Management of Keloid and Hypertrophic Scars

Annals of Burns and Fire Disasters - vol. XVIII - n. 4 - December 2005

MANAGEMENT OF KELOID AND HYPERTROPHIC SCARS

Edriss A.S., Měšťák J.

Department of Plastic and Reconstructive Surgery, Bulovka University Hospital, Prague, Czech Republic

SUMMARY. Scar management for the prevention of excessive scar formation has always been important but never so important as it is today. Optimal management continues to be an enigma for surgeons, and the best modality of treatment has been debated for many years. However, most studies have unfortunately been either retrospective or case report descriptions. Advances in scar management have been hampered by confusing or ambiguous terminology. There is no consensus on what amount of post-trau- matic skin scar formation is “normal” and what should be considered “hypertrophic”. In the World Health Organization’s ICD-9, there is no diagnostic code for hypertrophic scar - only keloid is listed. Yet the medical and scientic literature distinguishes them as different conditions. This confusion results in inappropriate management of scar formation, and occasionally contributes to de- cision-making related to elective or cosmetic surgery. Our experience suggests that there is no single treatment for scars that is adequate and that clinical judgement is very important when considering treatment and balancing the potential benets of the various treatments available. The goal of treating scars is to restore functionality, provide relief of symptoms, enhance cosmetics, and prevent recurrence. This article is based on our scientic and clinical experiences and focuses on over-the-counter options to manage keloid and hypertrophic scars.

Introduction some vaguely defined wound boundary. Such a classifi- cation scheme sets the stage for confusion, particularly Scars are a result of the natural healing process that when one of the disorders is classified as an inheritable occurs when the skin repairs itself after wounds, trauma, disease. Scientists investigating pathological scarring sug- burns, surgical incision, or disease. Normal skin tissue is gest that there are significant phenotypic differences be- replaced with scar tissue to close open wounds and pre- tween hypertrophic and keloid scars that may not be clin- vent infection. Scars can be painful, cause itching, and lim- ically obvious until they invade surrounding tissue.1 There- it mobility. Many scars are primarily a cosmetic concern, fore, while keloid scars are by definition hypertrophic, on- but their presence may have a significant negative impact ly a small percentage of large scars can be truly classi- on the affected individual’s self-esteem. Consequently, pa- fied as keloid. tients often seek treatment to reduce the visibility and discomfort of a scar. The wound healing process There are several types of scars, two of the commonest being hypertrophic and keloid scars. In the medical lit- In order to discuss hypertrophic and keloid scar patho- erature, a hypertrophic scar is generally described as an genesis and treatment, a review of the pertinent aspects overgrowth of scar tissue that remains within the bound- of wound healing is essential. Wound healing is a very aries of a wound. The wound boundary shrinks as more complex process that is tightly regulated to achieve wound scar tissue forms. Currently, no objective diagnostic crite- repair. The process can be categorized in three distinct ria have been formulated to indicate when a scar can be phases that have very different objectives: inflammation, considered hypertrophic. Keloid scars are densely col- proliferation, and maturation. Following the initial tissue lagenous, nonencapsulated, benign connective tissue neo- injury, inflammatory mediators known as cytokines are plasms. The size and shape of keloid scars have little cor- released from the injured tissue cells and wound blood relation with the extent of the skin wound. Large disfig- clot, after which the inflammatory phase initiates. The uring tumours often result from minimal skin trauma. amount of blood released, the extent of devitalized tis- Keloid scars, unlike hypertrophic scars, have a genetic ae- sue, and the bacterial content are important issues as the tiology. wound does not become sterile until it regains an ep- A commonly taught but confusing concept is that ithelium. keloids can be distinguished from hypertrophic scars by If the wound healing process is uncomplicated, the the extension of the scar beyond the wound border. This proliferation stage (also called the “transitional repair concept implies that a scar starts out as a hypertrophic stage”) begins several days after injury.2 Platelet degranu- scar and later becomes a keloid, when it has exceeded lation activates the coagulation cascade, and the resultant

