THOMAS P HABIF MD

Adjunct Professor (Dermatology)

Department of Surgery
Geisel School of Medicine at Dartmouth
and Dartmouth-Hitchcock Medical Center
Hanover and Lebanon, NH, USA

JAMES L CAMPBELL Jr MD MS
Adjunct Associate Professor (Dermatology)
Department of Surgery
Geisel School of Medicine at Dartmouth
and Dartmouth-Hitchcock Medical Center
Hanover and Lebanon, NH, USA

M SHANE CHAPMAN MD
Associate Professor (Dermatology)
Department of Surgery
Geisel School of Medicine at Dartmouth
and Dartmouth-Hitchcock Medical Center
Hanover and Lebanon, NH, USA

JAMES G H DINULOS MD
Associate Professor of Surgery and
Pediatrics (Dermatology)
Department of Surgery and Pediatrics
Geisel School of Medicine at Dartmouth
and Dartmouth-Hitchcock Medical Center
Hanover and Lebanon, NH, USA

KATHRYN A ZUG MD
Professor of Surgery (Dermatology)
Department of Surgery
Geisel School of Medicine at Dartmouth
and Dartmouth-Hitchcock Medical Center
Hanover and Lebanon, NH, USA

Content Strategist: Russell Gabbedy

Content Development Specialist: Joanne Scott
Content Coordinator: Trinity Hutton
Project Manager: Maggie Johnson/Anne Collett
Design: Stewart Larking
Marketing Managers (UK/USA): Helana Mutak
Contents
TOPICAL THERAPY
1. Basic principles of treatment
2. Topical corticosteroids

ECZEMA
3. Acute eczematous inflammation
4. Rhus dermatitis (poison ivy, poison oak, poison
sumac)
5. Subacute eczematous inflammation
6. Chronic eczematous inflammation
7. Lichen simplex chronicus
8. Hand eczema
9. Asteatotic eczema
10. Chapped, fissured feet
11. Allergic contact dermatitis
12. Irritant contact dermatitis
13. Fingertip eczema
14. Keratolysis exfoliativa
15. Nummular eczema
16. Pompholyx
17. Prurigo nodularis
18. Stasis dermatitis
19. Venous leg ulcers
20. Atopic dermatitis
21. Autosomal dominant ichthyosis vulgaris
22. Keratosis pilaris
23. Pityriasis alba

URTICARIA
24. Acute urticaria
25. Chronic urticaria
26. Physical urticaria
27. Angioedema
28. Mastocytosis (urticaria pigmentosa)
29. Pruritic urticarial papules and plaques of
pregnancy

ACNE, ROSACEA, AND RELATED DISORDERS

30. Comedonal acne
31. Pustular acne
32. Cystic acne
33. Perioral dermatitis
34. Rosacea (acne rosacea)
35. Hidradenitis suppurativa

PSORIASIS AND OTHER PAPULOSQUAMOUS

DISEASES
36. Psoriasis: hands and feet
37. Psoriasis: lesions
38. Psoriasis: nails
39. Psoriasis: special forms
40. Seborrheic dermatitis
41. Grover disease (transient acantholytic
dermatosis)
42. Pityriasis rosea
43. Lichen planus
44. Lichen sclerosus
45. Pityriasis lichenoides et varioliformis acuta
BACTERIAL INFECTIONS
46. Impetigo
47. Cellulitis
48. Folliculitis
49. Pseudofolliculitis barbae
50. Furuncles and carbuncles
51. Pseudomonas folliculitis
52. Otitis externa

SEXUALLY TRANSMITTED INFECTIONS

53. Syphilis
54. Chancroid
55. Genital warts
56. Genital herpes simplex
57. Pubic lice
58. Molluscum contagiosum

VIRAL INFECTIONS
59. Warts (verruca vulgaris)
60. Flat warts
61. Plantar warts
62. Molluscum contagiosum
63. Herpes simplex (cold sores, fever blisters)
64. Varicella (chicken pox)
65. Herpes zoster (shingles)
66. Hand, foot, and mouth disease

FUNGAL INFECTIONS
67. Candidiasis (moniliasis)
68. Candidal balanitis
69. Candidiasis (diaper dermatitis)
70. Candidiasis of large skin folds (candidal
intertrigo)
71. Tinea versicolor
72. Tinea of the nails
73. Angular cheilitis
74. Cutaneous fungal infections (tinea)
75. Tinea of the foot
76. Tinea of the groin
77. Tinea of the body
78. Tinea of the hand
79. Tinea incognito
80. Tinea of the scalp
81. Tinea of the beard

EXANTHEMS AND DRUG REACTIONS

82. Non-specific viral rash
83. Erythema infectiosum
84. Cutaneous drug eruptions

HYPERSENSITIVITY SYNDROMES AND

VASCULITIS
85. Erythema multiforme
86. Stevens–Johnson syndrome
87. Erythema nodosum
88. Cutaneous small vessel vasculitis
(hypersensitivity vasculitis)
89. Henoch–Schönlein purpura
90. Schamberg disease (Schamberg purpura)
91. Sweet syndrome
INFESTATIONS AND BITES
92. Scabies
93. Head lice (pediculosis)
94. Bee and wasp stings
95. Lyme disease
96. Rocky Mountain spotted fever
97. Flea bites
98. Cutaneous larva migrans

VESICULAR AND BULLOUS DISEASES

99. Dermatitis herpetiformis
100. Pemphigus vulgaris
101. Pemphigus foliaceus
102. Bullous pemphigoid

CONNECTIVE TISSUE DISEASES

103. Chronic cutaneous lupus
104. Acute cutaneous lupus erythematosus
105. Dermatomyositis
106. Scleroderma
107. Morphea

LIGHT-RELATED DISEASES AND DISORDERS OF

PIGMENTATION
108. Sun-damaged skin, photoaging
109. Polymorphous light eruption
110. Porphyria cutanea tarda
111. Vitiligo
112. Idiopathic guttate hypomelanosis
113. Lentigo, juvenile lentigo, solar lentigo
114. Melasma (chloasma, mask of pregnancy)

BENIGN SKIN TUMORS

115. Seborrheic keratosis
116. Skin tags
117. Dermatofibroma
118. Keloids and hypertrophic scars
119. Keratoacanthoma
120. Nevus sebaceus
121. Chondrodermatitis nodularis helicis
122. Epidermal cyst
123. Pilar cyst
124. Sebaceous hyperplasia
125. Syringomas

PREMALIGNANT AND MALIGNANT

NON-MELANOMA SKIN TUMORS
126. Basal cell carcinoma
127. Actinic keratosis
128. Squamous cell carcinoma
129. Bowen disease
130. Leukoplakia
131. Cutaneous T-cell lymphoma
132. Paget disease of the breast
133. Extramammary Paget disease
134. Cutaneous metastasis

NEVI AND MALIGNANT MELANOMA

135. Nevi, melanocytic nevi, moles
136. Atypical mole syndrome (dysplastic nevus
syndrome)
137. Malignant melanoma, lentigo maligna
138. Melanoma mimics
139. Congenital melanocytic nevi
VASCULAR TUMORS AND MALFORMATIONS
140. Hemangiomas of infancy
141. Vascular malformations
142. Cherry angioma
143. Angiokeratoma
144. Venous lake
145. Pyogenic granuloma
146. Kaposi sarcoma
147. Telangiectasias
148. Spider angioma (nevus araneus)

HAIR AND NAIL DISEASES

149. Androgenic alopecia (male pattern baldness)
150. Androgenic alopecia in women (female pattern
hair loss)
151. Alopecia areata
152. Trichotillomania
153. Fungal nail infections
154. Nail diseases:
a. Psoriasis
b. Paronychia, Pseudomas, infection, white
spots or bands
c. Ridging and beading, habit tic deformity,
onycholysis
d. Digital mucous cyst, nevi and melanoma,
hematoma

NEONATAL DISEASE
155. Erythema toxicum neonatorum
156. Miliaria
157. Cutis marmorata

CUTANEOUS MANIFESTATIONS OF
INTERNAL DISEASE
158. Acquired cutaneous paraneoplastic syndromes
159. Inherited cutaneous paraneoplastic syndromes
160. Acanthosis nigricans
161. Neurofibromatosis
162. Tuberous sclerosis
163. Granuloma annulare
164. Necrobiosis lipoidica
165. Pyoderma gangrenosum
166. Lasers in dermatology
167. Leishmaniasis
168. Leprosy (Hansen disease)
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 Basic principles of

DDx Ref  70 • 79 • 108

treatment 1 

Steroid atrophy. Atrophy with prominence of the

underlying veins and hypopigmentation after use
of a superpotent steroid applied daily for 3
months to treat psoriasis.

Long-term use of topical corticosteroids can

produce thinning of the skin, allowing easy
bruising.

Striae of the groin after long-term use of group V

topical steroids for pruritus. These changes are
irreversible.

Inappropriate application of a topical steroid

causes tinea cruris to flare (tinea incognito).
1 Basic principles of
treatment
DDx Ref  70 • 79 • 108
MAINTAINING THE SKIN BARRIER
• Functions of the skin: fluid homeostasis; protec-
tion from infection, toxin absorption, temperature
regulation and ultraviolet radiation. • Primary goal
of topical or systemic dermatologic therapy:
restore and maintain a normal skin barrier.
SKIN CLEANSING
Use mild soaps and cleansers (Cetaphil, Dove, Keri,
or Aveeno). Limit use of exfoliating brushes and fra-
granced soaps. Wash with tepid, not hot, water.
SKIN MOISTURIZATION
Moisturize immediately after washing. Use thicker,
oil-based ointments for excessively dry, damaged
skin. Use lotions to maintain healthy skin. Use exfo-
liating emollients containing glycolic acids (lactic
acid, salicylic acid) and urea to gently remove
scales. Examples of lubricating creams and lotions.
• Thicker creams and ointments: Vaseline petro-
leum jelly, Aquaphor ointment, CeraVe. • Lighter
creams: Acid Mantle, Cetaphil cream, DML cream,
Moisturel cream, Vanicream. • Lighter lotions:
Cetaphil lotion, DML lotion, Nutraderm lotion, Curél
lotion, Aveeno lotion, CeraVe lotion.
TOPICAL FORMULATIONS
Two main factors determine the effectiveness of a
topical medication: the drug and the vehicle (base).
Vehicles assist in drug delivery and have therapeutic
properties. • Vehicle examples: powders (drying),
ointments (moisturizing, form protective barrier,
increase skin penetration of drug), creams (cooling,
not occlusive), pastes (drying, less greasy), solutions
or lotions (drying, effective for hairy areas), gels or
foams (greaseless).
TOPICAL APPLICATION AND DOSING
Gently massage medication into skin in one thin
layer. No need for thick application: 1 g of cream
covers a 10 × 10-cm area. The amount of cream
applied to the finger from the distal skin crease to
the tip of an adult index finger is 0.5 g. Apply creams
once or twice a day. Skin location affects ease of
medication penetration. The following anatomic loca-
tions are organized in increasing difficulty of medica-
tion penetration: mucous membranes (easy
penetration) > scrotum > eyelids > face > torso >
extremities > palms and soles.
WET DRESSINGS
Useful to dry exudative (wet) skin diseases or debride
infected wounds. • Immerse a clean, soft cloth (such
as bed sheeting or shirt material slightly larger than
the treated area) in cool (antiinflammatory) or tepid
solution (e.g. tepid water, Burow’s solution). • Gently
wring out excess solution and apply wet cloth to skin.
• Leave dressing open to air and in place for 30 min.
• Repeat 2−4 times a day. • Discontinue when skin
becomes dry.
 Topical corticosteroids
DDx Ref  15 • 20 • 37
2 

Plastic wrap (e.g. Saran Wrap) with paper tape is

an effective method to increase penetration of
topically applied medications.

Ace wrap can be applied on top of this plastic

wrap to help keep the wrap in place.

Occlusion of the entire body. A vinyl exercise suit

is a convenient way to occlude the entire body.

Occlusion for extended periods of time may result

in secondary infection with pustules and
Staphylococcal folliculitis. Occlusion is stopped
and the patient is treated with oral antibiotics.
2 Topical corticosteroids
DDx Ref  15 • 20 • 37
DESCRIPTION
• Topical corticosteroids: used to treat inflamma-
tory dermatoses; safe and effective with proper use.
• Corticosteroid potency: organized into seven
groups based on their anti-inflammatory activity;
group I (strongest) to group VII (weakest).
GENERAL FACTS AND GUIDELINES
Important factors to consider when choosing steroid
strength are diagnosis, location, age, and patient’s
financial resources. Two weeks is adequate to see a
clinical response. Steroid concentrations reflect rela-
tive strength for a particular corticosteroid (triam­
cinolone 0.025%, 0.05%, 0.1%) and cannot be used
to compare strengths between corticosteroids. Fluor-
inated steroids (containing a fluorine atom) have an
increased potency and a tendency for side effects.
• Superpotent topical corticosteroids (group I):
use less than 45−60 g per week; use cyclic dosing
(2 weeks of therapy followed by 1 week of rest);
prescribe limited amounts; use for plaque psoriasis
and hand or foot eczema. • Group II−VII topical
corticosteroids: avoid undertreatment with weak
group VII topical corticosteroids (hydrocortisone) for
more difficult rashes; eyelid dermatitis and intertrigi-
nous areas respond quickly to group VI or VII
steroids.
METHODS OF APPLICATION
Simple
Firmly massage thin layer of topical corticosteroid
into the skin without the aid of an occlusive dressing.
Washing is not necessary before each application.
Occlusive
Occlusive dressings (e.g. Saran Wrap) hydrate the
stratum corneum and allow enhanced corticosteroid
absorption; allow for use of lower-strength corticos-
teroids. Occlusive dressings can be used during the
day for periods up to 2 h, or 8 h during sleep. Simple
applications can be alternated with applications
assisted by an occlusive dressing. Vinyl exercise
suits (sauna suits) are effective to occlude large body
surface areas. • Complications of occlusive dress-
ings: infection, folliculitis, and miliaria
STEROID−ANTIBIOTIC MIXTURES
Antifungal–corticosteroid combinations (Mycolog,
Lotrisone) are expensive and have limited uses. The
topical corticosteroid betamethasone dipropionate
found in Lotrisone is too strong for intertriginous
areas and can cause permanent striae.
POTENTIAL SIDE EFFECTS OF TOPICAL
CORTICOSTEROIDS
• Allergic contact dermatitis, burning, itching, irrita-
tion, dryness (largely due to the vehicle), hypertricho-
sis, hypopigmentation, miliaria and folliculitis, skin
breakdown, glaucoma, cataracts, rebound phenom-
enon (i.e. psoriasis becomes worse after treatment
is stopped), rosacea, perioral dermatitis, acne, skin
atrophy with telangiectasia, stellate pseudoscars
(arms), purpura, striae, skin blanching from acute
vasoconstriction, systemic absorption, tinea incog-
nito, impetigo incognito, scabies incognito. • Infants
are at increased risk for systemic absorption.
 Acute eczematous
inflammation
DDx Ref  11 • 16 • 75
3 

Acute eczema findings: erythema, edema, and

vesiculation or bullae. This is intensely itchy,
early-onset poison ivy. Acute contact allergy is
often characterized by vesiculation.

Acute eczematous reaction to 5-fluorouracil to

treat actinic keratoses. The skin is erythematous,
weeping, and edematous.

Erythema, edema, vesiculation, and pruritus—all

findings of acute eczematous inflammation.

Erythematous papules scattered on the upper

chest and arms. Biopsy showed a spongiotic
epidermis typical of acute eczematous
inflammation.
3 Acute eczematous
inflammation
DDx Ref  11 • 16 • 75
DESCRIPTION
Acute eczematous inflammation is characterized
clinically by erythema, edema, and vesiculation.
Weeping and oozing of acute lesions is typical. Pru-
ritus is often severe.
HISTORY
• Multiple causes, including allergic contact hyper-
sensitivity to specific plant allergens such as poison
ivy, oak, sumac. • Nickel, topical medicaments (such
as bacitracin, neomycin, benzocaine, fragrances),
preservatives in personal care products, and rubber
additives are also common causes of acute eczema.
Irritant dermatitis is common after repeated water,
solvent, or detergent exposure. • In an ‘id reaction’,
acute eczema with vesicles occurs at a distant site
(e.g. hands) from an active fungal infection (e.g. feet).
• Stasis dermatitis, scabies, irritant reactions, and
dyshidrotic and atopic eczema may present as acute
eczema. • If provoking factors can be avoided, erup-
tion improves over 7–10 days, clearing usually by
3 weeks. • Excoriation predisposes to infection
and causes serum, crust, and purulent material to
accumulate. Excoriation can result in secondary
staphylococcal infection, aggravation, and dermatitis
prolongation.
PHYSICAL FINDINGS
• Examination finds erythema, edema, vesiculation,
and weeping. Inflammation moderate to intense.
Tiny, clear, fluid-filled vesicles. Bullae may develop.
FURTHER EVALUATION
• Consider patch testing for delayed-type hypersen-
sitivity if distribution suggests a contact exposure; if
problem recurrent or refractory to therapy; or if
known occupational, hobby, or other exposure to
cutaneous allergens. • Consider mineral oil prepara-
tion for scabies, especially in eczema of new or
recent onset. Consider scraping scale for potassium
hydroxide examination for dermatophyte fungus
infection. Blood tests almost never helpful. •
Repeated bouts of acute eczema on the face or
exposed hands or arms suggest a contact allergic
problem—evaluate by patch testing. • Patch testing
to patient’s own toiletry products is recommended,
along with appropriate testing of occupational aller-
gens with specific allergen trays.
TREATMENT
• Cool, wet dressings and topical steroid creams
suppress inflammation and itching. Soak a clean
cloth in cool water or Burow’s solution, then place on
affected areas for 30 min. Apply an appropriate
topical steroid cream (group II or III), rub in well. •
Reserve oral corticosteroids for severe or generalized
acute eczema. Approximately 1 mg/kg q.d. initially,
tapering over 3 weeks. Too short a course may result
in recurrence and rebound. • Oral antihistamines
such as diphenhydramine (Benadryl) and hydroxyzine
(Atarax) can relieve itching; sedative effect promotes
sleep. • If secondary infection suspected, culture,
review sensitivity, and use an appropriate oral anti-
biotic for 10–14 days. • Remove all patient’s topicals
(lotions, topical over-the-counter medicaments, anti-
itch preparations); treat with topical steroids only or
bland emollients such as plain Vaseline. Keep skin
care and exposures minimal and simple.
 Rhus dermatitis (poison ivy,
poison oak, poison sumac)
DDx Ref  11 • 47 • 75
4 

Allergic contact dermatitis to poison ivy is often

arranged in linear streaks. Not all the dermatitis
will appear this way, but vesicles in a linear
distribution suggest plant contact dermatitis.

Poison ivy, oak, and sumac share common

allergenic catechols called urushiols. The
dermatitis they cause is intensely pruritic and can
erupt over several weeks.

Severe poison ivy. Intact and collapsed bullae on

intensely erythematous skin on the forearm.

Dried urushiol on the skin may leave behind a

telltale black ink-like mark.
4 Rhus dermatitis (poison ivy,
poison oak, poison sumac)
DDx Ref  11 • 47 • 75
DESCRIPTION
Poison ivy, oak, and sumac (Anacardiaceae family,
Toxicodendron genus) are the most common causes
of allergic contact dermatitis in the USA; they are rare
in Europe. Related plants grow in South-East Asia,
and Central and South America. The plant oleoresin
(lipid-soluble portion) contains highly allergenic cat-
echol chemicals (urushiols).
HISTORY
• Contact with leaf, stem, or root causes eruption
within 8–72 h of exposure in a previously sensitized
individual, 12–21 days for a person not yet sensitized
(primary sensitization). • Primary allergic sensitiza-
tion can result from plant exposure. After sensitiza-
tion, repeat exposure causes the rash more promptly.
• About 80% of American adults develop the rash if
exposed; 30–40% require prolonged exposure. About
10–15% will not become sensitized. • Not spread by
blister fluid or person to person.
PHYSICAL FINDINGS
• Findings vary with oleoresin contact quantity,
pattern of contact, individual susceptibility. • Pruritic,
edematous, linear erythematous streaks, usually
with vesicles and large bullae on exposed skin.
• Airborne particulate matter from burning plant can
cause intense facial erythema and marked edema;
eyelids can be dramatically swollen. • One clue is a
temporary black mark, from dried and oxidized
urushiol, on exposed skin. • Rash duration 10 days
to as long as 3 weeks.
TREATMENT
• Wash skin with soap to inactivate and remove
allergic oleoresin. Most effective if done within
15 min of exposure. • Cleanse exposed clothing and
tools with soapy water. • Short, cool tub baths, with
or without colloidal oatmeal (Aveeno), are soothing.
• Calamine lotion helps control itching. • Oral anti-
histamines (hydroxyzine or diphenhydramine) may
alleviate itching. Best at night to promote rest and
offer itch relief. • Cool tap water or Burow’s solution
compresses highly effective during blistering stage.
Apply for 15–30 min several times a day for 1–4 days
until blistering and severe itching controlled. Tap
water cool compresses useful for severe facial or
eyelid edema. • A medium-potency topical steroid
(group II–V) is generously applied after wet dressing.
If periorbital skin involved, a weaker topical steroid
(group VI–VII) is advised for limited duration (twice
daily for 7 days). • For severe, widespread inflam-
mation, oral prednisone 0.75–1 mg/kg q.d. every
morning, slowly tapered over 3 weeks. • Ivy Block
barrier cream can prevent or lessen dermatitis, but
must be applied before plant contact.
 Subacute eczematous
inflammation
DDx Ref  12 • 18 • 77
5 

Arm with subacute eczematous changes, which

include confluent erythema and secondary changes
of scaling, erosions, and crusts. Atopic dermatitis or
allergic contact dermatitis appears this way.

Nipple eczema is a finding in atopic dermatitis.

Subacute eczematous changes seen here are
scaling, erythema, fissuring, and crusting. The
skin appears dry.

Eczema around the eye area. The patient was

allergic to a component of her moisturizer. Fragrance
materials and preservatives in make-up and
toiletries can be acquired allergies at any time in life.

Ear with xerosis, erythema, and crusting typical of

subacute eczematous inflammation.
5 Subacute eczematous
inflammation
DDx Ref  12 • 18 • 77
DESCRIPTION
Subacute eczematous inflammation consists of itchy,
red, and scaling patches, papules, and plaques.
HISTORY
• May evolve from acute (vesicular) eczema. • Most
common clinical manifestation of atopic dermatitis.
• Itching variable; can be moderate to severe, or
rather mild. • Resolves without scarring when pro-
voking or contributing aggravating factors are
removed. May require treatment to resolve. • Exco-
riation and repeated exposure to aggravating condi-
tions (water, detergents, irritants, or other common
irritant or allergic offenders) convert this condition to
a chronic process. • Nummular eczema, fingertip
eczema, scabies, and fungal infections are derma-
toses that may present as subacute eczema. • Atten-
tion to exposures of irritants, allergens, and patient’s
overall skin care regimen is vital to addressing cause
and aggravating factors.
PHYSICAL FINDINGS
• Erythema, scaling, and itching occur; often, there
are indistinct borders. • Patchy redness may be faint
or intense.
TREATMENT
• Moisturizers are an essential part of daily therapy;
encourage frequent application. • Moisturizers are
most effective when rubbed in well and applied
directly after skin is patted dry following bathing.
• Emollients with simple formulations lacking the
most common allergy-associated ingredients (e.g.
Aveeno, Cetaphil, DML, Acid Mantle) are better than
lotions. Plain petroleum jelly is an excellent emollient.
• Infrequent washing with bar-type mild soap (e.g.
Dove, Cetaphil, Keri, Purpose, Basis) is also helpful.
• Group II–V steroid creams twice a day with or
without plastic occlusion. Occlusion hastens resolu-
tion while increasing absorption. Duration of occlusion
should be specified, limited, and supervised. • Alter-
native is steroid ointment applied twice a day without
occlusion. • Non-steroid topical immune modulators
tacrolimus (Protopic ointment 0.1, 0.03%) and pime-
crolimus (Elidel cream 1%) applied twice daily to
affected skin are especially useful in subacute eczema
of the face or periorbital eyelid skin. May initially cause
some stinging or burning, which subsides in a few
days. These therapies are useful for chronic manage-
ment of subacute eczema in atopic patients. • Tar
ointments and creams (many over-the-counter prepa-
rations) provide an alternative to steroid-resistant
lesions and are moderately effective. • Wet dressings
should be avoided, because they cause excessive
dryness. • Antibiotics (e.g. trimethoprim-sulfa,
cephalexin, dicloxacillin) for secondary bacterial
infections (usually Staphylococcus aureus, but sensi-
tivity should be checked). • Ask about occupation,
duties at home, and hobbies, as these may contribute
to ongoing skin irritation or allergy. Gloves are a useful
protective barrier in cases of repeated exposure to
water, irritants, or allergens. Vinyl gloves are best,
because they do not contain common rubber-related
allergens (gloves can be ordered online from http://
www.allerderm.com). Allerderm Ultimate N-Dex Free
Nitrile exam gloves do are non-latex, powder free,
accelerator and antioxidant free gloves with excellent
chemical resistance properties.
 Chronic eczematous
inflammation
DDx Ref  7 • 15 • 20
6 

Eczematous dermatitis of the distal fingertip. The

chronic problem has resulted in a horizontal nail
depression and scaling of the nail. Scaling,
erythema, and fissuring are seen.

Chronic eczematous dermatitis on the forearm.

There is confluent erythema, a moderate amount
of scaling, and an occasional crust. Vesicles are
not seen. This is very pruritic.

The palm is red, thickened and fissured. These

findings had been present for months.

The skin is red, thickened, dry, cracked and

excoriated. Rubbing and scratching should be
actively discouraged. Bland emollients such as
Vaseline should be substituted for other fragrance
or suspect preservative allergen-containing lotions
and creams.
6 Chronic eczematous
inflammation
DDx Ref  7 • 15 • 20
DESCRIPTION
Affected skin is inflamed, red, scaling, and thickened
(lichenified).
HISTORY
• There is moderate to intense, prolonged itching.
• Scratching and rubbing become habitual and may
be done subconsciously. • The disease becomes
self-perpetuating. • Scratching leads to thick skin,
which itches even more. • Atopic dermatitis, chronic
allergic or irritant contact dermatitis, habitual
scratching, lichen simplex chronicus, chapped and
fissured feet, nummular eczema, asteatotic eczema,
fingertip eczema, and hyperkeratotic eczema are
possible etiologies. • This process is the result of a
chronic dermatitis.
PHYSICAL FINDINGS
• Intense itching can lead to excoriations. • Inflamed,
itchy skin thickens, and surface skin markings
become more prominent. • Thick plaques with deep
parallel skin markings appear (lichenification).
• Sites commonly involved are those easily reached
or creased areas. • Common locations are the back
of the neck, popliteal fossae, ankles, eyelids, ano-
genital skin, palms, soles and legs in stasis derma-
titis. • Hyperpigmentation or hypopigmentation can
occur on affected skin.
TREATMENT
• Ointments penetrate lichenified skin well and are
generally more effective than creams on lichenified
skin. • Consider and evaluate for contact irritants and
allergens. Simplify the skin regimen, i.e. mild soaps,
bland emollients (petrolatum, Aquaphor, Aveeno,
Vanicream) only. Protopic ointment (tacrolimus) can
be helpful for involved lichenified chronic eczema on
the face. • Chronic eczematous inflammation is often
resistant to treatment; the key to success is breaking
the itch–scratch cycle through treatment and removal
of the cause or sources of aggravation. • A cool, wet
dressing on the affected skin for 20 min will help
soothe and diminish itch; it can be very helpful for
the nighttime itch urge. • Group I or II creams or
ointments applied twice a day can be effective (not
for face location). • Group II–V steroids are used with
plastic occlusion for 2–8 h. • Intralesional injections
(e.g. triamcinolone (Kenalog) 10 mg/mL) are very
effective; resistant plaques are reinjected at 3- to
4-week intervals. • Steroid-impregnated tape (e.g.
Cordran tape) should be left on for 12 h. • Chronic
rubbing or scratching is at least part of the problem—
address it and aim to diminish it.
 Lichen simplex chronicus
DDx Ref  18 • 20 • 37
7 

Dorsum of the hand with an erythematous plaque

that has overlying scale and fissuring. The skin is
thickened in lichen simplex chronicus, often from
chronic scratching or rubbing.

Erythema, scaling, marked xerosis, and angular

erosions indicating excoriation characterized this
lesion of lichen simplex chronicus.

The back of the neck is a common area for a

plaque of lichen simplex chronicus. The patient
often admits to repeated scratching of this area.

The perianal skin is thickened and pink, with

fissuring, due to chronic scratching. Cool
compresses, topical steroid ointment, and oral
antihistamine should help interrupt the itch–
scratch cycle.
7 Lichen simplex chronicus
DDx Ref  18 • 20 • 37
DESCRIPTION
Localized plaque of chronic eczematous inflamma-
tion created by habitual rubbing and scratching.
Frequently located on wrists, ankles, anogenital skin,
and back of neck.
HISTORY
More common in adults but may be seen in atopic
children. A typical plaque stays localized and shows
little tendency to enlarge. Once established, the
plaque does not usually increase in size.
PHYSICAL FINDINGS
• Findings include a sharply demarcated, deeply
violaceous or red scaly plaque with prominent skin
lines (lichenification). • Although this is a chronic
eczematous disease, acute changes of vesiculation
and weeping may result from sudden allergy to
topical treatments. • Moist scaling, serum, crust, and
pustules signal secondary infection. • Nodules,
usually smaller than 1 cm and scattered randomly on
the scalp, occur in patients who frequently pick at
the scalp. • Areas most commonly affected are con-
veniently reached, commonly the outer portion of
lower legs, wrists, ankles, posterior neck, scalp,
eyelids, fold behind the ear, scrotum, vulva, and
anal skin. • Infection can mimic lichen simplex
chronicus; consider potassium hydroxide examina-
tion. • Contact allergy may cause, lead to, or com-
plicate. Patch testing can be helpful.
TREATMENT
• Stress may play a role in some, and should be
explored, acknowledged and addressed. • The
patient should understand the problem will not
resolve until even minor scratching and rubbing are
stopped. • Scratching frequently takes place during
sleep, and the affected area may have to be covered.
• Treatment consists of a 5-min water soak followed
by the application of a topical steroid with medium
to high potency in an ointment base. • The treatment
of the anal area, genitalia, or fold behind the ear does
not require potent topical steroids; rather, these
areas should be treated with low-potency topical
steroids in ointment base. • For scalp lesions, apply
a group I or group II steroid gel such as fluocinonide
(Lidex) or a solution such as clobetasol (Cormax scalp
solution) twice each day for 2 weeks. • Moist, sec-
ondarily infected areas respond to oral antibiotics and
topical steroid lotion. • Nighttime itching can be
diminished with oral antihistamines such as diphen-
hydramine (Benadryl) or hydroxyzine (Atarax).
• Grenz ray (superficial X-ray therapy) can be helpful
but has limited availability. • Nodules caused by
picking may be very resistant to treatment, requiring
monthly intralesional injections with triamcinolone
acetonide (Kenalog 5–10 mg/mL). • Stress does not
cause the condition, but most definitely contributes
to aggravating and perpetuating it. Ask about stress,
address the role it can play, and seek avenues for
stress reduction.
 Hand eczema
DDx Ref  20 • 37 • 47
8 

Hand dermatitis. Erythema of the palms, with a

more focal area of scaling and pruritus. Search
for irritants, allergens, and history of atopy.
Consider occupational and other daily exposures.

Dorsum of the hand with patch of erythema,

some crusted vesicles, and some scaling.
Excoriation has caused the skin surface to break
in several areas.

Dermatitis with erythema, scaling, and crusting

on the palms and fingers. Consider irritants,
allergens, exposures, and care regimen specifics
in looking for causal or aggravating factors.

Erythema, yellow scaling, and fissuring

characterize this more psoriasis-like dermatitis on
the fingers.
8 Hand eczema
DDx Ref  20 • 37 • 47
DESCRIPTION
Common, often chronic, with multiple causative and
contributing factors. • Types: irritant (most common)
and allergic contact; atopic, keratolysis exfoliativa;
fingertip; hyperkeratotic; nummular; pompholyx
(dyshidrosis); and ‘id reaction’.
HISTORY
• Occupational risks: irritant exposure, frequent
wet work, chronic friction, work with sensitizing
(allergenic) chemicals. • Irritants: include chemical
irritants (e.g. solvents, detergents, alkalis, acids),
friction, cold air, low humidity. • Allergenic chemi-
cals from occupational and/or non-occupational
sources: immediate type 1 allergy (e.g. to latex, food
proteins); delayed type 4 allergy can develop to
rubber antioxidants and accelerators, nickel cobalt
and chromium, medicaments (bacitracin, neomycin,
hydrocortisone) and ingredients in skin products (e.g.
preservatives, fragrances, sunscreens, other addi-
tives). • Id reactions: eczematous eruptions to
distant fungal (dermatophytid) or bacterial (bacterid)
infection. • Endogenous factors: atopic diathesis
(allergic rhinitis, asthma, atopic eczema).
PHYSICAL FINDINGS
Variable presentation: acute, subacute, or chronic
eczematous lesions. The following findings may
prove useful. • Xerosis, erythema, burning > 
itching on dorsal or volar hands: evaluate for
irritant or allergic factors. • Nummular eczema:
allergy, irritation, or atopy can play a role; occasion-
ally, contact urticaria (type 1 allergy) is culprit.
• Recurrent, intensely pruritic vesicles on lateral
fingers and palms: suspect pompholyx. • Fingertip
eczema (dryness, splitting, tenderness, no itch):
suspect an irritant, an endogenous factor (atopy
during winter), or a frictional eczema. • Erythema,
scaling, itching in ‘apron’ (base of the fingers) of
palm: suspect atopy.
TREATMENT
• Frequent, generous application of a bland emollient
(white petrolatum, Aveeno, Hydrolatum, Aquaphor).
• Avoidance of irritants such as frequent hand
washing and water exposure, soaps, detergents, sol-
vents. If hand sanitizer can be used in place of
washing hands, it is less irritating and should be
recommended. Chronic frictional trauma also an irri-
tant. • Take protective measures (e.g. vinyl gloves
for wet or chemical work). • Medium- to high-potency
(groups II–IV) topical steroids twice daily. Ointments
preferred. Most effective when used intermittently.
• For severe dermatitis, a superpotent topical cortico­
steroid applied after wet dressings containing
Burow’s solution, twice a day for 3–5 days, followed
by a medium-potency topical cortico­steroid twice a
day for several weeks. • Other options include topical
tar hand soaks with Balnetar oil, two or three capfuls
diluted in water for 15–30 min twice daily, followed
by topical corticosteroid. • Systemic steroids (pred-
nisone 0.75–1 mg/kg q.d., tapering over 3-week
course) may occasionally be required. • Most improve
with irritant avoidance, frequent emollient use, and
occasional topical steroid treatment. • Refer to a
dermatologist if chronic and refractory. • Patch
testing indicated to evaluate for occupational and
environmental allergens if recurrent.
 Asteatotic eczema
DDx Ref  12 • 18 • 47
9 

A dry, cracked, almost fissured-looking skin

surface characterizes asteatotic eczema. Winter
and low humidity often prompt this condition in
the elderly. Daily bland emollient use is helpful.

Asteatotic eczema can be severe enough to result

in fissuring and heme crusting of the skin. This
condition is tender and uncomfortable.

The skin in asteatotic eczema is often described

as having a ‘cracked pavement’ appearance.

Asteatotic eczema with prominent follicular

inflammation.
9 Asteatotic eczema
DDx Ref  12 • 18 • 47
DESCRIPTION
Distinctive clinical pattern of eczematous dermatitis
caused by excessive dryness and chapping. Also
referred to as eczema craquelé.
HISTORY
Asteatotic eczema is a form of subacute eczematous
dermatitis that tends to be chronic and low grade,
with wintertime seasonal flares due to low humidity.
Peaks in late winter and improves in summer, espe-
cially in colder, drier climates. • More common in
patients with the atopic diathesis, more common in
older individuals. • Most patients have a history of
previous similar flares. • Any site may be affected,
although lower legs most commonly involved.
• Early, affected individuals often note that skin looks
and feels dry. • With progression, itch and increasing
inflammation become most prominent symptoms.
• Burning, stinging occur in advanced cases with
fissures, crusting.
PHYSICAL FINDINGS
• Clinical picture is a subacute eczematous derma-
titis. • Xerosis with accentuated skin markings are
features. • Inflammation, first subtle, becomes more
pronounced over time. • Faint, poorly defined ery-
thema progresses to fiery red, acute eczematous
papules. • Vesicles are not typically seen, although
excoriations are nearly universal. • Dry, thin desqua-
mation progresses toward a pattern termed eczema
craquelé, with thin superficial fissures. • With pro-
gression, the eczema develops acute features with
weeping, crusting, intense erythema.
TREATMENT
• Therapy is determined by stage (acute, subacute,
chronic) of asteatotic eczema and degree of inflam-
mation. • For xerosis, therapy consists of sensitive
skin measures, namely limited use of mild soap and
liberal use of emollients. • Petrolatum offers preserv-
ative-free choice as a lubricant; compliance may be
difficult. • Moisturizers containing lactic acid, urea,
or glycolic acid may also be useful. • Early inflam-
mation best treated topically with a medium-potency
corticosteroid, preferably in an ointment base.
• Therapy should be continued until erythema and
scaling resolve, about 2–3 weeks. Liberal use of
emollients should then be continued as prophylaxis
against recurrence. Bland, fragrance-free emollients
(Vanicream, Aveeno) or Cetaphil creams or hydrola-
tum are best. • Localized flares with acute eczema-
tous features of weeping and crusting should be
treated as acute eczema. Patients require close
follow-up during this stage, because localized flares
may become generalized. • Wet dressings with
Burow’s solution along with medium-potency topical
corticosteroid cream helpful. • Oral antibiotics may
be indicated for secondary impetiginization. • Once
weeping, induration, and crusting improve, stop wet
dressings. • A medium-potency topical corticoster-
oid ointment (group II or IV) should be continued
until redness and scaling resolve, approximately
2–3 weeks. Thereafter, sensitive skin care, including
daily bland emollient use, is helpful in limiting
recurrence.
 Chapped, fissured feet
DDx Ref  11 • 36 • 75
10 

The feet have a chapped appearance, with scaling

and fissures, which are often tender.

Both feet demonstrate affected skin that is more

prominent on weight-bearing surfaces. Vesicles
are typically absent, and a potassium hydroxide
test is negative for fungal elements.

This example of chapped, fissured feet is notable

for the increased skin lines and dry, cracked
appearance of the great toe.

The chapped, fissured foot at its worst, with

deep, painful fissures. A thick, bland emollient
applied twice daily helps rehydrate the skin and
heal the fissures.
10 Chapped, fissured feet
DDx Ref  11 • 36 • 75
DESCRIPTION
Findings include scaling, erythema, and tender fis-
suring of the plantar feet. Tendency for severe chap-
ping is age-related; it is most common in prepubertal
children but can occur in adults.
HISTORY
• Chapped, fissured feet are most common in early
autumn, when the weather becomes cold and heavy
socks and impermeable shoes or boots are worn.
• Symptoms include soreness and pain, less com-
monly asymptomatic. • Mean age of onset is 7 years;
mean age of remission is 14 years. • Symmetric
involvement of the soles. Inflammation may be con-
fined to just part of the soles. • Atopic dermatitis in
children occurs mainly on the dorsal toes. Children
with chapped, fissured feet complain of soreness and
pain. • Cracks and fissures appear in cases of long
duration. Pain becomes more intense than itching.
• The key to improvement lies in frequent, heavy
moisturization of the skin and prompt removal of
moist footwear. • Differential diagnosis includes
tinea pedis infection, allergic contact dermatitis,
psoriasis.
PHYSICAL FINDINGS
• Skin on the plantar feet—especially the weight-
bearing skin of the toes and metatarsal regions—is
dry, erythematous, scaly, and fissured. Fissuring may
be deep and very tender. • Chapping may extend to
the sides of the toes. • Eventually, the entire sole
may be involved.
TREATMENT
• Feet should be kept dry; avoid prolonged time in
moist, occlusive shoes. Excessive sweating and
occlusion often aggravate. • Apply thick emollient
ointment (Aquaphor, petrolatum, Cetaphil, Aveeno
cream) several times each day. • If the condition is
pruritic, topical steroids provide some relief. Group II
or III topical steroid ointments are applied twice a
day, preferably with plastic wrap occlusion at
bedtime, for 2–3 weeks. • A 15-min soak with tar
oil (Balnetar) is followed by the application of a lubri-
cating ointment or topical corticosteroid. • Preventive
measures include changing into light leather shoes
after removal of wet boots, alternating footwear
to allow complete drying, and changing socks
frequently if moist.
 Allergic contact dermatitis
DDx Ref  11 • 20 • 40
11 

Irritant dermatitis is common from tape. This

pruritic patch is dry and mildly erythematous. A
bland emollient and alternating the taped area will
help resolve it.

Eyelid dermatitis can be allergic, irritant, atopic,

or sometimes combinations of these. Patch
testing to a screening allergen series will help in
the assessment of allergic contact dermatitis.

Erythematous patch, with oozing and vesicles.

This is spreading contact allergy to bacitracin
which was applied to a minor wound.

Bilateral, symmetric erythematous patches.

Symptoms are pruritus, periodic flares, swelling,
vesiculation. Shoe or medicament allergy, or
additives from products used, are possible contact
allergens.
11 Allergic contact dermatitis
DDx Ref  11 • 20 • 40
DESCRIPTION
A delayed-type hypersensitivity. A form of eczema-
tous dermatitis. Sensitization required; specific to a
particular allergen. • Prototypes. Poison ivy, oak,
and sumac. • Common allergies. Metals (nickel,
chromate, cobalt); rubber additives in gloves and
shoes; preservatives or additives in skin products
such as creams, lotions, sunscreens, cosmetics, and
toiletries; fragrances; dyes; formaldehyde and related
chemicals; topical medicaments. Occupational expo-
sures to allergens can be significant.
HISTORY
• Initial exposure, primary sensitization results in
eczematous rash 14–21 days post exposure. If pre­
viously sensitized, rash 8–72 h later, but variable.
May last 3 weeks. Can occur even after prolonged
exposure. • Some patients develop multiple contact
allergies. • Can develop after years of exposure to
products and medications; new exposures also can
cause. • Hairdressers, dental care providers, health-
care workers, florists, and machinists at high risk.
• Other dermatoses (atopic dermatitis, stasis derma-
titis) may be aggravated by contact allergy.
PHYSICAL FINDINGS
• If acute, vesicles or bullae, edema, redness, and
often extreme pruritus. May be chronic, erythema-
tous, pruritic eczematous dermatitis. • Distributed at
sites of contact, at least initially. If exposure chronic,
dermatitis may spread beyond area of contact.
• Plant dermatitis typically in linear streaks. • Hands,
forearms, and face are most common sites. • Most
occupational allergic contact dermatitis affects the
hands. • Common facial involvement: pruritic patchy
erythema, asymmetric. Airborne matter (e.g. burning
poison ivy) results in rash on exposed skin. Photo­
allergic contact distribution: face, neck, forearms,
dorsal hands; spares submental, upper eyelid, pos-
tauricular. • Patch testing indicated if persistent or
recurrent eczematous dermatitis despite appropriate
topical therapy. Patch testing should be performed to
a broad panel of allergens including any relevant
occupational allergens, tested at proper concentra-
tion. Photopatch test patients with photodistributed
dermatitis.
TREATMENT
• Identification, avoidance of allergens is essential.
• If allergy suspected, start treatment, further evalu-
ate with patch testing. • Begin by simplifying skin
regimen and using topical corticosteroid of appropri-
ate strength for site (see topical therapy for eczema-
tous dermatitis). Treat with topical steroid for 2–3
weeks. Discontinue all moisturizers, lotions, and topi-
cals, except plain petrolatum. • Ointments rather than
creams preferred. No other topical products (except
plain petrolatum or prescribed corticosteroid) should
be used during treatment. • For severe or generalized
dermatitis, a 3-week tapering course of oral corticos-
teroids is appropriate. Avoid repeated use. • Some
allergens (i.e. hair dye and glues) penetrate gloves;
protection may not be adequate. • Some allergens
are associated with chronic dermatitis despite avoid-
ance. • Once an allergen is determined by diagnostic
patch testing, reviewing allergen exposures, educat-
ing about avoidance, and providing suitable alterna-
tives are vital to good outcome.
 Irritant contact dermatitis
DDx Ref  9 • 18 • 47
12 

The lips are xerotic and fissured; skin surrounding

the lips is erythematous, scaling and chapped
appearing. Repeated lip licking is the most
common cause of this irritant dermatitis.

Erythema, xerosis, and scaling are common with

irritant dermatitis. If no improvement using bland
emollients and medium-strength corticosteroid,
consider patch testing.

Irritant and allergic dermatitis often appear similar:

these hands show erythema, xerosis, scaling,
crusting. Look for irritants (repeated washing,
soap, solvent, detergent exposure) and allergens.

Dryness, fine scaling, and a faint erythema are

typical of a low-grade irritant dermatitis. Daily
bland emollient use is helpful.
12 Irritant contact dermatitis
DDx Ref  9 • 18 • 47
DESCRIPTION
An eczematous dermatitis often caused by repeated
exposure to mild irritants such as water, soaps, sol-
vents, heat, friction. Chronic exposure to mild irri-
tants is common and can result in eczematous
changes. Strong irritants include acids, alkalis, wet
cement; these chemicals can result in acute lesions
of chemical burns. Mild irritants cause dryness, fis-
suring, erythema; strong irritants produce an imme-
diate reaction of burning, erythema, edema, and
possibly vesiculation or ulceration.
HISTORY
• Atopic individuals predisposed and often have more
difficult to manage, prolonged course. • Most
common type of occupational skin disease. • Critical
history: employment, household duties, childcare,
hobbies. Jobs characterized by repeated wet work,
such as food service, healthcare, childcare, and hair-
styling, predispose. • Chronic friction, heat exposure
are other causes. • Common irritants: repeated
water exposure, detergents, acids, alkaline chemi-
cals, oils, organic solvents, oxidants, reducing
agents, coarse fibers. • Potential airborne irritants:
fiberglass, formaldehyde, epoxy resins, industrial
solvents, glutaraldehyde, sawdust. • May occur with
continuous exposure to mild irritants. Once irritation
threshold reached, persistent dermatitis results from
less exposure. • Low environmental humidity
reduces irritation threshold. • Continuous exposure
to moisture and wet–dry cycles in areas such as
hands, diaper area, or skin around a colostomy may
eventually cause eczematous inflammation. • May
become complicated by allergy over time.
PHYSICAL FINDINGS
• Most common site: hands. Other sites: eyelids, lips.
• Erythema, dryness, painful cracking or fissuring,
scaling. • Common: tenderness, burning. • Acute
irritant dermatitis may show papules and/or vesicles
on erythematous patchy background, with weeping
and edema. • Persistent dermatitis results in licheni-
fication, erythematous patches, fissures, excoria-
tions, scaling. • Hyperkeratotic form: scaling,
cracking, low-grade erythema may result from
repeated mechanical trauma, such as paper
handling. • Differential diagnosis: allergic contact
dermatitis, atopic dermatitis, psoriasis, tinea.
TREATMENT
• Early diagnosis, treatment, and preventive meas-
ures important to avoid chronicity. • Avoidance of or
decreased exposure to irritants is critical for skin
barrier recovery. • Frequently apply a bland emollient
such as Vaseline or Aquaphor to affected skin.
• Decrease number of wet–dry cycles resulting from
activities, such as repeated hand washing. • Cotton
gloves under vinyl gloves may offer good protection
(gloves can be ordered online at http://www.
allerderm.com). • Encourage appropriate gloves for
specific solvent or chemical exposure. • When occu-
pation deemed relevant, consult Material Safety Data
Sheet or seek expertise regarding best exposure and
protection information. • Use mildest cleanser
possible (Cetaphil, Dove, Aquanil). • For irritant hand
dermatitis, apply medium- or high-potency topical
steroid ointment twice a day for several weeks.
 Fingertip eczema
DDx Ref  7 • 16 • 36
13 

Excessive scaling (hyperkeratosis), erythema, and

painful fissures all characterize recurrent eczema
of the fingertips. If vesicles are present, consider
contact allergy.

Marked hyperkeratosis and painful fissuring of the

palmar and lateral aspects of the fingers.
Consider chronic friction, chronic irritant
exposures, or psoriasis.

A hyperkeratotic finger with tender areas where

plate-like scale has peeled away. It is typically
painful, not pruritic. Irritants should be avoided.
Systemic retinoids may help if emollients fail.

Mild fingertip eczema with increased linear

markings and xerosis. This often responds to
bland emollient or topical lactic acid lotion used
twice a day. Aggravated by paper handling and
low humidity.
13  Fingertip eczema
DDx Ref  7 • 16 • 36
DESCRIPTION
Common form of eczema limited to the fingertips.
One finger or several fingers can be affected. Itch is
limited or is absent often. Tenderness and burning
are common presenting complaints.
HISTORY
• Fingertip eczema is usually a recurring winter
problem but may occur all year round. • Uncommon
in children, it occurs most frequently in adults.
• Atopy may be a predisposing factor. • Irritant
chemicals or frictional contact may play a role.
Repeated frictional contact with paper handling has
been implicated as an aggravating factor. • A less
frequent etiology is allergic contact dermatitis to
plants, resins, glues. • Consider occupational and
hobby-related allergens, heat, repeated water expo-
sure, repeated wet–dry cycles, friction. • Cyanoacr-
ylate glue (Crazy Glue) is often used to seal the
fissured painful fingertip cracks; contact allergy to
this chemical is uncommon but possible. • May last
months or years, and can be very resistant to treat-
ment. • Precipitating factors often not easily or con-
sistently avoided. • Inflammation may start on the
fingertips but slowly spread to involve fingers and
palms.
PHYSICAL FINDINGS
• Dry, scaling, pink, fissured fingertips characterize
fingertip eczema. • Peeling reveals red, tender skin.
• Fingertips very dry, smooth, red, fragile. Inflamma-
tion tends to be chronic. • Vesiculation not typically
seen. • Process stops before the distal interphalan-
geal joint is reached.
TREATMENT
• Avoid repeated wet–dry cycles, irritating deter-
gents or solvents, heat, friction. • Manage as a sub­
acute or chronic eczema; irritants should be avoided
and affected areas must be lubricated frequently.
• Apply frequently a bland emollient such as Vase-
line. • A lactic acid cream (Lac-Hydrin or Amlactin
12% cream) may be helpful. • Medium-potency
topical steroids, with or without occlusion, give tem-
porary relief. • Cotton gloves and heavy moisturizers
at night can help. • Tar-based creams applied twice
each day may be tried if other measures fail. • Pro-
tection of hands and affected skin by repeated appli-
cation of petrolatum and use of cotton gloves can be
very helpful. • Decreasing irritation from repeated
hand washing and decreasing exposure to other irri-
tants is a cornerstone of treatment. Use household
gloves for wet work and cleaning duties. • Patch test
patient where occupational exposures to glues,
adhesives, resins, or plants (e.g. for florists, dental
hygienists, dentists) may be relevant, despite a lack
of history of contact with ‘new’ exposures.
 Keratolysis exfoliativa
DDx Ref  12 • 16 • 36
14 

The palm is barely erythematous, with a

serpiginous light desquamation. Itching is not
typical. Potassium hydroxide testing of the scale
is negative.

A severe form that recurred two or three times

each year. Palms were painful.

Fingers showing fine scaling and no erythema.

This scaling is often recurrent and occurs in
waves. The cause is unknown.

Palmar erythema, dryness, increased markings,

and fine ring-like arrangements of scaling are
present. This benign condition often responds well
to frequent emollient use.
14  Keratolysis exfoliativa
DDx Ref  12 • 16 • 36
DESCRIPTION
Keratolysis exfoliativa is a common, chronic, asymp-
tomatic, non-inflammatory, symmetric peeling of
palms and soles. The cause is unknown.
HISTORY
• Occurs most commonly during summer. • Often
associated with sweaty palms and soles. • Some
people have repeated episodes; others experience
this phenomenon only once. • Resolves in 1–3
weeks but may recur. • Improves with moisturization
and generally resolves with age.
PHYSICAL FINDINGS
• Scaling starts simultaneously from several points
on the palms or soles with 2–3-mm of round scale
that appears to have originated from a ruptured
vesicle; however, vesicles are not seen. • Scales
continue to peel and extend peripherally, forming
larger, roughly circular areas that resemble ring-
worm. The central area becomes slightly red and, in
a few cases, tender. • Scaling borders may coalesce.
• A potassium hydroxide examination is worthwhile
to exclude tinea infection.
TREATMENT
No therapy other than lubrication is required.
 Nummular eczema
DDx Ref  37 • 42 • 77
15 

Nummular eczema may look like ringworm or

psoriasis. The borders of ringworm and psoriasis
are usually sharply defined. The lesion borders
are indistinct in this case of nummular eczema.

The most common areas are the dorsa of the

hands, the lower legs, the upper extremities
(shown here), and the trunk. Men are most
commonly affected.

Sharply circumscribed erythematous plaque with

weeping surface. Nummular dermatitis may be a
solitary lesion, but more frequently there are
multiple similar lesions.

On the back there are scattered erythematous

plaques which are intensely pruritic, leading to
poor quality of life. This nummular eczema may
last many months and may be refractory to
treatment.
15  Nummular eczema
DDx Ref  37 • 42 • 77
DESCRIPTION
Round (coin-shaped) lesions of eczematous inflam-
mation, often chronic, treatment-refractory. Cause
unknown, occasionally allergic contact allergens are
relevant. Intensely itchy.
HISTORY
• Adults most often affected, men more than women.
• Onset usually gradual, with no clear precipitant and
no eczema history. • Often begins with few isolated
lesions on legs; with time, multiple lesions occur,
without particular distribution. • Lesions often
resolve or improve after use of topical corticosteroids
but recur in same area after steroid withdrawal. Can
become refractory even to high-strength topical
steroids. • Course variable, unpredictable; may be
chronic and relapsing for years. • Once lesions
established, they tend to remain same size and
recur on previously affected skin. • Differential diag-
nosis includes psoriasis, tinea, cutaneous T-cell
lymphoma.
PHYSICAL FINDINGS
• Sharply demarcated, round eczematous plaques on
trunk and extremities. • Weeping lesions and vesicu-
lation characterize flares. • Secondary infection can
result in disease flares. • A yellow, honey-colored
crust indicates secondary impetiginization. • Patch
testing reveals a relevant positive result in small per-
centage of cases (one-quarter to one-third). • Culture
may reveal Staphylococcus aureus. Antibacterial
treatment usually helps but does not often resolve
problem.
TREATMENT
• See Subacute eczematous inflammation or Chronic
eczematous inflammation. • Consider patch testing
in refractory cases. • Discontinue unnecessary
routine topical moisturizing products, over-the-coun-
ter oral medications, dietary supplements, herbal
preparations for at least 3–4 months. • Active tinea
pedis should be sought; treat tinea with antifungal
agents if present. • Use of medium-potency topical
steroid ointments and bland emollients (Aquaphor,
Vanicream, Vaseline) should be aggressive. • Apply
topical steroid twice a day for 2–3 weeks. Treat a
week or so longer than deemed necessary to resolve
lesion. • Efficacy of topical steroid increased by
occlusion with plastic wrap or sauna suit, or by
hydrating skin with a bath before applying medica-
tion. • Treat secondary infection with systemic
antistaphylococcal antibiotics, according to sensitiv-
ity results (e.g. dicloxacillin 250 mg q.i.d., cephalexin
250 mg q.i.d.). • Antihistamines can be prescribed
for itching. • Systemic corticosteroids should be
avoided for long-term management. • Refer refrac-
tory cases to a dermatologist. • Light therapy can
help resolve lesions when topical treatments have
failed. Narrow- and broadband ultraviolet B are best
choices for light therapy; can use psoralen plus ultra-
violet A if ultraviolet B therapy fails. • Topical aller-
gens such as fragrance and medicaments (bacitracin,
Neosporin, hydrocortisone) may drive some cases of
nummular dermatitis. Counsel against their use.
 Pompholyx
DDx Ref  3 • 11 • 36
16 

Bilateral palmar scattered vesicles that have

evolved to pustules. In pompholyx, the vesicles
usually erupt suddenly and in crops. Pruritus may
be present or absent.

Vesicles and pustules of dyshidrotic eczema in

varying stages of evolution. The differential
diagnosis is pustular psoriasis and contact
dermatitis. The feet often develop a similar eruption.

Severe hand eczema: marked erythema, vesicles,

and scaling. Contact allergy should be considered,
and the patient patch tested to a broad screening
series and occupational allergens.

Aftermath of a bout of dyshidrotic eczema: some

tender macules of healed epidermis; some diffuse
scaling and erythema; and an occasional
resolving, dry-appearing vesicle.
16  Pompholyx
DDx Ref  3 • 11 • 36
DESCRIPTION
Distinctive, chronic relapsing, vesicular eczematous
dermatitis of unknown etiology. Characterized by
sudden, recurrent eruptions of usually highly pruritic,
symmetric vesicles on palms, lateral fingers, and/or
plantar feet.
HISTORY
• Affected patients frequently have atopic back-
ground (personal or family history of asthma, allergic
rhinitis, or atopic eczema). • Moderate or severe
itching precedes a flare. • Hyperhidrosis (increased
sweating) often aggravates or accompanies. • Vesi-
cles resolve over 1–3 weeks. • Causes of this recur-
rent, sometimes disabling dermatitis are unknown;
provoking factors seem heterogeneous. Consider role
of atopy, occupational and/or other contact chemi-
cals, and distant tinea infection. • Systemic contact
allergens may play a role; some individuals with posi-
tive patch tests show vesicular reactions on hands
when challenged orally with nickel, cobalt, or chro-
mium. • Differential diagnosis: contact allergy, pus-
tular psoriasis, inflammatory tinea, ‘id reaction’ on
hands to tinea on feet, bullous pemphigoid, rarely
cutaneous T-cell lymphoma.
PHYSICAL FINDINGS
• Vesicles 1–5 mm, monomorphic, deep-seated,
filled with clear fluid. They erupt suddenly, symmetri-
cally on palms, lateral fingers, or plantar feet. • Rings
of scale and peeling follow eruption as itch dimin-
ishes. • Depending on phase of disease, clinician
may see only brown spots. When acute process ends,
skin peels, revealing a red, cracked base with brown
macules. • Chronic eczematous changes with ery-
thema, scaling, and lichenification may follow.
• Waves of symmetrically distributed vesiculation
can recur indefinitely. • For unknown reasons, the
chronic recurring eruption sometimes ceases with
time.
TREATMENT
• Initial treatment with cold compresses twice a day
with either tap water or Burow’s solution, followed
by medium- or high-potency steroid cream (group
I–III). • Prednisone 0.5–1 mg/kg q.d. tapered over
1–2 weeks is prescribed, but not frequently or as
maintenance. • Tacrolimus ointment (Protopic 0.1%)
rotating with a topical medium-strength corticoster-
oid (group II–III) twice daily for cycles of 3–4 weeks
can provide some relief. • Oral antihistamines can
alleviate pruritus. • Topical psoralen plus ultraviolet
A is a treatment option for frequent, refractory erup-
tions. • Elimination diets (such as a nickel-reduced
diet for nickel-allergic patients) may be worth a trial
in difficult cases. • If distant focus of tinea identified,
treat with topical antifungal medication (econazole or
terbinafine cream every day for 3 weeks) or short
course of oral antifungal medication (terbinafine
or itraconazole) of appropriate duration and dose.
• Moderating or eliminating stress can help and is
anecdotally curative for some. • For chronic or
severe disabling dyshidrotic eczema, consult a
dermatologist.
 Prurigo nodularis
DDx Ref  97 • 117 • 119
17 

Erythematous, discrete, rounded plaques with

central erosion and crust. There are sparse
eczematous patches nearer the elbow, but most
lesions are discrete.

Lesions are thick and severely eroded by picking

and scratching. The edges are hyperpigmented.

In neurotic excoriations, the linearity of the

lesions, oriented in a direction of a natural scratch
or ‘dig’, is common. These pink patches are
scars, some with fresh but recurrent excoriation.

Prurigo nodules have been scattered here. There

are old hypopigmented scars, hyperpigmentation,
and some discrete papules with crust and pink
nodularity. Intralesional steroid is often helpful.
17  Prurigo nodularis
DDx Ref  97 • 117 • 119
DESCRIPTION
Prurigo may be considered an idiopathic, papular or
nodular form of lichen simplex chronicus. In prurigo
nodularis, there are very pruritic firm papules and
nodules on easily accessed skin. Lesions are second­
ary to repeated, localized scratching and picking.
HISTORY
• Onset is usually gradual and occurs in setting of
pruritus. • Prurigo nodularis occurs primarily in
adults. • Stress is often anecdotally implicated. It
may perpetuate the problem and seems to relate
clinically to recurrence or flares. • Individuals with
atopy and diabetes may be predisposed. • Affected
patients may be compulsive ‘pickers’.
PHYSICAL FINDINGS
• Few to numerous dull, erythematous, or hyper­
pigmented nodules randomly distributed. Extensor
arms and legs are typically affected; the lumbosacral
area, nape of neck, and dorsal hands are reachable
areas that are typically involved. • Lesions are
created by repeated rubbing, picking, scratching.
• The small papules and nodules are red or brown,
hard, and often dome-shaped with a smooth,
crusted, or warty surface. • Often, there are clues to
a chronic process—hypopigmented scars or postin­
flammatory hyperpigmentation on skin accessible to
repeated scratching and picking. • Skin biopsy is
rarely necessary but may help confirm the diagnosis
when in question. • In generalized prurigo of recent
onset (less than 1 year), evaluate and exclude sys­
temic causes of pruritus. • Causes of generalized
pruritus include chronic renal disease, drug reac­
tions, hypothyroidism, occult liver disease (including
hepatitis C), HIV infection, occult malignancy (includ­
ing solid-organ metastatic disease and leukemia or
lymphoma). • Uncommon mimics of prurigo lesions
have been reported and include dermatitis herpeti­
formis, nodular scabies, metastatic cancerous
lesions, Langerhans cell histiocytosis, atypical lym­
phoproliferative diseases.
TREATMENT
• Medium- or high-potency topical corticosteroids
(groups II–IV) with plastic wrap occlusion to enhance
penetration and provide barrier to scratching. • Apply
corticosteroid-impregnated tape (Cordran) to lesions
every day. Covering lesions provides a barrier against
trauma of repeated scratching while medicating
underlying skin. • Apply topical superpotent steroids
twice a day to individual lesions for several weeks.
• Intralesional steroid injections (Kenalog 5–10 mg/
mL) can be given and repeated every 4–6 weeks if
needed. Hypopigmentation in dark skin may occur
from such treatment. • Pramoxine with hydrocorti­
sone (Pramosone ointment) or Sarna lotion may help
relieve intense pruritus. • Light therapy with ultra­
violet B, narrowband ultraviolet B, or psoralen plus
ultraviolet A can be considered for severe, general­
ized cases. • Cryotherapy sometimes successful.
• Excision of individual nodules is rarely performed
but sometimes a valid option.
 Stasis dermatitis
DDx Ref  11 • 47 • 77
18 

Recurrent stasis dermatitis. There is striking

edema, bright-red erythema, weeping and
scaling.

The lower leg has circumferential erythema and

scaling, with a tight appearance. The skin often
feels firm. This degree of stasis dermatitis
appears to be very chronic and untreated.

Subacute eczema with erythema and scale

present over a wide area. Varicosities are
scattered on the lower, medial foot.

