Differential Diagnosis of Melanoma:
- In a patient who has multiple pigmented lesions, a lesion with an appearance that is substantially different from the others (eg, dark brown rather than light brown, nodule rather than flat) may represent melanoma ("ugly duckling sign"). The "ugly duckling sign" has a sensitivity of up to 90% for melanoma.
- Vertical growth of a melanoma often corresponds to a palpable nodularity, as in this patient, and increases metastatic risk. The Breslow depth (distance from the epidermal granular cell layer to the deepest visible melanoma cells) is the most important prognostic indicator in malignant melanoma.
- Benign pigmented lesions are usually asymptomatic; therefore, biopsy should be considered for moles that itch or bleed, particularly in the presence of other concerning features.
If melanoma is suspected, the patient should undergo excisional biopsy with initial margins of 1-3 mm of normal tissue.
Classically a pigmented macule or plaque that is asymmetric and has irregular, notched, scalloped, or poorly defined borders. The lesion usually has shades of brown, tan, red, white, blue-black, or combinations thereof.
Hx: Backs of men and legs of women
ABCDE of Melanoma:
Asymmetry: a lesion that is not regularly round or oval.
Border irregularity: a lesion with notching, scalloping, or poorly defined margins.
Color variegation: a lesion with shades of brown, tan, red, white, or blue-black, or combinations thereof.
Diameter: a lesion >6 mm in diameter; although a high level of suspicion exists for a lesion >6 mm in diameter, early melanomas may be diagnosed at a smaller size.
*Evolution: a lesion that changes in size, shape, symptoms (itching, tenderness), surface (bleeding), or shade of color.
Superficial spreading melanoma presents as a variably pigmented plaque with an irregular border and expanding diameter ranging from a few millimeters to several centimeters. It can occur at any age and anywhere on the body, although it is most commonly seen on the back in men and on the legs in women. Most superficial spreading melanomas appear to arise de novo. Superficial spreading melanoma accounts for approximately 70% of melanoma cases.
Nodular melanoma presents as a dark blue or black “berry-like” lesion that expands vertically (penetrating skin). It most commonly arises from normal skin and is most often found in people age 60 years or older. Nodular melanoma accounts for approximately 15% of melanoma cases.
Dx: Excisional biopsy. Fully excising the lesion allows for both assessment of the degree of cytologic atypia and the depth of invasion (termed the Breslow depth), which is the most significant prognostic feature of melanomas and is used to guide therapy.
Lentigo maligna melanoma presents initially as a freckle-like, tan-brown patch. When confined to the epidermis, the lesion is called lentigo maligna type. The lesion may be present for many years before it expands and becomes more variegated in color. When it invades the dermis, it becomes melanoma. It most often arises in sun-damaged areas (face, upper trunk) in older people. Lentigo maligna melanoma accounts for approximately 10% of melanoma cases.
Acral lentiginous melanoma can present in a variety of ways, including as a longitudinal dark pigmented streak on a fingernail or toenail, dark pigmentation of a proximal nail fold, and dark pigmented patches on the palms or soles. This variant of melanoma is the most common type among Asian and dark-skinned people. Acral lentiginous melanomas account for only 5% of melanoma cases.
Basal cell carcinomas (BCC)
Basal cell carcinoma is the most common type of skin cancer (75% of all skin cancers) and usually presents as a pearly papule or plaque with small telangiectasias on sun-exposed areas (head and neck). The most important risk factors for the development of BCCs are fair skin and sun exposure (the same risk factors as for AKs), the two often occur in the same area.
Possible features of BCC include:
- Persistent open sore that bleeds, oozes, or crusts
- Reddish patch or irritated area (superficial BCC)
- Pearly or translucent nodule with pink, red, or white color (nodular BCC)
- Elevated or rolled border with central ulceration
- Pale scar-like area with poorly defined borders
Nodular BCC (~60% of BCC)
A skin-toned to 🀄pink, pearly translucent, firm papule with telangiectasias. May have rolled borders and a central depression with ulceration. The most readily recognized clue to the diagnosis of a BCC is a changing skin lesion, including ulceration or erosion that spontaneously bleeds. Often found on the head or neck.
Px: Sun-exposed areas face, neck, trunk legs.
Superficial BCC (~30% of BCC)
A well-defined, erythematous, scaling plaque or occasional papules with a thin pearly border. Larger lesions often have hemorrhagic crusts and occur predominately on the trunk. A complete skin examination to find other similar plaques may help distinguish the solitary lesion of superficial BCC from psoriasis.
