Infective Peritonitis

8/14/2019 Infective Peritonitis

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Infective peritonitis

Warunee PunpanichWarunee PunpanichInfectious Disease DivisionInfectious Disease Division

Queen Sirikit National Institute of Child HealthQueen Sirikit National Institute of Child Health

Grand Round 14 June 2006Grand Round 14 June 2006


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Infective peritonitis

Primary the peritoneal infection is not directly relatedto other intra-abdominal abnormalities.

Secondary an intra-abdominal process, such as a

ruptured appendix or a perforated peptic ulcer, isevident.

Tertiary a later stage of the disease, when clinicalperitonitis and signs of sepsis persist after treatment

for secondary peritonitis, and no pathogens or onlylow-grade pathogens are isolated from the peritonealexudate.


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Primary peritonitis, sometimes referred toas spontaneous bacterial peritonitis

(SBP): infection of the peritoneal cavity

without an evident source.


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Primary peritonitis may occur in childrenwithout predisposing disease particularly in children with cirrhosis and in 2% of

children with NS, (some reported in UTI)

Among 63 consecutive adult patients withcirrhosis and ascites studied prospectivelyusing optimal aerobic and anaerobic

bacteriologic techniques, primary peritonitiswas found in 5.


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BacteriologicCharacteristics

Several decades ago, the organisms reported to causeprimary peritonitis in children were Streptococcus pneumoniaeStreptococcus pneumoniaeand group A streptococciand group A streptococci.

By the 1970s the number of nephrotic children withstreptococcal peritonitis had declined.

The relative frequency of peritonitis caused by gram-negativegram-negativeenteric bacillienteric bacilli had increased.

In cirrhotic patients, microorganisms presumably ofentericentericorigin account for up to 69%origin account for up to 69% of the pathogens.


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E coliE coli is the most frequently recovered pathogen,followed by KlebsiellaKlebsiella pneumoniae, S.pneumoniae, and other streptococcal species,including enterococci.enterococci.

AnaerobesAnaerobes and microaerophilic organisms areinfrequentlyinfrequently reported.

In one series, sterile cultures occurred in 35%sterile cultures occurred in 35% ofpatients with clinical findings consistent withprimary peritonitis.


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Blood culturesBlood cultures were positive in one thirdone third of thesepatients.

The frequency of culture-negative ascitic fluidmay be decreased by inoculating blood-culturedinoculating blood-culturedbottles with ascitic fluidbottles with ascitic fluid at the bedside.

Bacteremia is present in up to 75%Bacteremia is present in up to 75% of patients

with primary peritonitis caused by aerobicbacteria.


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The hepatic reticuloendothelial system is known to be a majorsite for removal of bacteria from blood.

The decrease in phagocytic activity seen in alcoholic cirrhosisis proportional to the severity of the liver disease.

The characteristics of ascitic fluid in nephrosis and cirrhosispredispose to infection.

Opsonic activity, as reflected by low levels of complement andOpsonic activity, as reflected by low levels of complement andimmunoglobulinsimmunoglobulins, is reduced in the ascitic fluid.

Primary bacteremia, usually caused by coliforms.


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The onset may be insidious, and findings of peritonealirritation may be absent in an abdomen distended withascites.

Fever (>37.8C [100F]) is the most commonpresenting sign, 50 to 80%, and may be presentwithoutwithout abdominal signs or symptoms.

The ascitic fluid protein concentration may be lowbecause of (1) hypoalbuminemia and

(2) dilution of ascitic fluid with transudate from the portalsystem when there is cirrhosis or the portal vein is obstructed.


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The WBC in peritoneal fluid usually is greater than300 cells/mm3300 cells/mm3 (in 85% of cases, >1000/mm3), withPMN predominating in > 80% of cases.

Ascitic fluid pH < 7.35 and a lactate > 25pH < 7.35 and a lactate > 25 mg/dl weremore specific but less sensitive than a WBC> 500cells/mm3 using all three parameters together increased the diagnostic

accuracy.

Gram stainingGram staining of the sediment, when positive, is diagnostic,but it is negative in 60 to 80%negative in 60 to 80% of patients with cirrhosis andascites.


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Diagnosis

One ofexclusionexclusion of a primary intra-abdominal source ofinfection.

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 torespond within 48 to72 hours72 hours to appropriate antimicrobial therapy.

