HYPERTROPIC SCAR BY HERRY SETYA YUDHA UTAMA

CHAPTER 1

INTRODUCTION

Scar formation after injury is a normal process. It is the body's natural way of healing, by creating a connective tissue fibers such as collagen and deposits on the skin to close the wound. However in some cases the wound tends to swell, become swollen and sometimes red. These scars are known as hypertrophic scars. Scar hypertrophy is due to several reasons such as burns, scrapes, injections and tattoos. Another reason for the occurrence of hypertrophic scarring can be simple things like that can lead to the formation of acne scars, insect bites and accidents. Hypertrophic scarring can occur in individuals of all ages. However, in some cases, individuals tend to get hypertrophic scarring because they are genetically prone to it. Individuals with lighter skin is more susceptible to injury because the scars are more visible and prominent.

Scar hypertrophy is characterized by erythematous, pruritic, raised fibrous lesions that typically do not grow beyond the boundaries of the initial injury and may undergo partial spontaneous resolution. Scar hypertrophy often occurs after thermal injury and other injuries involving the deep dermis.

Hypertrophic scar looks like a keloid. Hypertrophic scars are more common. They do not get as large as keloids, and may fade with time. They occur in all racial groups. Keloids considered a benign tumor, but they are mainly cosmetic nuisance and never become malignant. Operates in keloid scarring usually stimulate more to form, so that people with keloids may have been told that nothing can be done to get rid of them.

LITERATURE REVIEW

1. Definitions

Scar is a proliferation of connective tissue in response to trauma. When scar bigger or wider than usual, or be "piled up", it is known as keloids or hypertrophic scars. Scar hypertrophy is where the changes are limited to the scar. Scar hypertrophy is a skin condition characterized by the accumulation of excess scar tissue in the local area. This disease can affect individuals of any ethnicity. However, more common in blacks, Asians and Hispanics.

2. Pathophysiology

Hypertrophic scars and keloids can be described as a variation of healing Typical injuries. In a typical wound, anabolic and catabolic processes achieve a balance of approximately 6-8 weeks after to harm. At this stage, the strength of the wound is approximately 30-40% compared to healthy skin. As time passes scars, scar tensile strength increased as a result of the progressive cross of collagen fibers. In this condition, the scar is usually hyperemic and may be thickened, but tends to subside gradually over several months until the scar flat, white, soft, perhaps stretched, adults have been developed.

When an imbalance occurs between anabolic and catabolic phases of the healing process, more collagen is produced than is degraded, and the scar is growing in all directions. The scar is raised above the skin and remain hyperemic. Excessive connective tissue is classified as a keloid or hypertrophic scars.

Kischer and Brody expressed collagen nodule into structural units identify scar hypertrophy and keloid. Nodule, which is absent from mature scars, contains a high density of fibroblasts and unidirectional collagen fibrils in a highly organized and distinct orientation. Additionally, keloids and hypertrophic scars is different from that of healthy skin by rich veins, high cell density (mesenchymal), and epidermal cell layer thickens. Efforts to clinically differentiate keloids from hypertrophic scar has proved difficult in the initial phase of formation. Clinical differences become more apparent as mature lesions. The most consistent histologic difference is the presence of broad, dull, pink bundles of collagen in keloids, which are not present in the scar hypertrophy.

Many theories were postulated regarding the mechanism of formation of keloids and hypertrophic scars, including allergic immunoglobulin E (IgE) mediated responses, leading to a decrease in the percentage of cross-linked collagen mature and increase collagen soluble fraction. A second theory implicates deficiency in the metabolism of melanocyte-stimulating hormone (MSH) or excess MSH as the initiator of the formation of keloids and hypertrophic scars. The increase in the formation of scar hypertrophy mediated MSH and subsequent related to certain periods of life, such as pregnancy and puberty, supports this theory. A third hypothesis concerns the possibility that microvascular occlusion and hypoxia may be responsible for the formation of keloids and hypertrophic scars. More recent studies have reported an increase in interleukin-6 (IL-6) expression in the pathophysiology of keloids and hypertrophic scars, and the role of insulinlike growth factor-1 (IGF-1) and IGF-1 receptor axis in keloid invasive activity.