Morpheaform BCC (~5-10% of BCC)
A skin-colored, waxy, scar-like area that slowly enlarges. Usually develops on the head or neck of an older person. The name is based on its resemblance to morphea (scleroderma).
Low-risk lesions on the trunk or extremities can be managed with electrodessication and curettage (ED&C). However, ED&C is not recommended for higher-risk lesions or for BCC on the face, where the resulting scarring and hypopigmentation are undesirable.
Nodular BCC on the trunk or extremities may be easily managed with standard surgical excision, typically with 3-5 mm margins.
Mohs micrographic surgery is employed more often for the face. Mohs surgery is characterized by sequential removal of thin skin layers with microscopic inspection to confirm that the margins have been cleared of malignant tissue. This technique currently has the highest cure rate for BCC and provides the least disruption to surrounding tissues, making it ideal for delicate or cosmetically sensitive areas (eg, perioral region, nose, lips, ears).
Squamous cell carcinoma (SCC)
Squamous cell carcinoma is the second most common skin cancer and occurs primarily on sun-exposed areas.
SCC should be suspected in patients with a rough, scaly nodule or nonhealing, painless ulcer that develops in the setting of a scar or chronic inflammatory lesion. Sun exposure is the most common cause of SCC, but other risk factors include radiation exposure; immunosuppression; and chronic wounds, burns, or scars.
Hx: Risk factors include smoking and alcohol consumption; for lesions that occur on the ear, lips, chronic sun exposure is an additional risk factor. SCC is especially common in patients who have a history of organ transplant and are on chronic immunosuppressive therapy. SCC in immunosuppressed patients is typically more aggressive, with an increased risk of local recurrence and regional metastasis.
SCC arising within a 🔥burn wound is known as a Marjolin ulcer. In addition, SCC has been seen within the skin overlying a focus of osteomyelitis, radiotherapy scars, and venous ulcers. SCC arising within chronic wounds tends to be more aggressive, so early diagnosis with biopsy is important for preventing metastatic disease.
Hx: Presents as a firm, isolated, flesh-colored, pink or red ulcerated keratotic macule, papule, or nodule commonly found on the scalp, neck, pinna, or lip (most common type of malignancy on the lips and oral cavity). Generally consist of red plaques or nodules that may be covered with scale, crust, and erosions. The lesions often become keratinized (with a thickened, rough surface) or ulcerate with crusting and bleeding.
Keratoacanthomas are red, volcano-like nodules with a prominent central keratin plug. They are considered to be a subtype of well-differentiated squamous cell carcinoma. They grow rapidly and may reach a size of several centimeters within a few weeks. Classic keratoacanthomas eventually stabilize in size and may spontaneously regress without treatment.
Bowen Disease: A solitary, sharply demarcated, pink to fiery red scaly plaque that resembles superficial BCC, psoriasis, or eczema. May have a keratotic surface. Most commonly occurs on sun-exposed areas.
The diagnosis of SCC should be confirmed with skin biopsy (punch, shave, or excisional) that includes the deep reticular dermis to assess the depth of invasion. Small or low-risk lesions are usually managed with surgical excision or local destruction (eg, cryotherapy, electrodessication); lesions that are high risk or located in cosmetically sensitive areas should be referred for Mohs micrographic surgery.
Actinic keratosis (AK)
Common erythematous scaly macules that typically occur on sun-exposed areas of older persons with fair skin.
AKs are premalignant (squamous cell precursor) lesions that occur in sun-damaged areas. Approximately 1% to 5% will develop into squamous cell carcinomas over time.
Early lesions (1-3 mm) often are felt, not seen, and have a rough sandpaper texture. Color ranges from skin-colored to pink to red to brown. Occur on sun-damaged skin. Early superficial BCC may look like early actinic keratosis. With time, superficial BCC develops a rolled border and actinic keratoses get a thicker keratotic scale.
Tx: Multiple treatment options are available, including cryotherapy (3 ten- second freeze thaw cycles), topical imiquimod, topical 5-fluorouracil, and photodynamic therapy.
Common nevi (moles)
Nevi can become elevated and may be irritated by clothing, causing inflammation and bleeding. Nevi can undergo progressive loss of color over time. By age 60 y, nevi may be flesh-colored, dome-shaped, soft papules. Even inflamed nevi do not have overlying telangiectasias.