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fibrin clot serves as a scaffold for the proliferation phase scarring in burn wounds that take longer than 21 days to of wound healing. During the proliferative phase, the num- heal. ber and density of fibroblasts in the extracellular matrix Hypertrophic scarring also occurs as the result of dy- increase, and the fibroblasts synthesize tissue components, namic mechanical skin tension acting on the healing wound. such as proteoglycans, fibronectin, and collagen. New ves- As a result of mechanical tension, scars located in certain sels and epithelium are formed as rapidly as possible to areas of the body (e.g. sternum, deltoid, and upper back) maximize the tissue replacement dynamics. All wound cells are frequently hypertrophic. This anatomical dependency are maximally active and are sensitive to factors that reg- seems to correlate with a pattern of skin tension.4 The char- ulate cell proliferation and protein biosynthesis. All the acteristic feature of hypertrophic scars is that they regress cells proliferate, and metalloproteinases are simultaneous- in time after injury, leaving behind, however, an unsight- ly released into the extracellular fluid to activate a matrix ly wide gap of thinned dermis between the wound edges. breakdown process. The balance between tissue degrada- A familial pattern of hypertrophic scarring has not been tion and biosynthesis permits remodelling of the provi- reported. However, populations with a higher skin melanin sional tissue and determines the net amount of scar tissue content are known to have a higher incidence of hyper- produced. trophic scars. These populations include people of African, When enough provisional tissue is generated, a turn- Asian, and Hispanic descent. Hormonal inuences are al- off signal is received that initiates the final stage of wound so known to be a factor, with hypertrophic scarring often healing, the maturation stage. This phase is characterized initiating at the onset of puberty or during pregnancy. Scar by cellular apoptosis and a shift in balance from scar re- tissue cells are sensitive to the inuences of the same modelling towards scar degradation.3 The process is ac- growth factors that drive normal tissue growth and devel- companied by extracellular matrix reorganization and re- opment. Schierle et al.5 reported an increase in testosterone duction. Metalloproteinases synthesized during the prolif- receptors in hypertrophic scars, which may contribute to eration stage continue to break down the extracellular ma- the formation of the scars during adolescence. trix at a rate largely determined by physical and biochemical factors in the matrix. The amount of extracellu- Keloid scars lar matrix biosynthesis is controlled by the need for tis- Although the diagnosis of keloid scar is often inap- sue strength and other operational parameters. Mechani- propriately applied to hypertrophic scars, the two lesions cal stress is an important contributory parameter in net can be differentiated at several levels. Unlike hypertrophic scar production. scars, the natural history of keloid scars is that they do not The most important known determinates of scar pro- regress with time following injury. Keloid tumours grow duction are the extent and duration of inflammation, the to reach a certain size and may remain that size inde- magnitude of mechanical tension acting on the scar, and nitely. They are thought to be a localized reaction to cu- the genetic phenotype of the individual concerned. Al- taneous trauma, although in many cases no recollection of though other factors may be important - and some are yet the inciting event can be discovered. While there is no unknown - scar management that is fundamentally based doubt that trauma to the skin, including surgical incision, on these three critical parameters can be effective in lim- can cause keloids, a variety of factors may increase their iting unnecessary scar formation in most cases. incidence. People with darker skin, including Asians and, more commonly, blacks, are more susceptible to keloid Pathological scars formation than whites. The general population ratio may be as high as 15 keloids in the black population to one in Hypertrophic scars the white population, which has led to at least one theory Several epigenetic causes of hypertrophic scarring have suggesting an abnormality in the metabolism of the been identified. Basically, factors that increase or prolong melanocyte-stimulating hormone. This theory would seem wound inflammation or wound tension predispose to hy- to point to a higher incidence of keloids at times of in- pertrophic scar formation. Such factors include wound increased melanocyte-stimulating hormone production, such fection, prolonged healing by secondary intention, and im- as during puberty and pregnancy. munologically foreign material present in the wound. Hy- Keloids may affect virtually any surface on the body, pertrophic scars begin as the result of an injury to the deep with the central chest, deltoid region, and back having the dermis, and they are especially pronounced in wounds that highest frequency. This has led some to conclude that mo- have a prolongation of the inflammatory and proliferative tion and tension play a large role in keloid formation. While phase of wound healing.2 The incidence of hypertrophic this may be implicated in some cases, the earlobes, a site scars following surgery is about 40-70% - it is higher (up of countless keloids and recurrences, are subject to mini- to 91%) following burn injury. Several reports conclude mal motion and tension forces, even after previous keloid that there is a substantially increased risk of hypertrophic excisions. Conversely, the central face rarely has hyper-

