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

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

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

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

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

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

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

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

Surgical infections’ origin Contact Aerial Hematogen Endogen Exogen

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

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

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

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

Necrotizing infections Spread along anatomically defined path Clostridial myonecrosis Necrotizing fasciitis

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

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

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

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

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

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

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

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

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)

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

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

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

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

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

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

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

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

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

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

Tetanus IV. Therapy ICU Absorbed Tetanus Toxoid (active immunization) TIG (3-6000 U im., passive immunization) Surgery Drugs (Barbiturates, cardiacs, ect.) Penicillin 10-40 MU/day

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