Editing Wound healing

== Stages ==

# Inflammation
## Haemostasis (damage limitation) - erythrocyte and platelet plug
## Inflammation - increased permeability, migration, and activation
### Initial neutrophils
### But healing is largely mediated by macrophages - arrive as monocytes within 24-48 hours of injury, release a lot of chemokines/cytokines
### Lymphocytes appear day 5-7 - seem to be related to downregulating healing as wound closes. Can be affected by drugs that suppress T-lymphocyte function (steroids, cyclosporine, tacrolimus)
### Can continue up to two weeks
# Proliferation
## Acute response is over - scaffolding laid for repair of wound - formation of granulation tissue (capillary bed, fibroblasts, macrophages, and collagen etc scaffolding)
## Growth factors secreted, primarily by macrophages, which recruit the fibroblasts
##
# Maturation/remodelling/epithelialisation
## Centripetal movement of the whole thickness of surrounding skin
## Complex interaction of ECM and fibroblasts (which have changed to become myofibroblasts)
## Remodelling occurs as type III collagen is largely replaced by mature type I collagen

== Wound classification ==
{| class="wikitable"
|Type 1 - clean
|
** Uninfected operative wound with no inflammation and no entering of special tracts
** Heal with negligible risk of infection
** Primary closure is best
|-
|Type 2 - clean contaminated
|
** Operative wounds where the respiratory, alimentary, genital, or urinary tracts were entered under controlled conditions
** Only minor spillage 
** Close primarily after wound toilet
|-
|3 - contaminated
|
** Open, fresh, accidental wounds
** Operative where non-purulent inflammation is present
** Operative with major break in sterile technique or spillage from GIT
** Need copious irrigation before delayed primary or sometimes primary closure
|-
|4 - dirty

|
** Infected, contaminated, or devitalised wounds (the organisms causing post-op infection were present prior to the operation)
** Includes perforated viscera
** Open wounds >12 hours
** Need to be converted to type 1 or 2 prior to closure
|}

== Primary intention ==

* Fibrinous adhesions between surfaces by 24 hours
* Granulation tissue grows in
* Collagen is laid down
* Wound contracts, scar forms
* 10% strength at day 5, 50% at day 21

== Secondary intention ==

* Clot on surface allows moist environment at base of wound
* Debrided by phagocytic WBCs
* Collagen produced by fibroblasts in a matrix of mucopolysaccharides - granulation tissue
* Myofibroblasts cause wound contraction
* Epithelium migrates to cover wound

== Management of clean surgical wounds ==

* Fibrin layer forms within the first few days, especially if subcuticular suture is used (takes a bit longer with staples)
* Dry gauze on top is only necessary for about three days; after that, can be uncovered, or dry gauze at most (opsite)
* Can bathe/shower (in clean water) after five days
* A red area of a surgical wound does not mean cellulitis - it means pus that needs to be drained. Drain it locally by removing a few sutures or staples and then continue to observe it. If the cavity probes elsewhere, may need to open further.
* Only give antibiotics if there is severe cellulitis or fascia is involved
* Wound swabs are generally unnecessary, unless the wound is becoming problematic and MRSA may be involved

== Chronic/non-healing wounds ==

* Occurs when the normal healing process is disrupted, most often because an underlying disorder causes a prolonged, unchecked pro-inflammatory state
* There often seems to be inhibition of growth factors and other negative implications on a cellular level


== Factors influencing wound healing ==
(>90% of ulcers are associated with either chronic venous insufficiency, arterial occlusive disease, or diabetic neuropathy)

=== '''Local''' ===

** Ischaemia
*** '''Inadequate inflow''' - vessel ligation, '''PVD,''' systemic hypotension
**** See separate topics
**** Use WIfI classification to determine severity and guide intervention
**** Toe pressure can be useful in guiding chance of wound healing
**** In general same principles apply as for other wounds - pressure offloading, debridement of non-viable tissue, infection control, moist wound healing
**** Leave adherent eschar or dry gangrene in place until revascularisation has occurred
**** After revascularisation, be aware of limb oedema
***** For grafts ending at popliteal level, below-knee IPC is useful
***** For grafts ending distally, a pedal compression boot is useful
**** Common for infection to develop as areas of eschar/dry gangrene heal - need to be followed closely. Some surgeons prefer to amputate necrotic digits or perform wide debridements of eschar a few days after revascularisation.
*** Dead tissue at wound edge
*** Overly tight or closely spaced sutures
*** Tension on wound edge
*** Smoking - 30% reduction in wound blood flow
** Tension
** Dead space
** Foreign bodies/contamination
** Infection
*** Collagenolysis increases, tissue pressure elevates
*** Mechanical and antibiotic therapy can decrease bacterial count, reduce inflammation, and allow wound closure
*** See separate topic: 'wound infection'
** Haematoma
*** Predisposes to infection and wound complications
** Local trauma
** Chronic tissue factors
*** '''Chronic venous insufficiency'''
**** Venous disease in any combination of anatomic sites may result in limb ulceration, including superficial venous insufficiency alone, however most of the time a venous ulcer is present, there is involvement of the deep venous system (see below)
****
**** Chronic upregulation of pro-inflammatory cytokines appears to mediate the development of tissue fibrosis and the clinical appearance of lipodermatosclerosis (which is believed to be a pre-ulcerative condition). Ulceration eventually occurs secondary to minor trauma.
**** Should have an USS to assess for this (saphenous reflux, perforator incompetence, and iliac outflow stenosis, etc)
**** Sustained high-strength compression of the limb is the basis for treatment of venous leg ulcers, and must be maintained throughout treatment. Results in healing in 60-70% of patients after 4-6 months.
**** Venous intervention is recommended whenever superficial venous reflux is a prominent component of the abnormal venous function. Limited evidence supporting the removal of varicose channels extending into the ulcer bed.
**** Other therapies have been studied including skin grafting, but this is only useful in select cases
*** Lymphoedema, ischaemia, scarring
** Sutures
*** Silk - nidus for infection
*** Too tight?
** Irradiation