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trophic scars or keloids but is subject to extremes of mo- lin levels, which lead to collagen degradation. Corticos- tion and tension during the normal activities of daily liv- teroid preparations used for intralesional injection have in- ing. Additionally, increased tension has been shown to included hydrocortisone, triamcinolon, and dexametasone, crease broblasts and myobroblasts in in vivo and in vit- with none proving to be particularly advantageous. Sever- ro studies.1 al concentrations between 10 and 40 mg/ml can be used. In steroid-sensitive areas (e.g. nose, eyelids, lips) that can Clinical management undergo dermal atrophy, 10 mg/ml should be used initial- ly. After the initial dose, the patient should return after 3 The management of scars should begin even before to 4 weeks, and the injection should be repeated at a sim- the surgical procedure and continue 12 to 24 months af- ilar or higher dose if required. The local adverse effects terwards. The rst consideration in the discussion of scar of steroid injections are associated with the dose given. treatment is prevention. We should know how to prevent These are hypopigmentation, dermal atrophy, teleangiec- scars and we should learn how to identify them immedi- tasia, necrosis, and ulceration. Doses of less than 120 mg ately and manage post-operative complications correctly. per month in adults and less than 80 mg per month in chil- To do this, we should have a thorough understanding of dren (6-10 years old) are recommended. The systemic ef- wound healing and skin biomechanics. fects of intralesional steroid therapy have been widely re- In the surgical setting, events occurring during the ported. A major disadvantage of using intralesional corti- management of the open wound are important. Careful and costeroid is the pain associated with the injection, which meticulous handling of tissue, evacuation of blood from can lead to patient noncompliance in the follow-up. the wound, and accurate wound edge alignment during clo- Long-acting synthetic glucosteroids such as triamci- sure, as well as precise suture placement, will reduce in- nolone are commonly used in the treatment of hypertrophic ammation and therefore also scarring. The choice of su- and keloid scars. Synthetic glucosteroids, applied topical- ture material is important because some sutures trigger ly, are weakly soluble in water but well absorbed in the more immune reaction than others. Monolament ab- epidermis in time - they diffuse slowly into the scar. Al- sorbable synthetic biopolymers produce the least reaction. ternatively, solutions of triamcinolone can be injected in Minimizing the tension acting on the wound by aligning 10-40 mg/ml concentrations.10 Both methods of delivery are the incision parallel to natural skin lines (when possible) effective in the majority of noninfected scars that exhibit or the use of local aps will also help to reduce the inci- symptoms such as pain and pruritis.11 dence of post-surgical hypertrophic scars. Steroids are not often useful in the treatment of older Over the past two decades, some fundamentally new scars, which are less metabolically active; they are also therapeutic approaches to scar management have been re- not routinely used as a scar preventative immediately af- ported. These new techniques have substantially augment- ter wound closure because of concern about wound infec- ed existing therapeutic approaches and continue to enhance tion or dehiscence. them. The use of existing therapeutic approaches has been reviewed in detail elsewhere and will not to be covered in The inammatory response can be regulated at sever- depth here. In the following paragraphs, we will attempt al different physiological levels before, during, and after to briey summarize some of these new concepts. We hy- inammatory gene expression. Before gene expression pothesize that wound healing is evolutionarily optimized there are transcription factors, such as NF-kB (nuclear fac- for speed of healing in dirty conditions, where a multiply tor-kB) that are activated by cell injury. After gene ex- redundant, compensating, rapid inammatory response with pression there are inducible enzymes, such as cyclo-oxy- overlapping cytokines and inammatory cascades allows genase (COX) regulation, and inhibition of histamine syn- the wound to heal quickly in order to prevent infection thesis. The most widely used anti-inammatory agents be- and future wound breakdown. long to the broad category of nonsteroid anti-inammatory drugs (NSAIDs). These inhibit either the NF-kB path- Prevention of the extension of inammation way or COX activity, or both. It is noteworthy that corti- Anti-inammatory agents. The inhibition of ECM and costeroids exert a broad anti-inammatory effect through inammatory protein production by corticosteroids is one inhibition of multiple inammation transcription factors of the best-established approaches to scar management. Se- NF-kB, AP-1 (activator protein-1), and NF-AT (nuclear rial steroid injections do not eradicate keloids; they can factor of activated T lymphocytes).12 however diminish pruritus and pain and soften the lesions. NF-kB is a rapid-response transcription factor that is Corticosteroids are effective in the majority of noninfect- involved in the cellular stress response. It is involved in ed scars that exhibit symptoms such as pain and pruritus. the upregulation of cell membrane receptors to inamma- Intralesional corticosteroids are believed to act by inhibit- tory peptides. It is also involved in the production of cy- ing broblast growth and decreasing alpha2 macroglobu- tokines, chemokines, and growth factors. NF-kB activation

