Syphilis is a sexually transmitted infection by the spirochete Treponema pallidum, transmitted through skin and mucosa, with manifestations in nearly every organ system.

CLINICAL MANIFESTATIONS

Regional lymphadenopathy appears within 7 days. Nodes are discrete, firm, rubbery, nontender, more commonly unilateral; may persist for months.

Lesions

A painless ulcer or chancre (1 mm to 2 cm) occurs on the mucocutaneous site of inoculation, and is a button-like papule that evolves to a painless erosion and then ulcerates with raised border and scanty serous exudate. The surface may be crusted. Extragenital chancres occur at any site of inoculation; lesions on the fingers may be painful. Even without treatment, chancre heals completely in 4–6 weeks, the infection either becoming latent or developing into secondary or tertiary syphilis.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is made clinically and may be confirmed with dark-field microscopy or serologically. The differential includes genital herpes, traumatic ulcer, fixed drug eruption, chancroid, and lymphogranuloma venereum.

MANAGEMENT

Treat with intramuscular benzathine penicillin G 2.4 million units in single dose or oral doxycycline 100 mg twice daily for 14 days, which is highly effective and prevents secondary or tertiary syphilis.

Impetigo is most often caused by Staphylococcus aureus or betahemolytic streptococcus group A. Bullous impetigo results from local production of epidermolytic toxin A-producing S. aureus. These are not typical human skin flora, but rather transiently colonize skin and cause superficial infections. Primary infections occur most often in children, though primary and secondary infections can occur at all ages.

CLINICAL MANIFESTATIONS

Superficial infections are often asymptomatic.

Lesions

Impetigo appears as erosions with golden-yellow crusts 1 to 3 cm in diameter and with central healing if lesions have been present for several weeks. Lesions are scattered, discrete, and may become confluent; satellite lesions occur by autoinoculation. Secondary infection is common. Bullous impetigo as shown appears as blisters containing clear yellow or slightly turbid fluid with an erythematous halo, on normal-appearing skin. With rupture, bullous lesions decompress. If roof of bulla is removed, shallow moist erosion forms. Ecthyma as shown is ulceration with a thick adherent crust that may be tender and indurated.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical, confirmed by culture. Differential includes excoriation, allergic contact dermatitis, herpes simplex, epidermal dermatophytosis, scabies, burns, porphyria cutanea tarda, venous stasis, and ischemic ulcers.

MANAGEMENT

Treat lesions with mupirocin and retapamulin ointment and prevent recurrences with benzoyl peroxide wash and/or application of mupirocin and retapamulin ointment to the nares. Check family members for signs of impetigo and encourage all close contacts to wash hands with ethanol or isopropyl gel. Systemic antibiotics.

While malignant melanoma of the anogenital region is rare, the prognosis is poor because of early metastases via lymphatic vessels. Additionally, because the anogenital area is often not checked for precancerous and cancerous lesions, diagnosis often occurs late in the course of disease.

CLINICAL MANIFESTATIONS

There are macules or papules with variegation of brown-black color, irregular borders, and often with papular elevation, or ulceration. Lesions in men occur on the glans (67%), prepuce (13%), urethral meatus (10%), penile shaft (7%), and coronal sulcus (3%), and in women on the labia minora and clitoris.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is made clinically and confirmed with lesional biopsy. Total excisional biopsy with narrow margins is optimal, though incisional or punch biopsy is acceptable when total excisional biopsy cannot be performed. Do not use shave biopsy, which does not show the level of invasion. The differential includes genital lentiginosis, old fixed drug eruption, SCC, hemangioma, and intraepithelial neoplasia (Bowenoid papulosis).

