Wound healing is a coordinated biological response that restores tissue integrity after injury. It is usually described in overlapping phases: haemostasis → inflammation → proliferation → remodelling. In clinical practice, the key questions are: is the wound clean, vascular, approximated, infected, under tension, or systemically disadvantaged?

Doctor’s framing: Healing fails when the wound cannot clear contamination, cannot generate granulation tissue, cannot epithelialise, or cannot remodel collagen. Diabetes, steroids, malnutrition, smoking, infection, ischaemia, oedema and repeated trauma are common reasons wounds stall.

⏱️ Core Phases of Wound Healing

Timeframe	Phase	Key cells / mediators	Clinical relevance
Immediate: minutes–hours	Haemostasis	Vasoconstriction, platelet plug formation, coagulation cascade, fibrin clot. Platelets release growth factors including PDGF and TGF-β.	The clot is not just a plug - it forms a provisional matrix for inflammatory cells and fibroblasts. Persistent bleeding, anticoagulation or haematoma can separate wound edges and increase infection risk.
0–3 days	Inflammatory phase	Neutrophils dominate early, especially in the first 24–48 hours. Macrophages then become dominant from around day 3 onwards.	Neutrophils kill bacteria and remove debris, but excessive inflammation damages tissue. Macrophages are essential: they clear dead tissue, coordinate fibroblast activity, promote angiogenesis and help transition the wound into proliferation.
3–10 days	Proliferative phase	Fibroblasts migrate in and deposit extracellular matrix. Early collagen is mainly Type III collagen. VEGF-driven angiogenesis forms new capillaries. Keratinocytes migrate across the wound surface.	Granulation tissue forms: pink-red, moist, vascular, fragile tissue rich in capillaries and fibroblasts. Poor granulation suggests infection, ischaemia, pressure, malnutrition, steroid exposure or uncontrolled diabetes.
Weeks–months	Remodelling / maturation	Type III collagen is replaced by stronger Type I collagen. Collagen fibres are cross-linked, reorganised and aligned along lines of tension. Matrix metalloproteinases remodel excess matrix.	Tensile strength gradually improves but usually reaches only around 70–80% of original strength. The wound never becomes as strong as uninjured tissue, which matters for hernia risk, dehiscence and scar counselling.
High-yield	Impaired healing	Diabetes, steroids, smoking, malnutrition, infection, ischaemia, anaemia and old age.	Diabetes impairs neutrophil function, angiogenesis and collagen deposition. Steroids reduce macrophage and fibroblast activity. Smoking causes vasoconstriction and tissue hypoxia.

✂️ Healing by Intention

Type	Typical situation	Healing pattern	Clinical pearl
Primary intention	Clean surgical incision or tidy laceration with well-apposed edges.	Minimal tissue loss, limited granulation tissue, rapid epithelialisation, small scar.	Best for clean, low-tension wounds. Examples: elective laparotomy incision, appendicectomy port site, C-section wound.
Secondary intention	Open wound, pressure ulcer, infected wound, abscess cavity, traumatic tissue loss.	More inflammation, more granulation tissue, wound contraction, slower epithelialisation and larger scar.	Needs careful dressing choice, exudate control, infection control, pressure relief and optimisation of nutrition/perfusion.
Tertiary intention Delayed primary closure	Contaminated or high-risk wound initially left open, then closed later once clean.	Allows drainage and reduction of bacterial burden before closure.	Useful after some traumatic wounds, contaminated abdominal wounds or infected wounds after debridement.

🔍 Practical Wound Assessment for Doctors

Patient factors: diabetes control, smoking, steroids/immunosuppression, nutrition, vascular disease, renal disease, anaemia, frailty.
Wound factors: site, size, depth, tissue loss, contamination, devitalised tissue, exudate, odour, surrounding cellulitis, pain, undermining or sinus formation.
Perfusion: check pulses, capillary refill, limb temperature, venous disease, oedema and pressure areas. Consider ABPI before compression if arterial disease is possible.
Infection: increasing pain, spreading erythema, warmth, swelling, purulent discharge, malodour, systemic features or failure to progress.
Mechanical issues: tension, pressure, shear, foreign body, haematoma, seroma, repeated trauma or poor offloading.

Ward pearl: A wound that is not healing is rarely “just slow”. Look actively for infection, ischaemia, pressure, poor glycaemic control, malnutrition, steroids, smoking, oedema or an unrecognised foreign body.