An exponential rate ofdecline in the number of ascitic fluiddecline in the number of ascitic fluidleukocytesleukocytes after the initiation of antimicrobial therapy forprimary peritonitisdifferentiate primary from secondarydifferentiate primary from secondarybacterial peritonitisbacterial peritonitis.


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Diagnosis

Paracentesis for smear and culture is indicatedin all cirrhotic patients with ascites and inchildren with gross proteinuria and abdominalpain.

However, paracentesis is not without hazard.

Major complications include perforation of the

bowel with generalized peritonitis or abdominalwall abscess and serious hemorrhage.


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Treatment

Cover enteric bacteria (mainly GNB)

and S pneumoniae.

3rd

gen cephalosporin BL-BI

BL-AMG

Carbapenem

Total duration of 14 days


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Treatment

In those cases in which there is a strong clinicalclinicalsuspicionsuspicion of primary bacterial peritonitis but all culturesculturesare sterile, antimicrobial therapy should be continued.are sterile, antimicrobial therapy should be continued.

Clinical improvement together with a significant declinedeclinein the ascitic fluid leukocyte count should occur after 24in the ascitic fluid leukocyte count should occur after 24to 48 hoursto 48 hours of antimicrobial therapy if the diagnosis iscorrect.

Antimicrobial therapy should be continued for 10 to 14continued for 10 to 14

daysdays if improvement is noted; however, shorter-course(5-day) therapy has been shown to be as efficacious.


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Clavulanic acid is a beta-lactam drug that acts as a

competitive "suicide" inhibitor"suicide" inhibitorof many plasmid-mediated and chromosomally mediated bacterialbeta-lactamases.beta-lactamases.

BL + BI


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Spectrum The gram-negative spectrum: all except

AmpC betalactamase, ESBL producing GNB. Many anaerobic bacteria including B fragilisanaerobic bacteria including B fragilis. S pneumo, S aureus, enterococcienterococci

Increased dosages of amoxicillin (for oralform or in hard-to-reach site) may benecessary to overcome penicillin-resistantS. pneumoniae.

Amoxy clavulanic acid


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An aminothiazolyl-acetyl side chain with an alphamethoxyimino group at the 7-position of the beta-lactamring enhanced antibacterial activity, against the

Enterobacteriaceae and increased stability against many of thebeta-lactamases.

It has no activity against B. fragilis and enterococci.

Ceftriaxone


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Collateral Damage

Ecological adverse effects of antibiotic

therapy the selection of drug-

resistant organisms and the unwanteddevelopment of colonization or

infection with MDR organisms.

Collateral Damage from Antibiotic Therapy CID 2004:38 (Suppl 4) S341

CID 2004:38 (Suppl 4) S341


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The risk of such damage can be assessed for different antibioticclasses by a variety of epidemiologic studies.

Piperacillin/tazobactam for first-line therapy for febrile neutropeniawas associated with a decrease in the prevalence of VRE.

Rahal et al. used extensive class restriction of cephalosporins as ameans of controlling ESBL-producing Klebsiella infections.

Collateral Damage from Antibiotic Therapy CID 2004:38 (Suppl 4) S341


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The use of a cephalosporin for manycondition was allowed only after approvalfrom the hospitals infectious disease service.

The use of all cephalosporins decreased by80%.

This was accompanied by a 44% reduction in

the incidence of ESBL-producing Klebsiellainfections.


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Furthermore, total hospital use ofcephalosporins plus aztreonam was directlycorrelated with the prevalence of ESBL-producing K. pneumoniae and multiresistantA. baumannii.

Several case-control studies have alsoshown a relationship between prior use of3GC and subsequent colonization orinfection with ESBL-producing organisms.


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Aminoglycosides, b-lactam/b-lactamase inhibitorb-lactam/b-lactamase inhibitorcombinations, and macrolides appearleastleastfrequently to be associated with subsequentinfection with multiresistant organisms.

Intervention studies showing that sustainedreduction in rates of infection with MDR organismscoincides with reduction in the use of certainantibiotic classes may be the closest thing to proof

of the concept that certain antibiotic classes are lesscertain antibiotic classes are lesssuitable than others as workhorse antibioticsuitable than others as workhorse antibiotictherapy.therapy.

Infective Peritonitis

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