Management of Scars.pd f

ETIOLOGY OF SCARS:
•Surgery
•Lacerations
•Burns
•Chronic wounds
•Acne
•Steroids

1. MANAGEMENT OF SCARS
Dr Wan Azman Sulaiman
Reconstructive Sciences
Health Campus USM

2. OUTLINE
•INTRODUCTIONS
•SCARS ASSESSMENT
•MANAGEMENT ALGORITHM
–NON-SURGICAL VS SURGICAL
•HYPERTROPHIC VS KELOIDS

3. Scars
A scar can be defined theoretically in terms
such as those in the Short Oxford English
Dictionary:
The trace of a healed wound, sore or burn. A fault
or blemish remaining as a trace of some former
condition or resulting from some particular cause.

4. Aetiology of scars
•Surgery
•Lacerations
•Burns
•Chronic wounds
•Acne
•Steroids

5. BURNS

6. SURGERY

7. Scar Medical terminology
•mature or immature and the scarring processes as
normal or abnormal.
•"Normal" scarring is the final result of the wound healing
process and is formed by the remodeled collagen after
inflammation and proliferation have abated.
•A normal scar is flat, relatively narrow, and slightly paler
than the surrounding skin.
•An abnormal, due to either local factors or genetic
tendency, an unfavorable scar can result.

10. Problem scars
•Restrictive
•Anatomic location
•Stretched
•Hypertrophic
•Keloid
•Psychological
•Social issues

13. Facial lines

14. Scar assessment

15. Scar Assessment

16. Non-surgical scar Mx

19. Surgical improvement
IMPROVEMENTS IN AN UNSATISFACTORY SCAR
•
•Improvement of the direction of the scar
•Division of the scar into smaller components
•Leveling effect
•Improvements in the local condition of the wound (compared with
the original)
•Halving in depth
•Halving in surface
•Camouflaging by alternating small scars with normal unscarred
tissue
•Creation of accordion-like elasticity

20. Serial vs tissue expansion

21. Prevention of scarring

22. Management algorithm

23. Keloids and Hypertrophic Scars

24. Scar Formation in Normal Wound Healing
•Scars mainly consist of bundles of collagen
synthesized by fibroblasts. Scars serve to fill
the tissue defect after injuries and help to
anchor the edges of the wound together.

25. Amount of scar tissue formed depends on various
factors
•Age
•? Race and genetics (especially keloids)
•Site of the wound
•Mechanism of wound healing
•Wound tension and stress
•Suture material
•Infection

26. Abnormal Scar Formations
•Keloids
•Hypertrophic Scars
•? Different spectrums of similar entity
•? 2 different entities

27. Aetiology of Abnormal Scar Formation
•True aetiology is unknown
•Increased incidence of keloids and hypertrophic scars in
dark-skinned races documented. However, the lesions
occur in all races.
•Genetic factor may be involved as family members are
frequently involved
•Immune factor –no direct evidence

28. Pathogenesis
•Excessive proliferation of endothelial cells and perivascular
myofibroblasts contraction contribute to microvascular contraction,
which leads to tissue hypoxia. This in turn stimulates excessive
collagen deposition
•Excessive collagen-producing fibroblasts are selected by the ‘stressed’
environment in the wound
•Decreased collagen degradation in the presence of collagenase
inhibitors e.g. α2-macroglobin
•Collagen fibers are arranged in haphazard and ‘highly stressed’
configuration. This is more prominent in keloids compared to
hypertrophic scars

29. Hypertrophic Scars
•Early onset after wounding (4 weeks)
•Self-limiting overhealing with scar formation confined to
the limit of the original wound
•With time, the scar can become flat and pale and reduce
in size
•Probably will not recur after adequate surgical excision

30. Keloids
•Usually late onset (3 months to several years)
•Exuberant scar tissue formation that extends beyond the
limit of the original wound.
•Usually do not regress spontaneously
•High incidence of recurrence after surgical excision

34. Assessment
•Clinical Assessment e.g. Vancouver Scar Scale
•Photographic Assessment
•Histological Assessment

35. Prevention
•Incision parallel to line of minimal skin tension
•Avoidance of large sutures and tight suturing
•Intradermal sutures to splint the wound
•Application of pressure
•Prevention of hematoma and infection

36. Treatments
•Need to ascertain the objective
•To eradicate symptoms e.g. discomfort or itchiness
•To improve esthetic appearance
•To correct functional disability
•Timing of treatment
•Combination of treatment modalities may be used

37. Mechanical Approach
•Application of local pressure with pressure garment,
pressure earring. Require prolonged application
•Lesions may recur when pressure is removed
•Massage
•Silicon gel sheet e.g. Cica-Care

38. Pharmacological Methods
•Intralesional injection of steroids: triamcinolone
acetonide (10 or 40mg/ml) injection with metal syringe. ?
role of local anesthesia.
•Sublesional injection
•Injections are staged 6 weeks apart
•May cause telangectasia, depigmentation, ulceration and
skin atrophy in repeated injections
•? Role of prophylactic injection

39. Surgical Approach
•Direct excision of scar tissue is associated with high
incidence of recurrence
•Role of Z or W plasty in reorientation of wound direction
in relation to skin tension. May cause new scar formation
•Double-breasted vest principle proposed by Millard
•Skin grafting

40. Others
•Radiotherapy
•Laser Therapy
•Cryotherapy
•Local Chemotherapeutic Agent
•Local vitamin E cream

55. References
•Plastic Surgery, 1990 Edition. McCarthy. Keloids and Hypertrophic Scars. 732-
747
•Beausang, Floyd, Dunn, Orton, Ferguson. A New Quantitative Scale for
Clinical Scar Assessment. PRS. 1998. 102(6): 1954-1961
•Niessen et al. On the Nature of Hypertrophic Scars and Keloids: A Review.
Plastic and Reconstructive Surgery. 104(5): 1435,1999.
•Thomas et al. International Clinical Recommendations on Scar Management.
Plastic and Reconstructive Surgery. 110(2):560, 2002.
•Adel et al. Widening of Scars: Foe Coaxed into a Friend? The Millard
Technique Revisited. Plastic and Reconstructive Surgery. 106(7): 1488, 2000