Surgery chapters
Wound healing and tissue repair
The phases of normal wound healing and the cells and growth factors involved, healing by first, second and third intention, factors that delay healing, managing acute and chronic wounds, and abnormal scars such as keloids.
- Healing has three phases: inflammatory (0 to 2–3 days; platelets, neutrophils, macrophages), proliferative (day 3 to week 3; fibroblasts, type III collagen, granulation tissue, angiogenesis) and remodelling (to a year or more; type I replaces type III).
- Scar strength peaks around 12 weeks at about 80% of normal skin and never fully recovers.
- Keloid spreads beyond the wound and does not regress; hypertrophic scar stays within it and improves with time.
On this page
Overview
Wound healing is the body's attempt to restore the integrity of injured tissue. In humans it is repair by scar, not true regeneration, and scarring can itself cause problems: adhesions, keloids, contractures and even cirrhosis in the liver.
A clean cut in a healthy patient follows a predictable sequence. Surgeons aim to achieve this primary healing, to recognise what delays it, and to manage acute wounds, chronic wounds and abnormal scars.
Phases of normal healing
Most texts describe three phases. Some add an initial haemostatic phase and a destructive (cleansing) phase in which macrophages clear debris.
1. Inflammatory phase (immediately to 2–3 days)
- Bleeding → vasoconstriction → platelet plug and fibrin clot.
- Platelets release ADP (aggregation), then from their alpha granules: PDGF, platelet factor 4 and TGF-β.
- These attract neutrophils (first 24–48 hours) and then macrophages.
- Histamine, serotonin and prostaglandins increase vessel permeability.
- Fibrin forms the first scaffold.
- Macrophages remove dead tissue and bacteria and direct fibroblasts in the next phase.
- Clinically: rubor, tumor, calor, dolor.
2. Proliferative phase (day 3 to about week 3)
- Fibroblasts dominate: they make collagen and ground substance (glycosaminoglycans, proteoglycans).
- Angiogenesis: new capillary loops grow in.
- Granulation tissue = new capillaries + fibroblasts + inflammatory cells in a loose matrix (red, granular, bleeds easily).
- Re-epithelialisation of the surface.
- Collagen is laid down randomly and is mainly type III.
- Wound contraction begins and can greatly shrink an open wound in the first 3 weeks.
- Fibroblasts need vitamin C to make stable collagen (hydroxylation of proline and lysine).
3. Remodelling (maturation) phase (week 3 to a year or more)
- Type I collagen replaces type III until about 4:1.
- Fibres realign along lines of tension; cross-linking increases.
- Vascularity falls; the scar becomes paler, flatter and softer.
- Myofibroblasts continue contraction.
- Tensile strength is greatest at about 12 weeks, about 80% of normal skin, and never returns to 100%.
| Phase | Time | Dominant cells | Key events |
|---|---|---|---|
| Inflammatory | 0 to 2–3 days | Platelets, neutrophils, then macrophages | Haemostasis, PDGF/TGF-β, clearing debris |
| Proliferative | Day 3 to week 3 | Fibroblasts, endothelial cells | Granulation tissue, type III collagen, angiogenesis, epithelialisation |
| Remodelling | Week 3 to 1–2 years | Fibroblasts, myofibroblasts | Type I collagen, realignment, gain in strength |
The macrophage is the key cell that links inflammation to repair; wounds heal poorly without macrophages, but can heal without neutrophils.
"Platelets plug, PMNs pick, macrophages manage, fibroblasts fill, myofibroblasts move (contract)."
Matrix metalloproteinases that remodel collagen are zinc-dependent. Zinc deficiency (e.g. long parenteral feeding) causes poor healing with a peri-oral and acral rash.
Classification of wound closure
| Type | What happens | Result |
|---|---|---|
| Primary intention (first intention) | Clean edges brought together soon after injury | Least inflammation, minimal scar |
| Secondary intention | Wound left open; heals by granulation, contraction and epithelialisation | More inflammation and proliferation, wider scar, slower |
| Tertiary intention (delayed primary closure) | Contaminated wound left open, then closed after a few days once clean | Scar between the two; reduces infection in dirty wounds |
"Delayed primary closure" and "tertiary intention" are the same thing. Wound contraction is the main feature of secondary intention.
