Wound Healing
Wound healing is a complex physiological process involving haemostasis, inflammation, proliferation, and remodelling. Understanding normal healing and factors that impair it is essential for surgical practice.
Key Facts
Four phases: Haemostasis (minutes), inflammation (days 1-5), proliferation (days 5-21), remodelling (weeks to months/years) Primary intention: Clean wound edges apposed (e.g., surgical closure); heals rapidly with minimal scarring Secondary intention: Wound left open to heal by granulation, contraction, and epithelialisation (e.g., abscess cavity) Tertiary intention (delayed primary closure): Wound left open initially (e.g., contaminated), closed surgically after 3-5 days Granulation tissue: Highly vascular connective tissue; appears red and beefy; a sign of healthy healing Tensile strength: Wound achieves ~80% of original skin strength by 3 months; never reaches 100% Factors impairing healing: Infection (most common), diabetes, malnutrition, smoking, steroids, immunosuppression, ischaemia, foreign bodies, radiation Hypertrophic scars stay within wound boundaries; keloid scars extend beyond — both result from excessive collagen deposition
Overview
Key Facts
Understanding wound healing physiology is fundamental to surgical practice. Identifying and addressing factors that impair healing optimises patient outcomes.
Epidemiology
Chronic wounds affect ~2-4% of the population. NHS spends ~£5 billion/year on wound management. ~200,000 patients have chronic leg ulcers. Surgical site infections affect ~3-5% of surgical wounds.
Aetiology
Types of wound:
- Incisional (surgical), laceration, abrasion, contusion, puncture, avulsion, burn
- Acute wounds: Expected to heal through normal phases
- Chronic wounds: Fail to progress through normal healing — stuck in inflammatory phase (e.g., venous ulcers, diabetic ulcers, pressure ulcers)
Pathophysiology
Phase 1 — Haemostasis (minutes):
- Vasoconstriction → platelet aggregation → fibrin clot → coagulation cascade
Phase 2 — Inflammation (days 1-5):
- Neutrophils (first 24-48 hours) → macrophages (day 2-5; KEY orchestrating cell)
- Phagocytosis, debridement, cytokine release (TGF-β, PDGF, VEGF)
Phase 3 — Proliferation (days 5-21):
- Fibroblasts → collagen synthesis (predominantly type III initially → type I replaces over months)
- Angiogenesis → granulation tissue formation
- Epithelialisation from wound edges/adnexal structures
- Wound contraction (myofibroblasts)
Phase 4 — Remodelling (weeks to ≥1 year):
- Type III collagen replaced by type I collagen
- Cross-linking increases tensile strength
- Maximum strength ~80% of normal skin at 3 months
Clinical Presentation
Normal Healing
- Progressive wound closure, decreasing inflammation
- Clean, pink granulation tissue
- Contracting wound edges (secondary intention)
- Decreasing pain and exudate
Impaired Healing
- Wound dehiscence (partial or complete)
- Chronic non-healing wound (>6 weeks without healing)
- Excessive exudate, necrotic tissue, biofilm
- Surrounding cellulitis (infection)
Abnormal Scarring
- Hypertrophic scar: Raised, red, stays within wound boundaries; may improve over 1-2 years
- Keloid scar: Extends beyond original wound; does not regress spontaneously; more common in darker skin, earlobes, sternum, shoulders
- Contracture: Excessive wound contraction → functional limitation (especially over joints)
Red Flags
- Wound dehiscence post-laparotomy with pink serous discharge ('pink fluid') — may herald evisceration
- Non-healing wound in elderly or diabetic — exclude malignancy (Marjolin's ulcer — SCC arising in chronic wound)
- Rapidly spreading cellulitis around wound — consider necrotising fasciitis
Differential Diagnosis
| Wound Type | Features | Management |
|---|---|---|
