Treatment outcomes for keloid scar management in the pediatric burn population
ABSTRACT Keloids scars are challenging problems facing many reconstructive surgeons and have proven to be resistant to many treatments. This is evident by the broad range of treatments available and implemented with inconsistent results. We reviewed our experience to better define the disorder and to evaluate the impact of specific treatment options as related to our patient population.
After obtaining Institutional Review Board approval, we examined the medical records of pediatric patients who were evaluated at our pediatric burn center between 2000 to 2008. All study subjects were identified as having keloid scars confirmed by clinical evaluation (raised scar extending beyond the margins of the original wound [1,2]). Treatments included excision and grafting [split thickness autograft (STAG) or full thickness autograft (FTAG)], excision and grafting with steroid injection, excision and primary closure, or excision and primary closure with steroid injection. Patients were included only if there was follow-up of 12 months or greater.
One hundred and ten subjects with a diagnosis of a keloid scar were identified. Twenty-six were treated with excision and skin grafting and 8 were treated with a steroid and surgery regimen. Of the patients treated with surgery and steroids, the treatment varied from an intra-operative injection to post-operative injections at 6-week intervals. The number of injections was determined by the administering surgeon and varied from one to three. Clinical end points were determined by the administering surgeon and included: (1) no further improvement in scar maturation or (2) absence of improvement. Recurrence was defined as return of a raised scar consistent with a keloid scar. The recurrence rate was 87.5% for patients treated with surgery and steroids and 80.0% for surgery only. This difference was not statistically significant.
Our data demonstrate that steroids do not significantly decrease recurrence in pediatric burn related keloids as compared to previously published series involving non-burn related keloids [3,5]. This further emphasizes that burn related keloids respond differently to conventional treatments that have proven successful in keloid scars from other mechanisms of injury. A consistent and effective treatment algorithm should be implemented in treating keloid scars from burn wounds.
- Burns: journal of the International Society for Burn Injuries 04/2013; 39(6). DOI:10.1016/j.burns.2013.01.024 · 1.84 Impact Factor
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ABSTRACT: Keloids are fibroproliferative scars that spread beyond the original wound boundary and are very resistant to treatment. Development of highly effective therapies requires a comprehensive understanding of the mechanisms regulating keloid formation. Previous studies indicated that keloid keratinocytes have abnormal expression of genes involved in differentiation and adhesion, and increased migration rates. The objective of the current study was to better understand the role of hyaluronan synthase 2 (HAS2) in keloid keratinocyte migration and gene expression. Keratinocytes were isolated from keloid scars and normal skin. Migration rates of keloid keratinocytes were quantified using an in vitro scratch assay. Expression levels of HAS2, related HAS1, and HAS3 genes, and genes aberrantly expressed in keloid keratinocytes, were quantified using real-time polymerase chain reaction. Treatment with 4-methylumbelliferone (4MU) was used to inhibit hyaluronic acid synthesis. The expression of HAS2 was significantly increased in keloid vs normal keratinocytes. Treatment with 4MU caused a dose-dependent reduction in keloid keratinocyte migration and HAS2 expression; HAS3 expression was moderately inhibited by 4MU and HAS1 was not expressed. Keloid keratinocytes displayed a motile phenotype in vitro, including loose colonies and widely separated refractile cells; this phenotype was normalized by 4MU. Further, 4MU altered gene expression in keloid keratinocytes. The results suggest that HAS2 overexpression contributes to increased migration and altered gene expression in keloid keratinocytes. Abnormal keratinocyte migration may contribute to the overhealing of keloid scars beyond the original wound boundaries. Therefore, inhibition of HAS2 expression using 4MU may represent a novel strategy for treatment of keloid scarring.Journal of burn care & research: official publication of the American Burn Association 09/2013; 35(1). DOI:10.1097/BCR.0b013e3182a2a9dd · 1.55 Impact Factor
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ABSTRACT: There is limited information available on the natural history and prognosis of keloid scars. To evaluate how keloid scars behave over time to develop prognostic information for patients. 34 patients in Manchester and Barbados (average age 34 years) yielding 126 keloids completed questionnaires about their lesions. 46 keloids (37%) were described by patients as resolved, meaning they were satisfactory in appearance, not symptomatic and not requiring treatment. In each case the scar remained visible. 36 (29%) lesions resolved following treatment. Ten (8%) resolved spontaneously. The median number of years to resolution with treatment was 11.4 and to spontaneous resolution was 5, this difference was statistically significant (p < 0.05). The median number of years since resolution with treatment was 3 and since spontaneous resolution was 18, this difference was statistically significant (p < 0.0001). Seventeen lesions (13%) were resolving with treatment. 63 (50%) remained active. Overall the median number of years scars persisted was 15. Keloids never completely disappear to leave skin with normal texture, however they can resolve (flatten and soften) so they no longer burden patients in approximately one third of cases. Scars resolving spontaneously do so early in the disease. Those that don't may resolve after many years of treatment. This data can provide prognostic information to patients, and a baseline for future therapeutic trials.Journal of Plastic Reconstructive & Aesthetic Surgery 10/2013; 67(1). DOI:10.1016/j.bjps.2013.10.014 · 1.47 Impact Factor