Intraabdominal infections

May 7, 2012Shahbaz Hasan

Reference source

• IDSA Guidelines• Diagnosis and Management of Complicated

Intra-abdominal Infection in Adults and Children

• CID 2010;50:133-64

Outline

• Classification• Microbiology• Pathogenesis• Prognosis• Management• Special situations

Classification

• Result of invasion and multiplication of enteric bacteria in the wall of a hollow viscus or beyond.

• Intraperitoneal: peritonitis, abscess.• Visceral: liver, spleen, kidney, pancreas,

tuboovarian• Perivisceral: gallbladder, appendix, colon• Interloop

Peritoneal cavity

PeritonitisType Definition Microbiology

Primary Due to bacterial translocation or hemtogenous seeding. No break in integrity of GI tract

Monomicrobial; coliforms or streptococci

Secondary Microscopic or macroscopic perforation

Polymicrobial; coliforms, gram-positive cocci and enteric anaerobes

Tertiary Persistent or recurrent peritoneal infection developing after treatment of secondary peritonitis

Nosocomial organisms; enterococci, staphylococci; resistant gram negative bacilli and yeast

Dialysis associated Seeding of peritoneum due to dialysis catheter or breaks in sterility

Usually monomicrobial; skin flora, yeast

MicrobiologyLocation Colony counts Flora

Stomach 1000 CFU/ml Gram positive, oral flora

Upper small gut Scant Same + coliforms

Distal small gut 1-100 million CFU/ml Coliforms + enterococcus + anaerobes

Colon 10-100 billion CFU/ml Coliforms + enterococcus + Anaerobes + streptococci

Conditions which can change the expected microflora

• Hospitalization• Prior exposure to antibiotics• Obstruction and stasis of the gut• Think of: Pseudomonas, drug resistant gram

negatives, enterococcus, yeast, staphylococcus

Role of enterococci and candida

• Enterococci are present in 20% of intraabdominal infections.

• Role in uncomplicated infections is debated• Important in setting of treatment failure and

nosocomial infections• Candida are important when present as the

sole or predominant isolate or when accompanied by fungemia.

Pathogenesis

1. Mixed infections: in rat models of peritonitis, E coli is responsible for initial sepsis and bacteremia. Anaerobes then lead to abcess formation in the surviving rats.

2. Host response• Massive exudate• Neutrophil influx• Fibrinogen release• Cytokine release

Prognosis

• Age• Comorbidities• Duration of contamination• Presence of foreign material• Type of microorganisms• Site of contamination• Mortality is 3% in setting of early abdominal

perforation. Increases to 60% in established peritonitis with organ failure

• Inadequate antimicrobial therapy doubles mortality

Management

• Early diagnosis: history, exam, data, imaging• Supportive measures: IV fluids, sepsis protocol• Source control• Antimicrobial therapy

Diagnosis

• Signs and symptoms• Lab tests: cbc, cmp, pancreatic enzymes,

cultures• KUB: free air, sentinal loops, blurring of psoas

shadow• Ultrasound: biliary, renal, pelvic• CT• Nuclear medicine.

Source control

• “Single procedure or series of procedures that eliminate infectious foci, control factors that promote ongoing infection, and correct or control anatomic derangements to restore normal physiologic function.”

Timing of source control

• Diffuse peritonitis: immediate• Hemodynamically stable patient without

peritonitis: delay of up to 1d is acceptable

Source control

1. Image guided drainage procedures2. Minimally invasive surgery3. Open laparotomy• Bowel decompression• Closure of perforation; resection of diseased

segment or organ• Drainage : drains; relaparotomy• Failure to achieve adequate source control is

associated with a worse clinical outcome.

