1. INFECTION AND SEPSIS Surrounded by pathogens
Infection is the exception
Protective from infection
Physical barriers
Chemical barriers
Immunological function

2. Physical and Chemical Barriers to Infection
Skin
stronger in hands and feet
sebaceous secretions lower pH
Mucous membranes
ciliary function
mucous barrier
acid mileu in stomach

3. Barriers breached in Surgery

4. Barriers Breached in Trauma

5. Immune Defense Humoral defense Cellular defense Cytokines
antibodies
complement
Cellular defense
Cytokines
potential for deleterious effects
Interaction of mechanisms

6. Breakdown of Host Defense
Physical, chemical and immunological breakdown -act synergistically
e.g. patient with
diabetes
immunosuppresion
surgery
Potential for deleterious effects

7. Fourniers Gangrene

8. Commensal Microbial Flora
Important for immune development
Occupy binding sites for pathogens
Provide mucobacterial barrier
Anerobic bacteria
present in greatest quantity in GIT
Greatest diversity
Prevent invasion by gram neg. aerobes

9. Breakdown of Host Defense - GIT Flora
Transmigration of bacteria
Lack of feeding
Overuse of antibiotics
Absence of bile
Protein malnutrition
Immune deficiency

10. ICU patient fed enteraly To preserve GIT integrity

11. Infection Manifestation
Local signs
pain,redness,swelling, warmth loss of function
Systemic signs
Fever, somnolence, confusion, ileus, hypotension
Lab tests
TW,­polymorphs, Cultures
Non infective- causes may manifest as infection

12. Common Infections Wound infection
Initial inoculum overwhelms host defense
Occurs at days post op
Factors
host - immune suppression, DM, renal failure
surgeon - technique
environment - contamination

13. Common Infections Types of Wounds
1. Clean - no viscus, no sterile breach
2. Clean contaminated - controlled entry into viscus
3. Contaminated - emergency bowel resection, perforated appendix
4. Dirty - heavy contamination / long duration
Antibiotics used
type 2 as prophylaxis
type 3,4 as treatment

14. Wound Closure Wounds Closure by Timing of closure primary intention
secondary intention
Timing of closure
delayed primary closure
secondary closure

15. Closure by Secondary Intention

16. Intraabdominal Infection
Defense
Bacterial clearance - stomata between mesothelial cells under diaphragm lead to lymph vessels
Phagocytosis - both resident and recruited phagocytes
Sequestration - by fibrin rich inflammatory exudate, with omentum/viscera

17. Intraabdomianal Infection
Signs of peritonitis
Pain
sharp in character, well localised at first
spreads to surrounding areas
involuntary guarding, rigidity
absent bowel sounds
Posture
lying still, rapid breathing ,no movement
General condition
ill, septic, dehydrated, hypotension

18. Intraabdominal Infection
Usually viscus perforation
colon worse than upper GIT
Isolates
aerobic - E. Coli, klebsiella other enterobacter, strep, enterococci, proteus, pseudomonas
anaerobic - bacteroides, Clostridium
Treatment is surgical and aggressive antibiotic treatment

19. Enterocutaneous Fistula

20. Common Post Surgical Infections
Pneumonia
Protein malnourished
upper abdominal wounds ® poor cough
bed bound - atelectasis
elderly
ventilator
Occurs from 3 days post op
careful clinical exam,CXR
Routine chest physiotherapy

21. Common Post Surgical Infections
Urinary Tract Infection
catheters
dehydration
Remove catheters early
Ensure hydration
Antimicrobial therapy

22. Common Post Surgical Infections
Catheter and prosthetic devices
I/v canulas
central lines
mesh
Skin organisms- S aureus, S epidermidis
Aseptic technique
Remove if infected

23. Less Common Post Surgical Infections
Necrotising soft tissue infection
Parotitis
Sinusitis
Tonsillitis

24. Treatment of Infection
General principles
incise and drain pus
antibiotics as needed
debride dead tissue
remove foreign bodies

25. Antibiotic Therapy Prophylaxis Short course to prevent infection
Must be on board before contamination
Antibiotics with activity against expected inoculation organisms
Avoid extended spectrum agents
Post op benefit not proven
Topical antibiotics - not proven

26. Antibiotic Therapy Empirical therapy based on clinical information
search for source must continue
limit duration of empirical therapy
use known institution pattern of infection
multi agent vs broad agent

27. Antibiotic Therapy Directed therapy target identified pathogens
choose suitable efficacy /minimal toxicity agent
cover aerobic and anaerobic if likelihood exist for both
extended spectrum as last resort

28. Multiple System Organ Failure
AKA - Gram neg. bacterial sepsis
30% mortality
Healthy and compromised host
3-13 cases per 1000 admissions
Nosocomial

30. Multiple System Organ Failure
Factors
Host compromise
Elderly, disability
Malnutrition
Antimicrobial therapy
Major surgery
Cavity manipulation
Immunosuppression e.g. steroids

31. MSOF Fever Acidosis, hypoxemia Disordered oxygen and substrate use
Hyperglycaemia
Decreased systemic vascular resistance
Elevated cardiac output
Hypotension

32. MSOF Evidence for LPS - endotoxin LPS
O antigen - specific for each organism
core LPS
membrane lipid A

33. LPS - EFFECTS non specific polyclonal b cell proliferation
macrophage activation, cytokine release
hypotension, hypoxemia
bacterial translocation
complement and coagulation activation
platelet and white cell margination

34. LPS - Mechanism Direct effect of bacteria Indirect (mediated) effect
trigger macrophages to release TNFa, IL-1, IL-6, aIFN
TNFa, IL-1, - primary mediators but may be deleterious in large amounts
aIFN- causes continued activation of macrophages
Permeability defects in microcirculation
ARDS, GUT, Hepatic, renal failure

35. Problem
A 23 year old man had a perforated appendix. Three days post op this was his temperature chart. What is your interpretation.

36. Problem What is your choice for antibiotic prophylaxis for
colorectal surgery
biliary surgery
upper GI surgery

37. Problem
A 75 year old diabetic had an operation for perforated diverticular disease. His wound was found to be infected on the 5th POD.
What factors may have contributed to this?