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Head and Neck Keloid: Treatment by Core Excision and Delayed Intralesional Injection of Steroid
J Oral Maxillofac Surg 65:1292-1296, 2007
Head and Neck Keloid: Treatment by Core Excision and Delayed Intralesional Injection of Steroid Peter Donkor, BDS, MDSc, MSc, FRACDS, FWACS, FGCS* Purpose: This report aims to describe a technique used by the author for the management of head and
neck keloid. Patients and Methods: This is a clinical review of patients presenting with new and recurrent keloid of the head and neck to the Maxillofacial Surgery Unit at the Komfo Anokye Teaching Hospital, Kumasi, Ghana. The surgical technique involved the intralesional excision of the bulk of the keloid. Primary closure of the ensuring defect was achieved at operation. At the time of suture removal between 10 and 14 days postoperative, 40 mg triamcinolone was injected into the residual lesion. The injection was repeated on 2 more occasions at monthly intervals. All patients were followed up for at least 2 years. Results: Eighteen patients were successfully treated with no sign of recurrence in any of them. The main complication was hypo-pigmentation at the site of the original lesion. Conclusion: The technique was found to be effective for the treatment of moderately sized new and recurrent keloid scars of the head and neck and is therefore recommended. © 2007 American Association of Oral and Maxillofacial Surgeons J Oral Maxillofac Surg 65:1292-1296, 2007
Keloid and hypertrophic scars are unique to humans, and result from excessive production of fibrous tissue during the healing of wounds. Keloids can occur anywhere on the skin and have a tendency to run in families. They occur in all races but are 15 times more common in patients with darker skin. Incidence is approximately 10% in high risk groups. Onset may be delayed at least 3 months after injury with progression but no resolution. Areas most commonly involved are the shoulders, neck, anterior chest, upper arms, and face.1-5 Clinically, there are differences in the presentation of hypertrophic scars and keloids. Hypertrophic scars are raised erythematous lesions confined within the boundaries of the original wound. On the other hand, keloids frequently persist at the site of injury, often
*Consultant, Maxillofacial Surgery Unit, Department of Surgery, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Komfo Anokye Teaching Hospital, Kumasi, Ghana. Address correspondence and reprint requests to Prof Peter Donkor: Maxillofacial Unit, Department of Surgery, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Komfo Anokye Teaching Hospital, 1 Bantama High Street, Kumasi, Ghana, West Africa; e-mail: [email protected] © 2007 American Association of Oral and Maxillofacial Surgeons
0278-2391/07/6507-0005$32.00/0 doi:10.1016/j.joms.2006.10.049
recur after excision, and always overgrow the boundaries of the original wound. Both disorders are manifestations of a loss of the control mechanisms that regulate wound healing, which include clot formation, inflammation, cell migration and proliferation, synthesis and release of cytokines and extracellular matrix proteins, and remodeling of the newly synthesized matrix. This aberrant healing results in a disordered architecture and excessive deposition of matrix proteins that accounts for the clinical picture.6-12 Histologically, keloids are characterized by excessive accumulation of collagen. This is because of an exaggerated response of fibroblasts to transforming growth factor (TGF-) that regulates the expression and deposition of collagenous extracellular matrix. Fibroblasts isolated from the keloid have been found to have higher levels of TGF- receptors. Other growth factors that stimulate fibrosis and occur in increased quantities in keloids include platelet-derived growth factor, interleukin-1, and insulin-like growth factor. These growth factors further inhibit the production of proteases required to maintain the balance between the production and degradation of fibrous tissue.6-8 Mast cells and other vasoactive mediators known to stimulate growth of fibrous tissue are also known to be present in excess in keloid scars as compared with normal tissue.9,10 Keloid fibroblasts have been found to show resistance to apoptosis, a situation that predisposes to increased cellularity.11,12 Thus, the combined actions of these cytokines on
1292
1293
PETER DONKOR
