Infective peritonitis

Warunee Punpanich
Infectious Disease Division
Queen Sirikit National Institute of Child Health
Grand Round 14 June 2006
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.
• 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.
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.
• 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.
• 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,
immunoglobulins is reduced in the ascitic fluid.

• Primary bacteremia, usually caused by coliforms.

• 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.
• 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.
 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.
peritonitis
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.
Treatment
• Cover enteric bacteria (mainly GNB)
and S pneumoniae.
• 3rd gen cephalosporin
• BL-BI
• BL-AMG
• Carbapenem

Total duration of 14 days

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.
 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.
 Amoxy clavulanic acid

• Spectrum
– The gram-negative spectrum: all except
AmpC betalactamase, ESBL producing GNB.
– Many anaerobic bacteria including B fragilis.
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.
 Ceftriaxone

• 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.

 “Collateral Damage”
CID 2004:38 (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 2004:38 (Suppl 4) • S341

• 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 2004:38 (Suppl 4) • S341

• 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.
• 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.
• “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.