GC178 An Ugly Wound Wound Healing; Wound Infection; Anti-septic Technique
Wound healing is the biological process of tissue repair that can be complicated by wound infection when microbial colonization overwhelms host defenses, necessitating proper antiseptic technique to minimize contamination and promote optimal tissue restoration.
Lecture Map: The Big Idea
This lecture — GC 178: An Ugly Wound — is a foundational surgical-science session that bridges basic science (wound healing physiology) with clinical practice (wound infection recognition, antiseptic technique, debridement). It is taught by a Plastic Surgery faculty member (Dr. D. M. Wong) and underpins virtually every surgical and many medical scenarios you will encounter.
Why does this matter? Every operation creates a wound. Every wound follows the same biological healing cascade. When that cascade is disrupted (by bacteria, ischaemia, malnutrition, etc.), wound complications ensue — the single most common surgical morbidity. Understanding this cascade from first principles lets you predict complications, prevent infection, and manage non-healing wounds logically.
- Etiology of wound
- Description of wound
- Physiology of wound healing
- Pathological wound healing
- Factors affecting wound healing
- Wound infection and prevention
- MCQ/EMQ: Phases of wound healing (timelines, collagen types), sterilization methods, wound classification, antiseptic agents, debridement types.
- SAQ: Clinical signs of wound infection, factors affecting healing, principles of antiseptic technique, management of infected wound.
- OSCE/Viva: Describe a wound, scrub technique, draping, debridement rationale.
Etiology of wound: External — Traumatic, Thermal, Chemical, Surgical. Local — Vascular, Pressure, Neuropathic, Infective, Malignant. [1]
High Yield — Classification of Wound Etiology
The lecture classifies wound causes into External and Local. This is a favourite short-answer framing: "List the causes of chronic wounds" or "What local factors cause non-healing ulcers?"
| Category | Subtype | Example | Why It Causes a Wound |
|---|---|---|---|
| External | Traumatic | Laceration, stab wound | Direct mechanical tissue disruption |
| Thermal | Burns (heat, cold, friction) | Protein denaturation → tissue necrosis | |
| Chemical | Acid/alkali burn, extravasation injury | Chemical destruction of cells | |
| Surgical | Incisional wound | Intentional controlled tissue division | |
| Local | Vascular | Venous ulcer (gaiter area), arterial ulcer (toes/pressure points) | Inadequate O₂/nutrient delivery or venous stasis → tissue breakdown |
| Pressure | Pressure sore/decubitus ulcer | Sustained pressure > capillary closing pressure (~32 mmHg) → ischaemic necrosis | |
| Neuropathic | Diabetic foot ulcer | Loss of protective sensation → unrecognised trauma → chronic wound | |
| Infective | Fungal skin infection, necrotizing fasciitis | Organisms directly destroy tissue | |
| Malignant | Marjolin's ulcer (SCC in chronic ulcer), fungating tumour | Tumour outgrows blood supply → central necrosis |
Slide-Specific Clinical Images Highlighted [1]
- Pressure sore and Venous ulcer — classic exam image recognition
- Partially healed burn wound with slough — slough = dead tissue that must be debrided
- Extravasation wound — chemical injury from IV drug leaking into tissues (e.g., chemotherapy, calcium gluconate)
- Fungal infection — local/infective cause of wound
2. Physiology of Wound Healing
Wound Healing: A complex interactive process involving a variety of cell types, soluble factors and matrix components. [1]
Fetus → regeneration. Neonate–Adult → fibrosis/scarring. [1]
Why? Fetal wounds heal in a sterile, amniotic fluid–bathed environment with a different cytokine profile (less TGF-β1, more TGF-β3, reduced inflammation). The result is scarless regeneration. After birth, the inflammatory response dominates, and healing proceeds through fibrosis — this is why adults scar.
