Appearance
14.4 — Wound Healing and Scars
A fetus in the first two trimesters heals skin wounds without any scar at all — the tissue is regenerated exactly as it was, with collagen restored in its original basket-weave arrangement.
That capacity is lost around the third trimester and never returns. Working out why is one of the more interesting open problems in the field, and the leading explanations centre on the fetus's low-inflammation environment and its different collagen and growth factor profile.
Every scar you have is the price of an immune system that arrived at the wound.
The four phases
1. Haemostasis — seconds to minutes.
Vessels constrict, platelets plug, the clotting cascade produces fibrin (Chapter 7.1).
And the clot is not merely a plug. It is a scaffold — cells migrate along the fibrin mesh — and a reservoir of growth factors released by the platelets, which start everything that follows.
2. Inflammation — days 1 to 3.
Neutrophils first, clearing bacteria and debris; macrophages from about day 2, clearing the neutrophils and switching the process toward repair (Chapter 13.4).
The macrophage switch is the pivotal event. A wound in which macrophages fail to change from the inflammatory to the repair phenotype does not heal, and this is a central mechanism in chronic wounds.
3. Proliferation — days 3 to 21.
Four things happen together.
Angiogenesis — new capillaries sprout into the wound, driven by the low oxygen at its centre. Which is why healing depends so completely on blood supply, and why anything reducing it stalls the process.
Granulation tissue forms — the red, bumpy, slightly bleeding surface of an open wound. It looks alarming and it is exactly what should be there: new vessels and new matrix.
Fibroblasts lay down collagen — initially type III, which is weaker and disorganised.
Epithelialisation — cells from the wound edges and from surviving hair follicles and glands migrate across the surface.
And they only migrate across a moist surface. Under a dry scab, cells must burrow beneath it, which is slower.
This is the entire basis of modern moist wound healing, established by George Winter's work in 1962, and it reversed the traditional advice to "let it dry out and breathe". A wound kept moist under an appropriate dressing epithelialises around twice as fast and scars less.
Wound contraction also occurs, with specialised fibroblasts pulling the edges together. Useful in a small wound and destructive in a large one, where it causes the contractures that limit movement after burns.
4. Remodelling — 3 weeks to 2 years.
Type III collagen is progressively replaced by stronger type I, and the fibres are reorganised along lines of tension.
And the strength figures matter for practical advice.
At 1 week, about 3 percent of original strength. At 3 weeks, about 20 percent. At 3 months, about 70 to 80 percent — and that is the maximum a scar ever reaches.
So a wound that looks completely healed at three weeks has only a fifth of its strength, which is exactly why surgical patients are told to avoid heavy lifting for six weeks, and why abdominal wounds burst when they are not.
A scar never regains full strength, and it never regains hair follicles, sweat glands or normal pigmentation.
Healing by first and second intention
First intention — the edges are brought together and the gap is minimal. A surgical incision or a sutured cut. Minimal granulation tissue, fast, fine scar.
Second intention — the wound is left open and heals from the base up. A large or contaminated wound, or one with tissue loss. Extensive granulation, considerable contraction, slower, larger scar.
And knowing which to choose is a genuine clinical decision rather than a preference.
Some wounds must not be closed, because closing them traps bacteria in an ideal environment.
Bites — particularly cat bites, which are deep puncture wounds inoculated with mouth flora, and human bites over the knuckles (Chapter 5.5).
Heavily contaminated wounds, and wounds presenting late — generally beyond 6 to 12 hours, or 24 hours on the face, which has a better blood supply.
Abscesses — which need drainage rather than closure. "Where there is pus, let it out" is one of the oldest and most reliable rules in surgery, and antibiotics without drainage generally fail because they penetrate a walled-off collection poorly.
Delayed primary closure is the compromise: leave the wound open for 3 to 5 days, allow the inflammatory phase to clear the contamination, then close it.
What impairs healing
Local factors:
Poor blood supply — the dominant one. Arterial disease, venous disease, pressure, and radiation damage all reduce it.