stimulating excess collagen production, inhibiting its degradation, and interfering with the programmed cell death of fibroblasts in keloids contribute to overgrowth of scar. Several techniques for treating keloids have been developed and are aimed at inhibiting collagen synthesis and accelerating the removal of excess collagen. The limited success of any 1 technique has given rise to numerous treatment protocols with variable results. These include intralesional steroid injection, surgical excision, cryotherapy, laser therapy, irradiation, mechanical compression dressings, silicone applications, ultrasound and heat, intralesional interferon injection, or combinations of techniques. Intralesional steroids13 act by suppressing the inflammatory response, diminishing collagen synthesis, decreasing mucinous ground substance production, and inhibiting collagenase inhibitors that prevent the degradation of collagen.13 Among the adverse effects of steroids are atrophy of skin, hypopigmentation, telangiectasia, and cushingoid effects from systemic absorption. Surgical excision14-17 may be combined with skin grafting, but recurrences range from 45% to 100%. Surgery has been found to be most effective when combined with steroid, irradiation, or pressure therapy. Cryotherapy18 and laser therapy,19 which are forms of surgical therapy, cause microcirculatory disturbances leading to tissue damage, especially fibroblasts. These therapies are most effective when combined with other treatment modalities. Radiation for the treatment of keloid results in reduced rate of fibroblast and endothelial cell proliferation.12,20-22 The risk of malignant transformation and other side effects, as well as cost, restrict its widespread use. It may be used either alone or in combination with surgical excision. Mechanical compression dressings23,24 reduce oxygen tension in the wound through the occlusion of small vessels, leading to reductions in tissue metabolism, fibroblast proliferation, and collagen synthesis. Silicone gel sheets and silicone occlusive dressings25-28 worn 24 hours a day for up to 1 year have been used for treating keloids. The mode of action is by increasing the temperature of the scar, thus increasing collagenase activity. Ultrasound and heat probably act by increasing collagenase activity. This reduces the collagen content of the scar, thus softening it.29 Intralesional interferon30 is believed to cause shrinkage of keloids by reducing fibroblast synthesis of collagen, reducing mucinous ground substance production and decreasing collagenase activity. There has been limited success with many of the techniques used in the treatment of keloids at our
institution. Some of these techniques include intralesional steroid injection, extralesional excision, extralesional excision with immediate skin grafting, extralesional excision and immediate postoperative steroid injection, massage, application of silicone sheets, and occlusive dressings. There is no experience with the use of irradiation, cryotherapy, and laser therapy for the treatment of keloids at our hospital. This report is based on the author’s experience with a technique that combines intralesional surgical excision with delayed intralesional injection of steroids in the management of keloids of the head and neck.
Patients and Methods This is a clinical review of a technique used by the author for the treatment of keloid scars of the head and neck in patients attending the maxillofacial clinic at the Komfo Anokye Teaching Hospital, Kumasi, Ghana since 1999. Some of the patients had recurrent lesions after undergoing previous treatment for keloids, including surgical excision and skin grafting, scar massage, silicone sheets and occlusive dressings, and intralesional steroid injections. Others had not had any prior treatment for their keloid.
Surgical Technique The procedure was carried out using either general or local anesthesia. Following skin preparation, the bulk of the central portion of the keloid was excised leaving a thin rim of keloid. The edges of the wound were then undermined to permit advancement. After hemostasis, the wound was closed primarily, sometimes under tension. Suture removal was performed at 10 to 14 days postoperation, after which the skin was cleaned with antiseptic and 40 mg triamcinolone injected into the residual lesion. The injection was repeated at 4-week intervals on 2 additional occasions, for a total of 3 injections. All patients were first
Table 1. DISTRIBUTION OF HEAD AND NECK KELOIDS
Location of Keloid
Number
Ear lobe Preauricular area Upper lip Lower lip Submandibular area Back of neck All sites
8 1 3 2 2 2 18
Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
1294
HEAD AND NECK KELOID
Discussion The technique described in this report is similar in principle to other surgical approaches that combine with postoperative steroid injections.14,15 There are, however, some differences. The excision of a keloid is intralesional and not extralesional. It deliberately aims to leave a thin rim of keloid on the wound edges. This modification avoids the risk of inducing an intense inflammatory response in the surrounding, unaffected “keloid-prone” skin, which could lead to the formation of new and possibly bigger keloid. In contrast to the report by Lee et al,17 it was observed in our series that intralesional excision of keloid without adjuvant steroid therapy resulted in overgrowth of the residual scar if the injections were started later than 3 weeks after surgery.
