1. Intraabdominal infections May 7, 2012 Shahbaz Hasan

2. Reference source IDSA Guidelines Diagnosis and Management of Complicated Intra-abdominal Infection in Adults and Children CID 2010;50:133-64

3. Outline Classification Microbiology Pathogenesis Prognosis Management Special situations

4. 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

5. Peritoneal cavity

6. Peritonitis TypeDefinitionMicrobiology PrimaryDue to bacterial translocation or hemtogenous seeding. No break in integrity of GI tract Monomicrobial; coliforms or streptococci SecondaryMicroscopic or macroscopic perforation Polymicrobial; coliforms, gram-positive cocci and enteric anaerobes TertiaryPersistent or recurrent peritoneal infection developing after treatment of secondary peritonitis Nosocomial organisms; enterococci, staphylococci; resistant gram negative bacilli and yeast Dialysis associatedSeeding of peritoneum due to dialysis catheter or breaks in sterility Usually monomicrobial; skin flora, yeast

7. Microbiology LocationColony countsFlora Stomach1000 CFU/ml Gram positive, oral flora Upper small gutScantSame + coliforms Distal small gut1-100 million CFU/mlColiforms + enterococcus + anaerobes Colon10-100 billion CFU/mlColiforms + enterococcus + Anaerobes + streptococci

8. 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

9. 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.

10. 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

11. 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

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

13. 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.

14. 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.”

15. Timing of source control Diffuse peritonitis: immediate Hemodynamically stable patient without peritonitis: delay of up to 1d is acceptable

16. Source control 1.Image guided drainage procedures 2.Minimally invasive surgery 3.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.

17. 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

18. Antimicrobial therapy 1.Polymicrobial 2.Start soon 3.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

19. Antimicrobials: betalactams AnaerobesE coliStreptococciEnterococciPseudomonas Amp-sulbact+?++No Pip-Tazo+++++ Cefoxitin++No CeftriaxoneNo++ CefepimeNo++ + Imipen/Mero /Doripen +++++ Ertapenem+++No

20. Antimicrobials AnaerobesE coliStreptococciEnterococciPseudomon AztreonamNo+ + Clindamycin+ (gram pos)No+ Flagyl+ (gram neg)No AminoglycNo+ +/No+ FQMoxiflox++No+ Tigecycline++++/NoNo

21. 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

22. 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.

23. 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

24. 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.

25. 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?

26. 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

27. A few days later…. Still running fever. Wbc and crp up Intraop cultures: E coli, enterococcus, c albicans

28. 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.

29. 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.

30. 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.

31. 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.

32. 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.