MANAGEMENT

Treatment is excision down to the fascia. For lesions <1 mm thick, ensure 1-cm margins from lesion edges and biopsy lymph nodes only if nodes are palpable. For lesions >1 mm thick, ensure 2-cm margins and biopsy sentinel lymph nodes. Follow excision with direct closure or repair with skin grafts. Perform lymphadenectomy only for nodal basins with occult tumor cells or if nodes are clinically palpable and suspicious for tumor. Consider adjuvant therapy if there is risk of recurrence (positive regional lymph nodes, advanced stage).

Most sexually active people are subclinically infected with HPV and 1% of sexually active adults, 15–19 years old, develop lesions. Infection may be dormant for years and become infectious intermittently. A recently developed vaccine to specific types may decrease the incidence of HPV-induced carcinoma.

CLINICAL MANIFESTATIONS

There is dysplasia of anogenital and oral skin and mucosa ranging from mild to severe. Warts can develop into squamous cell carcinoma. Recurrences are more commonly from reactivation than reinfection. In pregnancy, warts may increase in size and number, show increased vaginal involvement, and have an increased rate of secondary bacterial infection. Children delivered vaginally to mothers with genital HPV infection are at risk for developing recurrent respiratory papillomatosis.

Lesions

Lesions are called condylomata acuminata and range from barely visible papules to nodules to confluent masses on anogenital skin or mucosa and oral mucosa including external genitalia, perineum, cervix, and oropharynx. Lesions are skin-colored, pink, red, tan, or brown and may be solitary, scattered, or isolated, or form voluminous confluent masses.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical, occasionally confirmed by biopsy. The differential includes normal anatomic variants (sebaceous glands, pearly penile papules, vestibular papillae), squamous cell carcinoma, benign neoplasms (moles, seborrheic keratoses, skin tags, pilar cyst, angiokeratoma), inflammatory dermatoses (lichen nitidus, lichen planus), molluscum contagiosum, condylomata lata, folliculitis, and scabietic nodules.

MANAGEMENT

No therapy has been shown to eradicate HPV or prevent cervical or anogenital cancer. Treatment is more successful if warts are small and present for <1 year. Treatment options are guided by patient needs; avoid expensive therapies, toxic therapies, and procedures that result in scarring. Imiquimod 5% cream or podophylox 0.5% solution is effective and can be applied by the patient. Cryosurgery and intralesional podophyllin 10–25%, and trichloroacetic acid 80–90% are alternatives as is surgical removal or electrodesiccation.

The second most common form of melanoma in light-skinned people, NM occurs mostly in middle age and on less sun-exposed areas. From the start, this tumor is in a vertical growth phase, involving the dermis. NM is much more common in those of Japanese descent (eight times for frequent than superficial spreading melanoma) for unknown reasons.

CLINICAL MANIFESTATIONS

NM may arise in a preexisting nevus, but more commonly arises de novo from normal skin, evolves over a few months, and is often noted by the patient as a new “mole”.

Lesions

The lesion is a uniformly elevated thick plaque or an exophytic, polypoid or dome-shaped lesion, usually with smooth regular borders. The color pattern is usually not variegated, and the lesion is uniformly blue or blue-black or, less commonly, can be very lightly pigmented or nonpigmented (amelanotic melanoma). NM is the one type of primary melanoma that arises quite rapidly (a few months to 2 years) from normal skin or from a melanocytic nevus as a nodular (vertical) growth without an adjacent epidermal component, as is always present in lentigo maligna melanoma and superficial spreading melanoma. Early lesions are 1–3 cm in size but may grow much larger if undetected.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical, confirmed with dermoscopy and/or biopsy. Total excisional biopsy with narrow margins is optimal. When biopsy is positive, reexcision is required. Incisional or punch biopsy is acceptable when total excisional biopsy cannot be performed or when lesion is large, requiring extensive surgery to remove the entire lesion. Differential for blue/black lesions is hemangioma (long history), pyogenic granuloma, and pigmented basal cell carcinoma. Any “blueberry-like” nodule of recent origin should be excised or, if large, biopsied.