FIGURE 1. A, Ear lobe keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
reviewed at 6 months from the time of the last steroid injection and followed up for at least 2 years.
Results Thus far, 18 patients have been treated using this technique. They comprised an equal number of males and females. The keloid scars were distributed around the face including the ear lobe, preauricular area, upper lip, lower lip, back of neck, and submandibular area (Table 1). The largest scar was located at the back of the neck and had a widest dimension of 6 cm. In seventeen (94%) patients, the scars remained soft and flat with no sign of recurrence. Examples are presented in Figures 1, 2, and 3. However, all the scars remained hypopigmented. In 1 patient there was dehiscence of the wound on the third postoperative day that was successfully resutured. This patient, however, was lost to follow-up and did not complete treatment.
FIGURE 2. A, Neck keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
1295
PETER DONKOR
Experience with this technique has so far been limited to its use in the head and neck region. A major limitation lies in the need to achieve primary closure following excision of the keloid. This would not be possible where an extensive body surface area was affected. It is therefore recommended for use in small to moderately sized lesions that will permit primary closure of the wound after excision. This technique of surgical excision of small to moderately sized keloid scars of the face followed by delayed injection of steroid was found to be effective and is therefore recommended. Combining surgical debulking with delayed intralesional steroid ensures uninterrupted initial wound healing and a faster resolution of the keloid than if either treatment modality was used alone. Acknowledgment The author is grateful to Lucy Amoateng, Victoria Narh, Felicia Sarpong, Dr Bertha Gyau, and Dr Alex Oti Acheampong for their assistance.
References
FIGURE 3. A, Preauricular keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
While success with surgical techniques that combine with the injection of steroid immediately after excision of keloid have been reported, it has been our observation that this causes delayed wound healing. In the technique described in this report, the injection of steroid was delayed until the time of suture removal. This avoids any interference with initial wound healing. The technique is superior to intralesional steroid as a sole therapy in that by debulking the lesion, tissue resistance was less and subsequent injections were much easier. Furthermore, fewer injections were required for resolution of the keloid, and therefore the potential for any undesirable side effects of the steroid was reduced. The time required for the resolution of the keloid was also shortened. Another advantage of this technique is that it was successfully used for the treatment of previously untreated keloid, as well as recurrent keloid where other therapies had failed.