3. Epidemiology

Keloids can be derived dominant and autosomal recessive. Although it can occur in all age groups, rarely found in newborns or parents and has the highest incidence in individuals aged 10-20 years. Scar hypertrophy nothing to do with a family history or ethnic background as the keloid scar. However, both types of this scar, collagen levels higher than the average of scar tissue. Hypertrophic scars are usually formed in the ears, shoulders, and chest, but they can form other places on the body as well (Berman, 2010 and Jones, 2008).

Keloids and hypertrophic scars situated in a location that is largely cosmetic concern, but some keloids or hypertrophic scars can cause contractures, which may result in loss of functionality if the above joint or in significant disfigurement if located on the face. Keloids and hypertrophic scars can be both painful and itchy. Keloids and hypertrophic scarring associated with HLA-B14 genetic, HLA-B21, HLA-Bw16, HLA-Bw35, HLA-DR5, HLA-DQw3, and blood group A.

Keloids form more frequently in people of Polynesia and China than India and Malaysia. As many as 16% of people in a random sampling of black Africa is reported to have keloids. White people at least generally exposed. This prevalence has been reported to be higher in young women than in young men, perhaps reflecting the greater frequency of earlobe piercing among women. Keloids and hypertrophic scars affects both sexes equally in other age groups. Onset occurs most often in people aged 10-30 years. Keloids occur more frequently at the extremes of age, although an increasing number of presternal keloids have resulted from coronary artery bypass surgery and other procedures now do the same in age groups.

4. Physical Findings

This condition is characterized by the appearance of a thick red scar on the skin surface. It usually appears only on skin areas that have been recently injured or surgery. Keloid scar hypertrophy is different from growing indefinitely. Scar hypertrophy only appears on the site of injury or surgery. Scars are thicker and darker than the surrounding skin area. It usually occurs on the ear lobe, lower facial area, shoulders, chest and back. Scar hypertrophy may develop at any time. These scratches can arise even after the wound has healed on the skin area. In later stages, the scars can be itchy and painful. It becomes difficult to touch and change the texture or sensitive to changes in temperature. Friction with clothing and rough surfaces can also cause pain and discomfort.

Scar hypertrophy rising, often a darker color than the surrounding skin, but they remain within the parameters of the wound. Scar hypertrophy can be itchy, highly visible and can cause problems with the tightness and skin mobility. Over time these injuries tend to be better, often reducing the height and lighten in color. However, sometimes this does not happen. Hypertrophic scars remain confined to the areas of trauma and regress spontaneously within 12-24 months, although not necessarily complete regression.

5. Cause

The exact mechanism of pathogenesis of keloids and hypertrophic scars continue a puzzle for physicians and researchers, and there is no particular gene or set of genes have been identified; skin pigmentation, but the increase in the prevalence of keloid parallelization increases indicate a genetic basis or, at least, a genetic linkage. Trauma to the skin, both physical (eg, earlobe piercing, surgery) and pathological (eg, acne, chicken pox), is the main cause for the occurrence of scar hypertrophy identified. The presence of foreign material, infection, hematoma, or increased skin tension can also lead to the formation of scar keloid or hypertrophic scar in susceptible individuals.

Higher accumulation of collagen occurs in response to certain events, namely:

• Injections, Scar hypertrophy often occur after certain medical injections strong.

• Operations, is often visible scars appear after surgery. Many people found the scar develops into scar hypertrophy after surgery.

• Injuries, skin suffering from hypertrophic scar on localized wound.

• Acne, these scars are often the results of acne on the skin.

• Body Piercing, in many cases, hypertrophic scars arising after the piercing of the skin surface. Body Piercing is one of the main causes of hypertrophic scar.

6. Diagnosis

Scar hypertrophy mainly diagnosed by medical professionals with observing the physical appearance of the skin. In some cases, a skin biopsy may be needed to rule out the presence of cancerous conditions such as tumors.

During the early stages of a scar, it is often very difficult to distinguish keloids from hypertrophic scar. They both look similar and are caused by an overgrowth of the same network. As a mature scar, it is easier to distinguish between the two lesions. Keloids contain collagen widely, pink bundle that is not present in hypertrophy.

