You are in: eMedicine Specialties > Plastic Surgery > SKIN Skin, Benign Skin LesionsArticle Last Updated: Feb 17, 2006AUTHOR AND EDITOR INFORMATIONSection 1 of 7
  Author: Todd A Morton, MD, FACS, Consulting Staff, Department of Plastic Surgery, Kaiser Permanente Todd A Morton is a member of the following medical societies: American College of Surgeons Coauthor(s): Wayne Stadelmann, MD, Stadelmann Plastic Surgery, PC Editors: Shahin Javaheri, MD, Chief, Department of Plastic Surgery, Martinez Veterans Affairs Outpatient Clinic; Consulting Staff, Advanced Aesthetic Plastic & Reconstructive Surgery; Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; Jorge I de la Torre, MD, FACS, Professor of Surgery and Physical Medicine and Rehabilitation, Residency Program Director, Division of Plastic Surgery, University of Alabama at Birmingham; Director, Center for Advanced Surgical Aesthetics; Nicolas (Nick) G Slenkovich, MD, Practice Director, Colorado Plastic Surgery Center at Swedish Medical Center; Susan E Downey, MD, Clinical Associate Professor, Department of Surgery, Division of Plastic Surgery, University of Southern California Author and Editor Disclosure Synonyms and related keywords: benign skin lesions, skin disorders, skin lesion, dermatoses, acantholysis, acanthosis, dyskeratosis, erosion, exocytosis, hyperkeratosis, papillomatosis, spongiosis, ulceration, seborrheic keratosis, acrochordon, actinic keratosis, cutaneous horn, bowen disease, pseudoepitheliomatous hyperplasia, nevus sebaceus, Jadassohn, sebaceous adenoma, inverted follicular keratosis, trichoepithelioma, trichilemmoma, keratoacanthoma, keratinous cyst, dermoid cyst, pilomatrixoma, nevus, junctional nevi, compound nevi, intradermal nevi, blue nevus, pyogenic granuloma, psoriasis, discoid lupus erythematosus, scleroderma circumscriptum, neurofibromatosis, xeroderma pigmentosum, dystrophic epidermolysis bullosa, cutis laxa, cutis hyperelastica, Ehlers-Danlos syndrome, necrobiosis lipoidica diabeticorum, acne vulgaris, pyoderma gangrenosum INTRODUCTIONSection 2 of 7
  Some of the most common questions asked of medical professionals regard issues of skin and skin disorders. Most skin lesions are benign. It is important to become familiar with benign lesions to be able to distinguish them from premalignant or malignant dermatopathology. Similarly, the myriad of dermatoses may represent systemic illness or conditions requiring timely medical intervention. The purposes of this article are to review many of the most common conditions and to acquaint the reader with the clinical significance and treatment options. For excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center. Also, see eMedicine's patient education articles Psoriasis and Skin Biopsy. DEFINITIONSSection 3 of 7
Some definitions are necessary to enhance communication among clinicians and other medical personnel. Gross clinical terms
Histologic terms
BENIGN NODULAR LESIONSSection 4 of 7
Seborrheic KeratosisThis is also known as seborrheic wart, senile wart, and basal cell papilloma (see Images 1-2). Clinical Seborrheic keratosis (SK) is a common benign tumor in advanced and middle-aged persons. It is typically a raised papular lesion of variable color from light to dark brown. SKs may be smooth or wartlike with visible pitting. Common sites include the face, trunk, and extremities. The lesion also may be pedunculated or sessile. A variant known as dermatosis papulosa nigra occurs over the forehead and malar regions of individuals with black skin. The variant lesion occurs at an earlier age and is smaller and smoother than in persons with fairer skin. Etiology A familial predisposition is apparent with an autosomal inheritance. SK also may be a consequence of inflammatory dermatoses or malignancies. Leser-Trélat sign is the sudden eruption of pruritic SKs as a manifestation of GI malignancy. Histology The lesions exist in varying patterns. Generally, the lesion is exophytic with a flat base level with the epidermis. An increased number of basal cells typically is observed. These form cords and/or sheets of cells with cysts of keratin (horn cysts). When the cysts communicate with the surface, they are visible as keratin plug-filled pits. This assists in the differential diagnosis when discriminating SK from melanomas and nevi. All SKs have varying degrees of acanthosis, papillomatosis, and hyperkeratosis. Subtypes exist. Hyperpigmentation of the basal cells may occur with any type and further confound the diagnosis. Irritated SK is one subtype, characterized by a predominance of basal cells but with whorling sheets of squamous cells. This squamous metaplasia is a consequence of irritation and requires careful discrimination from basosquamous carcinoma. A dermal lymphocytic infiltrate also may be observed, corroborating the inflamed irritated variation. Inverted follicular keratosis is an endophytic variant associated with a pilosebaceous follicle. Squamous metaplasia also is frequently present. The inverted geometry of the lesion gives it its name. Treatment Many patients require no treatment. Curettage and cryoablation are the principal options. SKs generally are removed for cosmetic, pruritic, inflammatory, and pain complaints. When malignancy is suspected or diagnosis is indeterminate, an excision is required. Withhold wide local excision until malignancy is confirmed. AcrochordonThis is also known as skin tag, fibroepithelial polyp, fibroma molle, and fibroepithelial papilloma (see Image 3). Clinical This is a common tumor found in middle-aged and older persons. It is almost inconsequential except for the questions and concerns it can generate. These lesions have been observed to follow warts, SKs, and inflammatory skin conditions. Acrochordons occasionally are associated with pregnancy, diabetes mellitus, and intestinal polyposis syndromes. They tend to be located in the intertriginous areas of the axilla, groin, and inframammary regions as well as in the low cervical area along the collar line. They are soft fleshy papules and usually, although not necessarily, pedunculated. They vary from 1-6 mm. Etiology Whether this is a specific entity or a common pathway in healing and recovery of several nonspecific inflammatory conditions of the skin is debatable. Histology Acrochordons all consist of a thin squamous