22 120 Practical Plastic Surgery Suggested Reading 1. Chang P, Laubenthal KN, Lewis IInd RW et al. Prospective, randomized study of the efficacy of pressure garment therapy in patients with burns. J Burn Care Rehabil 1995; 16:473. 2. Gold MH. A controlled clinical trial of topical silicone gel sheeting in the treatment of hypertrophic scars and keloids. J Am Acad Dermatol 1994; 30:506. 3. Mustoe TA, Cooter RD, Gold MH et al. International clinical recommendations on scar management. Plast Reconstr Surg 2002; 110:560. 4. Poston J. The use of silicone gel sheeting in the management of hypertrophic and keloid scars. J Wound Care 2000; 9:10. 5. Rockwell WB, Cohen IK, Ehrlich HP. Keloids and hypertrophic scars: A comprehen- sive review. Plast Reconstr Surg 1989; 84:827. 6. Tang YW. Intra- and postoperative steroid injections for keloids and hypertrophic scars. Br J Plast Surg 1992; 45:371 Chapter 23 Practical Plastic Surgery, edited by Zol B. Kryger and Mark Sisco. ©2007 Landes Bioscience. Benign Skin Lesions Zol B. Kryger Introduction Although this chapter deals with benign skin lesions, a number of these condi- tions are premalignant and must be regularly evaluated and biopsied if they be- come suspicious. The benign lesions and disorders of the skin are tremendously diverse and extensive. This chapter focuses on the common lesions encountered by the plastic surgeon. Since many patients arrive with the question, “is this can- cer?” an attempt has been made to classify every lesion as benign or premalignant. Some common terminology used in describing disorders of the skin is listed in Table 23.1. Lesions of the Epidermis Seborrheic keratosis is a common lesion, particularly in the elderly on sun-exposed areas. Multiple lesions are usually present. It demonstrates variable pig- mentation and its borders have a sharp, “pasted on” appearance, allowing it to be scraped off with a scalpel. Clinically, it may be confused with melanoma; pathologi- cally, it appears similar to squamous cell carcinoma. It is benign and has no malig- nant potential, so shave excision or freezing is adequate. Actinic (solar) keratosis is a dysplastic, premalignant lesion. Like the sebor- rheic keratosis, multiple lesions may present in sun-exposed areas. It appears as a scaling, poorly demarcated plaque. Suspicious sites should undergo excisional bi- opsy. Multiple solar keratoses may be treated with topical 5-fluorouracil. Keratoacanthoma is a rapidly growing papule with a round, smooth, pink rim encircling a keratinous plug. It is premalignant, and some consider it to be a variant of squamous cell carcinoma. Diagnosis is made by excisional biopsy; treatment con- sists of wide local excision or injection with 5-fluorouracil. Occasionally, these le- sions regress spontaneously. Epithelial Cysts Epithelial cysts, previously termed sebaceous cysts, are epithelium-lined cysts filled with a keratinous and lipid core. They are benign and have several forms: Dermoid cysts are congenital cysts that usually occur along the midline or at the lateral end of the eyebrow. They represent developmental inclusion of the embry- onic epidermis. Like the teratoma, their core may contain material from all three germinal cell layers (e.g., glandular material, hair follicle, cartilage, bone). Patients with midline lesions of the face should undergo computed tomography to check for intracranial extension. Treatment consists of excision. Epidermoid cysts are firm, fluctuant nodules, often with a central comedo that represents an epithelial opening. They are variable in size. They contain a cheesy, 23 122 Practical Plastic Surgery lipid rich material and have a tendency to become infected. Treatment consists of excision during which the entire lining must be removed to avoid recurrence. Mildly infected cysts should be treated with antibiotics for one week prior to excision. Se- verely infected cysts should undergo incision and drainage. The pilar cyst, or trichilemmal cyst, is the epidermoid cyst equivalent on the scalp. Multiple epidermoid cysts can be seen in Gardner’s syndrome (familial poly- posis). Moles The nevocellular nevus (common mole) is a benign congenital