1. Alhady SM, Sivanantharajah K: Keloids in various races. A review of 175 cases. Plast Reconstr Surg 44:564, 1969 2. Ramakrishnan KM, Thomas KP, Sundararajan CR: Study of 1,000 patients with keloids in South India. Plast Reconstr Surg 53:276, 1974 3. Datubo-Brown DD: Keloids: A review of the literature. Br J Plast Surg 43:70, 1990 4. Crockett DJ: Regional keloid susceptibility. Br J Plast Surg 17:245, 1964 5. Nessen F, Spauven P, Schalkwyk J, et al: On the nature of hypertrophic scars and keloids: A review. Plast Reconstr Surg 104:1440, 1999 6. Abergel RP, Pizzurro D, Meeker CA, et al: Biochemical composition of the connective tissue in keloids and analysis of collagen metabolism in keloid fibroblast cultures. J Invest Dermatol 84:384, 1985 7. Kazeem AA: The immunological aspects of keloid tumor formation. J Surg Oncol 38:16, 1988 8. Ala-Kokko L, Rintala A, Savolainen ER: Collagen gene expression in keloids: Analysis of collagen metabolism and type I, III, IV, and V procollagen mRNAs in keloid tissue and keloid fibroblast cultures. J Invest Dermatol 89:238, 1987 9. Ehrlich HP, Desmouliere A, Diegelmann RF, et al: Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol 145:105, 1994 10. Kikuchi K, Kadono T, Takehara K: Effects of various growth factors and histamine on cultured keloid fibroblasts. Clin Lab Invest 190:4, 1995 11. Greenhalgh DG: The role of apoptosis in wound healing. Int J Biochem Cell Biol 30:1019, 1998 12. Meenakshi J, Jayaraman V, Ramakrishnan KM, et al: Keloids and hypertrophic scars: A review. Indian J Plast Surg 38:175, 2005 13. Kiil J: Keloids treated with topical injections of triamcinolone acetonide (kenalog). Immediate and long-term results. Scand J Plast Reconstr Surg 11:169, 1977 14. Shons AR, Press BH: The treatment of earlobe keloids by surgical excision and postoperative triamcinolone injection. Ann Plast Surg 10:480, 1983 15. Golladay ES: Treatment of keloids by single intraoperative perilesional injection of repository steroid. South Med J 81:736, 1988 16. Berman B, Bieley N: Adjunct therapies to surgical management of keloids. Dermatol Surg 22:126, 1996 17. Lee Y, Minn K-W, Baek R-M: A new surgical treatment of keloid: Keloid core excision. Ann Plast Surg 46:135, 2001
1296 18. Muti E, Ponzio E: Cryotherapy in the treatment of keloids. Ann Plast Surg 11:227, 1983 19. Sherman R, Rosenfeld H: Experience with the Nd:YAG laser in the treatment of keloid scars. Ann Plast Surg 21:231, 1988 20. Van den Brenk HAS, Minty CCJ: Radiation in the management of hypertrophic scars and keloids. Br J Surg 47:595, 1959 21. Edsmyr F, Larsson LG, Onyango J, et al: Radiation therapy in the treatment of keloids in East Africa. Acta Radiol Ther Phys Biol 13:102, 1974 22. Sallstrom KO, Larson O, Heden P, et al: Treatment of keloids with surgical excision and postoperative x-ray radiation. Scand J Plast Reconstr Surg Hand Surg 23:211, 1989 23. Sawadow Y, Soni K: Hydration and occlusive therapy for hypertrophic scars and keloids. Brit J Plast Surg 45:599, 1992 24. Carr-Collins J: Pressure techniques for the prevention of hypertrophic scar. Clin Plast Surg 19:733, 1992 25. Cheng JC, Evans JH, Leung KS, et al: Pressure therapy in the treatment of post-burn hypertrophic scar–A critical look into
HEAD AND NECK KELOID
26. 27. 28. 29. 30.
