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.
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. Melody MK 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.
Learning Objectives (from the slides) [1]
- Etiology of wound
- Description of wound
- Physiology of wound healing
- Pathological wound healing
- Factors affecting wound healing
- Wound infection and prevention
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 injury/ulcer | Pressure and tissue deformation, often with shear, exceed local tissue tolerance; risk depends on magnitude × duration, perfusion, sensation and tissue properties—not one universal “capillary closing pressure” [16] | |
| 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 |
Reading the Clinical Images [1]
- Venous ulcer — the slide shows a shallow, irregular gaiter-area ulcer with a mixed red/yellow bed and surrounding chronic venous skin change. Describe site, edge, bed, exudate and periwound skin before naming the cause.
- Pressure injury — central yellow slough/eschar with discoloured, moist periwound tissue signals full-thickness damage; inspect for undermining and offload immediately. A photograph cannot determine the deepest extent when slough/eschar obscures the base.
- Partially healed burn — pink epithelialising areas coexist with pale/yellow non-viable tissue; the mesh-like surface may represent a meshed graft. Do not call every pale area “slough” from colour alone—assess perfusion, adherence, sensation and evolution.
- Extravasation injury — focal wrist eschar with surrounding erythema is a time-critical infusion injury. Stop the infusion, leave/aspirate through the cannula if the local protocol directs, identify the drug, elevate/mark/photograph, use agent-specific measures and seek early specialist advice; treatment is not generic for every extravasated drug [22].
- Slide labelled “fungal infection” — the extensive abdominal eschar demonstrates invasive tissue necrosis, but appearance alone cannot identify fungus. Suspected invasive fungal wound infection requires urgent deep tissue histology/culture and source control.
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? Early-gestation fetal wounds can heal with minimal scarring because inflammation, extracellular matrix composition, cellular behaviour and cytokine signalling differ from postnatal healing (including a higher relative TGF-β3 response). The slide's simple fetus-versus-adult contrast is useful, but “sterile amniotic fluid” alone does not explain scarless healing, and this phenotype is gestation-dependent.
High Yield — Four Phases with Timelines
Examiners love to test the phase names, timelines, key cells, and collagen type transitions. Memorise the table below.
Slide-Era Schematic — Do Not Read as Literal Boundaries
One imported figure in the slides gives unusually broad phase labels [1]:
| Phase | Slide Timeline | Slide Function |
|---|---|---|
| Haemostasis | Day 1–3 | Stop bleeding |
| Inflammation | Day 3–20 | New framework for blood vessel growth |
| Proliferation / Granulation | Week 1–6 | Pulls the wound closed |
| Remodelling / Maturation | Week 6–2 years | Final proper tissue |
Use it only to remember overlap. Haemostasis begins within seconds to minutes, not on day 1; inflammation and proliferation overlap from the first days; remodelling can continue for many months. For exams, use the detailed table below unless a question explicitly reproduces the slide figure.
| 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) and phagocytose bacteria and debris. By about 48 hours, macrophages become prominent. They continue phagocytosis, release growth factors (PDGF, TGF-β1, VEGF, FGF), and help coordinate the transition to proliferation. Experimental macrophage depletion markedly impairs healing, but “healing stops without macrophages” is an overstatement; delayed healing in immunosuppression is multifactorial.
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) | Initially left open, then closed only after serial reassessment shows viable tissue and controlled contamination/infection | Selected contaminated wounds; timing is wound-specific rather than a fixed 3–5 days | Can reduce open-wound time when closure is safe |
| 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 injuries), persistent stimuli—such as ischaemia, oedema, unrelieved pressure/shear, repeated trauma and a high or pathogenic microbial burden/biofilm—maintain inflammation. Neutrophils and macrophages keep releasing pro-inflammatory cytokines and MMPs that break down the nascent ECM faster than fibroblasts can rebuild it. Colonisation alone is expected in an open wound and is not synonymous with infection.