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can be inhibited by several different agents. These agents tibrotic effect on scars. Antihistamines, particularly the include cyclosporin, tacrolimus, antioxidants, and salicy- H1 blockers, inhibit the inammatory response, resulting lates (including aspirin). Salicylic acid indirectly inhibits in reduced scar formation and increased comfort. The in- NF-kB expression by blocking the enzymes that lead to amed scar is scratched less, which will most likely re- dissociation of IKB (the activator of NF-kB) from the NF- duce the scar growth rate. Antihistamines are also known kB complex in the cytoplasm. This dissociation subse- to inhibit collagen synthesis. Diphenhydramine and hy- quently decreases the amount of inammation. Aspirin not droxazine are the most commonly used antihistamines for only inhibits the NF-kB pathway but also irreversibly in- scar management. We prefer the use of long-acting activates both COX isoforms. Salicylates (2-5%) are com- nondrowsy formulations such as loratadine or fexofena- monly used to control certain causes of dermatitis and are dine, which have the advantages of sustained action and routinely used in acne treatment products. Our experience fewer CNS side effects. increasingly suggests that topical application of salicylates to painful, itching scars is a practical approach to reduc- Inhibitors of gene transcription. The antimetabolities ing inammation. Topical aspirin should be used under a mitomycin-c and uorouracil inhibit cell proliferation by physician’s guidance, because some patients - particularly blocking DNA synthesis and transcription through com- asthmatics - may develop hypersensitivity. Vitamin D3, petitive inhibition of thymidylate synthesis.15 A single ap- which is also used to treat dermatitis, is another inhibitor plication in the rst few days after wound closure seems of NF-kB. The action of vitamin D3 is due to its affinity to be effective. Antimetabolite-induced apoptosis has also for the DNA promoter regions that transduce the NF-kB been demonstrated in Tenon’s capsule broblasts.16 These dissociation signals. To date, only one prospective uncon- agents are thus likely to be helpful in scar control. trolled study of topical salicylic acid has been reported. Nonetheless, the number of physicians prescribing top- Growth factor inhibition. The transforming growth fac- ical anti-inammatory agents is increasing. Our personal tor (TGF-b) family of proteins is centrally involved in reg- clinical experience has been very encouraging of the ef- ulating wound healing.8 The process of TGF-b synthesis fectiveness of topical 2% salicylic acid in managing pru- and release is activated by injury and, along with the ritic growing scars. platelet-derived growth factor, it has a central and critical role in the induction of wound healing. The binding of Prostaglandins are a group of potent, hormone-like sub- TGF-b to its receptor on broblasts causes broblast pro- stances that mediate a wide range of physiological func- liferation ECM structural protein synthesis and TGF-b syn- tions, such as the control of blood pressure and contrac- thesis. Mannose-6-phosphate and several other disaccha- tion of smooth muscle. The synthesis of prostaglandins is rides sterically limit TGF-b binding to its receptor and lim- also central to the inammatory response. The common- it scar formation in experimental wound-healing models.17 est strategy for prostaglandin synthesis blockade is pharmacological inhibition of cell membrane-bound COX.25 The acceleration of scar degradation agents and growth COX-1 is expressed constitutively throughout the body, factor inhibitors can limit scar production, and strategies especially in the stomach and kidneys. COX-2, however, to accelerate scar tissue degradation are also very useful. is expressed constitutively only in the brain and kidneys.28 This approach may be the best for the management of old- COX-2 synthesis is highly inducible by activation of NF- er hypertrophic scars and older keloids. The rate of tissue kB, which occurs at sites of injury or infection and plays breakdown can be increased by both pharmacological and an important role in brosis. The adverse side effects of physicochemical means. COX inhibition are minimized by the use of specic COX- 2 inhibitors, making them agents of choice for prolonged Occlusive dressings. After elastic pressure wrap dress- usage. The therapeutic value of these agents in rheumato- ing for the healing of burn scars was observed by Larson logical disease is well established, but their potential val- et al. to be effective in the reduction of scar hypertrophy,20 ue in the management of hypertrophic scarring has been 24 mm Hg pressure garments became the mainstay of scar a more recent consideration. Our reported experience sug- prevention. The action mechanism of pressure dressings is gests that COX-2 inhibitors reduce symptoms of pruritus unknown, because they remain effective even when they and may induce scar maturation and involution.14 Some lose their elasticity and pressure after several weeks of dai- popular topical consumer scar treatment products are de- ly use. Measurements show a decrease in wound rived from onion extract, which has anti-inammatory prop- metabolism, with an increase in collagen activity. The erties. drawbacks to their use are primarily related to thermal in- sulation and movement restriction. If continuous pressure Antihistamines are commonly used to control symp- (capillary pressure greater than 24 mm Hg) is applied to toms of scar pruritus, but they also seem to exert an an- a keloid day and night for 6 to 12 months, this can help

