pathophysiology and prevention of scar tissues - nata
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Pathophysiology and Prevention of Scar Tissues - NataTRANSCRIPT
Pathophysiology and Prevention of Scar
Tissues
Deny budimanAchmad p
Hendrikus bollyJocliedian GL
The Anatomy of Human Skin
Epidermis (5 layers)Keratinocytes provide protective
properties.
Melanocytes provide pigmentation.
Langerhans’ cells help immune system.
Merkel cells provide sensory receptors.
Dermis (2 layers)Collagen, glycoaminoglycans, elastine,
ect.
Fibroblasts are principal cellular constituent.
Vascular structures, nerves, skin appendages.
Hypodermis (fatty layer)Adipose tissue plus connective tissue.
Anchors skin to underlying tissues.
Shook absorber and insulator.
Eight Functions of Human Skin
1. Protect underlying tissues from injury: mechanical, heat, cold, biological.
2. Prevent excess water loss.
3. Act as a temperature regulator.
4. Serve as a reservoir for food and water: adipose tissue
5. Assist in the process of excretion: H20, Salt, Urea, Lactic Acid.
6. Serve as a sense organ for cutaneous senses: pain, heat, cold, pressure, touch.
7. Prevent entrance of foreign bodies: microorganisms.
8. Serve as a seat of origin for Vitamin D.
Phases of Wound Healing
1. Clotting2. Vascular
Response3. Blood
coagulation4. Inflammation5. Formation of
new tissue6. Epithelialisation7. Contraction &
Remodeling
Physiological Stages
1.) Inflammatory Phase Initial response to injury Day 1-4 post injury Characterized by rubor, tumor, dolor, calor Platelet aggregation and activation Leukocyte (PMNs, macrophages) migration, phagocytosis
and mediator release Venule dilation Lymphatic blockade Exudative In wounds closed by primary intention, lasts 4 days In wounds closed by secondary or tertiary intention,
continues until epithelialization is complete
2.) Proliferative PhaseDay 4-42Fibroblast proliferation
stimulated by macrophage-released growth factors
Increased rate of collagen synthesis by fibroblasts
Granulation tissue and neovascularization
Gain in tensile strength
3.) Remodeling Phase6wks-1 yearIntermolecular cross-
linking of collagen via vitamin C-dependent hydroxylation
Characterized by increase in tensile strength
Type III collagen replaced with type I
Scar flattens
The stages of healing
Abnormal Wound Healing
KeloidHypertrophic scarContractureTrauma
Keloids overgrowth fibrous tissue after
healing of a skin injury. Tissue extends beyond the borders
of woundNot usually regress spontaneouslyRecur after excision 3 months to
years The first description of keloids
Egypt in 1700 BCE. 1806, Alibert cheloide chele, or crab's claw lateral growth of tissue
Keloids
Hypertrophic scars
Erythematous, pruritic, raised fibrous lesions
Not expand over border of initial injury
Partial spontaneous resolution After thermal injuries and other
injuries that involve the deep dermis 4 weeks after trauma
Hypertrophic
Scar
Hypertrophic Scar / KeloidHypertrophic Scars Keloids
Occur soon after injury or surgery. May not develop for many months after injury or surgery.
Usually flatten spontaneously with time.
Remain elevated and do not spontaneously resolve.
Limited to the area of the original tissue damage.
Not confined and may overgrow wound boundary.
Size related to the injury. A minor injury may produce a large lesion.
Occur with motion and tension. Independent of motion.
Usually occur across flexor surface, for example joints.
Commonly occur on ear lobes, shoulders, pre-sternal skin and upper back.
May be improved with appropriate surgery.
May be worsened with surgery.
Few collagen fibres; nodular structures containing fibroblastic cells, small vessels and collagen.
Large, thick collagen fibres in closely packed fibrils.
Contracturescars that cross joints or skin creases
at right angles are prone to develop shortening
a serious functional consequence of excessive scar formation
occur when the scar is not fully matured, often tend to be hypertrophic, and are typically disabling and dysfunctional
common after burn injury across joints or skin concavities.