MANAGEMENT

Treatment is excision down to the fascia. For lesions <1 mm thick, ensure 1 cm margins from lesion edges and biopsy lymph nodes only if nodes are palpable. For lesions >1 mm thick, ensure 2-cm margins and biopsy sentinel lymph nodes. Follow excision with direct closure or repair with skin grafts. Perform lymphadenectomy only for nodal basins with occult tumor cells or if nodes are clinically palpable and suspicious for tumor. Consider adjuvant therapy if there is risk of recurrence (positive regional lymph nodes, advanced stage).

SJS and toxic TEN are both an acute life-threatening mucocutaneous reactions characterized by extensive necrosis and detachment of the epidermis. SJS and TEN are variants of the same idiopathic or drug-induced disease and differ only in the percentage of body surface involved.

CLINICAL MANIFESTATIONS

The time from first drug exposure to onset of symptoms is 1–3 weeks, though this occurs more commonly with challenge. A prodrome of fever, malaise, and arthralgia often occurs 1–3 days prior to eruption. Impaired alimentation, photophobia, painful micturition, and anxiety may occur.

Lesions

There is mild-to-moderate skin tenderness, conjunctival burning or itching, then skin pain, burning sensation, tenderness, and paresthesia. Mouth lesions are painful and tender. The prodromal rash is morbilliform and can be targetoid with or without purpura. Lesions rapidly become confluent; alternatively, there may be no individual lesions, but rather diffuse erythema and no rash. As the rash progresses, epidermis becomes necrotic with crinkled macules that enlarge and coalesce. This is followed by sheet-like loss of epidermis and raised flaccid blisters that spread with lateral pressure (Nikolsky sign) on erythematous areas. With trauma, full-thickness epidermal detachment yields exposed, red, oozing dermis resembling a second-degree thermal burn. Lips, buccal mucosa, conjunctiva and genital and anal skin are invariably involved. Eyes have conjunctival lesions including hyperemia, pseudomembrane formation, keratitis, corneal erosions, and later synechiae between eyelids and bulbar conjunctiva.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

The differential includes drug eruptions, erythema multiforme, scarlet fever, phototoxic eruptions, toxic shock syndrome, graft-versus-host disease, thermal burns, staphylococcal scalded-skin syndrome (in young children, rare in adults), fixed drug eruption, and exfoliative dermatitis.

MANAGEMENT

Early diagnosis and withdrawal of suspected drug(s) are very important. Patients are best cared for in an intermediate or intensive care unit. Manage replacement of IV fluids and electrolytes as for patients with extensive a third-degree thermal burn. However, less fluid is usually required as for thermal burn of similar extent. Systemic glucocorticoids early in the disease; in high doses, they are helpful in reducing morbidity or mortality. Late in the disease they are contraindicated. High dose intravenous immunoglubulin in early stages. Surgical debridement is not recommended.

Eye lesions should be treated early with erythromycin ointment.

Neisseria meningitides colonizes the human nasopharynx and spreads by person-to-person contact through respiratory droplets.

CLINICAL MANIFESTATIONS

The symptoms of meningococcal meningitis are those of typical bacterial meningitis, namely, fever, headache, stiff neck, and PMNs in spinal fluid.

Lesions

Small, pink, blanchable macules and papules occur soon after onset of disease. With vascular friability and hemorrhage, petechiae and ecchymoses are seen on ankles, wrists, axillae, mucosal surfaces, and conjunctivae. A cluster of petechiae may be seen at pressure points, and ecchymoses and purpura may progress to hemorrhagic bullae, undergo necrosis, and ulcerate. In severe cases, purpura fulminans may occur which consists of bizarrely shaped, confluent necrotic hemorrhagic lesions that are grayish to black. There may be disseminated intravascular coagulation in fulminant disease. Patients may become septic and peripheral gangrene can occur. Waterhouse-Friderichsen syndrome is fulminant meningococcal septicemia characterized by high fever, shock, widespread purpura, disseminated intravascular coagulation, thrombocytopenia, and adrenal insufficiency.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Definitive diagnosis requires isolation of meningococci from blood or local site of infection. The differential includes adverse cutaneous drug eruptions, vasculitis, Rocky Mountain spotted fever, and infective endocarditis.