Infection — prolongs the inflammatory phase and consumes resources.
Foreign bodies — including suture material, and this is why gravel or glass must be removed before closure.
Movement — which is why joints are splinted and why a wound over a joint scars more.
Desiccation — as above.
Systemic factors, and most of them are modifiable:
Smoking. Nicotine constricts vessels, carbon monoxide reduces oxygen delivery, and both impair collagen synthesis. Wound complication rates in smokers are roughly two to four times higher, and stopping for four weeks before elective surgery measurably reduces them. It is one of the highest-yield preoperative interventions available and one of the least often achieved.
Diabetes — impairs every stage: reduced blood supply, impaired neutrophil function, and glycation of collagen making it weaker.
Malnutrition. Protein for collagen, vitamin C — which is required by the enzyme that stabilises collagen, hence the reopening of old scars in scurvy (Chapter 4.2) — zinc, and adequate calories.
And nutrition is checked and corrected before elective surgery in high-risk patients, because it is cheap and effective and routinely overlooked.
Steroids and immunosuppressants — impairing inflammation and collagen synthesis. Vitamin A can partially counteract the steroid effect, which is a rare specific antidote in this area.
Age — slower, though the final result is usually satisfactory.
Chemotherapy and radiotherapy.
Obesity — poorer blood supply to fat, greater tension on the wound, and higher infection rates.
Chronic wounds
A wound that has not healed in the expected time, usually taken as four to six weeks — and typically stuck in the inflammatory phase.
Three types account for the great majority, and their appearance and location distinguish them.
Venous ulcers (about 70 percent of leg ulcers) — from chronic venous hypertension when the calf pump and valves fail (Chapter 6.6).
Above the ankle, usually on the inner side. Shallow, irregular, with a wet base. Surrounded by brown pigmentation and thickened skin. Relatively painless, and often improved by elevation.
And the treatment is compression, which is the most important sentence in this section. Graduated compression bandaging heals the majority of venous ulcers, and it works because it corrects the underlying pressure problem rather than treating the surface. Dressings alone do not heal them.
Compression must not be applied without checking the arterial supply first, which is done by comparing ankle and arm blood pressures — because compressing a limb with poor arterial flow causes tissue death.
Arterial ulcers — from inadequate arterial supply.
On the toes, heel or pressure points. Deep, punched-out, with a pale dry base. Painful, particularly at night and when the leg is elevated, and relieved by hanging the leg down — which is the opposite of a venous ulcer and is a genuinely diagnostic history.
The foot is cold with absent pulses.
And the treatment is to restore the blood supply — angioplasty or bypass. No dressing heals an ulcer without perfusion.
Diabetic foot ulcers — neuropathy plus arterial disease plus impaired healing (Chapter 11.8).
On the pressure points of the sole, and characteristically painless, which is why they are noticed late.
Treatment is offloading — removing pressure from the area, usually with a total contact cast — plus debridement, infection control and blood supply assessment.
And the prevention is where the effect is largest. Daily foot inspection, well-fitting shoes, never walking barefoot, and annual screening with a monofilament prevent a large proportion of diabetic amputations.
Pressure ulcers — from sustained pressure exceeding capillary pressure, so tissue is starved of blood.
They can begin within two hours, and they develop from the inside out — muscle and fat over a bony prominence die before the skin does, so what appears as a small area of skin damage frequently overlies far more extensive deep injury.
Sites: sacrum, heels, hips, elbows, and the back of the head.
And they are largely preventable. Repositioning, pressure-redistributing surfaces, keeping the skin dry, and nutrition. Pressure ulcers acquired in hospital are now treated as a marker of care quality rather than as an inevitability, and rates have fallen substantially where that view has been taken seriously.
Scars
Normal scar maturation: red and raised initially — because of the new blood vessels — then progressively paler, flatter and softer over 12 to 18 months.
Which means a scar should never be judged before a year, and surgical revision is generally deferred until then.
Hypertrophic scars — raised, red, itchy, staying within the original wound boundaries. Often improve over one to two years.