Contracture
Contraction Vs Contracture
Contraction: centripetal movement of the whole thickness of surrounding skin reducing scar
Myofibroblasts: special Fibroblasts express smooth muscle and bundles of actin connected through cellular fibronexus to ECM fibronectin, communicate via gap junctions to pull edges of the wound
Contracture: the physical constriction or limitation of function as the result of Contraction (scars across joints, mouth, eyelid)
Burn/Keloid causing contracture
Trauma / Chronic WoundsTraumatic injuries can be sustained
from heat (burns) and cold (frostbite) and are often a combination of partial and full thickness injuries
Traumatic wounds are usually sustained in a dirty environment and contamination can lead to prolonged healing and a higher incidence of infection.
Lacerations and open injuries older than 24h
Trauma / Chronic Wounds
Scar ClassificationMature Light-coloured and flat.Immature Red, sometimes itchy and painful, slightly elevated. Many will mature to
become flat and assume pigmentation similar to the surrounding skin, although they can be paler or slightly darker.
Widespread Stretched
Appear when the fine lines of surgical scars gradually become stretched and widened. Typically flat, pale, soft, symptomless scars often seen after knee or shoulder surgery. Stretch marks (abdominalstriae) after pregnancy are variants of widespread scars. No elevation, thickening, or nodularity which distinguishes them from hypertrophic scars.
Atrophic Flat and depressed below the surrounding skin. Generally small and often round with an indented or inverted centre. Commonly arise after acne or chickenpox.
Contractures Scars that cross joints or skin creases at right angles are prone to develop shortening or contracture. Occur when the scar is not fully matured. Often tend to be hypertrophic, and are typically disabling and dysfunctional. Common after burn injury.
Linear Hypertrophic
Red, raised and sometimes itchy. Confined to the border of the original surgery or trauma. Develops within weeks of surgery. May increase rapidly in size for 3-6 months and then, after a static phase, begin to regress. Mature to have an elevated, slightly rope-like appearance with increased width. Full maturation can take up to two years.
Widespread Hypertrophic
Common after a burn. A widespread red raised and sometimes itchy scar that remains within the borders of the original burn.
Minor Keloid A focally raised, itchy scar that extends over normal tissue. May develop up to one year after injury and does not regress without treatment. Surgical excision is often followed by recurrence.
Major Keloid A large, raised scar which may be painful or pruiritic. Extends over normal tissue and can continue to spread over many years.
Pathophysiology
variations of typical wound healing. typical wound equilibrium anabolic and
catabolic processes ( 6-8 weeks ) 30-40% strength
scar matures strength cross-linking of collagen fibers hyperemic and thickened subside gradually over months until a flat, white, pliable, possibly stretched, mature scar has developed.
Imbalance more collagen grows all directions elevated , hyperemic. keloid or hypertrophic scar.
Kischer and Brody collagen nodule unit of hypertrophic scars and keloids.
Collagen nodule high density of fibroblasts and unidirectional collagen fibrils in a highly organized and distinct orientation rich vasculature, high mesenchymal cell density, and thickened epidermal cell layer.
Clinically differentiate keloids from hypertrophic difficult in early phases of formation.
Histologic difference Keloid broad, dull, pink bundles of collagen
FrequencyOnly humans All age groups rarely found in newborns
or elderly persons Highest aged 10-20 years.Mortality/MorbidityMost sites cosmetic some can cause
contractures overlying a joint or in significant disfigurement if located on the face
Genetically HLA-B14, HLA-B21, HLA-Bw16, HLA-Bw35, HLA-DR5, HLA-DQw3, and blood group A
RacePolynesian and Chinese White persons are least commonly
affected.SexHigher in young females earlobe piercing Both sexes equally other age groups.Age10-30 years. Less frequently extremes of age,
increasing number of presternal keloids coronary artery bypass operations and other similar procedures now undertaken in persons in older age groups.
CLINICALHistoryNot cause symptoms tender,
painful, or pruritic, burning sensation. Origins of lesions
◦Keloids areas trauma past the areas above skin rarely into subcutaneous tissue.
◦Hypertrophic limited traumatized area regress 12-24 months not complete
Clinical findings of KeloidsSoft , rubbery and hard. Early lesions erythematous brownish
red paleDevoid hair follicles and adnexal glandsEnlarge rapidly months stop growing
stable or involute slightlyEars, neck, and abdomen pedunculatedCentral chest and extremities raised with
a flat surface, base wider than the top.Round, oval, or oblong with regular
margins clawlike configurations, irregular borders.
Joint contract.
Frequency of lesion sitesWhite persons Face cheek and earlobes Upper extremities, chest, presternal area,
neck, back, lower extremities, breasts, and abdomen.
