2. BR
AINSTORMING QUESTIONS
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1. What Are the Appropriate Procedures for Initial Evaluation of Patients
with Suspected Intra-abdominal Infection?
2. When Should Antimicrobial Therapy Be Initiated for
P
atients with Suspected or Confirmed Intra-abdominal
Infection?
3. What Are the Proper Procedures for Obtaining Adequate
Source Control?
4. When and How Should Microbiological Specimens Be
Obtained and Processed?
5. What Are Appropriate Antimicrobial Regimensfor Patientswith
Community-Acquired Intra-abdominal Infection of
High Severity?
6. What Constitutes Appropriate Antibiotic Dosing?
7. What Is the Appropriate Duration of Therapy for Patients with
Complicated Intra-abdominal Infection?
8. What P
atients Should Be Considered for Oral or Outpatient
Antimicrobial Therapy and What R
egimensShould Be Used?
9. How Should Suspected Treatment Failure Be Managed?
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3. Intra-abdominal Infections
Intra-abdominal infections are:
🞺 Contained within the peritoneal cavity or retroperitoneal space
Theperitoneal cavity extends from the undersurface of the
diaphragm to the floor of the pelvis and contains:
Thestomach
Small bowel
Large bowel
Liver
Gallbladder, and
Spleen
Structures resides in Retroperitoneum
🞺 Theduodenum,pancreas, kidneys, adrenal glands, great
vessels (aorta and vena cava), and most mesenteric vascular
structures
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4. Introduction #2
Intra-abdominal infections may be:
🞺 Generalized or localized
🞺 Complicated or uncomplicated, and
🞺 Community or healthcare-associated
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Peritonitis is defined as the acute inflammatory response of the peritoneal
lining to microorganisms, chemicals, irradiation, or foreign-body injury
An abscessis a purulent collection of fluid separated from surrounding
tissue by a wall consisting of inflammatory cells and adjacent organs.
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5. EPIDEMIOLOGY
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Intra-abdominal infection is the second most common cause of
infectiousmortality in the intensive care unit (I D SA 2009)
Peritonitis may be classified as primary(spontaneous bacterial
peritonitis)
🞺 an infection of the peritoneal cavity without an evident source in the
abdomen
Develops in up to 10% to 30% of patients with alcoholic cirrhosis
Secondary
🞺 Involve perforation of the GI tract
Tertiary
🞺 Occurs in critically ill patients and is infection that persists or recurs
at least 48 hoursafter apparently adequate management of
primary or secondary peritonitis
Epidemiologic data for secondary and tertiary intra-abdominal infections are
lessunderstood.
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6. ETIOLOGY
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Primary peritonitisin adults occurs most commonly in
association with:
🞺 Alcoholic cirrhosis or
🞺 Ascitescaused by post-necrotic cirrhosis
🞺 Chronicactive hepatitis
🞺 Acute viral hepatitis
🞺 Congestive heart failure
🞺 Malignancy
🞺 Systemiclupus erythematosus, or nephriticsyndrome
Abscessesare the result of chronic inflammation and may occur without
preceding generalized peritonitis
Appendicitisis the most frequent cause of abscess
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7. PATHOPHYSIOLOGY
Intra-abdominal infection resultsfrom:
🞺 Bacterial entry into the peritoneal or retroperitoneal spaces
Or
🞺 Bacterial collections within intra-abdominal organs
🞺 In primary peritonitis bacteria enter via:
Thebloodstream or the lymphatic systemby transmigration through the
bowel wall, through an indwelling peritoneal dialysis catheter, or via the
fallopian tubesin females
🞺 Insecondary peritonitis, bacteria mostoften enter the
peritoneumor retro peritoneumas a result of perforation of
the GI or female genital tracts
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8. Pathophysiology #2
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Peritoneal cavity is lubricated with less than 100 mLof
sterile, clear yellow fluid
🞺 Normally withfewer than 250 cells/mm3 (250 × 106/L),
🞺 A specific gravity below 1.016, and
🞺 Proteincontent below 3 g/dL (30 g/L).
