wound healing lutgardo caparas, md, fpapras, fpcs
TRANSCRIPT
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Wound Healing
Lutgardo Caparas, MD, FPAPRAS, FPCS
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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)
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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
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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)
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Classifying wounds
Wounds can be classifiedaccording to their nature:• Abrasion• Contusion• Incision• Laceration• Open• Penetrating• Puncture• Septic etc……………
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Classifying wounds
Abrasion
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Classifying wounds
Incision
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Classifying wounds
Laceration
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Classifying wounds
Open
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Classifying wounds
Septic
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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
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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
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The 3 Phases of Wound Healing
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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
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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
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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
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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)
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Remodeling phase
• Longest part of wound healing
• Lasts from 21 days to 1 year
• Wound contraction and collagen remodeling
• 70 to 80 % strength only
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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
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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.
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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.
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Practical Points and Clinical Applications
• Wound Closure– Choice of suture material.
• Tapes• Tissue Adhesives• Staples• Stainless Steel• Non-Absorbable Sutures• Synthetic Monofilaments• Synthetic Braided Sutures
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Practical Points and Clinical Applications
• 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.
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
• 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.
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Practical Points and Clinical Applications
• Wound Contraction– Process whereby open wound shrink– Different region of the body have different rate– Steriods inhibit the process of wound
contraction
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
• Nutrition– Protein depletion inhibits all phases of
healing, particularly fibroplasia and collagen synthesis
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Practical Points and Clinical Applications
• 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.
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
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
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Practical Points and Clinical Applications
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
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Practical Points and Clinical Applications
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
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Practical Points and Clinical Applications
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
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Practical Points and Clinical Applications
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
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Practical Points and Clinical Applications
• 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
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Practical Points and Clinical Applications
• 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
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Abnormal Response to Injury and Abnormal Wound Healing
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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)
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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
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Excessive scar formation
• Hypertrophic scarring
– Likely to produce dysfunctional contractures
– Etiology and pathogenesis uncertain
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Excessive scar formation
• Keloids– Differ from hypertrophic
scarring by the overgrowth of dense fibrous tissue beyond the borders of the original wound
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Good Scar
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Excessive scar formation
• Goals of treatment (Decrease the process of scar formation)– Steroid injections– Pressure therapy– Silicone sheeting and ointment– External beam irradiation– Scar revision (?)
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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
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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
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Treatment
• Radiation - Kills replicating stem cells and produces an obliterative
endarteritis
- Superficial, low-dose (approximately 1000 rad) can be administered to bulky recalcitrant keloids
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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
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Types of Skin Closure
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Elliptical Excision
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Closure of Wounds following Circular Excision
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Wound Care
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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)
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Fundamentals of wound care
• Hypoxia & wound healing– Hypoxic wounds heal longer– Hypoxia may result from wound edema,
necrotic tissue, bacterial load and hypothermia
– Impairs “oxidative burst”
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Fundamentals of wound care
• 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
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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
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Adjucts to wound treatment
• Hyperbaric Oxygen– Increases interstitial diffusion of oxygen,
improving microcirculation – Implications:
• decreases hypoxia distally• Improves ischemia
– Controversial benefits
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Adjucts to wound treatment
• 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
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Adjucts to wound treatment
• Dressings
– Gauze (wet-to-dry)
– Semiocclusive (Tegaderm)
– Hydrogels (DuoGel)
– Hydrocolloids (Duoderm)
– Foam dressings
– Alginates (Kaltostat)
– Antimicrobials (Flammazine)
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Future Modalities
• Use of autologous stem cells in the problematic wound healing
• Manipulation of healing response thru genetically altered mediators resulting in emperceptible scars
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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.