High Yield — Four Phases with Timelines
Examiners love to test the phase names, timelines, key cells, and collagen type transitions. Memorise the table below.
| Phase | Timeline | Key Events | Key Cells | Key Mediators |
|---|---|---|---|---|
| (1) Haemostasis | Immediate | Tissue injury → TF activates extrinsic clotting cascade; Platelets clump → platelet plug; Fibrinogen → fibrin | Platelets | Tissue Factor, thrombin, fibrin |
| (2) Inflammatory | Immediate – Day 5 | Platelet degranulation → PDGF, TGF-β; Phagocytosis by neutrophils (early) and macrophages (later) | Neutrophils (first 24–48h), Macrophages (48h onward — the "conductor" cell of wound healing) | PDGF, TGF-β, IL-1, TNF-α |
| (3) Proliferative | Day 4 – Day 21 | Fibrin matrix replaced by granulation tissue → Type III collagen; Fibroblasts proliferate, migrate, deposit ECM; Endothelial cells → neovascularization; Re-epithelialization — keratinocyte migration | Fibroblasts, Macrophages, Endothelial cells, Keratinocytes | PDGF, TGF-β1, VEGF, FGF |
| (4) Remodelling | Day 21 – 1 year | Programmed regression of blood vessels and granulation tissue; Wound contraction (myofibroblasts); Collagen remodelling — Type III → Type I | Myofibroblasts, Fibroblasts | MMPs, TIMPs |
Phase 1 — Haemostasis (Immediate): When tissue is injured, subendothelial collagen is exposed. Platelets adhere (via vWF), activate, and aggregate → platelet plug. Simultaneously, Tissue Factor (TF) on injured cells triggers the extrinsic pathway: TF + Factor VII → activation cascade → thrombin → converts fibrinogen to fibrin. The fibrin mesh stabilises the platelet plug. This forms the provisional matrix that all subsequent healing is built upon. Why is this important? Patients on anticoagulants or with coagulopathies have impaired haemostasis → haematoma → increased infection risk → impaired healing.
Phase 2 — Inflammatory (Immediate – Day 5): As platelets degranulate, they release PDGF and TGF-β — powerful chemotactic signals. Neutrophils arrive within hours (attracted by IL-8, complement fragments). They phagocytose bacteria and debris. By 48 hours, macrophages become the dominant cell. Macrophages are essential — they continue phagocytosis, release growth factors (PDGF, TGF-β1, VEGF, FGF), and orchestrate the transition to the proliferative phase. Without macrophages, wound healing essentially stops. This is why immunosuppression (steroids, chemotherapy) delays healing — these drugs impair macrophage function.
Phase 3 — Proliferative (Day 4–21): The fibrin matrix is gradually replaced by granulation tissue — a highly vascular, collagen-rich tissue. Three key processes occur simultaneously:
- Fibroplasia: Fibroblasts migrate in, proliferate, and deposit Type III collagen (immature, thin fibres).
- Angiogenesis/Neovascularisation: Endothelial cells sprout new capillaries (driven by VEGF, FGF). This is why healthy granulation tissue looks beefy red — it's packed with new capillaries.
- Re-epithelialization: Keratinocytes at wound edges and from residual skin appendages (hair follicles, sweat glands) migrate across the wound surface. They require a moist wound bed. This is why desiccation impairs healing — dry wounds slow keratinocyte migration.
Phase 4 — Remodelling (Day 21 – 1 year): The wound matures. Type III collagen is progressively replaced by Type I collagen (thicker, stronger, organised fibres). Excess blood vessels regress. Myofibroblasts (fibroblasts with smooth-muscle-like contractile properties) cause wound contraction, physically pulling wound edges together. Collagen cross-links increase, raising tensile strength.
Tensile strength of healing wound: maximum ~80% of normal skin. Collagen content plateaus during the proliferative phase, but tensile strength continues to increase during the remodelling phase (due to cross-linking and Type III → Type I transition). [1]
Exam Trap: Collagen Content vs Tensile Strength
The slide shows that collagen content peaks during the proliferative phase, but tensile strength continues to rise during the remodelling phase. This is because tensile strength depends not just on how much collagen is present, but on how it is organised (cross-linking, fibre alignment, Type I vs III ratio). A healed wound never reaches 100% of original strength — maximum is ~80%. [1]
From GC 192 (Plastic Surgery): Primary closure — wound closed with approximation of wound edges surgically. Delayed primary closure — wound remains open for few days before surgical closure (allows drainage, decreases infection risk in contaminated wounds, e.g., dog bite). Secondary closure (secondary intention) — wound closure by granulation, epithelialization and contraction (for infected/contaminated wounds, e.g., abscess). Prolonged inflammatory phase, healing with increased scarring and contracture. [3]
| Type | Mechanism | Indication | Scar Quality |
|---|---|---|---|
| Primary intention | Direct surgical approximation | Clean surgical wound | Minimal, linear scar |
| Delayed primary (Tertiary intention) | Left open 3–5 days → then surgically closed | Contaminated wound (e.g., dog bite, dirty trauma) | Better than secondary, reduced infection risk |
| Secondary intention | Granulation → contraction → epithelialisation | Infected wound, abscess cavity | More scarring, contracture |
Pathological healing: Arrested in inflammatory phase → chronic/non-healing wound (e.g., venous ulcer, diabetic ulcer). Arrested in proliferative phase → excessive granulation/hypertrophic scarring/keloid. [1]
Why does a wound get "stuck" in the inflammatory phase? In chronic wounds (venous ulcers, diabetic ulcers, pressure sores), persistent stimuli (ischaemia, bacterial colonisation, repeated trauma) maintain the inflammatory response. Neutrophils and macrophages keep releasing pro-inflammatory cytokines and MMPs that break down the nascent ECM faster than fibroblasts can rebuild it. The wound never transitions to effective proliferation.