Post-inflammatory changes of white, shiny

scarring on the medial lower leg, and golden
brown hyperpigmentation. Note the varicosities.
18  Stasis dermatitis
DDx Ref  11 • 47 • 77
DESCRIPTION
An eczematous dermatitis of the legs, associated
with edema, varicosed and dilated veins, and hyper-
pigmentation. It is chronic and commonly relapses.
HISTORY
• Often a prior history of deep venous thrombosis,
surgery, leg trauma, or ulceration. • Often a family
or personal history of varicose veins. • Patient com-
plaints include heaviness or aching in the legs aggra-
vated by prolonged standing or walking. • Legs are
swollen at the end of the day. • Dermatitis and
itching are a common finding and can be chronic.
PHYSICAL FINDINGS
• Dilated and tortuous veins frequently present on
affected leg. • Subacute and chronic eczematous
dermatitis appears on lower legs or surrounding a
venous ulcer. • Dermatitis is obvious and associated
with dry, fissured, erythematous skin. • Dermatitis
can become generalized (auto-eczemization) if
condition persists. • Edema, brown discoloration
(hemosiderosis), erosion, or ulceration is common.
• Troublesome pruritus; excoriation can potentiate
secondary infection. • White scars, sometimes
atrophic or stellate, on medial malleolus indicate
previous ulceration. • Stasis papillomatosis (elephan-
tiasis nostra) and verrucous hyperplasia found in
chronically congested limbs, occurring with local
lymphatic disturbances such as chronic venous
insufficiency, primary lymphedema (Milroy disease),
trauma, and recurrent erysipelas. • Secondary infec-
tion with Staphylococcus aureus (impetiginization)
common, especially in excoriated skin. • Color
duplex ultrasonography can confirm venous valvular
incompetence. • If a strong family or personal
history of multiple deep vein thrombosis, check the
clotting cascade (protein S, protein C, activated
protein C resistance, factor V Leiden, cryofibrino-
gens, and homocysteine level).
TREATMENT
• Apply cool water dressings 10–20 min twice a day
for acute exudative inflammation. • Apply group II–V
topical steroids twice a day (cream if acute, ointment
if chronic) for 2–3 weeks. • If indication of infection,
administer Domeboro (aluminium subacetate) wet
dressings and a course of oral antibiotic according to
culture and sensitivity. • For generalized dermatitis
(auto-eczematization), treat with an oral corticoster-
oid with 3-week taper. • Oral antihistamines (e.g.
hydroxyzine) 10–25 mg every 4–6 h as needed may
help control itching. • Lubricate with bland emol-
lients daily. More Vaseline-like bases—such as plain
petrolatum, Aquaphor, Aveeno, Cetaphil cream—are
preferable to lotions. Many popular moisturizers
contain fragrance and preservative ingredients that
may result in contact allergy. Simplify topicals.
• Compression (20–30 mmHg) with stockings (e.g.
Venosan, Sigvaris, Jobst or Ace wraps). More aggres-
sive compression (30–40 mmHg at the ankle) may
be required.
 Venous leg ulcers
DDx Ref  18 • 88 • 165
19 

Venous stasis ulceration with surrounding atrophy

blanche (white, scarred plaque surrounding the
small ulcer). Some cayenne pepper-like dermatitis
surrounding the ulcer, typical of venous stasis.

Medial lower leg with stasis ulceration that is

clean with base of healthy granulation tissue.
Note hyperpigmentation of surrounding skin and
its tight appearance, indicating chronicity.

Chronic stasis dermatitis with ulceration. Medial

malleolus shows a small clean ulcer, surrounding
scar from prior healing, lower leg dermatitis, and
some varicosities on the foot.

Stasis ulcer with small surrounding hyper­

pigmentation and small superficial varicosities,
typical of lower leg venous stasis. Support
stockings are of value.
19  Venous leg ulcers
DDx Ref  18 • 88 • 165
DESCRIPTION
A chronic, non-healing ulcer typically located on
medial aspect of lower leg in association with chronic
venous insufficiency.
HISTORY
• Occur in middle-aged and elderly. • Ulcer forma-
tion often sudden. • Preceding leg injury, slight
trauma, phlebitis, obesity, and deep vein thrombosis
are also important risk factors. • Slow healing over
weeks or months. • Venous leg ulcers can be a
chronic, recurrent, lifelong problem. • Ulcers may be
asymptomatic or mildly tender; do not typically cause
severe pain.
PHYSICAL FINDINGS
• Ulcer location: most often medial malleolus. Flat,
sharp, or slightly sloping borders, and shallow with
granulation tissue. • Edema, usually pitting, is
common; improves at night with leg elevation.
• Chronic edema, trauma, infection, and inflamma-
tion lead to fibrosis; skin has firm, non-pitting,
‘woody’ quality. • Ultimately, decrease in lower leg
circumference from fibrosis. • Legs swollen and
ache; pain worse with standing, better in morning.
• Vein varicosities often prominent. • Secondary
eczematous dermatitis (stasis dermatitis) often
present. • Often hyperpigmentation. • Ulcer remains
small; may enlarge rapidly without trauma. • Color
duplex ultrasonography identifies presence and
source of significant venous reflux. • Chronic lesions
are biopsied to rule out cancer (basal cell or squa-
mous cell carcinomas), and for tissue culture. Biopsy
should be performed if wound persists > 3 months.
• Cultures not usually helpful. • Differential diagno-
sis: arterial, neuropathic, infectious, neoplastic,
metabolic ulcers. Pyoderma gangrenosum, anti-
phospholipid or other coagulation disorder.
TREATMENT
• Leg compression, elevation above heart level for
30 min three or four times daily and at night. • Com-
pression with Ace wraps, graded compression
stockings (30–40 mmHg), or external pneumatic
compression. • Unna boots helpful; apply and
replace weekly. • Use group III–V topical steroids (for
7–14 days) for stasis dermatitis. • Heavy moistur­
izers (e.g. Aquaphor, petrolatum, Aveeno cream)
protect skin, help resolve dermatitis. • Pentoxifylline
(Trental) 400 mg t.i.d. can help lipodermatosclerosis.
• Debride ulcer crust and exudates. • A variety of
synthetic dressings are available. • Hydrocolloid
dressings (e.g. DuoDERM CGF) are effective, easy to
use as initial treatment. • Change dressing type if
healing is slow. • Treat exudative and draining ulcers
with absorbent dressing such as calcium alginate.
• Signs of malnutrition (e.g. low serum albumin level)
should be noted and corrected. • Aspirin 300 mg q.d.
may improve healing. • Consider ascorbic acid
(1–2 g q.d.), zinc sulfate (220 mg t.i.d.), and vitamin
E (200 mg b.i.d.). • Consider skin grafting for difficult
cases.
 Atopic dermatitis
DDx Ref  8 • 11 • 131
20 

Atopic dermatitis in a young toddler. The child

scratches the face by rubbing. Eczematous
patches are evident on both cheeks. Use of
emollients daily is helpful.

Atopic dermatitis has a predilection for the eyelids.

Affected eyelids are red and scaling, and develop
lichenification over time. Avoidance of irritants and
allergens is a good management strategy.

Eczematous dermatitis on dorsal forearm. The

prominent finding is lichenification; this indicates a
long-standing problem. Ointment-based treatments
will penetrate this thickened skin better.

A typical site for atopic dermatitis in childhood is

the flexure popliteal fossae and the antecubital
fossae. These erythematous scaling patches are
very pruritic and sometimes weeping.
20  Atopic dermatitis
DDx Ref  8 • 11 • 131
DESCRIPTION
An eczematous dermatitis, distressingly pruritic,
recurrent, often flexural, and symmetric.
HISTORY
• Major diagnostic criteria: pruritus; young age at
onset; flexural lichenification and linearity in adults;
facial and extensor involvement in infants; chronic
relapsing course; personal or family history of
asthma, allergic rhinoconjunctivitis, atopic derm­
atitis. • Minor, less specific features: xerosis,
ichthyosis, palmar hyperlinearity, keratosis pilaris,
immediate type 1 skin test responses, dermatitis of
hands and feet, cheilitis, nipple eczema, increased
susceptibility to cutaneous infections, perifollicular
accentuation. Most children outgrow, but some
develop chronic relapsing disease, especially retro-
auricular, eyelids, and hands.
PHYSICAL FINDINGS
• Often begins abruptly with erythema, severe
pruritus. • Red pruritic papules, patches of erythema,
scaling. • Acute lesions oozing and vesicular; sub­
acute lesions scaly and crusted; chronic lesions dull
red, lichenified, very pruritic. • Infant distribution:
cheeks, perioral, scalp, dorsal feet, elbows. • Chil-
dren: flexural; antecubital, popliteal, neck, wrists,
ankles. • Adults: flexural. Hand dermatitis may be
sole manifestation. Upper eyelids common site. Can
be diffuse and patchy. • Secondary infection with
Staphylococcus aureus resulting in flare or rash per-
sistence. Increased susceptibility to herpes simplex,
molluscum contagiosum, S. aureus, and fungal
infections. • Hypopigmentation and hyperpigmenta-
tion may result from inflammation. • Patch test if
dermatitis pattern changes or is refractory to treat-
ment. • Children with severe disease may have food
allergies. Rarely a problem for adults.
TREATMENT
• Frequent application of a plain, thick, greasy mois-
turizer (Vaseline, Aquaphor, Aveeno, Vanicream)
without fragrances or common sensitizing preserva-
tives is ideal. • Advise soft, light cotton clothing;
avoid wool, coarse fibers. • Keep environment cool.
• Oral antihistamines with sedative effects for pruri-
tus—such as diphenhydramine (Benadryl), hydro­
xyzine (Atarax), and doxepin—especially at night.
• Control or eliminate inflammation and infection.
• Topical corticosteroids of appropriate strength for
patient’s age and affected area are applied twice
daily to inflamed skin for 10–21 days (see Topical
therapy). • Second-line treatment: tacrolimus (Pro-
topic) ointment 0.03% for children aged 2–15 years,
and 0.03% and 0.1% for adults, or pimecrolimus
(Elidel) cream 1% twice daily for short-term and
intermittent long-term therapy. Helpful for atopic
dermatitis of face, eyelids, or limited involvement.
• Staph aureus is the usual flare provoking bacteria,
but sensitivity patterns are changing. Oral antibiotics
may be helpful; choice should be guided by culture
and sensitivity results. Topical mupirocin (Bactroban)
cream twice daily for 5 days if infection is limited.
• For acute lesions and severe flares, wet dressings
with Burow’s solution applied for 20 min 2–3 times
a day, followed by a topical steroid. • Consult der-
matologist for severe, refractory disease.
 Autosomal dominant
ichthyosis vulgaris
DDx Ref  9 • 12 • 20
21 

Ichthyosis vulgaris can have a cracked pavement

appearance, and can be inflamed, especially in
winter.

The scales are stuck on and will slough off and

renew again. Emollients with lactic acid can help
alleviate the dry appearance of ichthyosis
vulgaris.

Large, dark, platelike scales characterized this

ichthyosis, which is X-linked ichthyosis. Ichthyosis
vulgaris can look like this, although usually the
scales are not as dark.

Dried scaling skin of ichthyosis. X-linked

ichthyosis vulgaris is more evident in winter. The
thick scale may disappear in the summer.
21  Autosomal dominant
ichthyosis vulgaris
DDx Ref  9 • 12 • 20
DESCRIPTION
A disorder of keratinization characterized by dry,
rectangular scales resembling a cracked pavement;
these scales appear most prominently on the exten-
sor extremities. Associated with the atopic diathesis
in 50% of cases.
HISTORY
• Onset in early to middle childhood. • Condition may
improve with age or may persist throughout life.
• Scales more noticeable and often pruritic in the
winter, when humidity is low. • Autosomal dominant;
1 in 300 have the disorder. • May be confused clini-
cally with X-linked ichthyosis. • Differential diagno-
sis: dry skin, acquired ichthyosis as a manifestation
of HIV, malignancy, drugs, autoimmune disorders,
X-linked ichthyosis.
PHYSICAL FINDINGS
• Findings often mild. • Dry, small, rectangular
scales appear on the extensor extremities. Lower
extremities, particularly the anterior shins, often
more noticeably affected. • Affected skin has the
appearance of cracked pavement or fish scales.
• Characteristically spares the flexor surfaces.
• Usually asymptomatic but may become pruritic or
chapped in winter. • Palmar creases may be accen-
tuated. • Keratosis pilaris may also be present.
• Scaling rarely involves entire cutaneous surface.
• Scaling of the skin results from the retention of
scale rather than increased proliferation. • No tests
are routinely indicated, unless there is a question of
X-linked ichthyosis. • Skin biopsy is rarely per-
formed; when performed, it shows in a subset of
patients a decreased or an absent granular layer.
TREATMENT
• Often improves with age; infrequently, it resolves
completely. • Increased environmental humidity and
warmth often result in resolution or improvement.
• Regular application of moisturizing cream or lotion
decreases pruritus and improves skin appearance.
• Optimal time for applying moisturizer is immedi-
ately after bathing and hydrating the skin. • Emol-
lients containing lactic acid, urea, or alphahydroxy
acids help treat severe dryness and scaling.
• Ammonium lactate 12% (Lac-Hydrin, Amlactin)
lotion or cream very effective when applied daily.
 Keratosis pilaris
DDx Ref  20 • 31 • 48
22 

Keratosis pilaris is characterized by pink,

erythematous follicular papules, which are also
somewhat scaly.

Discrete erythematous and scaling follicular

papules on the lateral upper arms. This is a
benign process with a cosmetic impact that is
often distressing.

Tiny follicular papules on the lateral cheek. Atopy

often accompanies this condition.

Florid keratosis pilaris on the buttocks of a young

child. The erythematous papules involve
numerous follicles and are inflammatory.
22  Keratosis pilaris
DDx Ref  20 • 31 • 48
DESCRIPTION
Keratosis pilaris consists of rough, monomorphic,
tiny, follicle-based scaling papules most commonly
on the posterolateral aspects of the upper arms but
occasionally more widespread, including the anterior
and lateral thighs and the buttocks. It results
from mild follicular plugging and perifollicular
inflammation.
HISTORY
• Keratosis pilaris is very common in young children,
peaking in adolescence. • Probably more common in
atopic individuals. • Usually asymptomatic but may
be somewhat pruritic. • The unusual adult diffuse
pattern persists indefinitely. • Keratosis pilaris is
common on the face of children and is frequently
confused with acne. • Treatment is often desired
because of the visible typical location of keratosis
pilaris on the extensor upper arms and thighs, and
the troubling cosmetic appearance. Otherwise, the
condition is generally asymptomatic.
PHYSICAL FINDINGS
• Small, pinpoint follicular papules, and occasionally
pustules, remain in the same areas for years. • A red
halo appears at the periphery of the keratotic papule.
• The skin feels rough, like sandpaper. • Lesions
most commonly appear on posterolateral upper
arms, anterior and lateral thighs. Occasionally, the
condition is generalized and appears on trunk, exten-
sor arms and legs. • No laboratory tests necessary.
TREATMENT
• Many patients seek treatment for cosmesis,
because most often the lesions are asymptomatic.
• Keratosis pilaris often improves or resolves by
adulthood. • Scratching, wearing tight-fitting cloth-
ing, or undergoing treatment with abrasive washes
or gritty scrubs may aggravate the condition.
• Tretinoin (Retin-A) may induce temporary improve-
ment, but irritation is usually unacceptable. • Lac-
Hydrin cream 12% or lotion 12% twice a day can
reduce roughness and improve appearance. • Low-
potency topical steroids may be used in limited
courses to temporarily reduce the redness but
should not be used on a long-term basis. • The
recognition of keratosis pilaris helps avoid inappro-
priate treatment.
 Pityriasis alba
DDx Ref  15 • 71 • 111
23 

Hypopigmented macules and patches on the

extensor arm. This child is atopic. There was no
preceding inflammation evident, as is typical of
pityriasis alba.

Hypopigmented macules and patches on the

extensor upper arm. These lesions are
asymptomatic; the patient often seeks advice due
to cosmesis.

Pityriasis alba can be very subtle. It is commonly

located on the lateral cheeks and upper arms in
children and young adults. Atopic eczema may be
present elsewhere.

Hypopigmented macules, differential diagnosis

includes pityriasis alba, tinea versicolor, post-
inflammatory hypopigmentation, vitiligo, and rarely
hypopigmented cutaneous T-cell lymphoma.
23  Pityriasis alba
DDx Ref  15 • 71 • 111
DESCRIPTION
Asymptomatic, hypopigmented, fine scaling patches
with indistinct borders, typically on the lateral
cheeks. Affects the lateral cheeks, lateral upper
arms, and thighs. Occurs more frequently in young
children and usually resolves by early adulthood.
HISTORY
• Pityriasis alba is asymptomatic. • Children and
young adults are affected. • No history of prior rash,
trauma, or inflammation. • Affected individuals are
often atopic. • Loss of pigment is often more notice-
able and distressing in darkly pigmented people.
PHYSICAL FINDINGS
• White macules and patches are round to oval and
vary in size; they are generally 2–4 cm in diameter.
• A fine surface scale may be seen on close inspec-
tion. • Lesions are most common on the lateral
cheeks, lateral upper arms, and thighs. • Condition
more obvious in the summer and in darker skin
types, when affected skin does not tan.
TREATMENT
• Usually no treatment is recommended, as the
problem is benign and self-resolving. Emollient use
every day may help. • Reassure the patient that the
loss of pigment is not permanent. • Hypopigmenta-
tion usually fades with time. • Hydrocortisone cream
or ointment 1% applied for a limited time (a few
weeks) on affected skin may help patients who are
most distressed by the pigment irregularity.
 Acute urticaria
DDx Ref  11 • 85 • 91
24 

Non-pitting, edematous plaques erupted and were

generalized. Intense itching prevented sleep.
Adrenaline (epinephrine) was not effective.
Hydroxyzine 50 mg every 4 h provided relief.

Superficial, widespread, and confluent plaques

were moderately itchy. Fexofenadine (Allegra)
180 mg in the morning and hydroxyzine 25 mg
q.h.s. were effective.

Superficial plaques with clear dusky centers. The

borders are annular. Itching was moderate.
Fexofenadine (Allegra) 180 mg q.d. was effective.

Confluent thick urticarial plaques with a polycyclic

pattern. Intense hives may have a blue cyanotic
appearance. Itching was intense. Hydroxyzine
25 mg every 4 h was required for control.
24  Acute urticaria
DDx Ref  11 • 85 • 91
DESCRIPTION
By definition, acute urticaria resolves within 6 weeks.
Hives lasting longer than 6 weeks are called chronic
urticaria. Acute urticaria presents as non-pitting
edematous plaques or wheals. Pruritus is intense and
lasts up to 24 h. Urticarial vasculitis is painful and
purpuric variant, and lesions last longer than 24 h. A
biopsy confirms the diagnosis. Drugs and viral infec-
tions can be a cause of urticaria, as can foods,
injected medications or vaccines, bites or stings.
HISTORY
• People of all ages are affected. Hives are more
common in atopic individuals. • The onset is abrupt,
often with intense itching. • Drugs, foods, animal
hair, and airborne allergens are common causes. The
etiology is not discovered in many cases. • Labora-
tory studies are ordered only to confirm abnormal
findings on history and physical examination. Physi-
cal urticaria can be caused by vibration, cold, pres-
sure, and sunlight.
PHYSICAL FINDINGS
• Pink-to-red, or flesh-colored non-pitting, edema-
tous plaques may appear on any body surface. The
center of the lesions may be flesh-colored, pink, or
cyanotic. The borders are surrounded by a white or
red halo. The size is highly variable. Lesions are
round, oval, annular, or polycyclic. • The plaques
change size and shape by peripheral extension and
regression and may also migrate. • New lesions
appear as others resolve. • Bullae or purpuric lesions
appear with intense swelling. • The distribution is
usually generalized in the case of food, drug or viral
etiology but may be limited to the area of contact with
some exposures such as natural rubber latex, animal
dander, pollen, or during preparation or handling of
foods. • Linear lesions suggest dermographism
(physical urticaria).
TREATMENT
• Stop suspected triggers (e.g. medications, food,
inhalants). • H1 blocker antihistamines are used
initially. Hydroxyzine 10–25 mg every 4–6 h is the
most effective but causes sedation. Liquid hydrox-
yzine 10 mg/5 cc works faster. Doses as high as
100 mg every 4 h may be used. Many patients adapt
to the sedation after a few days of treatment. Non-
sedating H1 blockers are useful for the daytime hours.
• Loratadine (Claritin) 10 mg q.d. is non-prescription.
• Desloratadine (Clarinex) 5 mg q.d., cetirizine (Zyrtec)
5 mg or 10 mg q.d., and fexofenadine (Allegra)
60 mg b.i.d. or 180 mg q.d. are other treatment
options. • Prednisone (e.g. 60 mg for 2 days, 40 mg
for 5 days, and then 20 mg for 7 days) may be effec-
tive and is used when patients are not responding to
antihistamines. • Adrenaline (epinephrine) is admin-
istered for extensive, severe cases. • Cool baths with
colloidal oatmeal (Aveeno Soothing Bath) relieve
itching. Hot showers provide immediate relief but
should be avoided, as they only worsen the pruritus
afterward. • Topical steroids are minimally effective
in most cases.
 Chronic urticaria
DDx Ref  28 • 97 • 102
25 

Hives have a variety of patterns. Red, round

wheals with a dusky center are a very common
presentation. The border is elevated and center
is flat.

Lesions vary in extent from a few to hundreds of

plagues. They can be localized or cover wide
areas of the body. They can be sparsely
separated or dense and confluent.

Round plaques have expanded and become

confluent. The entire lower leg was swollen, itchy,
and painful. Large dense plaques sometimes
become dark blue in the centers.

Plaques that last longer than 24 h should be

biopsied to exclude the diagnosis of urticarial
vasculitis. Urticarial vasculitis lesions are painful
rather than itchy.
25  Chronic urticaria
DDx Ref  28 • 97 • 102
DESCRIPTION
Non-pitting, edematous plaques called wheals or
hives. Hives that last longer than 6 weeks are
defined as chronic urticaria. Erythema multiforme
may look like wheals (hives). Early bullous pemphig-
oid may present with urticarial plaques before bullae
formation.
HISTORY
Patients sometimes report that lesions appear at a
certain time each day. Most patients are young
adults. Cause determined in only few cases. If cause
unclear after routine history and physical examina-
tion, laboratory tests may be of limited use. Think
of the five ‘I’s when trying to find the cause.
• Ingestants (common): foods, additives, drugs
such as antibiotics or others that are relatively new
to the patient. • Inhalants: dust, feather, pollen.
• Injectants: drugs, stings, bites. • Infections: bac-
terial, viral, fungal, parasitic. • Internal diseases:
such as chronic infections, thyroid disease, lupus
erythematosus.
Individual lesions itch, resolve in less than 24 h.
Biopsy painful hives that last longer than 24 h to
exclude urticarial vasculitis.
PHYSICAL FINDINGS
• Red, non-pitting edematous plaques (wheals) in
various shapes and patterns. Lesions round, oval,
annular, or polycyclic. Wheals may coalesce to form
very large plaques. Size varies from a few millimeters
to greater than 10 cm. • Wheals resolve in less than
24 h. New lesions appear as older ones fading.
• Tests to consider: complete blood count, sinus
X-rays to evaluate for sinusitis, dental X-rays to
evaluate for an occult dental abscess, rapid strepto-
coccal test or pharyngeal culture, Mycoplasma titers,
and thyroid-stimulating hormone and thyroid micro-
somal antibody test for autoimmune thyroid disease.
TREATMENT
• Antihistamines. Hydroxyzine the most effective and
reliable. Hydroxyzine 10–25 mg can be administered
every 4 h, up to 100 mg every 4 h as needed. Many
patients adapt and are not sedated after taking medi-
cation for a few days. Others do not tolerate sedation,
so use hydroxyzine only in evening and a non-sedat-
ing antihistamine during day. • Many patients treated
with just non-sedating antihistamines. Non-sedating
H1 antihistamines include desloratidine (Clarinex
5 mg q.d.), cetirizine (Zyrtec 5 mg, 10 mg q.d.), and
fexofenadine (Allegra 60 mg b.i.d. or 180 mg q.d.).
In difficult cases, these may be combined with type
2 (H2) antagonists such as cimetidine 400 mg b.i.d.
or ranitidine 150 mg b.i.d. Several non-prescription
antihistamines are available. • Oral steroids consid-
ered for unresponsive cases. Effect not predictably
reliable, but sometimes very effective. • May try
empiric antibiotic therapy if occult infection, such
as a tooth abscess, suspected. Antibiotics rarely
effective.
 Physical urticaria
DDx Ref  24 • 25 • 97
26 

Stroke the skin of any patient complaining of hives.

Most patients with dermographism will form a
wheal and red flare minutes later. This establishes
the diagnosis. No other tests are required.

Pressure urticaria. Swelling may occur hours after

the application of pressure. Many patients with
chronic urticaria also have pressure urticaria.
Antihistamines may not be effective.

Cholinergic urticaria. Round papular wheals occur

shortly after exercise or exposure to heat. These
‘heat bumps’ are very common in young adults.

Cold urticaria. Application of a solid or fluid cold

stimulus to the skin produces swelling. Swimming
in cold water can result in massive swelling and
may be dangerous.
26  Physical urticaria
DDx Ref  24 • 25 • 97
DESCRIPTION
Physical urticaria is produced by various physical
stimuli and is common in young adults. Dermogra-
phism (‘skin writing’) and cholinergic urticaria (‘heat
bumps’) are the most common forms.
HISTORY
• Dermographism. Occurs in about 5% of the popu-
lation. Infections or antibiotics may trigger the
disease. It lasts for weeks, months, or years. Recur-
rences occur. • Pressure urticaria. Deep itchy or
painful swellings that occur a few hours after the
application of pressure. The disease lasts for years.
Many of these patients also have chronic urticaria.
Lesions can be induced by standing or walking.
• Cholinergic urticaria. Seen in young people and
very common. Occurs within 1–20 min of exercise or
from exposure to heat; gone in less than 30 min.
• Cold urticaria. Occurs in children and young
adults. Occurs within minutes of exposure to cold
water or cold objects; lasts about 30 min. Swimming
in cold water can initiate a massive, dangerous flare.
PHYSICAL FINDINGS
• Dermographism. Shows linear swelling in areas
that are scratched. Many patients who complain of
itching are dermographic. Streak the arm as a diag-
nostic test. Linear welts occur in minutes. Patients
may have linear hives and typical round hives.
• Pressure urticaria. Occurs on the feet, trunk, and
buttock from sitting, and presents as broad-based
areas of swelling. • Cholinergic urticaria. Heat
bumps are round, tiny wheals that may become con-
fluent and look like typical hives.
TREATMENT
The goal of treatment is to relieve symptoms. It is not
necessary or possible to completely eliminate the
hives or physical urticaria. • Dermographism. Con-
trolled with non-sedating antihistamines such as
fexofenadine (Allegra 180 mg) during the day and
hydroxyzine 10–25 mg q.h.s. Many patients can be
treated for 24 h with a single or b.i.d. dose of hydrox-
yzine. Patients adapt to hydroxyzine and may not
experience sedation after a few days of treatment.
Chronic suppression may be required. • Pressure
urticaria. Most patients do not require treatment.
Some are disabled by the disease and respond to
intermittent courses of prednisone. • Cholinergic
urticaria. Patients may have to limit exercise. Pre-
treatment before exercise with cetirizine (Zyrtec
10 mg) or hydroxyzine (10, 25, 50 mg) may help.
• Cold urticaria. Patients should avoid sudden
changes in temperatures. Immersion in cold water is
avoided. Cyproheptadine 4 mg (Pericatin), loratadine
10 mg (Claritin), and cetirizine 10 mg (Zyrtec) may
be effective.
 Angioedema
DDx Ref  24 • 84 • 85
27 

This patient had hives and angioedema. This is an

extensive case with very large plaques with deep
swelling. The major complaint was discomfort and
some itching.

The plaques of angioedema are uniform, tense,

non-pitting, and non-erythematous. The borders
may be well defined. These plaques lack the faint
white or red halo found with hives.

Swelling of the lips is a classic sign of

angioedema. Swelling may be massive and the
only manifestation of the disease.

Swelling of the palms is another highly

characteristic sign of angioedema. Circular lesions
may resemble erythema multiforme. Erythema
multiforme is not associated with swelling found
in angioedema.
27  Angioedema
DDx Ref  24 • 84 • 85
DESCRIPTION
Non-pitting, well-defined area of edema caused by
increased vascular permeability in subcutaneous
tissue of skin, mucosa. Airway obstruction with
laryngeal edema can be fatal. This most often occurs
in hereditary angioedema and angiotensin-convert-
ing enzyme (ACE) inhibitor-associated angioedema.
Colicky abdominal pain, nausea, vomiting, diarrhea
are the result of intestinal wall edema.
Several causes. • Idiopathic (most common).
• Immunologic IgE allergic reaction (foods, drugs,
stinging insect venom, pollen); hives often present.
• Non-immunologic medication-induced (e.g. ACE
inhibitors). • Hereditary (type 1, type 2). • Acquired
type 1, type 2 very rare.
Hereditary angioedema types 1 and 2 are auto-
somal dominant, associated with recurrent, self-
limited, chronic attacks. Inherited deficiency of
C1-esterase inhibitor (C1-INH) in both types. • Type
1 (80–85% of cases): serum levels of C1-INH low.
• Type 2: serum levels of C1-INH normal but C1-INH
functional assay low.
C4 (screening test during attacks) low during
attacks in both types. C1q normal in hereditary
angioedema, low in patients with very rare acquired
types 1 and 2.
HISTORY
• Hives, angioedema common. • Inquire about drugs
(especially ACE inhibitors), aspirin, non-steroidal
anti-inflammatory drugs, foods, insect stings, and
family history. • Angioedema may be painful; pruritus
minimal.
PHYSICAL FINDINGS
• Well-circumscribed, non-pitting edema of the
head, face, lips, tongue and larynx. Palms, soles can
be affected. Reaction similar to that of hives, but
significant swelling occurs in subcutaneous tissues
of skin and mucosa. • Clinical appearance tends to
be more dramatic than hives, can cause disfigure-
ment to point where patient is unrecognizable.
TREATMENT
• Most common forms of angioedema: idiopathic or
allergic. • Initial goal of therapy: airway manage-
ment. • Treat acute, severe attacks with adrenaline
(epinephrine). • Treat with hydroxyzine 10–50 mg
every 4–6 h. Liquid hydroxyzine 10 mg/5 cc works
faster. Doses as high as 100 mg every 4 h may be
used. Many patients adapt to sedation after a few
days. • Non-sedating H1 blockers do not work as well
but useful for daytime hours and milder cases. Lorat-
adine (Claritin) 10 mg q.d. is non-prescription.
Desloratadine (Clarinex) 5 mg q.d., cetirizine (Zyrtec)
5 mg or 10 mg q.d., and fexofenadine (Allegra)
60 mg b.i.d. or 180 mg q.d. • Prednisone (e.g.
60 mg for 2 days, 40 mg for 5 days, then 20 mg
for 7 days) may be effective, is used when patients
not responding to antihistamines. • Acute attacks
of hereditary and acquired angioedema treated
with C1-INH concentrate or fresh frozen plasma.
• Danazol and stanozol for long-term prophylaxis.
 Mastocytosis
(urticaria pigmentosa)
DDx Ref  24 • 46 • 63
28 

Very small 1–3-mm pigmented macules over the

bilateral thighs of this adult woman characteristic
of urticaria pigmentosa. Usually asymptomatic.
May be misdiagnosed as vasculitis.

There are many brownish-red macules and

patches. The infant was irritable and had difficulty
sleeping. Scratching lesions caused itching hives
and flushing.

A typical solitary lesion. This brown oval plaque

had been present for months. There were no
symptoms. There was no family history of
mastocytosis.

Stroking the lesion produced a wheal and intense

flushing around the hive (Darier sign). Stroking
releases histamine from mast cell granules,
confirming mastocytosis. No biopsy was
performed.
28  Mastocytosis
(urticaria pigmentosa)
DDx Ref  24 • 46 • 63
DESCRIPTION
Mast cell proliferation. Increased numbers of mast
cells in various organs. Most often seen in young
children and usually confined to skin. Often involves
skin and internal organs in adults. Mast cells store
histamine in granules. Histamine released by
scratching lesions or ingesting certain agents. Cause
unknown.
HISTORY
• Onset occurs between birth and 2 years in 55% of
cases. • Incidence: 1 in 1000 to 1 in 8000 live births.
• Typically improves gradually; usually clears spon-
taneously by puberty. • Mast cell disease that begins
after age 10 usually persists for life. • When disease
is systemic, gastrointestinal tract and skeletal system
most commonly involved, and there can be associ-
ated mast cell leukemia. • Pruritus is most common
complaint. Scratching lesions or emotional upset
stimulates histamine release and episodes of itching.
When large numbers of mast cell lesions are present,
pruritus can be severe and difficult to treat.
PHYSICAL FINDINGS
• Most common presentation is pediatric-onset,
localized cutaneous disease. • Brown, slightly ele-
vated, non-blanchable macules and patches averag-
ing 0.5–1.5 cm in diameter. • Lesions vary in
number. Most infants have one or a few. May resem-
ble café-au-lait spots. Other children have several or
many lesions that may be concentrated on the trunk.
• Erythema or whealing occurs when lesions are
scratched (Darier sign). • Blisters seen in infants.
• Biopsy shows mast cell infiltrates in the dermis.
Special stains performed on skin biopsy specimens,
such as toluidine blue or Giemsa, useful for identify-
ing histamine granules.
TREATMENT
• No cure; therapy is to relieve symptoms. • Skin
lesions may be treated with a strong topical cortico­
steroid for 1–6 weeks. Occlusion enhances penetra-
tion and is useful for localized symptomatic plaques.
• Intralesional injections with triamcinolone (Kenalog)
10 mg/cc are very effective. Solution may be diluted
with saline to avoid inducing atrophy at injection site.
• Corticosteroids may decrease or eliminate the
mast cells. • H1 (fexofenadine, loratadine, cetirizine,
hydroxyzine, diphenhydramine) and H2 antihist­
amines (cimetidine, ranitidine, famotidine) decrease
pruritus, flushing, gastrointestinal symptoms. •
Doxepin has potent H1 activity and can be used if
antihistamines fail. • Oral disodium cromoglycate
(400–800 mg q.d.) may alleviate pruritus, whealing,
flushing, diarrhea, abdominal and bone pain. • Oral
psoralen plus ultraviolet A therapy given four times
each week controls itching and whealing. Reserved
for adults not responsive to other treatment. • Avoid
non-immunologic agents that stimulate histamine
release, such as aspirin, non-steroidal anti-inflam-
matory drugs, codeine, morphine, polymyxin B, vanco­
mycin, succinylcholine, estrogens, radiocontrast
media.
 Pruritic urticarial papules and
plaques of pregnancy
DDx Ref  25 • 82 • 84
29 

The eruption appears suddenly in the third

trimester. Red papules begin, in 90% of cases, in
the striae of the abdomen.

Lesions rapidly spread to the abdomen and

increase in number. Itching is moderate to
intense, but there are no excoriations.

Lesions spread to the thighs, buttocks, chest, and

upper arms. They can be urticarial, vesicular, or
target-like, and resemble erythema multiforme.

Extensive eruption involving the entire trunk,

upper arm, and buttock. The eruption rapidly
cleared within 1 week of delivery.
29  Pruritic urticarial papules and
plaques of pregnancy
DDx Ref  25 • 82 • 84
DESCRIPTION
Pruritic urticarial papules and plaques of pregnancy
(PUPPP) is the most common dermatosis of preg-
nancy. It affects between 1 in 300 pregnant women.
Most cases show pruritic hive-like lesions on the
abdomen. The urticarial lesions of herpes gestationis
may be confused with PUPPP lesions. Direct immun-
ofluorescence skin biopsy can help differentiate the
two diseases. There are no immunofluorescence
findings with PUPPP. Herpes gestationis shows C3
with or without IgG in a linear band along the base-
ment membrane zone.
HISTORY
• PUPPP occurs primarily in primigravidas in the third
trimester. It can occur in the postpartum period.
• Mean duration is 6 weeks. • Itching is moderate
to intense. Intense itching lasts about 1 week. • The
eruption typically clears within 1 week of delivery.
• There are no fetal or maternal complications.
• Infants do not develop the eruption. • Recurrence
in subsequent pregnancies or with oral contracep-
tives is unusual.
PHYSICAL FINDINGS
• Lesions usually first appear in the striae on the
abdomen. They begin as red papules surrounded by
a pale halo but rapidly evolve to urticarial papules.
• Vesicles and erythema multiforme-like target
lesions may resemble the lesions of herpes gesta-
tionis. • The rash spreads in a few days to the thighs,
buttocks, chest, and upper arms. It spares the face,
palms, and soles. Most lesions consist of either
papules or hive-like plaques.
TREATMENT
• Treatment is supportive. • Antipruritic topical
lotions containing menthol (Sarna lotion) are sooth-
ing. • Medium-potency topical steroids (e.g. triam­
cinolone cream 0.1%) suppress inflammation.
• Antihistamines such as fexofenadine (Allegra)
control itching. • A short course of oral prednisone
can be safely prescribed for severe cases. • Ultravio-
let B is reported to be effective.
 Comedonal acne
DDx Ref  48 • 122 • 125
30 

Open comedones (blackheads) and closed

comedones are the first acne lesions to appear.
Some become inflamed and become papules or
pustules.

Closed comedones, or whiteheads, have a very

small orifice. This impedes drainage. They
respond slowly to treatment.

Open comedones remain for months. Stretch the

skin for support, and remove them with a
comedone extractor.

Open comedones in the ear are unsightly. They

respond slowly to topical treatment and can be
removed with a comedo extractor and gentle
pressure.
30  Comedonal acne
DDx Ref  48 • 122 • 125
DESCRIPTION
Comedones (whiteheads are closed comedones and
blackheads are open comedones) are the primary
lesions of acne. Sebum production increases, follicu-
lar wall cells fail to desquamate to the surface in the
normal manner, and Propionibacterium acnes grows
in the sebum-cell mixture and forms a plugged pore
or a microcomedo and then a visible comedo.
HISTORY
Acne begins with the development of comedones.
These appear before other signs of puberty.
PHYSICAL FINDINGS
• First, sebaceous glands become more active, and
the face and scalp become oily. • Blackheads and
whiteheads first appear on the nose. Later, they form
on the forehead, cheeks, and finally chin. Chest and
back tend to be the last areas affected. Comedones
also form in and behind the ears.
TREATMENT
Retinoids are comedolytic and are drugs of first
choice. Apply q.o.d., q.d., or b.i.d. as tolerated.
Creams are for dry skin and are less irritating. Gels
are for oily skin.
• Tretinoin: Retin-A gel (0.025%, 0.01%) 15 g,
45 g; Retin-A cream (0.1%, 0.05%, 0.025%) 20 g,
45 g.; Retin-A solution (0.05%) Less irritating:
Retin-A micro (0.04%, 0.1%) 20 g, 45 g. Less irritat-
ing: Adapalene (Differin) gel (0.1%, 0.3%) 45 g;
Differin cream, or lotion (0.1%) 45 g, 59 mL.
• Azelaic acid (Finacea gel) (15%) 15 g: comedo-
lytic and antibacterial. Adapalene is unaffected by
sunlight. Tretinoin and tazarotene cause sensitivity to
sun. Tazarotene is pregnancy category X.
Drying, peeling antibacterial agents are used
alone or in combination with retinoids. • Benzoyl
peroxide-clindamycin combinations: Benzaclin
gel 25 g, 50 g; Duac gel 45 g; Acanya gel 50 g.
• Benzoyl peroxide-tretinoin combinations: Vetlin
gel 30 g, Ziana gel 30 g, 60 g. Dapsone (Aczone gel)
(5%) 30 g, 60 g.
 Pustular acne
DDx Ref  34 • 48 • 50
31 

Papules, pustules, and comedones are intermixed.

Pustules are superficial and may break and drain.

Moderate papulopustular acne. The propensity to

scar varies among patients.

Widespread pustular acne is disfiguring, has the

potential to scar, and requires aggressive therapy
(often with isotretinoin).

The course and extent of acne are highly variable

and unpredictable. Chest and back involvement is
common. This severity of acne is an indication for
isotretinoin.
31  Pustular acne
DDx Ref  34 • 48 • 50
DESCRIPTION
Papulopustules evolve from comedos.
HISTORY
• Common in the teenage years; many adults
affected. • Lasts longer in women; more severe in
men • Patients often pick acne, creating scars (acne
excoriee). Deep lesions may also leave scars.
PHYSICAL FINDINGS
• Comedones, papules, pustules, cysts and scars,
involving the face, chest, back and arms. Post-
inflammatory pigmentation is common, especially in
darkly pigmented individuals.
TREATMENT
• Mild to moderate. Treat with topical antibiotics
and retinoids or topical antibiotics and sulfaceta-
mide/sulfur. • Moderate and severe. Treat with
topical antibiotics, sulfacetamide/sulfur and oral anti-
biotics. Consider isotretinoin for failures. • Women.
Oral contraceptives (e.g. Ortho Tri-Cycle, Alesse)
and Spironolactone 50–200 mg q.d. may be
effective. Check testosterone, follicle-stimulating
hormone, luteinizing hormone, dehydro-epiandros-
terone-S, prolactin in women with persistent acne or
irregular periods. • Topical antibiotics. See Come-
donal acne • Sulfacetamide/sulfur. Lotion 10–5%,
30, 60 g Many washes and topical preparations
• Retinoids: see Comedone acne. • Oral antibiot-
ics. Tetracycline 250 or 500 mg b.i.d.; Doxycycline
20, 50, 75, 100 mg q.d. or b.i.d.; Minocycline 50,
100 mg b.i.d.; Isotretinoin 10, 20, 30, 40 mg.
Isotretinoin is used in severe acne at dose of 0.75–
1 mg or 2 mg/kg q.d. for a course of 4–5 months. It
is highly teratogenic and there are restrictions on use
of this drug. iPLEDGE registry is required for patients
and prescribing physicians for isotretinoin use in
the USA.
 Cystic acne
DDx Ref  34 • 48 • 50
32 

Cysts are larger, deeper, and last longer than

papules and pustules. They may be painful and
always scar.

Moderate cystic acne. Scars from previous lesions

are evident.

Severe cystic acne. Some cysts have become

confluent. The disease is long-lasting, the
scarring severe.

The back, chest, and upper arms are frequently

affected. Cysts may become confluent and create
very large, painful lesions.
32  Cystic acne
DDx Ref  34 • 48 • 50
DESCRIPTION
Most likely form of acne to cause scars. Must treat
early with oral medications to avoid scars.
HISTORY
• Starts with cysts or evolves from papulopustular
acne. • Lasts for months or decades. • May require
repeated courses of isotretinoin.
PHYSICAL FINDINGS
• Deep, inflamed cysts occur on the face, chest, back
and shoulders. • Distribution and severity highly
variable.
TREATMENT
• Moderate: same approach as for moderate and
severe papulopustular acne. • Severe: May try brief
trial of medications used to treat moderate and
severe papulopustular acne. • Isotretinoin (Claravis,
Amnesteem, Sotret) 10 mg, 20 mg, 30 mg, 40 mg.
Start with low dosage (e.g. 10–40 mg q.d.) to avoid
acne flare. Dose of 1–2 mg/kg/day is most effective
for severe cystic acne, given over a total of 4–5
months. • Short course of prednisone is sometimes
used. • Inject triamcinolone 2.5–5 mg/mL into
painful inflammed cysts. • Oral contraceptives
(e.g. Ortho Tri-Cyclen, Alesse) may be beneficial.
• Spironolactone 50–100 mg b.i.d. may be helpful
for women. Isotretinoin is highly teratogenic and its
use is restricted in the USA to patients and their
physicians who participate in the iPLEDGE registry
program.
 Perioral dermatitis
DDx Ref  2 • 34 • 48
33 

Papules and pustules are confined to the perioral

area and spare a narrow zone around the
vermillion border. Many cases will be of less
intensity.

Eruptions of this intensity occur about 1 week

after stopping long-term treatment with topical
steroids.

Pinpoint papules may be found next to the

nostrils. This may be the only finding.

Pinpoint papules may be found lateral to the eyes.

This may be the only finding.
33  Perioral dermatitis
DDx Ref  2 • 34 • 48
DESCRIPTION
Distinct papular eruption of perioral and/or periocular
area found almost exclusively in women.
HISTORY
• Very common in women in their twenties and thir-
ties. • Asymptomatic or mild itching. • Appearance
is major complaint. • Persists for months. • May
follow long-term use of moderate to strong topical
steroids. • Often it is idiopathic.
PHYSICAL FINDINGS
• Pinpoint papules and pustules found typically adja-
cent to the angles of the mouth, on the chin, adjacent
to the alar creases, and lateral ocular canthi. • May
be limited to one of these areas. • May be mild
scaling. • Lesions next to nostrils may be only mani-
festation. • Wide variability in intensity. Worst cases
follow cessation of moderate to strong topical ster-
oids. • Sometimes occurs lateral to eyes.
TREATMENT
A 2-6-week course of oral antibiotics is reliable and
more effective than topical treatment. Re-treat or use
long-term suppression for persistent actively.
• Tetracycline 250 or 500 mg b.i.d. • Doxycy-
cline 50 mg, 75 mg, 100 mg b.i.d. • Minocycline
50 mg, 75 mg, 100 mg b.i.d. • Erythromycin 500 mg
b.i.d. • Trimethoprim/sulfamethoxazole 80–400 mg,
160–800 mg b.i.d.
Topical medication may control disease or main-
tain remission when applied q.d. to b.i.d. Use mild
preparations in this easily irritated area: • 10%
sodium sulfacetamide (multiple brands) q.d. • Met-
ronidazole: Noritate cream 1%, 30 g; Metrocream
0.75%, 45 g; metrolotion 0.75%, 59 mL; metrogel
1% 60 g; metronidazole 0.75%, gel 45 g, cream
45 g, lotion 59 mL. • Azelaic acid: Finacea gel 15%,
30 g, azelex cream 20%, 30 g, 50 g. • Clindamycin:
Cleocin T gel 1%, 30 g, 60 g; Cleocin T 1%, lotion
60 mL; clindagel 1%, 40 mL, 75 mL; Clindamax
lotion 1%, 60 mL; evoclin foam 1%, 50 g, 100 g. •
Aczone gel 5%, 30 g, 60 g.
Avoid strong topical steroids, routine use of
moisturizers and cosmetics.
 Rosacea (acne rosacea)
DDx Ref  2 • 31 • 104
34 

Classic presentation with papules and pustules on

forehead, cheeks, and nose. There is erythema
but few telangiectasias.

Erythema of the nose is highly characteristic of

rosacea. Pustules present on the cheeks. Acne
can present with the same lesions and
distribution.

Years of active inflammation permanently alter

the dermis and distort the structure of the nose.
This is called rhinophyma.

The eye is involved in about 50% of cases. Many

problems are reported; grittiness and mild
conjunctivitis are common complaints.
34  Rosacea (acne rosacea)
DDx Ref  2 • 31 • 104
DESCRIPTION
Facial acne-like eruption, but without comedones.
Does not scar like acne. Ocular disease common.
Flushing is common.
HISTORY
• More common in people of Celtic origin. • May
persist for years and require long-term suppression.
• Spicy foods, emotional situations, alcohol and sun-
light exacerbate. • Ocular grittiness and soreness
common.
PHYSICAL FINDINGS
• Erythema, telangiectasias, and pustules primarily
on forehead, cheeks, nose. • Telangiectasia not a
constant feature. • Difficult to make diagnosis if pus-
tules absent. • Long-term nasal disease distorts
nose (rhinophyma). • Conjunctivitis may occur.
TREATMENT
Few pustules and mild erythema are treated topi-
cally. This treatment minimally effective for ery-
thema. Erythema may be treated with laser. Topical
medication may control disease or maintain remis-
sion when applied q.d. to b.i.d. Use mild preparations
in this easily irritated area: • 10% sodium sulfaceta-
mide (multiple brands) q.d. • Metronidazole: Noritate
cream 1%, 30 g; Metrocream 0.75%, 45 g; metrolo-
tion 0.75%, 59 mL; metrogel 1%, 60 g; metronida-
zole 0.75%, gel 45 g, cream 45 g, lotion 59 mL.
• Azeliac acid: Finacea gel 15%, 30 g; azelex cream
20%, 30 g, 50 g. • Clindamycin: Cleocin T gel 1%,
30 g, 60 g; Cleocin T 1%, lotion 60 mL; clindagel
1%, 40 mL, 75 mL; Clindamax lotion 1%, 60 mL;
evoclin foam 1%, 50 g, 100 g. • Aczone gel 5%,
30 g, 60 g. Oral antibiotics. Very effective for
papules, pustules, and ocular involvement. Tetra-
cycline 250 or 500 mg b.i.d. • Doxycycline 50 mg,
75 mg, 100 mg b.i.d. • Minocycline 50 mg, 75 mg,
100 mg b.i.d. • Erythromycin 500 mg b.i.d. • Tri-
methoprim/sulfamethoxazole 80–400 mg, 160–
800 mg b.i.d. • Isotretinoin and prednisone. For
very severe cases.
 Hidradenitis suppurativa
DDx Ref  48 • 50 • 122
35 

Lesions may appear in the axillae, under the

breasts, in the groin and about the buttock. This
florid eruption under the breasts is more extensive
than most cases.

Groin lesions are frequently misdiagnosed as

boils. Look for the double comedones, as seen
here in the left groin, to support the diagnosis.

Early hidradenitis presents as recurrent boils.

These lesions smolder and recur to produce
communicating sinus tracts as the disease
pursues a relentless course.

Boil-like lesions occur in the axilla. Their numbers

vary greatly. This is a particularly extensive
eruption that has been relentless.
35  Hidradenitis suppurativa
DDx Ref  48 • 50 • 122
DESCRIPTION
A chronic disease that resembles boils. Forms sinus
tracts and heals with scarring. Occurs in the axillae,
anogenital regions, under the breasts. A disease of
follicles, not apocrine glands.
HISTORY
• More common in females. • Appears after puberty.
Most cases in second and third decade • Suspect
hidradenitis when women complain of ‘boils in the
groin’. • Worse in the obese. • Progressive and
relentless. • Great variation in severity. • Most
patients have a few boil-like lesions.
PHYSICAL FINDINGS
• Double or triple comedone is hallmark of disease;
may be first sign of disease. • Boil-like lesions
smolder and communicate to form sinus tracts that
disrupt the dermis and heal with haphazard cord-like
bands of scar tissue.
TREATMENT
• Incise and drain fluctuant cysts. • Intralesional
triamcinolone acetonide (Kenalog) 2.5–10 mg/mL
controls small cysts. • Tetracycline 250 or 500 mg
b.i.d. Doxycycline 50 mg, 75 mg, 100 mg b.i.d.
Minocycline 50 mg, 75 mg, 100 mg b.i.d. Erythro-
mycin 500 mg b.i.d. Clarithromycin 250 mg
b.i.d. Trimethoprim/sulfamethoxazole 80–400 mg,
160–800 mg b.i.d. Lower dosages are tried for main-
tenance • Isotretinoin most effective in early disease.
• Surgical excision of sinus tracts may be necessary.
• Weight loss helps. • Adalimumab, Infliximab, and
Etanercept for severe cases.
 Psoriasis: hands and feet
DDx Ref  8 • 16 • 75
36 

Psoriasis of the palms may be difficult to discern

from hand eczema. The silvery, dense, scaling
plaques are also seen in chronic hand eczema.

This same presentation of defined round scaling

plaques of the dorsum is seen in nummular
eczema.

Pustular psoriasis of the palms and soles. Lesions

are localized or may involve the entire palms or
soles.

Pustular psoriasis lesions resemble dyshidrotic

eczema. Pustules evolve to deep-set brown spots
and then into scaling papules.
36  Psoriasis: hands and feet
DDx Ref  8 • 16 • 75
DESCRIPTION
Chronic, inflammatory disease due to abnormal T-
lymphocyte function. Affects skin, scalp, joints, nails.
HISTORY
• Chronic course; exacerbations, remissions.
• Genetic predisposition. Environmental triggers
include stress, physical trauma, Streptococcus infec-
tions, drugs (lithium, beta-blockers, antimalarials,
corticosteroid withdrawal), HIV. • Nail involvement:
10–50% (see Psoriasis: nails). • Psoriatic arthritis
(rheumatoid factor-negative): 7–20%. May precede
skin disease.
PHYSICAL FINDINGS
Most common: chronic plaque psoriasis (see Psoria-
sis: lesions). Extent highly variable. Other presenta-
tions below. • Guttate. Common initial presentation
in children; follows group A streptococcal pharyngi-
tis. Sudden appearance of 0.3- to 1.0-cm papules
primarily on trunk, extremities. Spares palms, soles.
• Pustular. Rare, severe, unstable. Sterile pustules
arise on red base, coalesce to form pus lakes. Ery-
thema progresses in waves with desquamation;
patient may appear toxic with fever, skin pain. Gen-
eralized forms serious, potentially fatal. Oral steroid
withdrawal may precipitate. • Erythrodermic.
Uncommon. May be initial presentation or evolve
from chronic plaque disease. Localized progressing
to generalized erythema, little scale. Oral steroid
administration or withdrawal may precipitate. May
appear toxic (chills, skin pain). • Pustular psoriasis
of palms and soles. Chronic, localized, recurrent,
treatment-resistant. Sterile pustules evolve from red
base on palms, instep. Pustules do not rupture but
turn dark brown, scaly. Often painful, limiting mobil-
ity. • Scalp psoriasis. Common. Scale may be very
thick, anchored by hair. Plaque may extend beyond
hairline. Itching varies. • Intertriginous (inverse).
Flexural or intertriginous areas: gluteal fold, axillae,
under breasts, groin and genitalia. Smooth, red,
sharply defined plaques with macerated surface.
Superimposed candida infection in diabetic patients
and with topical steroids.
TREATMENT
Treatment similar to that for chronic plaque psoriasis,
with specific considerations. • Guttate psoriasis.
Treat streptococcal infection with penicillin or equiva-
lent. Skin lesions best treated with triamcinolone 0.1%
cream b.i.d. and narrowband ultraviolet B therapy.
• Pustular psoriasis. Requires specialist care by der-
matologist. Pustular flares respond to Neoral or Soria-
tane. Ultraviolet B and psoralen plus ultraviolet A useful
adjunctive therapies. • Erythrodermic psoriasis.
Best managed with Neoral, Soriatane, methotrexate.
Ultraviolet therapy and topical steroids helpful adjunc-
tive therapies. • Intertriginous (inverse) psoriasis.
Best managed with lower-potency group V topical
steroids to minimize atrophy risk. Use in cycles (e.g.
b.i.d. for 10–14 days, stop of 10–14 days). • Scalp
psoriasis. Treatment with tar (T-Gel, etc.) or salicylic
acid shampoos removes some scale. Diffuse scale:
apply Derma-Smoothe FS oil to scalp at bedtime,
cover with shower cap. Steroid gels (e.g. Lidex, Temo-
vate, Topicort), steroid foams (Olux, Luxiq), or solutions
(Cormax) penetrate hair into scale. Dovonex solution
60 cc b.i.d. on weekdays as tolerated.
 Psoriasis: lesions
DDx Ref  15 • 42 • 77
37 

The primary lesion is a red, scaling, defined

papule with varying amounts of silvery scale.

Intertriginous plaques, here in the gluteal cleft,

are often thin with minimal moist surface scale.

Thick inflamed plaques on the lower back with

thin scale and excoriation. Occipital scalp plaques
often have thick scale and well-defined borders.

Lesions may first appear on the knees, elbows,

and scalp. In contrast to eczema, thick psoriatic
plaques have a sharply defined border. Thick
scale with thin underlying inflammation respond
to topical keratolytic followed by topical steroid.
37  Psoriasis: lesions
DDx Ref  15 • 42 • 77
DESCRIPTION
Chronic, inflammatory disease due to abnormal
T-lymphocyte function. Affects skin, scalp, joints,
nails.
HISTORY
• Prevalence: 1–3%. • Men, women affected equally.
• Onset: any age, peaks late twenties, early fifties.
• Chronic. • Genetic predisposition. • Triggers:
stress, trauma, infections, drugs. • Psychosocial
impact severe.
PHYSICAL FINDINGS
• Usually pink to red, sharply defined, scaling
papules coalesce, forming plaques. Elbows, knees,
scalp most common. Scale adherent, silvery. Pin-
point bleeding when scale removed. • Presentations:
guttate, pustular, erythrodermic, inverse.
TREATMENT
Topical (chronic plaques)
• Topical steroids. Groups I–V. Fast, temporary
relief. Side effects: atrophy, telangiectasia. • Cal-
cipotriol/Calcipotriene. (Dovonex cream, Vectical)
ointment, 100 g, b.i.d. on weekdays as tolerated.
Group I or II topical steroids b.i.d., weekends.
• Taclonex ointment is a combination calcipotriene,
class II steroid for once daily use • Tazarotene.
Tazorac 0.05%, 0.1%, cream (15, 30, 100 g) or gel
(30, 100 g), q.h.s. Less frequently if irritation. Group
I–IV topical steroids q. morning for irritation. • Tar
preparations (over-the-counter). Low cost, effec-
tive. Limited by odor, irritation, clothing stains.
• Phototherapy: narrowband ultraviolet B (NB-
UVB). Dermatologists administer 2–5 times per week.
• Psoralen plus ultraviolet A (PUVA). Dermatolo-
gists administer 3 times per week until clear, then
tapered. Patient takes oral psoralen 1.5–2 h before
exposure. Very effective. Side effects: gastrointestinal
intolerance, sunburn, skin aging, skin cancer risk.
Systemic
Dermatologist-supervised. Combining topical,
systemic helps limit toxicity, enhance efficacy.
• Methotrexate. Given orally, average 7.5–15 mg/
week. Adjust dose to maintain control. Folic acid
1 mg q.d. (but not methotrexate days). Monitor com-
plete blood count (CBC), liver function tests (LFT);
periodic liver biopsy. Serious drug interactions pos-
sible. Side effects: nausea, anorexia, fatigue, oral
ulcerations, mild leukopenia, thrombocytopenia,
hepatotoxicity. • Ciclosporin (Neoral). Rapid, tempo-
rary control (severe psoriasis). Dosage 2.5–5.0 mg/kg
q.d. Monitor blood pressure, CBC, creatinine, magne-
sium, cholesterol, triglycerides. Many drug inter­
actions. Side effects: hypertension, nephrotoxicity.
• Acitretin (Soriatane). May combine with PUVA,
UVB. Orally, 10–50 mg q.d. Monitor triglycerides,
cholesterol, CBC, LFT, blood urea nitrogen, creatinine.
Side effects: teratogenicity, dry skin, myalgias,
arthralgias, pseudotumor cerebri, alopecia, increased
triglycerides. • Biologic immunomodulatory ther­
apy. Engineered human proteins target T-cell-
mediated inflammatory processes. Etanercept (Enbrel)
binds tumor necrosis factor-α. Patient-administered,
50 mg s.c. once weekly. Adalimumab (Humira) simi-
larly binds TNF-α. Patient-administered, 50 mg s.c.
every other week. Infliximab (Remicade), also a
TNF-α inhibitor is given intravenously every 8 weeks.
All three TNF-α inhibitors are approved for psoriatic
arthritis. Ustekinumab (Stelara) binds IL-12 and IL-23
thus interfering with T-cell function in psoriasis. In-
office dosing is every 12 weeks.
 Psoriasis: nails
DDx Ref  72 • 153 • 154a
38 

Surface pitting is the best-known sign of psoriatic

nail disease. Pits may be random but are often
linear.

Onycholysis. Separation of the distal nail plate

may be misdiagnosed as a Candida or fungal
infection.

Oil spot lesions. Brown-red spots represent

accumulation of serum under the nail.

Matrix lesions. Distortion of the entire nail plate

occurs when psoriasis involves the nail matrix.
The entire nail plate is affected.
38  Psoriasis: nails
DDx Ref  72 • 153 • 154a
DESCRIPTION
Distinct nail changes occur in psoriasis that support
the diagnosis when skin changes are equivocal or
absent. Psoriatic nail disease frequently misdiag-
nosed as nail fungal infection.
HISTORY
• Incidence varies from 10% to 50% in psoriasis
patients. • Nail involvement may occur as isolated
finding. • Fifty percent of patients complain of pain.
• Arthritis of the distal phalangeal joint may be
present.
PHYSICAL FINDINGS
Four distinct nail changes seen alone or in combina-
tion. • Pitting. Pitting in the nail plate is the most
common finding. Nail plate cells are shed like psori-
atic scale is shed, leaving tiny, punched-out depres-
sions on the nail plate surface. Pits evolve from
psoriasis in the superficial nail matrix. Pitted areas
emerge from under the cuticle and grow out with the
nail. Many other skin diseases cause pitting (e.g.
eczema, fungal infections, alopecia areata), or it may
occur as an isolated finding in a normal variation.
• Onycholysis. Psoriasis of the distal skin of fingertip
results in accumulation of yellow, scaly debris that
elevates the nail plate. Debris is often mistaken for
nail fungus infection. Psoriasis of the nail bed causes
separation of nail from nail bed. Unlike the uniform
separation caused by pressure on the tips of long
nails, the nail detaches in an irregular manner. The
nail plate turns yellow, simulating a fungal infection.
• Oil spot lesion. Psoriasis of the nail bed causes
localized separation of the nail plate. Cellular debris
and serum accumulate in this space. The brown,
yellow color observed through the nail plate looks like
a spot of oil. • Nail deformity. Extensive involvement
of the nail matrix results in a nail losing its structural
integrity, resulting in fragmentation, crumbling.
Gross alteration of the nail plate surface and nail bed
splinter hemorrhages are common.
TREATMENT
Nail psoriasis is difficult to treat. Nails may improve
when patients are treated with systemic agents such
as ciclosporin, methotrexate, acitretin, or biologic
agaents. • Triamcinolone acetonide. Intralesional
injections at monthly intervals into the matrix with
triamcinolone acetonide (Kenalog) (2.5–10 mg/mL)
delivered with a 30-gauge needle is the standard
treatment. Most patients lose interest in this painful
procedure. Subungual hyperkeratosis, ridging, and
thickening respond. Benefits are sustained for up to
9 months. Onycholysis and pitting less responsive. •
Tazarotene. Tazarotene 0.1% gel (Tazorac) applied
each evening for up to 24 weeks to fingernails. Medi-
cation can be used under occlusion or unoccluded.
Onycholysis responds in occluded and non-occluded
nails and pitting (in occluded nails). • Calcipotriene.
Dovonex 0.005% solution applied to the distal nail
and nail folds twice daily reportedly helps.
 Psoriasis: special forms
DDx Ref  15 • 42 • 77
39 

Guttate psoriasis. Numerous, generalized papules

may abruptly occur following streptococcal
pharyngitis.

Guttate psoriasis. Papules are 0.5–1 cm, red, and

covered with typical psoriatic silvery scale.

Erythrodermic psoriasis. This form is usually

generalized with minimal scale. Erythema is
intense and the patient loses body heat.

Pustular psoriasis. Numerous pustules arise from

a red base. The wave of scale appears as the
pustules evolve and expands outward.
39  Psoriasis: special forms
DDx Ref  15 • 42 • 77
DESCRIPTION
Chronic, inflammatory disease due to abnormal T-
lymphocyte function. Affects skin, scalp, joints, nails.
HISTORY
• Chronic course; exacerbations, remissions.
• Genetic predisposition with environmental triggers,
including stress, physical trauma, Streptococcus
infections, drugs (lithium, beta-blockers, antimalar-
ials, corticosteroid withdrawal), HIV. • Nail involve-
ment: 10–50%. • Psoriatic arthritis (rheumatoid
factor-negative): 7–20%. May precede skin disease.
PHYSICAL FINDINGS
Most common: chronic plaque psoriasis. Extent
highly variable. Other presentations below. • Guttate.
Common presentation in children; follows group A
streptococcal pharyngitis. Sudden appearance of
0.3- to 1.0-cm papules primarily on trunk, extremi-
ties. Spares palms, soles. • Pustular. Rare, severe,
unstable. Sterile pustules arise on red base and coa-
lesce, forming pus lakes. Erythema progresses in
waves; patient may appear toxic with fever and skin
pain. Generalized forms serious, potentially fatal. Oral
steroid withdrawal may precipitate. • Erythro­
dermic. Uncommon. May be initial presentation or
evolve from chronic plaque disease. Localized pro-
gressing to generalized erythema with little scale.
Oral steroid administration or withdrawal may pre-
cipitate. May appear toxic (chills and skin pain).
• Pustular psoriasis of palms and soles. Chronic,
recurrent, treatment-resistant. Sterile pustules
evolve from red base on palms, instep. Pustules do
not rupture but turn dark brown and scaly. Often
painful, limiting mobility. • Scalp psoriasis.
Common. Scale may be very thick, anchored by hair.
Plaque may extend beyond hairline. Itching varies.
• Intertriginous (inverse). Flexural or intertriginous
areas: gluteal fold, axillae, under breasts, groin.
Smooth, red, sharply defined plaques with macer-
ated surface. Superimposed Candida infection in
diabetic patients, with topical steroid use.
TREATMENT
Similar to that for chronic plaque psoriasis, with
specific considerations. • Guttate psoriasis. Treat
streptococcal infection with penicillin or equivalent.
Skin lesions best treated with triamcinolone 0.1%
cream b.i.d. with addition of ultraviolet B therapy.
• Pustular psoriasis. Requires specialist care by
dermatologist. Pustular flares respond to Neoral or
Soriatane. Ultraviolet B and psoralen plus ultraviolet
A useful adjunctive therapies. • Erythrodermic
psoriasis. Best managed with Neoral, Soriatane, or
methotrexate. Ultraviolet therapy and topical steroids
helpful adjunctive therapies. • Intertriginous
(inverse) psoriasis. Best managed with lower-
potency group V topical steroids to minimize atrophy
risk. Use in cycles (e.g. b.i.d. for 10–14 days, stop of
10–14 days). • Scalp psoriasis. Treatment with tar
(T-Gel, etc.) or salicylic acid shampoos removes
some scale. Diffuse scale: apply Derma-Smooth FS
oil to scalp at bedtime, cover with shower cap.
Steroid gels (e.g. Lidex, Temovate, Topicort), steroid
foams (Olux, Luxiq), or solutions (Cormax) penetrate
through hair into scale. Dovonex solution 60 cc b.i.d.
on weekdays as tolerated. Taclonex solution q.d.
 Seborrheic dermatitis
DDx Ref  20 • 81 • 104
40 

Classic presentation of greasy scale and erythema

involving the central face and glabella regions and
the brows.