7. Differential Diagnosis

a. Keloids

Keloids are reddish nodules that develop at the site of injury. After the injury occurred in both skin skin cells and connective tissue cells (fibroblasts) begin to multiply to repair the damage. The scar is composed 'connective tissue' of fiber-prone as stored in the skin fibroblasts to hold the wound closed. In keloid, fibroblasts continue to multiply even after the wound is filled keloid on the surface of the skin and form a large mound of scar tissue. Keloids are formed in any part of the body, although the upper chest, shoulders and upper back are very prone to keloids. Symptoms include skin pigmentation, itching, redness, unusual sensation and pain.

b. Dermatofibroma

Dermatofibroma is skin nodules of unknown etiology commonly occurring more frequently in women. Dermatofibroma often develops on the extremities (most of the lower leg) and usually without symptoms, although pruritus and unusual tenderness. Dermatofibroma usually occurs slowly and most often occurs as a solitary nodule on the extremities, especially the lower limbs, but each site skin is possible. Some lesions may be present, but only rarely are multiple (ie, 15 or more) tumor is found. This was shown some of the most frequent variants in the setting of autoimmune disease or altered immunity, such as systemic lupus erythematosus, Graves' disease, Down's syndrome, HIV infection, or leukemia and may be indicative of deteriorating immunoreactivity.

8. Treatment

Prevention is the key, but the treatment of hypertrophic and keloid scar treatment including occlusive dressings, compression therapy, intralesional corticosteroid injections, cryosurgery, excision, radiation therapy, laser therapy, interferon (IFN) therapy, 5-fluorouracil (5-FU), doxorubicin, bleomycin , verapamil, retinoic acid, 5% imiquimod cream, tamoxifen, tacrolimus, botulinum toxin, and treatment of over-the-counter (for example, garlic extract; a combination of hydrocortisone, silicon, and vitamin E). Other therapies include antiangiogenic factors, including vascular endothelial growth factor (VEGF) inhibitors (eg, bevacizumab), phototherapy (photodynamic therapy [PDT], UVA-1 therapy, narrowband UVB therapy), transforming growth factor (TGF) -Beta3, tumor necrosis factor (TNF) -alpha inhibitors (etanercept), and recombinant human interleukin (rhIL-10), which is directed to a decrease in collagen synthesis.

1. Occlusive dressings

Occlusive dressings including the provision of silicone gel and dressings, occlusive sheets nonsilicone, and tape Cordran. These measures have been used with varying success. Antikeloidal effect appears to result from a combination of occlusion and hydration, instead of silicon influences. Previous studies have shown that in patients treated with occlusive silicone sheet with a pressure of 24 hours / day to 12 months, 34% showed excellent improvement, 37.5% showed moderate improvement, and 28% showed no or little improvement.

2. Corticosteroids

Corticosteroids, especially intralesional corticosteroid injections, has become mainstay of treatment. Corticosteroids reduce excessive scarring by reducing collagen synthesis, synthesis glucosaminoglycan change, and reducing the production of inflammatory mediators and proliferation of fibroblasts during wound healing. Which is most commonly used corticosteroid triamcinolone acetonide is (TAC) in a concentration of 10-40 mg / mL administered intra-lesion for 4-6 weeks intervals.

3. IFN therapy

IFN therapy, including IFN alpha, IFN beta, and gamma IFN, has been demonstrated in in vitro studies to reduce the production of fibroblasts keloidal collagen types I, III, and VI mRNA. IFN alpha and IFN beta also reduces fibroblast production of glycosaminoglycans (GAG), which is a scaffold for dermal collagen deposition. IFN gamma increases the production of GAGs. IFN alpha, IFN beta, and gamma IFN has shown an increase in the activity of collagenase. Research has shown that IFN gamma modulate p53 pathway of apoptosis by inducing apoptosis-related genes. p53 is a protein synthesized following DNA damage. After the damage repaired, p53 is degraded. Mutations of this protein is believed to affect the cell to hyperproliferation, may lead to the formation of keloids. In addition, p53 is a potent suppressor of interleukin (IL) -6, a cytokine involved in hyperproliferative conditions and fibrosis.