its usefulness and fallacies by pressure monitoring. Burns Incl Therm Inj 10:154, 1984 Gold MH: A controlled clinical trial of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids. J Am Acad Dermatol 30:506, 1994 Fulton J: Silicone gel sheeting for the prevention and management of evolving hypertrophic and keloid scars. Dermatol Surg 21:945, 1995 Berman B, Flores F: Comparison of a silicone gel-filled cushion and silicon gel sheeting for the treatment of hypertrophic or keloid scars. Dermatol Surg 25:484, 1999 Shamberger R, Tabbot T, Tripton H, et al: The effect of ultrasonic and thermal treatment on wounds. Plast Reconstr Surg 68:860, 1981 Granstein RD, Rook A, Flotte TJ, et al: A controlled trial of intralesional recombinant interferon-gamma in the treatment of keloidal scarring. Clinical and histologic findings. Arch Dermatol 126:1295, 1990
Head and Neck Keloid: Treatment by Core Excision and Delayed Intralesional Injection of Steroid Peter Donkor, BDS, MDSc, MSc, FRACDS, FWACS, FGCS* Purpose: This report aims to describe a technique used by the author for the management of head and
neck keloid. Patients and Methods: This is a clinical review of patients presenting with new and recurrent keloid of the head and neck to the Maxillofacial Surgery Unit at the Komfo Anokye Teaching Hospital, Kumasi, Ghana. The surgical technique involved the intralesional excision of the bulk of the keloid. Primary closure of the ensuring defect was achieved at operation. At the time of suture removal between 10 and 14 days postoperative, 40 mg triamcinolone was injected into the residual lesion. The injection was repeated on 2 more occasions at monthly intervals. All patients were followed up for at least 2 years. Results: Eighteen patients were successfully treated with no sign of recurrence in any of them. The main complication was hypo-pigmentation at the site of the original lesion. Conclusion: The technique was found to be effective for the treatment of moderately sized new and recurrent keloid scars of the head and neck and is therefore recommended. © 2007 American Association of Oral and Maxillofacial Surgeons J Oral Maxillofac Surg 65:1292-1296, 2007
Keloid and hypertrophic scars are unique to humans, and result from excessive production of fibrous tissue during the healing of wounds. Keloids can occur anywhere on the skin and have a tendency to run in families. They occur in all races but are 15 times more common in patients with darker skin. Incidence is approximately 10% in high risk groups. Onset may be delayed at least 3 months after injury with progression but no resolution. Areas most commonly involved are the shoulders, neck, anterior chest, upper arms, and face.1-5 Clinically, there are differences in the presentation of hypertrophic scars and keloids. Hypertrophic scars are raised erythematous lesions confined within the boundaries of the original wound. On the other hand, keloids frequently persist at the site of injury, often
*Consultant, Maxillofacial Surgery Unit, Department of Surgery, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Komfo Anokye Teaching Hospital, Kumasi, Ghana. Address correspondence and reprint requests to Prof Peter Donkor: Maxillofacial Unit, Department of Surgery, School of Medical Sciences, Kwame Nkrumah University of Science and Technology, Komfo Anokye Teaching Hospital, 1 Bantama High Street, Kumasi, Ghana, West Africa; e-mail: [email protected] © 2007 American Association of Oral and Maxillofacial Surgeons
0278-2391/07/6507-0005$32.00/0 doi:10.1016/j.joms.2006.10.049
recur after excision, and always overgrow the boundaries of the original wound. Both disorders are manifestations of a loss of the control mechanisms that regulate wound healing, which include clot formation, inflammation, cell migration and proliferation, synthesis and release of cytokines and extracellular matrix proteins, and remodeling of the newly synthesized matrix. This aberrant healing results in a disordered architecture and excessive deposition of matrix proteins that accounts for the clinical picture.6-12 Histologically, keloids are characterized by excessive accumulation of collagen. This is because of an exaggerated response of fibroblasts to transforming growth factor (TGF-) that regulates the expression and deposition of collagenous extracellular matrix. Fibroblasts isolated from the keloid have been found to have higher levels of TGF- receptors. Other growth factors that stimulate fibrosis and occur in increased quantities in keloids include platelet-derived growth factor, interleukin-1, and insulin-like growth factor. These growth factors further inhibit the production of proteases required to maintain the balance between the production and degradation of fibrous tissue.6-8 Mast cells and other vasoactive mediators known to stimulate growth of fibrous tissue are also known to be present in excess in keloid scars as compared with normal tissue.9,10 Keloid fibroblasts have been found to show resistance to apoptosis, a situation that predisposes to increased cellularity.11,12 Thus, the combined actions of these cytokines on
1292
1293
PETER DONKOR