MANAGEMENT

Use third-generation cephalosporins (ceftriaxone or cefotaxime) as primary therapy. Alternatives (provided the strain is susceptible) include penicillin G, ampicillin, fluoroquinolone, or aztreonam. The usual duration of therapy is 7 days. In highly penicillin-allergic adults, administration of chloramphenicol (1 g IV every 6 hours) is preferable to risking cross-reactions with a third-generation cephalosporin. Provide supportive care to protect function of involved organs.

Nail involvement occurs in 10% of individuals with disseminated lichen planus, and nail lesions may be the only manifestation, and can destroy the nails. One, several, or all 20 nails may be involved (“twenty-nail syndrome,” where there is loss of all 20 nails without any other evidence of lichen planus elsewhere on the body).

CLINICAL MANIFESTATIONS

Onychorrhexis is seen (longitudinal ridging and fissuring of the nail plate with brittleness and breakage), though this is not a specific feature and can also be seen with aging. There are similar changes in lichenoid graft-versus-host disease. On the skin, the dorsum of the peripheral nail fold shows swelling with blue/red discoloration of proximal nail fold. There may be a small focus in the matrix, appearing as a bulge under proximal nail fold and a subsequent longitudinal red line: Thinned nail plate evolves into distal split nail (onychorrhexis). Matrix involvement is diffuse selective atrophy of nail plate with onychorrhexis and/or transverse splitting. A red lunula may be focal or disseminated, and transitory longitudinal melanonychia may occur. There may be a complete nail split. Pterygium formation (scar, matrix destroyed) is partial loss of the central nail plate, which presents as a V-shaped extension of skin of proximal nail fold adherent to nail bed. Acute progressive nail destruction leading to diffuse nail atrophy with and without pterygium leads to complete loss of nail (anonychia). In ulcerative lichen planus, there are bullae, erosions, hemorrhage, and scarring; in this form, cutaneous lesions are usually present on palms/soles.

Variants of the disease include 20-nail dystrophy of childhood, which resolves spontaneously; lichen planus-like eruptions following bone marrow transplant in graft-versus-host disease; drug-induced LP-like reactions, and permanent anonychia as the only manifestation of lichen planus.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Clinical appearance and LP lesions elsewhere on the body. Differential diagnosis includes all destructive nail diseases like psoriasis, Darier disease, onychomycosis.

MANAGEMENT

Treat nail lesions with intralesional triamcinolone and systemic glucocorticoids.

Varicose veins result from chronic venous insufficiency due to failure of centripetal return of venous blood and increased capillary pressure. Peak incidence of onset is 30–40 years, and women are affected three times more often than men. Varicose veins are an inherited characteristic aggravated by pregnancy, increased blood volume, increased cardiac output, increased venocaval pressure, and progesterone.

CLINICAL MANIFESTATIONS

There may be heaviness or aching of legs, which is aggravated by standing (dependency) and relieved by walking.

Lesions

Superficial leg veins are enlarged, tortuous, and have incompetent valves; these are best evaluated with the patient standing. “Blow-out” may be seen at sites of incompetent communicating veins. Varicose veins may or may not be associated with starburst phlebectasia usually overlying the area of an incompetent communicating vein. Superficial venectasias (spider phlebectasia) without a starburst pattern may be present, but most commonly are not a sign of chronic venous insufficiency.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is made with the tourniquet test, in which a tourniquet is applied to the leg that has been elevated to empty the veins; when the patient stands up and the tourniquet is released, there is instant filling of a varicose vein due to absent or ill-functioning valves. Doppler and color-coded duplex ultrasound detects incompetent veins and venous occlusion due to thrombus.