Congenital melanocytic nevus (CMN) is a benign proliferation of melanocyte cells. CMNs present within the first few months of life and are usually solitary, hyperpigmentedlesions with an increased density of overlying dark, coarse hairs. Initially presenting with flat homogenous hyperpigmentation, CMNs can grow during infancy and appear as heterogeneously pigmented and raised.
The risk of transformation to melanoma increases (up to 5%) with increasing size of a CMN, and large lesions are often removed surgically to reduce risk. Small lesions may be removed for cosmetic reasons given their low risk of melanoma transformation.
Nevus simplex and nevus flammeus are flat, blanchable, and erythematous vascular birthmarks. Nevus simplex lesions are typically located on the eyelids, glabella, and nape of the neck and fade with time; nevus flammeus lesions (port-wine stains) do not regress with time and are usually unilaterally located on the face.
Results from enlargement of the sebaceous oil glands, producing single or multiple small umbilicated pink or yellowish papules on the face. The main distinguishing features are the pink or yellowish color, the absence of telangiectasias, and the absence of translucency (“pearliness”) that is seen in BCCs.
Benign, 2- to 4-mm papules with a characteristic yellow color and central umbilication. Occur in clusters on the face without telangiectasia or bleeding.
Well-demarcated, smooth, reddish-violet patches that occur in elderly patients with significantly sun-damaged skin; they are indicative of skin fragility. They invariably arise from trauma, although often the inciting event is so mild as to escape notice. They typically occur on the dorsal arms and pretibial lower legs; patients on anticoagulant agents often have prominent lesions. They may heal with postinflammatory hyperpigmentation, which can sometimes mimic lentigo maligna.
Solar lentigines are brown macules and patches that occur in elderly fair-skinned persons in areas of substantial sun damage. They are benign but are indicative of a region that is at risk for developing skin cancer because they are a marker for sun exposure.
A chronic erythema and scaling of the lower lip caused by extensive sun damage. It is a precancerous condition. Appears as a rash rather than a tumor; however, any bulky area should be biopsied to rule out SCC.
Tx: Often treated with cryotherapy, topical 5-fluorouracil, or laser ablation to reduce the risk of malignant transformation.
- 5 "Ps": pruritic, 💜 purple/pink, polygonal papules & plaques
- Lacy, white network of lines (Wickham striae)
- Hepatitis C
- Medications: ACE inhibitors, thiazide diuretics
- Chronic symptoms
- Formation of lesions at sites of trauma (Köbner reaction)
- Spontaneous resolution within 2 years
- Topical high-potency glucocorticoids (eg, betamethasone)
- Widespread lesions: systemic glucocorticoids, phototherapy
The skin lesions in LP are characterized by the "5 P's": pruritic, purple/pink, polygonal papules and plaques. The lesions often show white, lacy markings known as Wickham striae and can form along lines of minor trauma or scratching (Köbner phenomenon).
LP is usually idiopathic, although it is often seen in patients with hepatitis C. However, drug-induced LP (lichenoid drug reaction) has been associated with a number of medications, including ACE inhibitors, thiazide diuretics, beta blockers, and hydroxychloroquine. Drug-induced LP typically has a more diffuse presentation than idiopathic LP, which is frequently limited to the flexor surfaces of the wrists and ankles, oral mucosa, and genitalia.
Treatment of drug-induced LP includes topical high-potency glucocorticoids and discontinuation of the offending medication. Some patients may develop recurrent bouts despite drug discontinuation, and residual hyperpigmentation is common.
a slow-growing type of melanoma most commonly seen on the face of older fair-skinned persons who have received a substantial amount of cumulative sun exposure with resultant evidence of sun damage. It has a prolonged radial growth phase and can be present for many years before developing an invasive component (vertical growth phase). Once it becomes invasive, the staging and prognosis are identical to those of other types of melanoma.
Ddx: Skin Infections (Bacterial)
A rapidly spreading deep subcutaneous dermis-based infection most often caused by S. aureus or group A streptococci.
Hx: Risk factors for lower extremity cellulitis include eczema, tinea pedis, onychomycosis, skin trauma (including insect bites, drug injection), chronic leg ulcers, long-standing diabetes mellitus, and edema. Risk factors for MRSA infection include recent close contact with persons having a similar infection, recent antibiotic use, recent hospitalization, hemodialysis, injection drug use, diabetes, and previous MRSA colonization or infection.