stimulating excess collagen production, inhibiting its degradation, and interfering with the programmed cell death of fibroblasts in keloids contribute to overgrowth of scar. Several techniques for treating keloids have been developed and are aimed at inhibiting collagen synthesis and accelerating the removal of excess collagen. The limited success of any 1 technique has given rise to numerous treatment protocols with variable results. These include intralesional steroid injection, surgical excision, cryotherapy, laser therapy, irradiation, mechanical compression dressings, silicone applications, ultrasound and heat, intralesional interferon injection, or combinations of techniques. Intralesional steroids13 act by suppressing the inflammatory response, diminishing collagen synthesis, decreasing mucinous ground substance production, and inhibiting collagenase inhibitors that prevent the degradation of collagen.13 Among the adverse effects of steroids are atrophy of skin, hypopigmentation, telangiectasia, and cushingoid effects from systemic absorption. Surgical excision14-17 may be combined with skin grafting, but recurrences range from 45% to 100%. Surgery has been found to be most effective when combined with steroid, irradiation, or pressure therapy. Cryotherapy18 and laser therapy,19 which are forms of surgical therapy, cause microcirculatory disturbances leading to tissue damage, especially fibroblasts. These therapies are most effective when combined with other treatment modalities. Radiation for the treatment of keloid results in reduced rate of fibroblast and endothelial cell proliferation.12,20-22 The risk of malignant transformation and other side effects, as well as cost, restrict its widespread use. It may be used either alone or in combination with surgical excision. Mechanical compression dressings23,24 reduce oxygen tension in the wound through the occlusion of small vessels, leading to reductions in tissue metabolism, fibroblast proliferation, and collagen synthesis. Silicone gel sheets and silicone occlusive dressings25-28 worn 24 hours a day for up to 1 year have been used for treating keloids. The mode of action is by increasing the temperature of the scar, thus increasing collagenase activity. Ultrasound and heat probably act by increasing collagenase activity. This reduces the collagen content of the scar, thus softening it.29 Intralesional interferon30 is believed to cause shrinkage of keloids by reducing fibroblast synthesis of collagen, reducing mucinous ground substance production and decreasing collagenase activity. There has been limited success with many of the techniques used in the treatment of keloids at our
institution. Some of these techniques include intralesional steroid injection, extralesional excision, extralesional excision with immediate skin grafting, extralesional excision and immediate postoperative steroid injection, massage, application of silicone sheets, and occlusive dressings. There is no experience with the use of irradiation, cryotherapy, and laser therapy for the treatment of keloids at our hospital. This report is based on the author’s experience with a technique that combines intralesional surgical excision with delayed intralesional injection of steroids in the management of keloids of the head and neck.
Patients and Methods This is a clinical review of a technique used by the author for the treatment of keloid scars of the head and neck in patients attending the maxillofacial clinic at the Komfo Anokye Teaching Hospital, Kumasi, Ghana since 1999. Some of the patients had recurrent lesions after undergoing previous treatment for keloids, including surgical excision and skin grafting, scar massage, silicone sheets and occlusive dressings, and intralesional steroid injections. Others had not had any prior treatment for their keloid.
Surgical Technique The procedure was carried out using either general or local anesthesia. Following skin preparation, the bulk of the central portion of the keloid was excised leaving a thin rim of keloid. The edges of the wound were then undermined to permit advancement. After hemostasis, the wound was closed primarily, sometimes under tension. Suture removal was performed at 10 to 14 days postoperation, after which the skin was cleaned with antiseptic and 40 mg triamcinolone injected into the residual lesion. The injection was repeated at 4-week intervals on 2 additional occasions, for a total of 3 injections. All patients were first
Table 1. DISTRIBUTION OF HEAD AND NECK KELOIDS
Location of Keloid
Number
Ear lobe Preauricular area Upper lip Lower lip Submandibular area Back of neck All sites
8 1 3 2 2 2 18
Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
1294
HEAD AND NECK KELOID
Discussion The technique described in this report is similar in principle to other surgical approaches that combine with postoperative steroid injections.14,15 There are, however, some differences. The excision of a keloid is intralesional and not extralesional. It deliberately aims to leave a thin rim of keloid on the wound edges. This modification avoids the risk of inducing an intense inflammatory response in the surrounding, unaffected “keloid-prone” skin, which could lead to the formation of new and possibly bigger keloid. In contrast to the report by Lee et al,17 it was observed in our series that intralesional excision of keloid without adjuvant steroid therapy resulted in overgrowth of the residual scar if the injections were started later than 3 weeks after surgery.