lesion derived from the melanocyte that occurs in clusters or nests. The junctional nevus, com- monly seen in children and younger adults, consists of cells confined to the epidermal-dermal junction. It is a smooth and flat nevus with irregular pigmenta- tion. The compound nevus has cells in both the epidermal-dermal junction and the dermis. It is usually raised and represents a progression from the junctional nevus. The intradermal nevus contains cells in clusters that are confined to the dermis. The Juvenile melanoma (Spitz nevus). usually occurs in children as a pale red papule on the face. Despite its name, it is a benign lesion. It is treated by excision with margins due to the risk of recurrence. The atypical mole, formery referred to as dysplastic nevus, is premalignant. It is unevenly pigmented and has irregular borders. The lesion is usually solitary and is clinically indistinguishable from melanoma. Atypical moles should be biopsied. The familial form, B-K mole syndrome, presents with hundreds of atypical moles and confers a 100% risk of malignant transformation. Patients must have an annual photographic examination of their entire bodies. Any lesions that change must be excised. The nevus of Ota is benign blue-grey macule that is found on the face in the V1 or V2 distribution of the trigeminal nerve. It is usually congenital and has a female predisposition. It is treated with laser therapy. Table 23.1. Terminology of various skin lesions and disorders Term Definition Size Papule A palpable elevated skin lesion < 1 cm Plaque A larger palpable elevated skin lesion > 1 cm Macule A flat, colored, nonpalpable lesion < 1 cm Patch A larger flat, colored, nonpalpable lesion > 1 cm Vesicle A fluid-filled blister < 0.5 cm Bulla A larger fluid-filled blister > 0.5 cm Hyperkeratosis Increased thickness of the stratum corneum variable Parakeratosis Hyperkeratosis with retained keratinocyte nuclei variable Acanthosis Thickening of the epidermis variable Hypertrophic scar Raised scar that is confined to the borders variable of the wound or incision Keloid Raised scar that extends beyond the borders variable of the wound or incision 23 123 Benign Skin Lesions The blue nevus is similar to an intradermal nevus in that it is composed of intradermal melanocytes. It presents as a well-defined papule that can be distin- guished from venous lesions by the fact that it does not blanch. Distinguishing it from Kaposi’s sarcoma or melanoma can be difficult. It has a very small risk of malignant degeneration. It is treated by excision. The freckle is a pigmented lesion that represents excessive melanin granule pro- duction without an increase in the number of melanocytes. Freckles are benign and have no malignant potential. Lesions of the Epidermal Appendages This group of miscellaneous benign lesions includes those derived from hair follicles and sebaceous, apocrine and eccrine glands. Most of the lesions requiring treatment occur in the scalp and face. They are summarized in Table 23.2. Lesions of the Dermis and Subcutaneous Fat A number of benign tumors occur in the dermis and subcutaneous tissue. Their behavior may range from completely benign to recurrent and locally aggressive. Lipomas are fatty tumors of the subcutaneous fat. They are soft, mobile and usually painless. They can range in size from one to tens of centimeters. Larger lipomas are more likely to recur; they are often classified as low-grade liposarcomas. Small lipomas do not need to be biopsied. Patients with very large lipomas should undergo MRI to determine whether local invasion has occurred. Treatment consists of total excision as lipomas may recur if not completely removed. Dermatofibromas are encapsulated intradermal masses that are painless, firm and mobile. They usually are less than 2 cm and occur on the extremities. Due to their accumulation of hemosiderin, they can display the range of colors seen in an evolving bruise. Treatment consists of excision, mostly for cosmetic purposes. They may recur if incompletely excised. The dermatofibrosarcoma protuberans is a locally aggressive, indolent, nodu- lar intradermal mass. It occurs on the trunk and thighs. They