Inflammation appears when hair is grown on the

scalp and beard. Inflammation is more extensive
in the elderly.

Seborrheic dermatitis may appear in the ears and

be indistinguishable from eczema and psoriasis.

Erythema and scale vary in extent and intensity in

the scalp. Scalp hairs become matted with
adherent scale and debris, requiring careful and
persistent debridement.
40  Seborrheic dermatitis
DDx Ref  20 • 81 • 104
DESCRIPTION
Common, chronic. Pattern varies with age. Possibly
caused by the yeast Pityrosporum ovale in those
genetically predisposed.
HISTORY
• All ages affected. Infantile disease is self-limited;
adult form tends to persist, with periods of remission
and exacerbation. • Severe in elderly, those with HIV
infection, patients with neurologic disease (e.g.
Parkinson disease, stroke). • Flares precipitated by
stress, fatigue, seasonal climate change.
PHYSICAL FINDINGS
• Infants have yellow, greasy, adherent scale on
scalp (cradle cap), with minimal redness. Diaper area
may be involved. Scale adherent to eyelashes and lid
margins with erythema seen in children. • Adults
have yellow, greasy scale on red base, localized in
patches or diffuse. Central face, eyebrows, scalp
margins, scalp, external ear canals, presternal area,
upper back.
TREATMENT
• Facial disease initially treated with antifungal
creams ketoconazole (Nizoral) 30 g q.d. or b.i.d. or
ciclopirox (Loprox) gel 30 g q.d. or b.i.d. • Skin and
scalp disease may be suppressed with daily facial
washing with zinc pyrithione ZnP bar soap or Head
& Shoulders shampoo; selenium sulfide (Selsun)
2.5% 120 mL; selenium sulphide 2.25% in a vehicle
containing urea and zinc pyrithiones (Selseb)
180 mL; sodium sulfacetamide/sulfur cleansers for
facial involvement. Scalp scale may be reduced with
salicylic acid shampoos (e.g. T-Sal) Scalp inflamma-
tion may also be suppressed with tar shampoos (e.g.
T-Gel) or corticosteroid shampoos (e.g. Clobex).
• Group VI steroid creams or lotions (e.g. Desonide
lotion 2 oz b.i.d.) for several days may be required
periodically if antifungal creams fail. • Dense scale
in children and adults may be removed with Derma-
Smooth FS lotion (peanut oil, mineral oil, fluocinolone
acetonide 0.01%) applied to the scalp, washed out
in the morning. Wetting the scalp before application
and using a shower cap will help penetration.
• Blepharitis may be suppressed with zinc- or tar-
containing anti-dandruff shampoos. Brief applica-
tions of 1% hydrocortisone cream may also be used.
 Grover disease (transient
acantholytic dermatosis)
DDx Ref  42 • 48 • 92
41 

The chest and upper abdomen is the most

common site. Lesions may appear on the upper
back, shoulders, and proximal extremities.

Discrete red-brown itchy papules are the common

presentation. Occasionally, lesions are vesicular
or pustular.

Grover disease may cover wide areas of the chest

and abdomen. Itching is typical but not a constant
feature.

Lesions resolve with postinflammatory

hyperpigmentation or hypopigmentation.
41  Grover disease (transient
acantholytic dermatosis)
DDx Ref  42 • 48 • 92
DESCRIPTION
Uncommon, papular, itchy disorder of the chest and
abdomen of unknown etiology. May persist for
months and years.
HISTORY
• Self-limited. • More common in white, middle-
aged men. • Itching is intermittent, mild to severe,
exacerbated by heat or sweating.
PHYSICAL FINDINGS
• Chest, lower rib cage, upper back, lumbar areas.
• Red-brown, keratotic papules that are often excori-
ated. • May spread to lateral neck, shoulders, upper
thighs. • Older patients will usually have longer-
lasting, more extensive eruptions.. • Lesions resolve
with postinflammatory hyperpigmentation or
hypopigmentation. • Biopsy may be required for
diagnosis.
TREATMENT
Itching is mild in some cases, and symptomatic relief
with mentholated lotions (Sarna) is all that is neces-
sary. Colloidal oatmeal baths may relieve itching.
Avoid strenuous exercise, excessive bathing, and
exposure to heat. • Group II–V topical steroids:
moderately effective, used as needed. • Oral vitamin
A: 50 000 international units t.i.d. for 2 weeks then
reduced to 50 000 international units q.d. for a
maximum of 12 weeks may be effective for extensive
and severely pruritic cases. • Isotretinoin: 40 mg
q.d. until controlled (2–12 weeks), then taper dosage
to 10 mg q.d. once patient improves and continue for
12 weeks. • Prednisone: 20 mg b.i.d. controls
extensive inflammation and itching; relapse after
stopping is common. • Antihistamines, oral antibi-
otics, dapsone: not effective.
 Pityriasis rosea
DDx Ref  39 • 45 • 53
42 

The primary lesion is an oval, salmon-colored,

1- to 10-cm plaque that forms a round collarette
of scale in the center.

Lesions are found on the trunk and usually spare

the face and extremities.

The number of lesions is highly variable. Plaques

may extend to the neck and proximal limbs.

Numerous lesions may appear. A concentration of

lesions on the groin and lower abdomen is highly
characteristic, especially in children.
42  Pityriasis rosea
DDx Ref  39 • 45 • 53
DESCRIPTION
Common, usually asymptomatic, seasonal, possibly
post-viral, possibly contagious, highly characteristic,
self-limited eruption.
HISTORY
• Most patients between the ages of 15 and 35.
• May begin with mild upper respiratory symptoms.
May or may not begin with a single lesion on the
trunk, the ‘herald patch’, which is larger than subse-
quent lesions. A few to numerous lesions then sud-
denly appear 1–2 weeks later. • Itching is mild or
absent. Itching may be intense in extensive cases.
• Lesions clear without treatment in 4–12 weeks.
PHYSICAL FINDINGS
• The lesion is a salmon-colored, oval plaque 1–2 cm
in diameter. The long axis of the oval lesions is ori-
ented horizontally. • Lesions are dark brown on
African-American skin and sometimes difficult to
see. • A round rim of scale rapidly forms inside the
border. • Plaques sometimes very large and mis­
diagnosed as fungal infection (ringworm). • Lesions
are located on trunk and proximal extremities, often
concentrated on lower abdomen. • Dark-brown
postinflammatory pigmentary changes may take
months to resolve in darker-skinned people.
TREATMENT
• Mentholated lotions (Sarna) or sprays (Eucerin Anti-
Itch) for itching. • Sun exposure or ultraviolet B light
in a dermatologist office hastens resolution. • Erythro­
mycin stearate 250 mg q.i.d. (for adults) or 25–
40 mg/kg in four divided doses in children for 2
weeks may clear the eruption. • Group V topical
steroids and oral antihistamines provide some relief.
• Prednisone (20 mg b.i.d. for 1 week) used for
extensive cases with intense itching.
 Lichen planus
DDx Ref  39 • 42 • 103
43 

Primary lesion (early): Skin-colored to red,

flat-topped papule with angulated border. White,
reticulated surface lines are called Wickham
striae.

Mineral oil accentuates the reticulated lines.

Lesions become purple, thicker, and more
numerous with time.

Papules appear most often on the flexor surfaces

of wrists and forearms, ankles, and lumbar
region. Lesions may be much more extensive.

White, lacy pattern on buccal mucosa. Similar

lesions appear on the penis and vaginal mucosa.
43  Lichen planus
DDx Ref  39 • 42 • 103
DESCRIPTION
Chronic, difficult to treat, characteristic eruption of
unknown etiology. Skin, scalp hair follicles, mouth,
penis, vaginal mucosa, and nails may be affected.
HISTORY
• Uncommon; rare in children. • Itching highly vari-
able. • Family history in 10%. • May last 2 or more
years. • May be drug-induced. • Oral lichen planus
degenerates to squamous cell carcinoma in 3% of
cases.
PHYSICAL FINDINGS
• Many different presentations. • Primary lesion is a
flat-topped, red to purple, angulated papule. Highly
characteristic lacy white lines (Wickham striae)
appear on the surface. Lines are accentuated by
mineral oil. • Most common presentation: papules on
flexor wrists and forearms, ankles, and lumbar
region. • Lesions may develop in areas of injury
(Koebner). • Lesions become thick and dark purple.
• Very thick lesions on shins are called hypertropic
lichen planus.
• Always examine the oral mucosa. Some
patients have a lacy white pattern on the buccal
mucosa. Similar lesions may appear on the penis and
vaginal mucosa. Erosive lesions may appear in
mouth and oral mucosa.
TREATMENT
• Group I or II topical steroids: confined to lesions
b.i.d. for 2 weeks, then stop for 1 week. • Intra­
lesional triamcinolone acetonide: Kenalog 5–10 
mg/mL for thick lesions. • Prednisone: for general-
ized skin or erosive mucosal involvement; a 4-week
course starting at 1 mg/kg q.d. and gradually
decrease dosage. • Triamcinolone acetonide in
adhesive base (Orabase): apply b.i.d. to oral
lesions. • Tacrolimus (Protopic): 0.1% ointment
b.i.d. sometimes effective for erosive mucosal
lesions. • Sedating antihistamines: for itching
(hydroxyzine 10–25 mg every 4 h). • Dapsone,
retinoids (Acitretin), ciclosporin: considered for
severe, recalcitrant disease. • Azathioprine or
hydroxychloroquine: for severe, recalcitrant oral
lesions.
 Lichen sclerosus
DDx Ref  43 • 107 • 133
44 

Primary lesion: ivory white, flat-topped papule

which, on skin, will develop a keratotic follicular
surface plug (delling).

Papules coalesce into atrophic plaques with a dull

or glistening, smooth or wrinkled surface. Focal
hemorrhage may occur in the plaque.

Painful vaginal mucosal lesions are atrophic and

fragile. Lesions often hemorrhage, erode, and
scar.

Penile lesions favor the glans and coronal sulcus

but may extend to the shaft. Fragile atrophic
lesions develop hemorrhages and erosions.
44  Lichen sclerosus
DDx Ref  43 • 107 • 133
DESCRIPTION
Uncommon, chronic disease of unknown etiology
that causes focal atrophy of skin, penis, and vagina.
HISTORY
• Skin lesions are rare and usually asymptomatic.
• Most cases involve vulva or penis (balanitis xerotica
obliterans). Genital disease occurs in young girls and
uncircumcised boys, and in women over 60 and older
uncircumcised men. • Women have itching, pain
with intercourse and urination. Men have inflamma-
tion of the foreskin, which if untreated leads to
narrowing of the foreskin. Irritation and infection
occur because the foreskin cannot be retracted.
• Squamous cell carcinoma develops in 3% of
mucosal lesions.
PHYSICAL FINDINGS
• Skin lesions begin as white papules with keratotic
follicular surface plugs (delling). They coalesce into
dull white, atrophic plaques with a fragile wrinkled
surface. Focal hemorrhage may occur. • Mucosal
surfaces are white, fragile, atrophic. Minor trauma
causes erosions, bleeding, and leads to scarring.
• Penile lesions occur on the glans and may extend
into the urethral meatus and to the shaft. • The white
atrophic changes of the vulva may extend to and
surround the anus. • Focal purpura and erosions are
common. Tissues shrink, scar, and distort normal
structures.
TREATMENT
• Protect mucosal surfaces with heavy lubricants
(e.g. Aquaphor). • Initial treatment: group V topical
steroid ointment or cream b.i.d. for 2 weeks. • Group
I topical steroid creams or ointments (clobetasol)
used for resistant vulvar disease, b.i.d. for up to 1
month then intermittently as needed. This super­
potent steroid must be used with caution. • The
non-steroidal anti-inflammatory agent tacrolimus
ointment (Protopic) 0.1% may control vaginal and
penile disease. It may be used for extended periods.
• Acitretin (20–30 mg q.d. for 16 weeks) effective for
severe vulvar disease.
 Pityriasis lichenoides et
varioliformis acuta
DDx Ref  64 • 84 • 85
45 

Lesions appear abruptly and are found primarily

on the trunk and proximal extremities. There may
be a few or more than one hundred discrete
lesions.

Lesions may be asymmetrically distributed on the

trunk.

Lesions may appear on the distal extremities and

the palms and soles.

Red-brown, round to oval papules develop central

necrosis, hemorrhage, and crust. Lesions are in
different stages of development, as is seen in
chickenpox.
45  Pityriasis lichenoides et
varioliformis acuta
DDx Ref  64 • 84 • 85
DESCRIPTION
Rare papular eruption of unknown etiology and two
variants. 1. Pityriasis lichenoides et varioliformis
acuta (PLEVA) or Mucha–Habermann disease:
acute form with rapid evolution of highly inflamed
lesions. 2. Pityriasis lichenoides chronica: chronic
form with slow evolution of mildly inflammatory
lesions.
HISTORY
• Occurs at any age; most cases in first, second, and
third decades. • Usually benign and self-limited but
may wax and wane for years. • PLEVA presents with
sudden onset of mildly itchy papules that rapidly
evolve to vesicles and hemorrhagic crusts. The erup-
tion clears in about 6 weeks. A severe form presents
with ulceronecrotic lesions, high fever, and myalgias
and other systemic symptoms. • The chronic form
appears over several days; chronically inflamed
lesions take 6–8 months to resolve.
PHYSICAL FINDINGS
• PLEVA: papules with adherent thin scale occur in
crops. Round to oval, reddish-brown papules vary in
size, become vesicular, and undergo hemorrhagic
necrosis usually within 2–5 weeks, often leaving
postinflammatory hyperpigmentation. Occurs most
often on trunk and proximal extremities; face, scalp,
palms, and soles sometimes involved. • Pityriasis
lichenoides chronica: occurs primarily on trunk and
consists of brownish-red papules with fine, mica-
like, adherent scale.
TREATMENT
• Erythromycin (30–50 mg/kg q.d. for several weeks)
or tetracycline is the most commonly used treatment.
Response unpredictable. Group I–III topical steroids
used b.i.d. provide some relief. Oral corticosteroids
or dapsone may be effective for acute form. • Pho-
totherapy with psoralen plus ultraviolet A and ultra-
violet B, or ultraviolet B or narrowband ultraviolet B
effective for chronic form. • Mentholated lotions
(Sarna lotion) relieve itch.
 DDx Ref  63 • 67 • 97
Impetigo
46 

Rounded, crusted papules and plaques on face.

Crust is yellow and heavy-appearing. Lesions
have some vesiculation at outermost edge.

Primary lesion is a flaccid, thin-roofed bulla. The

larger lesions are secondary; they are erosions
with peripheral collarette of scale, which is a
typical evolution of bullous impetigo.

Faint erythema and yellow, honey-colored crusting

of the nare base. Nasal carriers of S. aureus do not
typically show this change; the carrier state is
identified by inner nasal mucosa culture.

A collarette of scale surrounds pink, previously

infected skin. There are a few tiny vesicles and
some yellow crusting in this case of impetigo
affecting the fingers.
46  Impetigo
DDx Ref  63 • 67 • 97
DESCRIPTION
Impetigo is a common, contagious, superficial skin
infection produced by Streptococcus pyogenes and/
or Staphylococcus aureus. Bullous impetigo and non-
bullous impetigo are two forms. S. aureus is the
primary pathogen.
HISTORY
• Impetigo may occur after a minor skin injury such
as an insect bite, or within lesions of atopic or other
dermatitis. • Children in close physical contact have
higher infection rate. • Responsible staphylococci
may colonize nose, serving as reservoir for skin
infection. • Warm, moist climates and poor hygiene
predispose.
PHYSICAL FINDINGS
Lesions may be localized or widespread. Common on
face. • Bullous impetigo. Thin-roofed bullae may
turn from clear to cloudy. Bullae collapse, leading to
an inner tube-shaped rim with central, thin, honey-
colored crust. Lesions enlarge and often coalesce
with minimal surrounding erythema. Thick crust
accumulates over time. Lesions found in all stages.
• Non-bullous impetigo (crusted). Vesicles or pus-
tules rupture, exposing red, moist base. Scaling
border forms as round lesions enlarge. Honey-yellow
to white-brown crust accumulates as lesion extends
radially; little surrounding erythema. Satellite lesions
appear beyond periphery. Systemic symptoms infre-
quent. Lesions generally asymptomatic, painless.
Incidence of acute nephritis 2–5%; if nephri-
togenic streptococcal strain, rate varies between
10% and 15%. Rheumatic fever not reported as a
complication.
S. aureus a common infection with potential
complications, particularly if some immune suppres-
sion exists. Recurrence following therapy is common.
Culture typically grows S. aureus, less commonly,
group A Streptococcus.
TREATMENT
• For limited infection, mupirocin 2% ointment or
cream (Bactroban) t.i.d. for 10 days. • Neomycin-
bacitracin creams also effective. • For widespread
infections, oral therapy such as dicloxacillin 250 mg
or cephalexin (Keflex) 250 mg q.i.d. for 5–10 days.
Pediatric doses cephalexin 40–50 mg/kg t.i.d. for
10 days, amoxicillin plus clavulanic acid 20 mg/kg
t.i.d. for 10 days. For penicillin-allergic, azithromycin
given over 5 days (500 mg on day 1 and 250 mg on
days 2–5) or clarithromycin 250–500 mg b.i.d. for
10 days may be effective. • For recurrent impetigo,
seek occult S. aureus. Most common site is the
nares. Less commonly in perineum, axillae, and toe
webs. • Mupirocin 2% ointment for recurrent
disease, applied to nares b.i.d. for 5 days. Repeat
monthly for several months.
 DDx Ref  11 • 18 • 88
Cellulitis
47 

Typical cellulitis of an extremity. An erythematous

patch with edema. These findings were
accompanied by tenderness in the affected skin
and fever.

Cellulitis limited to distal nasal tip. The skin is

tender and swollen.

Sharply demarcated erythema, swelling, and

tenderness. Usual organisms are S. aureus and
group A β-hemolytic Streptococcus pyogenes.
Diabetes and lymphedema are risk factors.

Cellulitis of the pinna may result from infection

with Pseudomonas species or with staphylococci
and streptococci.
47  Cellulitis
DDx Ref  11 • 18 • 88
DESCRIPTION
Infection of dermis and subcutaneous tissues char-
acterized by fever, erythema, edema, and pain.
HISTORY
• Localized pain, redness, tenderness, swelling.
• Risk factors: diabetes, cirrhosis, renal failure,
chemotherapy, immune suppression, malignancy,
alcohol, malnourishment, HIV. • Surgical wounds and
trauma sites (e.g. bites, burns, abrasions, lacera-
tions, ulcers) are common locations. • Recurrent
episodes at sites of compromised venous or lym-
phatic circulation (i.e. stasis dermatitis). • Ear and
lower legs susceptible to recurrence.
PHYSICAL FINDINGS
• Expanding, red, swollen, tender or painful plaque
with indefinite border in a small or wide area.
• Palpation produces pain, rarely crepitus. • Occa-
sionally, vesicles, blisters, hemorrhage, necrosis, or
abscesses. • Regional lymphadenopathy sometimes;
lymphangitis common with Streptococcus pyogenes.
• Pre-existing lesion: ulcer, erosion, tinea, or derma-
titis may be entry portal.
TREATMENT
• Rest, elevation of affected extremity. • Empiric
antibiotic coverage: staphylococcal and streptococ-
cal organisms. • Treatment options: dicloxacillin
350–500 mg orally every 6 h, or oral amoxicillin/
clavulanate 875 mg/125 mg b.i.d. or 500 mg/
125 mg t.i.d. (adult dose), or first-generation cepha-
losporin, i.e. cephalexin 250–500 mg q.i.d., or azi-
thromycin 500 mg initial dose then 250 mg on days
2–5, or clarithromycin 500 mg every 12 h. • Severe
infection may require hospitalization, i.v. antibiotics.
Intravenous empiric therapy for group A streptococci
and Staphylococcus aureus with cefazolin 1.0 g
every 8 h or nafcillin 2 g every 4–6 h. • Clostridial
anaerobic cellulitis most commonly caused by
Clostridium perfringens, sometimes other clostridia.
Pain, soft tissue swelling, and systemic toxicity
occur; gas may be palpable or visible by X-ray. Treat-
ment with high-dose i.v. penicillin in addition to
prompt surgical exploration and debridement of devi-
talized tissue. • Infected decubitus ulcers: organisms
mixed bowel flora (Gram-negatives, streptococci,
anaerobes). • Infection of burns: organisms Pseu-
domonas aeruginosa, other Gram-negatives, S.
aureus, Candida. • Postsurgical cellulitis: Gram-
negative organisms, complicated by wound dehis-
cence and sepsis; coverage for S. aureus, group A
streptococci, Gram-negatives. • Gangrenous celluli-
tis involves extensive necrosis, is a rapidly progres-
sive cellulitis most commonly caused by group A
streptococci. Streptococcal gangrene most com-
monly at site of trauma. Painful erythema followed
by edema, bullae, necrosis; may be complicated by
rapid bacteremia and septic shock. • Dog and cat
bite cellulitis: treat with oral amoxicillin/clavulanic
acid 875 mg/175 mg b.i.d. for 7–10 days or
500 mg/125 mg t.i.d., or oral doxycycline 100 mg
b.i.d. for 10 days.
 Folliculitis
DDx Ref  41 • 77 • 92
48 

Pustules are typical of folliculitis. They are

monomorphic, 1- to 2-mm pustules with a bright
halo of erythema. They are classic of
staphylococcal folliculitis.

Numerous discreet bright-red papules surrounding

hair follicles are seen in this case of folliculitis on
the legs. Staphylococcus aureus can be spread by
shaving.

Follicular pustules on the chin may represent

bacterial or fungal infection. Consider culture.

Folliculitis on the buttocks. These lesions are

eroded, and the condition is pruritic, and
sometimes painful.
48  Folliculitis
DDx Ref  41 • 77 • 92
DESCRIPTION
Folliculitis means an inflammation of the hair follicle.
Common types: mechanical folliculitis from persist-
ent friction or tight clothing, bacterial folliculitis.
Bacterial folliculitis includes follicular impetigo, a
superficial form, and sycosis barbae, a deep form in
beard area. Fungal folliculitis is less common but can
result from untreated tinea corporis, or tinea infection
in beard or hair-bearing skin.
HISTORY
• Usually, eruption is abrupt. • Bacterial folliculitis
can spread by trauma, scratching, or shaving. • Vari-
able distribution; often scalp, arms, legs, axillae,
trunk.
PHYSICAL FINDINGS
• Dome-shaped pustules with small erythematous
halos arise in the follicle. May be tender. • Staphy-
lococcus aureus is most common infecting organism.
• Potassium hydroxide examination of the hair and
surrounding scale can exclude dermatophyte
infection.
Types
• Staphylococcal folliculitis. Most common form.
Pustules, usually without fever or other symptoms.
• Dermatophyte folliculitis (tinea of hair follicle).
Inflammatory papules and pustules with surrounding
scale and eczematous papules. Potassium hydroxide
examination of hair and surrounding scale is positive.
• Eosinophilic folliculitis. Pruritic, extensive follicu-
lar papules on face, neck, chest. Associated with HIV.
Diagnosis confirmed or suspected by biopsy. • Gram-
negative folliculitis. Acneiform eruption suddenly
worsens, becomes pustular. Chronic oral antibiotics
predispose. • Hot tub folliculitis. Erythematous
papules and pustules primarily on trunk. Pseu-
domonas from improperly sanitized hot tub.
• Mechanical folliculitis. From chronic frictional
exposure, such as tight pants, obesity. • Occlusion
folliculitis. From occlusion, i.e. exposure to oil,
greases, ointments. • Pityrosporum folliculitis. On
back and chest. Potassium hydroxide test positive for
short hyphae and round spores. • Steroid folliculitis.
Multiple monomorphic pustules and red papules
within 2 weeks of using systemic corticosteroids.
TREATMENT
• Minimize heat, friction, occlusion. • Frequent
change of razor. • Mupirocin (Bactroban) applied
three times daily for 5 days for limited involvement.
Treat intranasally also if culture confirms carriage of
S. aureus. • Oral antistaphylococcal antibiotics
(trimethoprim-sulfac, oxacillin, doxycycline, dicloxa-
cillin, cephalexin, cefuroxime) indicated for extensive
disease or for deep involvement of sycosis barbae.
But culture and sensitivity is important to antibiotic
choice, given increasingly methicillin resistant
staphylococcus. • Nasal carriage of S. aureus is a
common reason for recurrent bacterial folliculitis.
Treat the nasal carrier state. • Pityrosporum follicu-
litis: topical or oral antiyeast antibiotics such as
clotrimazole lotion and econazole cream. Two tablets
of ketoconazole 200 mg taken once, repeated after
1 week for widespread disease. • Follicular dermato-
phyte infection (Majocchi granuloma) responds best
to oral antifungal therapy.
 Pseudofolliculitis barbae
DDx Ref  31 • 48 • 81
49 

Multiple follicular pink papules in the beard

region. The lesions often resolve with
hyperpigmentation.

Numerous scattered inflammatory papules where

skin has been shaved. Leaving beard length long
prevents the problem of pseudofolliculitis. The
problem is often more severe on the neck.

Tiny hairs piercing the skin, each hair surrounded

by an erythematous halo. This reaction is not
infectious, rather a foreign body-type reaction to
coarse or curved hair piercing the skin.

Papules in an area of skin where the hairs are

shaved short. Some papules are pink and some
are hyperpigmented. Close shaving predisposes.
49  Pseudofolliculitis barbae
DDx Ref  31 • 48 • 81
DESCRIPTION
Pseudofolliculitis barbae is a papular and pustular,
foreign body, inflammatory reaction that can affect
any individual who has curly hair and regularly
shaves closely.
HISTORY
• Significant problem in predisposed individuals who
are required to shave closely. • Occurs commonly in
African-American people; can be chronic and dis­
figuring. • Most severely affected sites are neck and
beard areas. • Tends to be a chronic problem.
PHYSICAL FINDINGS
• Pseudofolliculitis barbae affects people with curly
hair or with hair follicles oriented at oblique angle to
skin surface. • A sharp, shaved, tapered hair reenters
skin as it grows and induces a foreign body reaction,
producing a microabscess. • Perifollicular red
papules or pustules occur most commonly in beard
area or any area where hair is shaved. • Lesions
painful and/or pruritic. Scarring and hyperpigmenta-
tion may result. • Keloid formation is frequent
problem.
TREATMENT
• Dislodge embedded hairs. A needle is inserted
under hair loop, and the hair is firmly elevated. • A
Buff Puff or toothbrush can be used to gently
massage in a circular fashion and dislodge ingrown
hair. • Discontinue shaving until inflammation under
control. • Topical azelaic acid cream (Finacea) helps
reduce hyperpigmentation and inflammation.
• Topical antibiotic preparations (clindamycin,
benzoyl peroxide 5% or 10%, erythromycin) reduce
bacterial colonization. Culture, and if staph. aureus
present, a short course of antistaphylococcal antibi-
otic appropriate for sensitivity may hasten resolution.
• Intralesional triamcinolone acetonide 2.5 mg/mL
used for persistent papules. Atrophy may result tem-
porarily. • Once lesions resolve, shaving may be
resumed. Avoid close shaves. • Shower before
shaving and keep the beard hair in contact with
warm water for at least 2 min. • Use thick-lathering
shaving gels (Aveeno Therapeutic Shave Gel, Edge
Gel for Tough Beards). • Bump Fighter razor (http://
www.asrco.com) cuts the hair slightly above skin
surface. • An electric razor can be used; avoid
‘closest’ shave setting. • Shave in the direction of
hair growth. • A moisturizing lotion should be used
after shaving. LactiCare-HC (1% or 2.5%) can be
used intermittently. • Topical eflornithine hydrochlo-
ride 13.9% cream (Vaniqa) applied twice daily retards
hair growth. Apply twice daily to affected skin.
• Depilatories (Nair, Neet) are effective alternatives
to shaving. Apply to skin for 3–10 min then wipe off.
Irritation limits use to once or twice weekly. • If
measures fail, discontinue shaving indefinitely.
• Laser-assisted hair removal can provide a safe,
effective means of treating recalcitrant cases.
 Furuncles and carbuncles
DDx Ref  32 • 35 • 122
50 

Furuncle: a bright-red nodule with several

pustules on the surface and a rim of erythema.

Furuncle on the chin. An erythematous tender

nodule that drained in the center, releasing
purulent exudate.

Tender inflammatory plaque that is fluctuant on

palpation and has several pustules on the surface
where the lesion is draining.

Furuncles may be multiple, as in this case. The

tender inflammatory nodules have spontaneously
drained. Culture is positive for Staphylococcus
aureus. Antibiotic sensitivity patterns are
changing; check when prescribing therapy.
50  Furuncles and carbuncles
DDx Ref  32 • 35 • 122
DESCRIPTION
• Furuncle. Walled-off, deep, painful, firm, or fluctu-
ant mass enclosing a collection of pus; often evolves
from superficial folliculitis. Staphylococcus aureus is
most commonly associated organism, but other
organisms (Escherichia coli, Pseudomonas aerugi-
nosa, Streptococcus faecalis) and anaerobes cause
lesions. Methicillin resistant Staph. aureus has
become an increasing problem. • Carbuncle.
Extremely painful, deep, interconnected aggregate of
infected, abscessed follicles.
HISTORY
• Uncommon in children. • Occlusion and hyper­
hidrosis, diabetes, immune defects are risk factors.
• High friction and sweating sites most often
affected, such as beltline, anterior thighs, buttocks,
groin, axillae, waist.
PHYSICAL FINDINGS
• Furuncle. Deep dermal or subcutaneous, red,
swollen, and painful mass later points toward skin
surface and drains through multiple openings.
• Carbuncle. Deep, tender, firm, subcutaneous, ery-
thematous papules enlarge to deep-seated nodules;
stable or become fluctuant within days. Fever may
be associated.
TREATMENT
• Warm dressings 15–30 min. • Incision, drainage
is primary management for fluctuant lesions. Local
anesthesia required. Iodoform gauze used for packing
drained lesions; remove daily followed by wound
cleansing. Follow up to ensure treatment response.
• Culture and sensitivity for large, advancing, or atypi-
cal complicated lesions. Oral therapy appropriate for
complicated cases but lesion must be cultured, with
antibiotic choice based on sensitivity results. • For
susceptible S. aureus some options include: Dicloxa-
cillin 250–500 mg q.i.d. for 10 days (adults).
Cephalexin 250–500 mg q.i.d. for 10 days (adults);
40–50 mg/kg t.i.d. (children). Amoxicillin and clavu-
lanate 875 mg b.i.d. for 10 days (adults); children
aged more than 3 months and weighing less than
40 kg can be given 45 mg/kg b.i.d. or t.i.d. Clin-
damycin 150–300 mg q.i.d. for 10 days (adults);
15 mg/kg q.i.d. for 10 days (children). Nafcillin
or oxacillin 2 g i.v. every 6 h for moderate to
severe infections. Incidence of methicillin-resistant
S. aureus is increasing; culture and sensitivity
increasingly important. Trimethoprim–sulfa or doxy-
cycline are often first-line options in cases of methi-
cillin-resistant S. aureus when oral therapy is
appropriate.
Recurrence
• Eradicate S. aureus carriage. Mupirocin cream
(Bactroban) or ointment applied to wounds and nares
b.i.d. for 5 days or rifampin 600 mg for 10 days and
either dicloxacillin 500 mg q.i.d. or trimethoprim–
sulfamethoxazole one double-strength tablet b.i.d.
for 10 days. • Methicillin resistance. Mupirocin 2%
in nares and wounds twice daily for 1–2 weeks, or
one trimethoprim–sulfamethoxazole double-strength
tablet b.i.d. orally for 10 days, and rifampin 600 mg
q.d. for 10 days. Betadine or chlorhexidine wash of
body, fingernails daily for 1–3 weeks and changing,
washing towels, bed sheets daily. Change wound
dressings frequently; clean or replace shaving tools
daily; avoid nose picking.
 Pseudomonas folliculitis
DDx Ref  48 • 65 • 97
51 

The primary lesion in Pseudomonas folliculitis is

the pustule. It is follicular with a bright red halo
surrounding it. There is usually a history of recent
hot tub use.

Bright-red swollen macules with a central pustule

on the trunk. Pseudomonas folliculitis is typically
under the area covered by a bathing suit. It is
often pruritic.

Pseudomonas folliculitis of the buttocks.

Bright-red macules with central pustules. The
lesions are all in the same stage of evolution. A
culture is helpful. Note similarity of lesions.

Scattered inflammatory papules that are nearly

resolved, concentrated in the area that was
covered by the bathing suit.
51  Pseudomonas folliculitis
DDx Ref  48 • 65 • 97
DESCRIPTION
Pseudomonas folliculitis is an acute, superficial skin
infection that follows exposure to contaminated
water. The urticarial red plaque with a central papule
or pustule is highly distinctive. Multiple lesions on the
trunk are typical. Also called hot tub folliculitis.
HISTORY
• Attack rate significantly higher in children than in
adults, possibly because children tend to spend more
time in the water. • Occurs 8 h to 5 days (or longer)
after using a contaminated pool (whirlpool, hot tub,
physiotherapy pool) or water slide, or a contaminated
loofah sponge. The attack rate is variable; 7–100%
of those exposed to Pseudomonas species develop
the disease. • Spread of infection from person to
person is unlikely. • Prolonged exposure to water,
excessive numbers of bathers, and inadequate pool
or spa care predispose to infection. • Desquamated
skin cells in the water provide a rich, organic nutrient
source for bacteria. • In most cases, eruption clears
in 7–10 days without treatment, but recurrent crops
of lesions may occur for as long as 3 months.
PHYSICAL FINDINGS
• Plaques are 0.5–3 cm, red, pruritic, round, and
urticarial with a central papule or pustule. • Sudden
onset. A few plaques to more than 50 occur primarily
on trunk. • Rash may be a follicular, maculopapular,
vesicular, pustular, or polymorphous eruption includ-
ing all these lesion types. • Rash most severe in
areas occluded by snug bathing suits. • Occlusion
and superhydration favor colonization of skin with
Pseudomonas aeruginosa. • Women who wear one-
piece bathing suits at an increased risk. • Rash
resolves, leaving round macules of postinflammatory
hyperpigmentation. • Fever, malaise, and fatigue
may occur during initial few days of eruption, but this
is uncommon. • P. aeruginosa serotypes 0:9 and
0:11 are most commonly isolated from skin lesions.
TREATMENT
• Infection self-limited; treatment usually not
required. • Other treatment options: A wet dressing
of acetic acid 5% (white vinegar) is applied for
20 min b.i.d. or q.i.d. Silver sulfadiazine cream (Sil-
vadene) can help. • Cases resistant to topical therapy
can be treated orally with ciprofloxacin (Cipro)
250–500 mg b.i.d. for 7 days. • Preventive meas-
ures: continuous water filtration eliminates desqua-
mated skin; maintain adequate chlorine levels;
change water in private hot tubs every 4–8 weeks;
drain public hot tubs daily. • Showering after using
the contaminated facility offers no protection.
 Otitis externa
DDx Ref  11 • 39 • 47
52 

The ear shows marked near confluence of

erythema of varying intensity. There is scale crust
and some weeping in the bowl of the ear.
A culture is warranted.

Severe external otitis of the entire ear. The ear is

swollen, tender, and crusted. A bacterial source
should be considered, and awareness of potential
contact allergens is prudent.

Mild inflammation with scaling and a faint pink

erythema anterior to the ear, suggesting psoriasis
or seborrheic dermatitis. This will usually resolve
with a mild topical steroid solution.

Intense inflammation of the pinna with swelling

and exudate. Pseudomonas was cultured.
Treatment was with levofloxacin.
52  Otitis externa
DDx Ref  11 • 39 • 47
DESCRIPTION
Otitis externa is an inflammation of the external audi-
tory canal, usually with secondary infection.
HISTORY
• A mild, self-limited form known as swimmer’s ear
is common in children. • Symptoms range from itch
and irritation to severe pain. • Mechanical cleansing
of the external canal and medicaments used to
relieve symptoms can mask or exacerbate the condi-
tion. • Ear wax forms a water-resistant barrier for the
thin skin that lines the canal, and inhibits bacterial
growth by maintaining a low pH environment. When
this protective barrier is disrupted, bacterial over-
growth can occur. • The usual pathogen is Pseu-
domonas, but mixed infections with Staphylococcus
and Pseudomonas species are common. • Swim-
mer’s ear typically caused by Pseudomonas species,
Enterobacteriaceae, or Proteus species. Acute infec-
tion usually due to Staphylococcus aureus. • Sec-
ondary infection with Candida species may occur but
is uncommon. • A rare and severe form of otitis,
referred to as malignant external otitis, may develop
in patients who have diabetes or who have had ear
surgery.
PHYSICAL FINDINGS
• External auditory canal is inflamed with erythema,
edema, and dull pain. • Keratin and inflammatory cell
debris accumulate within canal. • Most cases do not
progress. With progression, pinna becomes red, hot,
and edematous, and may develop purulent drainage.
• Cellulitis involves entire pinna and often extends to
preauricular skin. Pain becomes sharp and constant.
• External auditory canal should be cultured.
TREATMENT
• Treatment involves reestablishing the natural pro-
tective barrier. • Cellular debris is flushed from the
external canal with gentle irrigation. • An acetic acid
solution (VoSol otic solution or VoSol HC otic solution)
helps lower pH and inhibits bacterial and fungal
growth. • Ofloxacin otic solution 0.3% (Floxin otic
solution twice daily) or ciprofloxacin and hydrocorti-
sone (Cipro HC otic) are instilled twice a day. For
acute disease, culture to determine organism and
sensitivity. • Topical steroids, wet dressings using an
astringent such as Domeboro, or Bluboro wet dress-
ings applied for 30 min three times daily, and oral
antibiotics such as ciprofloxacin (Cipro) are valuable
when cellulitis involves pinna. • Avoid the more
common contact allergens (such as topical baci-
tracin, neomycin, hydrocortisone) and minimize other
topical products. • Discourage vigorous scratching,
rubbing, or mechanical debridement of external audi-
tory canal. • Malignant external otitis requires hos-
pitalization, administration of i.v. antibiotics, and
debridement, as well as consideration of a computer-
ized or magnetic resonance imaging scan to evaluate
possible osteomyelitis. • Otolaryngology consultation
recommended for malignant external otitis.
 DDx Ref  42 • 54 • 56
Syphilis
53 

Treponema pallidum is the organism responsible

for syphilis. Here, it is seen through a dark-field
microscope as a tightly coiled simple bacteria. It
is a member of the Spirochete family of bacteria.

Primary syphilis. Lesion begins as papule that under-

goes ischemic necrosis and erodes to form a 0.3-
to 2.0-cm, painless to tender, hard, indurated ulcer.
Base clean with scant yellow serous discharge.

Secondary syphilis, with the characteristic

findings of pink oval scaly patches on the palm
with slight hyperpigmentation. These findings may
also be seed the plantar feet.

Lesions of secondary syphilis have marked

tendency to polymorphism, with various types of
lesions presenting simultaneously. They have a
coppery tint and assume various shapes.
53  Syphilis
DDx Ref  42 • 54 • 56
DESCRIPTION
Syphilis (lues) is an infectious disease caused by the
spirochete Treponema pallidum. Spread sexually.
Can affect virtually every organ. Untreated, syphilis
passes through stages: primary, secondary, latent,
tertiary.
HISTORY
• Primary. Chancre acquired by direct contact. It
appears 21 days after exposure and is usually soli-
tary. Primary chancres resolve but the spirochete
remains. • Secondary. Begins 6 weeks after the
chancre and results from hematogenous and lym-
phatic spread of the spirochete. An influenza-like
syndrome with mucocutaneous lesions, hepat-
osplenomegaly, and generalized adenopathy occurs
and lasts 2–10 weeks. Skin changes of this stage are
easily confused with other skin diseases, especially
pityriasis rosea. • Latent. Results of serologic tests
are positive without evidence of active disease.
Tertiary. Characterized by small number of spiro-
chetes eliciting a large or brisk cellular immune
response. This manifests as cardiovascular and
central nervous system granulomas or gummas.
• Congenital. Yet another variant.
PHYSICAL FINDINGS
• Primary. Chancre is painless and begins as a
3-mm to 2-cm papule, undergoes ischemic necrosis,
and erodes. Occasionally it is tender, firm, and indu-
rated. Borders are raised, smooth, sharply defined.
Syphilitic chancres on the cervix may be asympto-
matic and undetected, may allow transmission. Pain-
less, non-suppurative regional lymphadenopathy
develops in 1–2 weeks. • Secondary. Characterized
by systemic, cutaneous, and mucosal signs and
symptoms. Fever, malaise, pharyngitis, adenopathy,
weight loss, and meningeal signs (headache)
common. Most common sign is a non-pruritic, gen-
eralized, pink, scaly, papular eruption in 80% of
patients. Symmetric, hyperpigmented, oval papules
with a collarette of scale appear on palms or soles in
most patients. Irregular alopecia of beard, scalp, and
eyelashes occurs—sometimes referred to as ‘moth-
eaten alopecia’. Moist, anal, condyloma lata lesions
are highly infectious wart-like papules characteristic
of syphilis. All secondary lesions are infectious with
direct contact or palpation. • Latent. Very few if any
clinical signs. • Tertiary. Gummas or granulomatous
lesions develop subcutaneously, expand and ulcerate
in the skin. These lesions also occur in liver, bones,
other organs. Direct detection of treponemes under
dark-field microscopy is diagnostic. Serologic
screening tests (rapid plasma reagin (RPR) or vene-
real disease research laboratory (VDRL)) are reactive
by day 7 of chancre and easy to perform.
TREATMENT
• In early disease, drug of choice is benzathine peni-
cillin G, 2.4 million U i.m. once. • In late disease,
drug of choice is benzathine penicillin G, 2.4 million
U i.m. once a week for 3 weeks. For patients allergic
to penicillin, doxycycline or tetracycline can be given.
• Successful therapy indicated by falling RPR titer.
 Chancroid
DDx Ref  46 • 53 • 56
54 

Several small, painful ulcers are usually present.

The base is purulent, in contrast to the chancre of
syphilis, which is not painful.

The ulcers have coalesced during a 4-week

period without treatment.

Wright’s stain of purulent material of the base of

the ulcer shows a chain of coccobacilli
characteristic of Hemophilus ducreyi.

Deep ulcers bleed easily and spread laterally.

They are highly infectious. Lymphadenopathy
occurs in 50% of cases.
54  Chancroid
DDx Ref  46 • 53 • 56
DESCRIPTION
Chancroid is an uncommon sexually transmitted
disease caused by Hemophilus ducreyi. It is charac-
terized by painful genital ulceration and inguinal
lymphadenopathy.
HISTORY
• More common in heterosexual men who obtain it
from prostitutes who are usually asymptomatic car-
riers. • Common in certain developing countries but
uncommon in the USA. • Coinfection with HIV is
common.
DISCUSSION
• H. ducreyi cannot be cultured on routine media.
Newly formulated transport media can maintain the
viability of the organism. A cotton swab is used to
obtain a specimen at the base of the ulcer, which is
then rolled over a glass slide. Gram-negative clumped
organisms, resembling a school of fish, can be seen
and are diagnostic. • High rate of coinfection with
HIV among patients with chancroid, so HIV test is
reasonable in these patients. Also consider syphilis
serologies. • Herpes simplex is the most common
form of genital ulceration in North America. However,
the combination of painful genital ulceration and
ulcerative or suppurative inguinal adenopathy is
highly suggestive of a diagnosis of chancroid in the
right clinical setting. • Treatment of chancroid should
not be delayed for culture results if the disease is
suspected. Prolonged genital ulceration from the
disease may increase the risk and susceptibility for
HIV transmission.
PHYSICAL FINDINGS
• A painful, red papule first appears at site of inocula-
tion, followed by a pustule, which may rupture,
forming an ulcer surrounded by a bright-red base.
• The ulcer of chancroid is deep, bleeds easily, and
may spread laterally. It is covered by a yellow-gray
fibrinous exudate. These ulcers are highly infectious
and may become multiple via autoinoculation. This
can occur on thighs, buttocks, and anal area.
• Patients may feel ill, with fever, anorexia, malaise.
Unilateral or bilateral inguinal lymphadenopathy
develops in 50% about 1 week after infection. Lymph
nodes may suppurate and ulcerate or resolve spon-
taneously. • Women may carry the organism but
display no clinically detectable lesions and have no
symptoms. Untreated cases either resolve spontane-
ously or become chronic and require a long time to
heal.
TREATMENT
• Azithromycin: 1 g orally in a single dose can be
curative. • Ceftriaxone: 250 mg i.m. in single dose
is also all that is needed. • Ciprofloxacin: 500 g
b.i.d. orally for 3 days. Erythromycin: 500 mg t.i.d.
orally for 7 days.
 Genital warts
DDx Ref  58 • 115 • 135
55 

Small grouped verrucous papules on the penile

shaft.

Genital warts are similar in appearance to

common warts, with a pink to flesh-colored
verrucous surface.

Multiple discrete warts on the shaft of the penis

begin as barely raised papillomatous elevations
and may coalesce into larger plaques.

Verrcous and filiform, pedunculated grouped

papules and the perianal opening.
55  Genital warts
DDx Ref  58 • 115 • 135
DESCRIPTION
Caused by infection of genital or anal skin by human
papillomavirus (HPV). Warts in these locations can be
difficult to eradicate, many are asymptomatic carri-
ers, can lead to carcinoma. Variation in wart charac-
teristics, recurrence, and response to treatment may
relate to individual’s immune response. Common.
HISTORY
• Spread rapidly over moist areas; may therefore be
symmetric on opposing surfaces of labia or rectum.
• Frequently recur after treatment. • Latent virus
exists beyond the treatment areas in clinically normal
skin. • Half of patients who have widespread infec-
tion with genital HPV and who practice orogenital sex
have oral condylomata. Lesions may be asympto-
matic. Magnification may be necessary to detect oral
lesions. • Genital warts in children may result from
sexual abuse. A child with warts on the hands can
transfer the warts to the mouth, genitals, anal area.
A mother with hand warts can transfer warts to child.
Sexual play among children another possible mode
of transmission. • HPV types 16 and 18 most strongly
associated with genital cancers.
PHYSICAL FINDINGS
• Lesions may vary by individual. Lesions tend to be
pale pink to white, rough, barely raised papules.
Others may have projections on a broad base.
Surface may be smooth, velvety, and moist, and
lacks the hyperkeratosis of warts found elsewhere.
• Lesions may coalesce in the rectal or perineal area
to form a large, cauliflower-like mass. • Warts may
extend into the vaginal tract, urethra, and rectum, in
which case a speculum or sigmoidoscope is required
for visualization, treatment.
TREATMENT
• Warts that are flat and inconspicuous, especially
on penile shaft and urethral meatus, can be difficult
to visualize without magnification. • Treatment dif-
ficult; multiple visits and treatments often necessary
for success. • Cryotherapy is most common initial
therapy. Repeat treatment usually performed in 2–3
weeks. Treatment painful; blisters may form. When
electrocautery and curettage used, a light touch with
monopolar electrocautery, after anesthesia, is effec-
tive for treating a few isolated lesions. Scarring is
possible with either treatment. • Imiquimod, Condy-
lox, and Cantharidin all topical methods of wart
removal but may require multiple applications and
courses. • Use of condoms may reduce transmission
to partners likely to be uninfected, such as new part-
ners. • Over 90% of cervical carcinomas are related
to HPV infection. For this reason, women who have
no visible external warts but have a sexual partner
with genital warts should have a complete gyneco-
logic examination and Pap smear.
 Genital herpes simplex
DDx Ref  53 • 54 • 70
56 

Primary herpes simplex lesions transform from

vesicles and pustules to grouped erosions on a
red base.

Large, painful ulceration with inflamed red border

and surrounding small grouped vesicles
consistent with herpes simplex.

The classic presentation of early recurrent herpes

with a group of vesicles of uniform size. A
prodrome of ching or pain is commonly reported.

Recurrent herpes. Vesicles have evolved to form

erosions on a red base. The patient reported that
similar lesions had been present in the same
location on other occasions.
56  Genital herpes simplex
DDx Ref  53 • 54 • 70
DESCRIPTION
Genital herpes simplex is a common sexually trans-
mitted disease caused by the herpes simplex virus
(HSV). Primary painful vesicular infection is followed
by recurrent outbreaks.
HISTORY
• Primary infection occurs 2–20 days after exposure;
influenza-like symptoms, fever, headache, malaise,
myalgia occur. In 3–4 days, vesicles develop. Tender
lymphadenopathy occurs in the second and third
weeks. • With recurrent infection, influenza-like
symptoms are less intense or absent. A chronic,
relapsing course is common. • Genital HSV transmis-
sion occurs via sexual contact; however, some cases
can be transmitted by people who are unaware that
they have the infection or are asymptomatic when
transmission occurs.
PHYSICAL FINDINGS
• Primary infection symptoms are more severe and
extensive than secondary infections. • Herpes
simplex presents with a red swollen plaque followed
by grouped vesicles that evolve into pustules and are
surrounded by a red edematous base. The pustules
rupture or break, may crust, and form shallow painful
erosions. Large confluent erosions and ulcers can
occur. • Lesions heal in 1–2 weeks. Hypopigmenta-
tion, hyperpigmentation, and sometimes scars may
be left behind. • Lymphadenopathy (painful) occurs
with primary infection.
TREATMENT
• Currently, there is no permanent cure for herpes
simplex. • Explains the natural history of the disease,
recurrent episodes, asymptomatic viral shedding,
and sexual transmission. • Systemic antiviral drugs
partially control symptoms and signs of herpes erup-
tions. These drugs neither eradicate latent virus nor
affect the risk, frequency, or severity of recurrences
after the drug is discontinued. • Initiate treatment
within 72 h of onset of signs and symptoms. Valacy-
clovir, famciclovir, and acyclovir can be given orally
and work best when given within 72 h of onset of
symptoms. • Cool, wet, water compresses may sup-
press inflammation. • Severe primary infections can
be treated intravenously for immunocompromised
patients if needed. • Recurrent infection can be
treated similarly as above. • Long-term suppressive
therapy with lower doses of valacyclovir, famciclovir,
acyclovir can be very helpful. Treatment is continued
for at least 6–12 months. If treatment is successful,
a trial without medication may be considered. Daily
suppressive therapy reduces the frequency of genital
herpes recurrences by at least 75% among patients
who have six or more recurrences per year. Suppres-
sive treatment reduces but does not eliminate
asymptomatic viral shedding.
 Pubic lice
DDx Ref  20 • 46 • 48
57 

Phthirus pubis (pubic or crab louse), with a short,

oval body and prominent claws resembling those
of sea crabs.

Small crab lice having a blood meal with

additional nits attached to pubic hair shafts.

Nit attached to hair shaft. Hard white concretions

which contain lice egg. Very difficult to remove.

Pubic lice infestation. Difficult to see individual

parasites without magnification. Inflamed bite
marks or purpuric macules are diagnostic clues.
57  Pubic lice
DDx Ref  20 • 46 • 48
DESCRIPTION
Caused by infestation with Phthirus pubis. The most
contagious sexually transmitted disease. The chance
of acquiring pubic lice from an infested partner is
more than 90%. Direct contact with an infected
human is the primary source of transmission.
HISTORY
• Fomite transmission from hats, brushes, and ear-
phones is common. • Most patients complain of
pruritus. • Many patients are aware that something
is crawling on the groin but are unfamiliar with the
disease and have never seen lice. • Up to 30% of
patients infested with pubic lice have at least one
other sexually transmitted disease. • Infested adults
may spread pubic lice or crab lice to the eyelashes
of children. Crab lice infestation in children should be
considered sexual abuse.
PHYSICAL FINDINGS
• Nits may be noticed before the lice. Nits, or lice
eggs, are firmly cemented to hair shafts. • Lice may
be difficult to see with close inspection or magnifica-
tion. • The pubic hair is the most common site of
louse infestation, but lice frequently spread to the
hair around the anus. On hairy persons, lice may
spread to the upper thighs, abdominal area, axillae,
chest, beard. Occasionally, gray-blue macules
(maculae ceruleae), varying in size from 1–2 cm,
are seen in the groin and at sites distant from the
infestation. Their cause is unknown, but they may
represent altered blood pigment. • Most infected
patients have very little if any inflammatory changes,
but those who delay seeking help may develop wide-
spread inflammation and infection of the groin with
regional adenopathy.
TREATMENT
Topical medication
• An over-the-counter (OTC) permethrin rinse 1% is
often the drug of first choice. It is applied and washed
off after 10 min. OTC synergized pyrethrin shampoos
are also used. Permethrin 5% is prescribed when
OTC treatment fails. It is left on the hair overnight.
• Lindane shampoo is left in for 5 min then washed
out; treatment is repeated in 1 week. It is used if OTC
treatment fails. Lindane-resistant lice have emerged.
• Malathion lotion is highly effective. It is applied to
dry hair and shampooed out after 8–12 h. All agents
attack the louse’s nervous system; however, young
nits are unaffected. Repeat treatment in 1 week.
Oral medication
• Ivermectin 200 µg/kg is given in a single oral dose
that is repeated in 10 days. • Ivermectin attacks
invertebrate nerve and muscle cells in the louse and
causes paralysis and death. It has selective activity
against parasites but no systemic effects on
mammals.
 Molluscum contagiosum
DDx Ref  55 • 56 • 135
58 

Lesions are usually discrete, white, and

dome-shaped. They lack the many small
projections found on the surface of warts.

Characteristic molluscum lesions vary in size,

usually flesh colored and umbilicated. Inflamed
lesions may be difficult to identify without these
characteristic lesions near by.

Molluscum is commonly found in the pubic area

in adults. Examine this area with magnification.
The hair obscures the view, and many lesions can
be hidden.

Molluscum spreads rapidly over warm, moist,

intertriginous areas on the upper thigh near the
vulva. In adults, this should be considered a
sexually transmitted disease.
58  Molluscum contagiosum
DDx Ref  55 • 56 • 135
Description
A poxvirus infection of the skin characterized by dis-
crete umbilicated papules. Genital molluscum conta-
giosum in adults should be considered a sexually
transmitted disease. Genital molluscum contagiosum
is common in children; sexual abuse is not necessar-
ily the cause.
History
• Very common in children. • Spread by direct
contact or autoinoculation. • Lesions tend to be more
numerous and spread rapidly in patients with atopic
dermatitis or those with a decreased skin barrier.
• Lesions may become extremely large or ‘giant’ and
disfiguring in patients with HIV.
Physical findings
• Discrete, 2- to 5-mm, slightly umbilicated, flesh-
colored, and dome-shaped lesions appear. The pubic
and genital areas are most commonly involved in
adults. Lesions are frequently grouped and cover a
wide area. • Inflammation, erythema, and scaling at
the periphery of a single or several lesions may
occur. This may be the result of inflammation from
scratching, or it may be a hypersensitivity reaction.
• Trauma may decrease the characteristic appear-
ance of some lesions. • Papules often camouflaged
by pubic hair. Most patients have just a few lesions,
which can be easily overlooked. The focus of exami-
nation is the pubic hair, genitals, anal area, thighs,
trunk. Lesions may appear anywhere except the
palms and soles. • Molluscum contagiosum lesions
are often confused with warts.
TREATMENT
• Genital molluscum lesions should be treated to
prevent spread through sexual contact. • New
lesions too small to be detected at first examination
may appear after treatment and require attention at
subsequent visit. • Small papules can be quickly
removed with a curette with or without local anesthe-
sia. • Cryosurgery with liquid nitrogen is the treat-
ment of choice for patients who do not object to the
pain. A conservative approach is necessary, because
excessive freezing produces hypopigmentation or
hyperpigmentation. • A small drop of cantharidin
0.7% (Cantharone) is applied with the stick end of a
cotton swab over the surface of the lesion, and con-
tamination of normal skin is avoided. This should be
washed off 4–6 h later. Lesions blister and resolve
without scarring. New lesions occasionally appear at
the site of the blister created by cantharidin. Hypop-
igmentation or hyperpigmentation may occur.
• Imiquimod 5% cream can be effective when
applied three times weekly at night for 2–3 months.
This is especially effective for treating facial mol-
luscum in children, where scarring procedures are
contraindicated.
 Warts (verruca vulgaris)
DDx Ref  58 • 115 • 135
59 

Warty hyperkeratosis is typically rough-looking

and white. Proximal and lateral nail folds affected.
Treatment is difficult and must be gentle enough
not to scar or damage the nail matrix.

Multiple rough, flesh-colored papules grouped

around the proximal nail fold. Biting this area is
discouraged, as it may spread the warts to other
areas, such as the lips or nails.

Wart treated with liquid nitrogen. A rim of normal

skin is also treated. The white freezing color
change should remain 15 s and be allowed to
slowly thaw; often the lesion is treated twice.

Partial resolution of a wart after liquid nitrogen

treatment. The central area is resolved, although
a rim of warty tissue remains. Allowing rim and
center to stay white 15 s may avoid this.
59  Warts (verruca vulgaris)
DDx Ref  58 • 115 • 135
DESCRIPTION
Benign epidermal overgrowths caused by human
papillomavirus (HPV). Transmitted by contact, often
at small skin breaks, abrasions, or other trauma.
HISTORY
• Variable onset from exposure: 1–6 months. • Dura-
tion variable; spontaneous resolution with time
typical. • In children, approximately two-thirds of
warts spontaneously regress within 2 years. • Warts
in immunocompromised persons can be widespread,
chronic.
PHYSICAL FINDINGS
• Flesh-colored papules evolve into dome-shaped,
gray-brown, hyperkeratotic, discrete, rough papules,
often with surface black dots. • Usually few, may be
numerous. • Common sites: hands, periungual skin,
elbows, knees, plantar surfaces. • Filiform warts are
finger-like growths on narrow or broad base, often
on the face. • HPV subtyping not routine, readily
available, or necessary for common warts. • Genital
HPV subtypes 16, 18, and 31 are high-risk subtypes
and account for approximately 75% of invasive
genital cancers. • Biopsy a non-resolving wart on
hand, periungual unit, or foot to rule out squamous
cell carcinoma.
TREATMENT
Multiple treatments available. No treatment is con-
sistently highly effective. Avoid painful treatment,
especially for children. No treatment is acceptable,
but patients seek treatment because of unsightly
appearance, fear of spread or enlargement, or dis-
comfort. Some options follow. • Duct tape cut to wart
size and applied. Leave for 6 days, remove, wash
skin, gently debride. Reapply, continue cycle for
1 month if necessary. • Over-the-counter topical
salicylic acid (15–40%) applied once a day. Occlu-
sion with tape increases penetration. Treatment
duration 8–12 weeks. Some options are Mediplast
(40% salicylic acid), DuoFilm solution (17% salicylic
acid) or patch (40% salicylic acid), and Occlusal HP
solution (17% salicylic acid). • Multiple visits often
necessary when treating with ablative therapy. Liquid
nitrogen cryotherapy: 15-s freeze time, repeat once.
Retreatment in 2–3 weeks. Side effects: pain, blister
after treatment. Caution treating warts around nail.
Older children may tolerate gentle cryotherapy; con-
sider for long-standing warts or if child-friendly treat-
ments have failed. • Imiquimod 5% cream (Aldara)
has limited use in common warts; efficacy limited by
poor penetration in non-mucosal skin. Treat with
liquid nitrogen, then apply a salicylic acid preparation
at night, and imiquimod in the morning with occlu-
sion. Continue 6–9 weeks. • Intralesional bleomycin
for refractory warts; efficacy limited. Contact immu-
notherapy of warts using dinitrochlorobenzene,
squaric acid, and Candida antigen used by some
dermatologists. • Limitations of laser surgery: pain,
potential scarring. • Filiform warts easiest to treat.
Local anesthesia can be used; lesion removal with
snip or curette.
 DDx Ref  62 • 115 • 127
Flat warts
60 

Flat warts are barely raised, flesh-colored to

brown, flat-topped papules. They typically occur
on the face, dorsum of the hands, or shins, and
can be spread by shaving.

Grouped pink flat-topped papules along a line that

suggests autoinoculation.

Multiple small flat-topped papules on the

vermilion.

Filiform wart on the lower lip. This type of wart

like flat warts is typical on the face in children.
Snipping the warty skin or freezing with liquid
nitrogen are potential treatments.
60  Flat warts
DDx Ref  62 • 115 • 127
DESCRIPTION
Flat warts are benign, cutaneous hyperproliferations
due to infection with human papillomavirus. Common
subtypes are types 3 and 10.
HISTORY
• Common in children and young adults. • Flat warts
spread in a local region often through mildly trauma-
tized skin, such as within an area of shaving.
• Duration may be lengthy; flat warts may be very
resistant to treatment. • Generally located in cos-
metically important areas where aggressive, scarring
treatment procedures must be avoided. • Immuno-
compromised patients often have a protracted
course.
PHYSICAL FINDINGS
• Pink, light brown, or light yellow papules are
slightly elevated and flat-topped. They vary in size
from 0.1–0.3 cm. May be few or numerous and often
occur grouped or in a line as a result of spread from
scratching. • Typical sites are forehead, back of
hands, chin, neck, legs. • Typically asymptomatic.
TREATMENT
• If sparse numbers of lesions, a salicylic acid prepa-
ration may be applied daily directly to each lesion.
This treatment is limited by irritation. Other options:
• Tretinoin cream 0.025%, 0.05%, or 0.1% applied
at bedtime over the entire involved area. The fre-
quency of application is adjusted to produce fine
scaling and mild erythema. Treatment may be
required for weeks or months. • Liquid nitrogen or a
very light touch with an electrocautery needle may
be performed for quick results. Flat warts may not
respond to cryotherapy, even after many treatment
sessions. • Imiquimod 5% cream (Aldara) applied to
affected skin at night. Decrease frequency of applica-
tion if excessive irritation. Treatment may be required
for weeks. • Applied once or twice a day for 3–5
weeks, 5-fluorouracil cream 5% (Efudex) may
produce dramatic clearing of flat warts. Persistent
hyperpigmentation may follow the use of 5-fluorou-
racil and is minimized by applying it to individual
lesions with a cotton-tipped applicator. • Inform
patients that flat warts are easily spread within areas
of shaving. Discourage shaving over affected skin.
• Unlike common warts, the face is a common loca-
tion for flat warts.
 Plantar warts
DDx Ref  128 • 135 • 137
61 

Plantar warts sometimes become confluent. The

warty tissue is rough and thick. The excessive
hyperkeratosis should be pared for topical
treatment to be effective.

Mosaic plantar warts meld together, in this case

in apposing skin. The warty tissue has spread
the virus from the plantar foot to the apposing
fifth toe.

Rough, flesh-colored, hyperkeratotic papules with

punctuate hemorrhages along the lateral toe. The
apposing toe is also affected. Most warts resolve
with time and development of cellular immunity.