🧫 Surgical Site Infection - UK Clinical Context

Superficial SSI: involves skin and subcutaneous tissue. Look for erythema, warmth, tenderness, swelling or purulent discharge.
Deep SSI: involves fascia or muscle. Consider if there is deep pain, wound breakdown, abscess, fever or systemic deterioration.
Organ-space SSI: involves deeper anatomical spaces opened during surgery, such as intra-abdominal abscess after bowel surgery.
Management principles: assess severity, remove sutures/staples if drainage is needed, obtain cultures when appropriate, drain pus, debride devitalised tissue and use antibiotics when cellulitis or systemic infection is present.
Antibiotics: should follow local antimicrobial guidance, allergy status, likely source and culture results. Source control is often more important than antibiotics alone.

⚠️ Complications of Wound Healing

Complication	What it means	Clinical clue
Dehiscence	Partial or complete separation of wound layers.	Serosanguinous discharge, “popping” sensation, visible separation; higher risk with infection, obesity, steroids, poor nutrition and raised intra-abdominal pressure.
Evisceration	Abdominal contents protrude through a dehisced wound.	Surgical emergency. Cover with warm saline-soaked sterile gauze and seek urgent surgical help.
Hypertrophic scar	Raised scar that remains within the wound boundary.	Often improves over time; associated with tension and prolonged inflammation.
Keloid scar	Excess collagen extends beyond the original wound boundary.	Common at sternum, shoulders, jawline and earlobes; more likely in darker skin types and younger patients.
Chronic wound	Wound stuck in inflammation or unable to progress through healing.	Think venous disease, arterial disease, diabetes, pressure injury, malignancy, infection or inflammatory disease such as pyoderma gangrenosum.

🧬 Why Diabetes and Steroids Matter

Diabetes: hyperglycaemia impairs neutrophil chemotaxis/phagocytosis, reduces angiogenesis, damages microvasculature and predisposes to infection.
Steroids: reduce inflammation, macrophage signalling, fibroblast proliferation and collagen synthesis; this can reduce wound tensile strength.
Malnutrition: protein deficiency limits collagen synthesis; vitamin C deficiency impairs collagen hydroxylation; zinc deficiency can impair epithelialisation.
Smoking: nicotine causes vasoconstriction, carbon monoxide reduces oxygen delivery and tissue hypoxia impairs collagen synthesis and bacterial killing.

🦴 Bone Healing

Haematoma phase: bleeding around the fracture creates a clot and inflammatory environment.
Inflammation: macrophages and neutrophils remove necrotic tissue and prepare the fracture site.
Soft callus: fibrocartilaginous callus bridges the fracture but is not mechanically strong.
Hard callus: woven bone replaces soft callus and gives increasing stability.
Remodelling: woven bone becomes lamellar bone, shaped by osteoblast and osteoclast activity according to mechanical stress.
Delayed union/non-union risks: smoking, diabetes, poor blood supply, infection, inadequate immobilisation, NSAID overuse in some contexts, and severe soft tissue injury.

🧠 Brain and Nervous System Healing

CNS neurons have very limited regenerative capacity. Recovery after stroke or traumatic brain injury relies more on plasticity, functional reorganisation and rehabilitation than true tissue replacement.
Microglia clear debris, while astrocytes contribute to glial scar formation.
Clinical significance: glial scarring can limit axonal regrowth but may also wall off injury and restrict spread of damage.
Complications: seizures, spasticity, cognitive impairment, mood disturbance and long-term disability.

🫀 Healing in Other Organs

Liver: hepatocytes can regenerate remarkably well if the extracellular matrix scaffold remains intact; chronic injury leads to fibrosis and cirrhosis.
GI tract: rapid epithelial turnover supports healing, but anastomotic breakdown risk rises with sepsis, steroids, malnutrition, hypoperfusion and tension.
Myocardium: infarcted cardiac muscle heals mainly by scar formation rather than regeneration, predisposing to impaired contractility and aneurysm formation.
Skin: epithelialisation, granulation tissue and collagen remodelling are strongly affected by moisture balance, bacterial burden and vascular supply.

✅ Exam and Ward Take-Home Points

Neutrophils arrive first; macrophages are the key coordinating cells that allow healing to progress.
Fibroblasts lay down Type III collagen first; remodelling replaces it with stronger Type I collagen.
Granulation tissue means new capillaries plus fibroblasts plus extracellular matrix.
Wound tensile strength never returns to 100%, even after successful healing.
Primary intention is fast with minimal scarring; secondary intention is slower with more granulation tissue, contraction and scarring.
Diabetes and steroids are classic exam answers for impaired wound healing.
Pus needs drainage: antibiotics alone are often insufficient if there is an abscess or infected collection.

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Wound healing