4. Extract onion

Onion extract, namely Allium cepa extract, and especially quercetin derivatives, are bioflavonoids with antibacterial, fibrinolytic, antihistamine-releasing, and antiproliferative effects on normal and malignant cells can be found in onions and apples, red wine, and black tea. Additional biological activities described include inhibition of Na + K + ATPase, protein kinase C, tyrosine kinase, HIV reverse transcriptase, and kinase pp60src. Inhibit enzymes involved in proliferation signaling pathways (Eg, phosphatidylinositol 3-kinase [PI-3K], 1-phosphatidylinositol 4-kinase), and it causes cell cycle arrest and apoptosis. In vitro studies have shown that quercetin inhibits keloid fibroblast proliferation, collagen synthesis, basal expression, and activation of several key proteins in insulinlike growth factor (IGF) -I, which is a potent mitogen and inhibitor of apoptosis that stimulates fibroblast proliferation and increase collagen synthesis.

5. The combination of therapeutic agents

The combination of therapeutic agents, made in theory to obtain the effect synergistic benefit in the treatment of keloids and hypertrophic scars, have been developed that contain hydrocortisone 0.5%, 0.5% vitamin E, and 12% silicon. Each of the three components has been demonstrated, in varying degrees, to be effective for the treatment of keloids and hypertrophic scars. Corticosteroids inhibit collagen synthesis, stimulates collagenase activity, increasing collagen degradation, decrease proliferation of inflammatory mediators in the wound, decrease fibroblast proliferation, and decreased synthesis of GAG. Silicone provide occlusion and hydration to the wound surface. Occlusion decreased collagen formation, mitogenic activity, and capillary formation. In addition, silicon induces a negative ionic charge on the surface of the wound, inhibiting the formation of collagen. Vitamin E has been postulated to inhibit collagen synthesis, stimulates the expression of collagenase, reduce fibroblast proliferation, and reduce inflammation in wounds.

6. Vitamin E

Vitamin E (tocopherol) is a lipid-soluble antioxidant with biological effectssome, including the reduction of reactive oxygen species, which inhibits healing and cause damage to the DNA molecule, the cellular membrane, and lipids. In addition, vitamin E (tocopherol) also alter the production of collagen and GAG and inhibit the spread of lipid peroxidation in cellular membranes, thereby acting as a membrane stabilizing agent. Only anecdotal reports indicate that vitamin E accelerates wound healing and improve the cosmetic appearance of scars.

7. Radiation Therapy

Use of radiotherapy to treat keloids still controversial. Although many studies have demonstrated the efficacy and decrease relapse rates, security radiotherapy has been questioned. In a retrospective study of x-ray therapy of 24 keloids shallow cut, the authors reported a recurrence rate of 53%. The use of irradiation 192 iridium (Ir) interstitial after excisional surgery resulted in a recurrence rate of 21% after 1 year. Excisional surgery and preoperative hyaluronidase solution (150 U / mL sodium chloride) followed by external radiation (7.2 to 10.8 Gy) had a recurrence rate of 0%. Adjunctive high-dose-rate brachytherapy (192 Ir) is used after excision and closure resulted in a recurrence rate of 12% after 26 months.

8. Surgery

Surgical treatments include cryotherapy, excision, laser therapy, and other light therapy.

·      Cryotherapy

Cryosurgical media (eg, liquid nitrogen) affect mikrovascular and cause damage to cells through intracellular crystals, causing tissue anoxia. Generally, 1, 2, or 3 freeze-thaw cycles lasting 10-30 seconds each are used for the desired effect. Treatment may be repeated every 20-30 days. Be careful to manage liquid nitrogen in a short application time for the possibility of reversible hypopigmentation. Cryotherapy can cause pain and permanent depigmentation in certain patients. As a single modality, cryosurgery causes total resolution without relapse in 51-74% of patients after 30 months of follow-up observations.