Why does a wound get "stuck" in the proliferative phase? If the proliferative phase is overactive or fails to transition to remodelling, excess collagen accumulates → hypertrophic scar (stays within wound boundaries, may regress) or keloid (extends beyond wound boundaries, does not regress, more common in darker skin, genetic predisposition).
Systemic Factors: Old age, Obesity, Chronic diseases (DM, anaemia, chronic renal disease), Malnutrition/malabsorption, Genetic factor, Smoking, Medications (steroids, immunosuppressants, chemotherapy). Local Factors: Infection, Pressure, Edema, Desiccation, Colonization, Hypoxia (post-RT, arterial insufficiency). [1]
High Yield — Factors Affecting Wound Healing
This is one of the most frequently examined lists in surgical principles. Both systemic and local factors are testable.
| Factor | Mechanism of Impaired Healing |
|---|---|
| Old age | Reduced cell proliferation, decreased collagen synthesis, impaired immune function |
| Obesity | Poor tissue perfusion of adipose tissue, increased wound tension, higher infection rate |
| DM | Microangiopathy → hypoxia; hyperglycaemia impairs neutrophil function; neuropathy → unrecognised injury |
| Anaemia | Reduced O₂ delivery to wound bed |
| CKD | Uraemia impairs immune function and platelet function; fluid overload → oedema |
| Malnutrition | Protein (albumin < 30 g/L), vitamin C (collagen hydroxylation), zinc (cell division, immune function) deficiency |
| Smoking | Nicotine → vasoconstriction → tissue hypoxia; CO → shifts O₂-Hb dissociation curve left; impairs macrophage function |
| Steroids | Suppress inflammatory phase, inhibit macrophage function, reduce collagen synthesis |
| Immunosuppressants/chemo | Impair immune cell function, reduce cell proliferation |
| Infection (local) | Bacteria consume O₂ and nutrients, release toxins/proteases that destroy ECM, prolong inflammatory phase |
| Pressure (local) | Exceeds capillary closing pressure → ischaemia |
| Oedema (local) | Increases diffusion distance for O₂ and nutrients |
| Desiccation (local) | Dries out wound bed → impairs keratinocyte migration |
| Colonisation (local) | Sub-clinical bacterial burden that can progress to frank infection |
| Hypoxia (local) | Post-radiotherapy (obliterative endarteritis), arterial insufficiency → fibroblasts and WBCs need O₂ |
6. Wound Infection
Wound infection: bacterial growth > 100,000 organisms per gram of tissue (10⁵/g). [1]
Why this threshold? Below 10⁵/g, the host immune system can generally control the bacterial burden without clinical sequelae (this is "colonisation"). Above 10⁵/g, bacterial load overwhelms local defences, toxins/enzymes destroy tissue, and clinical infection manifests. This threshold is also important for skin graft take — grafts placed on beds with > 10⁵ bacteria/g tissue will fail.
| Severity | Clinical Features | Slide Reference |
|---|---|---|
| Mild wound infection | Pain, Erythema, Edema, Increased temperature | [1] |
| Wound infection with skin necrosis | Above features + skin necrosis | [1] |
| Severe wound infection | Pus collection (abscess) | [1] |
| Burn wound infection | High risk due to loss of skin barrier, eschar provides culture medium | [1] |
| Fournier Gangrene | Necrotizing fasciitis of perineum/genitalia — surgical emergency, polymicrobial, rapidly progressive, high mortality | [1] |
High Yield — Fournier Gangrene
Fournier gangrene is necrotizing fasciitis of the perineum. It is a life-threatening surgical emergency requiring immediate aggressive surgical debridement + broad-spectrum IV antibiotics + supportive care. Delay in surgery = death. Risk factors: DM, immunosuppression, perineal/perianal infection, urethral catheterisation.
