Anatomy and Clinical Examination

Skin is made up of the epidermis, dermis, and subcutaneous layers ( Figure 58.1 ). The epidermis possesses the following appendages:

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  Eccrine glands

  
  
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  Apocrine glands

  
  
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  Sebaceous glands

  
  
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  Hair follicles

  
  
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  Nails***

Layers of skin that include adnexal structures and the origin of benign and malignant tumors.

Glands and hair follicles arise as “down growths” from the epidermis and project into the dermis. The two types of sweat glands are the eccrine and apocrine. Eccrine glands exist all over the skin. They start as a coil in the dermis and open onto the skin’s surface and secrete clear, watery fluid. The apocrine glands are large sweat glands that open into hair follicles, to which they are attached, but rarely directly, to the skin’s surface. They are also coiled tubular glands found mainly in the axilla that do not develop fully until puberty. Secretion is evoked in response to stress, pain, and fright. Sebaceous glands are found all over the body, except the palms and soles of the feet. They have no lumen, are multilobulated, appearing as a pouch hanging on the side of the hair follicle, and secrete a fatty sebum.

The dermis is divided into two parts: (1) papillary and (2) reticular. The papillary dermis lies up against the epidermis, and papillae project up into it so that the alternating areas of epidermis, which drop down into it, are called “rete pegs.” It is these pegs that help resist shear disruption between the dermal and epidermal layers. The reticular dermis is deeper, made of coarser bundles of connective tissue fibers, and extends to the subcutaneous layer; it contains:

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  Connective tissue fibers—collagen, elastin, and reticulin

  
  
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  Cellular elements—migratory cells (leukocytes, histiocytes) and fixed cells (fibroblasts, mast)

  
  
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  Blood vessels

  
  
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  Nerves and specialized nerve endings

  
  
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  Smooth muscle

  
  
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  Lymphatics

  
  
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  Ground substance

The epidermis is superficial to the basal lamina and is comprised histologically of four cell layers (five layers in the palm) ( Figure 58.2 ), as follows:

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  The basal layer (stratum basale) consists of a single layer of columnar cells that stain deeply basophilic. At haphazard intervals between these basal cells are melanocytes—clear cells with small nuclei. Melanin is produced through the conversion of tyrosine to dopa, facilitated by the enzyme tyrosinase. Melanocytes can multiply and form nests in the deep epidermis and even spread into the subadjacent dermis, where they lose the ability to synthesize melanin but retain the melanin-storing property and remain pigmented. These intradermal clusters are called “nevus cells” and give the appearance of nevi. Melanocytes are actually dendritic cells that connect to each other over distances. They are derived from the neural crest. Merkel cells, like melanocytes, are nonkeratinocyte intraepidermal cells. They also occur in the basal cell layer and are associated with sensory axons for slow-adapting mechanoreceptors and pressure sensors. They are found in hair follicles as well.

  
  
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  The malpighian (or prickle cell) layer (i.e., stratum spinosum) is made up of cells connected to each other by intracellular bridges, so artifactually (during tissue processing) give the spiny, or prickle, appearance of this layer.

  
  
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  The granular layer (stratum granulosum) is made up of a few layers of diamond-shaped cells filled with basophilic granules (keratohyalin).

  
  
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  The horny layer (stratum corneum) has cells with no nuclei, and they are continuously shed from the surface.

  
  
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  In the palm only, the clear layer (stratum lucidum) gives a translucent appearance to the skin. It is composed of up to five layers of “dead” keratinocytes; this layer is situated between the stratum granulosum and the stratum corneum. Cells are filled with eleidin, an intermediate form of keratin.

Cellular layers of the epidermis.

In epidermal cancers, this natural progressive maturation is lost and becomes disorderly and finally totally anaplastic. The relative invasiveness of such cancers is also seen first by invasion deep into the basement membrane, then by depth of invasion, next entering the papillary dermis, and on into the deeper reticular dermis. Thus, carcinoma in situ is a true cancer that is disorganized in its progressive epidermal cell maturation but nonetheless has not invaded through the basement membrane of the dermis.