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the keloid to regress. It is believed that constant pressure Induction of remodelling decreases soft-tissue cellularity, increases interstitial space, Apoptosis inducers. The density of keloid scar brob- and results in histologically looser collagen bundles. How- lasts does not decrease as a scar ages. Instead, keloids con- ever, since continuous pressure application is required (> tinue to produce thick collagen bundles in a nodular ar- 23.5 h per day), this regimen is difficult to institute. Ap- ray. They also produce high levels of the proteolytic en- plying direct pressure to keloid sites has long been cited zyme caspase-3.3 Sayah et al. proposed that the downreg- as clinically successful. We have had little success with ulation of apoptosis-related genes in broblasts could al- this treatment because of the discomfort and prolonged du- ter the broblast phenotype, leading to increased scar tis- ration required. Even pressure earrings are poorly accept- sue production.7 A pharmacological agent that could block ed in our practice and are rarely worn continuously by our the expression and ultimate production of caspase-3 could patient population. be very valuable in the treatment of hypertrophic and keloid Both hydrogel and silicon gel sheeting have also been scars. used to control scar formation. It is clear, however, that Radiotherapy. The mechanism of radiotherapy involves the release of silicone into the scar is not the mode of ac- the destruction of broblasts that are not replaced, leading tion. Several reports have shown that hydrogel sheeting is to a reduction in otherwise excessive collagen synthesis. equally effective as silicone and has fewer adverse side- A common concern is the potential for radiation- effects.22,23 Hydrogel sheeting has recently been approved induced malignancy. To avoid the risk, treatment portals by the FDA as substantially equivalent to silicone for the were carefully designed to prevent scatter from affecting treatment of hypertrophic scars. Hydrogels have the added nearby body structures. Using this technique, virtually no advantage of their use as a hydration vehicle, as also a radiation is received by the central nervous system or thy- higher heat capacity for maintaining a continuous scar tem- roid gland. Additionally, the radiation penetrates approxi- perature. Silicone gels and sheeting have been successful- mately 4 mm - about the thickness of an earlobe. In re- ly used to decrease the recurrence of keloids, hypertrophic current earlobe keloids that are not responsive to excision scars, and post-burn scars.1,3 Several studies are currently and steroid treatment, repeat surgical excision followed by under way to determine more accurately their mechanism radiation therapy within one week of excision should be of action, which is currently unclear. Importantly, this tech- an option, after careful discussion with the patient. In a nique is relatively inexpensive and non-invasive, and in patient who is less likely to follow up on a monthly ba- our experience has a high patient compliance and satis- sis for serial steroid injections over 6 months, post- faction rate. operative radiotherapy to the earlobe keloid can be a use- We use silicone sheets for large at-surface keloids as ful option for adjunctive treatment for recurrent ear lobe both an alternative and an adjunct to surgery. keloids. In recurrent keloids in other head and neck sites, post-operative radiation is more controversial. If a recur- Inducer of scar degradation rent keloid is present in the lower anterior neck, many sur- Calcium antagonists. Many organic calcium channel geons would be more reluctant to institute post-operative blockers (i.e. verapamil) induce collagenase production and radiotherapy because of the risk of radiation exposure to scar tissue degradation. They induce changes in broblast the thyroid gland. The mechanism of radiation-induced scar gene expression, resulting in decreased collagen synthesis control seems to be the apoptosis of proliferating cells in and increased collagenase production. These effects appear the scar tissue.28 Low-dose ionizing radiation is most of- to be mediated by interruption of the basic cellular G-pro- ten reserved as the method of last resort for the treatment tein signal transduction pathway that is critical to regula- of intractable keloid scars. This therapy utilizes 15-20 Gy tion of broblast behaviour.24 This pathway can be inter- of orthovoltage radiation divided into ve to six treatments. rupted at multiple points by a wide range of commonly Although radiation therapy alone is not adequate, if it is used drugs.25 Verapamil, injected in a cream base applied used in conjunction with surgical intervention the reduc- topically on the scar, avoids rebound scarring from the tion in recurrence may reach 25%, compared with a re- trauma of intralesional injections. If an injection is neces- currence rate of up to 80% with surgery alone. sary, the alternation of verapamil with cortisone injections at monthly intervals seems to generate an effective yet ro- Cryotherapy has also been used to treat keloids and bust response. hypertrophic scars. Some researchers have used cryother- Additional agents that may induce scar degradation in- apy before intralesional steroid injection to allow for oede- clude calcium channel blockers, calmodulin inhibitors (e.g. ma and cellular injury from cryotherapy to subside. Oth- triuoperazin), and specic protein kinase C (PKC) in- ers have used cryotherapy as an effective treatment for hibitors (tamoxifen). These agents are promising as treat- new keloids, reporting a good response in 74% of patients.5 ment for older, non-inamed scars that are no longer ac- An adverse effect of cryotherapy is hypopigmentation due tively remodelling. to the cold sensitivity of melanocytes. Thus, darker-skinned

