Dr. Puligandla -- Intraabdominal Infections

Question 1

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

Answer 1

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

Question 2

What generally determines if and IAI will be complicated or not

Answer 2

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

Question 3

Define primary peritonitis

Answer 3

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

Question 4

Define secondary peritonitis

Answer 4

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

Question 5

Define tertiary peritonitis

Answer 5

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

Question 6

Pathogens responsible for primary peritonitis (3)

Answer 6

Monomicrobial:

1. Gram-negative enterbacteriaceae
2. Streptococci

NOTE: Infected ascites in ESLD

Question 7

Pathogens responsible for secondary peritonitis (3)

Answer 7

Polymicrobial:

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

Question 8

Pathogens responsible for tertiary peritonitis (4)

Answer 8

Nosocomial organisms, including:

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

Question 9

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

Answer 9

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

Question 10

5 associated symptoms of IAI

Answer 10

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

Question 11

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

Answer 11

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

Question 12

3 comorbidities to be aware of in event of IAI

Answer 12

1. Diabetes
2. Vascular disease
3. Immunosuppression

Question 13

4 potential findings of IAI patient’s vital signs

Answer 13

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

Question 14

6 signs of peritonitis

Answer 14

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

Question 15

Describe the pathophysiology of fever

Answer 15

Question 16

6 lab tests to request in event of IAI

Answer 16

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

Question 17

3 IAI CBC findings

Answer 17

1. Anemia
2. Leukocytosis
3. Thrombocytopenia

Question 18

Blood gas findings for IAI

Answer 18

Metabolic derangement (i.e. acidosis)

Question 19

Electrolytes finding of IAI

Answer 19

Hyper or hypokalemia

Question 20

5 potential findings on plain radiograph in event of IAI

Answer 20

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

Question 21

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

Answer 21

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

Question 22

Define infection

Answer 22

Process of bacteria invading normally sterile host tissues

Question 23

Define sepsis and its effects (6)

Answer 23

Response to infection causing:

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

Question 24

SIRS temperature

Answer 24

> 38^oC or < 36^oC

Question 25

SIRS HR

Answer 25

\> 90 bpm

Question 26

SIRS respiratory findings

Answer 26

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

Question 27

SIRS WBC findings

Answer 27

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

Question 28

Is there infection in SIRS?

Answer 28

No

Question 29

Consequence of an unbalanced response from SIRS or sepsis

Answer 29

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

Question 30

2 critical pathophysiological events in SIRS and sepsis

Answer 30

1. Decreased peripheral vascular resistance 2. Decreased oxygen extraction

Question 31

2 effects of decreased peripheral vascular resistance

Answer 31

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

Question 32

2 effects of decreased oxygen extraction

Answer 32

1. Metabolic acidosis 2. Cellular damage

Question 33

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

Answer 33

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-

Question 34

Effect of pro-inflammatory mediators on microcirculation

Answer 34

Microvascular thromboses

Question 35

APC role

Answer 35

* Anti-inflammatory * Anti-apoptotic * Anti-thrombotic

Question 36

Consequence of reducing APC (3)

Answer 36

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

Question 37

3 methods of source control of IAI

Answer 37

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

Question 38

3 methods of controlling acute appendicitis

Answer 38

* 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

Question 39

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

Answer 39

Potential for malignancy (CT, endoscopy)

Question 40

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

Answer 40

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)

Question 41

4 potentially fatal organisms causing IAI

Answer 41

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

Question 42

5 organisms responsible for abscess in IAI

Answer 42

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

Question 43

Purpose of prophylaxis antimicrobial for treating IAI

Answer 43

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

Question 44

Empiric therapy combination in event of IAI (2)

Answer 44

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

Question 45

2 pathogens of IAI that are "low-risk"

Answer 45

1. *E. coli* 2. *Bacteroides*

Question 46

3 antibiotics for low-risk individuals with IAI

Answer 46

1. Ampicillin 2. Gentamicin 3. Metronidazole

Question 47

3 antibiotic regimens for high risk individuals with IAI

Answer 47

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

Question 48

2 adverse effects of anti-microbial therapy for IAI

Answer 48

* Ototoxicity * Nephrotoxicity (Aminoglycosides)

Question 49

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

Answer 49

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

Question 50

Reason for outcome variability of IAI

Answer 50

**_Genetic Heterogeneity Hypothesis_** ## Footnote Genetic predisposition = genetic variations that disrupt innate immune sensing of infectious organisms = impaired ability of immune system to infection and current medical treatment

Question 51

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

Answer 51

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