Scar Management Strategies in Wound Care

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August/September 2001

By Robert H. Demling, MD, and Leslie DeSanti, RN

Photo 1. Histologic appearance of hypertrophic scar at 2-3 months demonstrating dense collagen fibers in a tight uneven pattern. Lack of elasticity results.

Photo 2. Appearance of hypertrophic scar on deep hand burns allowed to heal over a 5 week period. Preferred initial care is skin grafting.

Photo 3. Prevention with early splinting of contracture formation due to scar formation.

Excessive scar tissue can be minimized when treating wounds through a variety of approaches, from pharmacology to massage.

Hypertrophic scar and keloids occur only in humans, making the study of pathogenesis and treatment more difficult. Both occur in males and females, being more common in the teenager or younger adult.^1-6

Hypertrophic scarring is seen in approximately 50% of wounds after surgery and more than 50% of healed deep burns. Onset is clinically evident by 4 weeks after trauma with progression over months and some late resolution. The scar is red, raised, and itchy, and typically occurs more where there is tension on the wound, especially nearby joints where contracture results. Incidence is greater with increased wound inflammation and a wound that is open for more than 3 weeks.^1-6

Keloids occur in all races but 15 times more often in patients with darker skin. The incidence is about 10% with a wound in the high risk groups. Onset is delayed at least 3 months after injury with progression but no resolution. The scar is also red, raised, and itchy. Areas most commonly involved are the shoulders, neck, anterior chest, upper arms, and face. Keloids also form even if a wound is closed rapidly, while hypertrophic scar does not occur with early wound closure.^1-6

Biochemical and Histological Characteristics

Both hypertrophic scars and keloids represent an aberration in the normal healing process. Although there are similarities in the biology of the scar, there are also distinct differences. Prolonged increased levels of the fibrosis growth factors transforming growth factor ß (TGF-ß), platelet-derived growth factor, interleukin-1 (IL-1), and insulin-like growth factor (IGF-I) are present in both with TGF-ß appearing to predominate.^5-7

Exaggeration of the inflammatory phase, in an open or infected wound or burn, increases the concentration of these growth factors known to produce increased fibroblast numbers and excess amounts of collagen and extracellular matrix.^5-7 Increased mast cells leading to increased release of histamines, known to stimulate growth of fibrous tissue as well as other vasoactive mediators, are also present in both types of excess scar compared to normal.^5-7

Both types of scar show an increase in the thickness of new epithelial layer but without rete pegs making the surface vulnerable to injury. The keratinocyte becomes a factor for fibrotic growth factors. In addition, an excess and prolonged neovascularization is found in both types of scar compared to normal scar. Fibroblasts are also found in increased numbers, leading to increased collagen deposition as well as normal matrix. These fibro- blasts are more sensitive to growth factors than normal skin. The released chondroitin develops sulfated side chains, which lead to a more rigid scar. Increased and persistent levels of chondroitin sulfate are present in both scars, located in the nodular areas of excess collagen. Both are characterized by increased water content, which increases scar firmness. A decrease in interferons, cytokines that downregulate collagen and matrix synthesis, is also noted. This abnormality leads to less collagenolysis and matrix degradation with remodeling.^5-7

The major differences relate not to the factors stimulating excess scar, but rather to the genetic etiology and self-perpetuation of keloids despite early aggressive prevention and treatment modalities. Keloids appear to have a life of their own, predestined by genetic traits combined with a wound. Fibroblasts continue to produce collagen and matrix even if everything is done right. Regression does not occur. Also, there is an invasion of normal surrounding tissue by the excess scar. Fortunately, contractures are less common than seen with hypertrophic scar.^5-7

SCAR ASSESSMENT

Scar results in significant functional and psychological impairments. There are a variety of methods to control and decrease scar formation, and in most patients, more than one approach is used. However, the assessment of the response of the scar process to the approach used is problematic as an accurate method for the objective quantitative assessment of scar remains to be developed.^8,9

Since scar is the sum of the response to injury, repair, and intervention, the scar is not a static process, but rather a dynamic one changing over time, especially during the first 18 months or until healing is complete.^8-9