epithelium surrounding a fibrovascular core. Treatment No treatment is required; however, acrochordons are removed for bleeding, irritation, cosmesis, and discomfort. They may be electrodesiccated, shaved, or removed with cryoablation. While some may become quite large, excision is unnecessary. Actinic KeratosisThis also is known as solar keratosis and senile keratosis. Clinical These lesions are rough appearing, scaly, erythematous papules or plaques. They occur on exposed surfaces (eg, face, hands, ears, neck, legs, thorax) of middle-aged persons with fair skin and a history of chronic sun exposure. These lesions may demonstrate certain excrescences of keratin, referred to as cutaneous horns. The rough texture of the lesion imparts to the skin a sandpaperlike consistency. The color may be red, yellow, brown, or gray. Actinic keratosis (AK) may bear a clinical resemblance to psoriasis, Bowen disease, or Paget disease. The most important attribute is its premalignant potential. A recognized but small prevalence (15-20%) of squamous cell carcinomas, which originate from AKs, exists. Etiology Ultraviolet solar damage is the most likely origin of this lesion. The epidermis experiences a sequence of atrophic, dysplastic, and hyperplastic alterations. Histology The actinic changes are limited to the interfollicular epidermis; the follicles and the intraepidermal portion of appendageal ducts are spared. The lower layers of the epidermis are the most affected. The stratum corneum undergoes parakeratosis and gives rise to cutaneous horns. The granular layer generally is obliterated except near follicle units. Tonguelike projections of the atypical epidermis may project into the dermis but do not violate the basement membrane. Also, not infrequently, the basal cells experience some reactive proliferation along with the recruitment of melanocyte activity. These features give AK a heavily pigmented appearance and the appearance of a basal cell malignancy. Actinic (solar) changes of the underlying dermis also may occur, and their presence helps in making the diagnosis. Treatment A variety of treatments are available. Excision is generally unnecessary. Cryoablation, curettage, and topical 5-fluorouracil (5-FU) have been used successfully. In the absence of their success, excision is appropriate. A relatively depigmented spot may remain. A resurfacing approach may be used with either carbon dioxide laser or dermabrasion. Topical steroids may be used in tandem with 5-FU to attenuate the inflammatory response. An important benefit of topical therapy is its ability to eliminate subclinical AKs adjacent to the clinically obvious ones. Cutaneous HornCutaneous horn also is known as cornu cutaneum. Clinical Cutaneous horn is an interesting clinical finding but not a unique pathologic entity. It is a feature of hyperkeratotic lesions (ie, AK, verrucae, SK, inverted follicular keratosis, epidermoid carcinoma). Bowen DiseaseBowen disease also is known as carcinoma in situ and squamous intraepidermoid neoplasia. Clinical Originally described by Bowen in 1912, these lesions involve predominantly skin unexposed to the sun (ie, protected). Classically, Bowen disease involves the genitalia. Itching is a common complaint. With vulvar involvement, the labia majora tend to be involved more than the labia minora. The lesions are scaly, crusted, erythematous plaques. This lesion is considered to be a carcinoma in situ without spread beyond the dermal-epidermal junction. Over time, as many as 10% of these lesions experience invasion. Squamous cell carcinoma from Bowen disease tends to be more aggressive than that which has degenerated from AKs, and metastases occur in as many as one third of patients. Its expression is associated with other skin and internal malignancies. When a lesion of similar clinical and histologic appearance is found in a sun-exposed location, it is referred to as an AK of the bowenoid type. Similarly, when found on the mucous membranes, particularly the glans of the penis, this lesion is referred to as erythroplasia of Queyrat. Etiology Efforts have been made to correlate arsenic and Bowen disease. The results have been inconclusive at best. Histology The hallmarks of Bowen disease are atypical epithelial changes. These include cytoplasmic vacuolization, nuclear hyperchromasia, multinucleated keratinocytes, cell dyskeratosis, increased mitoses, and acanthosis. Also, the pattern and strata of maturation are altered. The most significant finding is that despite the obvious atypia, the dermal-epidermal interface is preserved perfectly. Treatment Curettage and electrodesiccation traditionally have been used in small lesions; however, recurrence rates have been high. Surgical excision generally has been recognized as the standard treatment. Other techniques include cryoablation and irradiation. Pseudoepitheliomatous HyperplasiaAnother term for this lesion is pseudocarcinomatous hyperplasia. Clinical This lesion is believed to be a reparative process characterized by tongues of squamous epithelium growing downward into the dermis. It can be difficult to distinguish from squamous carcinoma. Certain conditions and infections also have been implicated, such as North American blastomycosis, bromoderma, pyoderma vegetans, tuberculosis, syphilis, granular cell tumor, Spitz and other melanocytic nevi, and granuloma inguinale. Etiology The presence of this lesion is a feature of trauma and irritation. History of these predisposing conditions may be critical to distinguishing and interpreting the histology to discriminate carcinoma from the benign lesion. Histology As mentioned, invading tongues of squamous epithelium extend into the dermis as thin anastomosing strands. One of the most significant discriminators from squamous carcinoma is the profound chronic inflammatory infiltrate, which accompanies the epithelium. Another important finding is the lack of anaplasia. Treatment A conservative approach is warranted. If the lesion cannot be determined to be benign, then treat it as a squamous carcinoma with appropriate margins. Nevus Sebaceus of JadassohnSee Image 4 for a photograph of this lesion. Clinical While this lesion often is included in tumors of the skin adnexum, it is actually an epithelial nevus. Nevus sebaceus of Jadassohn is a hamartomatous lesion