Wound Classification & Types

1. Classification by Aetiology (Mechanism)

• Bailey and Love's Short Practice of Surgery, 28th Ed.

2. Classification by Depth

• History (duration and temperature of exposure)
• Appearance (red, mottled, white/yellow/brown)
• Pin-prick test - if sensation is retained, the wound is superficial; if insensate, deep dermal or full thickness
• Pye's Surgical Handicraft, 22nd Ed.

3. Surgical Wound Classification (CDC/NRC System)

• Current Surgical Therapy, 14th Ed. | Bailey and Love's, 28th Ed.

4. Classification by Complexity

5. Classification by Chronicity

6. Open vs. Closed Wounds

• Open wounds heal by secondary intention - contraction, granulation tissue, and re-epithelialisation; more inflammation and scarring; risk of desiccation of exposed structures (tendons, bone, nerves)
• Closed wounds heal by primary intention (edges approximated by sutures/staples/glue); less inflammation, narrower scar, faster healing
• Delayed primary closure (tertiary intention) - contaminated wounds left open initially and closed at 3-5 days once infection risk decreases
• Roberts and Hedges' Clinical Procedures in Emergency Medicine

Summary: Key Classification Axes

Phases of Normal Wound Healing

Phase 1 - Haemostasis (Seconds to Hours)

• Vascular injury triggers intense arteriolar vasoconstriction (mediated by catecholamines and prostaglandins), followed by vasodilatation and increased capillary permeability
• Platelet adhesion to the damaged endothelium is mediated by glycoprotein receptors (GPIa/IIa) binding to exposed collagen, and GPIIb-IIIa binding fibronectin, vitronectin, and fibrinogen; von Willebrand factor (vWF) is essential for initial platelet-collagen contact
• Platelet activation triggers release from two organelles:
  • Alpha granules → PDGF, TGF-β, IGF-1, fibronectin, fibrinogen, thrombospondin, vWF
  • Dense bodies → serotonin and vasoactive amines → vasodilation and increased permeability
• Mast cells release histamine and serotonin, further increasing endothelial permeability
• Platelet membrane-bound factor V + factor X generate prothrombinase, activating thrombin, which converts fibrinogen to fibrin clot (the provisional wound matrix)
• The fibrin clot also acts as a scaffold for subsequent cell migration
• Growth factors released (PDGF, TGF-β, VEGF, PF4, CD40L) create a chemotactic gradient that recruits inflammatory cells and initiates the next phase
• Sabiston Textbook of Surgery | Schwartz's Principles of Surgery, 11th Ed.

Phase 2 - Inflammation (Days 1-4)

Neutrophils (PMNs) - first responders, peak day 1-2

• Arrive within hours of injury, peak at ~48 hours
• Primary functions: phagocytosis of bacteria and debris; release of reactive oxygen species (ROS) for bacterial killing; release of proteases (elastase, collagenase) to break down devitalised tissue
• Not essential for healing in clean wounds (animal models show healing can proceed without neutrophils if infection is controlled), but essential when contamination is present
• Apoptose and are cleared by macrophages as the wound becomes clean

Macrophages - the "master regulators," peak day 3-4

1. Phagocytosis of apoptotic neutrophils, bacteria, and foreign material
2. Reactive oxygen species - bacterial lysis
3. Nitric oxide - kills antibiotic-resistant bacteria
4. Cytokine secretion - IL-1, IL-2, IL-4, IL-12
5. Angiogenesis - via VEGF, promoting capillary budding
6. Cell recruitment - recruits fibroblasts and endothelial cells into the wound
7. Homeostatic regulation - wound repair, follicle regeneration

• M1 (classically activated) - pro-inflammatory; dominant early; kills bacteria; secretes TNF-α, IL-6
• M2 (alternatively activated) - anti-inflammatory; dominant later; promotes tissue repair, collagen synthesis, angiogenesis

Lymphocytes - appear late, peak day 7

• Modulate the transition from inflammation to proliferation
• T-helper cells secrete cytokines that regulate fibroblast activity

• Sabiston Textbook of Surgery | Schwartz's Principles of Surgery, 11th Ed.

Phase 3 - Proliferation (Days 4-21)

3a. Angiogenesis (new vessel formation)

• Activated endothelial cells degrade the basement membrane of post-capillary venules
• Endothelial cells migrate into the wound along the fibrin scaffold using integrin αvβ3 (binds fibrin, fibronectin, fibrinogen)
• PECAM-1 mediates cell-cell contacts as capillary tubes form
• Stimulated by: VEGF, FGF, PDGF, TGF-β
• Results in the formation of granulation tissue - a highly vascularised, red, moist tissue filling the wound

3b. Fibroplasia (collagen synthesis by fibroblasts)

• Fibroblasts migrate into the wound along the fibrin matrix from day 4, peaking ~day 7-10
• Driven by PDGF (the key fibroblast mitogen) and TGF-β
• Fibroblasts synthesise type III collagen initially (weaker, more flexible), and later convert to type I collagen (stronger)
  • Normal skin: 80% type I / 20% type III
  • Early wounds: increased type III collagen
• Collagen is secreted as procollagen, cleaved extracellularly to tropocollagen, and then assembled into collagen fibrils (10-300 nm) and fibers (micrometres)
• The wound matrix also contains fibronectin, hyaluronic acid, proteoglycans - forming the ECM scaffold
• MMPs (matrix metalloproteinases) regulate matrix remodelling; MMP-1 (collagenase) is induced by IL-1 and downregulated by TGF-β; plasmin activates procollagenase to collagenase

3c. Re-epithelialisation

• Keratinocytes at the wound edge flatten, lose their attachments, and migrate across the wound surface
• Stimulated by: EGF, KGF (FGF-7), TGF-α, IL-6
• Keratinocytes proliferate behind the migrating front and eventually restore the stratified squamous epithelium
• Wound contraction (in open wounds) - myofibroblasts (fibroblasts expressing α-smooth muscle actin) contract the wound edges together, reducing wound size

• Sabiston Textbook of Surgery | Schwartz's Principles of Surgery, 11th Ed.

Phase 4 - Maturation / Remodelling (Day 21 - 2 years)

• Type III collagen is replaced by type I collagen - fibrils become larger, cross-linked, and oriented along lines of tension
• Tensile strength increases progressively:
  • Day 7: ~10% of original skin strength
  • Day 21: ~30%
  • Day 60: ~80%
  • Maximum: ~80% of original strength is never fully recovered
• MMPs and TIMPs (tissue inhibitors of metalloproteinases) regulate this balance - MMPs degrade old collagen; TIMPs prevent excess degradation
• Excess capillaries regress - the wound becomes less red and less raised over time
• Myofibroblasts undergo apoptosis once contraction is complete
• The final scar is acellular, avascular, and less elastic than original skin

• Insufficient remodelling → dehiscence or chronic wound
• Excessive collagen deposition → hypertrophic scar (within wound margins) or keloid (beyond wound margins)
• Sabiston Textbook of Surgery | Schwartz's Principles of Surgery, 11th Ed.

Summary Table