Mosaic plantar warts scattered on the heel. Pain

or difficulty walking are indications for treatment,
although painful destructive or scarring treatment
should be avoided.
61  Plantar warts
DDx Ref  128 • 135 • 137
DESCRIPTION
Caused by human papillomavirus infection on plantar
foot. Infection frequently occurs at points of maximal
pressure, such as over heads of metatarsal bones,
heels, or toes. A wart cluster is referred to as a
mosaic wart.
HISTORY
• Human papillomavirus types 1, 2, and 4 are typi-
cally associated with plantar warts. • Hyperhidrosis
is associated with a more widespread distribution of
warts often refractory to treatment.
PHYSICAL FINDINGS
• Round, single or multiple, coalescing, flesh-
colored, rough, keratotic papules often look
depressed. • Punctate black dots, often seen on
paring, are capillary loops. • May be tender with
pressure. • Some are depressed, resembling numer-
ous small pits. • Biopsy may be indicated if rapidly
growing, ulcerated, atypical, or treatment-resistant;
squamous cell carcinoma or melanoma may mimic
a wart.
TREATMENT
Treatment often difficult; plantar warts can be refrac-
tory, recurrent. Often, multiple treatments required.
Plantar warts do not require therapy if painless.
Spontaneous resolution with time and development
of immunity is the rule. Multiple treatment options
exist, indicating no single best option.
Therapeutic options include the following. • Kera­
tolytic therapy with salicylic acid (DuoPlant,
Occlusal). A conservative initial treatment. Wart is
pared, soaked daily in warm water, and salicylic acid
preparation applied. Limitations: irritation, soreness.
May require 6–8 weeks. • Plasters with salicylic
acid 40% (Mediplast). Useful in treating plantar
warts. Leave on for 24–48 h and replace. May
require 6–8 weeks. • Imiquimod 5% cream
(Aldara). May hasten resolution; one method is to
use cryotherapy first, then apply imiquimod every
night under duct tape occlusion for 6–12 weeks.
• Blunt dissection. Fast, effective surgical treat-
ment (90% cure rate); usually produces no scarring.
Superior to both electrodesiccation and curettage
and excision, because normal tissue is not disturbed.
• Cryosurgery with liquid nitrogen. Nitrogen is
applied for 15–30 s twice to wart. Resultant painful
blister can interfere with mobility. Repeated light
applications of liquid nitrogen are optimal. Treatment
painful. • Carbon dioxide and pulsed dye laser
treatment. Expensive. Probably no more effective
than other treatments. • Electrodesiccation and
curettage. Infrequently chosen due to pain from
anesthesia, postoperative pain, risk of scarring.
• Bleomycin. 0.5 units/mL injected into wart to
achieve blanching. Wart size determines injection
quantity. Responsive warts show hemorrhagic
eschars that heal without scarring. Treatment very
painful; necrosis or severe vasospasm may occur.
Pregnancy a contraindication. An aggressive treat-
ment option reserved for those experienced in its
use.
 Molluscum contagiosum
DDx Ref  59 • 63 • 124
62 

Papules of molluscum contagiosum are somewhat

firm and flesh-colored to pink. They have a
central core, composed of hundreds of infectious
particles from which spread may occur.

Inflammation is evident in several molluscum

papules. This inflammation often leads to
resolution of the papules.

Molluscum papules in a child in the periorbital

region. Lesions can be spread by picking and
scratching. Treatment is difficult; lesions will
resolve with development of cellular immunity.

Grouped papules scattered on the buttocks and

thigh. Some of the lesions have been picked and
appear crusted.
62  Molluscum contagiosum
DDx Ref  59 • 63 • 124
DESCRIPTION
A poxvirus infection of the skin characterized by
discrete umbilicated papules. Genital molluscum
contagiosum in adults should be considered a sexu-
ally transmitted disease. Genital molluscum conta-
giosum is common in children; sexual abuse is not
necessarily the cause. More common if immune
suppressed.
HISTORY
• Very common in children. • Spread by direct
contact or autoinoculation. • Lesions tend to be more
numerous and spread rapidly in patients with atopic
dermatitis or those with a decreased skin barrier.
• Lesions may become extremely large and disfigur-
ing in patients with HIV.
PHYSICAL FINDINGS
• Discrete, 2- to 5-mm, slightly umbilicated, flesh-
colored, and dome-shaped lesions appear. The pubic
and genital areas are most commonly involved in
adults. Lesions are frequently grouped and cover a
wide area. • Inflammation, erythema, and scaling at
the periphery of a single or several lesions may
occur. This may be the result of inflammation from
scratching, or it may be a hypersensitivity reaction.
• Trauma may alter the characteristic appearance of
some lesions. • Papules often camouflaged by pubic
hair. Most patients have just a few lesions that can
be easily overlooked. The focus of examination is the
pubic area, genitals, anal area, thighs, trunk. Lesions
may appear anywhere except the palms and soles.
• Molluscum contagiosum lesions are often confused
with warts.
TREATMENT
• Genital molluscum lesions should be treated to
prevent spread through sexual contact. • New
lesions too small to be detected at first examination
may appear after treatment and require attention at
subsequent visit. Options: Small papules can be
quickly removed with a curette with or without local
anesthesia. • Cryosurgery with liquid nitrogen is the
treatment of choice for patients who do not object to
the pain. A conservative approach is necessary,
because excessive freezing produces hypopigmenta-
tion or hyperpigmentation. • A small drop of can-
tharidin 0.7% (Cantharone) is applied with the stick
end of a cotton swab over the surface of the lesion,
and contamination of normal skin is avoided. This
should be washed off 4–6 h later. Lesions blister and
may resolve without scarring. New lesions occasion-
ally appear at the site of the blister created by can-
tharidin. Hypopigmentation or hyperpigmentation
may occur. • Imiquimod (Aldara) 5% cream can be
effective when applied three times weekly at night
for 2–3 months. This is especially effective for treat-
ing facial molluscum in children, where scarring
procedures are contraindicated.
 Herpes simplex (cold
sores, fever blisters)
DDx Ref  46 • 48 • 52
63 

Recurrent herpes simplex. Grouped vesicles have

become cloudy on an erythematous base on the
buttocks. Herpes on the buttock is seen in a
woman.

Herpetic whitlow: grouped cloudy vesicles, several

with central umbilication. This recurrent eruption
is exquisitely tender.

Recurrent herpes simplex. Grouped tiny crusted

monomorphic erosions on the lower lip. The
lesions have a typical ‘punched-out’ appearance.

Atopic child with multiple tiny crusted vesicles on

lower lids and nose. Herpes simplex occurring in
an area of eczema can spread easily and be
severe. Oral antiviral treatment is indicated.
63  Herpes simplex (cold
sores, fever blisters)
DDx Ref  46 • 48 • 52
DESCRIPTION
DNA virus that causes a vesicular skin infection. Type
1 typically associated with oral infections, type 2 with
genital infections. Two infection phases: primary and
recurrent.
HISTORY
• Most primary infections asymptomatic. • Virus
spread by respiratory droplets, direct lesion contact,
or virus-containing fluid shed in people with no
evidence of active disease. • Symptoms 3–7 or
more days after contact. • Gingivostomatitis and
pharyngitis most frequent manifestation. • Pro-
drome: localized pain, tender lymphadenopathy,
headache, generalized aching, fever. • Tenderness,
pain, paresthesias, or burning before lesion onset in
area of primary infection. • Symptomatic primary
genital infection in women may include vulvovagin-
itis, vaginal and cervical erosions with pain, edema,
dysuria. Men or women may also experience procti-
tis, anorectal pain, discharge, constipation, or tenes-
mus. • During primary infection, virus ascends
through peripheral nerves to dorsal root ganglia,
where it becomes latent. • Reactivation spontaneous
or by local skin trauma (e.g. ultraviolet light exposure,
chapping, abrasion) or systemic changes (e.g.
menses, fatigue, fever).
PHYSICAL FINDINGS
• Grouped vesicles on erythematous base appear,
subsequently erode. • Primary: vesicles more
numerous, scattered; heal without scar. • Diagnosis
often clinical; may include culture, Tzanck smear, or
rapid direct fluorescent antibody test.
TREATMENT
Prevention of spread: discuss avoidance of sharing
glasses, avoid kissing while lesions are open,
condoms. Infections resolve without treatment.
Therapy based on patient needs. Consider suppres-
sive therapy if frequent and painful recurrences
(more than 6 recurrences a year). For pain relief:
tetracaine cream 1.8% (Cepacol Viractin cream; over
the counter). Sun protection with zinc oxide or sun-
block lip balm.
Oral antiviral agents. • Valacyclovir (Valtrex).
Initial episode: 1 g b.i.d. for 10 days. Recurrent:
500 mg b.i.d. for 3 days. Recurrent oral-labial infec-
tion: 1 g, two tablets b.i.d. for just 1 day. Suppres-
sive: 1 g q.d. If no more than nine recurrences a year,
alternative dose 500 mg q.d. • Famciclovir
(Famvir). Recurrent: 125 mg b.i.d. for 5 days. Sup-
pressive: 250 mg b.i.d. for up to 1 year. • Acyclovir
(Zovirax). Initial episode: 200 mg every 4 h five
times a day for 10 days. Suppressive: 400 mg b.i.d.
for up to 12 months. Alternative regimens: doses
ranging from 200 mg t.i.d. to 200 mg five times a
day. Recurrent: 400 mg every 8 h t.i.d. for 5 days.
 Varicella (chickenpox)
DDx Ref  45 • 63 • 84
64 

Primary lesion of chickenpox (varicella): a

discrete, clear vesicle with central umbilication; it
later turns cloudy, then develops a crust. There is
a flare of erythema around the vesicle.

The evolving chickenpox vesicle is crusty and

cloudy, and usually collapses in the middle.

Varicella lesions are diffusely scattered. The

lesions are very pruritic. Deep lesions may scar.

Varicella lesions in varying stages of development

and widely scattered. Before the exanthem, there
is typically fever, cough, and itchy eyes.
64  Varicella (chickenpox)
DDx Ref  45 • 63 • 84
DESCRIPTION
Highly contagious infection caused by the varicella-
zoster virus. Most commonly results in lifetime
immunity.
HISTORY
• Transmission via airborne droplets or vesicular
fluid. • Patients contagious from 2 days before rash
until all lesions crusted. • Incubation period approxi-
mately 14–16 days. • In children, prodromal symp-
toms absent or low-grade fever, headache, malaise;
fever, malaise, and generalized vesicular rash
develop and last 4–7 days. Photophobia may be
present. • Adolescents, adults, immunocompro-
mised persons have more severe disease and are at
risk for complications. • Moderate to intense pruritus
during vesicular stage. • Complications include bac-
terial superinfection, pneumonia, dehydration,
encephalitis, hepatitis. Most common neurologic
complication is ataxia secondary to cerebellar inflam-
mation. Roughly 15% of healthy adults develop
pulmonary involvement. • Maternal infection during
first 20 weeks of gestation poses risk of fetal con-
genital varicella syndrome.
PHYSICAL FINDINGS
• Lesions (vesicles, pustules, crusts) in all stages.
• Begins on trunk and spreads to face and extremi-
ties. Extent varies. • Starts as a 2- to 4-mm red
papule, then a thin-walled, clear vesicle appears.
Vesicle becomes umbilicated and cloudy, breaking
after 8–12 h. Crust forms as red base disappears.
New lesions cease after 3 days. Crusts fall off in
about 7 days. • Secondary infection or excoriation
may result in scar. • Vesicles in mouth or vagina
may form aphthae-like ulcers. • Pneumonia most
common serious complication in healthy adults.
Hepatitis most common complication in immunosup-
pressed patients. • Laboratory tests: Tzanck, direct
fluorescent antibody test, or culture in questionable
cases.
TREATMENT
Symptomatic: antipruritic lotions (e.g. Sarna). Oral
antihistamines (hydroxyzine). For severe infection,
i.v. acyclovir. Other antivirals, such as valacyclovir
1 g t.i.d. for 7 days and famciclovir 500 mg t.i.d. for
7 days, may have a role, although presently approved
in USA for varicella-zoster infection. • Adolescents
and adults. Early therapy with oral acyclovir
decreases time to healing, decreases fever duration,
reduces symptom severity, but does not alter viral
shedding. Therapy onset after first day of illness is
no value in uncomplicated cases. High morbidity rate
even in otherwise healthy patients with clinically
evident varicella pneumonia; i.v. acyclovir 10 mg/kg
every 8 h for 7 days may help. • Immunocompro-
mised patients. Those treated with acyclovir have
decreased morbidity from visceral dissemination;
modest effect on cutaneous disease. Acyclovir
10 mg/kg i.v. every 8 h for 7–10 days. Varicella-
zoster immune globulin recommended for post­
exposure prophylaxis. Administer within 96 h post
exposure.
 Herpes zoster (shingles)
DDx Ref  4 • 46 • 63
65 

The unilateral herpes zoster vesicles are typically

confined to one or two dermatomes. This is a T4
distribution. The primary lesion is an umbilicated
vesicle. Pain often precedes the eruption.

Herpes zoster vesicles turn cloudy; central

umbilication evident. The grouped lesions are
nearly confluent. The area may ultimately turn
necrotic if there is underlying immunocompromise.

An obvious dermatomal distribution of vesicles on

an erythematous base is classic of herpes zoster.
The area may itch or be very painful or
uncomfortable to even fine touch.

Involvement of the mandibular division of the fifth

cranial nerve with vesicles along this distribution.
Vesicles do not extend beyond the midline.
65  Herpes zoster (shingles)
DDx Ref  4 • 46 • 63
DESCRIPTION
Viral infection generally involving skin of single or
adjacent dermatomes. Result of reactivation of vari-
cella virus that entered cutaneous nerves during
earlier chickenpox.
HISTORY
• Incidence increases with age. • Age, immunosup-
pressive drugs, lymphoma, fatigue, emotional
upsets, and radiation therapy have been implicated
in virus reactivation. • Elderly at greater risk for
debilitating segmental pain, which can continue for
months. • Pain may simulate pleurisy, myocardial
infarction, abdominal disease, migraine. • Constitu-
tional symptoms, headache, photophobia, and
malaise may precede eruption by several days. Fever
uncommon.
PHYSICAL FINDINGS
• Pain, itching, or burning may precede eruption by
4–5 days. • Eruption may involve one or two adjacent
dermatomes. Non-contiguous multidermatomal
lesions more common in immunosuppressed.
• Begins with red swollen plaques of various sizes;
spreads to involve part or all of dermatome. • Vesi-
cles, varying in size, in clusters on erythematous
base, become cloudy with purulent fluid by day 3
or 4. • Vesicles either umbilicate or rupture before
crusting. • Elderly or debilitated patients may have a
prolonged, difficult course, with hemorrhagic blis-
ters, necrosis, secondary bacterial infection, exten-
sive scarring. • Complications can include peripheral
nerve palsies, encephalitis, myelitis, contralateral
hemiparesis.
OPHTHALMIC ZOSTER
• Involvement of ophthalmic nerve. • Rash extends
from eye level to skull vertex but does not cross
midline. • Vesicles on nose side or tip (Hutchinson
sign) associated with most serious ocular complica-
tions. • Of patients not treated with antiviral therapy,
50% will develop ocular complications (keratopathy,
episcleritis, iritis). Oral antiviral therapy results in
decreased frequency of late ocular complications.
• Refer to an ophthalmologist.
TREATMENT
• Topical therapy may be soothing: cool tap water in
a wet dressing, applied 20 min several times a day.
• Oral steroids may decrease acute pain but have no
effect on postherpetic neuralgia and can result in
complications. • Oral antiviral drugs decrease acute
pain, inflammation, vesicle formation, viral shedding.
• May reduce duration and severity of postherpetic
neuralgia by treating acute herpes zoster with vala-
cyclovir or famciclovir. • Treatment most effective
when started within first 48 h, but reasonable to
consider antiviral therapy if all lesions not yet crusted.
• Recommended oral dosage for adults: 7–10 days
of acyclovir (Zovirax) 800 mg five times a day, vala-
cyclovir (Valtrex) 1000 mg t.i.d., or famciclovir
(Famvir) 500 mg t.i.d. All three drugs safe, well toler-
ated. Adjust dose for renal insufficiency. • Empiric
treatment if older than 50, immunocompromised, or
trigeminal zoster.
 Hand, foot, and
mouth disease
DDx Ref  63 • 64 • 85
66 

Oral vesicles of hand, foot, and mouth. There are

painful, white, aphthae-like erosions on the
tongue, lips, and hard palate. Eating can be
painful.

Palmar and plantar vesicles appear cloudy with a

small red halo. These lesions may be tender or
asymptomatic. They may be sparse or numerous.

Typical vesicles of hand, foot, and mouth disease

on the heel. Pain may impede walking, although
generally this is a mild illness.

Multiple discrete cloudy vesicles with

inflammatory halos on the palm are characteristic
of hand, foot, and mouth disease.
66  Hand, foot, and
mouth disease
DDx Ref  63 • 64 • 85
DESCRIPTION
Highly contagious viral infection that causes aph-
thae-like oral erosions and a vesicular eruption on
hands and feet. The classic benign, self-limited form
of this disease is associated with coxsackievirus A16.
Enterovirus 71 is a picornavirus genetically related to
coxsackie A16. It can cause oral ulcers and similar
skin exanthem, but epidemic outbreaks have associ-
ated potentially serious neurologic and cardiopulmon­
ary complications, particularly in children under
4 years.
HISTORY
• Incubation period 4–6 days. Epidemics in summer
and autumn but may appear any time. • Usually
presents with acute stomatitis and mild fever. Mild
sore throat and malaise or abdominal pain for 1–2
days may occur. • About 20% of patients develop
submandibular lymphadenopathy, cervical lymphad-
enopathy, or both. • Children younger than 5 years
most commonly affected; rate of infection among
close household contacts is high. • Enterovirus 71
outbreaks commonly include fever, oral ulcers and/
or extremity rash, vomiting, cough.
PHYSICAL FINDINGS
• Number of oral aphthae-like erosions (3–6 mm)
varies from few to 10 or more. They are irregularly
distributed anywhere in oral cavity. More painful in
younger children. Each erosion lasts 3–5 days.
• Cutaneous lesions in coxsackie-induced hand, foot,
and mouth disease occur in two-thirds of patients
and appear less than 24 h after oral lesions. • Skin
lesions begin as 3- to 7-mm red macules that rapidly
become pale, white, oval vesicles with red areolae.
Vesicles have unique rhomboidal shape of ‘square
blisters’. May be a few or dozens. • Vesicles occur
on palms, soles, dorsal aspects of fingers and toes,
and occasionally on face, buttocks, legs. • Heal in
approximately 7 days, usually without crusting or
scarring. • Diagnosis usually made clinically; labora-
tory tests unnecessary for the benign presentation of
the disease.
TREATMENT
• Hand, foot, and mouth disease caused by cox-
sackie A16 usually mild and self-limited. Resolves
without treatment in about 10 days. • Oral ulcera-
tions painful in infants and interfere with feeding.
• Recent emergence of epidemics of hand, foot, and
mouth disease caused by enterovirus 71 are associ-
ated with varied neurologic syndromes, including
aseptic meningitis, Guillain–Barré syndrome, polio-
like paralysis, acute transverse myelitis, acute cer-
ebellar ataxia, intracranial hypertension, febrile
convulsions. Prodrome is 1–7 days before neurologic
disease and has fever, coryza, malaise, headache,
diarrhea. Two-thirds of those affected may have a
rash, often truncal; herpangina-type lesions may
occur in mouth.
 Candidiasis (moniliasis)
DDx Ref  11 • 48 • 63
67 

Macerated scale and fissuring favor interdigital

involvement.

Satellite papules within the moist environment of

body folds.

Papules coalescing into plaques studded with

pustules and fragile scale.

Mucosal involvement with exudates and

overgrowth of Candida. Diabetes is a predisposing
factor.
67  Candidiasis (moniliasis)
DDx Ref  11 • 48 • 63
DESCRIPTION
Skin and mucosal infection caused primarily by
Candida albicans.
HISTORY
• Candida species live among the normal flora of the
mouth, vaginal tract, lower gastrointestinal tract.
Candida reproduces through the budding of oval
yeast forms, forming elongated pseudohyphae. The
yeast infects only the outer layers of the epithelium
of mucous membrane and skin (stratum corneum).
Yeast grows best in a warm, moist environment.
Infection usually confined to mucous membranes and
intertriginous areas. • Factors that predispose to
infection include infancy, pregnancy, oral contracep-
tive use, systemic antibiotic therapy, diabetes, skin
maceration, topical and systemic steroid therapy,
decreased cell-mediated immunity.
PHYSICAL FINDINGS
• Primary lesion is a superficial pustule. The contents
of the pustule dissect horizontally under the stratum
corneum and peel it away. Clinically, this process
results in a red, denuded, glistening surface with a
long, cigarette paper-like scaling and advancing
border. Itching and burning are common symptoms.
• In potassium hydroxide wet mount preparation and
culture, the pseudohyphae and hyphae may be dif-
ficult to distinguish from dermatophytes. • Culture
results must be interpreted carefully, because the
yeast is part of the normal flora in many areas.
• Nickerson’s media is used to isolate and identify
Candida species.
TREATMENT
Azole antifungal creams such as miconazole, clot-
rimazole, ketoconazole, oxiconazole, or econazole
effective. Apply cream twice daily for 7 days. A single
150-mg dose of fluconazole also effective. Use
caution in diabetic patients on oral hypoglycemic
agents.
 Candidal balanitis
DDx Ref  11 • 12 • 39
68 

Classic presentation. White exudate forms in the

intertriginous spaces created by the foreskin
covering the shaft of the penis. The glans shows
no sign of infection.

Infection present for weeks. Highly characteristic

red papules and pustules present on glans. White
exudate covers the inflamed shaft. Painful fissures
occurred after repeated retraction of foreskin.

Chronic Candida infections may present with just

tenderness and dry, red, inflamed skin. The
characteristic white exudate may never appear.
The skin becomes fragile and sore.

This patient is circumcised but obese. An

intertriginous area was created by a skin fold; the
yeast thrived in the warm, moist space. Cool
compresses and ketoconazole cream were
effective.
68  Candidal balanitis
DDx Ref  11 • 12 • 39
DESCRIPTION
An acute and chronic infection of the foreskin and
glans penis caused by Candida organisms.
HISTORY
• Occurs more frequently in uncircumcised men.
• Intercourse with an infected woman is a potential
risk factor. Infections also occur without sexual expo-
sure. Obesity and diabetes are risk factors. Any
circumstance that encourages warmth and moisture
predisposes to infection. • Itching and pain vary from
mild to moderate; many cases are asymptomatic.
• Infection may recur. • Patients with psoriasis may
have a red inflamed penile shaft and glans that
appear to be infected with yeast.
PHYSICAL FINDINGS
• Yeast invades the superficial epidermis, producing
pustules and exudate. Acute infections start with
tender, pinpoint, red papules and pustules that
appear on glans and shaft. Pustules rupture under
the foreskin and are usually never seen. White, thick,
creamy exudate similar to that seen in Candida
vaginal infections may be present. Ulceration and
fissures follow if the infection persists. • Edema and
pain can be intense enough to limit retraction of the
foreskin. Some patients with chronic Candida infec-
tions have no exudate; rather, the shaft is sore and
fragile. • Potassium hydroxide examination reveals
numerous yeast forms. Culture of acute exudate
shows Candida species. Bacterial culture may reveal
coexistent bacterial infection.
TREATMENT
• Many antifungal creams rapidly effective. Apply
miconazole, clotrimazole, ketoconazole, oxiconazole,
or econazole cream twice daily for 7 days. Avoid
topical steroids or combination steroid-antifungal
creams. • A single 150-mg dose of fluconazole is as
effective as clotrimazole cream applied topically for
7 days. Itraconazole 200 mg q.d. for 3–5 days also
effective. • Consider circumcision in chronic or
recurrent cases.
 Candidiasis
(diaper dermatitis)
DDx Ref  12 • 20 • 48
69 

Trapped moisture from urine and feces as well as

alkaline pH break the skin barrier.

Compromised skin barrier is colonized by yeast

present in stool.

Fragile pustules break, leaving shallow erosions.

An artificial intertriginous area is created under a

wet diaper, predisposing the area to a yeast
infection with the characteristic red base and
satellite pustules.
69  Candidiasis
(diaper dermatitis)
DDx Ref  12 • 20 • 48
DESCRIPTION
Diaper dermatitis is a term that encompasses a
number of skin conditions causing red, scaly rashes
in the diaper area.
HISTORY
• Diapers occlude the skin, leading to skin macera-
tion and predisposing to skin infection and inflamma-
tion. Frequent diaper changes decrease incidence of
diaper dermatitis. Absorbent disposable diapers
effectively draw moisture away from the skin.
• Elevations in skin pH occur under occlusive condi-
tions when skin is in prolonged contact with urine
and stool, especially with diarrheal illness. Skin
breakdown results.
PHYSICAL FINDINGS
• Several causes of inflammation in the diaper area.
Irritant contact dermatitis is the most common diaper
area rash, with red, scaly, eroded, painful plaques on
convex surfaces and sparing of creases. Seborrheic
dermatitis affects the scalp and intertriginous areas,
including diaper area. Red, scaly plaques occur on
scrotum, penis, labia majora, pubis, inguinal and
gluteal folds. Psoriasis can be isolated to the diaper
area and appears identical to seborrheic dermatitis.
• Candidiasis is an acute infection of the superficial
layers of the skin. Can be either a primary cause of
diaper dermatitis, occurring as bright-red (beefy-red)
plaques in inguinal and gluteal folds, or secondary,
occurring in setting of seborrheic dermatitis or pso-
riasis. • Satellite pustules are hallmark of Candida
dermatitis. Pustules rupture to form a superficial col-
larette of scale. Chronic, poorly treated Candida
diaper dermatitis can form granulomatous nodules.
• Potassium hydroxide examination confirms pres-
ence of pseudohyphae and spores if present. Culture
results are often mixed with bacterial superinfection
as well as Candida species.
TREATMENT
• Therapy should be directed at minimizing wetness
in diaper area, with frequent diaper changes and
brief diaper-free periods. Barrier ointments such as
petrolatum, Aquaphor ointment, or 40% zinc oxide
ointment are useful for prophylaxis. Avoid cleaning
with irritating baby wipes. Apply 1% hydrocortisone
cream twice daily until inflammation controlled.
Pimecrolimus (Elidel) 1% cream and tacrolimus (Pro-
topic) 0.03% ointment are steroid-free anti-
inflammatory alternatives. • Treat Candida infection
with miconazole, clotrimazole, ketoconazole, oxico-
nazole, or Spectazole cream applied twice daily for
a week or two. Do not apply at the same time as
the anti-inflammatory therapy; consider alternating
applications with successive diaper changes.
• Recommend Pampers Rash Guard diapers (Procter
& Gamble), which reduce severity and frequency of
diaper rash by delivering petrolatum to diaper area.
 Candidiasis of large skin folds
(candidal intertrigo)
DDx Ref  12 • 39 • 48
70 

Yeast thrives in warm moist areas created by skin

folds. Pendulous breasts in older women
predispose. Red plaques appear, increasing in size.
Satellite pustules appear beyond plaque edge.

Candida infections of the axillae occur in the

obese, especially in warm humid weather. The
red plaques with satellite pustules occur just as
they do under the breasts and on groin.

Maceration causes pustules to rupture and skin to

scale. Painful fissures may develop at the base of
the skin fold.

A white fringe of scale may appear at the junction

where skin surfaces diverge and no longer touch.
Satellite papules and pustules are seen along the
edge of involved areas.
70  Candidiasis of large skin folds
(candidal intertrigo)
DDx Ref  12 • 39 • 48
DESCRIPTION
Intertrigo is skin fold inflammation. Many causes.
Psoriasis causes red, glistening plaques with macer-
ated scale. Groin and axillae commonly affected.
Seborrheic dermatitis looks just like psoriasis. Can
appear on scalp and intertriginous areas, especially
in infants. Accumulation of moisture in obese people
predisposes to skin irritation, eczema. These
compromised, warm, intertriginous areas frequently
colonized and infected with Candida species. Topical
steroid use favors yeast growth within fold areas.
HISTORY
• Warm, moist, intertriginous areas where skin
touches skin are a breeding ground for yeast. Skin
folds retain heat and moisture, providing suitable
environment for yeast infection. Infection occurs
under pendulous breasts, between overhanging
abdominal folds, in groin and rectal area, and in
axillae. • Infection occurs in winter, when warm tight
clothing promotes heat retention. Sweating and poor
hygiene promote infection in hot, humid weather.
• Persons with diabetes are predisposed.
PHYSICAL FINDINGS
• Most common finding: slowly evolving, red, moist,
glistening plaques extending to or just beyond limits
of apposing skin folds. Inflammation becomes more
intense with deep erythema. Erosions occur in
chronic cases. Painful fissures eventually form at
base of folds. • Acute infections show different
pattern. Begin with bright-red plaques in skin folds.
This pattern is commonly seen under breasts. Pus-
tules form but become macerated under apposing
skin surfaces, and develop into red papules with a
fringe of moist scale at border. Intact pustules may
be found outside apposing skin surfaces.
TREATMENT
• Topical medication effective in most cases.
• Warm, moist conditions must be eliminated.
• Apply antifungal cream in a thin layer twice a day
until rash clears. Miconazole, clotrimazole, ketoco-
nazole, oxiconazole, or econazole is applied in a thin
layer twice a day. • Daily application of a group VII
topical steroid suppresses inflammation and controls
itching and pain. • Use cool, wet, Burow’s or tap
water compress 20–30 min several times daily to
promote dryness. Apply compress right after applica-
tion of medication. Continue use until skin remains
dry. • Fluconazole 100 mg q.d. for 7 days used for
resistant cases. Potential drug interaction between
oral hypoglycemic agents and fluconazole requires
careful monitoring of blood sugars with concomitant
use. • Medicated or non-medicated absorbent
powder (Zeasorb) may be applied after inflammation
is gone. Powder absorbs moisture and acts as a dry
lubricant, allowing skin surfaces to slide freely, pre-
venting moisture accumulation in a potentially stag-
nant area. • Weight loss eliminates folds and avoids
recurrence.
 Tinea versicolor
DDx Ref  23 • 39 • 111
71 

Lesions begin as multiple small circular macules

in various colors (white, pink-brown) that enlarge
radially. Lesions may be inconspicuous in
fair-complexioned individuals during winter.

Extensive eruption in a dark-skinned person.

Lesions are lighter than normal skin; accentuated
when uninfected skin tans. Demonstrating the
fine scale helps differentiate from vitiligo.

Lesions may be pink or white in fair skinned

patients. This extensive eruption has spread down
onto the abdomen.

Lesion may be light to dark brown when scale

accumulates. Demonstrating scale by scraping
with a blade helps confirm the diagnosis.
71  Tinea versicolor
DDx Ref  23 • 39 • 111
DESCRIPTION
Common infection caused by the lipophilic yeast Pity-
rosporum orbiculare (Malassezia furfur). The organ-
ism is part of the normal skin flora.
HISTORY
• More common during years of higher sebaceous
activity (adolescence, young adulthood); very
common especially in tropical, semitropical regions.
Potentially transmissible; people with oily skin may
be more susceptible. Excess heat and humidity
predispose to infection. • May itch but usually
asymptomatic; appearance often major concern.
• Recurrences common (40–60%) after successful
treatment. • Adrenalectomy, Cushing disease, preg-
nancy, malnutrition, burns, corticosteroid therapy,
immunosuppression, oral contraceptives may lower
resistance, allowing this normally non-pathogenic
resident yeast to proliferate.
PHYSICAL FINDINGS
• Numerous small, circular, scaling papules on upper
trunk extending to the upper arms, neck, abdomen.
Facial involvement more common in children and
in persons of African descent. • Lesions hypo­
pigmented in tanned skin and pink or fawn-colored
in untanned skin. Lesions may be inconspicuous in
fair-complexioned people during winter. • Dyspig-
mentation persists several weeks after yeast elimi-
nated. • Potassium hydroxide examination of scale:
numerous hyphae that tend to break into short, rod-
shaped fragments intermixed with round spores in
grape-like clusters, giving ‘spaghetti and meatballs’
pattern.
TREATMENT
• Topical. For limited disease. Apply selenium
sulfide lotion 2.5% to entire skin surface from lower
posterior scalp area down to thighs; wash off in
10 min. This can be repeated every day for 7 con-
secutive days. Ketoconazole 2% shampoo is applied
to dampened skin, lathered, left on for 5 min, then
rinsed. This has clinical response rate of about 70%
when used as a single application or daily for 3 days.
Zinc pyrithione soap (ZNP bar) is applied in shower,
lathered, left on for 5 min, then rinsed off. Micona-
zole, clotrimazole, econazole, ketoconazole applied
to entire affected area at bedtime for 2–4 weeks is
effective. Patient should not bathe for at least 12 h
after treatment. • Oral. For extensive disease and
patients who do not respond to topical treatment or
who have frequent recurrences. Itraconazole 200 mg
q.d. for 5 days, taken with food to enhance absorp-
tion. Ketoconazole 400 mg in single dose or 200 mg
q.d. for 5 days, taken at breakfast with fruit juice.
Fluconazole 150 mg (two capsules per week for
4 weeks or two capsules as an initial dose to be
repeated after 2 weeks). Sweating may improve
transfer of oral ketoconazole and fluconazole to the
skin surface. Oral Lamisil not effective.
 Tinea of the nails
DDx Ref  153 • 154a • 154c
72 

Distal subungual onychomycosis. Various patterns

are produced as the fungus grows proximally.

White superficial onychomycosis. The surface of

the nail is soft, dry, and powdery, and can easily
be scraped away.

Proximal subungual onychomycosis.

Hyperkeratotic debris accumulates and causes the
nail to separate from the nail bed.

Distal subungual onychomycosis. A yellow to

brown color extends the full thickness of the nail.
72  Tinea of the nails
DDx Ref  153 • 154a • 154c
DESCRIPTION
Onychomycosis: fungal infection of fingernail or
toenail plate. Cause: many different species of
fungus.
HISTORY
• Trauma from tight-fitting shoes that are too short
predisposes to infection. • A large mass composed
of a thick nail plate and underlying debris may cause
discomfort with footwear.
PHYSICAL FINDINGS
There are four distinct patterns. Several patterns may
occur simultaneously. • Distal subungual onycho­
mycosis. Most common pattern. Fungi invade
distal area of nail bed. Distal plate turns yellow or
white as an accumulation of hyperkeratotic debris
causes nail to rise and separate from underlying bed.
• White superficial onychomycosis. Caused by
surface invasion of nail plate, most often by Tricho-
phyton mentagrophytes. Nail surface is soft, dry,
powdery, and can easily be scraped away. Nail plate
is not thickened. • Proximal subungual onycho­
mycosis. Microorganisms enter the area of posterior
nail fold cuticle, invade nail plate from below. Surface
remains intact. Hyperkeratotic debris causes nail to
separate. Trichophyton rubrum is most common
cause. • Candidal onychomycosis. Nail plate infec-
tion caused by Candida albicans is seen almost
exclusively in chronic mucocutaneous candidiasis, a
rare disease. Generally involves all the fingernails.
Nail plate thickens and turns yellow-brown.
All nails and skin are examined to rule out other
diseases that mimic onychomycosis.
Aspergillus, Cephalosporium, Fusarium, and
Scopulariopsis species, considered contaminants or
non-pathogens, can also infect nail plate. Multiple
pathogens may be present in a single nail.
In a potassium hydroxide wet mount, subungual
debris and nail plate are examined for hyphae.
Culture to establish presence of dermato-
phytes—organisms susceptible to itraconazole
(Sporanox), terbinafine (Lamisil), and fluconazole
(Diflucan).
TREATMENT
• Topical antifungal creams. Little value. • Oral
therapy. Highest success rate in fingernail and
toenail infections in young persons. • Systemic
therapy. From 50% to over 80% effective. Relapse
rate approximately 15–20% in 1 year. Indications for
treatment include pain with thick nails, functional
limitations, secondary bacterial infection, and
appearance. • Terbinafine (Lamisil) 250 mg q.d.
Administered for 6 weeks for fingernail infection,
12 weeks for toenail infection. Not effective for
some candidal species. • Itraconazole (Sporanox)
200 mg q.d. Prescribed for 6 weeks for fingernail
infection, 12 weeks for toenail infection. Pulse dosing
with 200 mg b.i.d. for 1 week on then 3 weeks off
another option. Fingernail infection: two or three
pulses. Toenail infection: three or four pulses.
 Angular cheilitis
DDx Ref  12 • 46 • 67
73 

Dry skin in winter and repeated lip licking

predispose to inflammation. Group VI topical
steroids and petrolatum-based barrier protectants
may control early cases.

Mixed infection evolves after several weeks.

Ketoconazole cream, mupirocin ointment, and group
VI topical steroids (to suppress inflammation) are
used in rotation every 6 h to treat yeast and bacteria.

Saliva is drawn into perioral skin folds of the

elderly. Repeated wetting–drying cycles chap and
inflame the skin. Daily applications of petrolatum-
based lubricants may protect fold from moisture.

Skin folds beyond the angles of the mouth may

also become moist with saliva. Topical antibiotics,
antiyeast creams, and group VI topical steroids
may all be needed. A cool wet compress is very
effective.
73  Angular cheilitis
DDx Ref  12 • 46 • 67
DESCRIPTION
Inflammation at the angles of the mouth is called
perlèche or angular cheilitis. The problem occurs
most often in the elderly. It becomes a chronic source
of discomfort.
HISTORY
• A moist, intertriginous space forms in skin folds at
the angles of the mouth as a result of advancing age.
Photodamage leads to deep facial and perioral wrin-
kles. Saliva flows into the angles, especially during
sleep. Repeated cycles of wetting and drying chap
the angle. Licking causes progression to eczema and
secondary mixed infection with Candida organisms
and/or staphylococci. • Recurrence is common,
because the anatomic defect is not easily corrected.
• The constant irritation, pain, and itching is very
distressing. • Patients taking isotretinoin develop
severe dry lips and angular cheilitis. • Young habitual
lip lickers, especially atopic patients, are at risk.
PHYSICAL FINDINGS
• Older patients develop a deep crease in the skin at
the mouth angle. Wetting leads to drying and crack-
ing. Licking accelerates the drying, and eczema
develops with erythema and scaling. • Chronically
inflamed skin becomes infected with staphylococci,
which produce papules and pustules. Chronically wet
skin is a breeding ground for Candida species.
• Painful fissures occur at the base of the skin fold.
Further progression leads to erosions and ulceration.
• Culture skin that does not respond to standard
therapy.
TREATMENT
A combination of medications is usually required.
Yeast, bacteria, and eczema must be controlled.
• Yeast is treated with the twice-daily application of
clotrimazole, miconazole, ketoconazole, or econa-
zole. • A group V–VI steroid cream or lotion, such as
desonide lotion 0.05%, is applied 4 h later and used
twice each day. Non-steroidal anti-inflammatory
agents such as Elidel 1% cream or Protopic ointment
0.1% are not as effective as steroid creams for con-
trolling acute inflammation but may be useful for
maintaining control in chronic cases. • Secondary
bacterial infection responds to mupirocin ointment or
oral antibiotics active against staphylococci. • Stop
treatment when inflammation is controlled. Then
protect the angles with heavy lubricants such as lip
balm (Chapstick) or ointment (Aquaphor, or plain
petrolatum or zinc oxide 20% ointment). Use during
the day and at bedtime.
 Cutaneous fungal
infections (tinea)
DDx Ref  39 • 42 • 47
74 

A very characteristic pattern of inflammation is

the active border of infection.

Dermatophytes appear as translucent, branching,

rod-shaped filaments (hyphae) of uniform width,
with lines of separation (septa) spanning the
width and appearing at irregular intervals.

Hyphae may be difficult to find in a potassium

hydroxide wet mount. Parker’s blue ink and other
stains easily stain the hyphae, rendering them
visible under low power.

Mosaic artifact. Lipid droplets between epithelial

cells simulate fungal hyphae in potassium
hydroxide wet mounts. Heat will make this
disappear.
74  Cutaneous fungal
infections (tinea)
DDx Ref  39 • 42 • 47
DESCRIPTION
Tinea is the clinical term for dermatophyte infection.
Dermatophytes can infect and survive only on dead
keratin; that is, the top layer of the skin (stratum
corneum), hair, nails.
HISTORY
Some species are able to infect the hair shaft in
addition to the skin.
• Endothrix pattern: fungal hyphae inside the
hair shaft. • Ectothrix pattern: fungal hyphae inside
and on the surface of the hair shaft.
Fungal spores are either large or small. The type
of hair invasion is classified as large-spored or small-
spored ectothrix, and large-spored endothrix.
PHYSICAL FINDINGS
• Dermatophytes produce various disease patterns
that vary with location: foot (tinea pedis), groin (tinea
cruris), body (tinea corporis), face (tinea faciei), hand
(tinea manuum), scalp (tinea capitis), beard (tinea
barbae), nails (onychomycosis). • Greatest numbers
of hyphae located in active border, which is best area
to get a sample for potassium hydroxide examination.
Active border is scaly, red, slightly elevated. Hold a
#15 surgical blade perpendicular to skin surface;
smoothly draw the blade against the scale. Place
scale on microscope slide and apply coverslip. Potas-
sium hydroxide (10% solution) is applied to edge of
coverslip and allowed to run under.
• With the microscope condenser moved down
away from the slide, scan entire area under coverslip
at × 10 power. Dermatophytes appear as translucent,
branching, rod-shaped filaments (hyphae) of uniform
width, with lines of separation (septa) spanning width
and appearing at irregular intervals. Uniform width
and branching distinguish hyphae from hair and other
debris. • Fungal culture necessary for hair and nail
fungal infections. Cultures usually become positive in
1–2 weeks. Three types of culture media used for
tinea. Sabouraud’s agar: allows growth of most fungi,
including non-dermatophytes; useful for nail infec-
tions, because detection of non-dermatophytes is
desirable. Mycosel agar: contains antibiotics to
prevent growth of bacteria and saprophytic fungi;
best for evaluation of hair tinea. Dermatophyte test
medium: supplied in vial kits, produces fast but
slightly less accurate results; yellow medium turns
pink in presence of dermatophytes in 6–7 days.
TREATMENT
Topical or systemic depending on site, extent of
involvement. Generally, hair and nail infections
require longer treatment. Specific sites are covered
in the chapters that follow.
 Tinea of the foot
DDx Ref  11 • 16 • 36
75 

Maceration of the fourth web is a very common

finding and is asymptomatic in most cases. Here,
the fungal infection has progressed out of the
web space and onto the sole.

The acute onset of erythema surrounding the web

indicates the acute inflammatory stage of the
fungal infection or a secondary bacterial infection.

Classic ‘ringworm’ pattern on the dorsal foot with

concentric active borders and intervening dry
powdery scale. Cracks and painful fissures may
eventually appear.

Tinea of the soles is sometimes red and inflamed.

It progresses on to the heels and dorsum of the
foot. Itching is usually moderate to intense.
75  Tinea of the foot
DDx Ref  11 • 16 • 36
DESCRIPTION
Tinea pedis (‘athlete’s foot’) is epidermal infection
with dermatophyte fungi. On webs, soles, dorsum.
Different inflammation patterns. Psoriasis, eczema,
bacterial infections appear similar.
HISTORY
• Occurs in genetically predisposed persons.
Common in adults, especially men. Uncommon in
children. • Infection persists, recurs. • Wet locker
room floor a possible infection source. • Acute,
chronic phases. • Interdigital infections often asymp-
tomatic. • Extension out of web on to dorsum may
result in acute erythema, secondary bacterial infec-
tion. • Infection of soles mildly itchy, persistent.
Difficult to produce long remissions.
PHYSICAL FINDINGS
Potassium hydroxide culture sometimes necessary
for diagnosis. Toe web infection (especially third,
fourth) common. Shoes compress toes, create warm,
moist environment. Infection produces white, dry or
macerated, dense, persistent scale. Bacterial sec-
ondary infection sometimes occurs. Three infection
patterns. • Ringworm pattern and acute vesicular
infections. On sides and dorsum of foot or extend
from webs. Itching common. • Dermatophytid or
‘id reactions.’ Allergic reactions to fungal infection,
sometimes misinterpreted as drug rash. Itchy vesi-
cles erupt at distant sites (palms, trunk, along sides
of fingers). Prompts examination of webs, sides of
feet. Chronic scaly appearance of entire sole occurs
with dry skin but often unrecognized tinea infection.
• ‘Moccasin’-type pattern. Difficult to treat, recurs.
Orange-brown soles are thick, scaly, tender, some-
times itchy. Same pattern on palms. Classic presen-
tation is infection of two feet, one hand, or two hands,
one foot. Toenail or fingernail fungal infection may
eventually occur.
TREATMENT
• Over-the-counter terbinafine (Lamisil) and
butenafine (Lotrimin Ultra) cream may be more effec-
tive than miconazole, clotrimazole; b.i.d., 2–6 weeks.
Chronic sole infections require at least 3–4 weeks.
Antifungal-corticosteroid combination creams,
lotions (e.g. Lotrisone) minimally effective. Econazole
active against tinea, some bacteria. Useful for macer-
ated, secondarily infected web spaces. • Treat acute
vesicular infections with cool Burow’s or tap water
dressings, 30 min several times daily. May apply
immediately after cream. • Treat acute, extensive
infections orally: terbinafine (Lamisil) 250 mg q.d.
(2 weeks), itraconazole (Sporanox) 200 mg b.i.d.
(1 week), Diflucan 150 mg once a week (3–4 weeks).
• Treat secondary bacterial infection with oral anti-
biotics. Treat id reactions at distant sites with cool
wet dressings, group V topical steroids, and (if
intense) short course of prednisone (1 mg/kg per day
q.d.), 5–10 days. • Wear wide shoes. Open web
space with small strand of lamb’s wool (Dr Scholl’s
Lamb’s Wool), cotton ball. • Powders, not necessarily
medicated, absorb moisture (Zeasorb). Apply to feet
rather than shoes. Change wet socks.
 Tinea of the groin
DDx Ref  12 • 39 • 70
76 

Infection starts in inguinal crease and spreads on

to thigh. One or both sides involved. Many patients
are unaware of infection. Fine scale is present over
surface; well-defined scaling border shown.

Fungal infections slowly progress. The advancing

border is red with a fringe of scale. To obtain a
specimen for potassium hydroxide examination,
scrape the border scale with a #15 surgical blade.

Think of Candida infections if patient presents

with erythema in the groin extending to scrotum
and thigh. Satellite pustules can occur with tinea;
more common in acute yeast infection.

Erythrasma is a bacterial infection that looks like

tinea. The brown-red patches fluoresce coral red
under a Wood’s light. Prescribe topical
clindamycin or benzoyl peroxide wash.
76  Tinea of the groin
DDx Ref  12 • 39 • 70
DESCRIPTION
Fungal infection of the crural fold that slowly migrates
on to the thighs is known as tinea cruris or ‘jock itch.’
HISTORY
• Common in adult men, occasionally seen in obese
women, rare in children. • Many infections are
asymptomatic. Itching increases when inflamed.
• Warmth and perspiration in summer and multiple
layers of clothing in winter predispose to infection.
Acute inflammation may appear shortly after wearing
tight clothing. • Steroid creams provide temporary
relief but will alter the typical presentation. Bizarre
patterns of inflammation called tinea incognito may
result. Prolonged use of steroid creams or combina-
tion steroid-antifungal preparations (e.g. Lotrisone)
can cause striae. This is an irreversible change.
PHYSICAL FINDINGS
• A unilateral or bilateral half-moon-shaped patch
with a well-defined scaling, and sometimes a vesicu-
lar border, begins in the crural fold and slowly
extends onto thighs. Skin within the border turns
red-brown, is less scaly, and may develop papules.
• The infection can extend onto the buttocks and
gluteal cleft. The scrotum is rarely involved. This is
in contrast to Candida infections, which extend on to
the thigh and scrotum and show pustules beyond the
border. • Intertrigo from irritation is symmetric,
involving both inner thigh and scrotum. There is no
active scaling border. Psoriasis resembles intertrigo.
• Erythrasma caused by Corynebacterium minutis-
simum infection presents as a brown, half-moon-
shaped plaque with a fine scale on the surface.
Wood’s light examination shows a coral-red fluores-
cence. • A clinical diagnosis of tinea will be made in
many cases. Specimens for potassium hydroxide
examination should be taken from the advancing
scaling border.
TREATMENT
• Infection improves or clears if warmth and moisture
are eliminated. • Most over-the-counter antifungal
creams are effective. Use creams that are active
against both Candida species and dermatophyte
fungi (econazole, ketoconazole, miconazole, clot-
rimazole). Apply twice daily for 10–14 days. • Moist,
itching infections improve rapidly with a cool, wet,
tap water or Burow’s dressing for 20–30 min two to
six times daily until skin has been dried. • Resistant
infections respond to itraconazole 200 mg b.i.d. for
1–2 weeks, terbinafine 250 mg q.d. for 1–2 weeks,
or fluconazole 150 mg once a week for 2–4 weeks.
• Steroid creams may be used for a few days to
control acute inflammation. Limit the amount pre-
scribed. Infection may get worse and striae will form
with chronic or repetitive use. • Absorbent powders,
not necessarily medicated (Zeasorb), help control
moisture and prevent reinfection.
 Tinea of the body
DDx Ref  15 • 20 • 42
77 

Classic ringworm infection pattern. Round to oval

plaque, sharp scaling border. Single lesion or
many. Eczema, psoriasis, impetigo may be
similar. Patients call anything round ‘ringworm.’

Initial plaque appeared eczematous; treated with

topical steroids. Acute inflammation occurred
when steroids were stopped. Potassium hydroxide
examination of border scale proved the diagnosis.

Tinea can progress for years with few symptoms.

Topical steroids had no effect. Follicular papules
indicate extension of infection into follicle depths.
Cleared by terbinafine 250 mg q.d. for 2 weeks.

The sharp scaling annular border in this

geographic plaque on the back is an important
clue to the diagnosis. Psoriatic and eczematous
plaques are more homogeneous and symmetric.
77  Tinea of the body
DDx Ref  15 • 20 • 42
DESCRIPTION
Tinea corporis: dermatophyte infection of face, body,
trunk, limbs. Other diseases present with round
lesions that look like ‘ringworm.’ Nummular eczema
and psoriasis lack scaly advancing border of tinea.
Pityriasis rosea has collarette of scale that does not
reach edge of red border as it does in tinea.
HISTORY
• Infections common in warm, humid climates.
• Lesions grow slowly for months or years, may
eventually cover very wide areas. • Itching minimal
to moderate for chronic infections, intense with
inflammatory lesions. Very large lesions tend to be
mildly itchy or asymptomatic. Patients may be
unaware of their presence. • Wrestlers unknowingly
transmit disease to opponents. • Infections can be
acquired from animals (cows and cats).
PHYSICAL FINDINGS
• Most common presentation: classic ringworm
pattern of infection. Lesions appear as round, flat
papules with a scaly raised border. Lesion slowly
expands in diameter. Plaques vary from a few cen-
timeters to huge lesions that may cover half of skin
surface. Slowly advancing, scaly border is highly
characteristic. May have red raised papules or vesi-
cles. Central area becomes red, purple, brown, or
hypopigmented and less scaly. Fungal hyphae invade
deep into follicle, produce red papules. With treat-
ment, scaling resolves before erythema fades.
• Deep inflammatory lesions usually occur from
infection with fungi from animals, such as Trichophy-
ton verrucosum from cattle. Localized, intensely
inflamed lesions have elevated, red, boggy, pustular
surface. Secondary staphylococcal infection possi-
ble. Destructive inflammatory process causes brown
hyperpigmentation, scarring. Postinflammatory dys-
pigmentation blends or disappears over several
months. • Potassium hydroxide examination shows
abundant hyphae. Perform fungal cultures of
inflamed lesions to establish the animal of origin.
TREATMENT
• Treat localized superficial infections with clotrima-
zole, miconazole, ketoconazole, econazole,
butenafine, or terbinafine applied twice each day for
at least 2 weeks. Continue treatment for at least 1
week after infection resolves. • Extensive lesions and
those with red papules require oral therapy. Red
papules indicate extension into hair follicle. Topical
medication may not penetrate deeply enough to be
effective. Treat with terbinafine (Lamisil) 250 mg q.d.
for 1–2 weeks, itraconazole (Sporanox) 100 mg q.d.
for 1–2 weeks or 200 mg q.d. for 1 week, or fluco-
nazole (Diflucan) 150 mg once a week for 2–4
weeks. • Griseofulvin (ultramicrosize) adult 333 mg
q.d. or b.i.d. for 2–4 weeks also effective. • Treat
secondary bacterial infection with oral antibiotics.
• Consider short course of prednisone for highly
inflamed lesions to minimize scarring.
 Tinea of the hand
DDx Ref  36 • 48 • 163
78 

Sharply defined, scaling borders. Infected first,

second, third nails. Misdiagnosed as eczema and
treated with topical steroids. Nails and skin
cleared with terbinafine 250 mg q.d. 6 weeks.

Topical steroids were prescribed and infection lost

characteristic tinea features. Scaling border and
surface scale disappeared. Plaque thickened and
became painful. This is called tinea incognito.

Thick palmar scale often considered dry skin.

Mildly itching infection similar to that on soles. One
hand involved typical. Check feet for same pattern.
Recurrence common even after oral medication.

Inflammation of webs occurs in those exposed to

moisture. Eruption eczematous (intertrigo) or
infected with dermatophyte fungi, Candida,
bacteria. Econazole cream treats fungi, yeast,
some bacteria.
78  Tinea of the hand
DDx Ref  36 • 48 • 163
DESCRIPTION
Tinea of the back of the hand has the same pattern
of infection as is seen on the body. May look like
eczema or psoriasis, especially if border indistinct.
Tinea of the palm is often misinterpreted by the
patient as just dry skin.
HISTORY
• Rarely seen in children. • Slowly progressive and
minimally symptomatic. • Often misdiagnosed as
eczema and treated inappropriately with topical ster-
oids. • Typical ringworm pattern of infection on the
back of the hand responds to treatment sooner than
the dry, thick palms.
PHYSICAL FINDINGS
• Tinea involving the back of the hand has all the
features of classic ringworm lesions on the body. A
raised, red, scaly, advancing border is typical.
Papules or vesicles may be present at the border or
in the central area. • Tinea involving the palm has
the same appearance as the dry, diffuse, keratotic
form of tinea on the soles. Patients with palm infec-
tions frequently have infected soles. The usual
pattern of infection is involvement of one hand and
two feet or of two hands and one foot. • Hyperkera-
totic tinea of the palms may be asymptomatic; the
patient may be unaware of the infection, attributing
the dry, thick, scaly surface to hard physical labor.
• Diagnosis is subtle and easily missed. The thick-
ened palms may be severely dry and develop cracks
and fissures. Fingernail fungal infection (onychomy-
cosis) may accompany tinea manuum. A potassium
hydroxide wet mount or fungal cultures prove the
diagnosis.
TREATMENT
• Infection of the dorsum and palms may respond to
topical antifungal creams such as terbinafine
(Lamisil) or butenafine hydrochloride (Lotrimin Ultra),
but oral medication is more reliable. Terbinafine
(Lamisil) 250 mg q.d. for 2 or 4 weeks, itraconazole
(Sporanox) 200 mg q.d. or 200 mg b.i.d. for 1–2
weeks, or Diflucan 150 mg once weekly for 2 or 4
weeks is effective. Ultramicrosize griseofulvin
250 mg or 330 mg b.i.d. for 3–6 weeks also effec-
tive. • Treatment of nail infections requires a 6-week
course of terbinafine or pulse dosing with itracona-
zole (200 mg b.i.d., 1 week on, 3 weeks off, for 2–3
months). • Reevaluate patients with palm infections
in 6 months; there is a significant recurrence rate.
 Tinea incognito
DDx Ref  12 • 37 • 70
79 

This fungal infection was misdiagnosed as

psoriasis. Group I topical steroids were
prescribed. The inflammation became confluent
and spread over much of the lower leg.

A diagnosis of eczema of the dorsum of the foot

was made and treated with a group IV topical
steroid. The misdiagnosed fungal infection spread
in a ringworm-like pattern.

Initial plaque appeared eczematous; treated with

topical steroids. Acute inflammation occurred when
steroids stopped. Potassium hydroxide examination
of border scale showed fungal hyphae.

A group V topical steroid was applied

intermittently after an incorrect diagnosis of
intertrigo. The dermatophyte fungal infection
flared with a yeast-like pattern with satellite
pustules. Note sparing of the scrotum.
79  Tinea incognito
DDx Ref  12 • 37 • 70
DESCRIPTION
Fungal infection whose clinical presentation has
been altered by application of topical corticosteroids.
Bizarre patterns of inflammation are produced by the
inappropriate use of these topical anti-inflammatory
agents. The fungal infection is most often misdiag-
nosed as eczema, psoriasis, pityriasis rosea, follicu-
litis, or rosacea.
HISTORY
• A cutaneous fungal infection is misdiagnosed as an
inflammatory skin rash. Topical steroids are pre-
scribed. These anti-inflammatory agents decrease
inflammation, and the eruption appears to be improv-
ing. The fungus, however, flourishes with cortisone-
induced local immunosuppression. The topical
steroid is stopped and the infection rapidly flares. The
cycle of treatment and flaring continues until infec-
tions with bizarre patterns spread over a wide area.
• The altered clinical picture is called tinea incognito.
• The intensity of itching varies. • Perform a potas-
sium hydroxide examination when a rash does not
respond as expected to topical steroids.
PHYSICAL FINDINGS
• Fungal infections of the dorsum of the hand or foot,
lower leg, face, and groin may not present with a
typical ringworm pattern of infection. The typical
sharp scaling border is not always present. • Infec-
tions become much worse in the presence of immu-
nosuppressive anti-inflammatory agents. • A well-
defined border may not be present, and a once-
localized process may expand over wide areas.
• Diffuse scale and erythema make the eruption look
eczematous and encourage further use of topical
steroids. • Papules and pustules appear inside and
outside the border and may represent a bacterial
infection. • Brown postinflammatory hyperpigmenta-
tion appears in time.
TREATMENT
Stop topical steroids. Superficial lesions respond to
antifungal creams (e.g. butenafine, clotrimazole,
miconazole, econazole, oxiconazole, terbinafine)
applied twice each day. Continue treatment for at
least 1 week after resolution of infection. Extensive
lesions or those with papules or pustules are treated
with oral therapy. • Lamisil: 250 mg q.d. for 2
weeks. • Sporanox: 100 mg, two tablets q.d. for
2 weeks. • Diflucan: 150 mg once a week for 2
weeks. • Griseofulvin (ultramicrosize): Adult
333 mg q.d. or b.i.d. for 2–6 weeks.
Secondary bacterial infection is treated with oral
antibiotics such as cephalexin 500 mg b.i.d.
Cool water wet dressings suppress inflammation
and control itching.
 Tinea of the scalp
DDx Ref  39 • 40 • 151
80 

Seborrheic dermatitis pattern. Fine white diffuse

or patchy scale-like dandruff. Hair shaft infection
then occurs; hairs break at surface, leaving
alopecia areas. Broken hairs look like black dots.

Black dot pattern. Well-demarcated areas of hair

loss appear. Infected hairs break, leaving black
dots on scalp surface. Little or no inflammation.
Occipital adenopathy may be present.

Inflammatory tinea capitis. The lesion near the

vertex is boggy, with a scaling and crusted
surface.

Inflammatory tinea capitis (kerion). A deep boggy

mass with pustules and exudate occurs in some
patients. The painful lesion heals with scarring
and permanent localized hair loss.
80  Tinea of the scalp
DDx Ref  39 • 40 • 151
DESCRIPTION
Caused by invasion of stratum corneum and hair
shaft with fungal hyphae. Most patients prepubertal
children. Localized scalp scale in children is a
common presentation for seborrheic dermatitis. This
is frequently diagnosed as tinea capitis.
HISTORY
• Most US cases caused by Trichophyton tonsurans.
• Microsporum canis infection acquired from pets
(particularly cats). M. canis-, M. audouinii-infected
hair fluoresces blue-green under Wood’s light.
• Poverty, crowded city living risk factors. Fungal
spores remain on clothing, combs, brushes, tele-
phones for long periods.
PHYSICAL FINDINGS
Four clinical infection patterns for T. tonsurans.
• Seborrheic dermatitis type. Diffuse, patchy scale
on scalp. Adenopathy may be present. Potassium
hydroxide examination often negative. Culture scale.
• Black dot pattern. Fungal hyphae invade hair
shaft. Hair then breaks at scalp surface. Broken
shafts like black dots (red if hair red). Round areas
of alopecia with scale present without inflammation.
Occipital adenopathy may be present. • Inflamma-
tory tinea capitis (kerion). Deep boggy round
masses with pustules, surface exudate. Fever, occip-
ital adenopathy, leukocytosis may occur. Intense
inflammation destroys hyphae; potassium hydroxide
wet mounts, fungal cultures often negative. May initi-
ate treatment based on clinical appearance without
laboratory proof of infection. • Pustular. Pustules or
scabbed areas without scaling, significant hair loss
may be present; look like scalp bacterial infection.
Cultures, potassium hydroxide wet mounts may be
negative.
TREATMENT
Examine siblings and adult household members.
Clean or discard contaminated objects such as
combs. Daily dosing with following drugs is effective.
• Griseofulvin. Taken with a fatty meal. Used for 2
weeks beyond the time that cultures and potassium
hydroxide preparations become negative (usually
6–12 weeks). • Terbinafine, itraconazole, or flu-
conazole. Taken for 4–8 weeks. Itraconazole and
fluconazole are available as a suspension. A single
dose of 150 mg once weekly for 4 weeks may also
be effective for older children.
Consider suppressing kerion inflammation with
prednisone 1–2 mg/kg q.d. or intralesional triamci-
nolone 10 mg/cc.
Shampoo with selenium sulfide 1% (Selsun Blue)
or ketoconazole (Nizoral) every other day for the first
2 weeks, then twice weekly throughout course of rest
of oral therapy. Shampoo is left on for 5 min. Other
family members should shampoo two or three times
weekly.
 Tinea of the beard
DDx Ref  31 • 33 • 40
81 

Ringworm infection pattern. Annular border covers

a wide area of cheek. Little inflammation in central
area of plaque. Specimens for potassium hydroxide
examination are best taken from the border.

Red papules were present for weeks. There was

some itching. A diagnosis of seborrheic dermatitis
was incorrectly made. Topical steroids were
ineffective.

Inflammation of the chin spread slowly for weeks.

A potassium hydroxide examination was positive
for fungal hyphae.

Bacterial folliculitis was the initial diagnosis, but

the pustular eruption failed to respond to several
different antibiotics. Hair were easily extracted
and showed numerous fungal hyphae.
81  Tinea of the beard
DDx Ref  31 • 33 • 40
DESCRIPTION
Fungal infections of the beard often misdiagnosed as
bacterial folliculitis. Diagnosis is then suspected only
when multiple courses of antibiotics are ineffective.
HISTORY
• Tinea is a slowly evolving disease, in contrast to
bacterial infections. • Infections often subtle with
little or no itching. • Deep infection of the follicle
causes pain and swelling. • Wrestlers and farmers
in contact with cows are at risk.
PHYSICAL FINDINGS
• Ringworm pattern. Lesions similar to the round
plaques found on body. Border is scaling and sharply
defined. Plaques may reach considerable size before
they are recognized. The hair follicles within the
plaque may also be infected. • Follicular pattern.
Deep follicular infection causes erythema, papules,
and pustules that resemble bacterial folliculitis. The
fungal infection smolders and slowly spreads. Oral
antibiotics may provide some relief by treating a sec-
ondary bacterial infection. Pustules and draining
nodules may lead to kerion formation and permanent
scarring. Regional lymphadenopathy may occur.
Obtain hair for examination and culture. Hairs
infected with fungi are easily and painlessly epilated.
Hairs in an area of bacterial folliculitis are extracted
with difficulty. Fungal cultures are required if the
diagnosis is suspected but cannot be confirmed by
potassium hydroxide examination. A positive culture
for Staphylococcus does not rule out tinea. The posi-
tive culture may represent a secondary bacterial
infection.
TREATMENT
• Topical antifungal agents are not reliably effective,
because they do not penetrate deep enough into the
hair follicle. • Adult men are treated with terbinafine
(Lamisil) 250 mg q.d. for 2–4 weeks, itraconazole
(Sporanox) 200 mg q.d. for 2–4 weeks, fluconazole
(Diflucan) 150 mg once a week for 3–4 weeks, or
ultramicrosize griseofulvin 250 mg or 330 mg b.i.d.
for 4 weeks.
 Non-specific viral rash
DDx Ref  20 • 24 • 84
82 

Viral exanthems present as red macules and

papules. They can appear on any skin surface
including the palms and soles.

Macules and papules may resemble hives. Viral

exanthem lesions persist for days, unlike hives in
which individual lesions last for less than 24 h.

Viral exanthem on the cheeks. Lesions are

macular and papular but lack the scale seen in
atopic dermatitis. Hives have a similar
appearance.