·      Excision

Applying basic handling techniques of soft tissue at the site of the primary wound repair. Be careful closure with minimal tension, parallel with the line of low tension skin. Use the buried sutures, if necessary, to layered closure and to reduce tension. When only feasible, apply a pressure dressing during the postoperative period immediately for injuries in patients who scar hypertrophy.

9. Laser Therapy

Carbon dioxide, argon laser, and Nd: YAG laser (1064 nm). ablation keloid and scar hypertrophy using carbon dioxide laser (10,600 nm) can be cut and burn lesions, creating a dry surgical environment with minimal tissue trauma. When used as a single modality, carbon dioxide laser is associated with a recurrence rate of 39-92%, and when the carbon dioxide laser in combination with injectable steroids postoperatively, it is associated with a recurrence rate of 25-74%. Similarly, the carbon dioxide laser, the 488-nm argon laser can cause shrinkage of the collagen through excessive local heat generation. Argon laser has been demonstrated 45-93% recurrence rate.

CHAPTER  4

CONCLUSION

Male 19 years came to the clinic complaining toes into four bottom enlarged scars. 3 months ago, the patient admitted that there is a lump in the area. 1 month ago on the lump there are wounds. The wound becomes increasingly enlarged, hot and reddish. The patient did not complain of itching or pain in the scar..

Past medical history has never had a complaint serupe although. Families of patients also experienced no similar complaints. the patient did not complain of pain or itching, only less comfortable in cosmetics from the standpoint of the patient's parents.

Clinical findings obtained erythematous papules appear shiny demarcated extends to the size varies according to the initial injury, hard consistency, tenderness, and is located in the digiti IV lower left foot.

Based on the clinical picture seen from the equivalent abnormal skin, these patients were diagnosed hypertrophic scar. Scar hypertrophy occurs because of an imbalance occurs between anabolic and catabolic phases of the healing process, more collagen is produced than is degraded, and the scar is growing in all directions. The scar is raised above the skin and keep hyperemi. Excessive connective tissue is classified as a keloid or hypertrophic scars .

 Scars mature, containing a high density of fibroblasts and unidirectional collagen fibrils in a highly organized and distinct orientation. Additionally, keloids and hypertrophic scars is different from that of healthy skin by rich veins, high mesenchymal cell density, and a thickened layer of epidermis cells. Does not exist or can not be found that genetic factors play a role.

The diagnosis is based on the observation intentions skin disorders. Do not do a biopsy to rule out a tumor because the lesion is not so big and obvious precipitating factor is a history of previous scar. Found kelaina intentions skin is visible nodules demarcated erythematous shiny elongated with sizes vary according to the initial injury, hard consistency, no tenderness, and is located in the lower left forearm extensor.

Treatment in this case is the provision of a combination of retinoic acid, and mederma. Retionoic acid serves to decrease collagen synthesis and skin elasti, and also shrink the sebaceous glands to the skin's oil production is reduced. Retinoic acid also stimulates new collagen deposition.

Mederma is an onion extract, namely Allium cepa extract, quercetin derivatives and in particular, are bioflavonoids with antibacterial, fibrinolytic, antihistamine-releasing, and antiproliferative effects on normal and malignant cells. Garlic extract also inhibits keloid fibroblast proliferation, collagen synthesis, basal expression, and activation of several key proteins in insulinlike growth factor (IGF) -I, which is a potent mitogen and inhibitor of apoptosis that stimulates fibroblast proliferation and increase collagen synthesis.

REFFERENCE

Alphonso, Marline. 2010. Hypertrophic scarring. Diakses dari  www.buzzle.com/articles/hypertrophic-scarring.html tanggal 25 April 2011

Arinudh. 2011. Hypertrophyc Scar-Causes, Treatment and Removal. Diakses dari  www.primehealthchannel.com tanggal 25 April 2011

Berman, Brian. 2010. Keloid and Hypertrophic Scar. Diakses dari  www.medscape- medline.com tanggal 25 April 2011

Jones, Carlotta. 2008. What is hypertrophic scar?. Diakses dari  http://ezinearticles.com tanggal 26 April 2011

Kokoska, Mimi. 2010. Keloid and Hypertrophic Scar. Diakses dari  www.medscape- medline.com tanggal 26 April 2011

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