Originally, Clark’s levels were applied descriptively to the depth of melanoma invasion into the papillary dermis, reticular dermis, and on into subcutaneous sites. However, Breslow’s levels of actual millimeter thickness of invasion have been found to be more accurate prognostically. In the subungual regions, rete pegs and papillary dermis are less well defined, and there is also no subcutaneous fat, which means that the distance of tumor penetration between epidermis and periosteum is very small. In this region especially, the Clark and Breslow measurements cannot be used as an effective treatment guide.

Benign and malignant skin tumors thus may arise from epithelial elements (in which case malignancies are termed carcinoma ) of the epidermis, as well as from the adnexae in the dermis (i.e., hair follicles and sweat glands) (see Figure 58.1 ). Basal cell carcinoma (BCC) is derived from the basal cell layer of the epidermis and squamous cell carcinoma (SCC) comes from the more superficial keratinocytes.

Epithelial cysts within the dermis may be a result of implantation into the dermis (epidermal inclusion cyst), from blocked gland ducts (pilosebaceous cysts), and/or from hair follicles (trichilemmal cysts). Connective tissue tumors (malignant forms are termed sarcomas ) may arise from the fibrous tissue of the dermis, such as dermatofibromas and the rarer dermatofibrosarcoma protuberans. Nerve-ending tumors and those relative to blood vessels also occur in the dermis (e.g., neuro­fibroma, glomus, Merkel cell). Hemangiomas and capillary stains and vascular malformations are discussed elsewhere in this book.

Having an understanding of skin anatomy and tumor location is helpful in arriving at a clinical diagnosis. Intraepidermal lesions may be plaquelike but are not elevated into papules or nodules (the hallmark of intradermal lesions). Junctional (between dermis and epidermis) lesions are also not elevated, as is the case with a junctional nevus—a flat pigmented lesion. Dermatofibromas and the more vertically invasive nodular melanomas, in contrast, are elevated into a nodule. Melanomas are pigmented (though not always) because their cell of origin is the melanocyte, which produces melanin. However, melanocytes also do pass melanin into adjacent basal and spongy cells, so both BCCs and SCCs may be pigmented.

Epidermal lesions often have an “irritated” surface that may be ulcerative or thickened. Hyperkeratosis is a thickening of the stratum corneum, leading to an exuberant, flaking, and cracked appearance of the skin as in actinic keratosis and verrucae (or warts). In acanthosis, there is a thickening of the stratum spinosum; it gives the skin a leathery, folded appearance and, if it is pigmented, is called acanthosis nigricans . This may occur in simple obesity but can be a marker for internal malignancy. Hyperkeratosis may be so pronounced as to become heaped up to form a cutaneous horn. It is most commonly associated with actinic keratosis but may have an underlying SCC or keratoacanthoma. Similarly, greasy scaling lesions, which have a “pasted on” appearance, are typical of seborrheic keratosis.

In contradistinction, dermal lesions form a papule or nodule. A dermal inclusion cyst retains its attachment to the overlying epidermis (i.e., a punctum) and a dermatofibroma arises in the superficial dermal layers, so the overlying epidermis adheres to the deeper lesion. In fact, there may be an overlying pressure necrosis from a dermatofibroma, leading to an almost pathognomonic feature of central umbilication. The nodule in dermatofibroma is hard, but a nodular nevus is soft and indents with the back end of a cotton-tipped applicator.

The lesions of the deeper dermis will not have an overlying epidermal adherence. Lesions that are deeply attached will be nonmobile. Physicians should always clinically assess skin cancers for deep fixation and lack of deep mobility because these imply a deep invasion.

Regional clinical evaluation of lymph node drainage basins for malignant lesions is also important, and one must have an understanding of this anatomy, including the superficial and deep lymphatics. Superficial lymphatics from the ulnar side of the hand may drain first into the supratrochlear nodes just proximal to the medial epicondyle, but most pass directly up to the axilla. Superficial radial lymphatics ascend to the deltopectoral glands and then on to the subclavicular axillary nodes.

Deep lymphatic vessels accompany the deep blood vessels (e.g., radial, ulnar, anterior and posterior interosseous), along which there may be lymph glands. Most pass up to the lateral axillary nodes. Thus, it is necessary to examine the forearm, epitrochlear, supratrochlear, and deltopectoral regions, as well as the axilla (i.e., medial, lateral, and apex) and supraclavicular lymph node drainage basins. When planning so-called “prophylactic” lymph node biopsy in the absence of palpable glands, physicians cannot rely on a seemingly logical ascent of lymph drainage up the extremity to the axilla, but must assess for the “sentinel” node that can be at any one of these potential sites.