Factors that impair healing
| Local | Systemic |
|---|---|
| Infection (the commonest local cause) | Malnutrition: protein, vitamin C, vitamin A, zinc |
| Poor blood supply (arterial or venous disease) | Diabetes mellitus |
| Foreign body, devitalised tissue, haematoma | Steroids and other drugs (chemotherapy, immunosuppressants) |
| Previous radiotherapy | Immune deficiency (HIV, chemotherapy) |
| Tension, movement, pressure | Smoking, jaundice, uraemia, old age |
| Site and mechanism (crush, avulsion), tissue loss | Malignancy |
Vitamin A partly reverses the impaired healing caused by corticosteroids.
Healing in specific tissues
- Bone: same phases, with periosteal and endosteal callus (osteoid mineralised by hydroxyapatite). Rigid fixation with accurate reduction gives primary bone healing with little callus; a gap gives secondary healing with callus and risk of delayed union or non-union.
- Nerve: Wallerian degeneration distal to the cut; proximally back to the last node of Ranvier. Sprouting axons are guided by growth factors; poor apposition gives a neuroma. Repair under magnification with fine (8/0 to 10/0) monofilament nylon.
- Tendon: nourished intrinsically (vincular flow, synovial diffusion) and extrinsically (adhesions to the sheath). Weak for the first 3–6 weeks: protect with a splint but allow early active movement to limit adhesions.
Types of wound: tidy versus untidy
| Tidy | Untidy |
|---|---|
| Cut by a sharp edge (incised) | Crushed or avulsed |
| Clean | Contaminated |
| Healthy tissue | Devitalised tissue |
| Rarely tissue loss | Often tissue loss |
The aim is to convert an untidy wound into a tidy one by debridement; repeated "second look" debridement may be needed (blast, missile, crush and earthquake injuries).
Managing the acute wound
- Assess the whole patient by ATLS principles; check tetanus status.
- Control bleeding by elevation and a pressure pad; do not clamp blindly (risk to nerves and vessels).
- Adequate analgesia or anaesthesia; tourniquet for hand and limb exploration.
- Cleanse and explore (to the limit of blood staining); X-ray for foreign bodies in puncture wounds.
- Debride dead tissue until it bleeds (spare nerves, vessels and tendons). Muscle viability: colour, contractility, bleeding (and consistency).
- Repair deep structures (tendon, nerve, vessel, bone) in tidy wounds.
- Skin cover without tension: direct closure, skin graft (needs a vascular bed) or flap (brings its own blood supply over bone, tendon or nerve).
Special wounds
- Bites: high bacterial load; clean, debride, give antibiotic cover for aerobes and anaerobes; usually leave open or close loosely. Human bites over the knuckle ("fight bite") can enter the MCP joint.
- Degloving: skin and fat torn off the deep fascia; extent is usually larger than it looks; excise skin until dermal bleeding is seen.
- Compartment syndrome: pain out of proportion, pain on passive stretch, sensory change; absent pulses are a late sign. Fasciotomy if signs present or pressure persistently above 30 mmHg. Late fasciotomy in old crush injury risks myoglobinuric renal failure.
- High-pressure injection injury: small entry wound, extensive deep damage; needs urgent wide exploration.
Chronic wounds
A chronic wound is one that has not healed within the time normally expected for its type, usually 3 weeks. Healing is most often stuck in the inflammatory phase.
Leg ulcers
Causes: venous hypertension (commonest), arterial disease (atherosclerosis, diabetic small vessel), vasculitis, trauma, chronic infection (TB, syphilis) and neoplasm.
A chronic ulcer that does not respond to treatment must be biopsied. Squamous cell carcinoma in a chronic ulcer or burn scar is a Marjolin ulcer.