MANAGEMENT

Injection sclerotherapy in which a sclerosing agent is injected into varicosities, followed by prolonged compression is effective. Vascular surgery may also be performed.

Impetigo is most often caused by Staphylococcus aureus or betahemolytic streptococcus group A. Bullous impetigo results from local production of epidermolytic toxin A-producing S. aureus. These are not typical human skin flora, but rather transiently colonize skin and cause superficial infections. Primary infections occur most often in children, though primary and secondary infections can occur at all ages.

CLINICAL MANIFESTATIONS

Superficial infections are often asymptomatic.

Lesions

Impetigo appears as erosions with golden-yellow crusts 1 to >3 cm in diameter and with central healing if lesions have been present for several weeks. Lesions are scattered, discrete, and may become confluent; satellite lesions occur by autoinoculation. Secondary infection is common. Bullous impetigo appears as blisters containing clear yellow or slightly turbid fluid with an erythematous halo, on normal-appearing skin. With rupture, bullous lesions decompress. If roof of bulla is removed, shallow moist erosion forms. Ecthyma is ulceration with a thick adherent crust that may be tender and indurated.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical, confirmed by culture. Differential includes excoriation, allergic contact dermatitis, herpes simplex, epidermal dermatophytosis, scabies, burns, porphyria cutanea tarda, venous stasis, and ischemic ulcers.

MANAGEMENT

Treat lesions with mupirocin and retapamulin ointment and prevent recurrences with benzoyl peroxide wash and/or application of mupirocin and retapamulin ointment to the nares. Check family members for signs of impetigo and encourage all close contacts to wash hands with ethanol or isopropyl gel.

Necrobiosis lipoidica is a cutaneous disorder often, but not always, associated with diabetes mellitus occurring in young adults though not uncommon in juvenile diabetics. Women are affected three times more often than men. One-third of patients have clinical diabetes, one-third have abnormal glucose tolerance only, and one-third have normal glucose tolerance. The severity is not related to the severity or control of diabetes.

CLINICAL MANIFESTATIONS

Necrobiosis lipoidica is slowly evolving and enlarges over months, persisting for years. There is cosmetic disfigurement, and lesions that develop ulcers are painful.

Lesions

The lesion starts as a brownish red or skin-colored papule that slowly evolves into a well-demarcated waxy plaque of variable size. The sharply defined and slightly elevated border retains a brownish-red color, whereas the center becomes depressed and acquires a yellow-orange hue. Through the shiny and atrophic epidermis, multiple telangiectasias of variable size are seen. Larger lesions are formed by centrifugal enlargement. Merging of smaller lesions creates a serpiginous or polycyclic configuration. Ulceration may occur within the plaques, and healed ulcers result in depressed scars. Burned-out lesions are tan with telangiectasia. There are usually 1 to 3 lesions; >80% occur on the shin; at times symmetric. Less commonly lesions are on feet, arms, trunk, or face and scalp; rarely they may be generalized.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

The lesions are so distinctive that biopsy confirmation is not necessary; however, biopsy may be required in early stages to rule out granuloma annulare (which frequently coexists), sarcoidosis, or xanthoma.

MANAGEMENT

Topical glucocorticoids with occlusion are helpful; however, ulcerations may occur with occlusion. Intralesional triamcinolone, 5 mg/mL, into active lesions or lesion margins usually arrests extension of plaques. Most ulcerations heal with local wound care; if not, excision of entire lesion with grafting may be required.

Cutaneous reactions to arthropod bites are inflammatory and/or allergic reactions, and are characterized by an intensely pruritic eruption. Patients are often unaware of having been bitten. Significantly, arthropods are vectors of many systemic infections.