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 / nutrition risk | Inadequate protein-energy and micronutrient intake can impair repair. Albumin < 30 g/L is not a stand-alone diagnosis of malnutrition: albumin and prealbumin fall with inflammation and illness, so use clinical assessment and validated nutrition screening [17] |
| 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/shear (local) | Tissue deformation and impaired perfusion depend on pressure magnitude, duration, shear and tissue tolerance; no single pressure threshold predicts injury [16] |
| Oedema (local) | Increases diffusion distance for O₂ and nutrients |
| Desiccation (local) | Dries out wound bed → impairs keratinocyte migration |
| Microbial burden/biofilm (local) | Colonisation is not itself infection, but pathogenic burden and biofilm may sustain inflammation and can progress to local or spreading infection |
| Hypoxia (local) | Post-radiotherapy (obliterative endarteritis), arterial insufficiency → fibroblasts and WBCs need O₂ |
6. Wound Infection
Historical slide rule: “Wound infection = bacterial growth > 100,000 organisms per gram of tissue (10⁵/g).” [1]
The 10⁵ CFU/g concept is a historical quantitative heuristic, not a universal diagnostic cut-off. Open wounds are normally colonised, and infection is diagnosed clinically from local inflammation, purulence, tissue breakdown, spreading cellulitis or systemic illness in context. Current infection guidance advises against using quantitative microbial counts to define infection; when culture will change management, collect an aseptic tissue specimen or aspirate after cleansing/debridement rather than relying on a superficial swab [14]. Graft take depends on perfusion, wound-bed viability, shear/haematoma and organism virulence as well as microbial burden—failure is not determined by one number.
| 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 necrotising infection of the perineal/genital fascia. The slide sequence is a powerful visual warning: early disease shows marked swelling and erythema with only a small black perineal focus, whereas the later operative image shows extensive perineal and abdominal fascial excision with testes preserved. A small skin lesion can therefore conceal deep spread. Resuscitate, start broad empiric IV antibiotics and obtain immediate surgical consultation/source control; imaging may define extent in a stable, equivocal case but must not delay surgery when suspicion is high [15].
Slide sequence: assess → debride/remove foreign material → microbiology → empiric then targeted antibiotics → dress → consider cavity management. [1]
Use a safer clinical checklist:
- Assess severity first — physiology and sepsis; wound site, size, depth, perfusion, pain, discharge, crepitus and rapidly progressive change. Pain out of proportion, bullae, skin anaesthesia, dusky change, systemic toxicity or gas demand urgent senior/surgical review. Ultrasound or CT can locate deeper collections in stable patients, but must not delay source control for suspected necrotising infection [15].
- Control the source — drain pus, remove infected foreign material where indicated, and debride devitalised tissue while preserving viable structures. The slide showing pus tracking between tissue planes is a source-control problem, not an antibiotics-only problem.
- Sample selectively — if microbiology will alter treatment, cleanse and debride first, then obtain deep tissue/curettage or aspirated pus aseptically; superficial swabs often recover colonisers [14].
- Use antibiotics for clinical infection — select empiric therapy from syndrome, severity, allergies, prior cultures and the local antibiogram, then narrow. Antibiotics do not replace drainage/debridement.
- Optimise healing — appropriate moist dressing, pressure relief, oedema and glycaemic control, perfusion assessment, analgesia and nutrition review.
- Manage cavities deliberately — do not blindly irrigate a sinus. Establish anatomy and a drainage plan; NICE does not recommend routine wound irrigation or intracavity lavage merely to prevent SSI [12].
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 is usually moist pink/red viable granulation tissue without loose necrosis or retained foreign material, with adequate perfusion and controlled infection. The target is indication-specific: do not automatically debride a stable, dry, adherent heel eschar without erythema/fluctuance when perfusion is poor or revascularisation is not feasible; offload and monitor it while assessing vascular status [21].