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patients are at increased risk for hypopigmentation. In ad- keloid could be excised in one stage or two stages. We dition, post-procedure healing can be prolonged, requiring noted that the defect would be too big to pull together and several weeks. that it would be tight if we excised it in one stage, and Laser therapy (continuous-wave or short-pulsed car- we therefore decided to cut half out at a time, removing bon dioxide, 585-nm ashlamp pulsed dye) has been an- the other half after four months. Monthly corticosteroid in- other approach to manage keloids and hypertrophic scars. tralesional injections (30 mg/ml) were used until the sec- However, the optimal time to institute laser treatment has ond part. After excision, the initial treatment included top- not been determined. Some have proposed that when the ical vitamin D3 (Diabonex) cream as an anti-inammato- laser treatment is initiated in the rst few weeks post-in- ry agent, and after checking for scar symptoms we used jury, further scar proliferation can be abated. Currently, silicon gel (Dermatix Si Gel) and pressure therapy to ac- when laser therapy is used, it is usually instituted in com- celerate scar maturation and degradation. The same steps bination with other therapy. Further studies with long-term were used in the second half. The nal scar looked better follow-up are needed to fully evaluate keloid and hyper- than the original keloid. trophic scar recurrence rate with laser therapy. Our charts were also used for hypertrophic scar pre- Interferon therapy has also been used for treatment, vention in patients with a predisposition for hypertrophic on the basis of the nding that interferons alpha, beta, and scarring who had undergone plastic operations. gamma inhibit collagen synthesis (collagen types I and III) Our charts were reviewed with regard to 10 patients in dermal broblasts. who had undergone treatment for histologically documented keloid or hypertrophic scars and as prevention in Surgical revision. The commonest indications for the 10 patients with post-plastic-operation risk factors. The ini- surgical removal of scars are as follows: large scars that tial treatments were individualized. The factors to consid- are unlikely to be completely managed by medical thera- er when choosing the optimal treatment were the site and py in a reasonable timeframe, scars that harbour painful size of the lesions, scar duration, symptoms, and previous furuncles, and scar contractures that hamper muscu- treatment (Figs. 1-5). loskeletal function.29 Although the outcome of surgery may be desirable in the short post-operative term, the surgical revision of hypertrophic or keloid scars is followed by a high recurrence rate. Adjunctive measures to reduce in- ammation, skin tension, and other factors are essential to reduce recurrence. The protocol for patients that require elective surgical excision is to identify effective scar control medications beforehand, and then to restart the medications immediately following surgery. A gentle surgical technique is also critically important, because inamed scar tissue produces a tremendous scar response to trauma. The use of lasers and other burning techniques for scar removal is very controversial.