CLINICAL MANIFESTATIONS

Lesions

Solitary or grouped papules (usually <1 cm), papulovesicles, or bullae arise at the site of the bite occurring immediately after two days after the bite and persist for >48 hours. Erythematous macules can also occur at bite sites and are usually transient. Vesicles may form on papules, and large urticarial plaques may occur. Excoriations are common and can result in painful erosions that may be secondarily infected, and may heal with hyper- or hypopigmentation and/or raised or depressed scars, especially in more darkly pigmented individuals.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical and the differential includes papular urticaria and allergic contact dermatitis, especially to plants such as poison ivy or poison oak.

MANAGEMENT

Give potent topical glucocorticoids for a short duration for intense pruritus. Oral glucocorticoids can be given for persistent pruritus. Provide supportive care and watch for any secondary cutaneous infections or systemic infections transmitted by the arthropod.

Dyshidrotic eczema is a special vesicular type of hand and foot dermatitis that may be acute, chronic, or recurrent.

CLINICAL MANIFESTATIONS

Pruritus and sometimes pain occur when lesions are present.

Lesions

There is sudden onset of many deep-seated pruritic, clear “tapioca-like” vesicles; large bullae can occur (pompholyx). Later, scaling fissures and lichenification may occur. Pustules, cellulitis, lymphangitis, and painful lymphadenopathy represent secondary infection.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

The diagnosis is made clinically and the differential includes contact dermatitis, fungal infections, and viral exanthems.

MANAGEMENT

Topical high-potency corticosteroids, intralesional triamcinolone 3 mg/mL for small areas; in severe cases a short course of prednisone: starting with 70 mg and tapering by 10 or 5 mg over 7 or 14 days; systemic antibiotics for secondary infection and PUVA either oral or as “soaks.”

Dominant ichthyosis is an autosomal dominant disease that begins at age 3–12 months, and is characterized by usually mild generalized xerosis with scaling that is most pronounced on the lower legs.

CLINICAL MANIFESTATIONS

Dominant ichthyosis is very commonly associated with atopy, and xerosis and pruritus are worse in winter months. Many patients have cosmetic concerns, particularly when hyperkeratosis is severe. Over 50% of patients also have atopy.

Lesions

Xerosis (dry skin) with fine, powdery scaling occurs, but larger, firmly adherent tacked-down scales in a fish-scale pattern also occur. There is diffuse general involvement, accentuated on the shins, arms, and back, but also on the buttocks and lateral thighs; the axillae and the antecubital and popliteal fossae are spared as is the face usually, although the cheeks and forehead may be involved. Keratosis pilaris is perifollicular hyperkeratosis with little, spiny hyperkeratotic follicular papules of normal skin color, either grouped or disseminated, mostly on the extensor surfaces of the extremities but, during childhood, also on cheeks. The hands and feet are usually spared, but palmoplantar markings are more accentuated (hyperlinear).

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is usually by clinical findings; abnormal keratohyalin granules are seen in electron microscopy. The differential includes acquired ichthyoses and all other forms of ichthyosis.

MANAGEMENT

Instruct patients to keep skin hydrated, which is best accomplished by immersion in a bath followed by the application of petrolatum. Urea-containing creams, which bind water in the stratum corneum, are also helpful. Propylene glycol (44–60% in water), 6% salicylic acid in propylene glycol and alcohol under plastic occlusion (beware of hypersalicism), α-hydroxy acids (lactic acid or glycolic acid), and urea-containing preparations (2–10%) are also effective. For severe cases, intermittent therapy with isotretinoin and acitretin is very effective, but careful monitoring for toxicity is required.

When lice infest the head, they feed on scalp and neck and deposit eggs (nits) on hair shafts.

Young lice hatch within 1 week, passing through nymphal stages, growing larger and maturing to adults over a period of 1 week. One female can lay 50–150 ova during a 16-day lifetime. Lice survive only for a few hours off scalp. Transmission is from head-to-head contact via shared hats, caps, brushes, combs, fabric-covered seats, and pillows. The head louse is not a vector of infectious disease.