are often painful and can be complicated by ulceration or superinfection. The overlying epidermis may appear waxy. Dermatofibrosarcoma protuberans tends to grow extensions into the surrounding dermis and fascia, creating a gross “cartwheel” appearance. Treatment consists of wide excision to encompass the extensions of the tumor. Metastasis has been described in neglected or incompletely excised lesions. Angiofibromas present as small, erythematous, telangiectatic papules, usually located on the cheeks, nose or around the lips. They are benign when solitary. Superficial excision is the standard treatment. When multiple, these papules may be associated with tuberous sclerosis (seizures, mental retardation, renal angiomyolipoma). Dermabrasion can offer some cosmetic improvement for pa- tients with multiple angiofibromas. Skin tags, also termed cutaneous papillomas, are soft and often pedunculated, arising from a central stalk. They may become infected or may necrose. Treatment consists of amputation at the stalk and electrodissection of the remaining base. They are benign and do not recur. Glomus tumors present as a painful, firm, blue nodules on the hands and feet, especially subungually. They are benign vascular hamartomas derived from the glo- mus body. Excision is often required due to the pain caused by pressure from these tumors. 23 124 Practical Plastic Surgery Table 23.2. Lesions of the epidermal appendages Lesion Tissue of Origin Clinical Appearance Location Treatment Apocrine cystadenoma Apocrine gland Translucent dome shaped papule Face Excision Chondroid syringoma Apocrine gland Firm, fixed painless nodule Face Excision Syringoma Eccrine gland Clear papule occuring in adults Periocular Laser, cautery or cryotherapy Eccrine poroma Eccrine gland Soft red nodule at any age Foot Excision Cylindroma Eccrine gland Smooth pink papule or plaque Scalp, forehead Excision Nevus sebaceus Sebaceous gland Linear yellowish plaque, onset at birth Forehead Excision Sebaceous adenoma Sebaceous gland Yellow nodule in adults Head, neck Excision Sebaceous hyperplasia Sebaceous gland Ulcerated yellow-white papules Face Laser, cautery or cryotherapy Pilomatricoma Hair follicle Firm nodule stretching the skin Face, neck, arms Excision Trichoepithelioma Hair follicle Pink, shiny papules or a plaque Face Excision Trichofolliculoma Hair follicle Skin colored papule with central hair Face, scalp Excision 23 125 Benign Skin Lesions Pearls and Pitfalls Although most of the lesions described in this chapter are benign, many are difficult to clinically distinguish from malignant tumors of the skin. Furthermore, some of the lesions, such as atypical moles, may remain unchanged for years be- fore undergoing dysplastic changes. Even the most experienced surgeon has been fooled on occasion by a lesion he was sure could not be malignant. These facts emphasize the importance of excisional biopsy of any suspicious skin lesion. Skin incisions should adhere to the principles of relaxed skin tension lines in the neck and face, and should be longitudinal in the extremities. The excision should be as complete as possible; any part of the lesion that appears to have been left behind should also be excised. All excisional biopsies should be sent to a pathologist. When applicable, specimens should be oriented with a marking stitch. Finally, it is the obligation of the surgeon to follow up on the pathology report and notify the patient of the results. Suggested Reading 1. Demis DJ, ed. Clinical Dermatology. 22nd ed. Philadelphia: Lippincott-Raven, 1995. 2. Kumer et al, eds. Robbins Basic Pathology. 6th ed. Philadelphia: WB Saunders, 1997. 3. Zarem HA, Lowe NJ. Benign growths and generalized skin disorders. In: Grabb and Smith’s Plastic Surgery. 5th ed. Philadelphia: Lippincott-Raven, 1997:141. 