Treatment: Wound assessment (clinical, imaging) → Adequate debridement / removal of foreign body → Wound swab for culture → Empirical antibiotics, streamline after culture results → Dressing of wound → Irrigation of a cavity/sinus if present. [1]
This is a systematic approach — learn it as a checklist:
- Assess — Look, feel, smell. Consider imaging (USS for superficial collection, CT for deep/organ-space infection).
- Debride — Remove all dead/necrotic tissue and foreign bodies.
- Culture — Wound swab (avoid wound edge — contamination with skin flora), pus aspiration, or tissue biopsy. Send for C/ST.
- Antibiotics — Start empirical (broad-spectrum), then narrow when sensitivities return.
- Dress — Appropriate wound dressing to maintain moist environment.
- Irrigate — If a sinus or cavity exists, irrigation dilutes bacterial load.
8. Wound Debridement
Debridement: Removal of necrotic tissue from wound bed to promote wound healing. It is a natural process that occurs in all wounds. [1]
Remove foreign body (hair, sutures, dirt) — foreign body is a physical barrier against epithelialization. Reduces bacterial burden. Remove exudate. Promotes effective inflammatory response for healthy granulation tissue.
Healthy wound bed to promote granulation and epithelialization. Healthy wound bed for reconstruction (skin grafts, flaps).
A healthy wound bed = pink/red granulation tissue, no slough, no necrotic tissue, no foreign bodies.
| Method | Description | Characteristics |
|---|---|---|
| Autolytic | Body's own enzymes (proteases) break down necrotic tissue | Slowest; uses moist dressings (hydrogels) to facilitate; selective; painless |
| Sharp debridement | Using scalpel/scissors at bedside | Quick, selective, requires skill; can be done under LA |
| Enzymatic | Topical enzymes (e.g., collagenase) applied to wound | Selective; moderate speed; useful when surgery contraindicated |
| Mechanical | Wet-to-dry dressings, irrigation, hydrotherapy | Non-selective (removes healthy tissue too); can be painful |
| Biological | Sterile maggots (larval therapy) — Lucilia sericata larvae | Selective; larvae secrete proteases that dissolve necrotic tissue only; also have antibacterial properties |
| Surgical debridement | By surgeons in OR. Sharp debridement by scalpel, scissors, curette. Tangential debridement by Watson's knife, Goulian knife. Hydrosurgery (Versajet). USG debridement (Sonoca). Non-selective, requiring anaesthesia, creates larger wound. | Most thorough; for large/deep wounds, burns, Fournier gangrene |
- Scissors, scalpel, curette — sharp debridement
- Watson knife, Goulian knife — tangential excision (shaving thin layers of dead tissue, especially in burns)
- Versajet Hydrosurgery System — high-pressure (up to 15,000 psi) high-velocity sterile saline stream; Venturi effect creates local vacuum on the debriding surface; power settings 1–10; 8–14mm aperture. Advantage: precise, tissue-selective.
- Sonoca (USG debridement) — ultrasound energy to disrupt necrotic tissue
9. Antiseptic Technique and Prevention of Wound Infection
Every surgical wound is contaminated by bacteria. Three sources: (1) Surgical team, (2) Patient, (3) Operative environment. [1]
High Yield — Three Sources of Surgical Wound Contamination
Examiners may ask: "Name the 3 sources of contamination in a surgical wound." Answer: Surgical team, Patient, Operative environment. Then detail the preventive measures for each.