CLINICAL MANIFESTATIONS

There is pruritus of the back and sides of scalp. Scratching and secondary infection is associated with occipital and/or cervical lymphadenopathy. Some individuals exhibit obsessive compulsive disorder or delusions of parasitosis after eradications of lice and nits. Head lice are identified by eye or by microscopy (hand lens or dermoscope) but are difficult to find. Most patients have a population of <10. Nits are the oval grayish-white egg capsules (1 mm long) firmly cemented to the hairs and vary in number from only a few to thousands. With current infestation, nits are near the scalp; with infestation of long standing, nits may be 10–15 cm from the scalp.

Lesions

Papular urticaria on the neck may occur on the neck and reflect immune sensitivity/tolerance. Secondarily, eczema, excoriation, and lichen simplex chronicus may occur as can secondary infection. A hypersensitivity rash, resembling a viral exanthema, may also occur.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical, confirmed by detection of lice. Lice infestation can mimic hair casts (inner root sheath remnants); hair lacquer, hair gels, dandruff (epidermal scales), piedra, and pruritus may also be caused by atopic dermatitis, impetigo, and lichen simplex chronicus.

MANAGEMENT

Topical

Insecticide creams including permethrin, malathion, pyrethrin, piperonyl, and butoxide.

Systemic

Oral ivermectin (200 μg/kg).

BCC is caused by UV irradiation and is the most common cancer in humans. BCC is locally invasive, aggressive, and destructive but slow growing. There is almost no tendency to metastasize unless there is dedifferentiation, for instance, after inadequate radiotherapy. However, on the head, muscle and bone may be destroyed and the tumor can invade to the dura mater. BCC occurs after age 40, is more common in men, and rare in people with brown/black skin.

CLINICAL MANIFESTATIONS

BCC is a slowly evolving, often asymptomatic lesion that erodes or bleeds upon mild excoriation. Most often it occurs on the face, especially around the ears and nasolabial folds. The scleroxing type is often on the trunk.

Lesions

Nodular Translucent or pearly, firm, smooth nodule or papules with telangiectasia; sometimes have erosions or stipples of melanin. Ulcerating Translucent, pearly, smooth ulcers with telangiectasia; often have a crust and rolled border. Sclerosing is as small patch of morphea or superficial scar, often ill-defined, skin-colored, whitish but also with peppery pigmentation. Sclerosing BCC can progress to nodular or ulcerating. Superficial multicentric type has thin pink or red plaques with threadlike borders and telangiectasia; there may be considerable scaling. Superficial multicentric BCC can give rise to nodular and ulcerating BCC. Pigmented BCC Brown to blue or black, smooth, glistening surface; hard, firm, round or oval lesion; may be cystic or umbilicated.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical with careful examination with a hand lens, palpation, and dermoscopy, confirmed histologically. Differential includes all smooth papules; if pigmented, superficial spreading and nodular melanoma; if ulcerated, all nonpainful firm ulcers including SCC and extragenital primary chancre of syphilis. Solar keratoses are differentiated from BCC by the lack of bleeding upon excoriation.

MANAGEMENT

Excisions and repair is the standard of care. Cryosurgery and electrosurgery are options only for very small lesions below the neck. Use radiation therapy only when surgery may cause significant disfigurement or in very old age. Superficial BCCs below the neck may be treated with cryosurgery or electrocautery with curettage, though both are scarring. Topical 5-fluorouracil and imiquimod cream five times a week for 6 weeks is effective, and nonscarring, but may not remove all tumor tissue.

A blue nevus is an acquired, firm, dark-blue to gray-to-black, sharply defined papule or nodule representing a localized proliferation of melanin-producing dermal melanocytes. There are three types: common, combined, and cellular. Common and combined types are benign. Cellular blue nevi are larger and have very rare tendency to become malignant.