FIGURE 1. A, Ear lobe keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
reviewed at 6 months from the time of the last steroid injection and followed up for at least 2 years.
Results Thus far, 18 patients have been treated using this technique. They comprised an equal number of males and females. The keloid scars were distributed around the face including the ear lobe, preauricular area, upper lip, lower lip, back of neck, and submandibular area (Table 1). The largest scar was located at the back of the neck and had a widest dimension of 6 cm. In seventeen (94%) patients, the scars remained soft and flat with no sign of recurrence. Examples are presented in Figures 1, 2, and 3. However, all the scars remained hypopigmented. In 1 patient there was dehiscence of the wound on the third postoperative day that was successfully resutured. This patient, however, was lost to follow-up and did not complete treatment.
FIGURE 2. A, Neck keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
1295
PETER DONKOR
Experience with this technique has so far been limited to its use in the head and neck region. A major limitation lies in the need to achieve primary closure following excision of the keloid. This would not be possible where an extensive body surface area was affected. It is therefore recommended for use in small to moderately sized lesions that will permit primary closure of the wound after excision. This technique of surgical excision of small to moderately sized keloid scars of the face followed by delayed injection of steroid was found to be effective and is therefore recommended. Combining surgical debulking with delayed intralesional steroid ensures uninterrupted initial wound healing and a faster resolution of the keloid than if either treatment modality was used alone. Acknowledgment The author is grateful to Lucy Amoateng, Victoria Narh, Felicia Sarpong, Dr Bertha Gyau, and Dr Alex Oti Acheampong for their assistance.
References
FIGURE 3. A, Preauricular keloid before treatment. B, After treatment. Peter Donkor. Head and Neck Keloid. J Oral Maxillofac Surg 2007.
While success with surgical techniques that combine with the injection of steroid immediately after excision of keloid have been reported, it has been our observation that this causes delayed wound healing. In the technique described in this report, the injection of steroid was delayed until the time of suture removal. This avoids any interference with initial wound healing. The technique is superior to intralesional steroid as a sole therapy in that by debulking the lesion, tissue resistance was less and subsequent injections were much easier. Furthermore, fewer injections were required for resolution of the keloid, and therefore the potential for any undesirable side effects of the steroid was reduced. The time required for the resolution of the keloid was also shortened. Another advantage of this technique is that it was successfully used for the treatment of previously untreated keloid, as well as recurrent keloid where other therapies had failed.