Theseconditions change drastically with peritoneal infection or
inflammation
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9. Pathophysiology #3
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Humoral and cellular defenses respond first; then the
omentum adheres to the affected area
🞺 When bacteria become dispersed throughout the peritoneum,
the inflammatory process involves most of the peritoneal lining
🞺 Thefluid and proteinshift into the abdomen(called third-
spacing) may be so dramatic that circulating blood volume is
decreased
Cause decreased cardiac output and hypovolemic shock
Fluid imbalance
🞺 With an inflamed peritoneum, bacteria and endotoxinsare
absorbed easily into the bloodstream (translocation), and this
may result in septicshock
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10. Pathophysiology #4
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🞺 Cytokines, suchas tumor necrosis factor-α (TNF-α), interleukin
(IL) 1, IL-6, IL-8, and interferon γ (INF-γ), are produced by
macrophagesand neutrophils
With uncontrolled activation of these mediators, sepsis may result
Fluid shifts, cytokines and endotoxin may result in hypovolemia,
hypoperfusion, and shock
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11. Microbiology of Intra-abdominal Infection
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Primary bacterial peritonitis isoften causedby a single
organism
🞺 In children, the pathogen is usually group A Streptococcus, E.coli,
Streptococcus pneumoniae, or Bacteroides species
🞺 When peritonitis occurs in association with cirrhotic ascites
E.coli is isolated most frequently
🞺 Other potential pathogens are:
Haemophilus influenzae, Klebsiella spp., Pseudomonas spp., anaerobes, and
S. pneumoniae
Occasionally, primary peritonitismay be caused by Mycobacterium
tuberculosis
Because of the diverse bacteria present in the GI tract,
secondary intraabdominal infectionsare often polymicrobial
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13. Microbiology of Intra-abdominal Infection #3
Bacterial Synergism
🞺 Thecombination of aerobic and anaerobic organisms appears
to greatly increase the severity of infection
Facultative bacteria may provide an environment conducive to the
growth of anaerobic bacteria by:
Promotion of an appropriate environment for anaerobic bacterial growth
through oxygen consumption
Production of nutrients necessary for anaerobes, and
Production of extracellular enzymes that promote tissue invasion by
anaerobes.
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14. CLINICALPRESENT
ATION
Primary peritonitis
🞺 General
The patient may not be in acute distress, particularly with
peritoneal dialysis
🞺 Signs and symptoms
The patient may complain of nausea, vomiting (sometimes with
diarrhea), and abdominal tenderness
Temperature may be only mildly elevated or not elevated in
patients undergoing peritoneal dialysis
Bowel sounds are hypoactive
The cirrhotic patient may have worsening encephalopathy.
Cloudy dialysate fluid with peritoneal dialysis
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15. Clinical presentation #2
Laboratory tests
🞺 The patient's white blood cell (WBC)countmay be only
mildly elevated
🞺 Asciticfluid usually containsgreaterthan300
leukocytes/mm3, and bacteria may be evident on Gram
stain of a centrifuged specimen
🞺 In 60–80% of patientswith cirrhoticascites,theGramstain
is negative
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16. Clinical presentation #3
Secondary Peritonitis
🞺 Signs and symptoms
Generalized abdominal pain
Tachypnea
Tachycardia
Nausea and vomiting
Temperature is normal initially then increases to 37.7°C to 38.8°C
Decreased urine output due to dehydration
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17. Clinical presentation #4
Physical examination
🞺 Voluntary abdominal guarding changing to involuntary
guarding and a "board-like abdomen"
🞺 Abdominal tenderness and distension
🞺 Faint bowel soundsthat cease over time
Laboratory tests
Leukocytosis (15,000–20,000 WBC/mm3, with neutrophils
predominating and an elevated percentage of immature
neutrophils (bands)
Elevated Hct and BUN because of dehydration
Patient progressesfrom early alkalosis because of
hyperventilation and vomiting to acidosis and lactic acidemia
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18. Treatment
Desired Outcome
1) Correction of the intraabdominal disease processes or injuries
that have caused infectionand the drainage of purulent
collections(abscesses).
