Clinical Reference / Therapeutic Strategies / Keloids and Hypertrophic Scars

Keloids and Hypertrophic Scars


Key Points

  • Scarring is a common complication of wound healing and presents across a broad clinical spectrum.
  • Hypertrophic scars stay within the boundaries of the original wound site and are transiently indurated or symptomatic. In contrast, keloids are defined as scars that grow beyond the boundaries of the original wound site and are often marked by significant, persistent thickening and are pruritic or painful.
  • There is limited evidence to support the use of a wide variety of strategies used for the treatment of keloids; intralesional corticosteroids and/or cryosurgery are the best therapeutic strategies supported by evidence and are interventions with good safety profiles.

Introduction

Scarring is a common complication of wound healing and presents across a broad clinical spectrum, including imperceptible to highly visible symptomatic scars. Hypertrophic scars are those that stay within the boundaries of the original wound site and are transiently indurated or tender to palpation. Keloids are defined as scars that grow beyond the boundaries of the original wound and are often marked by significant, persistent thickening. Both may occur between 3 and 12 months following the inciting skin trauma. Clinically, they are firm, raised and can be hyperpigmented or marked with telangiectasias. The ears, upper back and chest, and upper arms are common sites of hypertrophic or keloid scar formation; ongoing tension or movement across the wound healing site may predispose to their formation at these sites. Keloids are more common in certain populations, including those with a family history of keloid scars and individuals of Asian, African and Hispanic descent; in one study, dark-skinned individuals had a 15-fold increased risk to develop keloids than light-skinned individuals. Whereas hypertrophic scars involute by 6 months after their formation, keloids persist and even extend beyond the original margins. Keloids not only are disfiguring, but they also can be symptomatic, marked by pruritus, tenderness, or extreme hyperesthesia.

Initial Evaluation

Hypertrophic scars

Keloids

Differential diagnosis

Morphea

Lichen sclerosus et atrophicus (note genital and extragenital locations)

Dermatofibrosarcoma protuberans

Treatment

First-line therapy: Intralesional corticosteroids remain the first-line therapy for keloids and hypertrophic scars. They may be effective in 50-100% of cases but may be associated with recurrence in up to half of cases. Treatment of keloids with intralesional corticosteroids often requires multiple injections with ongoing monitoring for adverse effects (atrophy, telangiectasias, hypopigmentation).

First steps

  • Keloids can be softened progressively, and made less painful by injections of triamcinolone acetonide (such as Kenalog) 20 mg/cc directly into several adjacent sites within the lesion(s). Space injections approximately 0.5 to 1 cm apart.
  • Use a 1/2-inch, 30-gauge Luer Lock needle and tuberculin syringe to allow injection under pressure. Wear a face shield to avoid contact with back pressure spray.
  • Give injections at monthly intervals until the desired degree of involution and/or symptomatic relief is achieved.
  • If no change occurs after one injection with a concentration of 20 mg/cc, increase the dose to 40 mg/cc. If no change has occurred after three or four injections, consider surgical excision (see Alternative therapy).

Alternative therapy

  • If keloids do not respond or remain symptomatic, surgical excision is an alternative, although the lesions tend to recur (see Pitfalls).
  • There is mixed evidence supporting the use of silicone sheeting for scarring and it may be effective if used early in wound healing. In some trials, silicone sheeting was effective in 70-80% of cases to avoid keloid formation. The evidence for the efficacy of self-drying silicone gels is weaker.
  • Alternate therapies with limited evidence to support their use include: imiquimod 5% (used nightly for 8 weeks), laser ablation, cryosurgery, cryosurgery combined with intralesional corticosteroids, radiotherapy. Cryosurgery is an effective, widely available therapeutic strategy with an excellent safety profile that can be used in conjunction with intralesional corticosteroids.
  • Scar massage is anecdotally effective, and may be helpful in the management of postsurgical scars rather than in posttraumatic scarring; supporting evidence is limited.
  • Application of Vitamin E-containing oil to keloids is not supported by scientific evidence.

Pitfalls

  • Keloids tend to recur after excision, and can be very recalcitrant to all types of therapy. Note: Sites of keloids that occur after piercing should not be re-pierced after excision of a prior keloid.
  • Elective surgery should be avoided in individuals with a history of keloid formation, especially in sites where keloids are likely to occur, such as the ears, chest, shoulders, and upper back.

When to refer to a dermatologist

  • If the diagnosis of keloid or hypertrophic scar is not clear, especially if there is no history of prior trauma or inflammation. Note that the differential diagnosis of keloid-like lesions includes inflammatory conditions such as morphea and xanthomas, growths such as sarcomas, and even infections such as lobomycosis.
  • If the lesion is symptomatic.
  • If the lesion is not improving with multiple intralesional corticosteroid injections.
  • If the lesion requires surgical excision or intralesional chemotherapy.

Clinical Cases

Case 1

  • 16-year-old healthy male
  • Past medical history includes nodulocystic acne with scarring
  • Presents for management of acne scarring

Initial evaluation

  • Healthy-appearing male
  • Firm, raised, indurated papular and linear plaques noted across the jawline and chest
  • Diagnosis: keloids (secondary to acne)
  • Recommend intralesional triamcinolone (20 mg/cc) injections
  • Follow-up in 4 weeks

Four-week follow-up evaluation

  • Improved (lesions much smaller in size, flatter, softer)
  • No adverse effects noted: atrophy, telangiectasias
  • Repeat injections to several persistently thickened lesions
  • Several lesions require intralesional triamcinolone at 40 mg/cc
  • Follow-up in 4-week intervals (requires 4 additional visits to improve a majority of lesions)

Case 2

  • 18-year-old healthy female
  • No significant past medical history
  • Family history notable for keloid scarring
  • Presents for management of a keloid scar on the right earlobe at the site of a previous jewelry piercing
  • Reasons for presentation to the clinic include visual appearance and tenderness to palpation

Initial evaluation

  • Healthy-appearing female
  • Exophytic firm non-inflammatory tender nodule, approximately 1 cm diameter, on the right earlobe
  • Diagnosis: keloid
  • Treatment options discussed: intralesional corticosteroids, surgical excision, possibly both
  • Patient opts for intralesional corticosteroid (40 mg/cc, 0.2 cc injected)
  • Follow-up in 4 weeks

Four-week follow-up evaluation

  • Minimal softening of induration, without evidence of adverse effects such as atrophy or telangiectasias
  • Repeat injection of intralesional corticosteroid (40 mg/cc, 0.2 cc injected)
  • Follow-up in 4-week intervals

Follow-up evaluation

  • After several rounds of intralesional corticosteroid injection, the lesion remains persistently firm and indurated. The patient now opts for surgical excision.
  • Surgical excision followed by intralesional corticosteroid injection and pressure bandaging, with serial injections of intralesional corticosteroid due to early recurrence of the keloid (at 2-week intervals)
  • Recommend against repeat ear piercing or wearing jewelry close to the keloid site

References

Chike-Obi CJ, Cole PD, Brissett AE (2009). Keloids: pathogenesis, clinical features, and management, Semin Plast Surg, 23: 178-184.

Shin TM, Bordeaux JS (2012). The role of massage in scar management: a literature review, Derm Surgery, 38: 414-423.

Tziotzios C, Profyris C, Sterling J (2012). Cutaneous scarring: pathophysiology, molecular mechanisms, and scar reduction therapeutics, Part II, J Amer Acad Dermatol, 66: 13-24.