Pressure sores
- Occur when external pressure exceeds capillary occlusion pressure (about 30 mmHg).
- Commonest sites in order: ischium, greater trochanter, sacrum, heel, malleolus, occiput.
- Prevention: turn bed-bound patients at least every 2 hours; wheelchair users lift off for 10 seconds every 10 minutes; pressure-relieving mattresses.
| Stage | Description |
|---|---|
| 1 | Non-blanching redness, skin intact |
| 2 | Partial-thickness loss (epidermis and dermis) |
| 3 | Full-thickness loss into subcutaneous fat, not through fascia |
| 4 | Through fascia into muscle, bone, tendon or joint |
Negative pressure wound therapy (vacuum-assisted closure)
Foam in the wound, sealed with film, suction about −125 mmHg. It reduces oedema and bacterial count, increases blood flow and speeds granulation, preparing the bed for a graft or flap.
Scars
A new scar is pink, firm, raised and itchy; it matures over 1–2 years, becoming pale, soft and flat.
| Feature | Hypertrophic scar | Keloid |
|---|---|---|
| Extent | Within the original wound | Beyond the wound margins |
| Course | Improves with time | Does not regress; recurs after excision |
| Timing | Soon after injury | May appear months later |
| Associations | Wounds across tension lines, prolonged inflammation, burns, across joints | Dark skin, family history, sites such as sternum, shoulders, ear lobes |
| Histology | Excess collagen, more vascular | Thick, disorganised collagen, more type III |
Treatment (both are hard to treat): pressure garments, silicone gel sheets, intralesional triamcinolone, excision plus steroid or postoperative radiotherapy (high recurrence), laser for redness.
- Atrophic scar: pale, flat, stretched (common on the back).
- Contracture: scar across a joint or flexion crease tightens; treat with Z-plasty, grafts or flaps and physiotherapy.
- Avoidable scarring: scrub out dirt (prevents traumatic tattooing), align landmarks (vermilion border, eyebrow), use fine monofilament sutures removed early, or subcuticular closure.
Expect: the timing and dominant cells of each phase; growth factors from platelets (PDGF, TGF-β); type III to type I collagen; myofibroblasts and wound contraction; scar strength over time; primary, secondary and tertiary intention; vitamin C, zinc and vitamin A with steroids; infection as the commonest local cause of poor healing; keloid versus hypertrophic scar and their treatment; Marjolin ulcer; pressure sore sites and staging; compartment syndrome signs; and the principles of debridement.
Quick revision
- Inflammatory (0–3 days) → proliferative (3 days–3 weeks) → remodelling (to 1–2 years).
- PDGF and TGF-β from platelet alpha granules; macrophage is the essential cell.
- Granulation tissue = capillaries + fibroblasts + inflammatory cells.
- Type III collagen early; type I later (4:1); vitamin C needed.
- Myofibroblasts cause contraction (key in secondary intention).
- Strength about 80% of normal at 12 weeks; never 100%.
- Infection is the commonest local cause of delayed healing; steroids reversed partly by vitamin A.
- Keloid beyond margins, no regression; hypertrophic within margins, improves.
- Chronic ulcer not healing → biopsy (Marjolin ulcer).
Written by The House Job from standard references (Bailey & Love's Short Practice of Surgery, 27th edition).
FAQ
What is granulation tissue made of?
New capillary loops, fibroblasts and inflammatory cells in a loose matrix; it is pink, granular and bleeds easily.
Which cell causes wound contraction?
The myofibroblast, a fibroblast with contractile proteins, which pulls the wound edges together.
How strong is a healed scar?
Strength rises steadily to about 80% of normal skin by about 12 weeks and does not return fully to normal.
What is delayed primary closure?
Leaving a contaminated wound open for a few days and then suturing it once it is clean; it is also called healing by tertiary intention.
How is a keloid different from a hypertrophic scar?
A keloid grows beyond the wound margins and does not settle, while a hypertrophic scar stays within the wound and usually improves with time.