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Block G -- Infection > Dr. Puligandla -- Intraabdominal Infections > Flashcards

Dr. Puligandla -- Intraabdominal Infections Flashcards

1
Q

Describe the general cause of developing and intra-abdominal infection (IAI)

A

Invasion and multiplication of enteric bacteria in the wall of a hollow viscus and beyond

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2
Q

What generally determines if and IAI will be complicated or not

A

Whether the infection extends into the peritoneal cavity or other normally sterile regions of the abdomen

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3
Q

Define primary peritonitis

A

Peritoneal infection developing in the absence of a break in the integrity of the GIT, as a result of hematogenous or lymphatic seeding, or bacterial translocation

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4
Q

Define secondary peritonitis

A

Peritoneal infection developing in conjunction with an inflammatory process of GIT or its extensions, usually associated with microscopic or macroscopic perforation

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5
Q

Define tertiary peritonitis

A

A persistent or recurrent peritoneal infection developing are initial treatment of secondary peritonitis

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6
Q

Pathogens responsible for primary peritonitis (3)

A

Monomicrobial:

  1. Gram-negative enterbacteriaceae
  2. Streptococci

NOTE: Infected ascites in ESLD

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7
Q

Pathogens responsible for secondary peritonitis (3)

A

Polymicrobial:

  1. Aerobic gram-negative bacilli
  2. Gram-positive cocci
  3. Enteric anaerobes
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8
Q

Pathogens responsible for tertiary peritonitis (4)

A

Nosocomial organisms, including:

  1. Resistant gram negative bacilli
  2. Enterococci
  3. Staphylococci
    1. Yeast
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9
Q

6 types of causes of secondary bacterial peritonitis in the hospitalized patient

A
  1. Post-operative peritonitis
  2. Procedural complications
  3. Spontaneous GI perforation
  4. Intestinal ischemia
  5. Device-related infection
  6. Community-acquired infection
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10
Q

5 associated symptoms of IAI

A
  1. Fever
  2. Emesis
  3. Diarrhea or change in bowel habit
  4. Blood in stool
  5. Abdominal distension
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11
Q

3 associated medical problems that one must be aware of in the event of IAI

A
  1. Previous surgery
  2. Trauma
  3. Co-morbidities
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12
Q

3 comorbidities to be aware of in event of IAI

A
  1. Diabetes
  2. Vascular disease
  3. Immunosuppression
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13
Q

4 potential findings of IAI patient’s vital signs

A
  1. Tachycardia
  2. Hypotension
  3. Tachypnea
  4. Fever
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14
Q

6 signs of peritonitis

A
  1. Rebound
  2. Guarding
  3. Distension
  4. Reduced bowel sounds
  5. Abdominal wall changes
  6. Visible loops
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15
Q

Describe the pathophysiology of fever

A
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16
Q

6 lab tests to request in event of IAI

A
  1. CBC
  2. Blood gas
  3. Electrolytes
  4. Urea/creatinine
  5. Liver enzymes
  6. LFTs
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17
Q

3 IAI CBC findings

A
  1. Anemia
  2. Leukocytosis
  3. Thrombocytopenia
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18
Q

Blood gas findings for IAI

A

Metabolic derangement (i.e. acidosis)

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19
Q

Electrolytes finding of IAI

A

Hyper or hypokalemia

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20
Q

5 potential findings on plain radiograph in event of IAI

A
  1. “Free air”
  2. Intestinal obstruction
  3. Mucosal ischemia (“thumb-printing”)
  4. Contrast studies
    • Leak
    • Obstruction
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21
Q

4 things to identify in event of IAI in a CT scan

A
  1. Fluid collections
  2. Abscess
  3. Ischemic bowel
  4. Perfusion of vital organs
22
Q

Define infection

A

Process of bacteria invading normally sterile host tissues

23
Q

Define sepsis and its effects (6)

A

Response to infection causing:

  1. Pyrexia
  2. Tachypnea
  3. Tachycardia
  4. Hypoxia
  5. Hypermetabolism
  6. Organ(s) dysfunction
24
Q

SIRS temperature

A

> 38oC or < 36oC

25
Q

SIRS HR

A

> 90 bpm

26
Q

SIRS respiratory findings

A

Tachypnea (RR > 20 bpm, PaCO2 < 32 mm Hg)

27
Q

SIRS WBC findings

A

WBC > 12,000 or < 4,000 /ml, 10% bands

28
Q

Is there infection in SIRS?