=== '''General health''' ===

** '''Diabetes'''
*** Macrovascular disease and microangiopathy
*** Sensory neuropathy - repeated trauma
*** Immunosuppression
** Advanced age
** Malnutrition
*** Vitamin C
*** Vitamin A
** Mineral deficiencies
*** Zinc
*** Iron
** Immunosuppression
** Medications
*** Corticosteroids
*** Chemotherapy
** Smoking 
** Systemic illness

== Approach to a chronic/non-healing wound: ==

* Review all potential contributing factors from above
* Check for granulation tissue - most negative factors above will stagnate the wound in the inflammatory phase
* Remember that many rare causes of non-healing wounds can only be diagnosed with biopsy!
* Wagner classification system:
**
* Wound bed preparation:
** Debridement of non-viable tissue
*** Remove callus, eschar, fibrinous material, and slough. None of these have regenerative capacity, and they harbour bacteria, and prevent migration of healthy epithelium.
*** Chemical debridement is possible, mostly using collagenase, and this is most effective at removing a moderate amount of fibrinous slough from the wound base, but is ineffective against thick tissue or eschar
*** There are many methods of debridement, but none have ever been found to be superior to standard surgical debridement
** Identification and correction of bacterial involvement
*** Controversial as to whether wounds that are colonised but not clinically infected should be treated
*** Rutherford's says wounds with poor progress or any evidence of enlargement or infection should have quantitative cultures, and anything growing to >10^5 bacterial counts per cubic mm should be treated with systemic therapy, guided by sensitivities
*** It is advantageous to remove biofilms where possible
** Control of chronic inflammation
** Elimination of limb oedema
** Control of wound exudate

== Hypertrophic scars/keloids ==

* Excessive net collagen deposition
* Keloids '''grow beyond borders of original wounds'''
** Rarely regress
** Aetiology
*** Much more prevalent in dark skin
*** Genetics
** Pathogenesis
*** Disorganised type I and III collagen
** Clinical features
*** Often form at previous minor trauma/scars e.g. earlobes from piercings
*** Generally get bigger over time, do not regress
*** Often a/w pain and pruritis
** Treatment
*** Medical
**** Topical/intralesional corticosteroids
**** Radiotherapy (often in conjunction with surgery, however one big study didn't show any difference to recurrence rates if it was included)
*** Surgical
**** Consider if refractory to medical treatment for 12 months
**** Leads to recurrence of 45-100%
* Hypertrophic scars are raised scars '''within confines of original wound'''
** Occur with prolonged inflammation and tension
** Frequently regress spontaneously
** Well-organised type III collagen
** Prevent by avoiding wound tension, hydration/occlusion, and use of taping/pressure garments
*** Indicated in severe burns, mechanical trauma, necrotising infections, or grafting
** Treatment:
*** 6-12 weeks: pressure therapy
*** >6mo: silicone therapy, intralesional corticosteroids (triamcinolone acetonide, 10-40mh/mL injected into papillary dermis every 2-4 weeks until flat. Works >50% of patients
* Approach to hypertrophic scars/keloids:
** History - including other scars, family history
** Examination - can use Vancouver scar scale to give objective measure of scar
** Counsel patient about difficult nature of problem and define goals of therapy:
*** Relief of symptoms
*** Reduction of scar volume
*** Functional or cosmetic improvement
** Initial trial of intra-lesional triamcinolone acetonide at a concentration of 10 to 40mg/mL
*** Reduces volume
*** Improves pain and pruritis
*** Repeat treatment several times at 4-6 week intervals
*** Injections are painful. Can cause dermal atrophy, skin ulceration, hyperpigmentation, telangiectasia.
** Can try combination fluouracil and triamcinolone - 50-96% had a good response in one meta-analysis - but these studies are of low quality. Can cause pain and hyperpigmentation.
** Can trial pressure - there are special devices for earlobes. Limited evidence. May be beneficial in combination with surgery.
** Surgery - recurrence approaches 100% - however is probably lower if combined with peri-operative triamcinolone or fluorouracil
** Post-op radiation therapy. Evidence from retrospective observational trials.

[[Category:Skin, soft tissue and wounds]]
[[Category:Intern education]]