Case report

A 16-year-old boy (born in 1988) who developed a histologically documented keloid after left side hernioplasty Figs. 1, 2 - Before rst operation. Pre-operative view from antero- (in 1996) twice underwent the surgical removal of a re- posterior (left) and lateral (right) side. current raised expanding keloid at the site of a previous excision within one year of surgical excision (1998). The last treatment option (by another surgeon) was surgical removal and full-thickness skin graft from the contralateral site (2001). It was possible to observe the extent of post- operative inammation (partial dehiscence, redness). On admission, the patient was noted to have pruritus and pain. Within one year (2002) a keloid developed at the site of the full-thickness skin donation. According to our chart, the rst step was to assess the size and symptoms of the Figs. 3, 4 - Intra-operative view. Fig. 4 - Upside down view of ex- keloid and the laxity of skin, in order to determine if the Full-thickness skin graft. cised keloid.

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Fig. 5 - After removal of suture (2 weeks Fig. 6 - Keloid recurrence one year post-op. Fig. 7 - After removal of suture, 2 weeks post-op). Note the extent of inammation. post-op and immediate treatment as described previously.

Fig. 8 - Four weeks post-op. Surgical partial Fig. 9 - Seven weeks post-surgical excision Fig. 10 - Showing use of silicon gel and pres- excision (according to our chart). and other treatments as described. sure therapy.

Conclusion treated with either topical salicylates or oral COX-2 medications, or both, in order to control scar inammation. As research continues on the initiation and control of The use of topical verapamil (5-10%) has shown great the various stages of healing, it is important that we main- promise in inducing the degradation of older inactive scars tain up-to-date knowledge of the way advances in scien- and reduced the need of surgical intervention. Transepi- tic research are being applied in the clinical setting. Phar- dermal delivery of these topical agents in scar manage- maceutical products are being incorporated into wound ment has made it possible to effectively treat scar condi- dressing, and we should be able to select and use these tions that previously were refractory to conventional ther- appropriately if we are to achieve some benet for our pa- apy. We hope that this experience will lead to more ef- tients. Despite recent scientic progress, scar-related dis- fective therapeutic options for such patients. gurement and disability remain major ongoing medical In this article, we have attempted to briey summa- problems. Stripped of the conicting and confusing ter- rize and place into a conceptual framework the various ex- minology, hypertrophic and keloid scarring can be essen- isting and emerging therapies for hypertrophic scar disor- tially reduced to inammation-mediated dermal brosis. ders. We hope that