4. Slade J et al. Atypical mole syndrome: Risk factors for cutaneous malignant melanoma and implications for management. J Am Acad Dermatol 1995; 32:479. Chapter 24 Practical Plastic Surgery, edited by Zol B. Kryger and Mark Sisco. ©2007 Landes Bioscience. Basal Cell and Squamous Cell Carcinoma Darrin M. Hubert and Benjamin Chang Overview Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) comprise the vast majority of nonmelanoma skin cancers. Over one million white Americans are affected by these two entities yearly. They predominantly affect fair-skinned indi- viduals, and their incidence is rising rapidly. Etiology may be multifactorial, but sun exposure appears to play a critical role. When detected early, their prognosis is gen- erally excellent. However, both are malignant cutaneous lesions with inherent meta- static potential. Thus appropriate diagnosis, treatment and surveillance are of utmost importance. Malignant melanoma was discussed in the previous chapter. Premalignant Lesions The most common precursor of cutaneous squamous cell carcinoma is the ac- tinic keratosis, also known as the solar keratosis. It appears as a scaly, discrete, maculopapular lesion that arises primarily on sun-damaged skin. Palpation of these flat lesions may reveal roughness that is not apparent on visual inspection. Due to the potential for progression to SCC, actinic keratoses are commonly treated by curettage and electrodessication, liquid nitrogen or topical 5-FU (Efudex). Bowen’s disease is a type of squamous cell carcinoma-in-situ marked by a soli- tary, sharply demarcated, erythematous, scaly plaque of the skin or mucous mem- branes. A second form of squamous cell carcinoma-in-situ is erythroplasia of Queyrat, which appears as glistening red plaques on the uncircumcised penis. Both have the potential for progression to invasive carcinoma and should be resected completely with conservative surgery. Leukoplakia is a condition found on the oral mucosa commonly in association with smokeless tobacco use. These white patches may undergo malignant transforma- tion to SCC in 15% to 20% of cases if left untreated. Epidermodysplasia verruciformis is a rare autosomal recessive disorder in which the body is unable to control human papilloma viral infections. It manifests itself as flat wart-like lesions that frequently degenerate into SCC. A keratoacanthoma, on the other hand, grows rapidly to form a nodular, elevated lesion with a hyperkeratotic core. It may involute spontaneously or appear indistinguishable from a SCC, and early conservative excision is recommended. Tumor Staging All nonmelanoma skin cancers are staged by the TNM system established by the American Joint Committee on Cancer (AJCC). The staging system is shown in Table 24.1. Characteristics of the primary tumor (T), regional lymph node status (N) and distant metastasis (M) are considered. BCC rarely metastasizes, although it may be locally destructive. The malignant potential of SCC is real and is related to the size and location of the tumor, as well as the degree of anaplasia. 24 127 Basal Cell and Squamous Cell Carcinoma Basal Cell Carcinoma BCC is the most common skin cancer and, indeed, the most common malignancy in the United States and Australia. It outnumbers cutaneous squamous cell carcinoma by approximately four to one. Its origin lies in the basal layer of the epithelium or the external root sheath of the hair follicle. Classic teaching holds that BCC requires stro- mal participation for survival, not the malignant transformation of preexisting mature epithelial structures seen in SCC. Although its metastatic potential is very low, basal cell carcinomas exhibit oncogene and tumor suppressor gene characteristics that ques- tion this classic explanation. Basal cell carcinoma tends to follow the path of least resistance, spreading into adjacent tissues. It only rarely metastasizes to distant sites. Classification Multiple histologic classifications have been proposed for subtypes of BCC, how- ever, only the most common are mentioned here. Nodular BCC is the most common (45-60%), found typically as single translucent papules on the face. It is firm, may ulcerate, and often exhibits telangiectasia. Superficial BCC (15-35%) occurs as mul- tiple scaly lesions on the trunk. Lightly pigmented or erythematous, it may resemble psoriasis or eczema. The less common subtypes are usually more aggressive. These include infiltrative BCC (10-20%), morpheic BCC (9%), which is associated with the highest recurrence rate, micronodular