonitis, sometimes referred to as spontaneous bacterial peritonitis (SBP): infection of the peritoneal cavity without an evident source.
4. 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.
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.
6. 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.
7. Blood cultures were positive in one third of these patients.
The frequency of culture-negative ascitic fluid may be decreased by inoculating blood-cultured bottles with ascitic fluid at the bedside.
Bacteremia is present in up to 75% of patients with primary peritonitis caused by aerobic bacteria.
8. The hepatic reticuloendothelial system is known to be a major site for removal of bacteria from blood.
The decrease in phagocytic activity seen in alcoholic cirrhosis is proportional to the severity of the liver disease.
The characteristics of ascitic fluid in nephrosis and cirrhosis predispose to infection.
Opsonic activity, as reflected by low levels of complement and immunoglobulins, is reduced in the ascitic fluid.
Primary bacteremia, usually caused by coliforms.
9. The onset may be insidious, and findings of peritoneal irritation may be absent in an abdomen distended with ascites.
Fever (>37.8°C [100°F]) is the most common presenting sign, 50 to 80%, and may be present without abdominal signs or symptoms.
The ascitic fluid protein concentration may be low because of
(1) hypoalbuminemia and
(2) dilution of ascitic fluid with transudate from the portal system when there is cirrhosis or the portal vein is obstructed.
10. 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.
11. Diagnosis 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.
12. Diagnosis 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.
13. Treatment Cover enteric bacteria (mainly GNB) and S pneumoniae.
3rd gen cephalosporin
14. Treatment In those cases in which there is a strong clinical suspicion of primary bacterial peritonitis but all cultures are sterile, antimicrobial therapy should be continued.
Clinical improvement together with a significant decline in the ascitic fluid leukocyte count should occur after 24 to 48 hours of antimicrobial therapy if the diagnosis is correct.
Antimicrobial therapy should be continued for 10 to 14 days if improvement is noted; however, shorter-course (5-day) therapy has been shown to be as efficacious.
15. Clavulanic acid is a beta-lactam drug that acts as a competitive "suicide" inhibitor of many plasmid-mediated and chromosomally mediated bacterial beta-lactamases.
The gram-negative spectrum: all except AmpC betalactamase, ESBL producing GNB.
Many anaerobic bacteria including B fragilis.
S pneumo, S aureus, enterococci
Increased dosages of amoxicillin (for oral form or in hard-to-reach site) may be necessary to overcome penicillin-resistant S. pneumoniae.
17. An aminothiazolyl-acetyl side chain with an alpha—methoxyimino group at the 7-position of the beta-lactam ring
? enhanced antibacterial activity, against the Enterobacteriaceae and increased stability against many of the beta-lactamases.
It has no activity against B. fragilis and enterococci.
19. Why not Cef-3 ’?????????
21. “Collateral Damage” Ecological adverse effects of antibiotic therapy ? the selection of drug-resistant organisms and the unwanted development of colonization or infection with MDR organisms.
23. The risk of such damage can be assessed for different antibiotic classes by a variety of epidemiologic studies.
Piperacillin/tazobactam for first-line therapy for febrile neutropenia was associated with a decrease in the prevalence of VRE.
Rahal et al. used extensive class restriction of cephalosporins as a means of controlling ESBL-producing Klebsiella infections.
24. The use of a cephalosporin for many condition was allowed only after approval from the hospital’s infectious disease service.
The use of all cephalosporins decreased by 80%.
This was accompanied by a 44% reduction in the incidence of ESBL-producing Klebsiella infections.
26. Furthermore, total hospital use of cephalosporins plus aztreonam was directly correlated with the prevalence of ESBL-producing K. pneumoniae and multiresistant A. baumannii.
Several case-control studies have also shown a relationship between prior use of 3GC and subsequent colonization or infection with ESBL-producing organisms.
27. “Aminoglycosides, b-lactam/b-lactamase inhibitor combinations, and macrolides appear least frequently to be associated with subsequent infection with multiresistant organisms.”
Intervention studies showing that “sustained reduction in rates of infection with MDR organisms coincides with reduction in the use of certain antibiotic classes may be the closest thing to proof of the concept that certain antibiotic classes are less suitable than others as workhorse” antibiotic therapy.
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