Gianotti–Crosti syndrome. Pink papules on the

extensor surface of the extremities, with only mild
itching.
82  Non-specific viral rash
DDx Ref  20 • 24 • 84
DESCRIPTION
A viral exanthem is a rash caused by a systemic viral
infection; different viruses produce similar-appearing
rashes.
HISTORY
Season, exposure history, and local and regional epi-
demiology assist with diagnosis. • Winter: respira-
tory viruses. • Summer and fall: enteroviruses.
PHYSICAL FINDINGS
• Generalized erythematous macules and papules,
and urticarial (non-polio enteroviruses, respiratory
viruses) petechial rashes mimic more serious sys-
temic infection such as meningococcemia, per­
iorbital edema (Epstein–Barr virus), keratoconjunc-
tivitis (adenovirus), papular acrodermatitis of
childhood (Gianotti–Crosti syndrome)—monomor-
phic, discrete papules and vesicles coalescing on the
face, extremities, buttocks. • Unilateral laterotho-
racic exanthem (asymmetric periflexural exanthem)
occurs on lateral thorax, near axilla, and can spread
to other hemithorax and extremities. Papular purpuric
gloves and socks syndrome: petechial erythema on
palms and soles (parvovirus B19).
TREATMENT
Supportive: bland emollients, group V and VI topical
steroids, oral antihistamines.
 Erythema infectiosum
DDx Ref  20 • 82 • 84
83 

Facial erythema ‘slapped cheek’ is characteristic

of erythema infectiosum. Note sparing of the
nasolabial folds and perioral regions.

‘Fish net’ lacy erythema occurs 2 days after the

facial erythema on the extensor surface of the
arms.

This highly characteristic lacy red net-like pattern

last from a few days to 3 weeks. It may recur
over several weeks.

Lesions can appear as round, faint pink–orange

plaques with central clearing.
83  Erythema infectiosum
DDx Ref  20 • 82 • 84
DESCRIPTION
Common viral exanthem produces bright-red cheeks
and lacy erythema of arms. Caused by parvovirus
B19. Also called fifth disease or slapped cheek
syndrome.
HISTORY
• More prevalent in winter and spring; most common
in children 5–14 years old; community outbreaks;
transmitted via respiratory secretions, blood, or verti-
cally from mother to fetus. • Asymptomatic infection
common. • Latent period 4–14 days. • Arthralgias in
adults. • When rash appears, not considered infec-
tious. • Self-limited in most patients.
PHYSICAL FINDINGS
• Facial erythema gives slapped cheek appearance.
Warm, symmetric, erysipelas-like plaques on cheeks,
sparing nasolabial folds and circumoral region (cir-
cumoral pallor). Fades in 4 days. • Two days after
facial rash onset, a lacy erythema occurs on proximal
extremities, extending to trunk and buttocks. Fades
in 6–14 days. • Sunlight, hot water, physical and
emotional exertion exacerbate the rash. • Adult
women can develop arthritis or small joints of hands
and knees, similar to rheumatoid arthritis; lasts 2–4
weeks. Arthritis usually resolves in less than 4
months but may be chronic. Men usually do not
develop arthritis. • In adults, rash can be non-spe-
cific macular eruption or acrally located (stocking and
glove distribution). • Infection during pregnancy: risk
of fetal loss is 8–10%, greatest if infection before 20
weeks’ gestation.
TREATMENT
Non-steroidal antiinflammatory drugs for joint symp-
toms for most patients. No treatment required for
rash.
 Cutaneous drug eruptions
DDx Ref  24 • 82 • 85
84 

The torso and proximal extremities are the most

common locations for cutaneous drug reactions.
This patient has the typical rash characterized by
red papules coalescing to plaques.

Severe drug reaction. Rash often starts on torso

and can progress to full-body redness
(erythroderma).

The penis is a common location for a fixed drug

reaction. Sometimes they are bullous, causing
deep erosions as seen in this patient.

Thiazide diuretics can produce a photosensitive

drug eruption characterized by red edematous
plaque with ill-defined borders on a sun-exposed
surface.
84  Cutaneous drug eruptions
DDx Ref  24 • 82 • 85
DESCRIPTION
Common. Many different clinical patterns. Can mimic
various dermatoses.
HISTORY
Most patients are on multiple medications. Typical
sequence begins with fever followed by a rash
several hours later. Rash starts on face and torso,
spreading to extremities. Reaction can occur after
weeks or years without ill effect, but once sensitiza-
tion occurs a reaction may occur within minutes
to 24–48 h. Chemically related drugs may
cross-react.
Different drug reaction patterns. • Morbilliform:
most common drug eruption, begins 7–10 days after
starting drug, lasts 1–2 weeks. • Urticarial: frequent
causes—aspirin, penicillin, blood products; IgE-
mediated—immediate reaction; immune complex–
mediated (serum sickness) 4–21 days after drug
ingestion. • Internal–external reactions: topical
sensitization to a drug results in rash after oral intake
of drug. • Erythema multiforme and toxic epider-
mal necrolysis. • Exfoliative erythroderma.
• Fixed drug reactions: appear soon after exposure
and occur at same site after exposure; drug-induced
hyperpigmentation. • Lichenoid drug reactions:
latent period 3 weeks to 3 years. • Photosensitive
reactions: phototoxic (rash within 24 h of sun expo-
sure), photoallergic (rash after 48 h of exposure).
• Small vessel necrotizing vasculitis. • Chemo-
therapy-induced acral erythema: caused by
cytosine arabinoside, fluorouracil, doxorubicin, meth-
otrexate • Acute generalized exanthematous pus-
tulosis: rash within 5 days of ingestion; resolves in
15 days; penicillin most common.
PHYSICAL FINDINGS
• Morbilliform: red macules and papules that
become confluent; looks like a viral exanthem; starts
on trunk, spreads to extremities; can involve mucous
membranes, palms, and soles; often spares the face.
• Urticaria: hives, usually generalized. • Internal–
external: eczematous reaction, particularly in axillae
and groin. • Erythema multiforme and toxic epi-
dermal necrolysis reactions: target lesions and
widespread blistering and skin exfoliation; can
involve mucous membranes. • Exfoliative erythro-
derma: generalized redness and scaling. • Fixed
drug reactions: single or multiple round dusky-red
plaques. • Drug-induced hyperpigmentation:
brown to grey patches that can be in photodistributed
areas (amiodarone), scars (minocycline), mucosal
(zidovudine), flagellate pattern (bleomycin), melasma
(oral contraceptives). • Lichenoid drug reactions:
multiple flat-topped, itchy, violaceous papules;
may have oral involvement. • Photosensitive:
phototoxic—erythema and skin peeling confined to
sun-exposed sites (can cause onycholysis); photoal-
lergic—rash can spread to non-sun-exposed areas.
• Small vessel necrotizing vasculitis: palpable
purpura (especially lower legs). • Chemotherapy
acral erythema: tingling on the palms and soles
followed in a few days by painful, symmetric, well-
defined swelling and erythema. • Acute generalized
exanthematous pustulosis.
TREATMENT
Identify responsible drug and switch to chemically
dissimilar drug. Symptomatic and supportive
treatments.
 Erythema multiforme
DDx Ref  24 • 82 • 84
85 

Erythema multiforme is commonly seen on the

extremities, especially palms and soles. Iris or
target lesions are classically seen along with fixed
urticaria-like papules.

The central portion of the target lesion can appear

dark red, blister, and heal with scale crust.

Erythema multiforme shows numerous lesion

morphologies, urticaria-like papules, vesicles,
bullae, and target-shaped papules.

Target lesions on the palms can mimic a drug

hypersensitivity reaction. Itching with erythema
multiforme lesions is usually mild.
85  Erythema multiforme
DDx Ref  24 • 82 • 84
DESCRIPTION
Relatively common, acute—often recurrent—
inflammatory disease characterized by target-shaped
skin lesions.
HISTORY
• Commonly associated with herpes simplex, Myco-
plasma pneumoniae, and upper respiratory tract
infections. • Can be seen with contact allergens,
drugs, connective tissue diseases, physical agents,
X-ray therapy, pregnancy, internal malignancies.
• Reactivation of herpes simplex can produce recur-
rent erythema multiforme due to cytotoxic immune
response directed against keratinocyte-expressing
foreign viral or drug antigens. • Usually resolves in
1 month.
PHYSICAL FINDINGS
• Numerous lesion morphologies: target lesions,
erythematous macules and papules, urticaria-like
lesions, vesicles, bullae. • Target lesions begin as
dusky red, round macules and papules and are
1–3 cm. Can see symmetric pattern on palms, soles,
backs of hands and feet, and extensor aspect of
forearms and legs. • The center of the iris can appear
dark red, purpuric, or vesicular, and is due to acute
epidermal injury. Surrounding the central area is a
pale area of edematous skin, which is in turn sur-
rounded by a sharp, discrete ring of erythema.
• Lesions appear in crops, resolving in 1–2 weeks
without scarring. • Postinflammatory pigment
changes are common (hypopigmentation and/or
hyperpigmentation). • Bullae and erosions may be
present in the oral cavity. • Lesions are fixed and
may occur in areas of trauma (Koebner phenome-
non). • Skin biopsy: interface reaction with necrotic
keratinocytes.
TREATMENT
• Ruptured blisters and eroded skin respond to
topical antibiotics (bacitracin, Bactroban). • Wide-
spread erythema multiforme responds rapidly to 1–3
weeks of systemic corticosteroids. • Prednisone
40–80 mg q.d. initially until lesions resolve, followed
by taper. •Triamcinolone acetonide (40 mg) i.m. can
be effective • Can prevent recurrent herpes-associ-
ated erythema multiforme with oral acyclovir
(200 mg b.i.d. or t.i.d. or 400 mg b.i.d.), valacyclovir
(Valtrex) 500 mg q.d., or famciclovir (Famvir) 125 mg
b.i.d. as continuous suppressive therapy.
 Stevens–Johnson
syndrome
DDx Ref  24 • 82 • 84
86 

The palms, soles, dorsum of hands, and extensor

surfaces are most commonly affected.

Patients with Stevens–Johnson syndrome can

develop conjunctivitis. Meticulous eye care with
erythromycin ointment can prevent ocular
adhesions.

Mucosal involvement may include erythema,

edema, sloughing, blistering, ulceration, and
necrosis. Mouth erosions are painful and may
impede adequate nutrition.

Severe bullous form. Mucosal involvement can be

extensive, requiring tracheostomy.
86  Stevens–Johnson
syndrome
DDx Ref  24 • 82 • 84
DESCRIPTION
Severe blistering mucocutaneous syndrome, involv-
ing at least two mucous membranes.
HISTORY
• Occurs in all ages but more common in children
and young adults. • Thought to be due to cytotoxic
immune responses directed against keratinocytes
expressing foreign infectious (Mycoplasma pneumo-
niae) and drug antigens (phenytoin, phenobarbital,
carbamazepine, sulfonamides, aminopenicillins).
• Medications started within 1 month of disease
onset are more likely to cause Stevens–Johnson syn-
drome. • HIV infection, systemic lupus erythemato-
sus, and malignancies treated with radiation increase
the risk. • Can involve pulmonary, gastrointestinal,
renal, and central nervous systems.
PHYSICAL FINDINGS
• Erythematous papules, dusky-appearing vesicles,
purpura, and target lesions erupt acutely. • Lesions
can be tender and burn. Oral, genital, and perianal
mucosa develop bullae and erosions. • Thick hemor-
rhagic crusts can cover the lips. • Patients develop
conjunctivitis and are at risk for corneal ulceration
and uveitis. • Stevens–Johnson syndrome skin
lesions are more centrally distributed on the face and
trunk. Crops of lesions erupt for 10–14 days and
slowly subside for the next 3–4 weeks.
TREATMENT
• Identify and treat sources of infection, withdraw
suspected offending drugs, maintain fluid and nutri-
tional requirements, provide meticulous local wound
care. • Mucous membranes: frequent mouth rinses
and applications of petroleum jelly (Vaseline) or
Aquaphor. • Viscous lidocaine (Xylocaine) or Benad-
ryl elixir for pain. Topical erythromycin ointment to
the eyes prevents ocular adhesions. Treat eroded
skin like a burn: cleanse gently, remove necrotic
tissue, apply bland emollients. • Narcotics for severe
pain. • Intravenous immunoglobulins in selected
patients. • The use of systemic corticosteroids is
controversial. Corticosteroids may be beneficial in
certain cases. Sick children who have extensive
cutaneous, ocular and oral lesions may respond to
prednisone (20–30 mg b.i.d.) until new lesions no
longer appear; it is then tapered rapidly.
 Erythema nodosum
DDx Ref  24 • 50 • 97
87 

Pink, dusky, firm, painful nodules classically

occur on the pretibial surfaces.

Erythema nodosum nodules have ill-defined

borders.

Erythema nodosum can be accompanied by

edema.

Although the legs are the typical location,

erythema nodosum lesions can occur with varying
shapes on the arms, head, neck, and torso.
87  Erythema nodosum
DDx Ref  24 • 50 • 97
DESCRIPTION
Panniculitis characterized by tender pink nodules on
extensor surface of lower legs.
HISTORY
• In adults, five to six times more common in women,
with a peak onset at 20–30 years. In children, boys
and girls affected equally. Caused by a hypersensitiv-
ity reaction to various antigenic stimuli: bacteria,
viruses, fungi, parasites, drugs, malignancies, con-
nective tissue diseases. Streptococcal infections and
sarcoidosis commonly associated with erythema
nodosum. Half of cases are idiopathic. • Can be
associated with fever, malaise, diarrhea, headache,
conjunctivitis, cough. New crops of lesions usually
develop for 3–6 weeks, although rarely erythema
nodosum persists for months to years.
PHYSICAL FINDINGS
• Pink to dusky-red firm nodules with indistinct
edges occur symmetrically on the pretibial surfaces.
• Ankle and leg pain are common. Erythema
nodosum occurs on head, neck, torso, arms, thighs.
• Fades in 1–2 weeks without scars.
TREATMENT
• Associated diseases and infections should be
identified and treated. • Discontinue precipitating
medications. Symptomatic treatment with rest,
compressive bandages, and non-steroidal anti-
inflammatory drugs (indometacin, Naprosyn).
• Supersaturated potassium iodide and systemic
corticosteroids have been helpful for chronic recur-
rent erythema nodosum.
Cutaneous small vessel vasculitis
(hypersensitivity vasculitis)
DDx Ref  24 • 85 • 86
88 

The pretibial surfaces are often affected in

hypersensitivity vasculitis.

Lesions occur in crops. Early lesions may be

nonpalpable, late lesions are palpable and may
ulcerate.

Lower extremities become edematous and

papules coalesce in patients with severe
hypersensitivity vasculitis.

The dorsal aspect of the toe is a common location

to find hypersensitivity vasculitis.
88  Cutaneous small vessel vasculitis
(hypersensitivity vasculitis)
DDx Ref  24 • 85 • 86
DESCRIPTION
Group of disorders characterized by inflammation of
small blood vessels in the skin, primarily postcapil-
lary venules. The principle skin lesion is palpable
purpura.
HISTORY
• Precipitated by many infectious agents, drugs,
chemicals, and food allergens; associated with many
chronic connective tissue diseases and malignan-
cies. • In 60% of patients, no precipitating agent or
coexistent disease is identified. • Caused by deposi-
tion of IgG or IgM immune complexes in small post-
capillary venules, resulting in leukocytoclastic
vasculitis. • Commonly associated with arthralgias,
myalgias, fever, and malaise. Multiple organs can be
involved. • Most patients improve in 1 month, but
condition may be chronic in some.
PHYSICAL FINDINGS
• Early lesions are asymptomatic purpuric macules.
Older lesions coalesce and become edematous and
palpable, ranging in size from pinpoint to several
centimeters. • Purpuric papules, nodules, pustules,
vesicles, bullae, and ulcerations can occur. • Lesions
are more prominent on any dependent area or an
area under local pressure (e.g. the back and arms of
supine patients). They are uncommon on face,
palms, and soles. • Lesions can be itchy and painful,
and occur in crops. • Patients frequently develop
ankle and lower leg edema.
TREATMENT
• Removal of precipitating agents and appropriate
treatment of coexistent disease usually results in
resolution. • Local measures using topical steroids
and antibiotics help some patients. • Antihistamines
and non-steroidal anti-inflammatory drugs control
fever, myalgias, and arthralgias. • Systemic cortico­
steroids (prednisone 60–80 mg q.d.) are helpful for
managing systemic manifestations and skin ulcera-
tion. Rebound can be prevented with a slow taper
over 3–6 weeks. • Immunosuppressive agents
(cyclophosphamide, methotrexate, azathioprine,
ciclosporin) have been used when systemic cortico­
steroids fail.
Henoch–Schönlein purpura
DDx Ref  24 • 88 • 90
89 

Pinhead-sized to 2-cm purpuric papules

classically appear on the buttocks and lower
extremities. Edema of the hands and feet can be
prominent.

Skin lesions begin as symmetric pink papules that

evolve into purpuric papules; palpable purpura is
the classic cutaneous lesion of leukocytoclastic
vasculitis.

Although less commonly affected than children,

adults can develop Henoch–Schönlein purpura.

The buttock and lower extremities are classic

locations for purpuric papules seen with
small-vessel vasculitis. From Bolognia JL, Jorizzo JL,
Rapini RP, eds. Dermatology. London: Mosby; 2003.
89  Henoch–Schönlein purpura
DDx Ref  24 • 88 • 90
DESCRIPTION
An IgA immune complex small-vessel vasculitis
resulting in palpable purpura, joint pain, abdominal
pain, and glomerulonephritis.
HISTORY
• Ninety percent of affected individuals are younger
than 10 years old; boys 4–8 years old are at highest
risk. • Peak incidence during winter months; com-
monly follows an acute respiratory illness by 1–2
weeks, suggesting that infection is an important ini-
tiating factor. • Up to 2 weeks before purpura onset;
40% develop low-grade fever, headache, arthralgias,
and abdominal pain. • Most commonly affected
extracutaneous organs: joints (80%), gastrointestinal
tract (70%), kidney (45%). Scrotal pain can occur
before the purpura, mimicking testicular torsion.
• Self-limited in most, lasting less than 1 month.
Long-term prognosis determined by severity of renal
involvement.
PHYSICAL FINDINGS
• Symmetric pink to red macules quickly evolve into
purpuric papules ranging from pinhead-sized to
2 cm. • Buttocks and lower extremities are com-
monly involved sites. • Lesions occur in crops and
fade within 2 weeks. • Edema of hands and feet can
be prominent. • Children younger than 3 years old
develop striking edema around eyes, scalp, and ears.
TREATMENT
• Manage arthralgias with non-steroidal anti-
inflammatory drugs. Systemic corticosteroids and
immunosuppressive agents for severe renal and
gastrointestinal complications.
 Schamberg disease
(Schamberg purpura)
DDx Ref  18 • 84 • 88
90 

Distinct, orange-brown patches with numerous

petechiae are referred to as cayenne pepper
spots.

Irregularly shaped asymptomatic cayenne pepper

spots commonly on the lower extremities.

Schamberg disease is a lymphocytic capillaritis

resulting in petechiae and residual orange-brown
pigmentation.

New petechiae are pin-point and bright red.

90  Schamberg disease
(Schamberg purpura)
DDx Ref  18 • 84 • 88
DESCRIPTION
A lymphocytic capillaritis resulting in progressive
pigmented purpura, occurring most commonly on the
lower extremities.
HISTORY
• Lesions slowly evolve on the distal lower extremi-
ties and progress proximally. • In adults, men are
more commonly affected. In children, girls are more
commonly affected. • The lymphocytic capillaritis
suggests that this is a cell-mediated hypersensitivity.
• Schamberg disease is a chronic condition without
internal disease. • The vast majority of patients
improve with time.
PHYSICAL FINDINGS
• Patients develop multiple, distinct, orange-brown,
pinhead-sized ‘cayenne pepper’ macules with
numerous petechiae. Lesions occur symmetrically on
lower extremities and sometimes on upper body.
New petechiae are bright red, becoming violaceous
with age and leaving brown dots of hemosiderin pig-
mentation. • Schamberg disease can be asymmetric,
especially when seen in adolescence. • May be a
slight amount of erythema, scale, and itching.
TREATMENT
• Pigmentation can be covered with cosmetic creams
such as Dermablend. • No consistently effective
therapies, although the following have been admin-
istered: group V topical steroids, pentoxifylline
(Trental) 300 mg q.d. for 8 weeks, rutoside (oral bio-
flavonoid) 50 mg b.i.d. and ascorbic acid 500 mg
b.i.d. for 4 weeks.
 Sweet syndrome
DDx Ref  84 • 85 • 165
91 

Plum-colored plaques are sharply demarcated and

give a pseudovesicular appearance.

Plaques can ulcerate and be very painful.

Tender plaques that sometimes blister can occur

on any skin surface but are more common on the
head, neck, and extremities; the torso can be
involved in widespread cases.

Multiple red edematous sharply demarcated

plaques on the lower extremities.
91  Sweet syndrome
DDx Ref  84 • 85 • 165
DESCRIPTION
An acute inflammatory eruption characterized by
multiple pink to red tender plaques, associated with
fever, malaise, and leukocytosis.
HISTORY
• Occurs in adults of all ages (mean age 56 years);
uncommon in children. • Often preceded by an upper
respiratory infection. • In 15–20%, Sweet syndrome
is paraneoplastic (hematologic malignancy, solid
tumors) and may precede the malignancy by up to
6 years. Paraneoplastic Sweet syndrome affects
mucous membranes, tends to be recurrent, and
occurs more commonly in males. • Other associated
conditions include streptococcal infection, inflamma-
tory bowel disease, autoimmune disorders (Hashi-
moto thyroiditis, Sjögren syndrome), myelodysplastic
syndrome, and acute myelomonocytic leukemia.
Sweet syndrome has been associated with preg-
nancy. Systemic symptoms include fever higher than
38°C (50%), malaise, arthralgias or arthritis (62%),
eye involvement (conjunctivitis, episcleritis, iridocy-
clitis) (33%), and oral aphthae (13%). • Can be self-
limiting in some patients. A minority of patients (15%)
develop relapses for several years.
PHYSICAL FINDINGS
Erythematous, edematous, ‘juicy’ (pseudovesicular),
plum-colored papules and plaques erupt acutely, can
be painful, and favor the head, neck, legs, arms,
dorsal hands, and fingers.
TREATMENT
• Systemic corticosteroids (prednisone 0.5–1.5 mg/
kg q.d.) produce rapid improvement and can be
tapered over 2–6 weeks. • Minocycline 100 mg
b.i.d., or doxycycline 100 mg b.i.d., may be effective.
• Oral potassium iodide 15 mg/kg q.d. inhibits neu-
trophil chemotaxis and equals systemic corticoster-
oids in effectiveness. • Other therapies include
colchicine, dapsone, clofazimine, non-steroidal anti-
inflammatory agents, and ciclosporin.
 DDx Ref  20 • 48 • 156
Scabies
92 

Sarcoptes scabiei mite in a potassium hydroxide

wet mount (× 40). Even when scabies mites are
present in the skin, it can be difficult to get a
positive scabies prep.

Linear vesicle and burrows remain discrete, are

characteristic and differentiate scabies from other
vesicular diseases such as poison ivy.

Scabies mites like web spaces of the hands, feet

and genital areas, causing red inflamed
eczematous patches and burrows.

Secondary lesions, papules and nodules, may

occur on the scrotum, penis, groin, axillae and
buttocks. Mites may be absent from the lesions
but pruritus persists, causing scratching and
erosion of nodules.
92  Scabies
DDx Ref  20 • 48 • 158
DESCRIPTION
Intensely pruritic contagious human infestation
caused by Sarcoptes scabiei var. hominis mite.
HISTORY
• Patients complain of unremitting itching (worst itch
ever), cannot stop scratching. • Uncommon for
scabies to present in just one family member. Other
members, especially bed partners, also sympto-
matic. • Nodular lesions take longest to heal.
• Crusted scabies (thousands of mites) may be
source of epidemic scabies, may be seen in institu-
tionalized and nursing home patients. • Persistent
itching after adequate treatment due to a prolonged
allergic response, presence of residual fecal matter
and mite parts.
PHYSICAL FINDINGS
• Linear burrow is classic lesion. Burrow can be
curved or S-shaped, slightly elevated. Inflamed vesi-
cles and papules, 1–2 mm in size, also common
features. May also present with scattered inflamed
pustules, papules, and even larger nodules. • Indi-
vidual lesions may be excoriated. • Typical locations
are wrists, web spaces of hands, sides of hands and
feet, genital area, warm intertriginous regions,
abdomen. Scalp, palms, soles affected more often in
infants. Secondary lesions (most common) have
eczematous reaction pattern or secondary impetigo.
Unique, advanced clinical variant is crusted
(Norwegian) scabies. Patients—usually those with
dementia, Down syndrome, immunosuppression—
experience thick crusting and eczematous dermatitis,
especially on hands, feet. Burrows most likely found
in finger webs, wrists, sides of hands and feet, penis,
buttocks, scrotum, and palms and soles of infants.
• Can be misdiagnosed as insect bites, eczema,
impetigo. • Mites, eggs, feces can be identified in a
scabies preparation.
TREATMENT
• Apply permethrin (Elimite, Acticin) or lindane
(Kwell) to entire skin surface from neck down, includ-
ing under fingernails and toenails, and in umbilicus.
Wash off in 8–12 h. • Head and neck uncommonly
affected, but if lesions need treatment, take care to
avoid eyes, mouth. Wash all clothes, bedclothes at
time of application. House fumigation, extermination
unnecessary. • Single dose of oral ivermectin
(Stromectol, 6-mg scored tablet) (200 µg/kg) also
safe and effective for most patients. Repeating dose
2 weeks later may provide higher cure rate. • Topical
steroids may be used to control pruritus and inflam-
mation after treatment with scabicide. Can treat
persistent nodular lesions with intralesional steroids.
• Can treat secondary bacterial infections with
appropriate antibiotics. • Even adequately treated
scabies may continue to itch for days to weeks after
treatment, and does not need to be retreated in all
cases.vn
 Head lice (pediculosis)
DDx Ref  40 • 46 • 48
93 

Three kinds of lice with similar characteristics infest

humans. Body lice are largest. They are wingless
insects with three pairs of legs. Legs terminate in
sharp claws adapted for feeding and grasping.

Infestations of the eyelash are seen almost

exclusively in children. It may induce blepharitis
with lid pruritus, scaling, crusting, and purulent
discharge.

Head lice are most often found in the occipital

areas. Nits are deposited on the shaft 1 cm above
the scalp surface. Excoriated lesions may become
crusted and infected.

Nits are lice eggs that appear as white, firmly

attached bumps.
93  Head lice (pediculosis)
DDx Ref  40 • 46 • 48
DESCRIPTION
Infestation of hair of scalp, body, pubic region by
flattened, wingless lice insects. Variation in distance
between hair shafts by region corresponds to type of
lice infection. Pediculus humanus var. capitis causes
head lice. Infestation by Pediculosis corporis, also
called body lice. Infestation by Phthirus pubis: pubic
lice. Lice attach to skin, feed on human blood. Lay
eggs (nits) that attach to hair shaft about 1 cm above
scalp, hatch in 8–10 days. Head lice is highly conta-
gious. Direct contact is primary source of transmis-
sion. Head lice more common in children. Obligate
human parasites; cannot survive on other animals or
furniture. Does not carry any known human disease
but can transmit epidemic typhus and relapsing
fever. Feed on blood every 3–6 h. Females lay 7–10
eggs a day, live for about 1 month.
HISTORY
• Typically diagnosed by schoolteacher or school
nurse. • Fomite transmission via hats, brushes, ear-
phones is common. • Symptoms range from itching
of the neck to no symptoms. Posterior cervical aden-
opathy occasionally noted. • Infestation rare in
African-Americans. • Infestation of eyelashes seen
almost exclusively in children.
PHYSICAL FINDINGS
• Nits are small white eggs firmly cemented to the
hair. Nits are easier to visualize than lice. Head lice
can be seen on the hair shafts and scalp. • Diagnosis
usually not difficult but may require repeated exami-
nations. • Head lice have an elongated body similar
to body louse but smaller. • Secondary impetigo may
present with yellow or honey-colored crusting with
cervical adenopathy. • Lice may induce blepharitis
with lid pruritus, scaling, crusting, purulent
discharge.
TREATMENT
Standard topical treatment
• Permethrin rinse 1% (over-the-counter) often first-
choice drug. Permethrin 5% (Elimite) administered
for treatment failures. Leave on hair overnight
under shower cap. • Lindane (Kwell) shampoo is
alternative. Lindane-resistant lice have emerged.
• Malathion lotion 0.5% (Ovide) rapidly pediculicidal
and ovidicidal, and for resistance to other treatments.
• Repeat all above treatments in 1 week, because
younger lice may not be eradicated. A special nit
comb also helpful in the week following treatment.
• Treatment of all close family members controver-
sial but often recommended.
Alternative therapies
• Petrolatum (Vaseline), mayonnaise, or pomades
applied to scalp overnight under a shower cap
smother lice. • As last resort, shaving scalp can be
curative.
Oral treatments
• Ivermectin 200 mg/kg prescribed in a single oral
dose and repeated in 10 days. Causes paralysis and
death of the parasite. • It has selective activity
against parasites but no systemic effects on
mammals.
 Bee and wasp stings
DDx Ref  24 • 46 • 47
94 

Bee sting. Red to pink edematous hive-like

plaque. Honey bees are the most common source
of insect stings and can cause severe allergic
reactions.

A large urticarial plaque began to occur minutes

after the sting. The spot in the center is the sting
site. This lesion was treated with an ice-cold wet
compress to decrease swelling.

Severe local reaction to a sting with necrosis and

ulcerations at the site of the bee sting. Necrosis is
unusual. In this case, it is difficult to tell what
type of insect caused the sting.

Edematous reaction to stings across the backs of

the legs. Will last a few days before clearing up.
Pruritus or tenderness is characteristic.
94  Bee and wasp stings
DDx Ref  24 • 46 • 47
DESCRIPTION
Honey bees are the most common source of insect
stings; can cause severe allergic reactions. Honey
bee stinger separates from abdomen when stinging,
remains embedded in vertebrate tissue. Stingers of
other bees and wasps do not detach. Detached
stinger is useful diagnostic feature for distinguishing
honey bee stings.
HISTORY
• Initial sharp or painful sting lasts a few minutes,
followed by moderate burning. Symptoms resolve in
a few days. • Most reactions in children are mild.
Children with deeper dermal reactions still have a
benign course and are unlikely to have recurrent
reactions. Severe reactions more common in adults.
• Localized or systemic allergic reaction may
develop. Patients sensitized by prior stings may
develop large, local reactions, with edematous swell-
ing forming hours after the sting and resolving in a
few days. • Edema more prominent with head and
neck stings. Toxic systemic reaction may develop
hours after the sting. Vomiting, diarrhea, headache,
fever, muscle spasm, loss of consciousness can
occur. • Allergic anaphylactic reactions occur within
minutes to hours after sting; involve itching, hives,
shortness of breath, wheezing, nausea, abdominal
cramps. Most fatal bee and wasp stings occur in
hypersensitive persons older than 40 years who have
received a single sting on head or neck. Death
caused by respiratory dysfunction or anaphylaxis.
Multiple stings can kill non-allergic people. Estimated
median lethal dose of bee venom: 500–1500 stings.
PHYSICAL FINDINGS
• A hive or raised pink weal with a central pinpoint
red punctum appears minutes after the sting and
lasts for about 20 min. Angioedema may occur in the
area, which is a localized reaction that appears thick,
hard, and edematous over an area as large as 10–
50 cm. • Main differential diagnostic concerns are
bites from other insects.
TREATMENT
• Remove the stinger as fast as possible. The degree
of envenomation does not differ if the stinger is
scraped or pinched off. Delays of a few seconds in
removing the stinger lead to greater venom delivery.
• Localized non-allergic reactions are treated with
ice and cool compresses; allergic reactions may also
require antihistamines. • Treat severe generalized
reactions with aqueous adrenaline (epinephrine)
1 : 1000 (0.3–0.5 mL s.c.), repeated at 20-min inter-
vals if needed. If patient is hypotensive, an i.v.
1 : 10 000 dilution of adrenaline can be administered.
Preloaded adrenaline syringe kits (e.g. EpiPen Auto-
Injector, Anakit) are available. Can administer
antihistamine (e.g. Benadryl) 25–50 mg orally or
intramuscularly. • Venom immunotherapy highly
effective for those with systemic reactions.
 Lyme disease
DDx Ref  47 • 77 • 94
95 

Large 5-cm targetoid patch with central clearing,

bright-red expanding border and central bite
inflammation, characteristic of the erythema
migrans rash of Lyme disease.

Erythema migrans. ‘Bull’s-eye’ lesion. Bright-red

or pink expanding circulate patch with central
clearing. Bite mark is usually centrally located.

Multiple inflamed expanding erythematous

patches, with central bluish hue characteristic of
disseminated Lyme disease.

Embedded engorged tick.

95  Lyme disease
DDx Ref  47 • 77 • 94
DESCRIPTION
Tick-borne disease caused by spirochete Borrelia
burgdorferi. Has three stages. Can affect multiple
organ system. Cutaneous eruption called erythema
migrans. In Europe, other species of Borrelia also
cause Lyme like-disease. The ‘black-legged’ tick or
Ixodes species (I. scapularis and I. pacificus) are
the ticks responsible for transmitting Lyme disease
in the USA.
HISTORY
Like syphilis, Lyme disease affects many organs,
occurs in stages, and mimics other diseases. Disease
onset is 3–28 days after infective tick bite. Stages may
overlap or occur alone. • Stage 1: expanding target-
like patch (erythema migrans) and influenza-like
symptoms, including fever, headache, arthralgias.
• Stage 2: cardiac, neurologic symptoms. • Stage 3:
arthritis present, neurologic problems persist.
PHYSICAL FINDINGS
• Initial tick bite causes local inflamed bite reaction.
Bite may be painless. Tick must stay attached for at
least 24 h for infection to occur. • Skin changes,
erythema migrans the most characteristic, not
present in all cases. • Erythema migrans is a bright-
red, edematous, expanding eruption at site of inocu-
lation. Begins as small papule or patch with enlarging
ring if erythema. Central erythema gradually fades,
leaving a flesh-colored to light blue surface, rarely
vesicular. Erythematous patch remains flat, blanches
with pressure. May reach up to >10 cm in diameter.
Expanding border of erythema migrans may be
slightly raised. Many patients (20–50%) have multi-
ple concentric rings at sites of subsequent hematog-
enous dissemination. Erythema migrans lesions
usually fade within 3–4 weeks, even if untreated.
• Results of serologic testing for anti-Borrelia anti-
bodies by enzyme-linked immunosorbent assay
(ELISA) are positive at initial presentation in 25% of
infected patients, and positive in 75% of them 4–6
weeks later, even with antibiotic therapy. More spe-
cific Western immunoblot test used to corroborate
equivocal or positive results obtained with ELISA.
TREATMENT
• Preventing tick bites is first line of defense. Wear
protective garments, tuck pants into socks, wear
closed-toed shoes. DEET can be used on skin, or
permethrin (Permanone) on clothing. • Check to
detect ticks after hiking or yard work and remove ticks
as soon as possible. • Adults with early Lyme disease
should receive 21 days of treatment with doxycycline
(100 mg b.i.d.), amoxicillin (500 mg t.i.d.), or cefuro-
xime axetil (Ceftin) (500 mg b.i.d.). Amoxicillin (25–
50 mg/kg t.i.d.) or cefuroxime axetil (250 mg b.i.d.)
used for children under 8 years old. • Disease that has
progressed to stage 2 or 3 requires more intensive
treatment. IV ceftriaxone 2 g q.d. for 14 days for
advanced Lyme meningitis and neurologic disease.
• The prophylactic antibiotic treatment of tick bites is
common but controversial. A single dose of doxycy-
cline 200 mg, has been advocated by some. In most
circumstances, treating a person for tick bite alone is
not recommended.
 Rocky Mountain
spotted fever
DDx Ref  84 • 88 • 89
96 

A generalized petechial eruption that involves the

entire cutaneous surface, including the palms and
the soles but characteristically appears first on
the wrist and ankles.

Pinpoint palmar purpura of Rocky Mountain

spotted fever.

Rocky Mountain spotted fever is caused by an

obligate intracellular coccobacillus R. rickettsi. It
is transmitted by the bite of an infected
Dermacentor or Ixodes tick.

Rocky Mountain spotted fever presentation with

pink to red inflamed macules on the wrists, dorsal
hands and fingers, with early mild petechiae.
96  Rocky Mountain
spotted fever
DDx Ref  84 • 88 • 89
DESCRIPTION
Rocky Mountain spotted fever is a potentially lethal
disease caused by Rickettsia rickettsii, a short,
Gram-negative bacillary organism. Infection charac-
terized by acute onset of fever, severe headache,
myalgia, vomiting, and petechial rash. Transmitted
by ticks, usually Dermacentor and Ixodes species.
Organisms disseminate via the bloodstream and
multiply in vascular endothelial cells. Condition
occurs most commonly in the eastern USA and Brazil
in summer and early autumn.
HISTORY
• Tick bites are typically painless, so patient may not
recall a recent tick bite. • Travel to an endemic area
and recent outdoor activity are helpful clues. Incuba-
tion period on average 6–8 days after bite. An abrupt
onset of fever (95%), severe headache (90%),
myalgia (85%), and vomiting (60%) occur.
PHYSICAL FINDINGS
• Skin findings evolve and appear a few days after
fever. Signs of previous tick bite may not be found.
Rash is discrete and macular, blanches with pres-
sure, and becomes petechial in 2–4 days. It appears
first on the wrists and ankles, which is very charac-
teristic. Hours later, it involves the palms and soles
(75%), then becomes generalized. Rash does not
occur at all in about 15% of cases. • Multiple organs
are involved in severe disease. Hepatosplenomegaly
is present in 25–50%. Neurologic symptoms include
seizures, meningitis, cranial nerve palsies. Respira-
tory distress, gastrointestinal bleeding, myocarditis,
and retinal thrombosis rare but reported. • Fever
subsides in 2–3 weeks, and rash fades with residual
hyperpigmentation. Mortality rate in treated patients
is 4%, and 20% in untreated patients. Many of those
who die have a fulminant course and are dead in 1
week. • Indirect fluorescent antibody tests on acute
and convalescent sera fairly accurate, can confirm
diagnosis. • Systemic vasculitis and meningococ-
cemia are the two other major diagnostic considera-
tions in patients with Rocky Mountain spotted fever.
• Serologic evidence appears in second week of
infection. A titer greater than 1 : 128 is positive. The
leukocyte count can be high, low, or normal; throm-
bocytopenia, elevated serum hepatic aminotrans-
ferase level, and hyponatremia are common.
TREATMENT
• Start empiric treatment if Rocky Mountain spotted
fever suspected. Doxycycline 100 mg b.i.d. for at
least 7 days and at least 48 h after resolution of fever
is current treatment of choice. • Chloramphenicol
50 mg/kg q.d. is an alternative.
 Flea bites
DDx Ref  24 • 46 • 48
97 

Flea bites occur in a cluster or group, and appear

as small purpuric macules. They typically occur
on the lower legs. Fleas jump but cannot reach
higher than above the calf.

Some people are very sensitive to flea bites,

which result in large wheals or hive-like plaques.
This is referred to as papular urticaria.

A child’s flea bites were excoriated and became

infected. These lesions will heal with scars.

Fleas are tiny, red-brown, hard-bodied, wingless

insects that are capable of jumping approximately
60 cm. They live in rugs and on the bodies of
animals.
97  Flea bites
DDx Ref  24 • 46 • 48
DESCRIPTION AND HISTORY
The flea itself is a small, red-brown, hard-bodied,
wingless insect. It is flattened laterally so that it can
squeeze between hairs of hosts. Flea bites present
as pruritic macular or papular eruption on the legs,
and is self-limited. Depending on the patient’s sen-
sitivity, it may subside in days to weeks. The flea
eggs can lie dormant for over a year and can reacti-
vate because of the vibrations from footsteps. Pants
and socks may offer some protection.
PHYSICAL FINDINGS
• Initially, tiny red dots or bite puncta may be seen
in clusters or groups around the calves and ankles.
• Red to purpuric, raised urticarial lesions known as
papular urticaria develop in hypersensitive patients,
especially children. Pruritus can be intense in hyper-
sensitive patients. The persistent scratching can lead
to round, white scars after healing. • Diagnosis is
usually not difficult.
TREATMENT
• Bites are treated symptomatically. Topical anti-
pruritics such as Sarna lotion can help. • Infected
lesions require antibiotics. This is uncommon. • Mild
to moderately potent topical steroids are useful for
treating papular urticaria. • Fleas must be eradi-
cated. The infested animal, its bedding and rugs
must be treated.
 Cutaneous larva migrans
DDx Ref  11 • 46 • 75
98 

Each day, the trapped larva struggles a few

millimeters to a few centimeters laterally through
the epidermis, creating a serpiginous tract.

The 1-cm larva stays concealed ahead of the

advancing tip. Any skin surface can be affected
but the toes and soles of the feet are most
commonly affected.

During larval migration, the release of larval

secretions provokes a local inflammatory response.
Itching is moderate to intense. Secondary infection
or eczematous inflammation occurs.

Many larvae are present in the same area,

creating several closely approximated wavy lines.
98  Cutaneous larva migrans
DDx Ref  11 • 46 • 75
DESCRIPTION
Cutaneous larva migrans (creeping eruption) is a
migratory, hookworm larvae infectious condition
most often seen on feet. Ancylostoma braziliense is
the most common species in North America.
HISTORY
• Lesions typically begin about 3 weeks after beach
vacation in the Caribbean, Africa, South America,
South-East Asia, even southeastern USA. • Infection
can also occur in children who play in sandboxes,
carpenters and plumbers who work under houses.
• Larvae are indiscriminate; parasite can penetrate
skin when humans walk on moist, feces-contami-
nated sand. • If untreated, larvae die in 2–8 weeks,
but can persist up to a year. Larvae eventually
sloughed away as epidermis matures. • Typically,
resolution of migration and itching occurs within 2–3
days of therapy. May take a week or so for the more
intense allergic inflammatory response to resolve.
PHYSICAL FINDINGS
• Local pruritic, inflammatory eruption to the larval
secretions occurs within 3 weeks of infection. Larvae
cause the classic evolution into a serpiginous, red to
purple lesion with a 3-mm-wide tract. • Feet and
ankles most commonly involved, followed by but-
tocks, genitals, hands. • Itching moderate to intense;
sometimes secondary infection and eczematous
inflammation can occur. • Worm migrates about
2 cm daily. • Up to 30% blood eosinophil count has
been reported. • Chest X-ray may show patchy
infiltration.
TREATMENT
• Freezing the leading edge of the lesion with liquid
nitrogen is often ineffective. • Ivermectin 200 µg/kg
(average dose 12 mg) administered as a single oral
dose is effective. Lesions heal within 5 days of start-
ing ivermectin. A second round of treatment with the
same dose is given for relapses. • Albendazole,
either 400 mg q.d. or 200 mg b.i.d. orally for 7 days,
is effective and well tolerated. Its action is rapid;
pruritus disappears in 3–5 days and cutaneous
lesions disappear after 6–7 days of treatment.
• Thiabendazole 15% in a liquid or cream compound
is applied topically three times a day for 5 days. It is
applied to affected areas and 2 cm beyond the
leading edge, because the parasite is often located
beyond the clinical lesion. The preparation is often
difficult to obtain. • Antibiotics used for secondary
infection. • Topical or systemic steroids may be
needed to treat severe pruritus. Typically, resolution
of migration and itching occurs 2–3 days after
therapy has begun. It may take a week or so for the
more intense allergic inflammatory response to
resolve.
 Dermatitis herpetiformis
DDx Ref  48 • 85 • 102
99 

Vesicles appear singly or in clusters and resemble

herpes simplex. Patients scratch lesions, making
it difficult to find an intact lesion to biopsy.

Vesicles are symmetrically distributed and appear

on elbows, knees, occipital scalp, shoulders, and
buttocks.

‘Herpetiform’ refers to the typical grouping of

vesicles.

Skin biopsy shows subepidermal clefting and

papillary dermal tips stuffed with neutrophils and
occasional eosinophils in the upper dermis.
99  Dermatitis herpetiformis
DDx Ref  48 • 85 • 102
DESCRIPTION
A rare, chronic, intense and unremitting itching and
burning, vesicular and bullous dermatosis associated
with a gluten-sensitive enteropathy.
HISTORY
• Age of onset usually between the second and fifth
decades. • Rare in children. • Prevalence 11–39 per
100 000. • Affects males twice as often as females.
• Rare in black and Asian people. • Increased inci-
dence in association with human leukocyte antigens
DRw3, B8, and DQw2.
PHYSICAL FINDINGS
• Clustered vesicles and/or excoriations, erythema-
tous or urticarial papules, symmetrically localized to
the elbows, knees, sacrum, and occipital scalp. Less
often generalized. Oral lesions rare. • Gastrointesti-
nal involvement usually asymptomatic. Severity of
skin disease does not correlate with degree of intes-
tinal involvement. Small bowel biopsy shows villous
atrophy. Increased risk of small bowel lymphoma and
non-intestinal lymphoma. Risk is reduced with
gluten-free diet though 100% dietary compliance is
difficult to maintain. • Skin biopsy with immunofluo-
rescence recommended for all blistering diseases;
shows inflammatory infiltrate of neutrophils and
occasional eosinophils in upper dermis. • Direct
immunofluorescence of skin biopsy from adjacent
normal perilesional skin shows granular or fibrillar
IgA deposits in dermal papillae in 90% of cases.
TREATMENT
• Dermatologists are trained well in bullous disorders
and the biopsy techniques and tests required for
accurate diagnosis. • The goal of therapy is to arrest
blister formation and relieve itching. • Oral dapsone
100–150 mg q.d. relieves itching and burning within
48–72 h; maintenance dose varies in the range of
25–200 mg q.d. Check glucose-6-phosphate dehy-
drogenase before starting dapsone. • A gluten-free
diet can control the disease alone or allow decreased
requirement for oral medication.
 Pemphigus vulgaris
DDx Ref  41 • 85 • 102
100 

Oral erosions usually precede appearance of skin

blisters by several weeks.

Flaccid blisters rupture easily because the roof

consists of only a thin portion of upper epidermis
and is very fragile. Healing is with brown
hyperpigmentation, but without scarring.

Skin biopsy shows intraepidermal bullae or

acantholysis (separation of the epidermal cells)
and mild to moderate infiltrate of eosinophils.

Mean age of onset is 60 years, and

intraepidermal blistering involving the skin and
mucous membranes is common.
100 Pemphigus
DDx Ref 
vulgaris
41 • 85 • 102

DESCRIPTION
Rare, potentially life-threatening, autoimmune,
intraepidermal blistering disease involving skin and
mucous membranes. Often presents with only oral
involvement.
HISTORY
• Mean age of onset 60 years; men and women
affected equally. • Incidence estimated at 0.5–3.2/
1 000 000; highest in people of Ashkenazi Jewish
descent. • Oral erosions usually precede onset of
skin blisters by weeks to months. • Most patients
describe skin tenderness or irritation.
PHYSICAL FINDINGS
• Bullae vary from 1–3 cm in diameter. Initially local-
ized but eventually become generalized if untreated.
Bullae rupture easily because the vesicle roof is very
fragile, consisting of a thin portion of upper epider-
mis. • Applying pressure to small intact bullae
causes the fluid to dissect laterally (Asboe–Hansen
sign). Traction pressure on intact skin causes bullae
formation (Nikolsky sign). • Erosions heal without
scarring. • Painful oral erosions occur in 50–70%
of patients and are typically the initial presentation.
• Skin biopsy with immunofluorescence recom-
mended for all blistering diseases. Shows an intraep-
idermal bullae or separation of epidermal cells and
an infiltrate of eosinophils. • Direct immunofluores-
cence performed on two biopsies: one from the
edge of a fresh lesion, a second from an adjacent
normal area showing IgG and often complement
C3 in the intercellular substance areas of the epider-
mis. • Indirect immunofluorescence confirms circu-
lating serum IgG antibodies in 80–90% of patients
with active disease. These antibodies are directed
against desmoglein-3, an intracellular keratinocyte
adhesion molecule. Level of antibody reflects disease
activity.
TREATMENT
• Consider dermatology referral for suspected cases,
as both diagnosis and management require specialist
training. • Prednisone with an immunosuppressive
adjuvant agent such as azathioprine or cyclophos-
phamide is standard treatment. Goal of treatment is
to arrest blister formation. Starting dosages of pred-
nisone typically vary between 40 and 120 mg q.d.,
and are subsequently tapered to establish a minimum
dose that controls most disease activity. • Cyclo-
phosphamide (1.5–2.5 mg/kg q.d.) or azathioprine
(1.0–2.5 mg/kg q.d.) is initiated with or after starting
corticosteroids. • A negative direct immunofluores-
cence finding is a good indicator of remission. • IVIG
should be used in patients with severe pemphigus
where conventional therapy is contraindicated or the
disease has been refractory to conventional forms of
treatment. Treatment with IVIG results in a gradual
decline in pemphigus autoantibodies.
 Pemphigus foliaceus
DDx Ref  40 • 46 • 100
101 

Pemphigus foliaceus is an autoimmune,

intraepidermal blistering disease characterized by
crusted patches and erosions.

Skin biopsy shows intraepidermal bullae or

acantholysis (separation of epidermal cells) in
upper epidermis and mild to moderate eosinophil
infiltration.

Disease begins gradually on the face in a

‘butterfly’ distribution, or first appears on scalp,
chest, or upper back as localized or broad areas of
erythema, scaling, crusting, or occasionally bullae.

Vesicle roof is so thin that it ruptures. Serum

leaks out and desiccates, forming localized or
broad areas of crust. Intact thin-walled blisters
are sometimes seen near the edge of erosions.
101 Pemphigus
DDx Ref 
foliaceus
40 • 46 • 100

DESCRIPTION
Autoimmune, superficial, intraepidermal blistering
disease characterized by crusted plaques and
erosions.
HISTORY
• Age of onset varies more widely than in pemphigus
vulgaris. • No racial prevalence. • Pain, burning
more often reported than itching. • Sun, heat may
worsen signs and symptoms. • May be localized
for years or progress rapidly and become general-
ized, evolving into an exfoliative erythroderma; may
be fatal if untreated. • Increased incidence of
thymoma, myasthenia gravis, other autoimmune
disease. • Fogo selvagem is Portuguese for ‘wild
fire.’ It is an endemic form of pemphigus foliaceus
found in certain rural areas of Brazil and Colombia.
• Pemphigus erythematosus (Senear–Usher syn-
drome) may be a combination of localized (face
and other seborrheic areas) pemphigus foliaceus
and systemic lupus erythematosus. Many of these
patients have a positive antinuclear antibody, but few
have any other signs or symptoms of systemic lupus.
• Pemphigus foliaceus has been reported in approxi-
mately 5% of patients taking D-penicillamine or cap-
topril. Most cases are mild and may resolve once the
drug is stopped.
PHYSICAL FINDINGS
• Early pemphigus foliaceus may resemble sebor-
rheic dermatitis or other papulosquamous diseases.
Lesions appear in a ‘seborrheic’ distribution on face,
scalp, chest, or upper back. • Disease begins as
localized or broad continuous areas of erythema,
scaling, crusting, or occasionally bullae. • Vesicle
roof so thin that it ruptures. Serum leaks out and
desiccates, forming localized or broad areas of crust.
Intact thin-walled blisters sometimes seen near the
edge of erosions. Intact blisters not usually seen
but are sometimes near the edge of the erosions.
• Upper portion of the epidermis can be dislodged
with lateral finger pressure. • Skin biopsy with
immunofluorescence recommended for all blistering
diseases. Shows an intraepidermal bullae or acan-
tholysis (separation of epidermal cells) in upper
epidermis and mild to moderate infiltration of eosi-
nophils. • Direct immunofluorescence performed on
two biopsies: one from the edge of a fresh lesion, the
second from an adjacent normal area. IgG and com-
plement C3 are found in the intercellular substance
areas of the epidermis. • Indirect immunofluores-
cence on serum confirms circulating IgG antibodies
in approximately 75% of patients with active disease.
Antibodies are directed against desmoglein-1, an
intracellular keratinocyte adhesion molecule. Level
of antibody reflects disease activity. Antibodies of
pemphigus vulgaris can be distinguished from those
of pemphigus foliaceus by testing on two tissue
substrates.
TREATMENT
• Early localized disease may be managed with
group I–III topical steroids. • Active widespread
disease is treated like pemphigus vulgaris. Sun pro-
tection may be helpful.
 Bullous pemphigoid
DDx Ref  24 • 84 • 85
102 

Pemphigoid begins with a localized area of

erythema or with pruritic urticarial plaques that
gradually become more edematous and extensive.

The eruption is often symmetric and generalized.

The plaques turn dark red or cyanotic in 1–3 weeks,
resembling erythema multiforme, as vesicles and
tense bullae rapidly appear on the surface.

Bullae rupture within 1 week, leaving an eroded

base that does not spread and that heals rapidly.

Skin biopsy shows subepidermal bullae with an

infiltrate of eosinophils within the dermis and
blister cavity.
102 Bullous
DDx Ref 
pemphigoid
24 • 84 • 85

DESCRIPTION
Uncommon, autoimmune, subepidermal blistering
disease primarily affecting elderly.
HISTORY
• Most patients over 60. • No racial, gender preva-
lence. • IgG autoantibodies directed against
hemidesmosomal proteins present. Trigger factor for
formation of autoreactive antibodies unknown. Furo-
semide, captopril, some non-steroidal anti-inflam-
matory drugs implicated. • Untreated bullous
pemphigoid may remain localized, undergo sponta-
neous remission, or may rapidly generalize. • Remis-
sion rate: 30% at 2 years, 50% at 3 years.
Recurrences may be less severe than initial episode.
• Mortality rate (1 year): 19%. Mortality risk from
treatment side effects in addition to comorbidities.
PHYSICAL FINDINGS
• Most often a generalized blistering eruption with
predilection for intertriginous, dependent areas.
Begins as itching and hive-like preblistering rash
with localized area of erythema or with pruritic urti-
carial papules coalescing into plaques. Plaques turn
deeper red in 1–3 weeks as vesicles and bullae
rapidly appear on their surface. Bullae tense. Firm
pressure on blister will not result in extension into
normal skin, as occurs in pemphigus. Bullae rupture
within 1 week, leaving eroded base that does not
spread but heals rapidly. • Peripheral blood eosi-
nophilia possible. • Skin biopsy with immunofluores-
cence recommended for all blistering diseases.
Shows subepidermal bullae with an infiltrate of eosi-
nophils and sometimes neutrophils within dermis and
blister cavity. • Direct immunofluorescence of skin
sampled next to a blister confirms IgG and/or com-
plement C3 in a linear band at the basement mem-
brane zone in about 90% of cases. • Indirect
immunofluorescence demonstrates circulating
autoantibodies in sera of approximately 70% of
patients. Titers do not correlate well with disease
activity, unlike in pemphigus.
TREATMENT
• Team approach with dermatologist, primary care
provider, visiting nurse care if required. Goal of treat-
ment is to arrest blistering, decrease itching, protect
skin, limit secondary infection. • Prednisone proba-
bly treatment of choice (1.0–1.5 mg/kg q.d.) until
blistering ceases. Most cases controlled in 28 days;
can gradually taper dosage to 0.5 mg/kg q.d. (3
months), 0.2 mg/kg q.d. (6 months). • Forty percent
of patients respond to dapsone (100 mg q.d.) alone.
Addition of dapsone may help produce remission.
• Consider adjuvant immunosuppressive therapy
with cyclophosphamide or azathioprine if dapsone,
prednisone fail. • May control limited disease with
group I topical steroids. Apply twice daily until
lesions healed, and 2 weeks thereafter. • Steroid-
sparing agents include tetracycline 1.0–2.5 g q.d.,
minocycline 200 mg q.d., niacinamide 1.5–2.5 g
q.d.. • Control itching with hydroxyzine 10–50 mg
every 4 h as needed. Causes sedation. Use with
caution in elderly. • Bedridden patients benefit
from air mattress support, other skin-protective
measures.
 Chronic cutaneous lupus
DDx Ref  34 • 37 • 43
103 

The scarred plaques of chronic cutaneous lupus

have peripheral hyperpigmentation and central
violaceous pink scarring. The lip is also involved.

Typical lesion of cutaneous lupus, showing central

hypopigmented scarring and a peripheral rim of
pink scaling papules. This might be confused for
a skin cancer or actinic keratosis.

Scaling pink plaques, some with peripheral

hyperpigmentation, scattered in a sun-exposed
distribution on the face.

Lupus in the scalp, demonstrating alopecia. This

lesion shows erythema, follicular prominence, and
erosion. Discoid lesions in the scalp are a cause
of scarring alopecia.
103 Chronic
DDx Ref 
cutaneous lupus
34 • 37 • 43

DESCRIPTION
Most common form of cutaneous lupus erythemato-
sus. Lesions may be localized or widespread, and
consist of scaling erythematous papules and plaques,
often with central atrophy and scarring. Chronic cuta-
neous lupus lesions are not always discoid; this term
should no longer be used.
HISTORY
• Chronic lupus erythematosus more common in
women. • Perhaps more common in people with an
African-American background. • Peak incidence in
the fourth decade. • Trauma and ultraviolet light may
initiate and exacerbate lesions. • Photo sensitivity is
present in 50% of patients with discoid lupus ery-
thematosus. • Lower incidence of systemic disease;
1–5% of cases progress to systemic lupus erythema-
tosus. Patients with non-localized, widespread
disease are at greater risk of advancing to systemic
disease. • Scarring alopecia is permanent.
PHYSICAL FINDINGS
• Lesions may occur on any body surface, but scalp,
face, and ears are most common areas. • Begins
asymptomatically; there are well-defined, elevated,
red to violaceous, 1- to 2-cm, flat-topped plaques
with firmly adherent scaling. • Follicular plugs are
prominent; peeling the scale reveals an undersurface
that looks like a carpet penetrated by several carpet
tacks. • Epidermal atrophy gives the surface either
a smooth white or a wrinkled appearance. • Lesions
may be hypertrophic or verrucous; they may involve
palms and soles or the oral mucosa. • Lesions
endure for months; they either resolve spontaneously
or progress with further atrophy, ultimately forming
smooth, white, or hyperpigmented depressed scars
with telangiectasia and scarring alopecia. • Scalp
disease begins with erythema, scaling, and follicular
plugging. Hair follicles are destroyed, resulting in
irreversible, scarring alopecia. Hair loss is haphazard
in distribution. • Skin biopsy is helpful in making this
diagnosis.
TREATMENT
• Treatment options include group I–III topical ster-
oids, intralesional steroids, antimalarials (e.g.
hydroxychloroquine 200 mg b.i.d.), dapsone, or oral
corticosteroids. • Reasonable to start with a twice-
daily application of a topical steroid and assess result
after 6 weeks. If this fails, hydroxychloroquine could
be considered. • Treatment options for difficult
cases are methotrexate, azathioprine, thalidomide, or
isotretinoin. • Sunscreens are an essential aspect of
therapy. A broad-spectrum, water-resistant sun-
screen should be applied daily. • Some patients may
respond to tacrolimus ointment (Protopic).
 Acute cutaneous
lupus erythematosus
DDx Ref  5 • 84 • 105
104 

Violaceous malar plaques are evident, also

involving the nose but sparing the nasolabial
folds.

Violaceous patches and erosions in a

photodistribution on the face—the characteristic
‘butterfly’ rash. Evaluation for systemic disease is
essential.

Violaceous papules of acute lupus, nearly

coalescing in a photodistribution of the upper
chest and extensor arms.

Acute cutaneous lupus affecting the hands. The

lesions are violaceous macules and patches
scattered on the palmar surface.
104 DDx Ref  Acute cutaneous
lupus erythematosus
5 • 84 • 105

DESCRIPTION
Serious multisystem disease associated with autoan­
tibody formation. May involve skin, joints, or hemat­
opoietic, pulmonary, renal, or central nervous
system.
HISTORY
• Women affected more often than men, in a ratio of
8 : 1. • Occurs most frequently in people aged 30–40
years. • Sunlight exacerbates acute cutaneous lupus
erythematosus and may induce it. • A multisystem
disease; may be fever, arthritis, renal, cardiac, pul­
monary, and central nervous system involvement.
• Assessing lupus erythematosus rashes and catego­
rizing the process as chronic cutaneous lupus, sub­
acute cutaneous lupus, or acute lupus is vital to
effective and appropriate treatment. It involves
careful attention to systemic symptoms, and hema­
tologic, renal, and serologic evaluation. • Constitu­
tional symptoms of fatigue, weight loss, fever, and
myalgias are more often present in patients with
systemic disease.
PHYSICAL FINDINGS
• Superficial and indurated, non-pruritic, erythema­
tous to violaceous plaques appear on sun-exposed
chest, shoulders, extensor arms, and backs of hands.
• May be fine scaling on the surface, and obvious
follicular plugging. • In 10–50% of patients, a ‘but­
terfly’ rash appears over malar area and nasal bridge.
• Atrophy does not occur. • Nail fold capillary micro­
scopy reveals tortuous, ‘meandering’ capillary loops.
• The patient may have excess vellus hair at the
frontal margin (lupus hair) or diffuse hair thinning.
• Alopecia (scarring and non-scarring) occurs in 20%
of cases. • Obtain biopsy of lesional skin for routine
study. • Underlying systemic lupus erythematosus is
screened for by using an antinuclear antibody titer,
a complete blood count, a serum chemistry profile,
and urinalysis. Antibodies to dsDNA are associated
with acute cutaneous lupus.
TREATMENT
• Sunscreens are an essential aspect of therapy. A
broad-spectrum, water-resistant sunscreen should
be applied daily. • Topical steroids, groups II–V, may
be used twice daily on affected skin. • Immunomod­
ulators such as tacrolimus ointment (Protopic) may
be tried b.i.d. • Hydroxychloroquine 200 mg b.i.d. is
a standard treatment for systemic and cutaneous
disease. Response to therapy is slow, over 2–3
months. • Other options for systemic disease include
prednisone, azathioprine, cyclophosphamide, myco­
phenolate mofetil.
 Dermatomyositis
DDx Ref  84 • 104 • 109
105 

Violaceous hue and telangiectasias along the lid

margin characterize the heliotrope of
dermatomyositis.

Flat-topped violaceous papules, Gottron’s papules,

are seen on the knuckles and proximal phalangeal
joints.

Gottron’s papules are flat-topped papules that

may occur along the lateral fingers. They are
pathognomonic for dermatomyositis.

In this patient with dermatomyositis, a faint

violaceous blush is seen along the extensor arms.
The knuckles also have a characteristic
violaceous hue.
105 Dermatomyositis
DDx Ref  84 • 104 • 109

DESCRIPTION
Acquired, idiopathic connective tissue disease char-
acterized by proximal muscle weakness and charac-
teristic violaceous skin rash prominent on eyelids,
scalp, metacarpophalangeal joints, and bony promi-
nences. Roughly 10% have skin findings without
evidence of muscle disease. Amyopathic dermato-
myositis is skin disease in absence of muscle disease
over 6 months; 2 years required to confirm this.
HISTORY
• Twice as common in females. • At least 15% of
cases occur in children. • May present with gradual
onset of typical skin findings, or with a proximal
muscle weakness. • Patients often have difficulty
combing hair, ascending stairs, or rising from a chair
without using arms. • Cutaneous lesions often
precede muscle involvement by 3–6 months.
PHYSICAL FINDINGS
• Heliotrope rash refers to violaceous erythema of
eyelids. • Pathognomonic Gottron’s papules located
over bony prominences, particularly proximal inter-
phalangeal, distal interphalangeal, and metacar-
pophalangeal joints. Violaceous papules and plaques.
• Shawl sign refers to violaceous erythema over back
of neck, posterior shoulders. • Poikiloderma (ery-
thema, telangiectasia, hypopigmentation and hyper-
pigmentation, and atrophy) is typical finding in skin
of upper chest, posterior shoulders, buttocks, and
back. • Periungual changes: ragged cuticles, ery-
thema, telangiectasia. • Scalp findings include alo-
pecia, pruritus, erythema scaling. • Skin lesions
often pruritic. • ‘Mechanic’s hands’ refers to scaly
fissures and inflammatory changes on hands bilater-
ally. • Calcinosis rare but severe associated finding.
• Muscle involvement: proximal and symmetric.
• Dysphagia in 12–45%. Fatigue. • Elevation of
muscle enzymes. Creatine kinase to follow disease
activity. • Muscle biopsy or muscle imaging with
magnetic resonance imaging. • May be a paraneo-
plastic disease; older patients at greater risk for
associated malignancy. Screening and rescreening
for malignancy is important in patients older than 50.
TREATMENT
• Broad-spectrum sunscreens, sun-protective cloth-
ing, behavior modification. • Earlier intervention,
therapy with systemic corticosteroids results in
improved prognosis if muscle disease. • Systemic
corticosteroids (prednisone 0.5–1.5 mg/kg q.d.) are
treatment cornerstone, although rash may not
respond. • Hydroxychloroquine 200–400 mg q.d.,
alone or combined with quinacrine 100–200 mg q.d.,
results in skin improvement; response may be incom-
plete. • Steroid-sparing options for skin disease
include immune suppressive agents methotrexate
2.5–30 mg/week, intravenous immunoglobulin 2 g/
kg for 2 consecutive days. • Antihistamines for pruri-
tus (non-sedating during day or sedating at night).
• Second-line agents for muscle disease treatment
and steroid-sparing: methotrexate 25–50 mg/week,
azathioprine 2 mg/kg q.d., cyclosporine 5 mg/kg q.d.,
cyclophosphamide 2 mg/kg q.d., intravenous immu-
noglobulin 2 g/kg. • Passive range of motion exercise,
rest, proper nutrition, physical and occupational
therapy are important.
 Scleroderma
DDx Ref  107 • 110 • 148
106 

The skin on the fingers is tight and contracted,

with digital fingertip crusting indicating prior
calcification and ulceration. Mat telangiectasias
are scattered on the palms.