| Venous ulcer | Medial malleolus, shallow, irregular, lipodermatosclerosis | Compression bandaging (ABPI >0.8) |
| Arterial ulcer | Distal, punched-out, painful, pale base | Revascularisation, wound care |
| Diabetic ulcer | Plantar surface, painless (neuropathic), callus border | Offloading, MDT diabetic foot |
| Pressure ulcer | Over bony prominences, immobile patients | Pressure relief, nutrition, wound care |
| Malignant ulcer | Non-healing, raised/rolled edges, bleeding | Biopsy |
Diagnosis / Investigation
Bedside
- Wound assessment: Size, depth, tissue type (granulation, slough, necrotic), exudate, edges, surrounding skin
- Wound swab: If clinical infection suspected (not routine — treat clinically)
- ABPI: For leg ulcers — venous (>0.8) vs arterial (<0.5)
Bloods
- FBC: Infection, anaemia
- CRP: Infection
- HbA1c, glucose: Diabetes optimisation
- Albumin, pre-albumin: Nutritional status
- U&Es: Renal function
Imaging
- Duplex US: Venous ulcers (assess venous insufficiency)
- X-ray: Osteomyelitis, foreign body
- MRI: Deep infection, osteomyelitis
- Biopsy: Non-healing wound >6 weeks — exclude malignancy
Management
Optimise Healing Factors
- Nutrition: Adequate protein, calories, vitamin C (collagen synthesis), zinc
- Glycaemic control: HbA1c <58 mmol/mol
- Smoking cessation: Nicotine causes vasoconstriction, reduces oxygen delivery
- Remove/reduce: Steroids, immunosuppressants where possible
- Offloading: Pressure ulcers and diabetic foot ulcers
- Treat infection: Antibiotics only for clinical infection (cellulitis, systemic sepsis)
Wound Management
- Debridement: Sharp, autolytic (hydrogels), mechanical, enzymatic, biological (larval)
- Dressings: Match to wound type — alginate (exudative), foam (moderate exudate), hydrocolloid (low exudate), hydrogel (dry/necrotic)
- Negative pressure wound therapy (NPWT/VAC): Promotes granulation, reduces oedema; useful for complex wounds
- Compression: For venous ulcers (only if ABPI >0.8)
Surgical
- Skin grafting: Split-thickness (SSG) or full-thickness (FTSG) for wounds unable to close
- Flap reconstruction: For complex wounds requiring tissue bulk
- Fasciotomy: Compartment syndrome
Referral Criteria
- Non-healing wound >6 weeks — tissue viability/wound specialist
- Suspected malignancy — biopsy and 2WW
- Complex wounds — plastic surgery
- Diabetic foot — MDT diabetic foot team
Prognosis
- Primary intention wounds: Heal within 1-2 weeks
- Secondary intention: Variable — weeks to months depending on size, depth, patient factors
- Venous ulcers: ~70% heal within 6 months with compression; recurrence common
- Diabetic foot ulcers: ~50% heal within 20 weeks; ~15% lead to amputation
- Pressure ulcers: Prevention is more effective than treatment; mortality ~25-33% in hospitalised patients with Grade IV
- Wound strength: Never exceeds ~80% of original tissue
Other Relevant Information
Phases of Wound Healing
| Phase | Timing | Key Cells | Key Events |
|---|---|---|---|
| Haemostasis | Minutes | Platelets | Vasoconstriction, clot formation |
| Inflammation | Days 1-5 | Neutrophils, macrophages | Phagocytosis, cytokine release |
| Proliferation | Days 5-21 | Fibroblasts, endothelial cells | Collagen synthesis, angiogenesis, epithelialisation |
| Remodelling | Weeks-years | Fibroblasts | Collagen cross-linking, scar maturation |
Factors Impairing Wound Healing
| Factor | Mechanism |
|---|---|
| Infection | Prolonged inflammation, tissue destruction |
| Diabetes | Microangiopathy, neuropathy, immune dysfunction |
| Smoking | Vasoconstriction, CO reduces O₂ delivery |
| Malnutrition | Protein/vitamin C/zinc deficiency |
| Steroids | Suppress inflammation and collagen synthesis |
| Ischaemia | Reduced O₂ and nutrient delivery |
| Age | Slower cell proliferation, reduced immune function |