Dr. Puligandla -- Intraabdominal Infections Flashcards
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
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
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
Define secondary peritonitis
Peritoneal infection developing in conjunction with an inflammatory process of GIT or its extensions, usually associated with microscopic or macroscopic perforation
Define tertiary peritonitis
A persistent or recurrent peritoneal infection developing are initial treatment of secondary peritonitis
Pathogens responsible for primary peritonitis (3)
Monomicrobial:
- Gram-negative enterbacteriaceae
- Streptococci
NOTE: Infected ascites in ESLD
Pathogens responsible for secondary peritonitis (3)
Polymicrobial:
- Aerobic gram-negative bacilli
- Gram-positive cocci
- Enteric anaerobes
Pathogens responsible for tertiary peritonitis (4)
Nosocomial organisms, including:
- Resistant gram negative bacilli
- Enterococci
- Staphylococci
- Yeast
6 types of causes of secondary bacterial peritonitis in the hospitalized patient
- Post-operative peritonitis
- Procedural complications
- Spontaneous GI perforation
- Intestinal ischemia
- Device-related infection
- Community-acquired infection
5 associated symptoms of IAI
- Fever
- Emesis
- Diarrhea or change in bowel habit
- Blood in stool
- Abdominal distension
3 associated medical problems that one must be aware of in the event of IAI
- Previous surgery
- Trauma
- Co-morbidities
3 comorbidities to be aware of in event of IAI
- Diabetes
- Vascular disease
- Immunosuppression
4 potential findings of IAI patient’s vital signs
- Tachycardia
- Hypotension
- Tachypnea
- Fever
6 signs of peritonitis
- Rebound
- Guarding
- Distension
- Reduced bowel sounds
- Abdominal wall changes
- Visible loops
Describe the pathophysiology of fever
6 lab tests to request in event of IAI
- CBC
- Blood gas
- Electrolytes
- Urea/creatinine
- Liver enzymes
- LFTs
3 IAI CBC findings
- Anemia
- Leukocytosis
- Thrombocytopenia
Blood gas findings for IAI
Metabolic derangement (i.e. acidosis)
Electrolytes finding of IAI
Hyper or hypokalemia
5 potential findings on plain radiograph in event of IAI
- “Free air”
- Intestinal obstruction
- Mucosal ischemia (“thumb-printing”)
- Contrast studies
- Leak
- Obstruction
4 things to identify in event of IAI in a CT scan
- Fluid collections
- Abscess
- Ischemic bowel
- Perfusion of vital organs
Define infection
Process of bacteria invading normally sterile host tissues
Define sepsis and its effects (6)
Response to infection causing:
- Pyrexia
- Tachypnea
- Tachycardia
- Hypoxia
- Hypermetabolism
- Organ(s) dysfunction
SIRS temperature
> 38oC or < 36oC
SIRS HR
> 90 bpm
SIRS respiratory findings
Tachypnea (RR > 20 bpm, PaCO2 < 32 mm Hg)
SIRS WBC findings
WBC > 12,000 or < 4,000 /ml, 10% bands
Is there infection in SIRS?
No
Consequence of an unbalanced response from SIRS or sepsis
Pro-inflammatory processes can have far reaching effects outside area of injury –> multi-organ dysfunction
2 critical pathophysiological events in SIRS and sepsis
- Decreased peripheral vascular resistance
- Decreased oxygen extraction
2 effects of decreased peripheral vascular resistance
- Permeable capillaries (“leaky vessels”)
- Hypotension
2 effects of decreased oxygen extraction
- Metabolic acidosis
- Cellular damage
Describe the general process leading to multi-organ dysfunction (6)
- Insult
- Liberation of TNF and IL-1
- Activation of proteases within cells
- Mediators act on various receptors located on immune cells, in blood vessels, etc.
- Liberation of vast quantities of pro- and anti-inflammatory cytokines
- Imbalance of pro- > anti-
Effect of pro-inflammatory mediators on microcirculation
Microvascular thromboses
APC role
- Anti-inflammatory
- Anti-apoptotic
- Anti-thrombotic
Consequence of reducing APC (3)
- Increased activation of thrombin
- Development of intravascular thromboses or clot
- Further reducing organ function
3 methods of source control of IAI
- Drainage
- Debridement
- Definitive measures to control ongoing source of infection and restore anatomy and function
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
Reason for follow-up requirement of adults treated non-operatively for appendicitis
Potential for malignancy (CT, endoscopy)
Treatment for severe, diffuse peritonitis (perforation) (2)
- Emergency exploratory laparotomy to control the source of infection
- “Damage control” for patients in septic shock or trauma
- 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)
4 potentially fatal organisms causing IAI
- E. coli
- Enterobacter/Klebsiella
- Proteus
- Pseudomonas
5 organisms responsible for abscess in IAI
- Bacteroides
- Eubacteria
- Clostridia
- Peptostreptococci
- Peptococci
Purpose of prophylaxis antimicrobial for treating IAI
Protection against skin organisms (asminister <60 min before incision)
Empiric therapy combination in event of IAI (2)
- Clindamycin (G+, anaerobe)
- Gentamicin (G-)
2 pathogens of IAI that are “low-risk”
- E. coli
- Bacteroides
3 antibiotics for low-risk individuals with IAI
- Ampicillin
- Gentamicin
- Metronidazole
3 antibiotic regimens for high risk individuals with IAI
- Pipercillin/tazobactam
- Imepenem
- Ciprofloxacin/metronidazole
2 adverse effects of anti-microbial therapy for IAI
- Ototoxicity
- Nephrotoxicity
(Aminoglycosides)
4 causes of mortality from IAI (from most common to least)
- Complicated mixed infections
- Diffuse suppurative peritonitis
- Localized peritonitis
- Localized abscess
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
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