Diagnostic Procedures and Nonsurgical Treatment

Most cutaneous lesions do not require special imaging unless, for example, there is a large, deeply invasive skin cancer; in that case, magnetic resonance imaging (MRI) may be helpful in planning resection.

For small lesions, one may proceed directly to an excisional biopsy. However, many small lesions are noncancerous or only minimally invasive, so various diagnostic and/or treatment options are available. Once again, understanding the depth of cutaneous involvement is an important guide. Many epidermal lesions can be treated by shaving or curettage. Where indicated, one of these methods has an advantage over elliptical excision because the deeper dermal layers are not violated, and there is less likelihood of adverse scarring. This is, perhaps, not as critical in the hand as on more cosmetically important areas such as the face. Appropriate nonsurgical treatments may be as follows:

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  Patient surveillance —Total lesion ablation may not be feasible. Periodic clinical examination and follow-up photographs may detect malignant transformation. This course can be chosen when total excision of a large congenital nevus is impractical, when a patient has multiple dysplastic nevi, or for diffuse syndromal conditions with a high risk of development of cutaneous malignancy (e.g., xeroderma pigmentosum, basal cell nevus syndrome).

  
  
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  Topical medications —Diffusely spread conditions with malignant potential can be treated with topically applied 5-fluorouracil (5-FU) ( Figure 58.3 ). However, Bowen lesions and superficial BCCs or SCCs cannot be treated with 5-FU. Verrucae can be treated by topical application of podophyllin or keratolytic agents (e.g., salicylic acid). A 5% imiquimod cream (Aldera, Graceway Pharmaceuticals, Bristol, TN) is approved for treatment of superficial BCCs; it should be applied 5 to 7 times per week for up to 12 weeks. Incomplete data are available for its use for Bowen disease, SCC, or lentigo maligna melanoma.

  
  

  
  

  
  

  

  
  

  
  

  Topical application of 5-FU can be used to treat a variety of superficial epidermal lesions.

  
  
  
  
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  Curettage —A 5-mm curet is most commonly used, and curettage is performed after adequate local anesthesia. It yields material for histologic examination but does not allow assessment of tumor margins. Curettage permits safe removal of superficial lesions with minimal scarring and is amenable for actinic, seborrheic keratoses, and verruca vulgaris. It is an excellent treatment for subungual verrucae, leaving almost no residual nail deformity. Remove the nail plate in order to identify a deep curettage cleavage plane using loupe magnification ( Figure 58.4 ).

  
  

  
  

  
  

  

  
  

  
  

  A, Periungual verruca vulgaris on two fingers. B, The lesions here have been curettaged after nail plate removal. Reepitheliazation and normal nail growth will follow because the full-thickness epidermis has not been breached.

  
  
  
  
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  Cryosurgery —Intense cold is applied and all cells within the freezing wave are killed. Liquid nitrogen can remove warts, superficial keratoses, and actinic lentigines. It must be used with caution where there are adjacent peripheral nerves, such as on the volar finger and olecranon, as permanent freeze damage to the nerve can occur. Also, destruction to critical paronychial and nail bed structures can occur at the fingertip. Aesthetic results are otherwise usually excellent, but cryosurgery must be used with caution in dark-skinned patients because hypopigmentation may result. It causes little pain and rarely requires anesthesia. For the procedure, a cotton-tipped applicator is used, with cotton teased out and tapered. As liquid nitrogen runs down the applicator, skin at its tip turns white and the ice front spreads outward ( Figure 58.5 ). Application should cease when visible freezing extends just beyond the lesion.

  
  

  
  

  
  

  

  
  

  
  

  Diagrammatic representation of cryotherapy with cotton-tipped applicator dipped in liquid nitrogen.

  
  
  
  
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  Electrosurgery —Electrical energy is converted to heat by tissue resistance. An office hyfrecator is a good electrosurgical instrument and can be used to destroy seborrheic keratoses, skin tags, lentigines, and spider nevi.