Px: Characterized by a well-demarcated area of warmth, swelling, tenderness, and erythema. possibly accompanied by lymphatic streaking or fever and chills.
Tx: Cellulitis without Purulence: Probable β-hemolytic streptococci or MSSA; MRSA unlikely.
Oral : Dicloxacillin, Cephalexin, Clindamycin
Intravenous: Oxacillin, Nafcillin, Cefazolin, Clindamycin
Cellulitis with Purulence: Probable MRSA; risk factors for MRSAc; failure to respond to non-MRSA therapy:
Oral: Trimethoprim–sulfamethoxazole, Clindamycin, Doxycycline, Minocycline, Linezolid
Intravenous: Vancomycin, Linezolid, Daptomycin
A superficial skin infection involving the upper dermis and superficial lymphatics.
Px: It is usually erythematous in appearance (“St. Anthony's fire”) with well-demarcated borders and is almost always caused by group A streptococci.
Tx: Treatment is usually a β-lactam antibiotic (eg, penicillin or amoxicillin).
A pustular skin infection in the hair follicle. Causes include S. aureus and, less frequently, group A streptococci.
Px: Typically affects the beard, pubic area, axillae, and thighs.
Tx: Folliculitis often is effectively treated with local application of heat and a topical antibiotic (mupirocin, chlorhexidine cleanser).
“Hot tub folliculitis” infection is generally caused by Pseudomonas aeruginosa
or Pseudomonas cepacia. The condition is usually self-limited, and therefore reassurance is all that is necessary. Antibiotic therapy is only indicated in recalcitrant
cases, or if patients are symptomatic.
Furuncles (boils/skin abscess)
Tender, pus-containing nodules that commonly appear on the neck or in the axillae or groin but may occur at any skin site
Boil: infection of the hair follicle that extends into the dermis and subcutaneous tissues
Abscess: Pus collections in the dermis and deeper tissues
Hx: Nearly always are caused by S. aureus.
Dx: Cultures from purulent material can distinguish MRSA from methicillin-susceptible S. aureus (MSSA) and can guide treatment.
Tx: Warm compresses to facilitate drainage may be adequate therapy for small furuncles. Incision and drainage (I & D) is required for larger furuncles and all abscesses. Incision and drainage may be adequate therapy for skin abscesses, and systemic antibiotics are not routinely required. However, they may be indicated if the patient is febrile or immunocompromised, has diabetes, or is at risk for MRSA or if there is a surrounding cellulitis
A superficial infection of the skin (epidermis) characterized by a group of yellowish, crusted pustules. caused by staphylococci (staph aureus) or streptococci.
Hx: Predisposing factors include poor hygiene, neglected minor trauma, and eczema.
Tx: Limited disease usually can be treated effectively with topical mupirocin or bacitracin; more extensive disease can be treated with a cephalosporin, penicillinase-resistant penicillin, or β-lactam-β-lactamase inhibitor.
An ulcerative form of impetigo usually caused by streptococci or staphylococci.
Px: The classic findings are superficial, saucer-shaped ulcers with overlying crusts, typically on the legs or feet.
Tx: Effective treatment consists of cleansing with an antibacterial wash followed by topical mupirocin plus oral cephalexin, dicloxacillin, or clindamycin. If MRSA is suspected or there is β-lactam allergy, one should consider other options.
Ecthyma gangrenosum is an ulcerative infection involving the dermis usually caused by Pseudomonas aeruginosa.
Hx: It is usually seen in immunocompromised patients and may indicate pseudomonal sepsis.
Px: Classic findings are ulcers with a central gray-black eschar and erythematous halo, typically on the legs or feet.
Tx: Initial therapy usually involves an antipseudomonal penicillin plus an aminoglycoside.
Risk factors for dermatophyte infection
- Warm, humid environments
- Direct contact with infected person, fomites, or public showers
- Contact with animals (eg, kittens)
- Concurrent dermatophyte infection (autoinoculation)
- Occlusive clothing
- Peripheral artery disease
- Diabetes mellitus
- HIV infection
- Systemic glucocorticoid therapy
Caused by T. tonaurans
Tx: Systemic therapy is necessary for a cure,
Griseofulvin is considered the treatment of choice in the United States, and should be used for 4 to 8 weeks.