expressing elements of sebaceous and apocrine glands, defective hair follicles, acanthosis, and papillomatosis. It is a congenital lesion, usually present on the scalp and face. The lesion tends to enlarge with time. The malignant potential of this lesion has been estimated at 10-50%. Degeneration into basal cell carcinoma is most common; however, other malignancies include adnexal tumors and squamous carcinoma. The color tends to be yellowish orange. The lesion is raised slightly with a waxy appearance. When located on the scalp, it is devoid of hair. An accelerated growth phase may be observed during adolescence secondary to changes in the hormonal milieu. The natural history of this lesion includes an evolution from a smooth featureless lesion into a verrucous, thickened plaque with crusting and ulceration. This is believed to be a congenital lesion. Histology Microscopically, many sebaceous glands in a vascular stroma with abortive hair follicles are observed. Some of the sebaceous glands communicate with the surface directly. Treatment Complete surgical excision is the treatment of choice. Sebaceous AdenomaClinical Sebaceous adenoma is a nodular and lobulated lesion with peripheral generative cells and variable sebaceous differentiations as the center of the lesion is approached. It is not as organized as the patterns of sebaceous hyperplasia. This lesion is distinct from the hamartomatous variety encountered on the face of patients with tuberous sclerosis syndrome. Other associations between multiple sebaceous adenomas and GI adenocarcinomas recently have been described. Treatment Since sebaceous adenoma has no malignant potential, completely excise the lesion for diagnostic purposes only. Inverted Follicular KeratosisClinical Inverted follicular keratosis is believed to be an inflammatory variant of SK. It commonly is found on the faces and sun-exposed areas of elderly patients. Typically, this lesion is located on the upper eyelid. Anatomically, it represents an upside-down or endophytic process within the epithelium of a pilosebaceous follicle. The lesions tend to be single and present as a papule or nodule. Etiology This is an acquired lesion, similar to SK. Histology The hallmarks of this lesion are the plentiful squamous eddies. A papillomatous and acanthotic appearance is found reliably. The margins are discrete and lack the inflammatory component found in keratoacanthoma (KA). Treatment Since this lesion is benign, simple excision is adequate. TrichoepitheliomaClinical Trichoepithelioma is an uncommon benign lesion. It is generally pink to flesh colored. It is frequently multiple and is not ulcerative. These lesions tend to be recapitulations of hair follicles. Initially, they appear during adolescence. Typical areas for this lesion are the face and scalp and, less commonly, the trunk and neck. A certain familial incidence exists. While these lesions tend to be multiple, a solitary presentation also can be observed. In general, all the lesions are less than 8-10 mm. Histology This tumor is characterized by collections of basal cells that are similar to the hair bulb. It is also remarkable for the presence of numerous horn cysts. Both of these tend to be accompanied by an inflammatory stroma that is fibrous. Occasional calcifications and melanin granules also can be found. The abortive hair shafts and follicles are another characteristic of trichoepithelioma. Occasionally, a differential diagnosis from a basal cell carcinoma can be difficult to determine. The most significant distinguishing features are a papillary frondlike orientation of basaloid cells and epithelial tracts consisting of more than one layer of basaloid cells. Treatment Because of the multiplicity of the lesions, the treatment can be difficult, and occasionally palliation is the only achievable goal. Techniques involving cryoablation, dermabrasion, and trichloroacetic acid help control individual lesions and groups of lesions. Unfortunately, any treatment short of complete surgical excision results in the persistence or continued growth and enlargement of these lesions. TrichilemmomaClinical Trichilemmoma is a benign tumor with a pattern of globular glycogen-rich clear cells. Occasionally, keratinization in the center is identified grossly. These lesions have some unique and interesting associations, specifically papillomas of the oral mucosa, acrokeratoses, and, most significantly, tumors of the breast, thyroid, and GI tract. This is a condition known as Cowden disease, which is a multiple hamartomatous syndrome. Additionally, a rare carcinoma variant of trichilemmoma is known as trichilemmal carcinoma. KeratoacanthomaThis lesion is also known as molluscum sebaceum. Clinical KA is a well-known self-healing skin tumor. It is most well known for its rapid growth rate. In fact, this rate of growth is frequently adequate to allow the clinician to distinguish KA from malignancy because it grows much more quickly than carcinoma. The lesion is classically a dome-shaped mound with a central crater of keratin. It tends to occur in males more often than in females, with a male-to-female ratio of 3-4:1. KA appears to be a product of the infundibulum of the hair follicle. A predictable clinical sequence occurs, which consists first of the development of a spontaneous nodule that is red to flesh colored. The nodule undergoes an impressive growth phase over approximately 1-2 weeks. It reaches approximately 1-2 cm and grows much faster than skin cancers, as previously mentioned. KA develops a central keratin plug, followed by either a static or an involutional period. Subtypes have been described. A Gryzbowski-type KA presents with multiple lesions simultaneously. When lesions present in a typical distribution, again with multiple locations, KA tends to be referred to as a Ferguson-Smith type. When the lesion is observed in sun-exposed skin associated with AKs, it is referred to as an actinic KA. Further associations have been noticed, particularly with certain inflammatory dermatoses, certain congenital lesions, certain genetic diseases, scarring, and AKs. The KA actually may represent a highly or very well-differentiated squamous cell carcinoma. The continued growth and the clinical finding of regional lymph node metastasis in rare occasions support this belief. Etiology