CLINICAL MANIFESTATIONS

Lesions

Common or combined types are papules or nodules, blue-gray, blue-black, <10 mm in diameter. Cellular blue nevi are larger (>1 cm) and irregular.

DIAGNOSIS AND DIFFERNTIAL DIAGNOSIS

Diagnosis is clinical and may be confirmed on biopsy. The differential includes dermatofibroma, glomus tumor, nodular or metastatic melanoma, traumatic tattoo, and pigmented basal cell carcinoma.

MANAGEMENT

No treatment is needed for common or combined nevi. Cellular blue nevi should be excised.

Disseminated superficial actinic porokeratosis is the most common form of the very rare porokeratoses, more common in men than in women with an age of onset that is typically in the sixth decade.

CLINICAL MANIFESTATIONS

There may be mild pruritus and cosmetic concerns.

Lesions

There are uniformly small, annular flat papules ranging from 2 to 5 mm in diameter that are distributed symmetrically on the extremities and located predominantly in sun-exposed sites. The border of the lesions is well-demarcated and hyperkeratotic, usually <1 mm in height with a characteristic longitudinal furrow encircling the entire lesion. As lesions progress, the central area becomes atrophic and unhidrotic.

Typically the palms, soles, and mucous membranes are spared.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical and can be difficult. The differential includes Darier disease, heat rash (miliaria rubra), papular urticaria, scabies, dermatitis herpetiformis (here there is grouping and the lesions are symmetric), Pityrosporum or eosinophilic folliculitis, insect bites, and drug eruptions.

MANAGEMENT

Treat lesions topically with Class I topical glucocorticoids under occlusion for 4 hours. Systemic oral glucocorticoids and dapsone have been used with success, but relapses occur after withdrawal. Phototherapy UVB or photochemotherapy may be useful for patients who do not respond to topical glucocorticoids under occlusion. Isotretinoin has been used in refractory cases.

Spider angiomas are very common and occur at all ages. They are more common in girls and women and may be associated with hyperestrogenic states, such as pregnancy (one or more in two-thirds of pregnant women), in patients receiving estrogen therapy, e.g., oral contraceptives, or in those with hepatocellular disease such as subacute and chronic viral hepatitis and alcoholic cirrhosis. Lesions arising in childhood or pregnancy may regress spontaneously.

CLINICAL MANIFESTATIONS

Lesions

A red focal telangiectatic network of dilated capillaries up to 1.5 cm in diameter radiates from a central arteriole (punctum). The central papular punctum is the site of the feeding arteriole with macular radiating telangiectatic vessels. The lesion is usually solitary and occurs most often on the face, forearms, and hands. On diascopy, the radiating telangiectasia blanches and the central arteriole may pulsate.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical and the differential includes hereditary hemorrhagic telangiectasia, ataxia-telangiectasia, or telangiectasia in systemic scleroderma.

MANAGEMENT

Spider angiomas are a benign vascular malformation. Laser treatments and electrosurgery are both effective if treatment is desired for cosmetic effect.

Epstein-Barr virus emerges from latency in advanced HIV disease and causes benign mucosal hyperplasia. Occurs with CD4+ cell count <300/ L.

CLINICAL MANIFESTATIONS

The disease is asymptomatic, though patients may be concerned that it gives stigmatization of HIV disease.

Lesions

White or grayish-white, well-demarcated plaques with corrugated texture occur on the lateral and inferior surfaces of the tongue and are often present bilaterally. Lesions do not rub off or clear with adequate anticandidal therapy.

DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS

Diagnosis is clinical. The differential includes pseudomembranous candidiasis (thrush), geographic or migratory glossitis, tobacco-associated leukoplakia, mucous patch of secondary syphilis, and squamous cell carcinoma in situ.

MANAGEMENT

Oral hairy leukoplakia usually resolves with antiviral treatment and immune restoration. Lesions can also be treated with podophyllin 25% in tincture of benzoin applied to the lesion with a cotton-tipped applicator for 5 min.