Keloid scars — growing beyond the original wound, do not regress, and frequently recur after excision.
More common in darker skin, in people aged 10 to 30, and at particular sites: chest, shoulders, upper back and earlobes.
Which is why ear piercing is a common cause, and why anyone with a keloid history should be warned before elective procedures on those areas.
Treatments include silicone sheets or gel, intralesional steroid injection, pressure, and — for keloids — excision combined with another treatment, since excision alone usually makes them worse.
Contractures — a scar shortening and restricting movement, particularly across joints and after burns. Prevented by early physiotherapy and splinting, which matters far more than any later treatment.
What actually reduces scarring:
Reducing tension — closing in layers, and using techniques that take tension off the skin edge.
Cutting along Langer's lines where possible (Chapter 14.1).
Silicone sheets or gel, with reasonable evidence, applied for several months.
Sun protection. A new scar pigments readily and permanently, so sun exposure in the first year produces a permanently darker scar. This is simple, effective and rarely mentioned.
Keeping it moist and covered while healing.
And what does not have good evidence: vitamin E applied topically, which several trials found made outcomes no better and sometimes worse; and most commercial scar creams, whose benefit is largely from the massage and moisture rather than the ingredients.
Sutures, glue and dressings
Choosing a closure method is a matter of matching the wound.
Sutures — strongest, most precise. Removal timing balances scarring against strength: face 3 to 5 days, scalp 7 to 10, limbs 10 to 14, over joints and on the back 14 days.
Leaving them too long causes cross-hatched "railway track" marks; removing too early risks the wound opening.
Tissue adhesive (glue) — for small, clean, low-tension wounds, particularly in children. No removal needed, no injection required, and cosmetically equivalent for suitable wounds. Not for the eyelids or across joints.
Adhesive strips — for superficial low-tension wounds.
Staples — fast, used for the scalp and for long surgical incisions.
And a practical note: hair apposition works well for scalp lacerations — twisting strands of hair from either side together and securing with glue. No sutures, no removal appointment, and better cosmetic results.
Dressings are chosen by what the wound is doing.
Dry, low exudate → hydrocolloid or film. Moderate exudate → foam. Heavy exudate → alginate. Infected → antimicrobial dressings, silver or iodine. Cavity → packing, or negative pressure therapy.
Negative pressure wound therapy — a sealed dressing under suction — removes exudate, reduces oedema, draws the edges together and stimulates granulation. It has substantially improved the management of large complex wounds.
Tetanus
Belongs here because every wound raises the question.
Clostridium tetani spores are in soil and dust everywhere, and they germinate in wounds with low oxygen.
The bacterium does not spread. Its toxin does — travelling up nerves to the spinal cord, where it blocks the release of inhibitory transmitters (Chapter 11.2).
So the result is unopposed muscle contraction: lockjaw, the characteristic fixed grimace, arching of the back, and violent spasms triggered by minimal stimulation. Mortality is 10 to 20 percent even with intensive care.
Tetanus-prone wounds: puncture wounds, wounds contaminated with soil or manure, burns, wounds with devitalised tissue, and any wound presenting after six hours.
And the management follows two questions: is the wound tetanus-prone, and is the person fully immunised?
A fully immunised person with an up-to-date course is protected and needs nothing. An incompletely immunised person with a tetanus-prone wound needs both the vaccine and tetanus immunoglobulin — the immunoglobulin gives immediate protection while the vaccine response develops (Chapter 13.3).
Thorough wound cleaning and removal of dead tissue matters as much as either, because the spores cannot germinate in a clean, well-oxygenated wound.
Tetanus has become rare where vaccination is routine, and it remains a substantial cause of newborn death where deliveries are unhygienic and mothers are unvaccinated — maternal vaccination prevents it, which is one of the clearest wins available in maternal health.
What the next page fixes
The skin's conditions are among the most visible in medicine and among the most treatable. Chapter 14.5 closes this Part with the common skin diseases — acne, eczema, psoriasis, infections and skin cancer — and with the one skin change that everyone should be able to recognise.