this review will encourage the consis- This suggests that much insight into effective management tent use of less ambiguous terminology and more effec- can be gleaned from the medical literature pertaining to tive therapeutic strategies in the future. dermatological and rheumatological conditions, which al- It is probable that future developments in wound care so have a large inammatory gene expression component. will focus on the control mechanism involved in wounds With these concepts in mind, we have designed sev- and on the ways in which failures of these mechanisms eral scar management protocols now under clinical evalu- impair healing. Control of wound healing is complex, and ation. Under these protocols, summarized in the chart, pa- it is doubtful that any single solution to delayed healing tients with scars that are actively enlarging or itching are will be found.

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Chart - Keloid and hypertrophic scar management (by A. Edriss, based on scientic and clinical experience, but requiring a greater number of patients, long-time follow-up, and photographic documentation)

209 Annals of Burns and Fire Disasters - vol. XVIII - n. 4 - December 2005

RÉSUMÉ. La gestion des cicatrices pour prévenir leur formation excessive a toujours été importante, mais jamais comme aujourd’hui. La gestion optimale reste une énigme pour les chirurgiens, et on discute depuis nombreuses années sur la meilleure modalité de traitement. Cependant, la plupart des études ont été malheureusement ou rétrospectives ou des descriptions de cas particuliers. Le pro- grès dans le champ de la gestion des cicatrices a été ralenti par une terminologie confuse ou ambiguë. On n’est pas d’accord sur la quantité de la formation de cicatrices cutanées post-traumatiques que l’on peut considérer comme “normale” et ce que l’on peut considérer comme “hypertrophique”. Le ICD-9 de l’Organisation Mondiale e la Santé ne contient aucun code diagnostique pour la cicatrice hypertrophique - il cite seulement la cicatrice chéloïdienne. Mais la littérature médicale et scientique les distingue comme des conditions différentes. Cette confusion porte à une gestion inappropriée de la formation des cicatrices, et en certains cas contri- bue au processus pour la prise de décisions pour ce qui concerne la chirurgie élective ou cosmétique. Selon l’expérience des Au- teurs, il n’existe pas un seul traitement efficace, et le jugement clinique est très important quand on considère le traitement clinique et pèse les bénéces potentiels des divers traitements disponibles. Le but du traitement des cicatrices est de restaurer la fonctionna- lité, soulager les symptômes, améliorer l’aspect cosmétique et prévenir les récidives. Les Auteurs présentent leurs expériences scientiques et cliniques et décrivent les options commerciales pour la gestion des cicatrices chéloïdiennes et hypertrophiques.

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