Terbinafine, itraconazole, fluconazole, and ketoconazole can also be used. If fluconazole were to be used, the treatment duration would only be for 3 to 4 weeks.
Topical ketoconazole shampoo or selenium sulfide lotion may kill spores on the hair.
Tinea corporis (“ringworm”)
- Athletes who have skin-to-skin contact
- Humid environment
- Contact with infected animals (eg, rodents)
- Scaly, erythematous, pruritic patch with centrifugal spread
- Subsequent central clearing with raised, annular border
- First-line/localized: topical antifungals
- (eg, clotrimazole, terbinafine)
- Second-line/extensive: oral antifungals
- (eg, terbinafine, griseofulvin)
Tinea corporis is a cutaneous dermatophyte infectionmost commonly caused by Trichophyton rubrum. Patches of tinea corporis are typically annular but may become confluent to form a "flower petal" shape.
Patients with tinea corporis often have concurrent infection elsewhere on the body, hands (tinea manuum), groin (tinea cruris), or between the toes or sides of the feet (tinea pedis). Those with immunocompromising conditions (eg, HIV, diabetes mellitus) can have severe or widespread disease. Other risk factors include exposure to warm, moist areas (eg, public showers, swimming pools), contact with infected animals or people (eg, during sports participation), and wearing tight or occlusive clothing.
The diagnosis is confirmed using potassium hydroxide (KOH) preparation of skin scrapings. Most cases can be treated with topical antifungals (eg, terbinafine, clotrimazole); patients who fail topical therapy or have extensive disease may need systemic therapy (eg, oral terbinafine, fluconazole).
Caused by T mentagrophytes
Occurs in the groin
Tinea versicolor (pityriasis versicolor)
- Malassezia globosa skin flora grows in exposure to hot & humid weather
- Hypopigmented, hyperpigmented, or mildly erythematous lesions (face in children, trunk & upper extremities in adolescents & adults)
- ± Fine scale
- ± Pruritus
- KOH preparation shows hyphae & yeast cells in a "spaghetti & meatballs" pattern
- Topical ketoconazole, terbinafine, or selenium sulfide
Tinea versicolor (pityriasis versicolor) is a superficial fungal skin infection caused by Malasseziaspecies (nondermatophytic, lipid-dependent yeasts; eg, M globosa, M furfur). It is characterized by salmon-colored, hyper- or hypopigmented macules that are sometimes covered by fine scales, most commonly on the upper trunk and extremities. Hypopigmented areas are frequently noticed following sun exposure due to tanning of the surrounding skin.
Potassium hydroxide (KOH) preparation of skin scrapings shows large, blunt hyphae and thick-walled budding yeast ("spaghetti and meatballs" appearance). Topical treatment with selenium sulfide or ketoconazole is recommended, but the pigmentation changes can take months to resolve following treatment.
The true cause is multifactorial, but familial factors are involved. The key factors are follicular keratinization, angrogens, and Propionibacterium acnes. In acne, the kertatinization pattern in the pilosebaceous unit changes, and keratin becomes more dense, blocking the secretion of sebum. The keratin plugs are called “comedones.”
Hx: actors contributing to acne vulgaris include increased sebum production, follicular hyperkeratinization, bacterial colonization (Propionibacterium acnes), and, in some cases, an inflammatory response. Contributory factors to acne include certain medications, emotional stress, and occlusion and pressure on the skin, such as by leaning the face on the hands (acne mechanica).
Acne is not caused by dirt, chocolate, greasy foods or the presence or absence of any foods in the diet.
Tx: Initial management of comedonal acne without a significant inflammatory component includes:
Topical retinoids with the addition of:
- Organic acid preparations (eg, salicylic, azelaic, or glycolic acid) if initial therapy fails.
- Benzoyl peroxide, a widely used antibacterial agent, is another option for patients with comedonal acne, although it is preferred for inflammatory acne. Some patients with comedonal acne will develop inflammatory features, and benzoyl peroxide can be added at that time.
- Topical antibiotics (eg, erythromycin, clindamycin) is used in most patients with moderate or moderate-to-severe inflammatory acne require .
- Oral antibiotics (eg, tetracyclines) are reserved for patients with severe or nodular acne and for moderate inflammatory acne unresponsive to topical antibiotics. Oral antibiotics are also considered in patients with widespread inflammatory acne (eg, back, upper arms) that makes topical therapy impractical.