(1) Surgical Team [1]
Mask, Gloves, Eye shield/goggles, Face shield, Barrier gowns
Why each item matters:
- Mask: Prevents droplet transmission of oral/nasal flora to wound
- Gloves: Barrier between surgeon's hands and patient's tissues
- Eye shield/goggles/face shield: Protects surgeon from blood/body fluid splash (universal precautions)
- Barrier gowns: Prevents transmission of organisms from surgeon's body/clothing
Povidone-iodine (Betadine) — rapid onset of action, broad spectrum, short effect. Chlorhexidine gluconate — longer acting. Brushes: may cause skin abrasions.
| Agent | Onset | Spectrum | Duration | Notes |
|---|---|---|---|---|
| Povidone-iodine | Rapid | Broad (G+, G−, fungi, viruses, spores) | Short (washes off, inactivated by organic matter) | Allergic reactions possible; stains |
| Chlorhexidine gluconate | Moderate | Broad (less sporicidal than iodine) | Longer acting (binds to stratum corneum — residual activity) | Ototoxic (avoid near ear); less affected by organic matter |
Why brushes may be harmful: Vigorous scrubbing with brushes causes micro-abrasions on the surgeon's skin → disrupts the skin barrier → paradoxically increases bacterial shedding and risk of self-inoculation. Current practice favours alcohol-based hand rubs or gentle sponge application.
Gentle tissue handling. Careful haemostasis to prevent haematoma formation. Irrigation of surgical field to dilute/reduce bacterial load.
Why haemostasis matters: Haematoma = collection of blood = excellent culture medium for bacteria + impairs local immune cell function (high protein, iron-rich environment). Meticulous haemostasis reduces this risk.
(2) Patient Preparation [1]
The longer the hospital stay, the higher the chance of hospital-acquired infection. Pre-existing pneumonia, drip site or other catheterisation are sources of infection. Colonisation by antibiotic-resistant bacteria. Special attention: smoker, DM/CRF/immunosuppressant, aspirin/anticoagulants.
Why longer hospital stay = more infection: Prolonged hospitalisation → colonisation by hospital flora (often resistant organisms like MRSA, ESBL-producing Enterobacteriaceae). Same-day admission for elective surgery reduces this risk.
Hair adjacent to operative site to be removed. Shaving often causes injury to the skin, increasing wound infection rates. Perform as near to the time of surgery as possible. Clippers preferred.
Why clippers > razors: Razor shaving creates micro-cuts that bacteria colonise. Clippers cut hair without cutting skin. Evidence shows that shaving the night before surgery significantly increases SSI rates compared to clipping immediately before surgery.
Use sterilized sponge forceps to apply: Povidone iodine, Aqueous chlorhexidine gluconate, Alcohol-based chlorhexidine gluconate. Beware of accumulation and subsequent burn injury.
| Solution | Slide Name | Key Points |
|---|---|---|
| Povidone Iodine | Povidone Iodine | Broad spectrum; rapid onset; inactivated by organic matter |
| Aqueous Hibitane 0.05% | Aqueous Hibitane 0.05% | Chlorhexidine; for skin/wound prep |
| Aqueous Hibitane 0.015% | More dilute; for wound irrigation | |
| Alcoholic Hibitane | Alcoholic Hibitane | Chlorhexidine in alcohol; most effective for intact skin prep; fire risk under diathermy! |
Exam Trap — Alcohol-Based Antiseptics and Diathermy Burns
Beware of accumulation and subsequent burn injury — the lecture explicitly warns about this. Alcohol-based solutions that pool (e.g., in skin folds, around drapes) can ignite when diathermy is used. Always allow alcohol to dry completely before draping and using diathermy.
Protect from contamination from the periphery. Sterilized cotton drapes — protection diminished when wet. Plastic disposable drapes.
Why cotton drapes lose protection when wet: Moisture wicks bacteria through the cotton fibres ("strike-through") → breaks the sterile barrier. Plastic/disposable drapes are impervious to fluid.
Dirty trauma wounds. Entry into nasal cavity/oropharynx/bowel etc. Cardiac indications (heart valves/vegetations). Cover up source of contamination — nipple shield in breast implant insertion.
Integration with GC 098 and Surgical Principles [2][4]:
| Wound Class | Infection Risk | Examples | Prophylactic Abx |
|---|---|---|---|
| Clean | 1–2% | Thyroid, breast, hernia (without mesh) | Not usually required; use if implant/prosthesis inserted |
| Clean-contaminated | 5–10% | Biliary, GIT (prepared), urinary tract | Yes — until end of surgery |
| Contaminated | 15–20% | Unprepared colon, open fractures, spillage | Yes — until end of surgery |
| Dirty | 40–50% | Perforated viscus, faecal peritonitis, abscess | Full therapeutic course |
Timing: Administer at induction of anaesthesia (to achieve peak tissue levels at time of incision). Re-dose if surgery > 2× half-life of antibiotic or blood loss > 1.5L. [4]
Common agents: Augmentin (amoxicillin-clavulanate) or cefuroxime ± metronidazole. [4]
(3) Operative Environment [1]
(1) Outer zone — patient reception area. (2) Clean zone — area between reception and theatre suite. (3) Aseptic zone — the operating area. (4) Dirty zone — disposal areas and corridors.