Digital ulceration of the fingertips is a painful

consequence of the vascular insult of
scleroderma.

Mat-like telangiectasias are part of the CREST

syndrome. Other findings are Raynaud disease,
esophageal dysmotility, sclerodactyly and
calcification.

Oral contracture and narrowing of the mouth

orifice are seen in scleroderma, along with
mat-like telangiectasias.
106 Scleroderma
DDx Ref  107 • 110 • 148

DESCRIPTION
Idiopathic fibrosing condition with diffuse or limited
involvement. Diffuse involvement can affect entire
skin, associated with serious internal complications
from organ fibrosis and vascular abnormalities.
Localized variant associated with CREST syndrome
(calcinosis, Raynaud disease, esophageal dysmotil-
ity, sclerodactyly, and telangiectasia); more indolent
course.
HISTORY
• Rare. • More common in women. • Peak onset
between 30 and 50. • Men, older aged, black indi-
viduals have worse prognosis. • Interstitial lung
disease and pulmonary arterial hypertension are pul-
monary complications; lung involvement most
common cause of death. Shortness of breath and dry
cough are common presentations. • Renal involve-
ment affects 10–15% of patients. • Survival roughly
predicted by extent of skin involvement within 1 year
of diagnosis. • Best prognosis: sclerodactyly only.
Truncal involvement heralds worst prognosis.
PHYSICAL FINDINGS
• Raynaud’s phenomenon may precede onset of
scleroderma. • Early on, patients may complain of
intense pruritus; affected skin is erythematous and
swollen. Sclerosis occurs and skin is smooth, yellow-
ish, firm. Skin appears tight, bound down. Nail folds
may show dilated, tortuous capillaries. Earliest
changes may be most notable around mouth and on
hands; there is loss of the normal facial expression
lines, difficulty in opening mouth, and lips appear thin
with radial furrowing. Trophic ulceration, gangrene
may occur on fingertips. Diffuse calcification may
occur within skin. • Late changes: hyperpigmenta-
tion or depigmentation, often seen on upper chest.
Hair follicles often retain pigment while adjacent skin
hypopigmented. Alopecia late, partial or complete.
• Limited form associated with Raynaud disease may
precede sclerosis. • Heart, gastrointestinal tract,
lungs, kidneys may be affected. • Scleroderma renal
crisis typically occurs within first 5 years. • Calcino-
sis can ulcerate in late scleroderma or CREST.
• Associated antinuclear antibody patterns: homo­
geneous, speckled, nucleolar. Nucleolar most spe-
cific. • Scl-70 associated with truncal scleroderma,
pulmonary fibrosis; renal disease less common.
• Anticentromere antibody (speckled pattern) highly
specific for CREST syndrome. • Homogeneous
pattern: polymyositis–scleroderma overlap. • Anti-
bodies to ssDNA: linear scleroderma.
TREATMENT
• No reliable and effective treatment to reverse or
prevent fibrosis; treatment-refractory. Angiotensin-
converting enzyme inhibitors for scleroderma renal
crisis effective. • Multidisciplinary approach for man-
aging complications. Treat Raynaud disease with
behavior modification for cold avoidance, calcium
channel blockers nifedipine 10 mg b.i.d. or t.i.d. or
amlodipine 2.5 mg q.d. • Physical and occupational
therapies important. • For pruritus: Sarna lotion
or Pramosone lotion 2.5%. • No smoking, trauma
prevention. Meticulous wound care for ulceration.
• Patient education materials: Scleroderma Founda-
tion (http://www.scleroderma.org).
 Morphea
DDx Ref  44 • 118 • 163
107 

Irregularly shaped sclerotic plaque of localized

morphea. Note wax-like appearance, which is
also yellow with a surrounding faint hue of pink.

Multiple varying sized, hyperpigmented,

light-brown patches of morphea on the back.
These patches are soft and non-tender. The
inflammatory process is no longer active.

En coup de sabre morphea on central forehead. A

linear depressed sclerotic plaque extends from
hairline to brow. Underlying soft tissue atrophy
present. May be bony atrophy as well.

Violaceous oval patches of inflammatory phase of

morphea. Skin biopsy was characteristic.
107 Morphea
DDx Ref  44 • 118 • 163

DESCRIPTION
Idiopathic disease manifesting as sclerotic dermal
plaques with violaceous borders and central hypop-
igmentation. May be localized (more than two
plaques) or generalized (more than three plaques).
Generalized form accounts for 15%. Linear sclero-
derma accounts for 20% of localized scleroderma.
HISTORY
• More common in women than in men. • Mean
onset, 32 years. • Onset slow and insidious or rapid
and progressive. • Natural history unpredictable;
lesions may spontaneously resolve after several
years. • Although lesions may soften, hyperpigmen-
tation often chronic. • Patients with generalized
morphea may have asymptomatic internal organ
involvement; evaluation is individualized.
PHYSICAL FINDINGS
• Early lesions are typically inflammatory and viola-
ceous. Later lesions manifest hyperpigmentation,
fibrosis, atrophy. • In generalized morphea, a large
area may be involved; lesions often truncal but may
involve extremities. • Linear scleroderma more
common on extremities than on face. • En coup de
sabre is term for linear scleroderma affecting fore-
head and scalp. In Parry–Romberg syndrome (pro-
gressive facial hemiatrophy), soft tissue and bony
defects also apparent. • Skin biopsy can help confirm
clinical diagnosis; biopsy to deep fat or fascia may
be necessary if involvement is deep. • Eosinophilia
common. • Antinuclear antibody commonly positive
with generalized morphea.
TREATMENT
• As lesions may darken with sun exposure, advise
sun protection. • Emollients may be comforting.
• Education regarding the disease may be all that is
required, because there is no reliable effective treat-
ment. Reassure patient with plaque morphea that
condition is benign, does not involve internal organs.
• Mid- to high-potency topical steroid cream or oint-
ment (group II or III) may be helpful in some cases to
soften lesions and decrease pruritus. • Inflammatory
lesions can be injected with intralesional triamci-
nolone 5–10 mg/mL; caution, as intralesional steroid
injection may result in atrophy. • Calcipotriene oint-
ment (Dovonex) twice daily can be used in adults and
children; a reasonable trial of use is 8 weeks. • For
rapidly progressing symptomatic disease, consider
prednisone 20–40 mg q.d. for 6–8 weeks. Taper by
10 mg every other day if lesion improvement; this
does not alter natural history. • Hydroxychloroquine
400 mg q.d. for 4-month trial is reasonable. If
response, 200 mg q.d. maintenance dose consid-
ered. • Immune-suppressing medications, such as
methotrexate or cyclosporine, may be used for short-
term therapeutic trial of 3–6 months for inflamma-
tory, symptomatic, and/or progressive disease.
• Therapies with ultraviolet A1 (not widely available
in USA), systemic or bath psoralen ultraviolet A
reported effective in small uncontrolled trials.
 Sun-damaged
skin, photoaging
DDx Ref  30 • 106 • 113
108 

Degraded collagen cannot support hair follicles.

The follicles expand, accumulate sebum, and
form comedones.

Sun-induced wrinkling on the back of the neck

shows a series of criss-crossed lines.

Course wrinkling occurs following loss of elastic

tissue and collagen. The skin surface is firm,
smooth, and yellow.

Bleeding occurs with the slightest trauma to

sun-damaged surfaces of the forearms and
hands. The fragile skin tears easily.
108 DDx Ref  Sun-damaged
skin, photoaging
30 • 106 • 113

DESCRIPTION
Recognizable, morphologic changes in the skin
resulting from years of accumulated ultraviolet
radiation.
HISTORY
• No known innate gender difference in susceptibil-
ity. Persons with fair complexion (skin types 1 and 2)
at greatest risk. • Signs of photoaging apparent by
age 40. Progressive damage from years of sun expo-
sure continues. • Some actinic keratoses may
regress completely with sun protection and time.
PHYSICAL FINDINGS
• Skin appears older than its chronologic age, with
all skin components affected. • Face, lateral neck,
and dorsal hands more severely affected. Posterior
neck is also involved in male patients. • Poikiloderma
describes the combination of epidermal atrophy,
hyperpigmentation and hypopigmentation, and tel-
angiectasia. • Skin appears loose and without resil-
ience. Epidermis is thinned and dry. Pigmentation is
uneven and blotchy with lentigines. Fine wrinkles
lateral to the eyes and deep furrows form on fore-
head, at angles of mouth, and on posterior neck.
Telangiectatic blood vessels appear on ears and
lateral cheeks. Pilosebaceous units are prominent
and dilated with retained keratin (solar comedones),
especially lateral to the eyes. • The skin of the dorsal
hands and forearms bruises with minimal trauma
(solar purpura). • Skin beneath the chin is
unaffected.
TREATMENT
• Sun-protective clothing and regular use of sun-
screens slows the progression of solar damage. Sun-
protective measures alone improve photoaging,
prevent further damage, and reduce skin cancer risk.
• Topical retinoids such as tretinoin (Renova 0.01%,
0.05%) and tazarotene 0.1% (Tazorac) reverse some
photoaging over several months. Epidermal hyperk-
eratosis decreases, pigmentation becomes more
uniform and lighter, and new collagen is deposited
within the papillary dermis. Improvement is dose-
dependent and persists as long as the retinoid is
continued. • Various peeling agents can also improve
texture and appearance of sun-damaged skin. Alpha-
hydroxy acids reduce hyperkeratosis, promote epi-
dermal thickening and new collagen formation in
papillary dermis. Beta-hydroxy acids improve solar
comedones and epidermal texture. • Deeper peeling
agents such as trichloroacetic acid and phenol cause
full-thickness epidermal damage with intentional
wounding of papillary dermis. Wounding causes a
thin zone of scar formation (new collagen) in papillary
dermis, effectively reducing wrinkles. • Laser resur-
facing has a similar effect on papillary dermis.
 Polymorphous light
eruption
DDx Ref  84 • 104 • 105
109 

The papular type is the most common form. Small

papules are densely aggregated. The back of the
hands is the most common site.

Small papules are disseminated or densely

aggregated on a patchy erythema.

The papulovesicular type begins with urticarial

plaques from which groups of vesicles arise.

The papulovesicular type occurs primarily on the

arms, the lower limbs, and the ‘V’ area of the
chest.
109 DDx Ref  Polymorphous light
eruption
84 • 104 • 105

DESCRIPTION
Idiopathic, recurrent photodermatitis that comes on
acutely, usually in spring with first prolonged sun
exposure.
HISTORY
• Commonly referred to as sun poisoning or sun
allergy. • Occurs in all races, at any age, but most
common in young women, in whom the incidence is
as high as 10%. • Occurs in northern climates where
sun intensity increases in spring, and during winter
vacations while visiting southern, sunny resorts.
• Symptoms may include pruritus, malaise, chills,
headache, nausea. • Usually appears with first one
or two exposures to sunlight in spring. Ultraviolet A
is trigger in most cases, although the amount of
exposure needed to trigger a flare varies. • Heredi-
tary polymorphous light eruption occurs in Inuit and
Native American people. • Autosomal dominant
transmission with incomplete penetrance and varia-
ble expressivity.
PHYSICAL FINDINGS
• Initial symptoms are burning, itching, and erythema
on exposed skin such as upper chest, backs of
hands, extensor aspects of forearms, and lower legs.
Lesions appear 2 h to 5 days after sun exposure.
Tends to spare the face (except in hereditary form).
• Several clinical types. Papular type: most common;
small red dermal papules, disseminated or densely
aggregated, on patchy erythema. Plaque type:
second most common; superficial or urticarial
plaques. Papulovesicular type: least common; begins
with urticarial plaques from which groups of vesicles
arise. Affected patients develop the same clinical
type of polymorphous light eruption each year.
• Lesions persist for 7–10 days. • Light sensitivity
decreases with repeated sun exposure through the
summer and recurs the next spring. Most patients
have exacerbations each summer for many years.
TREATMENT
• Minimize sun exposure, especially between 10
a.m. and 2 p.m. • Sun-protective clothing available
from Sun Precautions (http://www.sunprecautions.
com) and similar companies. • Broad-spectrum,
ultraviolet A-blocking sunscreens, especially those
containing avobenzone, Mexoryl, titanium dioxide,
and zinc oxide. • Using group II–V topical steroids for
3–14 days relieves itch and fades lesions. • Oral
steroids (tapered gradually over 2 weeks) useful in
severe cases. • Hydroxychloroquine 400 mg q.d. for
first month and 200 mg q.d. thereafter for difficult
cases. • Controlled gradual exposure to sunlight or
to in-office ultraviolet B or ultraviolet A in early spring
can increase sunlight tolerance.
 Porphyria cutanea tarda
DDx Ref  11 • 46 • 102
110 

Blisters occur in sun-exposed areas such as the

face and neck and the dorsa of the hands and
forearms.

Clinical features: blistering in sun-exposed areas,

facial hypertrichosis, hyperpigmentation, and
sclerodermoid changes.

The classic representation, with erosions,

vesicles, and bullae localized to the backs of
hands.

Blisters formed on a non-inflamed base following

sun exposure. The blisters have healed with the
formation of milia.
110 Porphyria
DDx Ref 
cutanea tarda
11 • 46 • 102

DESCRIPTION
Most common form of porphyria, disorders of heme
synthesis resulting from deficiency of hepatic uropor-
phyrinogen decarboxylase activity.
HISTORY
• Porphyrias represent abnormalities in heme synthe-
sis pathway. Enzyme deficiencies result in increased
formation of metabolic intermediaries (porphyrino-
gens) just before specific enzyme defect. Each por-
phyria characterized by specific enzyme deficiency,
has distinct clinical characteristics. • Porphyrias
divided into disorders of bone marrow heme synthesis
(erythropoietic porphyrias), disorders of hepatic heme
synthesis (hepatic porphyrias). Acquired and familial
forms exist. • Porphyria cutanea tarda occurs when
heme biosynthetic pathway is compromised by exo­
genous agent. Acquired ‘sporadic’ form occurs as
complication of hepatic dysfunction or is induced by
alcohol, drugs, hormones. • Estimated prevalence: 1
in 25 000 in North America. • Alcohol and estrogens
associated with more than 80% of cases. Porphyria
cutanea tarda from alcohol abuse tends to be chronic
and relapsing until alcohol dependence addressed.
• Autosomal dominant transmission in familial por-
phyria cutanea tarda.
PHYSICAL FINDINGS
• Erythema, edema, vesicles occur in sun-exposed
areas such as face, neck, dorsa of hands, forearms.
Blisters rupture, leaving erosions and ulcers that heal
with scarring. Milia form in previously blistered sites.
• Chronic changes include facial hypertrichosis,
hyperpigmentation, skin fragility. Sclerotic changes
develop on face, neck, hands. • Skin biopsy confirms
subepidermal split and thickening of superficial
dermal vascular endothelium. • Direct immunofluo-
rescence shows deposition of IgG, IgM, and comple-
ment C3 surrounding blood vessels in papillary
dermis. • Fecal analysis shows elevated copropor-
phyrins. • A 24-h urine collection contains uropor-
phyrin in a ratio of about 4 : 1 to the coproporphyrin
fraction. Urine may have red-brown discoloration,
so-called port-wine urine, from high levels of porphy-
rin pigments; may show bright-pink fluorescence
under a Wood’s light. • Pseudo-porphyria usually due
to non-steroidal anti-inflammatory drugs and is clini-
cally indistinguishable from porphyria cutanea tarda.
Porphyrin studies are negative.
TREATMENT
• Complete elimination of alcohol and other hepato-
toxins can result in skin clearing in 2 months to 2
years. • Iron removal by phlebotomy is treatment of
choice. One unit of blood should be removed every
2–4 weeks until the hemoglobin drops to 10 g/dL or
until serum iron drops to 50 mg/dL. • Chloroquine in
very low dosages causes release of hepatic tissue-
bound uroporphyrin; subsequently, it is rapidly elimi-
nated by the plasma and excreted in urine.
• Measuring plasma uroporphyrin is effective way to
monitor progress of patients. Treatment should con-
tinue until plasma uroporphyrin drops below
10 mmol/L • Sunscreens containing Parsol or physi-
cal sun blockers containing titanium dioxide or zinc
oxide are moderately effective.
 DDx Ref  23 • 71 • 135
Vitiligo
111 

Examine the axillae, groin, and anal area in all

patients suspected of having vitiligo, as these
areas are commonly involved.

The genitalia and anal areas may be the first or

only areas affected and must be examined.

Loss of pigment may be partial or complete.

Complex trichrome patterns are typical.

Vitiligo on the back of the hand is resistant to all

forms of treatment.
111 Vitiligo
DDx Ref  23 • 71 • 135

DESCRIPTION
Disfiguring depigmenting disease that causes
melanocyte destruction. Etiology unknown but
thought to be autoimmune.
HISTORY
• One peercent of population affected; in 50%,
begins before age 20. Males, females affected
equally. • Positive family history in 30%. • Patients
relate first onset to aftermath of emotional stress,
illness, skin trauma (e.g. sunburn). Slowly progresses
over years in highly variable course. Some patients
have very stable disease; others progress at alarming
rate. • Depigmented areas at increased risk for
sunburn, subsequent skin cancers. • Can be devas-
tating for dark-skinned people, especially if cultural
implications present. Listen to patients’ concerns and
make all efforts on their behalf.
PHYSICAL FINDINGS
Two clinical types. • Type A. More common pattern,
involving fairly symmetric pattern of white depig-
mented 0.5- to 5.0-cm macules and patches with
well-defined borders. Borders may have red halo of
inflammation or rim of hyperpigmentation. Wood’s
light accentuates hypopigmented areas. Common
sites include dorsal hands and fingers, face, body
folds, axillae, genitalia. Predilection for orifices,
including eyes, nostrils, mouth, nipples, umbilicus,
anus. Occurs at sites of trauma (Koebner phenome-
non). Increased incidence of autoimmune thyroid
disease. • Type B. Segmental vitiligo. Limited to one
segment of body (e.g. one extremity). More common
in childhood. Skin biopsy shows absence of melano-
cytes and sparse lymphocytic inflammation.
TREATMENT
• Broad-spectrum sunscreens that contain avoben-
zone, Mexoryl, titanium dioxide, or zinc oxide. • Sun-
protective clothing available from Sun Precautions
(http://www.sunprecautions.com), similar compa-
nies. • Concealing and camouflaging agents, such
as Dermablend, Covermark, and Elizabeth Arden
Concealing Cream, effective but require practice
in application for good cosmesis. Suggest a local
qualified aesthetician as resource for color matching.
• Sunless or self-tanning lotions darken skin by
staining; work best for skin phototypes 2 and 3.
• Group I–V topical steroid ointments effective for
limited disease. Apply twice daily for 6 weeks, stop
for 2 weeks; repeat for two more cycles if no side
effects. Face and neck respond better than other
areas. • Tacrolimus ointment 0.1% (Protopic) effec-
tive in some cases. • Calcipotriol ointment (Vectical)
may be effective in combination with Excimer laser
(308 nm) therapy. •Pulse-dose systemic steroids
may arrest or slow rapidly progressing cases but
have potential side effects and risk. • Topical or
systemic photochemotherapy with psoralen plus
ultraviolet A light therapy somewhat effective. Nar-
rowband ultraviolet B light treatment may be effec-
tive. • Punch skin grafting for limited areas of
involvement may be helpful. • Patients with involve-
ment of > 40% of body surface may choose to
remove remaining normal pigment with 20%
monobenzone (Benoquin cream). Apply mono­
benzone twice daily, 6–18 months, to chemically
destroy all melanocytes in skin. Depigmentation irre-
versible, requiring patient to be informed, subse-
quent close attention to sun protection.
 Idiopathic guttate
hypomelanosis
DDx Ref  44 • 60 • 115
112 

Idiopathic guttate hypomelanosis is characterized

by 2- to 5-mm white spots with sharply
demarcated borders.

Idiopathic guttate hypomelanosis is a sign of

photodamage.

Idiopathic guttate hypomelanosis occurs in 50%

of 50- to 70-year-olds.

Macules are scattered on the exposed upper and

lower extremities.
112 DDx Ref  Idiopathic guttate
hypomelanosis
44 • 60 • 115

DESCRIPTION
Common asymptomatic dermatosis of unknown
etiology consisting of small white macules on sun-
exposed upper and lower extremities.
HISTORY
• Occurs in middle-aged and older people; in
50–70% of people over the age of 50. • More
common in women. • Higher prevalence in family
members; genetic predisposition likely. • Actinic
damage has been incriminated as major cause, but
a senile degenerative phenomenon may play a role.
• Although asymptomatic, this condition is cosmeti-
cally distressing. • Lesions stable in size and remain
fixed while the number of lesions increases with age.
PHYSICAL FINDINGS
• Macules are white and hypopigmented, 2–5 mm,
with regular borders and smooth to slight xerotic
scaling. • Macules are scattered on the exposed
upper and lower extremities. • Patients have associ-
ated signs of photoaging, including atrophy, lenti­
gines, and xerosis in the same areas.
TREATMENT
• Reassurance is all that is required for most patients.
Encourage sun protection with clothing, as sun-
screens are less effective than clothing. • White
macules can be camouflaged with tinted make-up,
such as Covermark or Dermablend. • Self-tanning
creams that contain dihydroxyacetone darken the
lesions, but the appearance is speckled and not
pleasing. • A light spray with liquid nitrogen may
partially fade the lesions, although there is the poten-
tial for worsening the dyspigmentation. • Intrale-
sional triamcinolone (2.5 mg/mL) infiltrated into
individual lesions may partially cause repigmentation
of lesions, although there is risk of atrophy.
• A qualified aesthetician skilled with spray tanning
can provide excellent cover-up.
 Lentigo, juvenile lentigo,
solar lentigo
DDx Ref  108 • 135 • 137
113 

Lentigines are common, benign, brown macules

on the sun-exposed skin of Caucasians.

Lentigines (liver spots) occur in sun-exposed

areas of the face, arms, and hands.

Labial lentigines occur on the vermillion border of

the lower lip. They have a smooth border and are
benign.

Reactive hyperplasia of melanocytes causes

persistent pigmentation in the form of lentigines
on the neck and upper back.
113 DDx Ref  Lentigo, juvenile lentigo,
solar lentigo
108 • 135 • 137

DESCRIPTION
Common, benign, brown macules occurring on sun-
exposed skin of white people.
HISTORY
Localized hyperpigmentation in three patterns: freck-
les (ephelides), juvenile lentigo, solar lentigo. While
similar in size, distribution, clinical appearance, the
three patterns differ in age of onset, clinical course,
relation to sun exposure. • Freckles. Appear in child-
hood. Occur as autosomal dominant trait. Usually
confined to face, arms, upper trunk. Increase in
number and slightly darken in summer; often fade
completely in winter. • Juvenile lentigines. Appear
in childhood with mean number of 30 lentigines in
each prepubertal child. Lesions do not increase in
number or size, or darken, in response to sunlight;
do not fade in absence of sunlight. Juvenile lentigines
also occur as characteristic feature of certain heredi-
tary conditions, such as Peutz–Jeghers, LEOPARD,
LAMB syndromes. • Solar lentigines. Common on
sun-exposed skin. Increase in number and size with
advancing age. Roughly 75% of white people over 60
have one or more lesions, which occur in setting of
actinic damage.
PHYSICAL FINDINGS
• Freckles. 1- to 2-mm, sharply defined, red or tan
to light brown macules with uniform color. Number
varies from few sparse lesions over nose and malar
cheeks to hundreds, with near confluence on sun-
exposed skin. Usually limited to face, arms, upper
trunk. Freckles show increased melanin within basal
layer keratinocytes. • Juvenile lentigines. Round to
oval macules, 2–10 mm in diameter, darker than
freckles, uniformly tan, or brown or black. Color
uniform, although pigment may have lacy or fine
grainy pattern. Juvenile lentigo has increased
number of non-nested melanocytes along dermoepi-
dermal junction. • Solar lentigines. Tend to be
larger (2–20 mm), oval to geometric macules,
uniform in color, although pigment may appear as
fine grains. May appear blotchy, although borders
should be sharply defined. Surrounding skin shows
actinic damage. Solar lentigines also show irregular
elongation of rete ridges, basal layer keratinocyte
hyperpigmentation, and increased numbers of junc-
tional melanocytes.
Juvenile lentigo persists year-round, with little
change over years, or may spontaneously resolve.
Solar lentigo usually persist; additional lesions may
appear elsewhere on sun-exposed skin. Lesions are
asymptomatic but may be of cosmetic concern.
TREATMENT
• Monitor existing lesions for interval change. Stable
lesions do not require treatment, but it may be
requested for cosmetic reasons. • New lesions best
prevented with sun-protective measures, including
sun avoidance, hats, clothing, sunscreens. • Hydro-
quinone solutions, tretinoin, azelaic acid creams are
helpful self-treatments. • In-office glycolic or trichl-
roacetic acid peels are of benefit in reducing hyper-
pigmentation over weeks to months. • Light
cryosurgery also effective but requires experience.
 Melasma (chloasma,
mask of pregnancy)
DDx Ref  84 • 103 • 113
114 

The upper lip and chin are the areas most

frequently affected by melasma.

The pigmentation develops slowly without signs of

inflammation and may be faint or dark.

Melasma occurs during the second and third

trimester of pregnancy and also in some women
taking oral contraceptives.

Melasma is a common complaint in women with

darker skin tones.
114 DDx Ref  Melasma (chloasma,
mask of pregnancy)
84 • 103 • 113

DESCRIPTION
Acquired brown hyperpigmentation of the face and
neck in genetically predisposed women.
HISTORY
• A common complaint in women of African, Hisp­
anic, and Asian descent. Roughly 10% of cases occur
in men. • The forehead, malar eminences, upper lip,
and chin are most frequently affected. • Pigmenta­
tion develops slowly and is more prevalent after
sunlight exposure. Prolonged heat exposure may
contribute to this condition as well. • Melasma
occurs during the second or third trimester of preg­
nancy and in some women taking oral contraceptives
or other exogenous estrogens. Usually after preg­
nancy or with discontinuation of contraceptives, the
pigment fades slowly over months to years.
PHYSICAL FINDINGS
• Symmetric macular eruption of brown hyperpig­
mentation. The intensity of the color varies, with
deeper pigmentation in darker-skinned people. Color
is usually uniform but more often blotchy and uneven.
• The edges of the patches can be irregular but well
defined. • No signs of inflammation.
TREATMENT
• Patients must be made aware that treatment
requires several weeks and strict sun protection.
Minimize sun exposure at midday and encourage
wearing of hats. Sunscreens of at least SPF 30 con­
taining avobenzone, Mexoryl, or physical blockers
such as titanium dioxide or zinc oxide that block both
ultraviolet A and B should be worn daily. • Combina­
tion products containing tretinoin, hydroquinone, and
fluocinolone (Tri-Luma) may be more effective and
more convenient. This is applied once each day for
8 weeks and may be used intermittently for up to 1
year. • Over-the-counter hydroquinone products are
at 2% concentrations (Porcelana). Prescription prod­
ucts include 3% (Melanex) and 4% (Claripel, Lustra,
Eldoquin Forte, and Solaquin Forte). Hydroquinone
can be an irritant and a sensitizer. • Tretinoin is also
effective as monotherapy. Tretinoin cream 0.025%,
0.05%, 0.1% (Retin-A) and tretinoin emollient cream
0.05% (Renova) enhance the effectiveness of hydro­
quinones. EpiQuin Micro contains 4% hydroquinone
and retinol. • Azelaic acid (Finacea gel) is safe during
pregnancy. • In-office superficial peels with glycolic
acid or intermediate peels with trichlroeacetic acid
require expertise. • May be used in combination with
tretinoin and hydroquinone at home.
 Seborrheic keratosis
DDx Ref  59 • 135 • 137
115 

Diffuse yellow and brown waxy papules and

patches over the back of this elderly man.

Large seborrheic keratosis waxy plaque with a

sharp border and verrucous changes centrally.

Lesions are often concentrated on the back, upper

chest, neck and inframammary areas. Rubbing
and chafing from clothing or from maceration in
this area can cause these lesions to be inflamed.

Smooth-surfaced lesions contain dark or light

round horn pearls embedded in the lesion or
protruding from the surface. Seborrheic keratoses
may mimic warts, nevi and melanoma.
115 Seborrheic
DDx Ref 
keratosis
59 • 135 • 137

DESCRIPTION
Common, benign, persistent, waxy brown epidermal
lesion with various clinical appearances. One of the
most common benign growths of the skin. Often
confused and misdiagnoses with other benign and
malignant lesions.
HISTORY
• Most people develop at least one or more sebor-
rheic keratosis in their lifetime. • Males and females
equally affected. • Lesions may be localized to areola
in men and women. • Tendency to develop multiple
seborrheic keratoses may be inherited.
PHYSICAL FINDINGS
• Seborrheic keratoses are typically multiple and can
arise at any site except palms and soles. • Size and
surface appearance of lesions vary considerably.
Most are between 0.2 and 2.0 cm. Lesions may be
flat or raised significantly. Surface may be smooth,
velvety, rough or verrucous. Retained keratin cysts
may be seen just under the surface within clefts.
Color of lesions extremely variable, including white,
pink, brown, and black; color may vary within single
lesion. Lesions tend to be oval, sharply demarcated,
and often oriented along skin cleavage lines. Most
have ‘stuck on’ appearance and waxy texture.
Surface tends to crumble when inflamed or picked.
• Raised or pedunculated seborrheic keratoses may
be indistinguishable from skin tags and compound
melanocytic nevi. Flat seborrheic keratoses may
mimic spreading pigmented actinic keratosis or
superficial spreading melanoma. If diagnostic doubt
exists, perform a skin biopsy. • Dermatosis papulosa
nigra is term used to describe seborrheic keratoses
of face seen more commonly in African-Americans.
Dermatosis papulosa nigra lesions are 1–2 mm,
dark-brown keratotic papules concentrated around
eyes and upper cheeks. • Stucco keratoses describe
the small, whitish seborrheic keratoses more com-
monly found on lower legs, ankles and feet of elderly
white people. The sign of Leser–Trélat is the sudden
explosive onset of numerous seborrheic keratoses in
association with internal malignancy, usually gastro­
intestinal malignancy.
TREATMENT
• Treatment may be indicated for symptomatic
lesions which are inflamed, irritated or bleeding.
Lesions may be removed when they are sympto-
matic; this usually occurs when they are located in
an area of friction and frequent trauma. • Removal
often requested for cosmetic reasons. Patients
should be informed that cosmetic removal of sebor-
rheic keratoses is not usually covered by medical
insurance. • Cryosurgery is effective for flat to mini-
mally raised lesions. Thicker lesions best removed
by cautery and curettage under local anesthesia.
• Hypopigmentation or hyperpigmentation are pos-
sible side effects of cryotherapy or any method of
removal. Residual scarring, if any, is minimal. Apply-
ing gentle pressure to the surrounding skin often
provides enough tension to allow for easy curettage
of lesions.
 DDx Ref  55 • 115 • 135
Skin tags
116 

Skin tags (acrochordons) are fleshy pedunculated

papules found in the intertriginous area. They are
usually soft and non-tender, but may become
inflamed and irritated with friction.

Skin tags are tiny, brown or skin-colored, oval

papules attached by a short, broad to narrow
stalk that become elevated with time, and
eventually come to protrude from a narrow base.

In the axillae, skin tags will be grouped together

in various sized from 1 to 3 mm, and various
degrees of pigmentation.

As a result of their location, skin tags may

become irritated by friction, jewelry, or clothing.
116 Skin tags
DDx Ref  55 • 115 • 135

DESCRIPTION
Skin tags, or acrochordons, are common, benign,
small, fleshy papules occurring in the skin folds.
HISTORY
• Roughly 25% of adults have at least one skin tag.
The majority of patients with skin tags have only a
few such lesions. Uncommon before the age of 30,
common thereafter. More common in overweight
persons. • There may be a familial tendency toward
multiple skin tags. • Undisturbed lesions are usually
asymptomatic. • Skin tags may become irritated by
friction, jewelry, or clothing. They may become
tender and may bleed when traumatized, twisted,
torn, or thrombosed.
PHYSICAL FINDINGS
• Skin-colored or slightly pigmented, 1- to 5-mm
fleshy, pedunculated papules. May be flat or filiform,
although most are soft, fleshy, and pedunculated
on a thin stalk. • Typically not difficult to diagnose.
• The axillae are the most common location. Also,
the neck, eyelids, and intertriginous areas such as
the inframammary and inguinal creases. • The over-
whelming majority of skin tags are benign and have
no internal disease association. However, skin tags
are part of the Birt–Hogg–Dubé syndrome, a rare
condition that includes trichodiscomas and fibrofol-
liculomas of the face, neck, and chest. Patients with
this syndrome may have associated renal cell carci-
noma, colonic adenomas, pulmonary cysts, and
medullary carcinoma of the thyroid gland.
TREATMENT
• Asymptomatic skin tags do not require treatment.
Patients often request removal for bleeding, tender-
ness, or cosmetic reasons. • Skin tags are best
treated by scissors excision with or without local
anesthesia. Electrocautery and cryosurgery can also
be used. • Many dermatologists feel that histologic
confirmation is usually not necessary, but submis-
sion of all skin tags for histologic review is a topic of
debate.
 Dermatofibroma
DDx Ref  118 • 136 • 137
117 

Dermatofibromas are commonly benign, firm

dermal nodules that arise spontaneously.

Early lesions are elevated, hard, and pink and

may be pruritic or tender. Typically, there is a ring
of hyperpigmentation peripherally.

Most dermatofibromas lesions are dome-shaped,

although some are depressed below the
surrounding skin surface.

Rarely, lesions may be blue or black as the result

of hemosiderin deposition and resemble
melanoma.
117 Dermatofibroma
DDx Ref  118 • 136 • 137

DESCRIPTION
Dermatofibromas are common, benign, firm, dermal
papules. The etiology is unknown. They seem to arise
spontaneously in adults and occasionally occur in
children. Controversy exists as to whether the lesion
represents a spontaneous benign neoplastic process
or reactive hyperplasia in response to injury.
HISTORY
• Dermatofibromas may be asymptomatic, but more
commonly tender or pruritic. Some patients note
itching when the lesion is first noted and attribute
this to an insect bite. Most patients do not recall a
specific trauma to the area. • These lesions occur
more often in women. • Most are asymptomatic, but
itching and tenderness is not uncommon. • Der-
matofibromas tend to persist indefinitely, while
remaining stable in size and appearance. They have
no malignant potential but can be confused with
various types of skin cancer.
PHYSICAL FINDINGS
• Dermatofibromas are discrete, firm, pink dermal
papules typically 3–7 mm in diameter. Rarely,
lesions may be larger than 3.0 cm. • Most dermatofi-
bromas are dome-shaped, although some are
depressed below the surrounding skin surface. The
lesion is fixed within the skin but movable over the
underlying subcutaneous fat. • On palpation, the
lesion feels like a firm button. Pinching a dome-
shaped dermatofibroma between two fingers causes
the lesion to dimple below the level of surrounding
skin. • Dermatofibromas are typically flesh-colored
to pink with a poorly defined rim of tan to brown
pigmentation. Rarely, lesions may be blue to black
as a result of hemosiderin deposition, which may
resemble melanoma. The surface may be smooth,
shiny or scaly and excoriated. • Although dermatofi-
bromas may arise on any cutaneous surface, most
are found randomly distributed on the extremities.
Rarely, dermatofibromas occur on palms or soles. •
Lesions are usually solitary; however, multiple
lesions can occur, especially on the legs. • Der-
matofibromas should be stable in size, appearance,
and color. If they are not, they should be biopsied to
confirm their benign nature.
TREATMENT
• Dermatofibromas do not require treatment unless
they are symptomatic, repeatedly traumatized, or
cosmetically bothersome. • Surgical excision with
primary closure is the treatment of choice for symp-
tomatic lesions. • If incompletely excised, the patient
should be warned of possible recurrence.
 Keloids and
hypertrophic scars
DDx Ref  117 • 122 • 126
118 

Nodular pedunculated keloid on the posterior

earlobe, common with ear piercing.

A keloid is a firm red to purple nodule with

telangiectasia that extends beyond the area of
trauma.

A keloid formed after an injury. The lesions were

injected with triamcinolone 10 mg/cc at intervals
of weeks. Early lesions respond better to
treatment than older lesions do.

Hypertrophic scars and keloids can arise at any

skin site. Most occur on the chest, hand, neck
and earlobe. Occasionally, keloids arise
spontaneously, without any preceding trauma.
118 DDx Ref  Keloids and
hypertrophic scars
117 • 122 • 126

DESCRIPTION
Hypertrophic scars are exuberant scars or healing
responses to trauma or injury. Keloids are scars that
extend beyond the area of trauma or injury. Most
common sites include chest, head, neck. Earlobe is
another common site. Surgery, burns, piercing, acne
are common insults.
PHYSICAL FINDINGS
• Early, normal scars are usually red to purple and
firm during initial weeks of healing. • Itching, tender-
ness are common for normal scars, hypertrophic
scars, keloids.
Hypertrophic scars
Larger and more elevated than normal scars and
present for a longer period of time. Have a similar
color and texture to those of normal scars. Surface
is smooth, dome-shaped, shiny with prominent
vessels. One portion of a scar may appear normal,
another portion hypertrophied. Unlike keloid scars,
they remain confined to site of injury. May regress
over time without treatment.
Keloids
By definition, keloid scars extend beyond the area of
trauma or injury. Firm, red to violaceous, large,
tender nodules. Usually hyperpigmented in African-
Americans, red to purple in white people. Depending
on type of original injury, lesion may be linear or
nodular. In rare instances, keloids may arise sponta-
neously. This usually occurs on chest and shoulders.
Keloid scars show no tendency toward regression
and tend to enlarge over time.
TREATMENT
• Patients with history of these scars should be dis-
couraged from cosmetic procedures and piercings.
Those requiring surgical procedures in areas at
increased risk of abnormal scarring should be
advised of this possibility, reminded at time of suture
removal. • Hereditary tendency determines who
develops hypertrophic scars. Parents of a child who
has a cutaneous procedure that results in such scar-
ring need reassurance and a management plan.
• Early abnormal scarring typically responds better
than older, less active scars. Early intervention
advised in these cases. • Intralesional corticosteroid
injection probably treatment of choice initially for
most. • Radiation therapy and more recently pulse-
dye laser therapy have been used for hypertrophic
scars, keloids. • Compression therapy and silastic
sheeting helpful but inconvenient. • Newer topical
silicon-containing gels have been marketed for the
treatment of hypertrophic scars, although efficacy in
all patients questionable. • Surgical removal or cor-
rection of hypertrophic scars and keloids requires
experience, careful monitoring. Keloid scars tend to
recur often, sometimes larger, after surgical removal.
• Combination therapy with intralesional steroids and
surgical excision is sometimes required. • Consider
referral to a dermatologist or plastic surgeon with an
interest in scar removal. • Hypertrophic scars and
keloids difficult to eradicate, no matter what proce-
dure is used.
 Keratoacanthoma
DDx Ref  17 • 62 • 128
119 

Keratoacanthomas begin as a smooth, dome-

shaped, red papule. Lesions grow rapidly.

Keratoacanthomas develop and grow rapidly,

forming a keratin-filled necrotic crater.

This lesion resembles both a keratoacanthoma

and a squamous cell cancer, which is typical of
advancing keratoacanthomas. It is best to treat
this lesion as a squamous cell carcinoma.

Keratoacanthomas are dome-shaped tumors with

a central crateriform crust that grows rapidly.
Typical locations include the face, neck, hands
and sun-exposed extremities.
119 Keratoacanthoma
DDx Ref  17 • 62 • 128

DESCRIPTION
Rapidly growing crateriform nodule with distinctive
clinical appearance. Best considered as a low-grade
squamous cell carcinoma.
HISTORY
• The peak incidence of keratoacanthoma is between
ages 50 and 70. This tumor is rare before 40 years
of age. • White people with fair complexions are
more often affected. • Typical locations include the
face, neck, dorsal hands, and sun-exposed extremi-
ties. It occurs on the legs more often in women.
• The lesion erupts rapidly and is often quite tender.
• Chemical exposure and human papillomavirus
have been implicated as a cause in animal models,
although their role in humans is controversial. • His-
torically, keratoacanthomas have been regarded as
benign regressing lesions; however, they should be
thought of as variants of squamous cell carcinoma
and treated as such.
PHYSICAL FINDINGS
A keratoacanthoma is a characteristic, solitary, flesh-
colored to red, 0.5- to 2.0-cm, crateriform nodule. A
central keratotic plug or depression conceals a deep
keratinous cavity. This plug or depression gives the
nodule its characteristic volcano-like shape. The
nodule is firm in texture, tender to palpation or pres-
sure, and can grow rapidly. Keratoacanthoma nearly
always appears on sun-damaged skin. Three growth
phases are described. • Proliferative phase: a soli-
tary papule appears suddenly and then rapidly grows
to its maximum size over 2–4 weeks. • Mature
phase: the lesion is stable in size and appearance
for weeks to months; it may appear crateriform if the
core has been partially removed. • Resolving phase:
the base becomes indurated, the central core is
expelled, and the base resorbs, leaving a pitted scar
over several months.
Rare cases of multiple keratoacanthomas have
been reported, both as an eruptive (Grzybowski) form
and as a familial adolescent (Ferguson–Smith) form.
Patients with Muir–Torre syndrome develop seba-
ceous adenomas, at times with keratoacanthoma
architecture. Such patients should be evaluated for
occult gastrointestinal malignancy.
Patients on immunosuppressive therapy after
organ transplant are at increased risk of developing
keratoacanthomas and invasive squamous cell car-
cinoma. Examination for enlarged lymph nodes
should always be performed in this patient
population.
TREATMENT
• Best to presume a diagnosis of squamous cell
carcinoma pending biopsy results and clinical follow-
up. • An excisional biopsy or shave removal should
be performed. It is important to biopsy deep enough
to evaluate the dermis for possible invasion. • Treat-
ment options include complete excision with clear
margins, and electrodesiccation and curettage for
smaller lesions. Any of these options is curative in
the vast majority of cases.
 Nevus sebaceus
DDx Ref  115 • 126 • 134
120 

Nevus sebaceus in a 30-year-old man. The

plaque has developed in to a large verrucous
yellow-pink nodule with a decrease in terminal
scalp hair.

This 12-year-old boy has reached puberty, and

the lesion has become thicker. This change at
puberty is expected and represents, in part,
sebaceous gland and epithelial hyperplasia.

Nevus sebaceus occurs most often on the scalp,

although lesions are also found on the face, neck,
and trunk.

The lesion is usually a solitary round to oval

plaque but it may be linear and disjointed.
120 Nevus sebaceus
DDx Ref  115 • 126 • 134

DESCRIPTION
Distinctive congenital lesion of the head (usually
scalp), composed of skin and appendageal compo-
nents. Nearly all nevus sebaceus lesions are present
at birth or appear in early childhood. Lesions change
clinically and histologically with age. Not all lesions
may be noticed at birth. At puberty, these nevi tend
to enlarge and may be noticed for the first time at
this point.
HISTORY
• Nevus sebaceus remains stable throughout child-
hood and undergoes predictable change at puberty.
• In the first few months of life, the sebaceous glands
are well developed as a result of maternal hormonal
stimulation, although surrounding hair structures are
incompletely differentiated. Thereafter and through
the rest of childhood, the sebaceous glands are small
in size and number; incompletely developed hair
structures may be seen. • With puberty, hormonal
influences bring about diagnostic changes. Seba-
ceous glands mature and increase in size and
density. Hair structures remain undifferentiated, and
papillomatous epidermal hyperplasia develops.
Ectopic apocrine glands may also be found deep
within the underlying dermis. • Appendageal tumors
may develop later in life within nevus sebaceus. Each
such tumor has its own histologic pattern. The most
common tumor is syringocystadenoma papilliferum,
a benign apocrine tumor seen in up to 20% of
lesions. Basal cell carcinoma is the second most
common tumor and most common malignancy that
develops in nevus sebaceus. It occurs in roughly 7%
of lesions, but rarely, if ever, metastasizes.
PHYSICAL FINDINGS
Nevus sebaceus is usually a solitary, yellowish to
flesh-colored plaque and occurs most commonly on
the scalp, forehead, or postauricular areas. It tends
to be linear or oval-shaped, measuring 1–3 cm in
diameter. The lesion evolves in three stages corre-
sponding to sebaceous gland maturation through
childhood, puberty, and adulthood. • In childhood,
the plaque is barely raised and has a velvety surface,
is hairless, pink to tan, and asymptomatic. • Around
puberty, the plaque tends to thicken, become larger
and more verrucous, and has a yellow-white and
pink-speckled appearance. Lesions at this stage are
easily traumatized and may be tender. • The third
stage of evolution occurs during adulthood. Nevus
sebaceus may be confused with linear epidermal
nevus clinically.
TREATMENT
• Excision of the entire lesion is recommended;
nevus sebaceus has a tendency to develop basal cell
carcinoma within the nevus after puberty. • Excision
is best performed just before puberty, when the
lesion is still small and the patient is old enough to
understand and tolerate the procedure. • A larger
lesion may be excised in stages without any concern
of inducing malignant change.
 Chondrodermatitis
nodularis helicis
DDx Ref  126 • 127 • 128
121 

The primary lesion is a firm, tender, red to pink

papule of 2–4 mm with a central keratotic
punctum. It is most often found on the upper
helix.

The central scale lacks the keratinous plug of

keratoacanthoma. Removal of the scale reveals a
small central erosion.

During the active stage, the base may become

red and swollen; pain is constant.

Chondrodermatitis nodularis helicis usually occurs

in those over 40; the incidence increases with
age. Lesions are occasionally found on the
antihelix.
121 DDx Ref  Chondrodermatitis
nodularis helicis
126 • 127 • 128

DESCRIPTION
An inflammatory process of the cartilage of the ear.
It is an exquisitely tender papule on the most lateral
edge of the helix or antihelix. Men are affected more
often than women. The helix is involved more com-
monly in men, and the antihelix in women.
HISTORY
• Most patients are in the habit of sleeping on the
affected side. Pressure from resting on a pillow
causes pain, forcing the patient to alter sleeping
position and affecting the ability to sleep comfortably.
• The etiology is unclear. Related to focal dermal
necrosis due to repetitive trauma. Over many years,
dermal injury may result from actinic damage, physi-
cal pressure, or a combination of both. The vascular
supply to this tissue is decreased, there is an inflam-
matory response, and damage is slow to heal.
Inflammation and granulation tissue reflect attempts
at healing the damaged collagen. • Without treat-
ment, the lesions persist indefinitely. • Recurrences
are common, even after aggressive therapy.
PHYSICAL FINDINGS
• The primary lesion is a firm, tender, red to pink,
2- to 4-mm papule with a central keratotic punctum.
The punctum has firm, adherent crust or scale,
resembling a small cutaneous horn. The surrounding
skin shows scale, actinic damage with atrophy and
telangiectasia. • Occasionally, there is more than one
lesion. • The universal symptom is pain described as
stabbing and sharp. • This condition is classically
found on the most prominent and lateral portion of
the auricle. • The major diagnostic consideration is
squamous cell carcinoma, which tends to be more
necrotic and less tender. A skin biopsy should be
performed, which is diagnostic. A biopsy also rules
out squamous cell carcinoma.
TREATMENT
• Any therapy must include efforts to relieve pressure
and trauma on the affected area to allow healing.
Patients who are able to sleep on their back should
be encouraged to do so. Pillows should be positioned
to minimize pressure on the ear. • Topical therapy is
rarely successful. • Intralesional steroids can be
effective in a minority of cases. Patients should
expect some residual discomfort after injection. •
Surgical removal of the lesion along with the inflamed
cartilage can be curative. A shave excision is directed
at removing all the surrounding inflamed tissue and
cartilage. Curettage and light electrodesiccation of
the base is performed, and the wound is allowed to
heal by secondary intention. Definitive therapy
involves surgical resection of the involved portion of
the pinna. • Recurrences are common after any of
the above therapies.
 Epidermal cyst
DDx Ref  30 • 50 • 123
122 

Epidermal cysts are yellow to gray, smooth, dome-

shaped nodules with a central punctum and contain
keratin. Epidermal cysts vary in size. Lesions of this
size will show little tendency to rupture.

Spontaneous rupture of the wall results in

discharge of a soft yellow keratin into the dermis.
A tremendous inflammatory response ensues and
the cyst becomes red, swollen and tender.

Epidermal cysts occur commonly on the back of

the ear and may become clustered. Posterior
neck and back are also common sites.

Smaller epidermal cysts can occur about the

eyelids and in areas of scar trauma.
122 Epidermal
DDx Ref 
cyst
30 • 50 • 123

DESCRIPTION
An epidermal cyst is a firm, subcutaneous, keratin-
filled cyst originating from squamous epithelium,
most often from a hair follicle infundibulum.
HISTORY
• Epidermal cysts arise spontaneously. • They occur
most commonly on the trunk, postauricular fold, and
posterior neck. Cysts frequently develop in areas of
friction and are usually solitary. • Most epidermal
cysts arise from the squamous epithelium of the hair
follicle. • Unlike pilar cysts, the epidermal cyst wall
is fairly delicate and thus prone to rupture. Rupture
is followed by a foreign body reaction to keratin
extruded into the dermis and acute inflammation.
Such lesions are tender and appear to be infected.
However, cultures are usually sterile.
PHYSICAL FINDINGS
• The firm, dome-shaped, pale-yellowish, intra­
dermal or subcutaneous cystic nodules range from
0.5 to 5.0 cm in size. • Cysts are somewhat mobile
but are tethered to the overlying skin through a small
punctum that often appears as a comedo. This
punctum represents the follicle from which the cyst
developed. • Inflamed epidermal cysts are warm,
red, boggy, and tender on palpation. Furuncles have
a similar appearance. Sterile, purulent material and
keratin debris drain to the surface. • If the inflam-
matory response is brisk enough to destroy the cyst
wall, then it is unlikely the cyst will recur. More
often, the inflammation subsides and the cyst recurs.
• Scarring often follows rupture, which makes the
cyst more difficult to remove. • Multiple epidermal
cysts occurring on the face, scalp, and back should
raise suspicion of Gardner syndrome in the appropri-
ate clinical setting. This very rare, autosomal domi-
nant condition is associated with colonic polyposis
and early malignant degeneration into adenocarci-
noma of the colon.
TREATMENT
• Epidermal cysts on the face may rupture and lead
to scarring. • The cosmesis of elective surgical exci-
sion must be weighed against a scar from potential
rupture. Such lesions are far more difficult to remove
once they have ruptured. • Asymptomatic epidermal
cysts occurring elsewhere do not require treatment.
Symptomatic or recurrent ruptured epidermal cysts
should be removed. • Ruptured, inflamed epidermal
cysts should be incised and drained under local
anesthesia. • Attempts should be made to remove
the cyst lining, by either curettage or blunt dissection.
• Recurrent epidermal cysts that have previously
ruptured and scarred are best excised along with the
surrounding scar once the inflammation has
subsided.
 Pilar cyst
DDx Ref  50 • 122 • 135
123 

Pilar cysts are commonly found on the scalp, may

interfere with hats or helmets, and are usually
removed when symptomatic.

This large pilar cyst exerted pressure against the

skin and has destroyed follicles.

Roughly 90% of cysts appear on the scalp, with the

remaining 10% on the face, neck, back, and
scrotum. Removal of scrotal pilar cysts can be
accomplished by incision, similar to ones on scalp.

Pilar cysts rupture less frequently than epidermal

cysts, as the pilar cyst has a thicker wall, making
it firm and less mobile.
123 Pilar cyst
DDx Ref  50 • 122 • 135

DESCRIPTION
Firm, subcutaneous, keratin-filled cyst originating
from outer root sheath of hair follicle. Most commonly
on scalp.
HISTORY
• Pilar cysts are less common than, but otherwise
similar to, epidermal cysts. • Roughly 90% are on
scalp; remaining 10% occur on face, neck, back,
scrotum. • Epithelium of outer root sheath undergoes
different form of keratinization than that of cutaneous
epithelium. • Almost always develop after puberty. •
Tendency to develop pilar cysts often has autosomal
dominant inheritance. • Usually multiple in 70% of
patients. • Persist indefinitely, grow slowly to a
stable size unless they rupture. • Rupture less fre-
quently than epidermal cysts, presumably because
pilar cyst has thicker wall. Rupture usually results
from external trauma. A brisk foreign body inflamma-
tory reaction follows, can be quite painful, resembles
a furuncle.
PHYSICAL FINDINGS
• Clinically indistinguishable from epidermal cysts,
differing only in distribution. Both present as a firm,
subcutaneous nodule, about 0.5 to 5.0 cm. • Pilar
cysts have no central punctum, unlike epidermal
cysts. When such a cyst is surgically dissected, the
pilar cyst possesses a tough, white-gray wall more
resistant to tearing than the wall of an epidermal
cyst. Pilar cyst wall separates easily and cleanly from
surrounding dermis. • If pilar cyst ruptures, area
becomes inflamed, red, tender, boggy on palpation.
• Large cysts may be cosmetically objectionable.
Some cysts are so large and tender they may inter-
fere with wearing hats, helmets. • Acute inflamma-
tion after rupture often misdiagnosed as infection.
Antibiotics of little value in such cases. • Incision and
drainage under local anesthesia improve comfort and
limit scarring. Elective excision before rupture pre-
vents this complication.
TREATMENT
• Easily removed with excision under local anesthe-
sia. An incision is made over the cyst, exposing the
glossy white external surface. Cyst wall is freed
easily from surrounding connective tissue by blunt
dissection. • At this stage, smaller cysts may be
expressed intact up through the incision by steady,
firm pressure on each side of incision. • Larger cysts,
which cannot be expressed in this manner, should
be incised and their contents removed by curettage.
Incised cyst wall is clamped and, through a combina-
tion of gentle traction and pressure on each side of
the incision, the now smaller, partially emptied cyst
is delivered through the incision. If sutures are
needed, they are placed and removed in 7–10 days.
 Sebaceous hyperplasia
DDx Ref  62 • 126 • 135
124 

Sebaceous hyperplasia is a common benign condi-

tion consisting of prominently enlarged sebaceous
glands on the face.

Yellow-white papules are commonly found on

the forehead and cheeks. The central pore is
almost a constant feature.

Sun damage has been suggested as a

contributing factor. Genetic factors probably play
a significant role as well.

The lesion begins as a 1- to 2-mm, soft, pale

yellow to skin-colored minimally elevated papule.
Enlarges over time, and may be confused with
basal cell carcinoma.
124 Sebaceous
DDx Ref 
hyperplasia
62 • 126 • 135

DESCRIPTION
Common benign condition consisting of prominently
enlarged sebaceous glands on the face.
HISTORY
• Occurs in both men and women. • Papules rarely
appear before age 30 but become increasingly more
common with advancing age. Roughly 80% of
patients over age 70 have at least one such lesion.
• Most lesions represent a single, hypertrophied
sebaceous gland with multiple lobules arranged
around a central enlarged sebaceous duct. • Lesions
occur in all skin types but are more easily seen in
lighter skin. • Etiology unknown. Genetic inheritance
plays a large role. Sun damage has been suggested
as a contributing factor. • Lesions are entirely
asymptomatic but persistent. • Papules can become
disfiguring and are mostly of cosmetic concern.
Patients are typically concerned that the lesions
represent basal cell carcinoma or other type of
skin cancer.
PHYSICAL FINDINGS
• Lesion begins as a 1- or 2-mm, soft, pale yellow
to skin-colored, minimally elevated papule. With
time, lesion attains a maximum size of 3–4 mm and
develops a central umbilication. • Mature papules
possess a distinctly yellow-orange color and are
more sharply defined from the surrounding skin. •
Papules may be solitary but are more commonly
multiple and scattered randomly on the forehead,
eyelids, nose, and cheeks. • Papules may yield
sebum from the central umbilication with palpation.
• An orderly array of fine telangiectasias may radiate
outward from the umbilication toward the periphery
of the papule. • Individual lesions may be confused
with basal cell carcinoma, small keratoacanthoma,
or molluscum contagiosum.
TREATMENT
• Treatment is not required but may be requested for
cosmetic reasons. • Cryosurgery, carbon dioxide
laser, electrodesiccation and curettage, and trichlo-
roacetic acid are all effective in ablating individual
lesions. • The sebaceous lobules located within the
superficial dermis must be destroyed for the treat-
ment to be successful. • Care must be taken to avoid
over-treatment so as to minimize the risk of perma-
nent scarring. • Reassurance is often all that is
needed for the patient with sebaceous hyperplasia.
 Syringomas
DDx Ref  62 • 126 • 135
125 

Syringomas are the most common tumor of the

intraepithelial eccrine sweat glands. Appear as
asymptomatic flesh-colored papules.

Syringomas occur on the eyelids, malar cheeks,

axillae, anterior chest, abdomen, umbilicus, and
vulva.

The lower lids are the most common area for

finding this appendage tumor. Lesions may be
removed with curved scissors to improve
appearance.

Papules are usually symmetrically distributed and

asymptomatic. May be extensive in Down
syndrome and trisomy 21.
125 Syringomas
DDx Ref  62 • 126 • 135

DESCRIPTION
Small, firm, skin-colored papules occurring most
commonly in women around the eyelids, upper chest,
and vulva. Syringomas are the most common tumor
of the intraepidermal eccrine sweat glands.
HISTORY
• These appendageal tumors develop after puberty
and increase in number throughout young adulthood.
• Lesions are asymptomatic, stable in size and
appearance, and persistent. • The autosomal domi-
nant inheritance of multiple syringomas is well estab-
lished. Syringomas occur with increased frequency
in individuals with Down syndrome or trisomy 21. •
Facial lesions are of cosmetic concern, and most
patients request removal of larger lesions. • The
patient may be concerned that the lesions are can-
cerous. • Women seeking evaluation of vulvar
lesions may be concerned that the lesions are genital
warts.
PHYSICAL FINDINGS
• Small, skin-colored to yellow, 1- to 2-mm, barely
raised papules, most commonly found on lower
eyelids. They also occur on malar cheeks, axillae,
anterior chest, abdomen, umbilicus, and vulva.
• Papules usually symmetrically distributed and
asymptomatic. • Syringomas persist indefinitely and
remain small. They have no potential for malignancy.
• They may resemble flat warts or sebaceous
hyperplasia.
TREATMENT
• Syringomas may be removed for cosmetic pur-
poses. • Electrodesiccation and curettage, laser
surgery, and trichloroacetic acid may be used, with
variable success. • Sharp dissection or scissor exci-
sion of lesions is easily performed under local
anesthesia. • All these procedures can lead to scar-
ring, so care and precision are warranted. • In some
patients, syringomas are too numerous to remove all
lesions completely.
 Basal cell carcinoma
DDx Ref  124 • 128 • 135
126 

Common features of a nodular basal cell

carcinoma with a smooth transleucent pink and
pearly nodule with a sharp border and
telangiectasias.

Superficial basal cell carcinoma spreads

peripherally, sometimes several centimeters, and
invades after considerable time. May resemble
patch of eczema or psoriasis.

A basal cell carcinoma may present as a slow to

heal ‘wound’ on the anterior shin with beefy-red,
smooth erosive nodule.

Nodular basal cell carcinomas are common on the

nose. This lesion had been present for many
months, ulcerated, then began to heal, which
further delays diagnosis.
126 Basal cell carcinoma
DDx Ref  124 • 128 • 135

DESCRIPTION
Basal cell carcinoma (BCC) is the most common cutane-
ous malignancy. Locally invasive, slow-growing, rarely
metastasizes (unless patient is immunocompromised).
Neither life-threatening nor trivial.
HISTORY
• More common after age 40. • Highest incidence in
the fair-skinned. • Cumulative sun exposure is primary
risk factor. Occur mostly on sun-exposed skin of face,
scalp, ears, neck. • Clinical variants include nodular,
pigmented, superficial, sclerotic basal cell carcinoma.
PHYSICAL FINDINGS
• Nodular BCC. Most common variant. A pearly white,
almost translucent, dome-shaped papule with overlying
telangiectasias. Papule or nodule enlarges slowly, may
become flattened in center or may develop a raised,
rolled, translucent border. Frequently ulcerates, bleeds,
becomes crusted in center. • Pigmented BCC. Contains
melanin, may therefore resemble melanoma. • Super-
ficial BCC. Least aggressive form. More commonly on
trunk, extremities. Circumscribed, round to oval, red,
scaling plaque resembles eczema, psoriasis, extramam-
mary Paget disease, or Bowen disease. • Sclerosing
BCC. Most subtle and least common variant. Smooth,
pale white to yellow papules. Resembles scar tissue.
Borders may be difficult to discern. Higher rate of
recurrence.
TREATMENT
Without treatment, BCCs persist, enlarge, ulcerate,
invade, destroy surrounding structures. Treatment deter-
mined by size and location of tumor, tumor variant,
patient’s concerns. Clinical aggressiveness correlates
with histologic pattern.• Electrosurgery involves electro-
desiccation and curettage of obvious tumor. The 5-year
cure rates approach 92%. • Primary excision is preferred
for non-facial, well-defined nodular. The 5-year cure
rates approach 90%. • Mohs micrographic surgery is a
highly specialized, tissue-sparing method of excision
used for difficult tumors with contiguous growth, espe-
cially BCCs. Mohs micrographic surgery is used for
recurrent BCC, histologically aggressive forms of BCC,
such as sclerotic BCCs, and tumors in anatomically
important locations such as around eyes, nasal ala,
mouth, and ears. Also used for tumors with high risk of
recurrence. Treatment of choice for sclerotic and recur-
rent BCC and most BCCs of the central face, near func-
tionally important structures. The 5-year cure rates
approach 99%.
Non-surgical options are increasing. These include
radiation therapy, photodynamic therapy, and topical
immune modulators. • Radiation therapy may be useful
for difficult-to-treat tumors, such as on eyelids, and for
patients unwilling or unable to tolerate surgery. The
5-year cure rates are roughly 90%. Hedgehog inhibitors
are newer oral medications that show great promise for
slowing down or inhibiting BCC progression, especially
for advanced and inoperable BCCs.
• Photodynamic therapy is an evolving chemothera-
peutic modality for superficial BCC that is not widely
available today but may be useful in the future.
• Topical imiquimod 5% cream is an immune
response modifier shown to be about 85% effective or
better for superficial BCC. It is less effective for nodular
BCC.
All patients with BCC require follow-up to monitor
for recurrence at the treated site, regardless of which
treatment is used, and for the development of new
tumors.
 Actinic keratosis
DDx Ref  115 • 126 • 128
127 

Multiple hypertrophic actinic keratosis scattered

diffusely over the dorsal hand. Some of the
thicker actinic keratoses may be difficult to
distinguish from squamous cell carcinoma.

Single 3–5-mm actinic keratosis with thick

hypertrophic scale centrally, that may be
palpable, and rough surrounding pink changes
peripherally.

Actinic keratosis may accumulate a dense scale

on the surface and become a cutaneous horn.
These lesions require excision.