Risks for failure of source control

• Advanced age• High severity of illness (APACHE II score >15)• Delay in initial intervention (>24H)• Comorbidity and degree of organ dysfunction• Low albumin level• Poor nutritional status• Degree of peritoneal involvement• Underlying malignancy

Antimicrobial therapy

1. Polymicrobial2. Start soon3. Use appropriate antibiotics• Uncomplicated: community acquired, normal

host, no prior antibiotics: think E coli, streptococci and bacteroides (lower GI)

• Complicated: nosocomial, prior antibiotics, immunocompromised host: also think of pseudomonas, enterococcus, yeast, staphylococcus

Antimicrobials: betalactams Anaerobes E coli Streptococci Enterococci Pseudomonas

Amp-sulbact + ? + + No

Pip-Tazo + + + + +

Cefoxitin + + No No No

Ceftriaxone No + + No No

Cefepime No + + No +

Imipen/Mero/Doripen

+ + + + +

Ertapenem + + + No No

AntimicrobialsAnaerobes E coli Streptococci Enterococci Pseudomon

Aztreonam No + No No +

Clindamycin + (gram pos) No + No No

Flagyl + (gram neg) No No No No

Aminoglyc No + No +/No +

FQ Moxiflox + + No +

Tigecycline + + + +/No No

Choice of therapy: uncomplicated (think E coli and B Fragilis)

• Amp-sulbactam (Unasyn) : no longer recommended as empiric therapy

• Cefoxitin or cefotetan• Ceftriaxone + flagyl or clindamycin• FQ + flagyl or clindamycin• Ertapenem• Tigacyl

Choice of antimicrobials: complicated (think pseudomonas, enterococcus, yeast,

staphylococcus)• Pip-tazobactam (Zosyn)• Antipseudomonal carbapenem:

Imipen/mero/doripen• Ceftazidime/cefepime + flagyl or clindamycin

+ vancomycin• FQ + flagyl or clinda + vancomycin• Also consider addition of antifungal coverage.

Duration of antimicrobials

• 1 day: early infection, no perforation, early removal of source

• 5-7 days: perforation, but good source control• 7-14 days: perforation, delay in source control• >14 days: abscess formation, inability to

properly control source, tertiary peritonitis

Case presentation

• 28 y WF, previously healthy, delivered her first baby (NVD) 4 weeks prior

• 1 wk PTA, underwent D/C for retained placental products. Gynecologist recognized a uterine perforation immediately and repaired on the spot. Sent home with po Augmentin.

• Returns to hospital with sepsis, diffuse peritonitis and found to have a large pelvic abscess + free air.

Management issues

• How will you control the source?• IR drainage?• Laparoscopic drainage?• Open lap?• What empiric antibiotics would you choose?• Is this uncomplicated or complicated?• Upper GI flora vs Lower GI flora?

Case continues

• Went for open laparotomy:• Findings revealed extensive peritonitis,

perforated colon.• Colon repaired and diverting colostomy;

drains left in pelvis and abdomen• Started on IV zosyn

A few days later….

• Still running fever. Wbc and crp up • Intraop cultures: E coli, enterococcus, c

albicans

Case continues

• Repeat imaging shows extensive fluid collections in pelvis, left paracolic gutter and around liver. Drained by IR

• Added fluconazole• Currently at Day 20 of antibiotics, still with

drains.

Pyogenic liver abcesses

• Incidence 10-20 cases per 100,000 hospital admissions

• Route: biliary> portal vein> hematogenous > contiguous focus > penetrating trauma

• Flora: upper GI• Aspiration + antimicrobials leads to high

success rates. Treat for 4-6 weeks.

Cholecystitis

• Infection complicates 20-50% of acute cholecystitis cases

• Untreated, complications include emphysematous cholecystitis, empyema of the gallbladder, liver abcesses and bacteremia

• Flora: generally gram negative bacilli and anaerobes• Immediate cholecystectomy or cholecystostomy is

indicated if gangrene or perforation are suspected, otherwise surgery is delayed for 6-12 weeks.

• Role of antimicrobials in uncomplicated cholecystitis is debatable.

Appendicitis

• Lifetime risk is 8.6% in men and 6.7% in women• Flora is colonic• Primary treatment is surgery• Antibiotics are given for 5-7 days for a perforated

appendix• Contained perforations are managed by

antibiotics, percutaneous drainage of the abcess followed by interval appendenctomy in 6-8 weeks.

Diverticulitis

• Flora is colonic• For small, well-localized, peri-diverticular abcess, a 7-

10d course of antibiotics is successful in 70-80%.• Emergent surgery is indicated for uncontrolled sepsis,

generalized peritonitis, persistent obstruction, failure to respond to medical treatment. Usually a two-stage procedure (Hartmann)

• Elective surgery is performed for fistula formation, recurrent attacks of diverticulitis or for complicated diverticulitis brought under control with medical therapy.