Why zones? Unidirectional flow from clean to dirty prevents contaminated materials from re-entering clean areas. Personnel, patients, and instruments should flow in one direction.
Maintain humidity/temperature/air circulation. Directional air flow. Air pumped into room through filters. Passed out through vents in the periphery and does not return.
Positive-pressure ventilation: Theatre air pressure > corridor pressure → air flows OUT of the theatre, not in. HEPA filters remove > 99.97% of particles ≥ 0.3μm. Laminar flow theatres (used for joint replacement) provide ultraclean air with < 10 colony-forming units/m³.
Minimal number of people should be in the operating room. Must not contaminate the sterile instruments.
Why limit personnel? Each person sheds ~10,000 skin squames/min, each carrying bacteria. More people = more bacterial shedding = higher airborne bacterial count.
Sterilization: Complete destruction and removal of all viable micro-organisms, including viruses and spores. Damage to organic substances. Applied to inanimate objects only. [1]
Key Distinction: Sterilization vs Disinfection vs Antisepsis
- Sterilization: Destruction of ALL organisms including spores — for inanimate objects
- Disinfection: Reduction of organisms to a safe level (may not kill spores) — for inanimate objects
- Antisepsis: Reduction of organisms on living tissue (e.g., skin prep, scrubbing)
Methods of Sterilization [1]
| Method | Conditions | Spectrum | Use | Key Points |
|---|---|---|---|---|
| Steam (Autoclave) | 134°C at 30 psi for 3 min, OR 121°C at 15 psi for 15 min | Effective against bacteria (including TB), viruses (HBV/HCV/HIV), heat-resistant spores (C. tetani, C. perfringens) | Standard surgical instruments | Gold standard; cheap; reliable |
| Ethylene Oxide (EtO) | Low temp 20–60°C, 2–24 hrs | Broad spectrum; highly penetrative, non-corrosive | Delicate items: electrical equipment, flexible fibre endoscopes | Toxic, irritant, mutagenic, carcinogenic — requires aeration period |
| Irradiation | γ-rays or accelerated electrons; 25 kGy | Broad spectrum | Large batches: catheters, syringes | Industrial use; not for routine hospital instrument sterilization |
High Yield — Autoclave Parameters
Know the two standard autoclave settings:
- 134°C / 30 psi / 3 minutes (flash sterilization — for rapid turnaround)
- 121°C / 15 psi / 15 minutes (standard cycle)
Both kill spores of C. tetani and C. perfringens.
From Surgical Principles [2][4]:
SSI Definition: Infection occurring at or near a surgical site within 30 days (or 90 days if implant). Timing typically 3–7 days post-op, rarely within first 72h (except GAS or Clostridium — these can cause fulminant early infection). [4]
Three anatomical levels:
- Superficial incisional — skin and subcutaneous tissue
- Deep incisional — fascia and muscle (increased risk of wound dehiscence)
- Organ/space — any part of the anatomy opened or manipulated during surgery
Clinical features of SSI [4]:
- Swinging fever
- Spreading erythema, localised pain
- Purulent discharge from wound
- Wound dehiscence
Investigations [4]:
- Wound swab/pus for C/ST (avoid wound edge — skin flora contamination)
- CT with contrast for deep/organ-space infection (rim-enhancing collection)
- Bloods: CBC, CRP ± blood culture
Exam Intelligence
| Trap | Correct Understanding |
|---|---|
| Confusing collagen content peak with tensile strength peak | Collagen content peaks in proliferative phase; tensile strength continues to rise in remodelling phase due to cross-linking and Type III→I transition |
| Thinking a healed wound regains 100% strength | Maximum tensile strength is ~80% of normal skin |
| Shaving the night before surgery | Increases infection rate — clip immediately before surgery |
| Using razor instead of clippers | Razor causes micro-cuts → increased SSI |
| Forgetting that alcohol-based preps are flammable | Must dry before draping/diathermy |
| Confusing sterilization with disinfection | Sterilization kills ALL organisms including spores; disinfection does not necessarily kill spores |
| Thinking ethylene oxide is safe | It is toxic, mutagenic, carcinogenic — used for heat-sensitive items only |
| Confusing antisepsis (living tissue) with sterilization (inanimate objects) | Antisepsis = living tissue; sterilization = instruments/objects |
| Fetus heals by scarring | No — fetus heals by regeneration (scarless) |
| Type I collagen in early wound | Early wound = Type III; remodelling converts to Type I |
- Chlorhexidine vs Povidone-iodine: Chlorhexidine has longer residual activity (binds keratin), less affected by organic matter. Povidone-iodine has faster onset but shorter duration and is inactivated by blood/pus.