Diffuse actinic damage of the lower vermillion lip

with a blunting of the junction between the red
vermillion border and the cutaneous lip with
advanced actinic damage and early erosive changes.
127 Actinic
DDx Ref 
keratosis
115 • 126 • 128

DESCRIPTION
Common, persistent, keratotic lesions with malignant
potential. Most commonly on sun-exposed areas of fair-
skinned elderly patients, with significant sun exposure.
Over time, actinic keratoses evolve into squamous cell
carcinoma (SCC) or basal cell carcinoma (BCC).
HISTORY
• Result of years of cumulative sun exposure and kera­
tinocyte damage. • Progressively more common after
age 40. • Spontaneous regression occurs. • About
10–20% of actinic keratoses (AKs) progress to SCC or
BCC over several years. Multiple AKs indicates a history
of significant sun exposure and increased risk of skin
cancer.
PHYSICAL FINDINGS
• AKs are found along with other signs of chronic sun
exposure, such as uneven pigmentation, atrophy or thin-
ning, telangiectasias. Predominantly on face, head,
neck, dorsal hands. • Initially present as poorly defined
area of redness or telangiectasia. Over time, become
more defined and develop thin, adherent, yellowish or
transparent scale. • Easier to detect by palpation than
by observation. • Scale becomes progressively thicker,
yellow. Retained scale may form elongated keratinous
structure or cutaneous horn. Such advanced lesions may
be difficult to distinguish from squamous cell carcinoma
without biopsy. • Spreading pigmented AK: AKs with
fine reticulated pigmentation. May mimic solar lentigo,
melanoma in situ. • Hypertrophic AK: firm, thick, ele-
vated keratotic AK that may indicated progression to true
SCC. More aggressive treatment required. Actinic
cheilitis: sun-induced keratinocyte atypia, lower lip.
Focal crusting, scaling, along with blurring of vermilion
border—appears whitish, gray. Actinic lesions in this
location can be subtle clinically, behave aggressively.
• AKs of lower legs frequently multiple, hyperkeratotic,
distributed over large area. Numerous lesions may form
on dorsal hand.
TREATMENT
• Patients with multiple AKs require frequent follow-up.
• Visible or detectable lesions represent fraction of total
number of atypical keratinocytes present. • Most of
atypia scattered within sun-damaged skin and below
level of clinical detection. • Multiple AKs indicates that
patients are much more likely to develop more lesions
with time. • Application of liquid nitrogen (cryotherapy)
to solitary, superficial lesions is most common removal
method. • Patients with significant photodamage, mul-
tiple and recurrent lesions, present difficult treatment
problems. • Topical 5-fluorouracil 5% useful in reducing
number of atypical keratinocytes. Erythema will appear
if AKs present. Followed by burning and oozing. Treat-
ment may be stopped before completing 3-week course
if inflammation too intense. • Diclofenac sodium
(Solaraze) gel, imiquimod (Aldara) 5% cream, and photo­
dynamic therapy are other methods used to treat an
entire area of photodamaged skin, multiple AKs and
reduce skin cancer risk. • All therapies have a potential
risk of post-procedure hypopigmentation, scar forma-
tion, especially in darker-skinned patients. Clearly
explain this to patient before treatment. • Carbon dioxide
laser vermillionectomy and topical 5-fluorouracil 5%
cream possible treatments for actinic cheilitis. • Squa-
mous cell carcinoma can develop from AK, especially
with thicker lesions, lesions non-responsive to treat-
ment, and lower lip lesions. Consider biopsy to look for
invasive SCC in patients who do not respond appropri-
ately to treatment and in recurrent or hypertrophic AKs.
 Squamous cell carcinoma
DDx Ref  59 • 119 • 126
128 

Squamous cell carcinoma is commonly found on

the ears. The thick smooth mass had been
present for over 1 year. Dense scale has formed
on the surface.

A hard mass was present for 2 years. Erosion and

bleeding prompted a visit to the physician.

This lower lip tumor appears to be a superficial

actinic keratosis. Palpation revealed a large firm
mass in the dermis. Biopsy showed squamous
cell carcinoma.

Retention of dense scale on a hard mass

suggests the diagnosis of squamous cell
carcinoma.
128 Squamous
DDx Ref 
cell carcinoma
59 • 119 • 126

DESCRIPTION
Invasive, primary cutaneous malignancy arising from
keratinocytes of skin and mucosal surfaces. Most
commonly on the sun-damaged area of the head,
neck, hands of elderly. Can occur at any location.
Lesions may develop from precursor actinic kera-
toses or de novo. Second most common form of skin
cancer; 20% of all primary cutaneous malignancies.
Lifetime risk estimated to be 5–15%; > 200 000 new
cases of primary squamous cell carcinoma (SCC) in
USA each year, 2500 deaths annually.
HISTORY
• Occur on sun-exposed skin from years of accumu-
lated actinic damage. • In men, 90% of cutaneous
SCCs—nearly 80% in women—occur on head,
neck, hands. SCC on legs more often in women.
• White people with fair skin at greatest risk. • Ultra-
violet radiation (sunlight) is the primary cause of most
SCCs. Other factors include arsenic, tobacco, chemi-
cals, chronic inflammation, chronic infections,
chronic immunosuppression, burn scars, human
papillomavirus infection. • Incidence doubles with
each 8–10° decline in latitude. • Ultimately, tumors
metastasize, via the lymphatics, to other organs.
PHYSICAL FINDINGS
• Typically occur on sun-exposed areas. Found
within a background of sun-damaged skin with
atrophy, telangiectasia, blotchy hyperpigmentation.
• Early invasive SCC may have appearance of
hypertrophic actinic keratosis. Red, poorly defined
base and adherent, yellow-white cutaneous horn.
• Untreated lesion becomes larger, more raised,
developing into a firm red nodule with necrotic
crusted center. • May arise de novo, appearing as
sharply defined, smooth, dull-red, firm, dome-
shaped nodule with crusted center. Removal of crust
reveals central cavity filled with necrotic keratin
debris. • Keratoacanthoma now considered a variant
of invasive SCC. Most consider keratoacanthoma a
low-grade form of SCC. • Diagnosis based on histol-
ogy. • Metastases usually to regional lymph nodes.
Detected within 2–3 years. Palpable regional lymph
nodes suggest metastatic disease.
TREATMENT
• Excellent long-term prognosis for adequately
treated SCC. • Increased risk of developing additional
primary skin malignancies. • Metastatic rate of SCC
arising on sun-exposed skin: 2–6%. • Patients on
immunosuppressive therapy after organ transplanta-
tion at higher risk for all cutaneous malignancies,
especially SCC, 5–10 years after transplantation.
• Treatment of primary SCC involves wide local exci-
sion with histologic confirmation of margins. Mohs
micrographic surgery may be useful for specific sites,
such as the central face, where tissue sparing impor-
tant. • Palpation of regional lymph nodes mandatory
for all patients. • Lymph node biopsy indicated for
suspected nodal disease. • May consider radiation
therapy when surgical resection not feasible.
• Careful follow-up at regular intervals recom-
mended for all patients.
 Bowen disease
DDx Ref  15 • 37 • 133
129 

Bowen disease is a slowly growing lesion with in

situ or intraepithelial atypical squamous cells.
This plaque looks like psoriasis.

The diagnosis of Bowen disease is often not

made until after biopsy. This plaque looks like
actinic keratosis.

Bowen disease of the penis showing a mild pink

to red inflammatory patch on the glans; may be
confused with psoriasis or lichen planus. If
diagnostic doubt exists, confirm with biopsy.

Bowen disease may arise in sun-exposed and

sun-protected areas. It may be patch or
plaque-like and resemble eczema or psoriasis.
129 Bowen disease
DDx Ref  15 • 37 • 133

DESCRIPTION
An intraepidermal (in situ), primary cutaneous malig-
nancy arising from keratinocytes of the skin. Consid-
ered an early variant of squamous cell carcinoma.
Arises in both sun-exposed and sun-protected areas.
Etiologies include ultraviolet light (actinic), chemicals
such as arsenic, and human papillomavirus.
HISTORY
• Lesions are persistent and slowly enlarge over
months to years. Slow progression ultimately leads
to invasion. • They are minimally symptomatic, and
patients often delay seeking care. • Unlike actinic
keratoses (partial thickness), Bowen disease repre-
sents full-thickness replacement of the epidermis
with tumor cells. Bowen disease is less common and
a potentially more aggressive lesion.
PHYSICAL FINDINGS
• Solitary, barely raised, red plaque with adherent
dry scale or irregularly fissured, adherent scale.
Border is slightly elevated and very well demarcated.
Little if any inflammation is present. • May resemble
a single plaque of psoriasis or eczema. • Focal areas
of pigmentation may resemble pigmented basal cell
carcinoma and lentigo maligna. • Over many years,
the plaque extends laterally, becoming an invasive
squamous cell carcinoma. • Erythroplasia of Queyrat
is also squamous cell carcinoma in situ occurring on
the glans penis. These lesions are red, sharply
defined, and have a moist, glistening surface. Analo-
gous in situ lesions occur on the vulva. These lesions
can progress into squamous cell carcinoma. Erythro-
plasia of Queyrat has a greater tendency toward
invasion and metastases, estimated at 10–30%.
TREATMENT
• Bowen disease should be treated as invasive squa-
mous cell carcinoma until proven to be in situ squa-
mous cell carcinoma by biopsy. • Destruction or
excision of Bowen disease is optimal. Other treat-
ment modalities include curettage, cryosurgery,
topical 5-fluorouracil, and imiquimod cream. • Close
follow-up after any treatment is mandatory. Any
areas suspicious for recurrence should be biopsied
or excised without delay.
 Leukoplakia
DDx Ref  43 • 67 • 127
130 

Leukoplakia is a common, sometimes chronic

condition of the oral mucosa.

Leukoplakia usually appears after the age of 40,

and prevalence approaches 8% after age 70.

Leukoplakia. The white patches are slightly

elevated and well demarcated.

Leukoplakia 2 weeks after treatment with topical

5-fluorouracil.
130 Leukoplakia
DDx Ref  43 • 67 • 127

DESCRIPTION
Leukoplakia is a descriptive clinical term reserved for
white patches or plaques occurring on the mucosal
surfaces pending definitive diagnosis. It is a descrip-
tive clinical term, not a definitive diagnosis. The term
is often misused to designate a premalignant
condition.
HISTORY
• A common, sometimes chronic condition of the oral
mucosa. • Occurs more frequently in men than in
women. • Usually appears after age 40, and the
prevalence approaches 8% after age 70. • Most
lesions are asymptomatic.
PHYSICAL FINDINGS
• Leukoplakia begins as a single small, well-defined,
translucent to white, slightly elevated papule. • Indi-
vidual lesions may resolve completely, recur, or
progress. Multiple papules may coalesce into larger
plaques over time. • Uneven hyperkeratosis or small
erosions may develop. • Focal red areas or discrete
papules termed erythroplakia may develop within
plaques, giving a speckled appearance. • Lesions
may occur anywhere on the oral mucosa but are
most commonly found on buccal mucosa and lower
lip. • Differential diagnosis includes candidiasis, oral
hairy leukoplakia, white sponge nevus, lichen planus,
squamous cell carcinoma.
TREATMENT
• Encourage patients who use tobacco products to
stop. • Any area of change within the leukoplakia
patch, especially areas of erythroplakia, should be
biopsied without delay. • Localized areas of epithelial
dysplasia may be treated by cryosurgery, electrocau-
tery, or topical 5-fluorouracil. Combinations of these
therapies are sometimes used. • Areas demonstrat-
ing squamous cell carcinoma, either in situ or inva-
sive, are best treated with surgical excision. Close
clinical follow-up, including lymph node examination,
is required. • Indefinite close clinical follow-up is
required after treatment to detect recurrence early.
This includes inspection of other areas of the oral
mucosa, as well as regional lymph node examination.
• Progression to squamous cell carcinoma develops
in 15–20% of all patients with leukoplakia.
 Cutaneous T-cell
lymphoma
DDx Ref  15 • 37 • 77
131 

Early lesions are red with subtle scale or fine

wrinkles. They persist for months with little
peripheral extension and are often diagnosed as
eczema.

Infiltration of the entire skin produces thickened

red skin with or without scale. These features are
subtle, not always clinically diagnostic, and may
require a biopsy for diagnosis.

Pink to red, slightly scaly patches of early mycosis

fungoides; may be present for months or years, and
misdiagnosed as eczema. Biopsy can help differentiate
these subtle changes of cutaneous T-cell lymphoma.

Tumors develop from pre-existing plaques or

erythroderma. Tumors can vary in size; some
become huge.
131 DDx Ref  Cutaneous T-cell
lymphoma
15 • 37 • 77

DESCRIPTION
Also known as mycosis fungoides, this is a distinct
helper T-cell lymphoma of skin. T-lymphocytes
invade the skin, lymph nodes, peripheral blood,
internal organs.
HISTORY
• Evolves through several stages: early or pre-myco-
sis fungoides, patch, plaque, tumor stage. Stage
varies from patient to patient. • Sézary syndrome is
the blood or leukemic form. More common in men,
African-Americans. Typically diagnosed in fifth or
sixth decade.
PHYSICAL FINDINGS
• Parapsoriasis. Controversial term used to describe
pre-mycosis fungoides phase. Looks very similar to
patch-stage cutaneous T-cell lymphoma (CTCL). May
be a precursor stage, but it may not respond to
repeated courses of topical steroids, and persist for
months or years. • Patch stage. Appears eczema-
tous. Red to pink, scaly, atrophic, mottled, telangiec-
tatic eruption. • Plaque stage. Dusky-red to brown,
slightly elevated patches, plaques. Often located on
‘bathing trunk’ area: buttocks, hip, upper thighs.
Inner aspects of upper arms, legs (skin folds) involved
early. Shape of individual plaques varies: round,
oval, arciform, or serpiginous, with central clearing.
• Tumor stage. Red-brown expanding nodules, vari-
able in size, may be ulcerated. • Sézary syndrome.
Erythroderma and generalized scaling. Palms, soles
may be thickened. Alopecia, ectropion common. Infil-
tration of entire skin produces red, thickened skin
with increased scale (exfoliative dermatitis) or
without scale (erythroderma). Peripheral node
enlargement, generalized pruritus also common.
Frequently misdiagnosed as atopic dermatitis.
Other skin diseases resembling CTCL include plaque
and pustular psoriasis, drug eruptions, allergic
contact dermatitis.
TREATMENT
Stage-related. Referral to dermatologist or oncologist
is recommended for staging, treatment. • Patch,
plaque stages. Topical chemotherapy (nitrogen
mustard, carmustine), psoralen plus ultraviolet A,
ultraviolet B, total-body electron beam therapy, inter-
feron, combination of these therapies used. • Tumor
stage. Spot radiation, interferon can be effective.
• Erythroderma or Sézary syndrome. Extracorpor-
eal photopheresis, interferon, methotrexate, pred-
nisone, cyclophosphamide (Cytoxan), combinations
of these therapies used, along with supportive care
if needed. • Generally, course and prognosis relate
to disease stage and are extremely variable. Early
CTCL and patch stages can last many years without
progression to tumor development, adenopathy,
internal organ involvement. Some patients simply
have smoldering inflammatory changes resembling
eczema that are kept under control with topical ster-
oids. At the other end of the spectrum is progression
to plaque and tumor stage, visceral organ infiltration.
Necrosis, ulceration of plaques, tumors common in
progressive cases. May eventually involve lymph
nodes and viscera; if no response to treatment, CTCL
can be fatal.
 Paget disease
of the breast
DDx Ref  20 • 129 • 137
132 

Early Paget disease. There is erythema and scale

in the center of the nipple. The areola is not
involved.

The disease begins insidiously in one breast with

a small area of erythema on the nipple that drains
serous fluid and may form a crust.

Malignant cells migrate through the epidermis,

and the disease becomes initially apparent on the
areola and much later on the surrounding skin.

The process appears eczematous, but the plaque

is indurated and has sharp margins, which remain
relatively fixed for weeks.
132 DDx Ref  Paget disease
of the breast
20 • 129 • 137

DESCRIPTION
An uncommon, distinctive clinical presentation of
intraductal carcinoma of the breast. It is the most
common cutaneous presentation of breast cancer.
However, only represents 5% or less of all breast
cancer cases.
HISTORY
• Occurs almost exclusively in women and is rare in
men. • Incidence increases with age, reflecting the
incidence of breast cancer. • An insidious onset,
lasting months to years, usually in the fourth to sixth
decades. • May be asymptomatic. • Often misdiag-
nosed as nipple eczema. Should be suspected in
cases of nipple eczema that do not improve after the
use of topical corticosteroids. • Prognosis deter-
mined by breast cancer staging and therapy. The
5-year survival rate exceeds 90% when neither a
breast mass nor regional lymph nodes are palpable.
The 5-year survival rate is roughly 40% when an
underlying breast mass is palpable.
PHYSICAL FINDINGS
• Lesions are pink to red, sharply demarcated, irreg-
ularly shaped, scaly patch or plaque. The nipple,
areola, and surrounding skin may be involved. • Most
often it is unilateral, but it can be bilateral. • Initially,
induration is minimal. Over time, induration, infiltra-
tion, and nodularity develop. • An underlying breast
mass is palpable in roughly 50% of cases. • Eventu-
ally, there is local destruction of the nipple and areola
with retraction. • Underlying intraductal carcinoma is
found in the affected breast. • The contralateral
breast should also be examined carefully. The risk of
cancer in the second breast is increased in patients
who already have cancer in one breast. • The
regional lymph nodes are rarely palpable unless a
palpable breast mass or superficial ulceration is
present. • Skin biopsy confirms the presence of
Paget cells, which are large, round, pale, mucin-
producing cells within the epidermis. Deep biopsy
may show continuity with an underlying intraductal
carcinoma. • Differential diagnosis includes erosive
adenomatosis of the nipple, Bowen disease, superfi-
cial basal cell carcinoma, tinea, Candida, and contact
dermatitis.
TREATMENT
• Perform skin biopsy for all dermatoses involving
the nipple that do not respond to topical therapy or
that persist for more than 1 month. A skin biopsy
should be performed to confirm the diagnosis.
• Breast and nodal examination indicated for all
patients with Paget disease of the breast. • Mam-
mography should be performed on both breasts.
• Referral to a breast cancer surgeon should be
made for further evaluation of any palpable breast
mass. • For biopsy-confirmed breast carcinoma,
treatment can include surgery, radiotherapy, chemo-
therapy, and hormonal therapy as indicated.
 Extramammary
Paget disease
DDx Ref  37 • 70 • 129
133 

Extramammary Paget disease is a rare

intraepidermal adenocarcinoma that presents on
the scrotum in men and vulva in women. It may
be misdiagnosed as eczema or tinea.

The disease appears as white to red, scaling or

macerated, infiltrated, eroded or ulcerated plaque
most frequently observed on the labia majora and
scrotum.

Three biopsies were taken before malignant cells

were demonstrated at the periphery of this
chronic ulcer at the base of the scrotum.

White eroded plaque with ill-defined borders on

the labia are features of extramammary Paget
disease that can be confused with lichen
sclerosis.
133 DDx Ref  Extramammary
Paget disease
37 • 70 • 129

DESCRIPTION
Intraepidermal adenocarcinoma involving anogenital
or axillary skin. Occurs in areas where apocrine
glands are found. May be divided into two groups
based on source of underlying primary adenocarci-
noma. • Most cases represent adenocarcinoma in
situ with extension of primary adenocarcinoma in situ
from adnexal structures. Apocrine gland carcinoma
is the most common associated malignancy. • A
minority of cases reflect an intraepidermal spread of
tumor cells from non-cutaneous adenocarcinomas,
via local or lymphatic spread. Urogenital and rectal
carcinomas are the most common associated non-
cutaneous adenocarcinoma. Local contiguous or
regional lymphatic spread of these carcinomas leads
to intraepidermal invasion.
HISTORY
• Rare before age 40. • More common in women
than in men. • On vulva and perineum in older
women. In men, scrotum, penis, anal and perianal
skin most commonly affected. • May extend to
involve lower abdomen, inguinal folds, buttocks,
thighs. • Lesions slowly and relentlessly increase
in size.
PHYSICAL FINDINGS
• A red to white-gray plaque with a velvety or scaly
surface is typical. The plaque is sharply demarcated
and has irregular borders. The lesion may appear
eczematous or lichenified. Scaling, erosion, and
serous exudate may occur. • Most often unilateral.
• Differential diagnosis includes eczema, psoriasis,
intertrigo, tinea, Candida, lichen simplex chronicus,
and Bowen disease. • Depending on site of origin,
the non-cutaneous primary adenocarcinoma may be
visible and palpable. Regional lymph nodes are
usually not palpable early in the course of the
disease. • Unlike Bowen disease, dermal invasion
and regional metastases appear to occur earlier in
the disease course. • Fewer than 25% of all patients
with extramammary Paget disease have an under­
lying non-cutaneous malignancy. Of those patients
with underlying malignancy, 25% eventually die from
the underlying malignancy. • Most common sites of
metastases are the inguinal and pelvic lymph nodes,
followed by liver, bone, lungs, brain, bladder, pros-
tate, and adrenal glands. Regional and widespread
metastases may develop from any one of the primary
sites.
TREATMENT
• Local excision with obvious clear margins of the
involved areas is standard. • Although lesions appear
sharply defined clinically, histologic confirmation of
margins is vital. Surrounding, clinically normal-
appearing skin may also be involved. • High recur-
rence rate, even after excision with apparently
appropriate margins. • May be benefit from Mohs
micrographic excision as initial procedure. • Dissec-
tion of palpable regional lymph nodes may be war-
ranted. • Radiotherapy also an option for difficult
cases, recurrent disease.
 Cutaneous metastasis
DDx Ref  47 • 117 • 145
134 

Cutaneous metastases occur in 0.7–9.0% of all

cancer patients. Cutaneous metastasis occurs in
24% of all breast cancer patients.

About 75% of skin metastases in male patients

occur on the head, neck, and anterior chest and
abdomen.

In female patients, about 75% of skin metastases

occur on the anterior chest or abdomen.

Most cutaneous metastases do not have a distinct

clinical appearance. Most present as a cluster of
discrete, firm, painless nodules on the trunk or
extremity.
134 Cutaneous
DDx Ref 
metastasis
47 • 117 • 145

DESCRIPTION
Occurs in 0.7% of cancer patients. Detection alters
disease staging, therapy. Cutaneous metastases pre-
senting as first sign of malignancy occur most fre-
quently with lung, kidney, ovarian tumors. • Women:
most common cancers causing cutaneous metasta-
sis are breast (70%), colon (9%), melanoma (5%),
lung (4%). • Men: most common cutaneous meta-
static cancers are lung (24%), colon (19%), melanoma
(13%), oral squamous cell carcinoma (12%).
Abdominal wall is most common site for tumors
presenting as metastatic disease. Scalp metastases
in men tend to be from lung or kidney and present
early. Scalp metastases in women tend to be from
breast and present late. Facial metastases tend to be
from oral squamous cell carcinoma, renal cell carci-
noma, lung and breast cancer. Eyelid metastases
tend to be from breast or melanoma. Neck metas-
tases more often direct extensions from deep nodes
from lung, oral squamous cell carcinoma, or breast
carcinoma. Most cutaneous metastases lack a dis-
tinct clinical appearance.
PHYSICAL FINDINGS
Breast cancer
Cutaneous metastasis is presenting sign in 3.5% of
all breast cancer, occurs in 24% of cases. Seven
distinct patterns of metastatic breast cancer.
• Inflammatory metastatic carcinoma. Resembles
erysipelas over anterior chest in absence of fever.
• En cuirasse metastatic carcinoma. Diffuse,
morphea-like induration of skin of chest (‘encase-
ment in armor’). • Telangiectatic metastatic
carcinoma. Violaceous papulovesicles resemble
lymphangioma circumscriptum. May be pruritic. May
resemble vasculitis. • Nodular metastatic carci-
noma. Multiple firm papules or nodules appear on
anterior chest. May resemble melanoma or pig-
mented basal cell carcinoma. • Alopecia neoplas-
tica. Asymptomatic, non-inflammatory, circular
areas of alopecia. • Paget disease of the breast.
Sharply defined plaque of erythema and scaling on
breast, suggesting eczema, but eruption is persist-
ent. Represents a direct spread from underlying
breast cancer. • Most common representation of
cutaneous breast metastasis is an aggregate of dis-
crete, firm, non-tender, skin-colored nodules.
Lung carcinoma
Localized single nodule or cluster of non-specific,
red-purple-brown nodules, most often on anterior
chest, abdomen and back.
Colon and rectal carcinoma
Usually presents on abdomen and perineum as ero-
sions, ulcerated nodules associated with cutaneous
fistulas.
Melanoma
Cutaneous metastatic melanoma appears small, 2-
to 5-mm, blue to black papules with ‘blueberry-like’
appearance. Skin is most common primary site of
melanoma, followed by ocular and mucosal sites.
Renal cell carcinoma
Typically presents on head and neck region as
well-circumscribed, bluish to brown nodule with
prominent vascularity.
Oral squamous cell carcinoma
Usually occurs in men with known primary tumor.
Presents as multiple nodules on head and neck
region.
 Nevi, melanocytic
nevi, moles
DDx Ref  115 • 117 • 142
135 

This is a common presentation for a scalp nevus.

There is no pigment, and the surface is lobulated.

Halo nevus. A white halo appeared around a

benign-appearing nevus. The nevus then slowly
disappeared over a 3 year period.

A junction nevus with a slightly raised, brown,

uniform surface. The lesion had been present for
years.

A dermal nevus with horn pearls on the surface. It

is stuck on to the surface and has the consistency
of a seborrheic keratosis.
135 DDx Ref  Nevi, melanocytic
nevi, moles
115 • 117 • 142

DESCRIPTION
Benign growths composed of melanocyte-derived
nevus cells, classified by age of onset, arrangement
of nevus cells within skin.
HISTORY
• Nevi are ubiquitous; most adults have 12–20.
• Incidence of acquired nevi peaks during adoles-
cence. Few appear after age 30. • Most acquired
nevi appear on sun-exposed skin, are asymptomatic.
Consider nevi in sun-protected areas suspicious.
• May become darker during puberty, during preg-
nancy. • Acquired nevi begin as flat, round, uniformly
colored papules. Nevi mature by expanding laterally
and symmetrically. • Usually elevate and lighten over
time, eventually becoming a skin-colored papule.
PHYSICAL FINDINGS
• Junctional nevi. Flat or slightly raised brown to
tan macules, mostly in children. Nevus cells cluster
at dermoepidermal junction. Nevi of palms, soles,
genitalia, mucosa usually junctional. • Compound
nevi. Raised pigmented papules. Nevus cells found
at dermoepidermal junction and within dermis. Can
have irregular border but are symmetric. • Intra­
dermal nevi. Usually elevated, fleshy, pigmented
papules, but may contain no pigment. Nevus cells
found within dermis, sometimes extending into sub-
cutaneous fat. • Nevus spilus. Similar to a café-
au-lait spot but contains small, monomorphic, dark
brown junctional nevi. • Blue nevi. Solitary, dark
bluish papules usually on head, neck, buttocks. Color
due to intensely pigmented melanocytes in deep
dermis. • Spitz nevus. Reddish pink, dome-shaped,
smooth papule found usually on face, scalp, limbs of
children. While benign, Spitz nevi contain pleomor-
phic nevus cells. Most dermatologists favor complete
removal. • Halo nevi. Occur primarily during adoles-
cence. A pre-existing nevus develops surrounding
hypopigmentation then gradual disappearance of
nevus. Halo nevi appear to be a host response
directed against nevus cells. • Recurrent nevus
phenomenon. May occur at site of previously par-
tially removed nevus. Random pleomorphic nevus
cells along with scar can be suspicious for melanoma.
Most melanocytic nevi are benign and follow the
course of maturation described above. Nevi that
deviate from this pattern are suspicious and biopsy
is warranted.
TREATMENT
• Assess all nevi regularly, carefully, singly and in
aggregate. • Most benign nevi symmetric, less than
6 mm in diameter, with well-defined, regular border,
uniform color. • Regard nevi appearing different from
others on same patient with suspicion. • Biopsy
suspicious nevi. • Examine entire cutaneous surface.
• Educate patients to self-examine all skin areas
periodically. Review changes to watch for.
 Atypical mole syndrome
(dysplastic nevus syndrome)
DDx Ref  115 • 117 • 137
136 

Atypical mole syndrome consists of multiple

clinically atypical nevi, together with an increased
risk of melanoma. It occurs as a familial
syndrome.

The fried egg pattern for an atypical nevus.

The center is dark and raised with a lighter,
less distinct scalloped border.

The pigmentation of atypical nevi has several

distinct patterns. Here, there is a broad
homogeneous white center with a hyper­
pigmented rim.

Here, the hypopigmented and hyperpigmented

components are intermixed. Magnification with
dermoscopy showed that the pigmentation was
uniform.
136 DDx Ref  Atypical mole syndrome
(dysplastic nevus syndrome)
115 • 117 • 135

DESCRIPTION
Multiple clinically atypical nevi, with increased
melanoma risk. Familial syndrome or sporadic.
HISTORY
• As familial syndrome, affected members have
many irregular nevi, multiple family members with
melanoma. Inheritance appears autosomal dominant
with variable penetrance. • Nevi were considered
marker for risk of developing melanoma. • Syndrome
is uncommon. • Solitary atypical nevi common,
prevalence of 5–20%. • Males, females equally
affected. • Atypical nevi not present at birth; begin
appearing in childhood. Unlike common acquired
nevi, which stop appearing after age 30, atypical nevi
continue to appear in adulthood. • While sun expo­
sure favors appearance of nevi, lesions also develop
in sun-protected areas. • Most affected people have
> 50 nevi, some of which appear atypical. • Striking
heterogeneity from one nevus to another. • Atypical
nevi regarded as along continuum between benign
and malignant melanocytic neoplasms. Likelihood of
an individual atypical nevus subsequently developing
into melanoma cannot be estimated. Lifetime
melanoma risk estimated at 1.3%. Risk for persons
with atypical nevi, but without family history of
melanoma, estimated at 6%. Risk increases to 15%
in patients with atypical nevi and family history of
melanoma. Persons with familial atypical nevi have
150-fold increased risk of developing melanoma by
age 70, 500-fold increased risk if patient has already
had melanoma.
PHYSICAL FINDINGS
• Atypical nevi usually larger (6–15 mm in diameter),
with irregularly outlined, indistinct border. Color
varies: pink, tan, brown, black. Surface irregular,
may contain central or eccentric papule surrounded
by a prominent macular component. • Affected
persons often have nevi in sun-protected areas.
• Pathologists often use terms such as mild to
moderate atypia when describing these lesions. This
does not mean that they are or would have evolved
into a melanoma.
TREATMENT
• Patients with atypical nevi should have routine
full-skin examinations after puberty, with follow-up
every 3–12 months. Consider dermatologic referral
for regular monitoring of nevi. Examine entire cuta­
neous surface. Also examine family members.
• Changing lesions should be biopsied. • Emphasize
patient education and awareness. Teach patients to
perform regular skin self-examinations. • Consider
photomapping to assist patient in self-monitoring
between visits.
 Malignant melanoma,
lentigo maligna
DDx Ref  115 • 136 • 142
137 

Melanoma represents 4% of all cancers in men

and 3% of all cancers in women. This innocuous
pigmented lesion on the nose was shown to be
lentigo maligna on biopsy.

It cannot be overemphasized that melanomas vary

considerably—no single color or change is diagnostic.
This melanoma has areas of inflammation (red),
regression (white), and deeper pigment (blue).

Lesions tend to be greater than 6 mm in diameter,

flat, and asymmetric, with varying coloration. This
advanced lesion shows ulceration.

Lesions appear and tend to spread laterally within

the skin over a few years, before nodules develop
within the lesion and necrosis develops, as shown
here in this acral lentiginous melanoma.
137 DDx Ref  Malignant melanoma,
lentigo maligna
115 • 136 • 142

DESCRIPTION
An increasingly common malignancy of
melanocytes.
HISTORY
• Lifetime risk of melanoma is 1 in 75. Risk factors
include skin types 1 or 2, atypical nevi, personal or
family history of melanoma, history of blistering
sunburn, large congenital nevi. • Thirty percent
of melanomas develop within a pre-existing nevus.
• The thinner the melanoma, the better the
prognosis.
PHYSICAL FINDINGS
Melanomas vary in appearance. No single color or
change is diagnostic. When melanoma develops in a
pre-existing lesion, there is usually a focal color
change. Four clinical subtypes of melanoma are rec-
ognized. • Superficial spreading melanoma. Most
common subtype. Occurs most often on trunk and
extremities. Lesions usually flat, asymmetric, with
varying colors. Tends to spread laterally. • Nodular
melanoma (10–15%). Tends to occur on extremities
as raised, brown to black, rapidly growing papules.
• Lentigo maligna and lentigo maligna melanoma
(5–10%). Represent in situ melanoma and progres-
sion to invasive melanoma. Develop over years on
sun-exposed white skin, most often on face. Lesions
flat, brown, mottled. • Acral lentiginous melanoma
(7%). Occurs on hands and feet, including nails of
people with darker skin types. Lesion similar in
appearance to lentigo maligna.
Amelanotic melanoma (2%). Describes a non-
pigmented melanoma of any subtype. The lesion is
an innocent-appearing, enlarging, pink-red papule.
TREATMENT
• Biopsy report should state diagnosis, anatomic site,
Breslow level (vertical thickness), whether margins
are involved. Breslow level is single most important
prognostic factor. Ulceration is the second most
important prognostic factor. • Palpate regional
nodes. Suspicious nodes should be evaluated by
nodal biopsy. Best biopsy technique is complete exci-
sion of entire lesion. Shave biopsy not recommended.
May consider incisional or punch biopsy for large
lesions or lesions in cosmetically important areas.
The most suspicious area should be included in
biopsy. • Once melanoma confirmed by biopsy, reex-
cision with appropriate surgical margins is deter-
mined by Breslow. Melanoma in situ requires margin
of 0.5 cm. A 1.0-cm margin recommended for tumors
up to 2.0 mm thick; a margin of 2.0 cm recom-
mended for tumors up to 4.0 mm thick. Sentinel node
biopsy is performed for thicker tumors. Sentinel
lymph node status predicts risk of recurrence and
mortality. • Adjuvant treatment for advanced disease
often recommended with interferon. • Follow-up
examination is performed at regular intervals.
Includes visual examination of entire skin surface,
palpation of regional and distant nodes, and palpation
of liver.
 Melanoma mimics
DDx Ref  115 • 142 • 145
138 

Seborrheic keratosis with an irregular border and

a white area that mimics regression in a
melanoma. The white surface horn pearls support
the diagnosis of seborrheic keratosis.

Seborrheic keratosis. A large, multicolored lesion.

Magnification showed scale over the entire
surface and black horn pearls imbedded in the
dark thick areas.

Seborrheic keratosis. The lesion is black with an

irregular notched border. The large, black, surface
horn pearls support the diagnosis of seborrheic
keratosis.

Seborrheic keratosis. A dome-shaped, black

lesion that mimics nodular melanoma. Black
surface horn pearls support the diagnosis of
seborrheic keratosis.
138 Melanoma
DDx Ref 
mimics
115 • 142 • 145

DESCRIPTION
Melanocytic or non-melanocytic skin lesions that may
clinically and/or histologically resemble melanoma.
HISTORY
• Benign melanocytic nevi may be clinically suspi-
cious for melanoma. • Roughly 30–50% of melano-
mas arise in pre-existing melanocytic lesions. • Nevi
classified as junctional, compound, intradermal
based on location of nevus cells within skin. • Most
nevi symmetric, sharply defined, less than 6 mm at
greatest diameter, usually one dominant color,
usually asymptomatic. Nevi that develop symptoms
or change appearance (size, shape, color) are suspi-
cious. • Atypical nevi often larger than 6 mm at
greatest diameter, tend to have indistinct borders,
variegated pigmentation.
PHYSICAL FINDINGS
• Blue nevi are benign melanocytic nevi with nevus
cells located deep within dermis. Blue to black color
may suggest melanoma. Blue nevi are defined, uni-
formly color, stable in appearance. • Combined nevi
are blue nevi associated with overlying benign junc-
tional, compound, or intradermal nevus. Combined
nevi are solitary, asymmetric with focal pigmenta-
tion. • Traumatized nevi often have hemorrhagic
crusting suggesting ulceration. Patients are usually
aware of trauma. • Nevi previously biopsied can
develop recurrent nevus phenomenon, with melano-
cyte hyperplasia on scar that resembles melanoma
clinically and histologically. Review of original biopsy
helps exclude melanoma diagnosis. • Pigmented
basal cell carcinoma contains melanin pigment.
Amount of melanin and its distribution vary. Lesions
often pink with focal blue to gray pigment, or jet
black. • Seborrheic keratoses often contain varying
amounts of melanin. Pigmentation uneven, asym-
metric; can grow rapidly. Lesions vary from flat to
verrucous; white to pink to jet black. • Spreading
pigmented actinic keratosis displays fine reticulated
pigmentation, thin scale. Lesions appear on sun-
damaged skin, simulate lentigo maligna melanoma.
• Vascular lesions, including cherry angiomas,
angiokeratomas, hemangiomas, can be red, purple,
black. • Friction injury to heel (talon noir) or nail
trauma may produce hemorrhage. Hemosiderin may
be present, suggesting melanin pigment. • Lesions
that mimic melanoma clinically are discriminated
from melanoma histologically. • Nevus cells of Spitz
nevus may be pleomorphic, indistinguishable from
melanoma cells on histologic grounds. Lesion archi-
tecture, patient’s age help discern Spitz nevus from
melanoma. • Lentigo maligna can be quite subtle,
can resemble benign junctional nevi histologically.
Junctional nevi are lesions of childhood; junctional
nevi from an adult are best considered suspicious.
TREATMENT
• Biopsy suspicious lesions. Histology often discerns
melanoma from lesions clinically suspicious for
melanoma. • Histologic mimics of melanoma include
malignancies derived from non-melanocytic cells.
Special stains reveal origin of malignant cells. •
Melanocytic lesions that mimic melanoma histologi-
cally, such as Spitz nevus, recurrent nevus, require
clinicopathologic correlation. • Management and
follow-up depend on histologic diagnosis.
 Congenital
melanocytic nevi
DDx Ref  135 • 136 • 137
139 

Congenital nevi are benign skin tumors composed

of melanocyte-derived nevus cells. Many lesions
have a pebbled surface and course terminal hair.

Congenital nevi with uniform surface

characteristics and light pigmentation have little
chance of degenerating into melanoma.

Congenital nevus with speckled surface showing

uniform, darkly pigmented papules on a lightly
pigmented background.

Congenital nevi may have a papular surface that

mimics cobblestones. Hyperpigmented brown
papules are uniformly distributed over the surface.
139 DDx Ref  Congenital
melanocytic nevi
135 • 136 • 137

DESCRIPTION
Benign growths composed of melanocyte-derived
nevus cells, present at birth or appearing by age
2 years. Considered a type of birthmark. Many
variants.
HISTORY
• Any melanocytic nevus present at birth or appear-
ing during infancy is considered a congenital melano-
cytic nevus. Roughly 1% of newborns have at least
one. • Nevi may increase in size, become more
heavily pigmented during puberty. • Usually asymp-
tomatic but may be irritated by clothing, external
trauma.
PHYSICAL FINDINGS
• Usually brown, raised, with an irregular verrucous
surface. Most have increased terminal hairs. Size
varies greatly. Depending on their location, large
lesions may be disfiguring. • Mongolian spots are
poorly defined patches colored blue-black to gray,
more commonly seen in the sacral region of new-
borns of darker skin. • Congenital nevi are usually
compound nevi with nevus cells at the junction and
in the dermis. Nevus cells may extend into fat, invest-
ing adnexal structures and blood vessels. • Mongo-
lian spots are equivalent to blue nevi histologically,
with pigmented spindle-shaped nevus cells deep in
the dermis. • Most congenital melanocytic nevi are
benign and follow the usual course of maturation.
Nevi that deviate from this pattern are suspicious,
and biopsy is warranted. Mongolian spots often fade
in early childhood. • The risk of malignant degenera-
tion occurring in congenital melanocytic nevi is con-
troversial. There is general agreement that risk of
malignant change is increased in congenital nevi with
diameters greater than 20 cm. Lifetime risk is esti-
mated at 5–8%. The risk of melanoma developing in
smaller congenital nevi is uncertain but is likely
increased in lesions larger than 2 cm. • Many der-
matologists favor elective excision of congenital nevi
when feasible, usually around the time of puberty.
Careful histologic review is needed by a qualified
dermatopathologist.
TREATMENT
• Assess all the patient’s nevi. • Educate patients
and parents on how to perform self-examination of
the skin; encourage them to do so on a regular basis.
Combine the teaching of self-examination techniques
with the screening skin examination. Review changes
to watch for, including symptoms of itching and ten-
derness, with the patient. • Benign nevi are usually
symmetric with well-defined borders, uniform in
color. Congenital nevi should increase in size in pro-
portion to the patient’s growth through adolescence.
Pigmentation should remain uniform. • Photography
helpful for following nevi. • Biopsy suspicious nevi.
• Large congenital nevi may be disfiguring, depend-
ing on location. Plastic surgery referral should be
considered for giant congenital nevi. Removal may
require serial procedures with tissue expanders.
 Hemangiomas of infancy
DDx Ref  141 • 143 • 145
140 

Ulceration is one of the most common

complications of hemangiomas of infancy. Midline
lumbar and sacral lesions can be associated with
underlying vertebral and spinal cord anomalies.

This early lesion on the dorsal aspect of the hand

and fingers involuted without treatment and
without functional loss of the hand.

The head and neck regions are the most common

locations for hemangiomas of infancy. This large
parotid hemangioma required oral steroids,
intralesional steroids, and surgical excision.

This plaque hemangioma involving the medial

cheek and nasal dorsum resolved completely
within 5 years. The patient had a 2-month course
of oral corticosteroids.
140 Hemangiomas
DDx Ref 
of infancy
141 • 143 • 145

DESCRIPTION
Benign red, purple, or blue vascular neoplasms due
to endothelial hyperplasia occurring within the first
year of life.
HISTORY
• Most common vascular tumor of infancy (1–3% of
newborns and 10% of 1-year-olds); 30% noticeable
at birth, most detected within the first 3 weeks of life.
Deeper lesions noted within first month of life; pre-
dictable pattern of growth, stabilization, and involu-
tion. • Half of all hemangiomas resolve by age 5.
• Lesion size, depth, location do not affect rate of
involution. • Most infants have single lesion; multiple
lesions in 15–20%. • Visceral involvement possible.
• More common in girls, premature infants, and head
and neck region; can damage function of eyes, ears,
mouth when located near these organs. • Mandible
(beard distribution) hemangiomas of infancy can be
associated with glottic hemangiomas. Large seg-
mental facial hemangiomas can be associated with
malformations of other organs (PHACES syndrome:
posterior fossa malformations, hemangioma, arterial
anomalies, coarctation of the aorta and cardiac
defects, eye anomalies, and sternal defects). Midline
hemangiomas of infancy can be associated with
underlying bony, soft tissue abnormalities. • Other
complications: pain, ulceration, infection.
PHYSICAL FINDINGS
• Nascent (early) hemangiomas of infancy appear flat
and pale white, with a few telangiectasias and large
dilated blood vessels. Growing hemangiomas appear
bright red (superficial) or blue (deep), feel firm and
rubbery. • The surface color of deeper lesions can
be very subtle. • Involuting hemangiomas become
slate-gray and begin to soften.
TREATMENT
• Follow closely for complications. • Avoid scarring
procedures, except when medically necessary to
prevent permanent deformity. • Ulcerations: gently
cleanse with mild soap, apply thin layer of a topical
antibiotic such as mupirocin 2% ointment (Bac-
troban), metronidazole gel (MetroGel), or bacitracin
ointment; cover with air-permeable barrier dressing
such as polyurethane film dressing, Tegaderm, and
OpSite. Barrier creams such as zinc oxide 20% oint-
ment, Desitin ointment, A&D ointment can be used
for the perineum and other sites not amenable to
topical dressings. Regranex (platelet-derived growth
factor) speeds healing and decreases pain. • Pulsed
dye laser for ulcerations can be useful but can
worsen ulceration in a small percentage. • Systemic
prednisone or prednisolone 2–3 mg/kg orally, given
as a single morning dose, is a widely used therapy
for complicated lesions. • Propranolol given at a dose
of 2 mg/kg/day divided b.i.d. or t.i.d. • Other medical
therapies include intralesional and topical corticos-
teroids, and topical beta-blockers such as timolol
maleate. • Embolization, surgical resection, and
radiation are sometimes used for complicated
hemangiomas.
 Vascular malformations
DDx Ref  139 • 143 • 146
141 

Capillary malformations can involve segments of

the skin.

Capillary malformations develop a cobblestone

appearance to the surface with age.

Laser treatment can be very effective to treat

large segmental port-wine stains.

Children with port-wine stains involving the first

division of the trigeminal nerve are at risk for
central nervous system, ocular, and bony
involvement (Sturge–Weber syndrome).
141 Vascular
DDx Ref 
malformations
139 • 143 • 146

DESCRIPTION
Anomalies of blood and lymphatic vessels due to
abnormal development and morphogenesis.
HISTORY
• Present at birth but might not become noticeable for
months, sometimes years. • Classified by vessel type
(capillary, venous, arterial, lymphatic, mixed
(common), arteriovenous) and flow characteristics
(slow or fast). • Increase in size in proportion to
patient’s somatic growth. • Most sporadic, not inher-
ited. Inherited types include multiple glomuvenous
malformation, blue rubber bleb nevus syndrome (both
autosomal dominant). • Ten percent of infants with
large facial capillary malformations, especially involv-
ing trigeminal nerve V1 (forehead and upper eyelid),
are at risk for underlying eye (glaucoma in 30–70%)
and central nervous system (seizures in 70–80%)
involvement (Sturge–Weber syndrome). • Large
cervicofacial lymphatic malformations can compro-
mise airway. • Arteriovenous malformations can
cause cardiac failure due to shunting; head and neck
arteriovenous malformations can cause seizures and
focal neurologic deficits. • Capillary malformations
can darken with age, develop a cobblestone appear-
ance. • Extensive venous and arterial malformations
can involve deeper structures (e.g. muscle) and be
a source of local or disseminated coagulopathy.
• Vascular malformations may cause alterations in
underlying bone and soft tissue, resulting in functional
disability. • Lymphatic malformations can be compli-
cated by pain, swelling, intralesional bleeding,
infection.
PHYSICAL FINDINGS
• Capillary malformations (slow flow). Macular
staining occurs commonly on the eyelids (‘angel
kiss’), forehead, and nuchal area (‘stork bite’). Capil-
lary malformations can be more substantial and
involve a segment and/or segments of skin innervated
by the trigeminal nerve (V1–V3). • Venous malfor-
mations (slow flow). Blue and spongy-appearing.
Enlarge with Valsalva maneuver. Can be painful. May
contain hard calcified nodules called phleboliths.
• Lymphatic malformation (slow flow). Small
lymphatic channels (microcystic) or large channels
(macrocystic) can be localized or diffuse. Lymphangi-
oma circumscripta (microcystic) consists of small
(1–5 mm) discrete, clear to blood-tinged papules that
look like vesicles (‘frog spawn’). Cystic hygroma
(macrocystic) commonly occurs in the cervicofacial
region. • Arterial malformations (fast flow). Arterial
malformations (aneurysm, stenosis, arteriovenous
malformation) can cause minimal skin signs (pink
stain), or they can produce massive swelling, ulcera-
tion, and necrosis. Arteriovenous malformations can
be quiescent for years only to cause disability through
blood shunting in puberty. Arteriovenous malforma-
tions most common in head and neck region.
TREATMENT
• Pulsed dye laser for capillary malformations.
• Compression stockings, low molecular weight
heparin, hydrotherapy, massage, and physical
therapy for coagulopathies associated with venous
malformations. • Laser surgery, surgical resection,
embolization, and sclerosis are used alone or in
combination to treat complicated vascular
malformations.
 Cherry angioma
DDx Ref  137 • 143 • 146
142 

Early lesions are bright-red, smooth, dome-

shaped papules.

Early lesions occur mostly on the trunk.

Older lesions develop gray strands of fibrosis,

producing a multilobulated appearance.

Cherry angiomas may mimic pigmented nevi and

melanoma. Magnification or dermoscopy can be
helpful to distinguish the two.
142 Cherry angioma
DDx Ref  137 • 143 • 146

DESCRIPTION
Benign vascular neoplasm found in nearly all people
older than 30 years.
HISTORY
• Lesions appear gradually in adulthood and are
asymptomatic. • Multiple eruptive cherry angiomas
have been associated with bromide exposure,
sulfur mustard gas, and the glycol ether solvent
2-butoxyethanol. • The sudden appearance of mul-
tiple lesions may warrant a search for occult malig-
nancy, especially for small tumors capable of
hormone production (those in the pancreas, small
bowel, and respiratory system). • Undisturbed cherry
angiomas persist indefinitely. • Superficial trauma
may produce bleeding. • Isolated reports of patients
with hundreds of cherry angiomas arising in associa-
tion with pregnancy, and also in patients with ele-
vated prolactin levels, suggest that hormonal factors
may play a role.
PHYSICAL FINDINGS
• A few to hundreds of discrete, 0.5- to 5.0-mm,
smooth, dome-shaped to polypoid papules occur
mostly on the trunk but can be found on the head,
neck, and extremities. • Early smaller lesions are
cherry red, deeper larger lesions maroon.
TREATMENT
Ablation with electrocautery, laser surgery, cryosur-
gery, or by simple scissor excision carries slight risk
of scarring and dyspigmentation.
 Angiokeratoma
DDx Ref  55 • 135 • 137
143 

Angiokeratomas result from dilatation of

superficial blood vessels and epidermal
thickening.

The classic lesion is a compressible, blue-black,

discrete papule with a scant amount of scale.

Angiokeratoma occurring on the buttocks in a

patient with angiokeratoma corpus diffusion.

Angiokeratoma of Fordyce occurs on the scrotum

and vulva. It appears in midlife and is permanent.
143 Angiokeratoma
DDx Ref  55 • 135 • 137

DESCRIPTION
Red to purple, scaly papules formed by dilatation of
superficial blood vessels and epidermal thickening.
HISTORY
Common and most often seen as multiple lesions
restricted to specific body sites. Undisturbed angiok-
eratomas persist indefinitely. Surface trauma often
results in bleeding but not resolution. Four clinical
variants • Angiokeratoma corporis diffusum
(Fabry disease). In childhood and adolescence, boys
develop episodic bouts of fever associated with
severe pain in the extremities and abdomen, brought
on by exercise and temperature changes; these
crises can precede the angiokeratomas. Girls experi-
ence minor symptoms. Other affected organs: brain
(transient ischemic attacks and stroke), heart (myo-
cardial infarction), kidney (renal failure). Men usually
die by age 50. Most males and many carrier females
develop distinctive corneal opacities. X-linked reces-
sive inborn error of metabolism caused by a defi-
ciency of the lysosomal enzyme α-galactosidase A.
Other lysosomal enzyme deficiencies (galactosidase-
β1-fucosidase, β-mannosidase, neuraminidase) can
produce similar symptoms. • Angiokeratoma of
Fordyce. Most common. Asymptomatic multiple
angiokeratomas symmetrically distributed on
scrotum and vulva. Appears in mid life and persists
indefinitely. Scrotal angiokeratomas may be associ-
ated with inguinal hernia, varicosities of leg, or vari-
cocele; thus increased venous pressure thought to
play a role. Vulvar angiokeratomas develop at a
younger age in pregnant woman or with use of oral
contraceptives. • Solitary or papular angiokerato-
mas. Occur equally in both sexes. Commonly occur
as a single lesion on the legs of young adults; they
may be multiple and occur in any location. Papular
angiokeratomas are larger than the other variants
and easily traumatized. • Angiokeratoma of Mibelli.
Symmetric, grouped, multiple, occurring on the
backs of fingers and toes. Appear during childhood
and adolescence, continue to increase in number.
More common in females. May be associated with
chilblains or pernio. Inherited in an autosomal domi-
nant manner.
PHYSICAL FINDINGS
A deep red to maroon, or blue to black, sharply
defined papule of 0.5–1.0 cm. • Early lesions: light
in color, soft, and easily compressed. • Older
lesions: dark, warm, and raised, with surface scale.
TREATMENT
Cosmetically concerning and traumatized lesions can
be treated with excision, electrosurgery, and laser
surgery.
 Venous lake
DDx Ref  113 • 137 • 145
144 

Venous lakes can mimic melanoma; however,

they lose their color when compressed. The lower
lip is a common location for a venous lake.

Venous lakes are more common on sun-exposed

areas such as the lower lip. Multiple venous lakes
can occur.

Raised venous lakes can be itchy and sore, and

can easily bleed when traumatized.

Lesions may occur on the ear.

144 Venous lake
DDx Ref  113 • 137 • 145

DESCRIPTION
Small, blanchable, dark-blue to purple papule result-
ing from a dilated vein.
HISTORY
• Common on sun-exposed skin of elderly patients,
especially white men. • Acquired sun damage and
subsequent loss of dermal elasticity (solar elastosis)
cause venous lakes. • They persist and increase in
size with time.
PHYSICAL FINDINGS
• Asymptomatic, dark-blue to purple, soft papule
(2–10 mm) that blanches with pressure. • Multiple
lesions may be present on the mucosal surface of the
lip, especially the lower lateral vermilion border. •
Lesions may be found on the ears; itchy and sore
lesions suggest thrombosis. • Traumatized lesions
bleed easily and form a hemorrhagic crust.
TREATMENT
• Reassurance. • Traumatized or cosmetically con-
cerning lesions and lesions that interfere with eating
or speaking should be treated; recurrence is
common. • After anesthetizing with local or regional
anesthesia, the venous lake is unroofed with iris scis-
sors and cauterized. Lasers are also effective.
 Pyogenic granuloma
DDx Ref  126 • 134 • 137
145 

The fingers are a common location for pyogenic

granulomas, leading to the theory that trauma is
an important initiating factor.

Pyogenic granuloma on the finger. Lesions on the

fingers reoccur more frequently than in other
locations.

This dome-shaped papule has mucoid drainage;

however, it is not infected.

Pyogenic granuloma near the fingernail.

145 Pyogenic
DDx Ref 
granuloma
126 • 134 • 137

DESCRIPTION
An exophytic, dome-shaped papule made up of pro-
liferating capillaries separated by thick fibrous bands
and surrounded by an epithelial collarette. Also called
lobular capillary hemangioma.
HISTORY
• More common in children and young adults, less
common in the elderly. • Cause unknown, but lesions
occur at sites of trauma and during pregnancy, sug-
gesting an important role for trauma and hormones.
• Seen in increased frequency in acne patients
treated with isotretinoin. • Pyogenic granulomas
arise suddenly, attain a stable size, and persist
without treatment, although some lesions spontane-
ously regress within 6 months. Larger, deep-seated
lesions may recur with treatment. • Rarely, multiple
satellite lesions can occur.
PHYSICAL FINDINGS
• Yellow to deep red, glistening, dome-shaped to
polypoid papules of 3–10 mm. • Lesions grow
rapidly, bleed profusely, and can be covered with
yellow crust and surrounded by a collarette of scale.
They can ‘fall off’ only to regrow. • Gingival lesions
occurring during pregnancy are referred to as epulis
gravidarum. • Lesions are more common on the
head, neck, and fingers.
TREATMENT
• Treated by biopsy followed by electrodesiccation
and curettage of the base and border of the lesion.
• Most resolve with a single crateriform scar; recur-
rences occur in a few patients. • Rarely, multiple
satellite lesions develop at and around the site of a
previously treated pyogenic granuloma. This occurs
most often on the shoulder and trunk in younger
patients.
 Kaposi sarcoma
DDx Ref  108 • 142 • 145
146 

Kaposi sarcoma lesions can have varying

morphologies, including multiple purple papules
and plaques, and can be widespread, depending
on the clinical variant.

Classic Kaposi sarcoma occurs on the lower

extremities; in this patient, lesions are located on
the foot. Early lesions can look like malignant
melanoma.

AIDs-related Kaposi sarcoma. Early lesions are

flat plaques.

Kaposi sarcoma related to immunodeficiency

syndrome is more widespread. Lesions on the
lower extremities can appear eczematous. This
patient has violaceous papules coalescing to
plaques.
146 Kaposi sarcoma
DDx Ref  108 • 142 • 145

DESCRIPTION
A malignancy of lymphatic endothelial cells associ-
ated with a gamma herpesvirus, human herpesvirus
8 (Kaposi sarcoma-associated herpesvirus). Four
clinical and epidemiologic subsets: classic, endemic,
immunosuppression- or transplant-associated, and
epidemic- or AIDS-associated.
HISTORY
Four clinical variants. • Classic. Sporadic, slowly
progressive; occurs predominantly in 50- to 70-year-
old men of eastern European or Mediterranean
descent. • Endemic. Regions are eastern and south-
ern Africa. Up to 50% of all childhood soft tissue
tumors due to Kaposi sarcoma. Children develop
an aggressive lymphadenopathic form. • Immuno-
suppression- or transplant-associated. Organ
transplant recipients at risk. Patients of Mediterra-
nean and eastern European descent are at increased
risk for immunosuppression-associated Kaposi sar­
coma, supporting the theory of genetic predisposi-
tion. • Epidemic-associated. The most common
AIDS-associated cancer and is 20 times more
common in homosexual men than in those who
acquired HIV by another means (e.g. through hemo-
philia). Patients with AIDS-related Kaposi sarcoma
often have systemic involvement, particularly of the
gastrointestinal tract (stomach and duodenum).
Fever, night sweats, and weight loss may be present.
PHYSICAL FINDINGS
Various morphologies (macules or patches, papules
or plaques, nodules). • Classic. Starts with purple
patches on the distal lower extremities that progress
proximally and become multifocal. Individual lesions
darken and thicken, eventually becoming brown and
verrucous. Lesions on the lower legs can look ecze-
matous and ulcerate. Early Kaposi sarcoma nodules
can feel soft; older nodules can feel firm. • Endemic
(within Africa). Involves lymph nodes in people
with localized nodular lesions. Occurs most com-
monly in men and children. • Immunosuppression-
associated. Morphologically similar to classic Kaposi
sarcoma. Lesions typically improve and sometimes
resolve with cessation of immunosuppressive
therapy. • AIDS-associated. Lesions have a predi-
lection for the face (especially nose, eyelids, ears),
torso, and oral mucosa (especially hard palate).
TREATMENT
• Classic Kaposi sarcoma. Single lesions: surgical
excision. Multiple lesions localized to one area: radia-
tion. Extensive or recurrent lesions: combination
therapy with surgery, radiation, and chemotherapy.
• Endemic. Radiation and chemotherapy. • Immu-
nosuppression-associated. Modification or discon-
tinuation of the immunosuppressive therapy produces
regression of Kaposi sarcoma. Radiation and chemo-
therapy useful when immunosuppressive therapy
modification fails. • AIDS-associated. Radiation
therapy : large, localized, and/or ulcerative lesions.
Cryosurgery (3-week intervals): superficial Kaposi
sarcoma. Intralesional vincristine. Antiretroviral
therapy : alone or in combination with radiation or
systemic therapy, such as cytotoxic drugs (Paclit-
axel) and interferon alpha, directed against Kaposi
sarcoma.
 Telangiectasias
DDx Ref  34 • 108 • 126
147 

Multiple punctuate telangiectasias on the palms

and fingers can be seen in connective tissue
disorders such as CREST syndrome.

Close-up view shows dilated arterioles coalescing

to form a telangiectasia.

Numerous telangiectasias involving the lips and

tongue can be a sign of hereditary hemorrhagic
telangiectasia or CREST syndrome.

Multiple telangiectasias appear on the sun

exposed cheeks in predisposed individual.
Patients with rosacea may also have erythema
and pustules.
147 Telangiectasias
DDx Ref  34 • 108 • 126

DESCRIPTION
Common asymptomatic dilatations of capillaries,
venules, and arterioles within the subpapillary
plexus.
HISTORY
Occur in various clinical settings.
Primary telangiectasia
• Hereditary hemorrhagic telangiectasia (Osler–
Rendu–Weber syndrome). Autosomal dominant.
Telangiectasias on mucosae, skin, and internal
organs. Earliest sign: recurrent epistaxis in child-
hood. Characteristic telangiectasias occur in early
adulthood and are prominent on tongue, palate, nasal
mucosa, palms, soles, nail beds. Normal lifespan.
Increased risk of life-threatening hemorrhage.
• Hereditary benign telangiectasia. Autosomal
dominant. Widespread telangiectasias. No mucosal
or internal organ involvement. No associated bleed-
ing diathesis. • Ataxia telangiectasia (Louis–Bar
syndrome). Autosomal recessive condition with pro-
gressive cerebellar ataxia, telangiectasias, immune
dysfunction. The earliest sign, ataxia, is evident
when the child begins to walk, and usually by the
age of 3 years. Telangiectasias appear later on
conjunctivae, face, neck, upper trunk by age 5. Café-
au-lait macules, skin ulcerations, poikiloderma, pre-
mature gray hair, dry skin, sclerodermatous skin
changes, eczema, and hirsutism may also occur.
Caused by defective DNA repair of chromosomal
breakages. • Generalized essential telangiectasia.
Women affected more often than men. Telangiecta-
sias first appear on legs and then gradually, progres-
sively, and symmetrically extend to involve trunk and
arms. • Unilateral nevoid telangiectasia. Unilateral
dermatomal distribution of fine telangiectasias. Most
common dermatomes are the trigeminal and the third
and fourth cervical nerves. May be congenital or
acquired. Congenital: males more than females.
Acquired: females more than males. Can begin
during puberty and pregnancy, and resolve in adult-
hood and after delivery, suggesting causative role for
estrogen.
Secondary telangiectasias
• Basal cell carcinoma, rosacea, collagen vascular
disorders, corticosteroid atrophy, CREST, sclero-
derma, chronic graft-versus-host disease. • Second-
ary telangiectasias occur in the setting of altered
dermal connective tissue as a result of injury or
chronic inflammation. Damage may be from
ultraviolet radiation (actinic damage), ionizing radia-
tion, or treatment with topical or intralesional
corticosteroids.
PHYSICAL FINDINGS
• Non-palpable pink to red dilated dermal vessel with
a diameter of 1 mm or less; easily blanched with
diascopy. • Lesions may appear as discrete vessels
or clustered as telangiectatic ‘mats.’
TREATMENT
Telangiectasia may be ablated with laser surgery or
pinpoint electrocautery. Individual lesions may
require several treatments.
 Spider angioma
(nevus araneus)
DDx Ref  34 • 108 • 126
148 

The lower eyelid is a common location for these

tortuous angiomas. The face, hands, and fingers
are common locations in children.

Spider angiomas are dilatations of a pre-existing

blood vessel; notice the tortuous small blood
vessels leading into the dorsal aspect of the nose.

Spider angiomas blanch with pressure. Multiple

spider angiomas can be seen on sun-exposed
surfaces, with liver disease, and with pregnancy.

Spider angioma with long vessels leading to the

center. The vessels were destroyed for cosmetic
purposes with careful, conservative
electrocautery.
148 DDx Ref  Spider angioma
(nevus araneus)
34 • 108 • 126

DESCRIPTION
Asymptomatic blanchable pink papule due to a
central dilated arteriole and very fine radial branches.
HISTORY
• Found in 10–15% of normal adults and children. •
Seen with increased frequency in pregnancy and
chronic liver disease (states of relative estrogen
excess). Lesions arising during pregnancy tend to
resolve after the birth. Those found in patients with
liver disease are persistent. • Spider angiomas are
due to dilatation of a previously existing vessel rather
than a neoplasm. • Spider angiomas arising during
pregnancy and those occurring in children tend to
disappear spontaneously over a period of 3–4 years.
PHYSICAL FINDINGS
• A central, slightly raised, bright-red vascular
papule from which fine blood vessels radiate. • Firm
pressure easily blanches the radiating vessels,
whereas the central papule is less easily blanched.
Pulsation of the central papule with this technique
confirms the arteriolar nature of the papule. • Most
commonly seen on face, neck, upper trunk, upper
arms, hands, fingers.
TREATMENT
• Most resolve spontaneously and do not require
treatment. • For persistent, cosmetically bothersome
lesions, pulsed dye laser or electrocautery are effec-
tive. • There is a slight risk of dyspigmentation and
scarring, and lesions may recur.
 Androgenic alopecia
(male pattern baldness)
DDx Ref  151 • 152
149 

Early pattern loss on the vertex.

Early pattern loss with frontal recession.

Extensive loss on the vertex, frontal hair is

retained.

