II.2 Características particulares del proyecto
II.2.5 Operación y mantenimiento
These single or multiple, discrete, dry, rough, adherent scaly lesions occur on the habitually sun-exposed skin of adults. They can progress to SCCIS, which can then progress to invasive SCC (Fig. 11-1). For a full discussion of this condition, see Section 10.
Synonym: Solar and actinic keratosis is syn- onymous.
Section 11 Precancerous Lesions and Cutaneous Carcinomas
227
Figure 11-1. Solar keratoses and invasive squamous cell carcinoma Multiple, tightly adherent dirty looking
solar keratoses (see also Figs. 10-25 to 10-27). The large nodule shown here is covered by hyperkeratoses and hemor- rhagic crusts; it is partially eroded and firm. This nodule is invasive squamous cell carcinoma. The image is shown to demonstrate the transition from precancerous lesions to frank carcinoma.
Cutaneous Horn ICD-9: 702.2 ° ICD-10: L85.8
■ A cutaneous horn (CH) is a clinical entity havingthe appearance of an animal horn with a papular or nodular base and a keratotic cap of various shapes and lengths (Fig. 11-2).
■ CHs most commonly represent hypertrophic solar keratoses. Non-precancerous CH formation can also occur in seborrheic keratoses and warts. ■ CHs usually arise within areas of dermatoheliosis
on the face, ear, dorsum of hands, or forearms, and shins.
■ Clinically, CHs vary in size from a few millimeters to several centimeters (Fig. 11-2). The horn may be white, black, or yellowish in color and straight, curved, or spiral in shape.
■ Histologically, there is usually hypertrophic actinic keratosis, SCCIS, or invasive SCC at the base. Because of the possibility of invasive SCC, a CH should always be excised.
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Part I Disorders Presenting in the Skin and Mucous MembranesFigure 11-2. Cutaneous horn: hypertrophic actinic keratosis A hornlike projection of keratin on a slightly raised
base in the setting of advanced dermatoheliosis on the upper eyelid in an 85-year-old female. Excision showed invasive SCC at the base of the lesion.
Arsenical Keratoses ICD-9: 692.4 ° ICD-10: L85.8
■ Appear decades after chronic arsenic ingestion(medicinal, occupational, or environmental exposure).
■ Arsenical keratoses have the potential to become SCCIS or invasive SCC. These are currently being seen in West Bengal and Bangladesh where drinking water may still contain arsenic.
■ Two types: punctate, yellow papules on palms and soles (Fig. 11-3A); keratoses indistinguishable from actinic keratoses on the trunk and elsewhere. These are often associated with small SCCIS of the Bowen-type and hypopigmented slightly depressed macules (“raindrops in the dust”) (Fig. 11-3B). ■ Treatment—as for solar keratoses.
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Squamous Cell Carcinoma in Situ
ICD-9: 173.0 ° ICD-10: M8070/2
■ Presents as solitary or multiple macules, papules,or plaques, which may be hyperkeratotic or scaling.
■ SCCIS is most often caused by UVR or HPV infection.
■ Commonly arises in epithelial dysplastic lesions such as solar keratoses or HPV-induced squamous epithelial lesions (SIL) (see Sections 27 and 34). ■ Pink or red, sharply defined scaly plaques on the
skin are called Bowen disease; similar but usually non-scaly lesions on the glans and vulva are called
erythroplasia (see Section 34).
■ Anogenital HPV-induced SCCIS is referred to as
Bowenoid papulosis.
■ Untreated SSCIS may progress to invasive SCC. With HPV-induced SCCIS in HIV/AIDS, lesions often resolve completely with successful antiretroviral therapy and immune reconstitution.
■ Treatment is topical 5-fluorouracil, imiquimod, cryosurgery, CO2 laser evaporation, or excision,
including Mohs micrographic surgery.
Section 11 Precancerous Lesions and Cutaneous Carcinomas
229
A
B
Figure 11-3. Arsenical kerato- ses (A) Multiple punctate, tightly
adherent, and very hard keratoses on the palm. (B) Arsenical kerato-
ses on the back. Multiple lesions are seen here ranging from red to tan, dark brown, and white. The brown lesions are a mix of arsenical kera- toses (hard, rough) and small sebor- rheic keratoses (soft and smooth). The difference can be better felt than seen. The red lesions are small Bowenoid keratoses and Bowen disease (SCCIS, see Fig. 11-4). The white macular areas are slightly de- pressed and represent superficial atrophic scars from spontaneously shed or treated arsenical keratoses. The entire picture gives the impres- sion of “rain drops in the dust.”