  
  
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  Electrodesiccation and curettage —A curet is used to scrape the lesion down to dermis. Scraping is then paused to use a hyfrecator. This causes electrocoagulation (electrodesiccation) of the raw surgical surface. The process is usually repeated three times or until the surgeon is comfortable with the margins. The technique’s effective use depends on clinical experience but has advantages: (1) good cosmetic results, (2) rapid recognition of a recurrence because the lesion is not obscured by a wound closure or flap, and (3) a straightforward office procedure. It can be used for multiple superficial lesions that would otherwise be difficult or tedious to treat with multiple excisions. It is useful for seborrheic keratoses and viral warts but also has been used for multiple superficial BCCs, keratoacanthoma, and Bowen disease. For larger lesions, sometimes scarring can be obvious.

Before ablative surgery, a histologic diagnosis should always be obtained using the following as needed. In some cases, the biopsy process actually may be the curative treatment for smaller lesions.

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  Shave biopsy —This may totally excise the lesion and be curative or just serve as a diagnostic biopsy. Lesion elevation by the mechanical effects of a wheal of local anesthetic and pinching between thumb and index finger above the plain of the surrounding tissue enables a full-thickness shave biopsy down to dermis. This can be done with a scalpel or a razor blade ( Figure 58.6 ). Shave biopsies are not suitable for neoplasms that clinically appear to infiltrate dermis and generally not for pigmented lesions with a suspicion for melanoma.

  
  

  
  

  
  

  

  
  

  
  

  

  
  

  
  

  A, B, Diagrammatic illustration of shave biopsy. The lesion is plumped up first by local anesthetic infiltration and then by pinching the skin between the index finger and thumb. Tangential excision of the lesion is thus facilitated. C, D, Clinical demonstration of shave biopsy.

  
  
  
  
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  Punch biopsy —This may be incisional or excisional, if the lesion is small enough for the punch to fit around. Variable-sized cutting punches are available from 1.5 to 6 mm (4 mm is the most frequently used). Local anesthetic is first injected. When the circular punch incision reaches subcutaneous fat, the punch is removed. The small cylinder of tissue is then lifted and its base transected at the level of the subcutaneous tissue with small iris scissors ( Figure 58.7 ). Sutures are generally not used. Sampling error is minimized by careful choice of the site to be biopsied.

  
  

  
  

  
  

  

  
  

  
  

  A, Different size punches (3 mm, 4 mm, 5 mm). B, Illustration that shows how the cutting punch creates a cylinder of tissue that can then be lifted up and cut loose. C, D, The core of tissue can be lifted up by fine forceps or by piercing it with the tip of a hypodermic needle.

  
  
  
  
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  Elliptical incisional or excisional biopsy— If the lesion is too large to make an excisional biopsy impractical, incisional biopsy with a margin of adjacent normal skin is performed. Provided that subsequent excision is performed in a timely manner for histologically proven malignant conditions, prior incisional biopsy does not alter the natural history of melanoma and other cutaneous malignancies. Incisional biopsies should be done longitudinally so that the resulting scar, which may need to be excised later, does not compromise subsequent excision of a potential malignancy.

  
  
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  Elliptical excision —This is usually designed in the line of least skin tension to facilitate linear closure. If the line of least skin tension is difficult to assess, simply excise around the lesion perimeter with appropriate margins and the wound will gape into an ellipse, indicating skin tension; then simply excise the “dog ears” ( Figure 58.8 ).

  
  

  
  

  
  

  

  
  

  
  

  Method of “dog-ear” excision following elliptical excision of a lesion.

  
  
  
  
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  Subungual lesions and longitudinal melanonychia —Remove the nail plate and perform either incisional or excisional longitudinal removal depending on the ability to finely repair the nail bed in a tension-free manner after lateral undermining.

Surgical Lesion Excision

Such excisions range from simple elliptical ones and tumor closure, through excision with frozen section assessment of margins, to Mohs micrographic surgery. If the lesion is small and there is abundant surrounding tissue laxity, then excision and linear closure may be permissible. If permanent sections reveal a persistent tumor, then reexcision of the scar is a simple matter. However, if a surgeon is planning a complex wound closure by tissue rearrangement or flap coverage, or if the lesion has complex invasion or is difficult to evaluate clinically by inspection and palpation (e.g., recurrence or certain infiltrative lesions), then intraoperative frozen section analysis of tumor margins is wise or resort to Mohs micrographic surgery.