Various infections have been implicated, including viral sources. Also, mineral oil and tar products historically have had some importance. However, the most common denominator appears to be sun exposure. Histology KA is determined easily when a number of its critical elements are demonstrated. A lesion with an overall hemispheric shape with a keratin-filled crater and overhanging edges is highly characteristic of KA. Mitotic figures are present, secondary to the accelerated growth. Basaloid cells are found toward the periphery. Eosinophils also may be common. An overall slight mild pleomorphism is detected. In general, the epithelium is well differentiated and has an abundant ground glass cytoplasm. At the margin, evidence of a pushing edge is present. This is characterized by an inflammatory rind with extension into the muscle. Perineural and vascular invasion also can be observed. These features make this lesion occasionally difficult to discern from an epidermal carcinoma. Immunohistochemical staining can help differentiate the two. Filaggrin is a histidine-rich protein that is found in the horny and granule layers of the dermis. It is ubiquitous in KA but is apparently uncommon in carcinoma. When the biopsy specimen lacks the central keratin plug and the other characteristic anatomy is difficult to determine, this lesion may be confused with squamous cell carcinoma. The biopsy findings, clinical history, and a description of the gross physical appearance greatly facilitate in making this diagnosis. Treatment While the lesion is generally self-limited, intervention commonly is desired. Intervention is preferred because of the potential cosmetic compromise with the healing of the lesion. Surgical excision, curettage, and electrodesiccation have been the traditional approaches to this lesion. Because KA can be removed in total with surgical excision, which provides an adequate pathologic specimen, this is generally the treatment of choice. Keratinous cystThis lesion is also known as a sebaceous cyst, wen, atheroma, or steatoma. Clinical For many years, keratinous cysts have been misnamed and referred to incorrectly as sebaceous cysts. Historically, two essential types have been identified. The most common type is known as an epidermoid or epidermal inclusion cyst. This represents approximately 90% of keratinous cysts. The second most common type is termed a pilar or trichilemmal cyst. Cornified epithelium, a very well-demarcated granular layer, and multiple lamellae of keratin without calcification characterize the epidermoid cysts. These lesions can be found in almost any location. Variations found in the extremities, particularly the fingers and toes, may be a traumatic form of inclusion. In contrast, the pilar cyst occurs almost exclusively on the scalp. Its hallmark is a trichilemmal keratinization pattern. This pattern is different from the lamellated form because the well-defined granular layer is lacking. Additionally, focal calcification is common. Amino acid analysis of both types of cysts demonstrates that the epidermoid cyst is most likely to originate from the infundibular portion of hair follicles. Another conclusion is that the trichilemmal cyst tends to have an origin from the epithelium of the hair follicle that is at or distal to the level of sebaceous ducts. In this location, no typical granular layer is present. Treatment The treatment of choice is excision. However, when the cyst is acutely inflamed, incision and drainage is frequently the best approach. Following the resolution of the infection, the lesion is excised. The lesion nearly always is accompanied by a central communicating punctum, which is frequently obvious in the skin surface. They must be excised with an ellipse of skin in continuity. Other techniques of removal include punch biopsy aspiration followed by curettage and avulsion of the cyst wall. Dermoid cystThe dermoid cyst is a variation of the keratinous cyst. Treatment Several treatment options exist for these cysts. If the cyst is acutely inflamed or infected, incision and drainage is the wisest choice initially. This may be followed by a definitive excision when the inflammation is resolved. An alternative technique following drainage involves the application of phenol to the lining of the cyst. Facial cysts initially may be attended to with aspiration by a 2-mm punch biopsy. Through this small aperture, the cyst lining then may be avulsed. Curettage is also a useful adjunct. The standard remains simple excision with an ellipse of skin involving the cutaneous punctum over the lesion. PilomatrixomaPilomatrixoma is also known as pilomatricoma and the calcified epithelioma of Malherbe. Clinical Pilomatrixoma is a variation of the epidermal cyst and should be included in the differential diagnosis. It is a relatively uncommon tumor. It tends to occur on the neck, head, and upper extremities of children and young adults. Typically, it presents as a solitary subcutaneous nodule, with attachment to the skin and occasional episodes of inflammation and pain. Histology The lesion is a nodular subepidermal tumor with elements of hair matrix. Intensely basophilic-staining cells are found peripherally, and eosin-favoring cells are near the center. Also present are shadow or ghost cells, which are cells with eosinophilic cytoplasm with what appear to be vacuolated areas from where the nuclei formerly were present. Treatment Simple surgical excision is the cornerstone of treatment. The lesion has a friable capsule. While extremely rare, a malignant counterpart has been named the malignant pilomatrixoma or pilomatrix carcinoma. NevusGeneral The definition of a nevus can be expanded to include any congenital lesion that is circumscribed to well defined. The term also occasionally has been used as a synonym for mole. A mole is defined as a shapeless mass. Most nevi appear when individuals are aged 2-60 years and have a predictable evolution. They rarely undergo activation or malignant degeneration. Nevi tend to be more common on the head, neck, and trunk. However, a great deal of variability exists with regard to size, shape, and even amount of hair present. Nevomelanocytic nevi, which are the most common, classically and clinically are categorized in 3 different ways: junctional, compound, and intradermal subtypes.
