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Infective peritonitis

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E coli is the most frequently recovered pathogen, followed by Klebsiella pneumoniae, S. pneumoniae, and other streptococcal species, including enterococci. – PowerPoint PPT presentation

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Title: Infective peritonitis


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 (gt37.8C 100F) 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, gt1000/mm3),
    with PMN predominating in gt 80 of cases.
  • Ascitic fluid pH lt 7.35 and a lactate gt 25 mg/dl
    were more specific but less sensitive than a WBCgt
    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
  • BL-BI
  • BL-AMG
  • Carbapenem

Total duration of 14 days
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
BL BI
  • Clavulanic acid is a beta-lactam drug that acts
    as a competitive "suicide" inhibitor of many
    plasmid-mediated and chromosomally mediated
    bacterial beta-lactamases.

16
Amoxy clavulanic acid
  • Spectrum
  • 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
Ceftriaxone
  • An aminothiazolyl-acetyl side chain with an
    alphamethoxyimino 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.

18
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19
Why not Cef-3 ?????????
20
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21
Collateral Damage
CID 200438 (Suppl 4) S341
  • Ecological adverse effects of antibiotic therapy
    ? the selection of drug-resistant organisms and
    the unwanted development of colonization or
    infection with MDR organisms.

Collateral Damage from Antibiotic Therapy CID
200438 (Suppl 4) S341
22
What would you do if you lost everything?
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.

Collateral Damage from Antibiotic Therapy CID
200438 (Suppl 4) S341
24
  • The use of a cephalosporin for many condition was
    allowed only after approval from the hospitals
    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.

25
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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.

28
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