Subjective assessment includes various factors that contribute to the patient's own evaluation (visual and tactile contributions), which includes both perception and attitude (body image). Objective assessment includes the physical characteristics of size, shape, volume, color, texture, and probability. In addition, structural, mechanical ,and physiologic characteristics are included. The Vancouver Scar Scale is a commonly used method that attempts to quantify most of these parameters. Despite an attempt at objectivity, all objective markers are very much dependent on the examiner's expertise and perceptions, and assessment will vary considerably between different examiners.^8-9

Future approaches currently being tested include two-dimensional and three-dimensional imaging techniques and computer vision algorithms. A range scanner is a device that allows acquisition of 3-D data and can accurately estimate scar volume. This approach can also be used to assess pliability.^8-9

PREVENTION AND TREATMENT

We know very little about the pathogenesis of a scar. However, a greater number of treatment modalities have become available. This fact is certainly the case with scar management but no treatments work well enough to be deemed standard. Wound closure and scar excision. The earlier a wound is closed by a skin graft (preferably thick), tissue flap, or any approach, the less the risk of hypertrophic scar. This is not the case with keloid, which can form even after very early wound closure.

A simple excision of either an established hypertrophic scar or keloid has a very high recurrence rate (over 50%). The exception for hypertrophic scar appears to be tension-releasing procedures, eg, z-plasties to release burn contractures or burn scar removal with tension-free closure where results are much better. Keloid recurrence also remains a major problem, although the addition of corticosteroids to the edges of the excision decreases recurrence. Therefore, surgical approaches to late scar need to be combined with other approaches.^4,6,10

Laser surgery. This promising approach to both hypertrophic scar and keloids uses a laser beam to cause a thermal tissue reaction, which can heat the injury or coagulate specific tissues. The CO2 and argon lasers are ineffective. However, the newer flash lamp-pumped pulse dye laser selectively decreases scar blood flow with a demonstrated improvement of more than 50% in over 50% of cases. A more pliable, less pruritic, and less erythematous scar results.^4,6,10

Cryotherapy. Comparable to laser therapy, cryotherapy results in microcirculatory disturbances leading to tissue damage, especially fibroblasts. Positive response is seen in 50% to 70% of patients, which is comparable to laser therapy. Treating early hypertrophic scars has the best results. Keloids are less responsive.^4,6,10

Typically, these surgical approaches are combined with other modalities, such as corticosteroids and other pharmacologic approaches and biophysical therapies like pressure, to optimize results.

Biophysical Therapeutics

The biophysical basis for therapeutic efficacy in scar management remains controversial, especially the relevance of abnormal biochemical pathways and their pharmacologic modifications. However, these approaches have become the standard of care for hypertrophic scar control-both prevention and treatment. Keloids in general respond minimally to these approaches.^10-14

1. Compression pressure

The use of fitted elastic garments to generate about 24 mm Hg on the hypertrophic scar was popularized more than 20 years ago, especially for burn scar. Pressure, if used 18-24 hours a day for at least 6 months, appears to have at least partial success in producing a thinner, more mature, and more pliable scar in over 50% of patients. The garments should be used as soon as the wound is closed. The pressure decreases scar blood flow, decreasing protein deposition, increasing lysis, decreasing edema and chondroitin sulfate, and increasing mast cell stability. The latter is likely the reason for decreased itching with compression. However, it is clear that the initial measured pressure lasts only for a very short time as tissue edema decreases, lessening the pressure. Yet a positive effect persists. Recent theories include an increase in scar tissue temperature due to the tight garment weave. Increased temperature, even by 1°C, will significantly increase collagenolysis and scar maturation, thus the use of heating as a treatment modality.^10-14

2. Ultrasonic or microwave heating

Used to soften scar and loosen still-stiff joints, ultrasonic or microwave heating decreases the tensile strength of a scar, and appears to reduce collagen content possibly by increasing collagenase activity; some benefit is seen in at least half the patients.^10-14

