wound healing lutgardo caparas, md, fpapras, fpcs

Wound Healing

Lutgardo Caparas, MD, FPAPRAS, FPCS

Skin: structure and function

• Largest organ of the body• Primary function is

protective• Composed of several

layers– Outer Epidermis and

Stratum Corneum– Dermis, containing the

capillary network– Subcutaneous layer

(hypodermis, adipose layer)

Skin: structure and function

• Thickness varies from a thin membrane at internal flexures (e.g. elbows), to thicker at the soles of the feet which bear considerable pressures

• Hair follicles, sebaceous glands, and sweat glands pass through the epidermis, but arise from the dermal layer

Classifying wounds

A wound can be defined as:

“A cut or break in the continuity of

any tissue, caused by injury or

operation”

(Baillière’s 23rd Ed)

Classifying wounds

Wounds can be classifiedaccording to their nature:• Abrasion• Contusion• Incision• Laceration• Open• Penetrating• Puncture• Septic etc……………

Classifying wounds

Abrasion

Classifying wounds

Incision

Classifying wounds

Laceration

Classifying wounds

Open

Classifying wounds

Septic

What is wound healing?

• Repair or reconstitution of a defect in an organ or tissue, commonly the skin

• A global response to injury to re-establish homeostasis and to stabilize the entire organism’s physiology

Wound healing

• All wounds heal following a a specific sequence of phases which may overlap

• The process of wound healing depends on the type of tissue which has been damaged and the nature of tissue disruption

• The phases are:– Inflammatory phase– Proliferative phase– Remodelling or maturation phase

The 3 Phases of Wound Healing

Inflammatory phase

• Begins immediately following tissue injury

• Prioritizes attainment of the ff:1. Hemostasis

2. removal of dead tissues

3. prevention of colonization of microbial pathogens

Inflammatory phase (cont…)

• The healing response starts at the moment of injury – the clotting cascade is initiated

• The inflammatory phase is characterised by heat, swelling, redness, pain and loss of function at the wound site

• Early (haemostasis)• Late (phagocytosis)• This phase is short lived in the absence of

infection or contamination

Proliferative phase

• Occuring from days 4 to 21

• Prioritizes the ff:– Re-epithelialization– Increase in fibroblast

cells– Production of fibrin

matrix that is gradually replaced by granulation tissue

– Formation of new blood vessels

Proliferative phase (cont…)

• Epithelialization• The epidermis immediately adjacent to the wound edge

begins to thicken within 24hrs after injury• In approximated incised wounds re-epithelialisation is usually

complete within 48hrs.

• Characterised by the formation of granulation tissue in the wound

• Granulation tissue consists of a combination of cellular elements including:

• Fibroblasts, • Macrophages• Endothelial cells forming new capillaries (angiogenesis)

Remodeling phase

• Longest part of wound healing

• Lasts from 21 days to 1 year

• Wound contraction and collagen remodeling

• 70 to 80 % strength only

Remodeling phase (cont…)

• Wound maturation• New collagen forms, changing the shape of the

wound and increasing the tensile strength• During the remodelling process there is a gradual

reduction in cellularity and vascularity of the reparative tissue

• Wound contraction• Only undesirable where it leads to unacceptable

tissue distortion and an unsatisfactory cosmetic result

• Wound contraction usually begins from day 5 and is complete at approx. day 12 - 15

Fetal Healing

• Closed fetal healing wounds heal rapidly and without scar formation.

• Open fetal skin wounds do not contract.• Amniotic fluid, rich in extracellular matrix

components, such as hyaluronic acid and fibronectin, inhibit the wound contraction process.

• Fetal skin wound are relatively hypoxic and neutropenic are devoid of acute inflammation, and manifest minimal fibrolastic infiltration and proliferation.

Practical Points and Clinical Applications

• Debridement and Irrigation– Mechanical Debridement – Physiologic Saline Irrigation

• Tissue Injury and Blood Supply– Ischemic wounds heal poorly and become

infected.– Well-vascularized tissues heal well.


• Wound Closure– Choice of suture material.

• Tapes• Tissue Adhesives• Staples• Stainless Steel• Non-Absorbable Sutures• Synthetic Monofilaments• Synthetic Braided Sutures


• Suturing Techniques– Interrupted – Continuous – Subcuticular

* The importance of meticulous hemostasis, atraumatic handling of tissues, and avoidance of dead space cannot be overemphasized as prerequisites for uncomplicated healing.