Special variances and subtypes of nevi exist. The first of these is the blue nevus. The blue nevus tends to be a small discrete lesion, typically located in the head and neck and occasionally on the upper extremity. A variant form of this has manifestation on the buttock and sacrococcygeal areas. In general, the blue nevus has abundant melanin pigment. It is located entirely within the dermis. No epidermal or junctional component is present. If the pigment is misinterpreted as hemosiderin, blue nevus occasionally can be misdiagnosed as a benign fibrous histiocytoma. Two predominant types of blue nevi exist, the common and the cellular blue nevus. The cellular blue nevus is a special variety characterized by being larger with more intense pigmentation. Its distribution tends to be in the buttock and sacrococcygeal areas. Its subtypical import is that it must be distinguished from a malignant melanoma. The confusion surrounds the increased degree of pigmentation. After the sacrococcygeal and buttock areas, other regions of expression include the scalp, face, and backs of the hands and feet. Histologically, it is distinguished from melanoma by the absence of peripheral reaction and stigmata of invasion and by the lack of atypical junctional activity or mitotic figures. The natural history is that of a benign course, which is occasionally recurrent locally. Regional lymph node involvement has been demonstrated and is of concern; however, patients generally are cured by primary excision. Additionally, a malignant variant of the blue nevus exists. Pyogenic GranulomaThis is also termed granuloma telangiectaticum (see Image 5). Clinical Pyogenic granuloma is a rapidly proliferating solitary lesion known for its bleeding tendencies. An association with trauma is frequent. While the size varies, it is usually less than 1 cm in greatest dimension. Typical locations include the face, fingers, and thorax. Clinically, melanoma must be excluded. Histology Multiple dilated capillaries with prominent swollen endothelial cells are observed. Edema is present in the stroma. A pedunculated gross appearance is common. Treatment The approach varies but excision is the mainstay of treatment. A biopsy confirming the diagnosis frequently is obtained. Performing curettage and electrodesiccation is another option. Recurrence may be a problem. Other lesions For information on hypertrophic scars and keloids, please see the articles Wound Healing, Widened and Hypertrophic Scars and Wound Healing, Keloids. BENIGN DERMATOSESSection 5 of 7
Psoriasis Psoriasis (see Image 6) is one of the most common dermatoses. Its prevalence varies from 0.5-3% of the US population. It appears as a chronic, bilaterally symmetric, erythematous plaquelike lesion with a silvery scale covering. The lesions classically are located over the extensor surfaces, including the elbows, knees, back, and scalp. Confluent generalized lesions also may occur. Its etiology eludes modern medical science. A multifactorial inheritance pattern is suggested. These factors include familial clusters, trauma, hemolytic streptococcal infection, and endocrine changes. However, most cases occur without a precipitating event. Psoriasis is characterized by exceedingly rapid turnover of skin. This occurs on the order of 7-10 times faster than the normal 28-day cycle of skin renewal. The histomorphologic characteristics include parakeratosis and acanthosis. Characteristics but not pathognomonic findings are spongiform pustules of Kogoj and Munro microabscesses. A spongiform pustule is a local subcorneal neutrophil collection in intercellular spaces. Munro microabscesses are intracorneal collections of 4 or more neutrophils. Psoriasis occasionally is associated with other systemic illnesses, particularly psoriatic arthritis. Psoriatic arthritis occurs in approximately 5-10% of patients with psoriasis. A clinical entity known as psoriasis vulgaris may occur anywhere on the skin including the extensor surfaces, lumbosacral areas, intergluteal cleft, and the glans of the penis. Males may be affected in approximately one third of cases. Typically, mucosal surfaces are spared. A plaquelike salmon-colored lesion is the most common finding clinically. Changes of the nails include dimpling, onycholysis, pitting, thickening, and crumbling. At some point, as many as one third of patients may develop a Köbner phenomenon, which is a condition in which new insult or skin trauma is greeted with a development of psoriatic lesions. Greater risk of postsurgical infections also is found due to a higher-than-normal bacterial colonization of the skin and psoriatic lesions. Therapy consists of systemic and topical forms and phototherapy. Prior to elective procedures, psoriasis should be clinically optimized. Discoid lupus erythematosus Discoid lupus erythematosus and systemic lupus erythematosus are clinically distinct entities. Discoid lupus is a chronic, relatively common dermatitis with clinical presentation more common in women than in men. It presents with erythematous plaques that vary from an atrophic to hyperkeratotic appearance in the region of the face, scalp, neck, extremities, and trunk. These may be exacerbated by sunlight. Histologically, these lesions are characterized by a hyperkeratosis with some atrophy of the epidermis and degeneration of the basal layer. However, none of the histologic findings are particularly pathognomonic. A band of lymphocytic infiltrates can be found along the dermal-epidermal junction. Melanin pigmentation may be discontinuous in extending to the papillary dermis. The follicles and other adnexa commonly tend to be surrounded with an intense lymphocytic infiltrate. Periodic acid-Schiff (PAS) stains demonstrate thickening of the epidermal basement membrane; however, this is nonspecific. Immunofluorescence of immunoglobulin G, immunoglobulin M, immunoglobulin A, and complement demonstrates a lupus band test. This occurs predominantly in the basement membrane and is found in the clinically