Black persons Earlobes, face, neck, lower extremities,
breasts, chest, back, and abdomen.Asian persons, Earlobes, upper extremities, neck, breasts,
and chest.
CausesEnigma no specific gene or set of genes Trauma primary Foreign material, infection, hematoma, or
increased skin tension in susceptible individuals.
Lab StudiesBiopsy diagnosis
TREATMENT
Medical CareNo single therapeutic modality is
best Individual Prevention keyPrevention :
◦Avoid nonessential cosmetic surgery ◦Minimal tension surgical wound◦Incisions not cross joint spaces.◦Avoid midchest incisions◦ incisions follow skin creases
Standard treatments
Occlusive dressings silicone gel sheets and dressings, nonsilicone occlusive sheets, and Cordran tape. occlusion and hydration
Previous studies silicone occlusive 24 h/d, 12 months,
34%excellent, 37.5% moderate, and 28% no or slight improvement
semipermeable, semiocclusive, nonsilicone-based dressings 8 weeks, 60% flattening of keloids, 71% reduced pain, 78% reduced tenderness, 80% reduced pruritus, 87.5% reduced erythema, and 90% were satisfied with the treatment.
• Compression therapy pressure thinning Reduction cohesiveness of collagen
• Button compression, pressure earrings, ACE bandages, elastic adhesive bandages, compression wraps, spandex or elastane (Lycra) bandages, and support bandages.
60% of patients treated with these devices showed 75-100% improvement.
Corticosteroids• Intralesional injections • Reduce collagen synthesis reducing
production of inflammatory mediators and fibroblast proliferation
• Triamcinolone acetonide (TAC) 10-40 mg/mL/4-6 week Response 50-100%, recurrence 9-50% (+) excision, postoperative intralesional TAC reccurence < 50%.
• Complications atrophy, telangiectasia formation, and pigmentary alteration
New treatments intralesional interferon, 5-FU, doxorubicin, bleomycin, verapamil, retinoic acid, imiquimod 5% cream, tacrolimus, tamoxifen, botulinum toxin, TGF-beta3, and rhIL-10.
Interferon therapy • Alfa, beta, and gamma reduce
production of collagen types I, III, and VI mRNA.
• Alfa and Beta reduce glycosaminoglycans (GAGs) deposition of dermal collagen
• Increase collagenase activity Gamma modulates p53 apoptotic
pathway mutations hyperproliferation keloid formation
• Interferon injected into the suture line prophylactic for reducing recurrences.
5-Florouracil• Inhibits fibroblastic proliferation reduce
postoperative scarring • Effective hypertrophic scars and small
keloids. Doxorubicin (Adriamycin)• Irreversibly inactivates prolyl 4-
hydroxylase inhibit collagen alpha-chain assembly excessive scarring
Bleomycin • Injections necrosis of keratinocytes
with a mixed inflammatory infiltrate.
Tamoxifen, Synthetic nonsteroidal antiestrogen Inhibit proliferation of keloid fibroblasts
and their collagen synthesis in monolayer cultures.
Reduce TGF-alpha, and its isoform TGF-alpha1, production
Radiation therapyControversial some studies efficacy
and decreased recurrence rates safety ?
Surgical CareCryotherapyCryosurgical liquid nitrogen
microvasculature cell damage Possibility of reversible
hypopigmentation, pain and permanent depigmentation
51-74% total resolution, no recurrences
Laser therapyCarbon dioxide laser (10,600 nm)
dry surgical environment with minimal tissue trauma.
Recurrence rates 39-92% (+) postoperative injected steroids recurrence rates 25-74%.
Argon laser (488 nm), Nd:YAG laser (1064 nm), pulsed dye laser (585 nm)(treatment of choice)
Excisional surgeryLeast amount of soft tissue
minimize traumaClosure minimal skin tension
full- and split-thickness skin grafts
Remove source postoperative inflammation trapped hair follicles, foreign material, hematomas, or infectious areas.
Recurrence rates surgery alone range from 45-100%.
Effective combined with external radiation, steroid injection, pressure therapy, or a combination
Z-Plasty
LengthensReorients
FOLLOW-UPHigh rate of recurrence 1 year follow
up Close follow-up monitoringPreventionAvoid sharp traumaMinimize inflammation acne or
surgery.Complicationsinfection.PrognosisKeloids rarely resolve spontaneously Excision treatment alone recur
(>50%).
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