When performing a simple tumor excision under local anesthesia, first determine tumor extent by loupe magnification inspection and palpation; mark the tumor margin together with the anticipated excision margin. Do this before local anesthetic infiltration because the presence of anesthesia distorts the tissues ( Figure 58.9 ).

A, The margin around a pigmented lentigo maligna lesion is marked prior to infiltration of local anesthetic. B, Resulting soft tissue wound. C, If clear clinical margins are ensured, a flap reconstruction may possibly be performed; this shows the outline of a Limberg transposition flap. D-H, However, always select the simplest and most effective method of wound closure. Wound edge undermining reveals that the wound can be closed directly. Subcuticular wound closure is performed after deep dermal closure, and dog-ear excision; the wound is supported by adhesive strips. Final outcome is shown in H .

Mohs micrographic surgery is generally reserved for certain widespread lesions with margins that are difficult to interpret clinically and where optimum conservation of uninvolved tissue is necessary such as with diffuse Bowen lesions ( Figure 58.10 ). In contrast to the conventional bread-loafed sectioning of the excised specimen, Mohs surgery involves tangential layered excisions and creating maps of the residual tumor for further excision until the whole lesion is excised. It is applicable to recurrent carcinomas, high-risk squamous carcinomas, tumors with ill-defined clinical margins (e.g., dermatofibrosarcoma protuberans), and in areas where maximal conservation of tissue is required to preserve function.

A, B, Bowen carcinoma. It is difficult to define the tumor margins by clinical inspection. Mohs surgery is performed (C, D) and skin grafting done (E), with the long-term outcome shown in F and G .

Epidermal Lesions

Seborrheic Keratosis

These lesions are more common in middle-aged and elderly patients. Lesions are usually centrally located, thus are more frequently seen on the upper arm and chest than on the hands. The depth of pigmentation is related to the amount of sun exposure. Occasionally, they mimic melanoma and require diagnostic biopsy. Seborrheic keratoses are benign flat lesions that take on a characteristic greasy scale and appear to have been “stuck” onto the skin’s surface ( Figure 58.11 ). Because they are entirely epidermal lesions, treatment takes advantage of their superficiality and includes curettage, shave biopsy, or application of liquid nitrogen. Given that these treatments do not invade the dermis, the potential for scarring is minimal.

Characteristic appearance of seborrheic keratoses on dorsum of the hand.

Pigmented Epidermal Lesions

Moles

Most common moles (nevi) do not require any specific treatment unless malignant transformation is suggested by enlargement, darkening pigmentation, or ulceration—“ABCD”: asymmetry, border irregularity, color variation, diameter greater than 6 mm. Palmar nevi were thought to be prone to malignant transformation, but this view has changed. Incidences of palmar nevi occur in 13% of whites and 29% of blacks, making routine excision of nevi in these locations both impractical and unnecessary.

Giant hairy congenital nevi occur most often on the face and bathing trunk area but can occur on the upper extremity ( Figure 58.12 ). It is unclear what the precise risk is for malignancy developing in giant congenital nevi. A systematic review suggests a range of 0 to 9%. The highest risk of malignant transformation with these lesions is actually during childhood and prepuberty, unlike the general incidence of melanoma, which is after puberty. Smaller congenital nevi are generally excised. However, excision of larger nevi may be less practical and require use of skin expansion, flaps, or skin grafting to close large wounds. Where excision is not feasible, periodic cancer surveillance and biopsy of suspicious areas must be done.

A, Arm giant hairy nevus. B, Large tissue expanders have been placed in the lateral chest wall. C, Most of the lesion is able to be excised at the first stage and a large wraparound chest wall pedicle flap is used for reconstruction (D) .

Dysplastic Nevus Syndrome

This occurs in both sporadic and familial forms ( Figure 58.13 ). There are multiple atypical nevi varying from 10 to more than 100, occurring mostly on the upper trunk. Lesions are often greater than 1 cm in diameter with irregular and variegated colors. Microscopic appearance is characteristic with large, atypical melanocytes that are spindle or epithelioid in type. The papillary dermis shows fibroplasia. It is impractical to excise all the lesions. Excision of a representative lesion can confirm a pathologic diagnosis. Such patients must be carefully observed and suspicious lesions excised.