uninvolved non–sun-exposed skin in patients with this autoimmune process. Topical treatment of this occurrence has involved a combination of steroid and antimalarial drugs such as hydroxychloroquine. Despite efforts to control a disease topically, scarring and healing visible portions of the face may require the attention of a plastic surgeon. Classic reconstruction efforts have been successful using either a full-thickness skin graft or adjacent local flaps after medical control is achieved. As with all chronic scarring processes, the possibility of malignant degeneration into a squamous carcinoma has been reported. As with most dermatoses, daily protection from solar exposure is essential. Scleroderma circumscriptum These lesions often are defined on the trunk or an extremity in a dermatome. A particular manifestation of this is the face and paramedian forehead. These lesions appear to be violations that are lilac-colored and isolated. Occasionally, pruritus is associated. Scleroderma circumscriptum may be widespread and chronic and it may involve the digits of the hand. Clinically, it almost always is distinguished from the systemic form of scleroderma, also known as progressive systemic sclerosis. Histologically, the significant change appears to be in the amount of collagen found. This collagen deposition is indistinguishable from normal collagen levels. The type and proportion of collagen (type 1 or type 3) are similar to those found in the healthy dermis. A special situation known as scleroderma en coup de sabre is associated with progressive hemifacial atrophy in children. This is manifest with atrophy of the skin, subcutaneous tissues, muscle, and bone. Occasionally the process is spontaneously resolving. It can be unpredictable in its clinical course. While it remains destructive and progressive, this condition is observed. In its burnout quiescent phase, the treatment of choice is self-tissue augmentation. In systemic scleroderma, the classic acrosclerotic form is observed generally in women aged 20-50 years. This can be associated with vasospastic or Raynaud phenomenon of the hand. These hand lesions are remarkable for a fixed partial flexion with extreme limitation of motion. Skin becomes inelastic and bound with ulcerations over fingertip and joint surfaces. Because of its progressive and incurable nature, conservation and therapy are recommended. Some medical regimen approaches include medical sympathetic block and episodic steroids with systemic effect, although neither has been shown to be beneficial. A patient with scleroderma requiring an operation requires great concern in planning. The wound healing conditions are tenuous at best. Ulcers should be managed with careful debridement and skin grafting as permitted. Neurofibromatosis Also known as Von Recklinghausen disease, this is a relatively common disorder with a frequency of approximately 1 in 3000. Nearly 50% of patients with neurofibromatosis have a definable autosomal dominant transmission pattern. The remaining cases appear to be due to mutations. While the penetrance is 100%, the expressivity is variable. Clinical patterns include multiple neural tumors anywhere on the body. Numerous pigmented skin lesions occur. The classic café au lait spots predominate. Additionally, pigmented iris hamartomas (ie, Lisch nodules) are common. Bone lesions and intracranial and GI lesions and symptoms may be identified. While pigmentary changes may occur at birth, the tumor formation is most aggressive during puberty. The severity of the disease is associated loosely with the age at which symptoms or tumors are found. Central and peripheral neurologic deficiency may follow the progressive growth of these lesions in their mass effect. With respect to surgery, the most common indications are excisions of symptomatic lesions or the accompanying soft tissue facial deformity. Frequently, because of critical and eloquent locations, removal of the masses is subtotal. While malignant degeneration is recognized in multiple neurofibromas, practically, it is unfeasible to excise all lesions in most patients. When masses are found at the cerebellopontine angle, this creates the clinical condition recognized as an acoustic neuroma. While café au lait spots may be found in the healthy population, the presence of 6 or more spots in an aggregate of more than 1.5 cm in greatest dimension establishes the diagnosis of neurofibromatosis. Clinical course is difficult to predict. An association of severity with youthful onset appears to exist. However, to the plastic surgeon, the most significant manifestations of the disease are the multiple and varied facial deformities. The therapeutic plan essentially involves excising the lesions that are bothersome or visible. Occasionally, only palliative partial resection can be accomplished. Bony involvement of the facial skeleton also creates a difficult problem. Total satisfactory excision of all symptomatic lesions seldom is accomplished. Xeroderma pigmentosum Xeroderma pigmentosum is an autosomal recessive disorder in which the individual is left essentially unprotected from ionizing radiation. The mechanism is well understood and involves the absence of certain DNA repair mechanisms for pyrimidine dimers that have been formed following actinic radiation change. Within the patient, ultraviolet exposure develops the full spectrum of actinic injury. Basal and squamous cell carcinomas and malignant melanomas may be found. Additionally, pigmentary changes and hyperkeratoses are ubiquitous within the skin surface. Mainstays of therapy include protection from solar radiation, topical chemotherapeutic agents such as 5-FU, excision or dermabrasion of involved skin, and vigilant surveillance of all premalignant and malignant lesions. These strategies have been successful in expanding the lifespan beyond early adulthood for patients with xeroderma pigmentosum. Dystrophic epidermolysis bullosa This is a rare hereditary disease of epithelial