BCC (15%) and adenoid BCC (precise incidence unknown). Table 24.1. Staging of nonmelanoma skin cancers according to the TNM system established by the American Joint Committee on Cancer (AJCC) Primary Tumor (T) TX Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1 Tumor 2 cm or less in greatest dimension T2 Tumor more than 2 cm, but not more than 5 cm in greatest dimension T3 Tumor more than 5 cm in greatest dimension T4 Tumor invades deep extradermal structures (e.g., cartilage, muscle or bone) Regional Lymph Nodes (N) NX Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1 Regional lymph node metastasis Distant Metastasis (M) MX Distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasis Staging System Stage 0 Tis N0 M0 Stage I T1 N0 M0 Stage II T2 N0 M0 T3 N0 M0 Stage III T4 N0 M0 Any T N1 M0 Stage IV Any T Any N M1 24 128 Practical Plastic Surgery Risk Factors Exposure to ultraviolet radiation appears to play a major role in the development of BCC. A thorough history during the preoperative evaluation should investigate this, making special mention of any significant sunburns during childhood or ado- lescence. Other risk factors include exposure to radiation or chemical carcinogens such as arsenic, Fitzpatrick skin type 1 or 2 (fair skin), increasing age, male sex, xeroderma pigmentosum, albinism and immunosuppression. Patients with basal cell nevus syndrome may develop multiple basal cell carcinomas. This syndrome, known eponymously as Goltz-Gorlin syndrome, is characterized by odontogenic keratocysts, palmar or plantar pits, cleft lip or palate, rib anomalies and areas of ectopic calcification. Nevus sebaceous lesions also predispose to BCC. As hairless yellow plaques present at birth, these lesions are typically found in the head and neck region. They may undergo malignant transformation in 10% of cases. Special mention should be made of the importance of the “H-zone” of the face. This designation, roughly in the shape of an “H,” is defined by the preauricular regions and ear helices, nasolabial folds, columella and nose and lower eyelids. BCC lesions located in this area are associated with both a higher risk of recurrence and greater morbidity as a consequence of treatment. Treatment There are several modalities available for the treatment of BCC. For a given lesion, one must weigh the treatment in terms of effectiveness in eliminating the malignancy against the functional and cosmetic implications before choosing the appropriate route. First, surgical excision involves the full-thickness removal of the lesion, down to subcutaneous fat, along with a rim of “normal” tissue. Current literature recom- mends margins of 3 mm for small (<10 mm) and 5 mm for larger (10-20 mm) BCC of the face. For lesions found in any other location, margins of 5 mm are recom- mended. These wounds are typically either closed primarily or allowed to heal by secondary intention. For lesions located in delicate areas of the face, such as the eyelids, where removal of a margin of normal tissue may have profound functional consequences, Mohs micrographic surgery may be indicated. This technique has demonstrated the highest cure rates of any treatment modality. Cure rates of 99% for primary BCC and 93-98% for recurrent BCC have been demonstrated with the use of Mohs surgery. The technique of Mohs surgery is discussed in detail below. An additional accepted treatment is cryotherapy, which is typically followed by curettage and healing by secondary intention. Local anesthesia is used, and the lesion is rapidly frozen with liquid nitrogen. There is no histological control with this method, and the tissue typically becomes initially very edematous. Its use has been advocated particularly near underlying cartilage. Recurrence rates of 3.7-7.5% have been reported. Curettage and electrodessication have been employed in the past, with recur- rence rates of 3.3% for low risk lesions to 18.8% for high risk ones. Due to unac- ceptably high recurrence rates, poor cosmetic outcome and lack of histological control, it is generally not accepted as a first line therapy for BCC. Radiation therapy has also been used to treat BCC, but the