• Suture Removal– 3 to 5 days on the face– 7 to 10 days on the extremities and trunk

• Regaining Tensile Strength– Injured Skin, tendon, and fascia never regain

their normal, or uninjured, strength.– 70 – 80%

• Resutured Wound– Secondary wound phenomenon– Maximal in the second or third week


• Epithelialization– Mechanism of healing in split-thickness skin

graft donor sites, dermabrasions, and partial-thickness burns.

– Process is enhanced in a moist environment, saline or emollient dressings are beneficial.

– Topically applied vitamin A reverse the inhibitory effect of steroids on epithelialization.


• Wound Contraction– Process whereby open wound shrink– Different region of the body have different rate– Steriods inhibit the process of wound

contraction


• Hemodynamics– Hypovolemia, hypoxia, increased blood

viscosity, low flow states, and anemia have been implicated in delayed healing

– Healing is generally unaffected however if hematocrit levels are not less than 15 g/dl and normal blood volume is maintained


• Nutrition– Protein depletion inhibits all phases of

healing, particularly fibroplasia and collagen synthesis


• Vitamin A – Lysosomal labilizer (stimulates inflammation)– Important in maintenance of epithelial integrity– Counteracts steroid inhibition of epithelialization– Effective topically

• Vitamin B – Cofactors in important enzyme systems– Deficiency inhibits antibody formation and the

bactericidal function of leukocytes.


• Vitamin C– Cofactor in the synthesis of collagen

(hydroxylation of proline)– Modifies the inflammatory reaction, inhibits

collagen synthesis, and interferes with leukocyte function

• Vitamin D– Essential for calcium homeostasis


• Vitamin E– Lysosomal stabilizer (inhibits inflammation)– Enhances absorption, storage and use of

vitamin A

• Vitamin K– Required for synthesis of clotting factor VII, IX

and X


• Minerals– Calcium, magnesium, copper, maganeses, iron and

zinc function as enzyme cofactors– Specific deficiencies must be corrected to ensure

normal wound repair– Iron is essential for the hydroxylation of proline– Copper is necessary for normal cross-linking of

collagen– Plasma zinc levels less than 100 mg/dl result in

delaying healing, altered intracellular bactericidal activity, and decreased host resistance


Impaired HealingCauses

Disease states – Malnutrition

Acute Infection – Depressed capillary migration

- Decreased phagocytosis

- Increased angiogenesis and

granulation tissue formation

- Decreased epithelialization

- Decreased wound contraction

- Increased collagen metabolism


CausesDiabetic Patients – Regional Ischemia caused by

large vessel occlusive disease

- Local Ischemia caused by

increased blood viscosity

secondary to increased red

cell rigidity, aggregation and

stagnation

- Soft tissue hypoxia resulting

from increased affinity of

Glycosylated hemoglobin for

oxygen


CausesDiabetic Patients – Progressive and poorly understood

diabetic neuropathy

- Impaired phagocytosis secondary to

altered opsonic capacity

- Abnormal polymorphonuclear

leukocytes, macrophages and

lymphocytes

* Amputations can frequently be avoided by combining skills of the vascular surgeon in distal revascularization procedures and the plastic surgeon in aggressive flap closure of indolent ulcers


CausesDrugs

1) Steroids – Retard epithelialization and contraction at

any time

- Inhibit normal fibroplasia, collagen synthesis

and neovascularization

2) Chemotherapeutic Agents – Nitrogen Mustard

- Retard inflammation

3) Lathyrogens – Penicillamine, Beta-Aminopropionitrile

- Interfere with the cross linking of collagen

4) Colchicine – Slows cellular collagen transport,

suppresses epithelialization, retards

contraction


CausesRadiation – Inhibits all aspect of healing

- Maximal effect if administered 36 hours after

wounding

- Principal mechanism – Destruction of replicating

and differentiating stem cells and the initiation of

a progressive obliterative endarteritis

Smoking – Precise mechanism are not yet understood, both

nicotine and carbon monoxide implicated

- Untoward effects of smoking may be minimized by

cessation of smoking at least 2-3 weeks before

surgery and 1-2 weeks after surgery


• Methods of Promoting HealingA) Growth Factors

– Extract growth factors from platelet

- Interact directly with cell receptors in the wound

- Stimulate active growth of granulation tissue, capillaries

and epithelium.