2) T
o achieve a resolutionof infection without major organ
system complications and adverse drug effects
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19. General Approach to Treatment
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A. Prompt drainage of the infected site
B. Hemodynamic resuscitation and support of vital organ functions,
and
C. Early administration of appropriate antimicrobial therapy to treat
infection not eradicated by surgery
* large volumesof IV fluids are required to restore vascular volume
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20. Non-pharmacologic Treatment
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Drainage Procedures
Fluid Therapy
🞺 Patients should be evaluated for signs of hypovolemia,
hypoperfusion, and shock
Treatmentgoals during the first 6 hoursor resuscitation:(a) central
venouspressure(CVP)8 to 12 mmHg,(b) meanarterial pressure
(MAP) ≥65 mmHg, and (c) maintain urine output ≥0.5 mL/kg/h
The Surviving Sepsis Campaign: International Guidelines for Management
of Severe Sepsis and Septic Shock recommendation
In patients with significant blood loss, blood transfusion may be
indicated
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21. Timing of Initiation of Antimicrobial Therapy
🞺 Antimicrobial therapy shouldbe initiated oncea patient
receives a diagnosis of an intra-abdominal infection or once
suchan infection is considered likely.
For patients with septic shock, antibiotics should be administered as
soon as possible
🞺 For patients without septic shock, antimicrobial therapy
should be started in the emergency department
🞺 Satisfactory antimicrobial drug levels shouldbe maintained
during a source control intervention
Complicated Intra-abdominal Infection Guidelines • CID 2010:50 (15
January)
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22. Pharmacologic Treatment
Antimicrobial Experience
🞺 Selection of antimicrobials for intra-abdominal infections are
the following:
Antimicrobial regimensusedfor secondaryinfections shouldcovera
broad spectrum of aerobic and anaerobic bacteria from the GI tract
Single-agent regimens(suchasanti-anaerobic cephalosporins,
extended-spectrum penicillins with β-lactamase inhibitors, and
carbapenems) are as effective but have the benefit of being less
nephrotoxic compared to combinations of aminoglycosides with
antianaerobic agents
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23. Pharmacologic Treatment #3
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Resistanceisnowprevalent amongB.fragilis to clindamycinand
cefotetan and E.coli to ampicillin–sulbactam and quinolones and
therefore these agents should not be routinely used empirically for
complicated intraabdominal infections
If susceptible, antimicrobial treatment can be completed orally with
amoxicillin–clavulanate, metronidazole with either ciprofloxacin or
levofloxacin, or moxifloxacin
Four to seven days of antimicrobial treatment is sufficient for most
intraabdominal infections with adequate source control
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25. Recommendations for Empiric Antimicrobial Therapy for Health Care–Associated
Complicated Intra-abdominal Infection
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26. Cont’d…
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🞺 Ampicillin-sulbactam is not recommended for use because of
high rates of resistance to this agent among community-
acquired E.coli
🞺 Cefotetan and clindamycin are not recommended for
use because of increasing prevalence of resistance to these
agents
among the Bacteroidesfragilisgroup
Complicated Intra-abdominal Infection Guidelines • CID 2010:50 (15
January)
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27. Initial Intravenous Pediatric Dosages of Antibiotics for Treatment of
Complicated Intra-abdominal Infection
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28. SuspectedTreatment Failure
🞺 Extra-abdominal sourcesof infection and noninfectious
inflammatory conditions should also be investigated if the
patient isnot experiencing a satisfactory clinical responseto a
microbiologically adequate initial empiric antimicrobial
regimen
🞺 Forpatients who do not respond initially and for whom
a focus of infection remains, both aerobic and anaerobic
cultures should be performed from 1 specimen, provided it is of
sufficient volume(at least 1.0 mLof fluid or tissue)and is
transported to the laboratory in an anaerobic transport system
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29. Evaluation of Therapeutic Outcomes
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Thepatient shouldbereassessedcontinually to
determine the successor failure of therapies
Most patients should show improvement within 2 to 3
days
At 24 to 48 hours, aerobic bacterial culture results
should return
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