1. Alhady SM, Sivanantharajah K: Keloids in various races. A review of 175 cases. Plast Reconstr Surg 44:564, 1969 2. Ramakrishnan KM, Thomas KP, Sundararajan CR: Study of 1,000 patients with keloids in South India. Plast Reconstr Surg 53:276, 1974 3. Datubo-Brown DD: Keloids: A review of the literature. Br J Plast Surg 43:70, 1990 4. Crockett DJ: Regional keloid susceptibility. Br J Plast Surg 17:245, 1964 5. Nessen F, Spauven P, Schalkwyk J, et al: On the nature of hypertrophic scars and keloids: A review. Plast Reconstr Surg 104:1440, 1999 6. Abergel RP, Pizzurro D, Meeker CA, et al: Biochemical composition of the connective tissue in keloids and analysis of collagen metabolism in keloid fibroblast cultures. J Invest Dermatol 84:384, 1985 7. Kazeem AA: The immunological aspects of keloid tumor formation. J Surg Oncol 38:16, 1988 8. Ala-Kokko L, Rintala A, Savolainen ER: Collagen gene expression in keloids: Analysis of collagen metabolism and type I, III, IV, and V procollagen mRNAs in keloid tissue and keloid fibroblast cultures. J Invest Dermatol 89:238, 1987 9. Ehrlich HP, Desmouliere A, Diegelmann RF, et al: Morphological and immunochemical differences between keloid and hypertrophic scar. Am J Pathol 145:105, 1994 10. Kikuchi K, Kadono T, Takehara K: Effects of various growth factors and histamine on cultured keloid fibroblasts. Clin Lab Invest 190:4, 1995 11. Greenhalgh DG: The role of apoptosis in wound healing. Int J Biochem Cell Biol 30:1019, 1998 12. Meenakshi J, Jayaraman V, Ramakrishnan KM, et al: Keloids and hypertrophic scars: A review. Indian J Plast Surg 38:175, 2005 13. Kiil J: Keloids treated with topical injections of triamcinolone acetonide (kenalog). Immediate and long-term results. Scand J Plast Reconstr Surg 11:169, 1977 14. Shons AR, Press BH: The treatment of earlobe keloids by surgical excision and postoperative triamcinolone injection. Ann Plast Surg 10:480, 1983 15. Golladay ES: Treatment of keloids by single intraoperative perilesional injection of repository steroid. South Med J 81:736, 1988 16. Berman B, Bieley N: Adjunct therapies to surgical management of keloids. Dermatol Surg 22:126, 1996 17. Lee Y, Minn K-W, Baek R-M: A new surgical treatment of keloid: Keloid core excision. Ann Plast Surg 46:135, 2001
1296 18. Muti E, Ponzio E: Cryotherapy in the treatment of keloids. Ann Plast Surg 11:227, 1983 19. Sherman R, Rosenfeld H: Experience with the Nd:YAG laser in the treatment of keloid scars. Ann Plast Surg 21:231, 1988 20. Van den Brenk HAS, Minty CCJ: Radiation in the management of hypertrophic scars and keloids. Br J Surg 47:595, 1959 21. Edsmyr F, Larsson LG, Onyango J, et al: Radiation therapy in the treatment of keloids in East Africa. Acta Radiol Ther Phys Biol 13:102, 1974 22. Sallstrom KO, Larson O, Heden P, et al: Treatment of keloids with surgical excision and postoperative x-ray radiation. Scand J Plast Reconstr Surg Hand Surg 23:211, 1989 23. Sawadow Y, Soni K: Hydration and occlusive therapy for hypertrophic scars and keloids. Brit J Plast Surg 45:599, 1992 24. Carr-Collins J: Pressure techniques for the prevention of hypertrophic scar. Clin Plast Surg 19:733, 1992 25. Cheng JC, Evans JH, Leung KS, et al: Pressure therapy in the treatment of post-burn hypertrophic scar–A critical look into
HEAD AND NECK KELOID
26. 27. 28. 29. 30.
its usefulness and fallacies by pressure monitoring. Burns Incl Therm Inj 10:154, 1984 Gold MH: A controlled clinical trial of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids. J Am Acad Dermatol 30:506, 1994 Fulton J: Silicone gel sheeting for the prevention and management of evolving hypertrophic and keloid scars. Dermatol Surg 21:945, 1995 Berman B, Flores F: Comparison of a silicone gel-filled cushion and silicon gel sheeting for the treatment of hypertrophic or keloid scars. Dermatol Surg 25:484, 1999 Shamberger R, Tabbot T, Tripton H, et al: The effect of ultrasonic and thermal treatment on wounds. Plast Reconstr Surg 68:860, 1981 Granstein RD, Rook A, Flotte TJ, et al: A controlled trial of intralesional recombinant interferon-gamma in the treatment of keloidal scarring. Clinical and histologic findings. Arch Dermatol 126:1295, 1990