Dr. Puligandla -- Intraabdominal Infections Flashcards Preview

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

Flashcards in Dr. Puligandla -- Intraabdominal Infections Deck (51)
1

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

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

2

What generally determines if and IAI will be complicated or not

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

3

Define primary peritonitis

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

4

Define secondary peritonitis

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

5

Define tertiary peritonitis

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

6

Pathogens responsible for primary peritonitis (3)

Monomicrobial:

  1. Gram-negative enterbacteriaceae
  2. Streptococci

NOTE: Infected ascites in ESLD

7

Pathogens responsible for secondary peritonitis (3)

Polymicrobial:

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

8

Pathogens responsible for tertiary peritonitis (4)

Nosocomial organisms, including:

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

9

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

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

10

5 associated symptoms of IAI

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

11

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

  1. Previous surgery
  2. Trauma
  3. Co-morbidities

12

3 comorbidities to be aware of in event of IAI

  1. Diabetes
  2. Vascular disease
  3. Immunosuppression

13

4 potential findings of IAI patient's vital signs

  1. Tachycardia
  2. Hypotension
  3. Tachypnea
  4. Fever

14

6 signs of peritonitis

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

15

Describe the pathophysiology of fever

16

6 lab tests to request in event of IAI

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

17

3 IAI CBC findings

  1. Anemia
  2. Leukocytosis
  3. Thrombocytopenia

18

Blood gas findings for IAI

Metabolic derangement (i.e. acidosis)

19

Electrolytes finding of IAI

Hyper or hypokalemia

20

5 potential findings on plain radiograph in event of IAI

  1. "Free air"
  2. Intestinal obstruction
  3. Mucosal ischemia ("thumb-printing")
  4. Contrast studies
    • Leak
    • Obstruction

21

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

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

22

Define infection

Process of bacteria invading normally sterile host tissues

23

Define sepsis and its effects (6)

Response to infection causing:

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

24

SIRS temperature

> 38oC or < 36oC

25

SIRS HR

> 90 bpm

26

SIRS respiratory findings

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

27

SIRS WBC findings

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

28

Is there infection in SIRS?

No

29

Consequence of an unbalanced response from SIRS or sepsis

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

30

2 critical pathophysiological events in SIRS and sepsis

  1. Decreased peripheral vascular resistance
  2. Decreased oxygen extraction

31

2 effects of decreased peripheral vascular resistance

  1. Permeable capillaries ("leaky vessels")
  2. Hypotension

32

2 effects of decreased oxygen extraction

  1. Metabolic acidosis
  2. Cellular damage

33

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

  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

Effect of pro-inflammatory mediators on microcirculation

Microvascular thromboses

35

APC role

  • Anti-inflammatory
  • Anti-apoptotic
  • Anti-thrombotic

36

Consequence of reducing APC (3)

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

37

3 methods of source control of IAI

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

38

3 methods of controlling acute appendicitis

  • 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

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

Potential for malignancy (CT, endoscopy)

40

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

  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

4 potentially fatal organisms causing IAI

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

42

5 organisms responsible for abscess in IAI

  1. Bacteroides
  2. Eubacteria
  3. Clostridia
  4. Peptostreptococci
  5. Peptococci

43

Purpose of prophylaxis antimicrobial for treating IAI

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

44

Empiric therapy combination in event of IAI (2)

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

45

2 pathogens of IAI that are "low-risk"

  1. E. coli
  2. Bacteroides

46

3 antibiotics for low-risk individuals with IAI

  1. Ampicillin
  2. Gentamicin
  3. Metronidazole

47

3 antibiotic regimens for high risk individuals with IAI

  1. Pipercillin/tazobactam
  2. Imepenem
  3. Ciprofloxacin/metronidazole

48

2 adverse effects of anti-microbial therapy for IAI

  • Ototoxicity
  • Nephrotoxicity

(Aminoglycosides)

49

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

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

50

Reason for outcome variability of IAI

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

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

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