^{3. Gel sheeting}

Form-fitted silicone gel sheets held in place by elastics and worn at least 18 hours a day for several months also appear to increase scar maturation and decrease hypertrophy. Although the mechanism was initially thought to be due to pressure or increased temperature, neither appears to occur. Silicone itself is not playing a role as the same results occur with the use of a hydrogel. Current evidence suggests that maintaining scar hydration is the common element, although the effect of hydration on decreasing scar is unclear.^10-14 However, the fitted sheet also takes tension off the wound, a known stimulant of scar. Early use has the best results.^10-14

4. Scar massage

This approach is usually combined with several other modalities. Deep massage reportedly stretches fresh scar and breaks down the cement or matrix holding the scar contracted. Massage therapy appears most beneficial in preventing contractures. However, massage also mechanically stimulates fibroblast synthesis of collagen. Therefore, this approach must be combined with an anticollagen synthesis approach to be of significant benefit.^10-14

Pharmacologic Therapy

Nonsteroidal anti-inflammatory agents have been shown to decrease fibrosis through inhibition of IL-1 and prostanoids, known to stimulate fibrosis. However, data verifying clinical efficacy in controlling excess scar are lacking.^15-20

Antihistamines have been shown to be effective not only in controlling pruritus, but also suppressing histamine-induced tissue proliferatives. Topical agents such as doxepin cream would likely be more effective as the concentration in the scar would be greater. In addition, doxepin (Prudoxin) is 800 times more potent than diphenhydramine as an antihistamine.^15-20

Some newer antiallergic drugs also inhibit the release of histamine and prostanoids from wound mast cells. These agents, except for some mild sedation, are very safe. Corticosteroids are, of course, used to control hypertrophic scar and keloids by injection into the scar itself. However, the corticosteroids, except for stabilizing mast cells, are not acting as an anti-inflammatory agent, but rather by inhibiting protein synthesis.^15-20

Corticosteroids are the main agent in the protein synthesis inhibitors category. These agents, when injected into scar, decrease fibroblast proliferation, decrease angiogenesis, and inhibit collagen synthesis and also extracellular matrix protein synthesis. Complications include pain on injection, thinning of surrounding skin if the steroid spreads to normal tissue, systemic absorption, and recurrence of scar at a later date.^15-20

Interferons are known to reduce the production of major scar forming growth factor TGF-ß Both intravenous and intralesion injections of interferon have shown significant clinical benefits on reducing hypertrophic scar and keloid. Popularity to date is hampered by high cost and unfamiliarity with this approach. Agents that inhibit collagen cross-linking would decrease scar rigidity and collagen deposition. The most promising agent in this category is topical putrescine, which has been reported to decrease hypertrophic scars with no side effects.^15-20

Stimulation of proteolytic enzyme synthesis works by increasing the degradation rate of collagen and matrix proteins. Calmodulin and protein kinase C inhibitors have been shown to be somewhat effective, but further data are needed. Calcium channel blockers inhibit the incorporation of protein into extracellular matrix protein. Several studies have reported an increased rate of scar degradation.^15-20

Prevention of Wound Contracture

A major complication of hypertrophic scar formation is contracture formation as scar tends to form across areas of movement and tension, especially joints.

Prevention of hypertrophic scar includes early wound closure. However, additional standard biophysical measures include approaches to avoid contractures that can impair movement.

The etiology and optimum management of fibroproliferative disorders leading to excess scar remain highly controversial. However, it is quite possible to develop a working knowledge of these processes and thereby select the most appropriate prevention and treatment modality. But it is clear that accepting historical practice standards is not appropriate, as there are no established effective standards. Assimilation of new knowledge as well as new management skills is necessary to render optimum scar management.

Robert H. Demling, MD, is the director, and Leslie DeSanti, RN, is a research nurse at the Burn Center, Brigham and Women's Hospital, Boston.

REFERENCES

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Border WA, Noble NA. Mechanisms of disearse: transforming growth factor ß in tissue fibrosis. N Engl J Med. 1994;331:1286-1292.
Erlich HP, Krummel TM. Regulation of wound healing from a connective tissue perspective. Wound Repair Regener. 1996;4:203-210.
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August/September 2001