The lecture slides illustrate healthy granulation tissue as a red-to-pink, moist, granular wound surface — this appearance confirms the wound bed is ready for reconstruction (skin grafts, flaps) or can proceed to epithelialisation. [1]
| 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 | Monofilament pad or appropriately selected irrigation/physical removal | Often non-selective and potentially painful. Routine wet-to-dry gauze traumatises new tissue and is generally not a preferred maintenance dressing |
| Biological | Sterile maggots (larval therapy) — Lucilia sericata larvae | Selective; larvae secrete proteases that dissolve necrotic tissue only; also have antibacterial properties |
| Surgical debridement | Scalpel, scissors, curette; tangential excision; hydrosurgery or ultrasound-assisted methods in selected wounds | Fastest source control for extensive/deep necrosis. It can be selective in skilled hands; anaesthesia, blood loss and removal of viable tissue are procedure-dependent risks |
"Chronic wounds usually get trapped in the inflammatory stage of wound healing; however, aggressive debridement transforms chronic wounds to acute wounds and therefore complete healing." — Wilcox et al., Frequency of Debridements and Time to Heal (312,744 wounds) [1]
The slide's chart comes from a large retrospective cohort: a shorter interval between debridements was associated with shorter healing time, whereas intervals over two weeks tracked with longer healing [1]. It supports regular reassessment and debridement when indicated, but does not prove that a universal weekly schedule causes faster healing; wound complexity and treatment selection may confound the association.
- Scissors, scalpel, curette — sharp debridement
- Watson knife, Goulian knife — tangential excision (shaving thin layers of dead tissue, especially in burns)
- Tangential burn excision image — sequentially shave eschar until a viable dermal endpoint with uniform punctate bleeding is reached. The before/after slide also reminds you to anticipate major blood loss and secure haemostasis; bleeding alone is not proof that all remaining tissue will survive.
- Versajet Hydrosurgery System — the slide shows a saline jet with local Venturi suction that cuts and evacuates debris. Its clinical value is controlled, layer-by-layer debridement around contours; product pressure, handpiece size and power setting are device parameters, not the biological endpoint.
- 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 against vegetative organisms; not reliably sporicidal under routine skin-prep conditions | Limited residual effect | Formulation and site matter; stains |
| Chlorhexidine gluconate | Rapid | Broad against vegetative organisms; not sporicidal | Longer acting (binds to stratum corneum — residual activity) | Ototoxic (avoid near ear); less affected by organic matter |
Current surgical hand preparation: remove rings/bracelets/watches, clean beneath nails, and use either an antimicrobial soap or a persistent-activity alcohol-based surgical hand rub for the manufacturer's stated duration. A brush is not required and vigorous brushing can abrade skin; artificial nails should not be worn [20].
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.
Current practice: do not remove hair routinely. If hair would interfere with the operation or dressing, use a single-use electric clipper with a disposable head on the day of surgery; do not use a razor [11][12].
Use sterilized sponge forceps to apply: Povidone iodine, Aqueous chlorhexidine gluconate, Alcohol-based chlorhexidine gluconate. Beware of accumulation and subsequent burn injury.
The product photographs are historical examples, not a current prescribing chart:
| Slide-era product | What the image teaches | Current interpretation |
|---|---|---|
| Povidone-iodine | An iodophor preparation | A valid alternative where alcohol-based chlorhexidine is unsuitable; formulation and site matter |
| Aqueous Hibitane 0.05% | A dilute chlorhexidine product | Do not infer suitability for an open wound from the old label; follow the current registered product and local policy |
| Chlorhexidine 0.015% + cetrimide 0.15% | A historical combined aqueous solution | Not a universal wound-irrigation prescription |
| Alcoholic Hibitane | Chlorhexidine in alcohol for intact-skin preparation; the old label also mentions “emergency instrument disinfection” | Do not use skin antiseptic to sterilise instruments. Critical instruments require a validated sterilisation process [13] |
For intact skin, WHO recommends an alcohol-based chlorhexidine solution unless contraindicated [11]. Use the locally approved concentration and manufacturer instructions. Keep chlorhexidine away from the eyes, brain/meninges and middle ear; do not use intact-skin alcohol preparations on mucosa or open wounds. Allow full drying and prevent solution pooling beneath the patient or drapes [11].