A

No

29
Q

Consequence of an unbalanced response from SIRS or sepsis

A

Pro-inflammatory processes can have far reaching effects outside area of injury –> multi-organ dysfunction

30
Q

2 critical pathophysiological events in SIRS and sepsis

A
  1. Decreased peripheral vascular resistance
  2. Decreased oxygen extraction
31
Q

2 effects of decreased peripheral vascular resistance

A
  1. Permeable capillaries (“leaky vessels”)
  2. Hypotension
32
Q

2 effects of decreased oxygen extraction

A
  1. Metabolic acidosis
  2. Cellular damage
33
Q

Describe the general process leading to multi-organ dysfunction (6)

A
  1. Insult
  2. Liberation of TNF and IL-1
  3. Activation of proteases within cells
  4. Mediators act on various receptors located on immune cells, in blood vessels, etc.
  5. Liberation of vast quantities of pro- and anti-inflammatory cytokines
  6. Imbalance of pro- > anti-
34
Q

Effect of pro-inflammatory mediators on microcirculation

A

Microvascular thromboses

35
Q

APC role

A
  • Anti-inflammatory
  • Anti-apoptotic
  • Anti-thrombotic
36
Q

Consequence of reducing APC (3)

A
  1. Increased activation of thrombin
  2. Development of intravascular thromboses or clot
  3. Further reducing organ function
37
Q

3 methods of source control of IAI

A
  • Drainage
  • Debridement
  • Definitive measures to control ongoing source of infection and restore anatomy and function
38
Q

3 methods of controlling acute appendicitis

A
  • Appendectomy (open or laparoscopic)
  • Antibiotics only if gangrenous or perforated
  • Drainage of associated intra-abdominal abscesses
    • At time of initial OR post-op under image guidance
39
Q

Reason for follow-up requirement of adults treated non-operatively for appendicitis

A

Potential for malignancy (CT, endoscopy)

40
Q

Treatment for severe, diffuse peritonitis (perforation) (2)

A
  1. Emergency exploratory laparotomy to control the source of infection
    • “Damage control” for patients in septic shock or trauma
  2. Second look operation in 24-48 hours once patient is stable
    • May be required to re-evaluate bowel viability (i.e. ischemic bowel –> resect necrotic)
41
Q

4 potentially fatal organisms causing IAI

A
  1. E. coli
  2. Enterobacter/Klebsiella
  3. Proteus
  4. Pseudomonas
42
Q

5 organisms responsible for abscess in IAI

A
  1. Bacteroides
  2. Eubacteria
  3. Clostridia
  4. Peptostreptococci
  5. Peptococci
43
Q

Purpose of prophylaxis antimicrobial for treating IAI

A

Protection against skin organisms (asminister <60 min before incision)

44
Q

Empiric therapy combination in event of IAI (2)

A
  1. Clindamycin (G+, anaerobe)
  2. Gentamicin (G-)
45
Q

2 pathogens of IAI that are “low-risk”

A
  1. E. coli
  2. Bacteroides
46
Q

3 antibiotics for low-risk individuals with IAI

A
  1. Ampicillin
  2. Gentamicin
  3. Metronidazole
47
Q

3 antibiotic regimens for high risk individuals with IAI

A
  1. Pipercillin/tazobactam
  2. Imepenem
  3. Ciprofloxacin/metronidazole
48
Q

2 adverse effects of anti-microbial therapy for IAI

A
  • Ototoxicity
  • Nephrotoxicity

(Aminoglycosides)

49
Q

4 causes of mortality from IAI (from most common to least)

A
  1. Complicated mixed infections
  2. Diffuse suppurative peritonitis
  3. Localized peritonitis
  4. Localized abscess
50
Q

Reason for outcome variability of IAI

A

Genetic Heterogeneity Hypothesis

Genetic predisposition = genetic variations that disrupt innate immune sensing of infectious organisms = impaired ability of immune system to infection and current medical treatment

51
Q

3 points of rationale for studying gene single nucleotide polymorphisms (SNPs) in critical illnesses

A

Seek to identify:

  • Potential markers of susceptibility, severity and clinical outcome
  • Potential markers for responders and non-responder in clinical trials
  • Targets for therapeutic intervention

Block G -- Infection (23 decks)

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