1. Wound healing, surgical infections, gas gangrene, tetanus
Csaba Kósa, M.D.
Department of Surgery

2. Wound healing Cover the wound, substitute damaged tissues
Conditions: clear wound, good oxigene supply, adequate macrophag function
First intention or primary
Repair without complication
Second intention or secondary
Formation of granulation tissue
Eventual migration of epithelial cells
Infected (bacterial or abacterial) wounds and burns

3. Phases of wound healing
Inflammation : 2-3 days, macrophags, gel formation, thrombocyte aggregation, capillarisation
Prolifaration: 4-7 days, fibroblasts, ganulation, collagen and elastin reticulation
Reparation and scar: 8. day, wound contraction, epithelisation

4. Healing failure
Impaired perfusion and oxygenation are the most common causes
Oxygen!
Profoundly influenced by local blood supply, vasoconstriction and factors that govern perfusion

5. Impaired healing
Disorders of inflammation – excessive and inadequate inflammatory responses can cause problems
Anti-inflammatory corticosteroids, immune suppressants, cancer chemotherapeutic agents
Malnutrition – weight loss, protein depletion

6. Surgical techniques Technical errors!
Tissues should be protected from drying, contamination
Clean, sharp dissection
Gentle handling of tissue
Postoperative care!

7. Surgical infections Definition
Occupies an unvascularized space in tissue or an operated site
Appendicitis, empyema, abscess ect.
Unlikely to respond to conservative treatment
It can be a vicious circle

8. Pathogenesis Elements An infectious agent Susceptible host
A closed, unperfused space

9. Surgical infections’ origin
Contact
Aerial
Hematogen
Endogen
Exogen

10. 1. Infectious agents Staphylococcus aureus Klebsiella
Enteric organisms
Anaerobs
Bacteroides, peptosterptococci
Clostridiums
Smear and culture is important!
if there is any suspicion

11. Risk factors Immunosuppression body AIDS, burn, diabetes, anergy, ect.
2. Susceptible host
Risk factors
Immunosuppression body
AIDS, burn, diabetes, anergy, ect.

12. 3. Closed space Denominators are: Poorly perfused tissue
Local hypoxia, Hypercapnia
Acidosis
Spaces with narrow outlets:
Gallbladder, appendix, intestines

13. Spread of infections Necrotizing infections Abscesses
Phlegmons and superficial inf.
Spread via lymphatic system
Spread via bloodstream

14. Necrotizing infections
Spread along anatomically
defined path
Clostridial myonecrosis
Necrotizing fasciitis

15. Abscesses enlarge, killing more Leukocytes contribute to necrosis
tissue
Leukocytes contribute to necrosis
by lysosomal enzymes

16. Phlegmons and superficial infections
Contain little pus, but much
edema
Spread along fat planes with the
features of necrosis and
abscesses

18. Spread via lymphatic system
infective agents are streptococcus and staphylococcus
Lymphangitis
Lymphadenitis

19. Spread via bloodstream
Causes metastatic abscesses
Empyema
Endocarditis
Liver abscess
Brain abscess
Pylephlebitis (septic thrombosis of the portal vein)

20. Complications Fistulas (abdominal infections) Suppressed wound healing
Immunosuppression (consumptional immunopathy)
Superinfection – antibiotic resistency

21. Bacteriaemia and septicaemia
-Bacteria are in the blood
-Infections, manipulations
- Bacteria and endotoxins in
the blood
-clinical features: chill, fever,
hypotension, shock

22. Sepsis I. Diagnosis Physical examination (locally): Erythema
Induration
Warmth
Tenderness

23. Sepsis II. Diagnosis Laboratory findings: Leukocytosis CRP, PCT
Acidosis
Blood cultures

24. X-ray (chest, abdominal) Ga 67 labeling leukocytes (scintigraphy)
Sepsis III.
Diagnosis
Imaging studies:
X-ray (chest, abdominal)
Ultrasound
CT scan
Ga 67 labeling leukocytes (scintigraphy)

25. Incision, drainage, excision
Sepsis IV.
Treatment
Locally:
Incision, drainage, excision
Circulatory enhancement:
Antibiotics:
First
Second
Nutritinal support:

26. Clostridial infections I.
Anaerobic, sporulating, Gram+ bacteria
Cl. welchii seu perfringens 80%
Cl. hystolyticum40%
Cl. septicum 20%
Mixed infections

27. Clostridial infections II. Predisposing factors
War injury
Dirty wound
Necrotic wound
Poor tissue perfusion
Arterial stenosis

28. Clostridial infections III.
Pathomechanism
Poorly vascularized tissues
Toxins
Proteolytic ensymes (capillary damage)
Local symptoms
Genereal symptoms

29. Clostridial infections III.
Clinical classification
Simple contamination
Gas abscess (Welch’s abscess)
Crepitant clostridial cellulitis
Localized clostridial myositis
Diffuse clostridial myositis (gas gangrene)
Edematous gangrene

30. Clostridial infections IV. symptoms, diagnosis
Latent period of hours to 3 days
Local:
Pain, oedema
Brownish colour
Gravy-like secretion
Crepitation, sweet smell
Myonecrosis
General:
Fever, tachycardia, delirium
Hypotension, fluster, Shock
MOF

31. Clostridial infections V.
Treatment
Wide surgical exploration
Necrectomy
H2O2 locally
Antibiotics (Penicillin, Metronidazole)
ICU

32. Tetanus I. Cause:
Clostridium tetani: spores survive for years, getting into wounds in anaerobic circumstances propagate and produce toxins:
tetanospasmin
tetanolysin
neurotoxin

33. Tetanus II. Predisposing factors
War injury
Dirty wound
Necrotic wound
Poor tissue perfusion
Arterial stenosis

34. Tetanus III. Diagnosis 2-21 days latent period
Limitation of movements of jaws
Painful muscle spasm-trismus
Laryngospasm
Stiffnes of the neck
Tonic spasms and convulsions
Presence of non treated wound

35. Tetanus IV. Therapy ICU Absorbed Tetanus Toxoid (active immunization)
TIG ( U im., passive immunization)
Surgery
Drugs (Barbiturates, cardiacs, ect.)
Penicillin MU/day

36. Tetanus V. Prevention Active immunisation TIG
Absorbed Tetanus Toxoid (booster vaccination every 10 years)
Correct surgical treatment