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.
The slide identifies operations with predictable contamination (for example entry into the oropharynx or bowel) and implant-related precautions. Translate that into a procedure-specific protocol, not one antibiotic list:
| Wound class | Current interpretation |
|---|---|
| Clean | Prophylaxis is often unnecessary, but may be indicated for particular procedures or prosthetic/implant surgery |
| Clean-contaminated | Give procedure- and flora-appropriate prophylaxis according to the local guideline |
| Contaminated | Prophylaxis and/or therapeutic antibiotics depend on the mechanism, source control and evidence of established infection |
| Dirty/infected | Treat established infection and obtain source control; this is treatment, not prophylaxis alone [12] |
Give prophylaxis early enough to achieve bactericidal tissue levels at incision—WHO recommends administration within 120 minutes before incision, accounting for drug half-life and infusion time [11]. Follow local guidance for agent selection, weight-based dose and intra-operative redosing (for a long case, major blood loss or drug half-life). Do not routinely continue prophylaxis after the operation or because a drain remains [11][12]. The slide's “cardiac indications” refers to a separate question of infective endocarditis prophylaxis, not an extension of SSI prophylaxis.
(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 helps keep corridor air from entering an operating room; filter class, air-change rate and pressure relationships are engineering specifications governed by local standards. The slide's directional-flow diagram is conceptually useful, but laminar airflow should not be presented as an SSI-prevention requirement for total arthroplasty: WHO recommends against using it for that purpose [11].
Minimal number of people should be in the operating room. Must not contaminate the sterile instruments.
Why limit personnel? Movement and door opening disturb airflow and increase particles shed from people and clothing. Keep traffic and unnecessary personnel to a minimum, while preserving the staff required for safe care.
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)
Choose the processing level by intended use (Spaulding principle) [13]:
| Item class | Contact | Minimum processing |
|---|---|---|
| Critical | Enters sterile tissue or the vascular system | Sterilisation |
| Semicritical | Contacts mucosa or non-intact skin | At least high-level disinfection; sterilise when feasible/product-directed |
| Noncritical | Contacts intact skin only | Low- or intermediate-level disinfection according to contamination and policy |
Methods of Sterilization [1]
| Method | Conditions | Spectrum | Use | Key Points |
|---|---|---|---|---|
| Steam (Autoclave) | The slide gives 134°C/3 min and 121°C/15 min examples | Sporicidal when the validated cycle is achieved | Heat/moisture-stable critical instruments | Preferred where compatible; exposure depends on steriliser, load, packaging and instrument instructions [13] |
| Ethylene Oxide (EtO) | Low-temperature gas cycle followed by aeration | Sporicidal validated process | Selected critical heat/moisture-sensitive devices | Penetrative but toxic and slow. Flexible GI endoscopes are generally semicritical devices processed by high-level disinfection unless their instructions require sterilisation [13] |
| 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 Are Cycle-Specific
The slide's 134°C/3 min and 121°C/15 min values are useful historical examples of saturated-steam exposure. They are not interchangeable universal cycles: packaged versus unwrapped items, load configuration and device design change the validated time. Follow the steriliser and instrument manufacturers' instructions and monitor the cycle [13]. Avoid the old term “flash sterilisation”; immediate-use steam sterilisation is not a routine substitute for adequate inventory and full processing.
From Surgical Principles [2][4], reconciled with current surveillance criteria:
CDC/NHSN surveillance window: superficial incisional SSI is monitored for 30 days for all procedure categories. Deep-incisional and organ/space SSI use a 30- or 90-day window depending on the procedure category—not simply “90 days if an implant is present” [18]. These are surveillance definitions, not a reason to dismiss a clinically infected wound outside the window.
SSI may present early or late. There is no reliable rule that “most occur on days 3–7” or that only GAS/Clostridium cause infection within 72 hours; assess the wound and physiology whenever concerning features arise.