230
Part I Disorders Presenting in the Skin and Mucous MembranesEtiology
UVR, HPV, arsenic, tar, chronic heat exposure, and chronic radiation dermatitis.
Clinical Manifestation
Lesions are most often asymptomatic but may bleed. Nodule formation or onset of pain or tenderness within SCCIS suggests progression to invasive SCC.
Skin Findings. Appears as a sharply demar-
cated, scaling, or hyperkeratotic macule, pap- ule, or plaque (Fig. 11-4). Pink or red in color, slightly scaling surface or erosions, and can be crusted. Solitary or multiple. Such lesions are called Bowen disease (Fig. 11-4).
Red, sharply demarcated, glistening macu- lar or plaque-like SCCIS on the glans penis or labia minora are called erythroplasia of Queyrat (see Section 36). Anogenital HPV-induced SCCIS may be red, tan, brown, or black in color and are referred to as Bowenoid papulo-
sis (see Section 36). Eroded lesions may have areas of crusting. SCCIS may go undiagnosed for years, resulting in large lesions with annu- lar or polycyclic borders (Fig. 11-5). Once inva- sion occurs, nodular lesions appear within the plaque and the lesion is then commonly called
Bowen carcinoma (Fig. 11-5).
Distribution. UVR-induced SCCIS commonly arises within a solar keratosis in the set- ting of photoaging (dermatoheliosis); HPV- induced SCCIS, mostly in the genital area but also periungually, most commonly on the thumb or in the nail bed (see Fig. 10-33 and 34-16).
Laboratory Examination
Dermatopathology. Carcinoma in situ with loss
of epidermal architecture and regular differen-
tiation; keratinocyte polymorphism, single cell dyskeratosis, increased mitotic rate, and multi- nuclear cells. Epidermis may be thickened but basement membrane intact.
Diagnosis and Differential Diagnosis
Clinical diagnosis confirmed by dermatopatho- logic findings. Differential diagnosis includes all well-demarcated pink-red plaque(s): Num- mular eczema, psoriasis, seborrheic keratosis, solar keratoses, verruca vulgaris, verruca plana, condyloma acuminatum, superficial BCC, amelanotic melanoma, and Paget disease.
Course and Prognosis
Untreated SCCIS will progress to invasive SCC (Fig. 11-5). In HIV/AIDS, resolves with successful antiretroviral therapy (ART). Lymph node metastasis can occur without demonstra- ble invasion. Metastatic dissemination from lymph nodes.
Management
Topical Chemotherapy. 5-Fluorouracil cream ap-
plied every day or twice daily, with or without tape occlusion, is effective. So is imiquimod, but both require considerable time.
Cryosurgery. Highly effective. Lesions are usu-
ally treated more aggressively than solar kera- toses, and superficial scarring will result.
Photodynamic Therapy. Effective but still cum-
bersome and painful.
Surgical Excision Including Mohs Micrographic Surgery. Has the highest cure rate but
the greatest chance of causing cosmetically disfiguring scars. It should be done in all lesions where invasion cannot be excluded by biopsy.
Section 11 Precancerous Lesions and Cutaneous Carcinomas
231
A
B
Figure 11-4. Squamous cell carcinoma in situ: Bowen disease (A) A large,
sharply demarcated, scaly, and erythematous plaque simulating a psoriatic lesion.
(B) A similar psoriasiform plaque with a mix of scales, hyperkeratosis, and hemor-
232
Part I Disorders Presenting in the Skin and Mucous MembranesFigure 11-5. Squamous cell carcinoma in situ (SCCIS): Bowen disease and invasive SCC: Bowen carci- noma A red to orange plaque on the back, sharply defined, with irregular outlines and psoriasiform scale represents
SCCIS, or Bowen disease. The red nodule on this plaque indicates that here the lesion is not anymore an in situ lesion but that invasive carcinoma has developed.
invasive Squamous Cell Carcinoma
ICD-9: 173.0 ° ICD-10: M8076/2-3
■ SCC of the skin is a malignant tumor ofkeratinocytes, arising in the epidermis. ■ SCC usually arises in epidermal precancerous
lesions (see above) and, depending on etiology and level of differentiation, varies in its aggressiveness. ■ The lesion is a plaque or a nodule with varying
degrees of keratinization in the nodule and/or on the surface. Thumb rule: undifferentiated SCC is soft and has no hyperkeratosis; differentiated SCC is hard on palpation and has hyperkeratosis.
■ The majority of UVR-induced lesions are differentiated and have a low rate of distant metastasis in otherwise healthy individuals. Undifferentiated SCC and SCC in immunosuppressed individuals are more aggressive with a greater incidence of metastasis.
■ Treatment is by surgery.