Transcript Intraabdominal infections

Intraabdominal infections
May 7, 2012
Shahbaz Hasan
Reference source
• IDSA Guidelines
• Diagnosis and Management of Complicated
Intra-abdominal Infection in Adults and
Children
• CID 2010;50:133-64
Outline
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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
Peritonitis
Type
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 Usually monomicrobial;
to dialysis catheter or
skin flora, yeast
breaks in sterility
Microbiology
Location
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
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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
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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
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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
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Image guided drainage procedures
Minimally invasive surgery
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
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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
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Polymicrobial
Start soon
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
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No
Pip-Tazo
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Cefoxitin
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No
No
No
Ceftriaxone
No
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No
No
Cefepime
No
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No
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Imipen/Mero +
/Doripen
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Ertapenem
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No
No
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Antimicrobials
Anaerobes
E coli
Streptococci Enterococci
Pseudomon
Aztreonam
No
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No
No
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Clindamycin
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No
No
Flagyl
+ (gram neg) No
No
No
No
Aminoglyc
No
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No
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FQ
Moxiflox
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No
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Tigecycline
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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
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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
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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
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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 710d 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.