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]:
- If microbiology will change treatment, aspirate pus or obtain a cleansed/debrided deep tissue specimen; use a superficial swab only when a better specimen is not feasible and interpret colonisers cautiously [14]
- 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 |
| Routine pre-operative hair removal | Leave hair in place; if it interferes, clip on the day of surgery—never razor-shave [11][12] |
| 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 |
| All fetal wounds heal scarlessly | Scar-minimal healing is most characteristic of early gestation; it is gestation- and context-dependent |
| 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 debridement is selective and usually comfortable but slow. Surgical debridement is rapid and can achieve source control; selectivity and anaesthetic requirement depend on depth, extent, technique and patient factors.
- 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
- Diagnose clinically: increasing pain, erythema, oedema, warmth, purulence, tissue breakdown or systemic illness. The slide's > 10⁵ organisms/g threshold is historical, not a universal diagnostic cut-off.
-
Treatment of infected wound
- Assess severity/perfusion → urgent source control when needed → deep/aspirate culture if it will change care → syndrome-appropriate antibiotics → wound care and optimisation.
-
Debridement methods
- Autolytic, sharp, enzymatic, mechanical, biological (maggots), surgical. Endpoint = healthy granulation tissue.
-
Prevention (3 sources)
- Surgical team (hand preparation, gown/gloves, technique), patient (optimise comorbidities, leave hair or clip only if needed, antisepsis, draping, indicated prophylaxis), environment (theatre zones, airflow, behaviour, instrument processing).
-
Antiseptic agents
- Povidone-iodine (rapid onset, short duration) vs Chlorhexidine (longer acting). Alcohol-based agents — fire risk with diathermy.
-
Sterilization
- Steam is preferred for compatible critical instruments; use the validated device/load cycle rather than treating the slide's two settings as universal. Ethylene oxide is a toxic low-temperature option for selected critical devices; irradiation is mainly industrial.
-
Wound classification
- Clean → clean-contaminated → contaminated → dirty/infected. Prophylaxis is procedure-specific; a dirty/infected wound needs treatment and source control, not “more prophylaxis”.
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) [11] WHO. Global Guidelines for the Prevention of Surgical Site Infection, 2nd ed. (2018) [12] NICE NG125. Surgical site infections: prevention and treatment — Recommendations [13] CDC. Guideline for Disinfection and Sterilization in Healthcare Facilities: Summary Recommendations [14] IWGDF/IDSA. Guidelines on the Diagnosis and Treatment of Diabetes-related Foot Infections (2023) [15] IDSA. Practice Guidelines for the Diagnosis and Management of Skin and Soft Tissue Infections [16] International Pressure Injury Guideline. Etiology of Pressure Injuries [17] ASPEN. The Use of Visceral Proteins as Nutrition Markers: An ASPEN Position Paper [18] CDC NHSN. Surgical Site Infection Event Protocol, January 2026 [19] BAETS/Difficult Airway Society/ENT-UK. Management of haematoma after thyroid surgery: systematic review and multidisciplinary consensus guidelines [20] CDC. Clinical Safety: Hand Hygiene for Healthcare Workers [21] International Pressure Injury Guideline. Prevention and Treatment of Pressure Ulcers/Injuries, 2019 edition with November 2023 update [22] NHS England. Guidelines for the Management of Extravasation of Systemic Anti-Cancer Therapy
GC177 A Thyroid Nodule Benign Thyroid Nodules; Thyroid Cancer
Thyroid nodules are discrete lesions within the thyroid gland, classified as benign (colloid nodules, adenomas) or malignant (papillary, follicular, medullary, or anaplastic carcinoma), evaluated by ultrasound characteristics and fine-needle aspiration cytology.
GC179 Anal Pain Perianal Lesions And Sepsis
Anal pain with perianal lesions and sepsis encompasses conditions such as perianal abscesses, fistulae, fissures, and thrombosed hemorrhoids that may present with localized pain, swelling, and potential systemic infection if inadequately treated.