risk of radiation dermatitis, increased risk for future skin malignancy, and lack of histological control have discouraged its current use. Squamous Cell Carcinoma Risk Factors Similar to BCC, cutaneous SCC typically occurs in areas of skin receiving the greatest sun exposure. The etiology appears to be the result of UVB radiation 24 129 Basal Cell and Squamous Cell Carcinoma (wavelength range of 290-320 nm), which produces thymidine dimers in the DNA of the p53 tumor-suppressor gene. Fair-skinned individuals, albinos and those with xeroderma pigmentosum seem to be at particularly increased risk. Other risk factors include infection with human papillomavirus, chronic immunosuppres- sion such as that seen in the organ-transplant population, exposure to chemical carcinogens such as arsenic, and exposure to ionizing radiation. Chronically in- flamed or damaged skin may predispose to carcinoma as well, termed Marjolin’s ulcer. These are most commonly squamous cell carcinomas, and they can arise in long-standing, chronic wounds such as pressure sores, fistulae, venous ulcers, lymphedema and burn scars. Recurrence and Metastasis The metastatic potential of SCC is greater than that of BCC, and the relative risk of recurrence and metastasis can be assessed according to characteristics of the lesion. The most important predictor is size of the tumor, with lesions greater than 2 cm in diam- eter recurring at a rate of 15% and resulting in metastasis at a rate of 30%. Anatomic location predicts greater malignant potential, especially the lip and ear, but also the scalp, forehead, eyelid, nose, dorsum of the hands, penis and perineum. Other features associated with higher risk of recurrence and metastases are rapid tumor growth, host immunosuppression, prior local recurrence, depth of invasion greater than 4 mm or into the subcutaneous tissues and location in a Marjolin’s ulcer. Perineural invasion denotes a particularly poor prognosis and is lethal in a majority of patients by five years. Treatment With the exception of cryotherapy, treatment options for SCC are similar to those for BCC. However, there have been no randomized controlled trials compar- ing the efficacy of the various techniques. Direct surgical excision has demonstrated a recurrence rate of approximately 8% and metastatic rate of 5% at five years. Some authors have advocated surgical margins of 4 mm for low risk lesions and 6 mm for high-risk lesions whenever feasible. Mohs surgery has demonstrated the highest cure rates, about 97% for primary SCC, and is especially recommended for high-risk lesions. Due to lack of histological control and unacceptable cure rates, curettage with cautery, cryosurgery and radiotherapy are not recommended. Mohs Surgery Mohs micrographic surgery (MMS) was developed by Dr. Frederic Mohs in the 1930s. Dermatologists with specialized fellowship training in Mohs surgery typi- cally perform the technique today. Fresh-tissue horizontal frozen sections are the hallmark of the procedure. Another salient feature is that the surgeon who performs the excision also interprets the histological results. The process can be summarized briefly in the following steps: 1. Gross debulking of the tumor 2. Excision of a narrow (2-3 mm rim) of normal tissue, beveled at 45˚ at the edges 3. Color-coding of specimen to mark margins and orientation 4. Mapping of the specimen and division into sections 5. Frozen-section processing in on-site laboratory 6. Microscopic examination 7. Repeat cycle if any residual tumor is noted 8. Healing by secondary intention, primary closure, skin graft or flap closure [...]