surfaces including skin and mucosa. Its most obvious clinical characteristic is a bullous formation in the skin following essentially minimal trauma. This heals with scarring and aggressive contracture. The incidence is approximately 1 in 300,000 live births. One half of the physiobiologic mechanisms that have been discovered include an excessive activity of a particular epidermal collagenase and fibroblasts with supranormal contractile abilities. Of greatest clinical significance is the involvement of children's hands. A continued unrelenting cycle of injury followed by scarring and contracture with creeping epithelialization occurs until the interdigital and web spaces are completely encased in an epidermal cocoon. A progressive atrophic scar results in the stepwise and eventual total loss of use of the digits of the hand. While recognizing that variable clinical expression of this disorder exists, all individuals with dystrophic epidermolysis bullosa have some degree of functional loss. While the mucosal services of the hypopharynx and esophagus also are involved, they appear to be less significantly involved clinically than the exposed surfaces of the hands and fingers. A pathognomonic sign of this is the appearance of blisters with minimal trauma referred to as the Nikolsky sign. While no medical or surgical cure exists for this affliction, some modicum of benefit has been discovered with the vigorous use of topical steroid therapy. Surgical treatments are frustrating, and one of the larger series of these treatments has been developed at the Ormond Street Hospital for Children in London. In this facility, a highly specialized multidisciplinary approach is used in the perioperative setting to protect all of the epithelial tissues. One significant clinical contribution from these large series has been the knowledge that within the epithelial cocoon, the digits remain surprisingly mobile with a greater than expected active and passive range of motion. Skin grafts are used to close the intervening epithelial defects and they actually heal quite normally. Generally, the donor site heals in an essentially typical fashion. Another significant clinical observation has been the chronically colonized condition of the blister fluid with beta-hemolytic streptococci. Despite early excellent successes with surgical management, the final common pathway appears to be a recrudescence of the recurrent minor trauma and epithelial encasement. For this reason, treatment is considered only temporary. Cutis laxa Cutis laxa is a rare disorder that is principally in the skin but also can involve other organ systems. The pathologic defect consists of degeneration of the elastic fibers of the dermis. Two types have been recognized. One is autosomal dominant and manifests only in the skin. The other type has a recessive inheritance pattern and is associated with fascial deficiencies in the inguinal and ventral areas. Other manifestations include chronic obstructive pulmonary disease (COPD), bladder and GI diverticulosis, great vessel aneurysms, and cardiac abnormalities. These many manifestations, particularly the cardiopulmonary involvement, severely limit the patient's operative candidacy. Clinically, patients with cutis laxa are recognized by the extreme elasticity of their skin, which permits it to literally hang in sheets of loose folds. Microscopically, a decrease in the number of fibers as well as their size is noted. While the skin is loose, it is not any more fragile. It heals essentially normally and has relatively little elasticity. In some operative candidates, satisfaction can be found with operative correction of the excessive redundant skin. In particular, rhytidectomy has been performed with some satisfaction. Repeated excisions of redundant skin can be beneficial in some patients. Cutis hyperelastica (Ehlers-Danlos syndrome) This entity is common to contortionists in that the hyperelasticity and flexibility of the skin and joints permit the achievement of grotesquely exaggerated positions. Some of the 8-10 forms that are described are recessive and some are dominant in their inheritance. The basic defects in these patterns tend to be either a defect in the synthesis of type 3 collagen, a deficiency of the lysyl hydroxylase enzyme preventing cross-linkage, or the procollagen-N-peptidase enzyme deficiency, which impairs the aggregation of collagen fibers. An X-linked recessive form is the result of a possible deficiency in the lysyl-oxidase enzyme. All patients have variable fragility of the skin and blood vessels. Their response to injury is poor, with easy bruising and blister and hematoma formation following minimal shear injury. Similarly, they heal very poorly. Simple lacerations result in large separated wounds that tend to retract. The overall tensile strength in the skin is poor and fails to adequately hold suture material. An important distinction remains between Ehlers-Danlos syndrome (cutis hyperelastica) and cutis laxa. Elective procedures should be discouraged in patients with Ehlers-Danlos syndrome because of the poor healing of the skin. The elasticity has some variance in that younger individuals appear to have normal elasticity, but with aging, the skin becomes more relaxed and redundant. Necrobiosis lipoidica diabeticorum Necrobiosis lipoidica diabeticorum (see Image 7) is a plaquelike, depressed, atrophic yellow lesion typically found in patients with diabetes. It has a strong association with diabetes and actually may be a clinical prodrome of the onset of the disease systemically. It rarely is found in locations other than the lower extremities and seldom is found in the absence of diabetes. The lesion tends to progress from a red plaquelike area to one with atrophy that occasionally may ulcerate. Controlling the diabetes does not tend to modulate the clinical outcome of this lesion. Successful management occasionally has required resection and skin grafting of the involved areas. Acne vulgaris The word acne is