- Hypertrophic scar vs Keloid: Hypertrophic stays within wound margins and may regress. Keloid extends beyond wound margins, does not regress, has genetic predisposition.
- Autolytic vs Surgical debridement: Autolytic is selective and painless but slow. Surgical is non-selective but thorough and fast — used for large necrotic wounds.
Past Paper Questions
Stem: "A 50-year-old lady underwent laparoscopic cholecystectomy for acute gangrenous cholecystitis. She developed wound infection and subhepatic abscess. She eventually recovered but lost 5 kg. (a) List three clinical signs of hypermetabolism she might have when she developed wound infection and subhepatic abscess. (3 marks) (b) What are the contributory reasons for the weight loss? Name three. (3 marks) (c) What would be the MOST APPROPRIATE treatment to make her recover from the complications of cholecystectomy? (4 marks)"
Answer/Rationale:
- (a) Signs of hypermetabolism: Tachycardia, fever/pyrexia, tachypnoea (± sweating, warm peripheries). These reflect the systemic inflammatory/metabolic response to infection (increased catabolism, increased O₂ consumption).
- (b) Weight loss reasons: Increased catabolism (hypermetabolism from sepsis), reduced oral intake (anorexia of infection, post-operative ileus, nil by mouth), muscle wasting (protein catabolism for gluconeogenesis — surgical stress response). Also: increased energy expenditure, possible malabsorption.
- (c) Treatment: Drainage of subhepatic abscess (percutaneous or surgical) + appropriate antibiotics (empirical then targeted based on culture) + nutritional support (enteral preferred, parenteral if enteral not feasible) + wound care/debridement of infected wound.
Stem: "There are multiple modes of transmission of different microbes causing 'hospital' outbreaks. (a) Name the MOST COMMON multidrug resistant gram-positive bacteria transmitted by contact... (b) ...gram-negative bacteria... (c) ...yeast... (d) ...bacterial cause of infectious diarrhoea... (e) Name three microbes commonly transmitted by airborne route... (f) Name three viruses transmitted by blood products..."
Answer/Rationale:
- (a) MRSA (Methicillin-resistant Staphylococcus aureus)
- (b) ESBL-producing Enterobacteriaceae (or Acinetobacter baumannii / CRE depending on local epidemiology)
- (c) Candida auris
- (d) Clostridioides difficile
- (e) Airborne: Mycobacterium tuberculosis, Measles virus (rubeola), Varicella-zoster virus (± SARS-CoV-2)
- (f) Blood: HBV, HCV, HIV
Relevance to this lecture: Sterilization by autoclave is effective against HBV/HCV/HIV and spore-forming Clostridium. Understanding hospital-acquired organisms links to why we have theatre zones, scrubbing protocols, and antisepsis.
Stem: "Surgical antibiotic prophylaxis for total hip replacement."
Answer: B. Cefazolin
Rationale: Joint replacement is a clean procedure with implant insertion. The main organisms to cover are skin flora (S. aureus, CoNS). Cefazolin is a first-generation cephalosporin with excellent Gram-positive coverage and is the standard surgical prophylaxis for orthopaedic implant surgery. Augmentin/cefuroxime would also be acceptable in some protocols but cefazolin is the standard answer for orthopaedic prophylaxis.
Stem: "A woman had known hyperthyroidism and large multinodular goitre, and she had total thyroidectomy done. A suction drain is inserted post-operatively. What is the purpose of keeping a surgical drain for this woman?"
Answer: D. To reduce haematoma formation by draining blood and serous fluid
Rationale: Post-thyroidectomy haematoma is dangerous because it can cause airway obstruction (neck is a confined space). The drain itself prevents haematoma by allowing blood/serum to exit. Option B describes the consequence of haematoma (airway obstruction) but that is prevented by removing the fluid (option D), not by "releasing pressure." The drain does not deliver antibiotics (A) or monitor thyroxine (C).