- Epidermal Cell Derived Factor (EDF)

- Fibroblast stimulating factor (TGF-B)

- PDGF


• Methods of Promoting HealingB) Hyperbaric Oxygen Therapy

- Strong stimulus for angiogenesis

- Therapeutic adjunct in oxygen-deficient wounds, such as lower extremity ulcers, extensive burns, and ischemic skin flaps

C) Methods for Immunosuppressed Patients

- Cytokines and Lymphokines

- Biologic skin substitutes

Abnormal Response to Injury and Abnormal Wound Healing

Inadequate scar formation

• Failure to replace a tissue defect with a scar

• Treat underlying defect in scar formation– E.g. pressure sores

(treat underlying pressure and infection problem to progress wound to granulate and heal)

Excessive regeneration

• Overexhuberant attempts of the body to heal, resulting in a disordered and uncontrolled growth– E.g. neuroma formation and cutaneous

psoriasis• Tx: decrease cellular proliferation and

regeneration

Excessive scar formation

• Hypertrophic scarring

– Likely to produce dysfunctional contractures

– Etiology and pathogenesis uncertain


• Keloids– Differ from hypertrophic

scarring by the overgrowth of dense fibrous tissue beyond the borders of the original wound

Good Scar


• Goals of treatment (Decrease the process of scar formation)– Steroid injections– Pressure therapy– Silicone sheeting and ointment– External beam irradiation– Scar revision (?)

Treatment

• Prolonged Pressure greater than 22 mm Hg (capillary hydrostatic pressure) flattens and soften exuberant scars

Eg: Jobst garments

Silastic sheeting

• Pressure decreased collagen synthesis, increasing degradation and stimulating remodeling along lines of stress

Treatment

• Steroid Injection - Reduce local collagenase inhibitors (i.e., increase

collagenolysis)

- Triamcinolone injection

- Maximal dose of Triamcinolone every month

- 40mg for infants and children aged 1-5 years

- 80mg for children aged 6-10 years

- 120mg for adults

Treatment

• Radiation - Kills replicating stem cells and produces an obliterative

endarteritis

- Superficial, low-dose (approximately 1000 rad) can be administered to bulky recalcitrant keloids

Treatment

• Surgery

- Coincide with relaxed skin tension lines

- Divide complex scar into smaller components

- Leveling contour deformities

- Lengthening Tight Scars• Elliptical excision and closure • Z-Plasty • W-Plasty• VY-Plasty• Dermabrasion and Dermaplaning• Skin Grafts and Flaps

Types of Skin Closure

Elliptical Excision

Closure of Wounds following Circular Excision

Wound Care

Fundamentals of wound care

• Age & wound healing– There is a decline in wound healing rates in

the elderly (aged fibroblast and endothelial cells)

– Decreased growth factors

– Decreased ability to survive in hypoxic and toxic stresses

– Needs supplementation (antibiotics, Vit C)


• Hypoxia & wound healing– Hypoxic wounds heal longer– Hypoxia may result from wound edema,

necrotic tissue, bacterial load and hypothermia

– Impairs “oxidative burst”


• Bacteria & wound healing– All wounds are contaminated, – Bacterial load of 105 interferes with wound

healing except B-hemolytic streptococcus (wherein few amounts of this bacteria causes severe infection)

– contaminated wound– Increase production of

toxins and proteases

Adjucts to wound treatment

• Debridement– Prepares the wound for healing by reducing

bioburden

• Negative-Pressure Wound Therapy– Vacuum Assisted Closure (VAC)– Decreases edema and increases chemical

mediators beneficial to wound healing


• Hyperbaric Oxygen– Increases interstitial diffusion of oxygen,

improving microcirculation – Implications:

• decreases hypoxia distally• Improves ischemia

– Controversial benefits


• Growth Factors– Becaplermin (Regranex)

• This is a Platelet-Derived Growth Factor derivative used for treating diabetic foot ulcers and irradiated wounds (applied as topical dressing)

• Not available locally

• Enzymes– Enzymatic debriding agents that selectively

digest necrotic tissues• Eg, papain, urea, Zolrox (Daikin’s solution)

– Not a substitute for surgical debridement


• Dressings

– Gauze (wet-to-dry)

– Semiocclusive (Tegaderm)

– Hydrogels (DuoGel)

– Hydrocolloids (Duoderm)

– Foam dressings

– Alginates (Kaltostat)

– Antimicrobials (Flammazine)

Future Modalities

• Use of autologous stem cells in the problematic wound healing

• Manipulation of healing response thru genetically altered mediators resulting in emperceptible scars

Conclusion

• Wound care is becoming more complex as the range of wounds increases

• Correction of the underlying causative factors is essential and multidisciplinary

• Overall patient benefit with the different wound healing strategies remains to be determined.

wound healing lutgardo caparas, md, fpapras, fpcs

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