- Oral isotretinoin is indicated for nodular acne, severe acne, or moderate recalcitrant acne. 🕷
In addition, since both tetracycline and isotretinoin cause pseudotumor cerebri, the two medications should never be used together.
Drug-induced acne (also called steroid-induced folliculitis or steroid acne)
Drug-induced acne is typically associated with systemic 🌑 glucocorticoids but can also be caused by topical glucocorticoids, glucocorticoid-sparing agents (eg, azathioprine, cyclosporine), and a variety of other drugs (eg, anticonvulsants, antituberculous drugs).
In contrast to acne vulgaris (which displays lesions in various stages of development and typically occurs on the face in adolescents), drug-induced acne can be seen in any age group, is characterized by monomorphic papules without associated comedones, and commonly involves the upper back, shoulders, and upper arms. Some patients may have small pustules, but lesions are found in the same stage of development, and scarring cystic and nodular lesions are not seen. Drug-induced acne does not respond to typical acne treatment but improves rapidly on discontinuation of the offending agent.
Acute urticaria (hives)
Urticaria is due to mast cell activation in the superficial dermis, which increases release of multiple mediators (eg, histamine) that cause pruritus and localized swelling in the upper layers of the skin. Urticaria can be accompanied by angioedema, which is due to mast cell activation in the deeper dermal and subcutaneous tissues (eg, face, hands, and buttocks).
Etiologies of acute urticaria include infections (viral, bacterial, and parasitic), nonsteroidal antiinflammatory drugs, and IgE-mediated (eg, antibiotics, insect bites, latex, food) or direct (eg, narcotics, radiocontrast medium, muscle relaxers) mast cell activation. However, nearly 50% of patients have no known cause (idiopathic urticaria). Chronic urticaria can be due to physical stimuli (eg, cold temperature, skin pressure), serum sickness, or systemic disorders (eg, autoimmune disease, vasculitis, malignancy).
Patients with acute urticaria usually develop well-circumscribed and raised erythematous plaques with central pallor. The lesions can be oval, round, or serpiginous, and up to several centimeters in diameter. Patients usually have intense pruritus that can persist at night. Individual lesions appear and enlarge over minutes to hours before disappearing within 24 hours.
An H1-blocking nonsedating antihistamine (e.g., cetirizine [Zyrtec]), which will stop the likely allergic cause of her urticaria.
A short course of systemic glucocorticoids may also be helpful for patients with widespread or highly symptomatic involvement. In persistent cases, an H2-blocking antihistamine is sometimes added, although the effectiveness of doing so has not been established.
Topical corticosteroids can occasionally provide additional relief for symptomatic urticarial lesions
❗Concerning features: wheezing; stridor; and lip, tongue, or eyelid swelling; dyspnea, difficulty clearing secretions, or hemodynamic instability
Tx: Administration of epinephrine would be indicated.
Atopic Dermatitis (eczema)
Atopic dermatitis (eczema) is a very common condition characterized by pruritus, erythema, and scaly lesions on the skin. Pathogenesis involves epidermal dysfunction due to improper synthesis of stratum corneum components. Allergens can enter the disrupted skin barrier and generate an inflammatory response. Excessive bathing, dry environments, stress, overheating, and irritating detergents can trigger flares.
Eczematous lesions usually begin with pruritus alone and evolve to erythematous papules and scaly plaques. Severe lesions may have serous exudates and crusting.
Infants typically have lesions in the distribution of the face, scalp, and extensor surfaces of the extremities. The lesions can also be seen in flexural creases in older children and adults.
Treatment includes trigger avoidance, frequent application of thick bland emollients, and use of hypoallergenic cleansers for bathing and laundry. Moderate and severe eczema may require topical anti-inflammatory ointments (eg, hydrocortisone).
Dermatofibroma (DF) is due to fibroblast proliferation causing isolated or multiple lesions, most commonly on the lower extremities. The etiology is unknown, but some patients may develop lesions after trauma or insect bites. Typical lesions are nontender and appear as discrete, firm, hyperpigmented nodules that are usually <1 cm in diameter. The lesions have a fibrous component that may cause dimpling in the center when the area is pinched ("dimple" or "buttonhole" sign).
Diagnosis of DF is made clinically based on the appearance of the lesion. Treatment (cryosurgery or shave excision) is usually not required unless the lesion is symptomatic, bleeds, or changes in color or size. Patients may also request treatment for cosmetic reasons or because of recurrent cuts when shaving the legs.