Stem: "A man presented to A&E with a stab wound. (a) List three features that must be recorded in the description of the stab wound. (6 marks) (b) List two features that help to differentiate self-inflicted injury from assault injury. (4 marks)"
Answer/Rationale:
- (a) Description of wound: Site/location, Size (length × width × depth), Shape/orientation, Depth, Edges (clean/ragged), Surrounding tissue condition (bruising, erythema). Also: presence of foreign body, bleeding status.
- (b) Self-inflicted vs assault: Self-inflicted wounds tend to be on accessible areas (anterior forearm, anterior chest, anterior abdomen), superficial and multiple parallel "hesitation marks", clothing often removed. Assault wounds tend to be deeper, on areas the victim cannot reach, with defensive injuries on hands/forearms, torn clothing over wound.
Relevance: The lecture covers wound description and etiology (traumatic — external).
- GC 192 (Plastic Surgery) [3]: Expands on primary/secondary/delayed primary closure and the reconstruction ladder (direct closure → skin graft → local flap → distant flap → free flap).
- Surgical Principles (Dr IYH Wong) [2]: Reinforces CDC wound classification (Clean → Dirty), antibiotic prophylaxis, and wound healing principles (free of tension, good apposition, free of infection, good vascular supply, healthy tissue).
- CFB WCS27 Surgical Infection [5]: Expands on SSI definition, timing, types.
- GC 237 (Musculoskeletal Infection): Open fracture wound management parallels debridement principles here.
- GC 231 (Open Fracture): Gustilo classification and wound management in open fractures — debridement principles are identical.
High Yield Summary
Wound Healing Phases: Haemostasis (immediate) → Inflammation (0–5d, neutrophils then macrophages, PDGF/TGF-β) → Proliferation (4–21d, Type III collagen, granulation, angiogenesis, re-epithelialization) → Remodelling (21d–1yr, Type III→I collagen, myofibroblast contraction, max 80% tensile strength).
Pathological healing: Arrested in inflammatory phase = chronic wound. Arrested/excessive in proliferative phase = hypertrophic scar/keloid.
Wound infection threshold: > 10⁵ organisms/g tissue. Signs: pain, erythema, edema, warmth ± pus, necrosis.
Treatment of infected wound: Assess → Debride → Culture → Empirical Abx (streamline later) → Dress → Irrigate.
Debridement methods: Autolytic, sharp, enzymatic, mechanical, biological (maggots), surgical. Endpoint = healthy granulation tissue.
Prevention (3 sources): Surgical team (scrub, gown, technique), Patient (optimise comorbidities, clip not shave, antisepsis, drape, prophylactic Abx), Environment (theatre zones, airflow, behaviour, sterilization).
Antiseptic agents: Povidone-iodine (rapid onset, short duration) vs Chlorhexidine (longer acting). Alcohol-based agents — fire risk with diathermy.
Sterilization: Autoclave (134°C/3min or 121°C/15min — kills spores), Ethylene oxide (low temp, for delicate items, toxic), Irradiation (γ-rays, 25 kGy, for large batches).
Wound classification: Clean (1–2%), Clean-contaminated (5–10%), Contaminated (15–20%), Dirty (40–50%).
Active Recall - Lecture Notes
[1] Lecture slides: GC 178. An ugly wound Wound healing; Wound infection; Anti-septic technique.pdf [2] Lecture slides: 2022 07 29 Surgery Surgical Principles (Dr IYH Wong).pdf [3] Lecture slides: GC 192. I want to look better Plastic and reconstructive surgery.pdf [4] Senior notes: Maksim Surgery Notes.pdf (Surgical wounds, pp. 23–29, 343–344) [5] Lecture slides: CFB WCS27_Surgical Infection.pdf [6] Senior notes: Ryan Ho Fundamentals.pdf (Ulcer description, p. 159) [7] Past papers: 2020 Fourth Summative SAQ.pdf (Q3) [8] Past papers: 2023 Fourth Summative SAQ.pdf (Q3) [9] Past papers: 2024 Fourth Summative SAQ.pdf (Q12) [10] Past papers: 2025 Fourth Summative MCQ.pdf (Q18, Q53)
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