A, B, Child with multiple dysplastic nevi on trunk and upper and lower extremities, including plantar and palmar surfaces (acral nevi).

Acral nevi (nevi occurring on the thickened palmar skin) can have histologic findings that may mimic dysplastic nevi.

Longitudinal Melanonychia

This term refers to the dark streaking of the nail caused by melanin deposits in the nail plate. Acral nevi that involve the nail matrix can present in this way. In dark-skinned patients, longitudinal melanonychia is common and is simply caused by increased melanin production by normal melanocytes. A longitudinal full-thickness nail bed biopsy is required for a suspicious lesion after removal of the nail plate and repair of the hyponychial nail fold and nail bed. Suspicious new lesions for potential melanoma include those in older patients (50–70 years), a longitudinal band >3 mm in width, change in lesion color and size, involvement of a single digit, nail dystrophy, and extension to the periungual skin (Hutchinson sign) ( Figure 58.14 ).

A, Nail has become completely involved by dark pigmentation. B, Nail plate has been removed to reveal germinal matrix nail bed pigmentation. Biopsy showed cellular atypia but no invasive melanoma. This was treated by nail bed surgical ablation and full-thickness skin grafting. C, Subungual melanoma showing Hutchinson sign with pigmentation encroaching on the proximal eponychium.

Dermal Lesions

Such lesions are often elevated to be classified as macules or papules and nodules. The following list describes some.

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  Dermatofibroma (histiocytoma) is a fibrous tumor that involves the dermis. They most frequently occur on the extremities. It is usually solitary, slow growing, and firm and attached to overlying skin but freely mobile in relation to deeper subcutaneous tissues. They may have a depressed central “umbilication.” Occasionally, dermatofibroma may be dark brown and be clinically confused with malignant melanomas. When indicated, simple excision can be done ( Figure 58.15 ).

  
  

  
  

  
  

  

  
  

  
  

  A, Dark-colored dermatofibroma showing central “umbilication.” B, Finger dermatofibroma.

  
  
  
  
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  Digital fibrokeratoma (acral fibrokeratoma) usually occurs on the acral surfaces of the hands. They are characteristically a hornlike projection with a raised collar of skin at the base. The overlying epidermis is hyperkeratotic and the dermis demonstrates increased fibrosis. They may mimic fibromas, eccrine poromas, and pyogenic granuloma. Treatment is by excision, though reappearance may occur.

  
  
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  Epidermal inclusion cysts arise from occluded pilosebaceous follicles, with some arising from traumatic displacement of epidermal cells into the dermis ( Figure 58.16 ). The skin is elevated over the underlying lesion and adherent to it. Central keratin-filled punctum may be seen. They are asymptomatic but may become secondarily infected. The preferred treatment is excision to include the entire epidermal lining.

  
  

  
  

  
  

  

  
  

  
  

  A, Patient who had prior fingertip traumatic amputation now presents with an apical finger mass. B, Radiograph shows pressure indentation of the distal phalanx. C, Fingertip inclusion cyst is excised. D, E, Palmar finger inclusion cyst.

  
  
  
  
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  Pilomatricoma (or calcifying epithelioma of Malherbe) occurs as a solitary tumor in the upper extremities of children and young adults ( Figure 58.17, A, B ). It is usually a nondescript small dermal nodule (0.5-cm diameter), and the foci of calcification are seen histologically. Treatment consists of surgical excision

  
  

  
  

  
  

  

  
  

  
  

  A, Small, slightly tender, and erythematous lesion over dorsum of proximal phalanx of little finger. B, Characteristic calcification of pilomatricoma is seen histologically. C, Patient with neurofibromatosis. D, E, Patient has a simple tender digital neurofibroma which is excised.

  
  
  
  
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  Neurofibroma may occur as an isolated dermal lesion or as part of a more diffuse neurofibromatosis ( Figure 58.17, C–E )

  
  
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  Infantile digital fibromatosis occurs at the tips of the fingers (but not the thumb). These may be single or multiple, as “kissing” lesions on adjacent digits ( Figure 58.18 ). They may cause functional deformity. Histologically, there are characteristic eosinophilic cytoplasmic inclusion bodies. Wide excision is required to minimize return but risk of recurrence is high.

  
  

  
  

  
  

  

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