... Am 1990; 23( 5):88 9-9 7 2 Gallico IIIrd GG Biologic skin substitutes Clin Plast Surg 1990; 17 (3) :51 9-2 6 3 Jones I, Currie L, Martin R A guide to biological skin substitutes Br J Plast Surg 2002; 55 (3) :18 5-9 3 4 Hauben DJ, Baruchin A, Mahler D On the history of the free skin graft Ann Plast Surg 1982; 9 (3) :24 2-5 5 Petruzzelli GJ, Johnson JT Skin grafts Otolaryngol Clin North Am 1994; 27(1):2 5 -3 7 6 Place... in plastic surgery (Skin grafting) Grabb and Smith’s Plastic Surgery 5th ed Philadelphia: Lippincott-Raven, 1997:1 7-9 7 Ratner D Skin grafting From here to there Dermatol Clin 1998; 16(1):7 5-9 0 8 Thornton JF Skin grafts and skin substitutes Selected Readings in Plastic Surgery 2004; 10(1): 1-2 4 27 Chapter 28 Burns: Initial Management and Resuscitation Baubak Safa and Mark Sisco Epidemiology Of the 2 -3 ... Primary Tumor T1 ≤ 1 mm T2 1-2 mm T3 2-4 mm T4 > 4 mm -a: no ulceration or level II/III; -b: ulceration or level IV/V N = Regional Lymph Node Status N0 No nodal involvement N1a One microscopic positive node; N1b: one macroscopic positive node N2a 2 -3 microscopic positive nodes; N2b: 2 -3 macroscopic positive nodes N3 >4 nodes, matted nodes, or nodal involvement as well as in-transit mets M = Distant Metastases... regenerate sufficiently, aesthetically and functionally to cover an open wound Examples include full-thickness or deep partial-thickness burns as well as large exposed surfaces from surgical or traumatic Practical Plastic Surgery, edited by Zol B Kryger and Mark Sisco ©2007 Landes Bioscience 146 Practical Plastic Surgery extirpations Skin grafts and skin substitutes are commonly used to provide coverage over... TBSA of a burn victim Partial-Thickness Burns (Second Degree) Partial-thickness burns may involve a wide spectrum of dermal injury and present a diagnostic dilemma Superficial partial-thickness burns involving the uppermost layers of the dermis may only be slightly more serious than a superficial burn A deep partial-thickness burn, however, may behave in a similar fashion to a full-thickness burn and... low-grade consumptive coagulopathy but are not a cause of the Kasabach-Merritt syndrome Although it is classically stated that 50% involute by age 5, true involution likely is complete before this Most of the changes that occur 140 Practical Plastic Surgery Table 26.2 Syndromes associated with vascular lesions Syndrome PHACES Sturge-Weber syndrome Klippel-Trenaunay syndrome Parkes Weber syndrome Blue-rubber... the skin All full-thickness burns need surgical excision and skin grafting Burn Triage The American Burn Association has defined the criteria used in triaging burns to be admitted and treated in a specialized burn unit: • Partial- and full-thickness burns >10% TBSA in patients under 10 or over 50 years of age • Partial- and full-thickness burns > 20% TBSA in other age groups 28 • Full-thickness burns... biopsy with a 1-2 mm rim of normal skin in an elliptical shape If the lesion is large (over 1.5 cm), or in a location where skin removal is critical, an incisional biopsy 133 Melanoma Table 25.1 Guidelines for surgical margins during excision of malignant melanomas Type of Lesion Dysplastic nevus Lentigo maligna/melanoma in situ Melanoma 0-1 mm thick Melanoma 1-2 mm thick Melanoma 2-4 mm thick Melanoma... treatment For patients with metastases, surgery is palliative and systemic therapy is the mainstay of treatment 135 Melanoma Table 25.2 A simplified version of the TNM classification and staging scheme for malignant melanoma according to the American Joint Committee on Cancer (AJCC) Stage Stage I Stage II Stage III Sage IV Definition T 1-2 N0 M0* T 3- 4 N0 M0 Any T with N 1 -3 M0 Any T with any N M1 T = Thickness... Apligraf 27 152 Practical Plastic Surgery Table 27.1 Continued Product Integra Indications for Use For treatment of life-threatening, full-thickness or deep partialthickness skin burns where sufficient autograft is not available at the time of excision or not desirable due to the physiologic condition of the patient Epicel (cultured epitheilial autografts) For treatment of deep dermal or full-thickness . Definition Stage I T 1-2 N0 M0* Stage II T 3- 4 N0 M0 Stage III Any T with N 1 -3 M0 Sage IV Any T with any N M1 T = Thickness of the Primary Tumor T1 ≤ 1 mm T2 1-2 mm T3 2-4 mm T4 > 4 mm -a: no ulceration. cm Melanoma 0-1 mm thick 1 cm Melanoma 1-2 mm thick 1-2 cm (2 cm preferable; 1 cm in aesthetically important areas) Melanoma 2-4 mm thick 2 cm Melanoma >4 mm thick 2 cm 25 134 Practical Plastic Surgery ity. range of 29 0 -3 20 nm), which produces thymidine dimers in the DNA of the p 53 tumor-suppressor gene. Fair-skinned individuals, albinos and those with xeroderma pigmentosum seem to be at particularly