a derivative of the Greek word acme, referring to the prime of life. This corresponds with the usual age of onset of acne, which tends to be in early puberty. More than 80% of adults have some experience with acne. Clinically significant lesions consist of an open comedone, which corresponds to the term blackhead. Closed comedones correspond to whiteheads. Additional inflammatory lesions include pustules and papules. The most aggressive forms of acne have chronic scarring coexisting with active inflammatory foci. The fundamental unit of involvement is the diseased pilosebaceous system. The location of acne manifestation is defined by the distribution of the pilosebaceous glands. Adolescence causes endocrine maturation of the adnexal elements, resulting in an accumulation of cellular products within the ductile systems. In addition to the cellular products are coexistent microorganisms, most commonly Propionibacterium acnes and Staphylococcus epidermidis. In discussing the pathogenesis, the most common pathophysiologic condition is believed to be that of increased end-organ sensitivity to androgen stimulation. The organism P acnes also has been demonstrated to produce a lipase that hydrolyses lipases to free fatty acids. These free fatty acids have been shown to produce inflammation in comedones when applied to rabbit ears or when injected intradermally in humans. Additionally, P acnes may have complement activation contributions, further increasing the inflammation. Additionally, a pathophysiologic cycle occurs with respect to the keratinized layer of the sebaceous duct. In normal uninflamed ducts, the keratinized epithelium is loosely adherent and easily separates up to the skin surface as it is regenerated from deeper layers. In the acne condition, these follicular cells are cohesive and coalesce to form retention hyperkeratosis, a physical obstruction to the pilosebaceous unit. This leads to back pressure and the leakage of sebum and bacteria into the dermis across the epithelialized surface, stimulating the inflammatory response. Clinically, the features of acne can have many forms. Closed comedones are approximately 1-3 mm in diameter. Open comedones are approximately 2-5 mm in diameter, and this dark core is a packed combination of melanin, oxidized lipids, keratin, and bacteria. Occasionally, several adjacent units may coalesce and create deep dermal abscesses. The treatment objectives are decreasing the count of P acnes, decreasing the hyperkeratosis, and decreasing the sebum production. Topical antibiotic preparations and those with systemic effect have been used, as have sebum antagonists. Benzyl peroxide is a common bactericidal with a free oxygen radical moiety as its active mechanism. It simultaneously decreases the organism concentration and the amount of free fatty acids available on the surface. Because it is a keratolytic, enhanced global skin blood flow is recognized. All transretinoic acid (tretinoin) is a topical preparation with established efficacy. The primary mechanism is to decrease retention hyperkeratosis by limiting cohesiveness of the keratinized layer. This regimen results in the thinning of the stratum corneum to approximately one half of its usual thickness. Topical tetracycline, erythromycin, and clindamycin also have been used. The pustular and papular forms respond better to these antibiotics than the cystic or comedonal forms. Tetracycline and erythromycin share similar efficacy in the systemic sense because both are concentrated in the sebaceous gland and follicle. Both also limit leukocyte chemotaxis to decrease the inflammatory milieu. Isotretinoin (13-cis-retinoic acid) has revolutionized treatment. This compound reduces sebaceous gland size by 50% and function by more than 90%. It inhibits keratinocyte proliferation and permits thinning of the epidermis. However, it is indicated only for severe cystic acne. During a regimen, serum lipoproteins should be monitored since as many as 25% of patients may develop hypertriglyceridemia. Lastly, isotretinoin is a known teratogen. The scarring of acne tends to be of two different types, either the broad-based depression or the ice-pick lesion. Treatment usually centers on making the scar borders less distinct with techniques such as dermabrasion, laser abrasion, and chemical peeling. Subcutaneous collagen injections can be a useful adjunct. Frequently, it is best to excise ice-pick lesions. Because of the significant changes in epidermal thickness by isotretinoin therapy, efforts to resurface by dermabrasion or laser should be deferred for at least 1 year to afford the skin the opportunity to recover. Pyoderma gangrenosum While pyoderma gangrenosum (see Image 8) is associated with ulcerative colitis, 50% of the time it occurs without inflammatory bowel disease. Other associations include ulcer diathesis, diverticular disease, rheumatoid arthritis, pulmonary and hematologic illnesses, and carcinoid tumors. Approximately 20-25% of cases are uniquely pyoderma gangrenosum. The lesions typically are undermined ulcerations in association with abscesses in a necrotizing process. Physiologically, the wound is more like a progressive vasculitis than an infection. However, gram-positive and gram-negative bacterial species have been cultured from these chronic wounds. Streptococcal and Proteus species appear to be involved frequently. Topical antimicrobials and those with systemic effect are effective to some degree in controlling the disease. The mainstay of management appears to be anti-inflammatory regimens of steroids with local and systemic effect as well as azathioprine. Surgical caveats remain minimal debridement and limitation of all forms of skin trauma and irritation. The slightest cutaneous injury may evolve into a disastrous area of necrosis. MULTIMEDIASection 6 of 7
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Skin, Benign Skin Lesions excerpt Article Last Updated: Feb 17, 2006 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
