Practical Scar Care

The first consideration in scar treatment is prevention. Events that occur during the management of the open wound are influential. Providing a healthy environment for the wound to heal is most important.

Once the wound is closed, treatment can begin to prevent too much scarring. Over the past two decades, several new therapeutic approaches to scar management have been reported. These new approaches promise to add substantially to existing therapies.

Anti-Inflammatory Agents
Limiting inflammation is paramount to scar reduction. Inhibition of inflammation using corticosteroid injections is one of the oldest and most established approaches to scar management. The broad effects include inhibition of protein synthesis, including collagen and other extracellular matrix proteins. However, the adverse side effects of repeated injections, as well as the frequent occurrence of skin depigmentation are major drawbacks to this approach. Steroids are not effective for treatment of older, asymptomatic scars that are less metabolically active.

Although non-steriodal anti-inflammatory drugs (NSAIDS) have been used to prevent internal scarring in arthritis for decades, they have only recently been used for hypertrophic and keloid scar management. In our experience, the newer type-2 cyclooxygenase inhibitors are very effective in reducing symptoms of pruritus. They also seem to induce scar maturation and involution.

Salicylic acid and acetylsalicylic acid (aspirin) are powerful anti-inflammatory medications that are commonly used to treat skin inflammation-related ailments. Salicylates (2-5%) are commonly used to control skin inflammation and are routinely used in acne treatment products. We have found topical salicylates to be among the most effective anti-scar agents. These agents should not be used on open wounds. Topical aspirin should be used under a physician's guidance since some patients, particularly asthmatics, may develop hypersensitivity.

Anti-histamines are commonly used to control symptoms of scar pruritus. However, they have other important anti-scar properties. Anti-histamines, particularly the H1 blockers, inhibit the inflammatory response resulting in reduced scar formation and increased comfort. Patients are less likely to scratch inflamed scars, which reduces the scar growth rate. Finally, anti-histamines in high doses are well known to inhibit collagen synthesis

Inhibitors of Gene Transcription
The anti-cancer drugs mitomycin-c and 5-fluorouracil inhibit population growth of cells by blocking DNA replication. A single application in the first few days after wound closure seems to be effective in scar reduction under laboratory conditions. Further investigation will be needed to determine how this approach can be used clinically.

Acceleration of Scar Degradation
While steroids and NSAIDs act to limit scar production, other strategies act to induce or accelerate scar degradation. This approach may be the best for management of older hypertrophic scars and older keloids. The rate of tissue breakdown can be increased by both pharmacologic and physicochemical means.

Occlusive Dressings
After elastic pressure wrap dressings applied to healing burn scars were observed to be effective in the reduction of scar formation, 20-24 mm Hg pressure garments have become the mainstay of scar prevention. The mechanism of action of pressure dressings is unknown because they remain effective even when they lose elasticity and pressure several weeks after daily use. Measurements show a decrease in wound metabolism with an increase in collagenase activity. Drawbacks to their use are primarily related to their thermal insulation and movement restriction.

Hydrogel and silicone sheeting have been used to control scar formation. Like elastic garments, the mechanism of action is not known, but hypotheses reported in the literature include induction of scar hypoxia, increased hydration of the epidermis covering the scar and increased scar temperature. Several reports have shown that hydrogel sheeting is equally effective as silicone and has fewer adverse side effects. Hydrogel sheeting has been approved by the FDA as substantially equivalent to silicone for treatment of hypertrophic scars. Hydrogels have the added advantage of dual use as a drug delivery vehicle, as well as a higher heat capacity for buffering scar temperature.

Mechanical Tension Blockers
Calcium channel blockers and other calcium antagonists have been shown to induce changes in fibroblast gene expression resulting in decreased collagen synthesis and increased collagenase production. These effects appear to be mediated by interruption of the basic cellular communication pathways that are critical to regulation of scar fibroblast behavior. Verapamil, injected in the lesion, has been shown to induce scar degradation in the skin, fascia and periocular scars. These agents hold promise as treatment for established, non-inflamed scars that are no longer actively remodeling.

Tissue Heating
Both ultrasound and diathermy methods are commonly in use to soften scars in muscle and joints after injury. Although this approach is well established and effective, these devices are not widely used to treat skin scars, but the technology may be further developed.

Radiation
The density of fibroblasts in keloid and hypertrophic scars is higher than normal. In normal scars, fibroblasts are present in high numbers initially, but decrease as the wound enters the maturation stage. Ionizing radiation is another established method of therapy for hypertrophic scarring and keloids. Ionizing radiation activates several signaling pathways in the nucleus subsequent to the damage of DNA, as well as signalling pathways at the level of the cell membrane, which causes cell death. The primary mechanism of radiation induced scar control seems to be apoptosis of proliferating cells. Low dose ionizing radiation is most often reserved as the method of last resort for the treatment of intractable keloid scars. This therapy utilizes 15-20 Gy of ortho-voltage radiation fractionated in 5 to 6 treatments. Although radiation therapy alone is not adequate, if used in conjunction with surgical intervention, reduction in recurrence may reach 25% compared with a recurrence rate of up to 80% with surgery alone.

Surgical Removal
The most common indications for surgical removal of scars are the following: large scars that are unlikely to be substantially reduced using medical therapy within a practical timeframe; scars that harbor infection; and scar contractures that hamper movement function. Surgical revision of hypertrophic or keloid scars is associated with a high recurrence rate. Gentle surgical technique is critically important because inflamed scar tissue produces a tremendous scar response to trauma. Adjunctive measures to reduce inflammation, skin tension and other factors are essential to reduce recurrence. Use of lasers and other burning techniques for scar removal is very controversial.

In order to reduce the scar recurrence rate after surgery, effective scar control medications should be initiated pre-operatively and continued post-operatively. Our experience suggests that most patients with scars large enough to require surgical excision require both systemic COX-2 inhibitors and long-acting H1 anti-histamines to induce scar degradation and reduce recurrence. Increasingly, we find that topical application of NSAIDS to healing wounds will be the most practical approach. Trans-epidermal delivery of these agents is enhanced by the application of an occlusive barrier such as hydrogel sheeting.

Conclusion
Hypertrophic and keloid scarring can be essentially reduced to inflammation mediated dermal fibrosis, suggesting that there is much insight into effective management that can be gleaned from dermatological and rheumatologic conditions of similar pathophysiology. Patients today expect and require superior clinical outcomes compared to those acceptable in the past.