Extensive loss on the frontal, vertex and crown

areas.
149 DDx Ref  Androgenic alopecia
(male pattern baldness)
151 • 152

DESCRIPTION
A genetically predetermined, androgen-dependent
loss of hair, primarily of the frontal, vertex, and scalp
crown but may be total.
HISTORY
• A physiologic occurrence induced by androgens in
genetically predisposed men. • Pattern of inheritance
is probably polygenic. • Can begin any time after
puberty; usually expressed by age 40. • Progression
and various patterns of hair loss have been classified
by Hamilton. Triangular frontotemporal recession
occurs normally in most young men (type 1) and
women after puberty. First signs of balding are
increased frontotemporal recession accompanied by
midfrontal recession (type 2). Hair loss in a round
area on the vertex follows, and the density of hair
decreases, sometimes rapidly, over top of the scalp
(types 3–7).
PHYSICAL FINDINGS
• Terminal hair follicles are transformed into vellus-
like follicles. Terminal hair is replaced by fine, light,
vellus hair, which is shorter and has a reduced dia­
meter. • With time, further atrophy occurs, leaving
scalp shiny and smooth. Follicles disappear. • Begins
with bitemporal thinning that progresses to an
M-shaped recession. • There is a loss of hair focally
in crown of the scalp, which may extend to total hair
loss in the central scalp. • There is increased growth
of secondary sexual hair (that on chest, in axillae, and
in pubic and beard areas).
TREATMENT
• Minoxidil (Rogaine). A topical 2% or 5% solution
available over the counter. It is applied to a dry scalp
twice a day. Ideal candidates are men under 30
years. Regrowth takes 8–12 months. May help stop
further loss but must be used continually to preserve
growth. • Finasteride (Propecia) 1 mg. An oral pre-
scription medication taken daily. It works by blocking
5α-reductase in the scalp. No laboratory tests neces-
sary. It must be used daily and chronically to stabilize
or reverse balding. Decreased libido and erectile
dysfunction occur in less than 2% of men taking
finasteride. Contraindicated for women. • Hair
transplants. Have been used successfully for years
to permanently restore hair. Hair weaves have been
refined in a process whereby strands of human hair
are applied to a thin nylon filament anchored to the
scalp with the patient’s own hair. Another option is
surgical: an anteroposterior elliptic excision of bald
vertex scalp with primary closure can provide an
instant hair effect.
 Androgenic alopecia in women
(female pattern hair loss)
DDx Ref  151 • 152
150 

Usually, the most obvious hair loss is from the

frontal scalp. From Haber RS, Stough DB, eds. Hair
Transplantation. London: Saunders; 2006.

The Christmas tree pattern indicates hair loss

from the frontal scalp exceeding loss from
occiput.

Diffuse thinning without inflammation on the

crown of the scalp.

Widening of the part. Diffuse thinning without any

scalp inflammation.
150 DDx Ref  Androgenic alopecia in women
(female pattern hair loss)
151 • 152

DESCRIPTION
Common hereditary, central, diffuse hair thinning
that begins at a relatively early age. This is in contrast
to postmenopausal hair loss that begins in women
in their fifties, sixties, or seventies. Affected scalp
hairs have shortened anagen cycle and progressive
miniaturization of hair follicles.
HISTORY
• Inheritance is poorly understood; clearly a genetic
predisposition. • May affect 6–25% of premeno­
pausal women. • Women rarely become completely
bald. • Hereditary hair thinning can begin in teenage
years; two peaks of onset, in twenties and forties.
• Gradual hair loss, not abrupt or massive. • Menses
normal, regular. Heavy menses cause iron deficiency
and increased hair shedding. Pregnancies normal; no
infertility or galactorrhea. • Certain drugs cause hair
thinning. Hair regrows when drug is stopped.
PHYSICAL FINDINGS
• Gradual hair loss on scalp crown with retention of
normal hairline. • Widening of part often earliest
visible change. Usually most obvious loss in frontal
scalp. • Christmas tree pattern of loss indicates hair
loss from frontal scalp exceeding loss from occiput.
• Increased spacing between hairs, often pencil
eraser-sized areas lacking hairs. • Many hairs
miniaturized (thin and short). • Hair diameter
becomes thinner. • Biopsy sometimes performed to
rule out diffuse form of alopecia areata or telogen
effluvium. • Most do not require hormonal evalua­
tion. Typically, no signs of hyperandrogenemia, and
serum androgen levels normal. • Dehydroepiandros­
terone sulfate, serum-free or total testosterone, and
prolactin levels should be determined if one or more
present: irregular menses, hirsutism, virilization,
cystic acne, galactorrhea, infertility. A subset may
have polycystic ovarian disease and insulin resist­
ance. • Other tests: thyroid-stimulating hormone. If
heavy menses, serum iron, total iron binding capac­
ity, and ferritin.
TREATMENT
• Topical 2% minoxidil solution (Rogaine) may be
effective in some. It is applied twice a day for a trial
of 6 months. If effective, must be continued for per­
sistent effect. If there is no response, 5% solution is
used twice daily; this is approved for use in men.
• Patients with abnormal laboratory studies can be
referred to an endocrinologist or a gynecologist. • No
restrictions on frequency of washing, combing, hair
coloring, or permanents. • Women with androgenic
alopecia who desire an oral contraceptive should use
a progestin with little androgenic activity, such as
norgestimate or ethynodiol diacetate.
 Alopecia areata
DDx Ref  53 • 80 • 152
151 

Localized alopecia areata: round, discrete patches

of hair loss. The scalp is smooth without scaling,
erythema, or scarring.

Alopecia areata in the beard skin can be subtle

and noted only as adjacent shaved hairs regrow.
Affected beard area skin is smooth; the round
patch is hairless without inflammation.

Alopecia areata of the occiput. This large hairless

patch is characteristically round and devoid of
hair.

Alopecia areata can affect any site of hair-bearing

skin. Here, it has resulted in loss of eyelash hairs.
151 Alopecia
DDx Ref 
areata
53 • 80 • 152

DESCRIPTION
A non-scarring hair loss. Typically rapid onset in
sharply defined, usually round or oval area. Loss may
be diffuse or focal, or band-like at scalp margins.
HISTORY
• Most common in children and young adults.
• Sudden hair loss in areas that are sharply demar-
cated, 1–4 cm. • Eyelashes and beard may be
involved, and (rarely) other parts of the body. • Total
hair loss of the scalp (alopecia totalis) is most fre-
quent in young people; may be accompanied by
cycles of growth and loss. • Total hair loss of the
body (alopecia universalis) is very rare. • Regrowth
in 1–3 months; may be followed by loss in other
areas. • Prognosis for total regrowth, if limited
involvement, is good.
PHYSICAL FINDINGS
• Most common pattern: patchy. Other patterns:
ophiasis (band-like loss at scalp margins) and
ophiasis inversus (spares scalp periphery, involves
crown). Diffuse pattern least common. • Skin typi-
cally very smooth but may have short hair stubs.
• Tapered hairs resembling exclamation points best
seen at margin of circular loss. • New regrowth may
be fine and white. • Diffuse fine nail pitting in up to
30%. • Biopsy if the clinical presentation not typical.
Findings include peribulbar lymphocytes, miniatur-
ized follicles, telogen to vellus hair ratio of 1.5 : 1, and
increased telogen and catagen follicles. • May be
associated, but not caused by with thyroid disease,
pernicious anemia, Addison disease, vitiligo, lupus
erythematosus, ulcerative colitis, diabetes mellitus,
Down syndrome. • Differential diagnosis: trichotillo-
mania, tinea capitus, syphilis, telogen effluvium,
diffuse androgenetic alopecia.
TREATMENT
• In most areas, hair regrows and no treatment is
needed. • Group I topical steroids applied twice a day
are minimally effective. Used in cycles, such as 2
weeks of treatment, 1 week of no treatment. Other
options: • Intradermal injection of triamcinolone
acetonide (Kenalog) 2.5–10 mg/mL is effective.
Injections may be repeated at 4-week intervals.
Atrophy is major side effect. Reserved for patients
with a few small areas of hair loss. • Squaric acid
dibutyl ester is used by some specialists, but contact
allergy can be severe. • Intravenous pulse of methyl­
prednisolone may be effective in patients with rapidly
progressing, extensive multifocal disease. • Oral
corticosteroid therapy does not prevent spread or
relapse of severe alopecia areata. Regrowth is rarely
maintained off therapy. • A hair prosthesis should
be considered and strongly encouraged for patients
with diffuse loss when emotional distress is high.
• A network of support groups across the USA is
available to help patients cope: Alopecia Areata
Foundation (http://www.alopeciaareata.com).
 Trichotillomania
DDx Ref  53 • 80 • 151
152 

Hair loss occurs in patches that are usually smooth,

without inflammation, and sharply angulated. In
this case, the loss is nearly complete in a round
patch, mimicking alopecia areata.

Note the bizarre shape of the hair loss, the

general retention of the frontal hairline, and some
short broken hairs.

A sharply angulated pattern of alopecia is a

telltale sign of an ‘outside job’. As in alopecia
areata, the scalp is not inflamed, not scaling, and
there is no evidence of scarring.

As in the other figures, the hair loss in

trichotillomania may not be complete, with some
broken hairs evident, and some patchy regrowth.
152 Trichotillomania
DDx Ref  53 • 80 • 151

DESCRIPTION
Recurrent pulling of one’s hair, resulting in significant
hair loss. Urge to pull hair is overwhelming; after hair
pulling, anxiety is relieved temporarily. It may involve
many hours each day of pulling the hair, or thinking
about pulling it. Often the ‘puller’ does not admit to
this habit.
HISTORY
• Trichotillomania is a habit tic most commonly found
in young children. It is also seen in adolescents and
adults. • Female to male ratio is 2.5 : 1. • Hair is
twisted around finger, pulled, and rubbed until it is
extracted or broken. • Favorite sites are easily
reached areas: frontoparietal scalp, eyebrows, eye-
lashes. • First manifests during inactive periods,
perhaps while watching television or before falling
asleep. • Parents seldom notice the behavior. • Often
associated with underlying anxiety, depression, low
self-esteem. • Can be a chronic problem and often
resolves spontaneously. • Affected area has an
irregular angulated border, and the density of hair is
greatly reduced, but the site is never bald as in
alopecia areata. • Multiple visits to providers and
specialists seeking a diagnostic answer are typical
for this condition; a biopsy can be helpful and sup-
portive of this diagnosis.
PHYSICAL FINDINGS
• There is a patch of hair loss with an irregular,
angulated border. • Hair density is greatly reduced;
the involved area is not completely bald and smooth,
as in alopecia areata. • Short broken hairs of
varying lengths are randomly distributed in involved
site. • Potassium hydroxide test rules out non-
inflammatory tinea capitis. • Plucked hair shows no
telogen hair roots (100% in the active growing
anagen phase). • Gentle hair traction produces no
more hair loss. • Skin biopsy reveals a marked
increase in catagen hairs.
TREATMENT
• Treatment often delayed, or not sought, because
of embarrassment. • Response is best to combina-
tion therapy including psychopharmacology, psycho-
therapy, and behavior modification (such as habit
substitution), rather than psychotherapy alone. • The
child’s attention should be diverted when hair is
being pulled. • Parents and physician should be
accepting and supportive rather than judgmental and
punitive. • Extensive involvement or persistence
requires psychiatric evaluation. Psychotherapy can
be helpful. • Trichotillomania shares features with
obsessive-compulsive disorder, including response
to medication. • Clomipramine (Anafranil), fluoxetine
(Prozac), and pimozide (Orap) can be effective;
however, not all patients respond fully to psycho­
pharmacology alone.
 Fungal nail infections
DDx Ref  38 • 154
153 

Distal subungal onychomycosis. Scrapings from

distal aspect under nail plate are often positive in
KOH. If negative KOH, consider culture prior to
treatment.

White superficial onychomycosis. Chalky white

scrapings taken from the nail surface are KOH
positive.

Proximal subungal onychomycosis. The nail

surface is smooth. The infection is beneath the
nail plate.

Multiple finger nails affected by onychomycosis. A

positive KOH or culture is advised before
treatment. Infection can be spread to skin by
scratching.
153 Fungal nail infections
DDx Ref  38 • 154

DESCRIPTION
Onychomycosis: fungal infection of fingernail or
toenail plate. Cause: many different species of
fungus.
HISTORY
• Trauma from tight-fitting shoes that are too short
predisposes to infection. • A large mass composed
of a thick nail plate and underlying debris may cause
discomfort with footwear.
PHYSICAL FINDINGS
There are four distinct patterns. Several patterns may
occur simultaneously. • Distal subungual onycho­
mycosis. Most common pattern. Fungi invade distal
area of nail bed. Distal plate turns yellow or white as
an accumulation of thick scaling debris causes nail
to rise and separate from underlying bed. • White
superficial onychomycosis. Caused by surface
invasion of nail plate, most often by Trichophyton
mentagrophytes. Nail surface is soft, dry, powdery,
and can easily be scraped away. Nail plate is not
thickened. • Proximal subungual onychomycosis.
Microorganisms enter the area of posterior nail
fold cuticle, invade nail plate from below. Surface
remains intact. Hyperkeratotic debris causes nail to
separate. Trichophyton rubrum is most common
cause. • Candidal onychomycosis. Nail plate infec-
tion caused by Candida albicans is seen almost
exclusively in chronic mucocutaneous candidiasis, a
rare disease. Generally involves all the fingernails.
Nail plate thickens and turns yellow-brown.
All nails and skin are examined to rule out
other diseases, such as psoriasis, that mimic
onychomycosis.
Aspergillus, Cephalosporium, Fusarium, and
Scopulariopsis species, considered contaminants or
non-pathogens, can also infect nail plate. Multiple
pathogens may be present in a single nail. In a potas-
sium hydroxide wet mount, subungual debris and nail
plate are examined for hyphae. Culture to establish
presence of dermatophytes— organisms susceptible
to itraconazole (Sporanox), terbinafine (Lamisil), and
fluconazole (Diflucan).
TREATMENT
• Topical antifungal creams. Little value. Poor nail
penetration.. • Oral therapy. Highest success rate
in fingernail and toenail infections in young persons.
• From 50% to over 80% effective. Relapse rate
approximately 15–20% in 1 year. Indications for
treatment include pain with thick nails, functional
limitations, secondary bacterial infection, and argu-
ably, appearance. • Terbinafine (Lamisil) 250 mg
q.d. Administered for 6 weeks for fingernail infection,
12 weeks for toenail infection. Not effective for some
candidal species. • Itraconazole (Sporanox)
200 mg q.d. Prescribed for 6 weeks for fingernail
infection, 12 weeks for toenail infection. Pulse dosing
with 200 mg b.i.d. for 1 week on then 3 weeks off
another option. Fingernail infection: two or three
pulses. Toenail infection: three or four pulses.
Nail diseases: Psoriasis
DDx Ref  38 • 154
154a 

Nail pitting is a change seen in psoriasis. The

nails appear to have a tiny ice pick depression.

Affected by psoriasis, this nail has distal

subungual hyperkeratosis, onycholysis, and a
yellow-brown color change termed oil spot lesion,
due to serum accumulation.

All five fingernails are affected with psoriasis.

There is onycholysis and some yellow-brown
discoloration typical of oil spot change.

The oil spot sign of psoriasis is a brown color.

Often, there are other psoriasis findings such as
onycholysis or pitting.
154a  NailDDxdiseases:
Ref 
Psoriasis
38 • 154

DESCRIPTION
Nail changes are characteristic of psoriasis, and the
nails of all patients with suspect psoriasis should be
examined. Psoriasis of the nails may be the only sign
that the patient has psoriasis; these patients may
have no skin lesions.
HISTORY
• The incidence of nail involvement in psoriasis
varies from 10–50%. • Nail involvement may be the
only sign of psoriasis, but it usually occurs simultane-
ously with skin disease. One or several nails may be
involved. • Pain may restrict activities.
PHYSICAL FINDINGS
• Pitting is the most common finding. There may be
a few or many pits, and they are haphazardly distrib-
uted on the nail plate surface. • Onycholysis is sepa-
ration of the nail from the nail bed. Separation begins
at the distal groove or under the nail plate and may
involve several nails. The separated nail appears
yellow and is often misinterpreted as a fungal infec-
tion. • Subungual scaly debris may accumulate
under the distal nail plate. The yellow-white debris
elevates the distal nail. This also is commonly mis-
taken for nail fungus infection. • Surface distortion
of the nail plate occurs when psoriasis affects the
nail matrix. • Oil spot lesions are yellow-brown spots
seen through the nail surface. Psoriasis of the nail
bed causes serum and scaling debris to accumulate
under the nail plate. • Nail psoriasis may have a very
similar appearance to tinea of the nail unit. Culture
of nail clippings or subungual debris, potassium
hydroxide preparations, and nail biopsy will help
establish the diagnosis of fungal nail infection. Nail
biopsy is performed by submitting nail clippings to
the laboratory for histologic identification of hyphae
to rule out fungal infection.
TREATMENT
• Many topical agents (calcipotriol, tazarotene, and
anthralin) have been tried, but results are discourag-
ing. • Intralesional injections at monthly intervals into
the matrix and lateral nail folds are effective but
painful. Triamcinolone acetonide (Kenalog) 2.5–
5 mg/mL is delivered with a 30-gauge needle. The
procedure is painful and most patients do not con-
tinue. • Treatment of skin disease with systemic
agents such as tumor necrosis factor inhibitors adali-
mumab, etanercept, or other immune suppressive
such as ciclosporin, methotrexate, or acitretin will
improve the nails, but not indicated for nail disease
alone.
Nail diseases: Paronychia, Pseudomas
infection, white spots or bands
DDx Ref  38 • 154
154b 

Acute paronychia. The pus is collecting in the

lateral nail fold and should be drained. The most
common cause is Staphylococcus aureus.

Chronic paronychia presents as swelling and

tenderness of the proximal and lateral nail folds.
The problem often occurs if there is repeated wet
work. Candida is the most common cause.

Separation of the nail from the nail bed results in

a warm moist space that predisposes to
Pseudomonas infection (green color) under the
nail. Soaking the finger makes it worse.

White spots in the nail plate, a very common

finding, possibly result from cuticle manipulation
or other mild forms of trauma. Psoriasis of the
mid-nail matrix can also produce this change.
154b  DDx Ref  Nail diseases: Paronychia, Pseudomas
infection, white spots or bands

38 • 154

ACUTE PARONYCHIA
• Bacterial infection of proximal and lateral nail fold
causes rapid onset of pain, swelling. • Caused by
trauma and manipulation, or may occur spontane-
ously. • Pus accumulates behind cuticle or deeper in
lateral nail folds. • Drain pus by inserting the pointed
end of a comedone extractor or similar instrument
between nail fold and nail plate. Pain is abruptly
relieved. • Deeper infections may require incision to
drain abscess. • Small confined abscesses may
respond to just drainage. Larger abscesses with sur-
rounding erythema treated with antistaphylococcal
antibiotics.
CHRONIC PARONYCHIA
• Contact irritant exposure is major cause. Bakers,
dishwashers, surgeons, dentists at risk. • Many or
all fingers are involved. Tenderness, erythema, and
mild swelling about the proximal and lateral nail
folds. • Cuticle disappears, leaving space between
proximal nail fold and nail plate exposed to infection.
Manipulation of the cuticle accelerates the process.
• Bacteria and yeast grow in the warm moist space
under the proximal nail fold. • Chronic inflammation
causes nail plate to be distorted, but it remains unin-
fected. • Psoriasis may have an identical appear-
ance. • Goals of treatment are to avoid irritation and
to suppress inflammation and infection. • Protect by
wearing vinyl gloves with cotton glove underneath
(http://www.allerderm.com). • Group V topical ster-
oids and not oral antibiotics are mainstay of treat-
ment. • Fungoid tincture (miconazole) is applied
twice daily to proximal nail fold and allowed to flow
into the space created by the absent cuticle. Cuticle
may never re-form in patients with long-standing
inflammation. • Fluconazole (150 mg q.d.) for 1–2
weeks may control treatment-resistant cases. Short
courses of fluconazole may have to be repeated as
the infection recurs.
PSEUDOMONAS INFECTION
• Separation of the nail plate (onycholysis) exposes
a damp, macerated space between nail plate and nail
bed. • Pseudomonas thrives in this warm moist
space and stains the nail plate undersurface green-
black. Little discomfort or inflammation, as occurs
with subungual hematoma. • Apply a few drops of a
bleach mixture (one part chlorine bleach to four parts
water) under the nail three times daily. Vinegar
(acetic acid) may also be used. • Cut unattached nail
to eliminate damp space under the nail.
WHITE SPOTS OR BANDS
• White spots in the nail plate are common. • Prob-
ably a result of repeated low-grade trauma. • The
spots or bands eventually grow out and disappear.
Patients often misinterpret this finding as a fungal
infection.
Nail diseases: Ridging and beading,
habit tic deformity, onycholysis
DDx Ref  38 • 154
154c 

Longitudinal ridging is common in aging. Beading

occurs at all ages but is more common in the
elderly. The beads cover part or most of the plate
surface and are arranged longitudinally.

Horizontal nail plate indentations along the length of

the nail are the hallmark of habit tic nail deformity.
Repeated trauma from a habit of rubbing or pushing
on the proximal nail fold causes this.

Distal separation of the nail plate from the nail

bed is called onycholysis. Some causes are
trauma, psoriasis, tinea, and phototoxic drug
reaction.

Distal splitting of the nail plate is a common

complaint without a simple fix. Hydration of the
plate with a thick emollient can be helpful.
154c  DDx Ref  Nail diseases: Ridging and beading,
habit tic deformity, onycholysis

38 • 154

RIDGING AND BEADING

• Longitudinal ridging is a common aging change
that is occasionally seen in young people. Beading
occurs at all ages but is more common in the elderly.
• The beads cover part or most of the plate surface
and are arranged longitudinally. • Patients may sand
or buff the nail to smooth the surface. • Elon nail
conditioner (http://www.ilovemynails.com) prevents
dryness and cracking.
HABIT TIC DEFORMITY
• Biting or picking a section of the proximal nail fold
of the thumb with the index fingernail is a common
habit. Other nails can be affected. • Linear bands of
horizontal grooves extend up the nail surface. Nail
rippling from chronic eczema of the proximal nail fold
causes a similar appearance. • Patients who can
stop this habit will eventually regrow normal nails.
ONYCHOLYSIS
• Onycholysis is the separation of the nail from the
nail bed. It is more common in women with long
nails. Vigorous cleaning under the nail accelerates
the process. • Separation begins at the distal end
and slowly progresses proximally. • The non-adher-
ent portion of the nail is white, yellow, or green-
tinged. • Causes include psoriasis, trauma to long
nails, Candida or Pseudomonas infections, internal
drugs, contact with chemicals, maceration from pro-
longed immersion, and allergic contact dermatitis
(e.g. to nail hardener or adhesives). • Screen patients
with unexplained onycholysis for hyperthyroidism
and asymptomatic thyroid disease. • Treat by cutting
the separated portion of the nail. This promotes
dryness and discourages infection under the nail. Do
not soak the fingertip. • Avoid exposure to contact
irritants. • Yeast grows in the space between the nail
and nail bed. Use liquid topical agents (e.g. fungoid
tincture that contains miconazole). Consider oral
fluconazole (Diflucan) for resistant cases. A short
course of fluconazole (e.g. 150 mg every day for 5–7
days) may have to be repeated as the nail grows out.
DISTAL PLATE SPLITTING
• Brittle nails and splitting are found in 20% of adults.
• The splitting into layers or peeling of the distal nail
plate resembles the scaling of dry skin. • Nails, like
the skin, dry in the winter. Repeated water immer-
sion encourages the process. Vinyl gloves protect
during wet work. • Rehydrate the nail by soaking in
water. Then apply a thick lubricant such as Aquaphor
ointment or Elon nail conditioner (http://www.ilove-
mynails.com). These are found in some pharmacies.
• The B-complex vitamin biotin (2.5 mg q.d.) may
improve nail plate thickness and integrity.
Nail diseases: Digital mucous cyst,
nevi and melanoma, hematoma
DDx Ref  38 • 154
154d 

A flesh-colored, almost translucent, rounded cystic

papule is present on the distal fingertip. Such digital
mucous cysts can compress the matrix and result
in a longitudinal nail plate depression.

Digital mucous cyst: incision with a #11 surgical

blade. A clear, sometimes blood-tinged, viscous,
jelly-like substance exudes when the cyst is
incised.

Melanoma: Hutchinson sign. Pigment that extends

on to the nail folds is a sign of subungual
melanoma. In this case, the pigment extension is
marked.

Trauma to the nail plate can result in subungual

hemorrhage. The hemorrhage is trapped by the
nail plate; the resultant pressure can be tender
until relieved by drainage.
154d  DDx Ref  Nail diseases: Digital mucous cyst,
nevi and melanoma, hematoma

38 • 54

DIGITAL MUCOUS CYSTS

• Digital mucous cysts are focal collections of mucin
lacking a cystic lining. • These dome-shaped, pink-
white structures occur on the dorsal surface of the
distal phalanx of middle-aged and elderly people.
• A clear, viscous, jelly-like substance exudes when
the cyst is incised. • Cysts on the proximal nail fold
compress the nail matrix cells and induce a longitu-
dinal nail groove. • Surgical excision by a qualified
hand surgeon to remove lesion if painful. Otherwise,
these benign lesions should be left alone.
NEVI AND MELANOMA
• Junctional nevi can appear in the nail matrix and
produce a brown pigmented band. Brown longitudi-
nal bands are common in black people but rare in
white people. • Melanoma of the nail can occur
anywhere around or under the nail. • The lesion
may present as a pigmented band that increases in
width. The spontaneous appearance of such a band
is noteworthy and concerning; such lesions should
be biopsied. • Benign subungual nevi are rare in
white people, so subungual nevoid lesions should
be regarded as malignant until proved otherwise.
• Hutchinson sign is the periungual extension
of brown-black pigmentation from longitudinal
melanonychia on to the proximal and lateral nail
folds. It is an important indicator of subungual
melanoma. • When there is suspicion of subungual
melanoma, biopsy should not be delayed. A derma-
tologist or plastic surgeon familiar with nail biopsy
techniques is best to perform this procedure.
SUBUNGUAL HEMATOMA
• Trauma to the nail plate may cause immediate
bleeding and pain. Bleeding may cause separation
and more pain. • Puncture the nail surface with a
red-hot paper clip tip to drain the blood. • Trauma to
the proximal nail fold causes hemorrhage that may
not be apparent for days. The nail plate may emerge
from the nail fold with bloodstains and mimic
melanoma.
 Erythema toxicum
neonatorum
DDx Ref  48 • 64 • 67
155 

Macules, papules and pustules appeared 24

hours after birth in this healthy baby. Gram stain
of the pustules showed numerous eosinophils.
The eruption resolved without treatment.

In some cases, pustules are sparse.

An extensive case with red papules on an

erythematous base. A few pustules were also
present.

Scattered papulovesicles with an erythematous

flare. A smear of intralesional material showed
greater than 90% eosinophils.
155 DDx Ref  Erythema toxicum
neonatorum
48 • 64 • 67

DESCRIPTION
A common, benign, transient, pustular eruption seen
in the newborn period.
HISTORY
• Occurs more commonly in healthy term infants
than in premature and low birth weight infants.
• Cause unknown. • Rash resolves within 3 weeks
of life without any adverse sequelae.
PHYSICAL FINDINGS
• Lesions appear as blotchy macules that develop
into superficial pink papules and pustules, taking on
a flea-bitten appearance. • Macules can coalesce to
form large pink patches studded with only a few to
hundreds of pustules. • Can occur anywhere on the
skin, but face, arms, buttocks, and torso most fre-
quently involved. Palms and soles rarely affected.
• Overall, erythema toxicum neonatorum can wax
and wane, with individual lesions appearing to occur
in crops. • Individual lesions can disappear in hours
or last for up to 2 weeks.
TREATMENT
• No treatment required. • Parents should be
reassured.

Figure 1, 2 and 3 from Eichenfield LF, Frieden IJ, Esterly

NB. Textbook of Neonatal Dermatology. Philadelphia:
Saunders; 2001.
Figure 4 from Bolognia JL, Jorizzo JL, Rapini RP, eds.
Dermatology. London: Mosby; 2003.
 DDx Ref  48 • 67 • 155
Miliaria
156 

Miliaria crystallina. Clear, superficial vesicles

developed in this patient that was covered with
blankets in warm weather.

Miliaria crystallina. Lesions occurred in crops and

were confluent. Many vesicles have ruptured and
the skin is desquamating.

Miliaria rubra. Intense pruritus occurred in this

neonate who was over dressed. Nonconfluent red
papules about the neck where friction had
occurred. Lesions resolved spontaneously.

Miliaria profunda is characterized by small

non-erythematous papules and pustules occurring
on the trunk and extremities.
156 Miliaria
DDx Ref  48 • 67 • 155

DESCRIPTION
Clear to red papules that result from obstruction of
eccrine sweat ducts.
HISTORY
Very common in newborns and infants who are
‘bundled’ or placed in warm environments, and in
febrile infants. Miliaria can last for hours to days.
Three types. • Miliaria crystallina. Eccrine obstruc-
tion at level of stratum corneum. Most common type
in newborns. Caused by warming lights and tight
bundling. • Miliaria rubra. ‘Prickly heat’ or ‘heat
rash.’ Intraepidermal eccrine obstruction. Redness
due to release of local inflammatory mediators.
• Miliaria profunda. Dermal–epidermal eccrine duct
obstruction. Rare in newborns. Cause unknown,
although a polysaccharide produced by certain
strains of Staphylococcus epidermidis may play a
role.
PHYSICAL FINDINGS
• Miliaria crystallina. Multiple subtle ‘dewdrop’
superficial vesicles that easily break. Common in
intertriginous areas such as neck folds, face (espe-
cially forehead), and trunk. • Miliaria rubra. Non-
follicular pustules and vesicles. Same distribution as
for miliaria crystallina. • Miliaria profunda. Small
non-erythematous papules and pustules occurring
on trunk and extremities.
TREATMENT
Cool bath and avoidance of tight bundling.
 Cutis marmorata
DDx Ref  104 • 140 • 141
157 

Cutis marmorata telangiectatica congenita, a

vascular malformation associated with skin
atrophy. Unlike typical cutis marmorata, it does
not resolve with skin rewarming.

Cutis marmorata telangiectatica congenita can

occur in a dermatomal distribution and be
associated with malformations of other organ
systems.

Cutis marmorata telangiectatica congenita in this

child was an isolated skin finding.

Skin atrophy and reticulated blood vessels are

notable in this view.
157 Cutis marmorata
DDx Ref  104 • 140 • 141

DESCRIPTION
Benign, transient skin mottling that resolves with
rewarming.
HISTORY
• A common, normal, vascular reaction pattern seen
in both full-term and preterm infants due to an exag-
gerated vasomotor response to decreased core body
temperature. • Must be distinguished from persistent
mottling seen in Down syndrome, trisomy 18,
hypothyroidism, neonatal lupus, and septic shock.
PHYSICAL FINDINGS
• Blanching mottled or lace-like erythema. •
Resolves with rewarming • Occurs on trunk and
extremities.
TREATMENT
• Rewarming results in complete resolution of ery-
thema. • Parents should be reassured.
 Acquired cutaneous
paraneoplastic syndromes
DDx Ref  91 • 105 • 115
158 

Sign of Leser–Trélat: the sudden appearance or

increase in number and size of seborrheic
keratosis on non-inflamed skin has been reported
to be a sign of internal malignancy.

Dermatomyositis: heliotrope erythema of the

eyelids (heliotrope: violet) can be paraneoplastic
condition. This can be misdiagnosed as eyelid
dermatitis.

Sweet syndrome. Acute tender erythematous

plaques and pseudovesicles, and occasional
blisters.

Paraneoplastic pemphigus. Widespread

polymorphous eruption with papules and blisters.
There were painful oral ulcerations. Total
resection of the neoplasm may cure the disease.
158 DDx Ref  Acquired cutaneous
paraneoplastic syndromes
91 • 105 • 115

Involve cutaneous findings attributed to internal

malignancy.
PRURITUS
• Symptom of many dermatoses, but in absence of
skin findings may indicate occult malignancy. • More
common in gastrointestinal and lymphoreticular
malignancies, especially Hodgkin disease. • May not
be associated with obvious skin changes. • Patients
may scratch or may show linear erosions or excoria-
tions distributed in reachable areas.
SIGN OF LESER–TRÉLAT
• Sudden, eruptive appearance of numerous sebor-
rheic keratoses may indicate internal malignancy.
Exceedingly rare and ominous entity known as sign
of Leser–Trélat. • Adenocarcinoma of gastrointesti-
nal tract is most common. • Lesions generalized,
small, inflamed, monomorphic keratoses.
DERMATOMYOSITIS
• Adults with dermatomyositis more likely to have
internal malignancy than age-matched controls.
• Prevalence estimated at 5–50%, with greatest
prevalence among older patients. • Most common
associated malignancies are in breast, ovary, lung,
gastrointestinal system. • Dermatomyositis may be
associated with proximal muscle weakness. • Find-
ings of dermatomyositis include Gottron’s papules,
periocular heliotrope or violaceous discoloration,
photosensitive violaceous eruption, poikiloderma,
periungual telangiectasia.
SWEET SYNDROME
• Also called acute febrile neutrophilic dermatosis.
• Recurrent, painful eruption associated with fever,
leukocytosis, arthralgias. • Women affected more
commonly. • May be associated with infection or
with hematologic malignancy, most often acute
myelogenous leukemia. • Lesions red, edematous,
pseudovesicular plaques, coalescing papules. Vary
from 0.5 to 5.0 cm, tender to palpation.
PARANEOPLASTIC PEMPHIGUS
• Presents as sign of internal malignancy, most
often hematologic and chronic lymphocytic leukemia.
• Paraneoplastic pemphigus presents as ocular
inflammation, oral erosions, generalized erythema
multiforme-like bullous lesions, denuded areas with
crusting.
CARCINOID SYNDROME
• Episodic, intense flushing of face, neck, upper
body, caused by release of vasoactive mediators
from carcinoid tumors into systemic circulation.
• Most arise in small bowel, usually appendix. May
also arise in lung. • When carcinoid tumors metas-
tasize to liver, mediators have access to systemic
circulation. • Carcinoid syndrome presents as acute
flushing of face, neck, chest lasting about 30 min.
Flushing episodes often associated with dyspnea,
abdominal cramping, diarrhea.
GLUCAGONOMA SYNDROME
• Rare, clinically distinctive syndrome consisting of
a dynamic generalized cutaneous eruption associ-
ated with a glucagon-secreting alpha-cell tumor of
pancreas. • Necrolytic migratory erythema describes
eruption of glucagonoma syndrome. Eruption gener-
alized but favors groin, buttocks, thighs. Bright
dermal erythema is polycyclic, followed by flaccid
bullae that desquamate, leaving denuded areas and
collarette of scale. Process is dynamic, changing,
extending each day.
 Inherited cutaneous
paraneoplastic syndromes
DDx Ref  119 • 122 • 126
159 

Various cutaneous lesions, such as cysts, fibrous

tumors, and hair follicle tumors, may be
associated with internal malignancy.

Large sebaceous gland tumors are yellowish

umbilicated tumors that can be associated with
colonic polyps in Muir–Torre syndrome.

Cowden syndrome. Multiple mucosa-colored

papules on the tongue. From Bolognia JL, Jorizzo JL,
Rapini RP, eds. Dermatology. London: Mosby; 2003.

Cowden syndrome (multiple hamartoma).

Hamartoma of the skin and mucosa occurs in
90% of cases. Cobblestoning of the gingiva is a
characteristic finding.
159 DDx Ref  Inherited cutaneous
paraneoplastic syndromes
119 • 122 • 126

Inherited cutaneous paraneoplastic syndromes

involve cutaneous findings associated with heritable
or genetically related conditions that carry an
increased risk of internal malignancy.
COWDEN SYNDROME
• Cowden syndrome, or multiple hamartoma syn-
drome, is a rare, under-diagnosed disorder affecting
multiple organ systems. • Affected individuals
develop benign and malignant tumors. • Breast
cancer occurs in more than 30% of female patients.
Thyroid carcinoma is also common. • Characteristic
varieties of facial and oral papules develop during
early adulthood. • Facial papules are 1–3 mm,
smooth, skin-colored, and concentrated around eyes,
nose, malar cheeks, and mouth. Biopsy usually con-
firms the papule as a trichilemmoma, which is char-
acteristic of Cowden syndrome when multiple. • Oral
mucosal papules are 1–3 mm, smooth, and white,
coalescing into a cobblestone pattern on tongue and
gingiva. • Punctate keratoses of palms and soles
occur in roughly half of patients. • Female patients
suspected of having Cowden syndrome should have
regular breast examinations, mammograms, and
very close follow-up. Prophylactic bilateral mastec-
tomy has been suggested by some.
GARDNER SYNDROME
• An autosomal dominant condition consisting of
multiple epidermal cysts and fibrous tumors of the
skin and subcutaneous tissue, and associated intes-
tinal polyposis. • Intestinal polyps are usually limited
to the colon. • Malignant degeneration of polyps
occurs in 50% of patients. • There is usually a family
history of colon cancer. • Individuals develop multi-
ple epidermal cysts, most commonly on face and
scalp. • Discrete fibrous tumors of the skin are rarely
symptomatic. • Multiple pilar cysts of the scalp are
not associated with Gardner syndrome.
MUIR–TORRE SYNDROME
• An autosomal dominant condition with multiple,
benign, cutaneous, sebaceous tumors and colonic
polyps with increased risk of malignant degenera-
tion. • Muir–Torre syndrome is suggested by the
presence of multiple benign tumors of the sebaceous
glands, including sebaceoma, sebaceous adenoma,
and basal cell carcinoma with sebaceous differentia-
tion. Of these, the most specific for Muir–Torre is the
sebaceous adenoma. • Patients also develop kerato­
acanthomas with distinctive sebaceous differentia-
tion. • Sebaceous hyperplasia is a common condition
in otherwise healthy people, and is not considered
part of the Muir–Torre syndrome. • Patients sus-
pected of having Muir–Torre syndrome or Gardner
syndrome should undergo colonoscopy.
 Acanthosis nigricans
DDx Ref  70 • 115
160 

Acanthosis nigricans is a thickened velvety

hyperpigmentation of flexural skin.

Brown velvety elevated plaque on the nuchal

region, characteristic of acanthosis nigricans.

The areola can also be involved. The surface is

rough, warty, or papillomatous. Darkening or
hyperpigmentation is characteristic.

Verrucous and slightly inflamed changes of

acanthosis nigricans in the flexural areas;
coincident skin tags are not unusual.
160 Acanthosis
DDx Ref 
nigricans
70 • 115

DESCRIPTION
Thickened, velvety hyperpigmentation of flexural
skin. Most commonly associated with obesity and
diabetes. Less common associations are other endo-
crine disorders, medications, and occult malignancy.
Acanthosis nigricans is a marker for insulin
resistance.
HISTORY
• Patients usually complain of an asymptomatic, dirty
appearance to the skin folds that is not removed with
vigorous washing. • Usually, there is a gradual onset
when it is associated with diabetes and obesity. •
Malignancy-associated acanthosis nigricans devel-
ops more rapidly and suddenly. • Attempts to rub,
scrub, or remove the skin changes are futile. • There
may be a family history of the eruption.
PHYSICAL FINDINGS
• There is a symmetric, velvety brown thickening of
the skin. • The surface is rough, warty, or papillo-
matous, and may look unwashed or neglected. • The
axillae and posterior neck are the most common
areas involved. The crural folds, beltline, dorsal
fingers, umbilicus, mouth, and breast areolae are
also commonly involved. • Severity varies from mild
to extensive. • Usually asymptomatic. • The vulva is
commonly affected in obese, hirsute, hyperandro-
genic, insulin-resistant women. • HAIR-AN syndrome
is hyperandrogenism, insulin resistance, and acan-
thosis nigricans.
TREATMENT
• Acanthosis nigricans can be caused by medications
such as estrogens and nicotinic acid. Other endo-
crinologic disorders, such as pineal gland tumors, are
possible etiologies. • The eruption is usually asymp-
tomatic and does not require treatment. • Reducing
thick lesions in areas of maceration may decrease
the odor and promote comfort. • Lac-Hydrin, a 12%
lactic acid cream, is applied twice a day. Retinoic
acid (Retin-A cream or gel) applied each day, or less
often if irritation occurs, can be helpful. • No treat-
ment is uniformly effective at eradicating the skin
changes completely.
 Neurofibromatosis
DDx Ref  113 • 126 • 135
161 

Lisch nodules are pigmented, melanocytic, iris

hamartomas. They increase in number with age
and are asymptomatic. Slit-lamp examination is
essential for differentiations from iris freckles.

Neurofibroma tumors are usually not present in

childhood, but they begin to appear at puberty.
Tumors increase in both number and size as the
patient ages.

Neurofibromatosis is characterized by café-au-lait

macules, neurofibromas, and axillary and groin
freckling. Axillary freckling is also called Crowe
sign.

Multiple large café-au-lait macules are

characteristic in neurofibromas. More than 6
lesions larger than 5 mm strongly suggests the
diagnosis.
161 Neurofibromatosis
DDx Ref  113 • 126 • 135

DESCRIPTION
An inherited disorder of the skin and central nervous
system made up of at least seven clinical variants.
Neurofibromatosis type 1 is the most common
variant. It is also called von Recklinghausen disease.
HISTORY
• Inheritance is autosomal dominant; however, 50%
of cases arise from a new mutation. • Incidence
is estimated at 1 in 3000. • Affects both genders
equally. • Pathogenesis is believed to be a defect in
the neurofibromin gene.
PHYSICAL FINDINGS
• Typically pink to flesh-colored, soft, pedunculated
papules that may be tender. • The number present
varies from a few to hundreds or thousands in severe
cases. • Dermal and subcutaneous neurofibromas
can be present around 5 years of age, but typically
start appearing around puberty and increase in
number with age and with pregnancy. • Café-au-lait
macules (CALMs) are randomly distributed tan to
brown patches that increase in number and size in
the first 5 years of life; more than six CALMs over
5 mm in diameter suggests the presence of neuro­
fibromatosis type 1. • Axillary or inguinal freckling
(Crowe sign) is specific to the disease. • Plexiform
neurofibromas occur along the course of peripheral
nerves, creating large, tender nodules or poorly
demarcated masses, often with overlying hyper­
pigmentation and hypertrichosis. • About 20% of
neurofibromatosis patients have plexiform neuro­
fibromas. When present, these tumors are highly
diagnostic. • Malignant degeneration of cutaneous
neural tumors occurs in 2% of patients but is rare
before age 40. • Lisch nodules are asymptomatic iris
hamartomas and occur in more than 90% of neuro­
fibromatosis patients over age 6. Because Lisch
nodules are rare in the general population, their pres-
ence in patients older than 6 years and suspected
of having neurofibromatosis is virtually diagnostic.
• Optic gliomas, astrocytomas, meningioma, ves-
tibular schwannoma (acoustic neuroma), and epend-
ymomas also commonly occur in neurofibromatosis
patients. • Non-central nervous system tumors
occurring in neurofibromatosis type 1 include neuro­
fibrosarcoma, rhabdomyosarcoma, pheochromocy-
toma, and Wilms tumor. • Skeletal abnormalities
include short stature, scoliosis, sphenoid wing dys-
plasia, and macrocephaly. Renovascular abnormali-
ties may include renal artery stenosis.
TREATMENT
• A multidisciplinary approach with regular follow-up
by the primary care physician, ophthalmologist,
neurologist, and dermatologist is best. • Head
circumference and blood pressure should be moni-
tored closely in children. • Hypertension in a child
may indicate renal artery stenosis. In an adult, it
may suggest pheochromocytoma. • First-degree
relatives should be screened for cutaneous and oph-
thalmologic signs of neurofibromatosis. • Genetic
counseling of patients and their families is
recommended.
 Tuberous sclerosis
DDx Ref  32 • 111 • 139
162 

The shagreen patch. There is usually one lesion,

but several may be present. They are soft,
flesh-colored to yellow plaques with an irregular
surface that has been likened to pig skin.

Hypomelanotic macules (oval or ash leaf shaped)

are randomly distributed, with a concentration on
the arms, legs, and trunk.

Periungual fibromas are conical, pink, firm

projections from posterior nail folds of the fingers
and toes. They appear around the time of puberty
and persist indefinitely.

Adenoma sebaceum is the most common

cutaneous manifestation of tuberous sclerosis.
The lesions consist of smooth and firm 1- to
5-mm, yellow-pink papules with fine
telangiectasia.
162 Tuberous
DDx Ref 
sclerosis
32 • 111 • 139

DESCRIPTION
An uncommon genodermatosis with characteristic
features of the skin and central nervous system, as
well as multiple other organs. Also called Bourneville
disease and epiloia.
HISTORY
• Incidence estimated at 1 in 10 000. • Equal gender
distribution. • Spontaneous mutations account for
75% of cases; 25% are autosomal dominant. • Two
separate genes have been implicated. • About 40%
of affected individuals have normal intelligence; the
remainder have subtle to mild mental retardation.
• Cutaneous manifestations may not correlate with
mental ability. • Premature death occurs rarely, most
often from status epilepticus or malignant brain
tumor.
PHYSICAL FINDINGS
• Typically presents at or just after birth. • Earliest
signs are ‘ash leaf’ hypopigmented macules, usually
found on trunk or extremities. These should be exam-
ined with a Wood’s lamp. Polygonal, hypopigmented
‘confetti’ macules are also common, especially in the
pretibial area. • Facial angiofibromas, also called
adenoma sebaceum, appear in early childhood and
increase in number throughout adolescence. These
benign hamartomas are smooth, firm, pink, 1- to
5-mm papules appearing on nasolabial folds, cheeks,
and chin. They may be misdiagnosed as acne. • The
shagreen patch is a connective tissue nevus seen
in roughly 80% of patients. Typically located in the
lumbosacral area, it is a 1- to 5-cm, white to yellow
plaque with a pebbled surface. • Periungual fibromas
or angiofibromas are conical, pink, firm projections
from the posterior nail folds of the fingers and
toes. They appear around the time of puberty and
persist indefinitely. • Associated non-skin findings
include cortical tubers, paraventricular calcification,
subependymal hamartomas, and astrocytomas.
• Seizures occur in 75% of patients with central
nervous system lesions. • Infantile spasms and
mental retardation are also part of the syndrome.
• Retinal hamartomas (phakomas) may be seen.
• Angiomyolipoma, multiple renal cysts, cardiac
rhabdomyoma, enamel pits, gingival fibromas,
phalangeal cysts, periosteal thickening, and pulmo-
nary cysts may be present.
TREATMENT
• Complete physical examination with routine follow-
up by the primary care physician is important.
• Imaging studies should be performed to look for
cardiac, renal, and central nervous system tumors.
• Referral to a pediatric neurologist, including long-
term follow-up, should be considered for seizure
management. • Baseline ophthalmologic evaluation
should be performed. • Carbon dioxide laser ablation
or shave removal of facial angiofibromas can signifi-
cantly improve cosmetic appearance and self-image.
• If needed, special educational planning should help
an individual reach maximal potential. • Careful
cutaneous and general examination of first-degree
relatives, as well as genetic counseling, is
recommended.
 Granuloma annulare
DDx Ref  43 • 77 • 131
163 

Over time, the papules and patches of granuloma

may coalesce in to large confluent areas.

The ankle is a common site for granuloma

annulare, as are the dorsal hands and fingers.
Although rare, granuloma annulare can be
generalized.

Granuloma annulare lesions are pink to

flesh-colored annular patches or plaques, with an
elevated border and central clearing. It is often
misdiagnosed as ringworm.

Solitary red to pink arcuate plaque on the dorsal

hand knuckles with raised border, no scale and
central clearing, characteristic of granuloma
annulare.
163 Granuloma
DDx Ref 
annulare
43 • 77 • 131

DESCRIPTION
A slowly progressive, self-limited, granulomatous-
like dermal skin disease. Characterized by round or
annular plaques that may initially resemble tinea and
spontaneously disappear over time. There is both a
localized and more rare, generalized form.
HISTORY
• About 70% of patients with granuloma annulare are
younger than 30 years, and 40% are younger than
15 years. • Duration is highly variable. • The condi-
tions in half of patients resolves within 2 years, but
40% experience recurrence at the same site.
• Lesions tend to be asymptomatic. Patients become
more concerned when multiple lesions in multiple
areas develop and expand.
PHYSICAL FINDINGS
• The disease begins with an asymptomatic, flesh-
colored papule that undergoes central involution.
Small, firm, flesh-colored or violaceous papules then
develop in a ring-like fashion. • Over months, a ring
of papules coalesce into a concentric annular plaque
that slowly increases in diameter up to 5 cm. • The
localized form, most common in young women, is
most frequently found on the lateral or dorsal sur-
faces of the hands and feet. Individual lesions may
persist for many years then vanish, only to appear
later in life at the same or different locations.
• Disseminated or generalized granuloma annulare
occurs in adults and appears with numerous flesh-
colored or violaceous papules, some of which form
annular rings. The papules may be accentuated in
sun-exposed areas. The course is variable but may
persist for many years. • Granuloma annulare is most
often confused with tinea. • Granuloma annulare is
rarely associated with diabetes mellitus.
TREATMENT
• Localized lesions are asymptomatic and are usually
left untreated. • Superpotent topical steroids used
daily in 2- to 3-week intervals are sometimes effec-
tive. Lower-potency topical steroids can be occluded
for shorter periods of time. • Intralesional triam­
cinolone acetonide can be injected only into the
elevated border. This is predictably effective and
induces long periods of remission. • Disseminated or
generalized granuloma annulare has been reported
to occasionally respond to dapsone, isotretinoin,
etretinate, hydroxychloroquine, and niacinamide.
 Necrobiosis lipoidica
DDx Ref  18 • 87 • 163
164 

Necrobiosis lipoidica begins as a pink to

violaceous oval asymptomatic patch that expands
slowly. There is central atrophy of the patch with
mild inflammation at the periphery.

Later, there is chronic inflammation and central

ulceration followed by healing with bound-down
scars. Treatment with intralesional corticosteroids
may help control the spread of eruption.

More than 50% of patients with this condition are

insulin-dependent. The majority of patients are
female. The eruption is confined to the anterior
surfaces of the lower legs in most cases.

One should look for diabetes mellitus in newly

diagnosed cases, as symptoms may be subtle or
subclinical.
164 Necrobiosis
DDx Ref 
lipoidica
18 • 87 • 163

DESCRIPTION
An inflammatory condition of degenertive collagen.
When present, necrobiosis lipoidica is often associ-
ated with diabetes; therefore it is called necrobiosis
lipoidica diabeticorum. However, only 1–2% of
patients with diabetes develop necrobiosis lipoidica.
HISTORY
• More than 50% of individuals with necrobiosis
lipoidica also have insulin-dependent diabetes.
• Skin lesions may appear years before the onset of
diabetes. • Lesions usually develop slowly and are
often asymptomatic. • Onset may occur at any age,
but the disease most commonly starts in the third or
fourth decade. • About 75% of those affected are
women.
PHYSICAL FINDINGS
• Lesions are usually limited to the anterior shins but
may be seen on calves and thighs, and rarely on the
arms, hands, feet, and scalp. • They begin as round,
violaceous patches and slowly expand. The advanc-
ing border is red, and the central area turns a char-
acteristic orange-yellow brown. The central area
atrophies and shows a shiny, waxy surface with
prominent telangiectasias. • Ulceration may occur,
particularly after trauma, in about 15% of cases.
These ulcers are exquisitely tender. • The number
or severity of lesions or ulcerations has not been
correlated with the degree of diabetic control. • The
course is unpredictable. Lesions usually heal with
atrophic scarring, or can be chronic and recurrent.
TREATMENT
• Topical and intralesional steroids slow the inflam-
mation but may promote further atrophy. Middle- to
high-potency corticosteroids can be used under
occlusion. • Intralesional injections of triamcinolone
acetonide 10 mg/mL can be helpful. • A short course
(5–6 weeks) of oral corticosteroids can be considered
if disease activity and symptoms are severe, but this
is rarely the case. • Pentoxifylline (Trental) 400 mg
t.i.d. has been advocated by some and has been used
in combination with low-dose aspirin for ulcerating
necrobiosis lipoidica. • Skin grafting can be per-
formed for extensive disease.
 Pyoderma gangrenosum
DDx Ref  50 • 91 • 131
165 

Large asymmetric ulceration with yellow fibrinous

debris centrally and bright-red to violaceous
inflamed and undermined border peripherally,
characteristic of pyoderma gangrenosum.

The pustule or papule will break down, evolving

into erosions/ulcers with multiple crater-like
holes. These ulcerated plaques consist of small
fistulous tracks from which drainage occurs.

The legs are the most common site. New lesions

form at sites of injury in a phenomenon called
pathergy. Multiple lesions are typical.

Differentiation from other diseases causing ulcers

is sometimes very difficult. Malignancies may
present as ulcerations with exactly the same
appearance; biopsy uncertain.
165 Pyoderma
DDx Ref 
gangrenosum
50 • 91 • 131

DESCRIPTION
A necrotic, painful, non-infective, inflammatory skin
disease characterized by rapidly enlarging, painful
ulcerations on the legs.
HISTORY
• Ulcerative pyoderma gangrenosum lesions may
begin spontaneously or at the site of trauma. • Most
cases occur between 25 and 55. • The disease is
commonly associated with inflammatory bowel
disease (Crohn disease and ulcerative colitis); pyo-
derma gangrenosum patients should be evaluated for
inflammatory bowel disease. • It is less commonly
associated with rheumatoid arthritis, chronic active
hepatitis, IgG monoclonal gammopathy, myelo­
dysplasia, paraproteinemia, myeloid leukemias, and
myeloma. • Pathergy (enlargement of the lesion) with
trauma is typical in pyoderma gangrenosum. Post-
surgical pyoderma gangrenosum may masquerade
as wound infection, poor healing or dehiscence.
PHYSICAL FINDINGS
• Most common sites are lower legs, buttocks,
abdomen. • Lesions begin as a very tender, red or
dusky macule, papule, pustule, nodule, or bulla. The
initial lesion is often described as a pustule or
inflamed red nodule that then ulcerates, forming an
extremely painful, sharply marginated, violaceous-
bordered ulcer with a purulent base. • The edge of
the ulcer is characteristically elevated or under-
mined. • Expansion occurs rapidly. • Multiple lesions
are usually present. Eventually, lesions may coalesce
into larger ulcers with crater-like holes with small
fistulous tracks. • Lesions gradually heal with irregu-
lar, cribiform, or stellate scarring.
TREATMENT
• In general, many patients with pyoderma gan-
grenosum have a chronic relapsing course, even with
adequate treatment. • Although eradication of the
disease is the ultimate treatment goal, most regi-
mens aim to reduce dependence on steroid therapy.
• Hospitalization may be necessary for severe cases.
• Analgesia is often required. • Most patients require
combination therapy with multiple immunosuppres-
sants. • High-dose systemic oral (1–3 mg/kg) or i.v.
(1 g/day) steroids for 3–10 days should be adminis-
tered initially to try to quickly suppress the immune
response. • Ciclosporin (3–5 mg/kg) may be the best
short term, non-steroidal immunosuppressant for
pyoderma gangrenosum, and can be used in combi-
nation with systemic steroids in the appropriate
patient. In recent years, tumor necrosis factor-alpha
inhibitors, such as infliximab, adalimumab and
etanercept have been used to treat pyoderma
gangrenosum with dramatic success, and may
allow reduction or complete cessation of systemic
steroids. • Dapsone, mycophenolate mofetil, azathio-
prine, minocycline, clofazimine, and thalidomide
have been used anecdotally with variable results.
• Intravenous immunoglobulin is yet another drug
used for pyoderma gangrenosum that is poorly
studied but has been successful in some patients.
• Intralesional steroids (Kenalog 10–40 mg/cc) can
be used for small or single lesions, but care must be
taken not to injure the skin. • Local compresses with
Burow’s solution or silver nitrate 2 or 3 times daily.
• Superpotent topical steroids and tacrolimus (Pro-
topic) 0.1% ointment has been used with some
success.
 Lasers in dermatology
166 

Dark red to violaceous telangiectasias over the

nose before treatment.

Improvement in telangiectasias after three

treatments with the pulsed dye laser.

Long-standing port wine vascular stain on the left

forehead before treatment.

Improvements in the port wine vascular stain after

two treatments with the pulsed dye laser.
166 Lasers in dermatology
INTRODUCTION
Laser light is, by definition, monochromatic (single
wavelength), coherent (waves in phase) and colli-
mated (waves travel in parallel). In the skin, laser
energy is absorbed by chromophores, which include
water, melanin and oxygenated hemoglobin. Selec-
tive photothermolysis is a more specific and targeted
laser energy delivery that improves effectiveness and
reduces thermal damage and potential scarring. For
almost all therapies, multiple treatments are required
for full benefit.
USE OF LASERS IN DERMATOLOGY
• Pigmentation. Photopigmentation: lentigoes or
solar freckles on sun exposed areas of face and
hands. Treatments which can destroy melanin
pigment include intense pulsed laser (500–1200 nm)
and alexandrite laser (755 nm). • Blood vessels.
Facial telangiectasias, rosacea, hemangiomas, port-
wine stains. Pulsed dye laser (585–595 nm), best for
vascular lesions of all types, may leave some bruising
and require several treatments for complete removal,
especially with port-wine stains. Nd : YAG laser
(1094 nm) also has a role in blood vessel removal,
especially spider veins of the legs. • Hair. Alexandrite
laser (755 nm), most commonly used for hair follicle
destruction, is best on dark hair and light skin. Mul-
tiple treatments required. • Tattoo. Dark tattoo inks
are easier to remove than lighter colors (light yellow,
orange and red). Various lasers may have potential
to remove darker tattoo pigments but KTP (532 nm)
laser is most useful. • Wrinkles and hytids. Skin
tightening and wrinkle removal is achieved due to
water acting as a chromophore in the skin. Carbon
dioxide laser (10 600 nm), with either conventional or
fractionated laser techniques, can heat the dermis
quickly, cool relatively fast and stimulate collagen
formation in the dermis resulting in tightening and
rhytid reduction. • Destruction. Ablation or destruc-
tion of skin, tumor or other unwanted growths can
also be achieved using water as the chromophore in
the skin and an ablative carbon dioxide laser
(10 600 nm), however scarring may occur. Can also
be used for tumor destruction, actinic cheilitis and
other types of benign tumor (e.g. large nevi). • Hair
removal in dark skin. Nd : YAG (1064 nm) laser is
used to remove dark hair in dark-skinned individuals,
especially for those with pseudofolliculitis barbae.
COMPLICATIONS AND LIMITATIONS
Burning and scarring with any type of laser is pos-
sible. Pigment change, either hypo- or hyperpigmen-
tation, can occur and depends on the baseline skin
color, degree of pigmentation or sun exposure,
before and after treatment. Ablation, destruction, or
burning of the retinal and iris pigment as well as
burning and blistering of darker skin types can also
occur.
 Leshmaniasis
167 

Phlebotomus sandfly vector of Old World

leishmaniasis. Courtesy of Centers for Disease Control
and Prevention, Atlanta, GA, USA.

Small single shallow ulceration with rolled border at

the edge of the nasal mucosa of L. braziliensis. From
Bolognia, JL, Jorizzo JL, Schaffeer, JV, eds. Dermatology. 3rd
edn. London, Saunders; 2012. Courtesy, Kalman Watsky, MD.

An inflamed and ulcerated ear of L. mexicana, or

chiclero ulcer, may lead to cartilage destruction.
From James WD, Berger T, Elston DMD, eds. Andrew’s
Diseases of the Skin. 11th edn. London, Saunders; 2011.

A typical ulcer of L. major, with a shallow ulcer

and rolled border. From Magill AJ, Ryan ET, Hill DR,
Solomon T. eds. Hunter’s Tropical Medicine and Emerging
Infectious Diseases. 9th edn. London, Saunders; 2013.
167 Leshmaniasis
DESCRIPTION
A parasitic, protozoal infection, caused by several
Leishmania species and transmitted by the sandfly.
Acquired in tropical and subtropical areas of the
world. Variable clinical presentations.
HISTORY
• The intracellular protozoan Leishmania species is
considered endemic in tropical and subtropical areas
of South America, Asia and Africa, also some Mediter-
ranean countries. • More common in developing
countries. • Children commonly affected. • The
sandfly (Phlebotomous or Lutzomyia) bite is the major
mode of transmission. Leishmania are found in a
flagellated promastigote stage within the midgut of
the sandfly, transmitted to humans by the bite of the
female sandfly. Incubation times range from 1–24
months from time of bite to clinical symptoms.
• Classified by geographic area, specific species and
clinical presentation. • Old World leishmaniasis
(Europe, Asia, Africa): L. tropica, L. major, L. infantum,
L. donovania. • New World leishmaniasis (Americas):
L. mexicana, L. amozonesis, L. braziliensis.
PHYSICAL FINDINGS
• The major types of clinical presentations: cutane-
ous (skin only), mucocutaneous (skin and mucosal
surfaces), diffuse cutaneous and visceral. • The clini-
cal spectrum depends on the type of species and the
cell-mediated immune response of the host.
SKIN FINDINGS
• Cutaneous leishmaniasis. Most common form,
usually Old World type. • Red non-tender papule,
2–4 mm, at site of bite. • Multiple lesions may occur.
• Papule slowly enlarges over 2–3 months into a
2–4 cm plaque with crust, may ulcerate and develop
a firm violaceous border, persisting for many months.
• May heal spontaneously with or without a scar.
• Mucocutaneous leishmaniasis. New World type.
• Nasopharyngeal involvement, extension of cutane-
ous disease. • Inflammation of the mucosa with
hemorrhage and painful discharge. • Diffuse cuta-
neous leishmaniasis. Numerous parasites within
the skin; poor host immune response to parasite.
• Many non-ulcerative nodules evolving from satel-
lite papules around initial lesion. • Visceral leish-
maniasis (kala azar). Bone marrow, liver and
spleen involvement. • Fever, pain, lymphadenopathy,
hepatosplenomegaly and pancytopenia. • Slow to
very fast progression, poor prognosis.
TREATMENT
• Depends on species of leishmaniasis and infection
location. • Early diagnosis, speciation and detection
of systemic involvement are important. • L. major
(e.g. Iraq) is a self-limited form and may resolve
within a year without treatment. L. tropica (e.g.
Afghanistan) may cause aggressive or chronic
disease and require systemic therapy. • Systemic
therapy including antimonials (meglumine antimoni-
ate, sodium stibocloconate) is usually the first choice.
• Amphoteracin B, azole antifungals (fluconazole,
kenoconazole), dapsone, rifampin and allopurinol are
other options. • Proper monitoring for toxicities of
these medications is required. Assistance from an
infectious disease specialist may also be helpful.
 Leprosy (Hansen disease)
168 

Anesthetic hypopigmented patches with inflamed

border on the shins of borderline leprosy. From
Peters W, Pasvol G. Atlas of Tropical Medicine and
Parasitology, 6th edn. Mosby; 2007.

Diffuse lepromatous leprosy macules with little

inflammation. From James WD, Berger T, Elston DMD,
eds. Andrew’s Diseases of the Skin. 11th edn. London,
Saunders; 2011.

Loss of digits from chronic anesthesia, trauma,

neurotrophic atrophy and eventual resorption of
bone and soft tissue. From Peters W, Pasvol G. Atlas of
Tropical Medicine and Parasitology, 6th edn. Mosby; 2007.

Infiltrated nodules of the forehead and face

resulting in leonine facies of lepromatous leprosy.
From Peters W, Pasvol G. Atlas of Tropical Medicine and
Parasitology, 6th edn. Mosby; 2007.
168 Leprosy (Hansen disease)
DESCRIPTION
• A chronic infectious mycobacterial disease affected
the skin and nerves, caused by Mycobacterium
leprae. • It mainly affects the poor, in underdevel-
oped countries. It carries the most negative stigma
the world has known. • There are several clinical
variants, from mild to severe, which fluctuate
depending on the number of mycobacteria and the
host’s cell-mediated immune response. • Multidrug
therapy, which includes sulfonamides, has reversed
the course of the disease.
HISTORY
• This infection has been recorded though out the
history of the world, from the ancient cultures of
Egypt, China, India, the Middle Ages and to the
present. • It affects millions worldwide, mostly the
poor, who live in crowded conditions, in developing
countries. • Named after Hansen in the 1870s, for
his extensive clinical, epidemiological and microbio-
logical studies of the M. leprae organism. • Many
classifications, including Ridley and Jopling, based
on the polarity of the disease (1966), and WHO,
based on paucibacillary and multibacillary disease
(1997). Treatment with systemic sufonamides
changed the course of the disease.
PHYSICAL FINDINGS
• The spectrum of clinical signs and symptoms
depends on the stage of the infection and host
immunity. • Categorized as lepromatous, borderline-
lepromatous, borderline-borderline, borderline-
tuberculoid, tuberculoid. • Lepromatous leprosy:
most inflammatory, multibacillary, poor cellular
immune response. Macules, papules and nodules
symmetrically over the cooler areas of the face, ears,
wrists, elbows, knees and buttocks. Lesions may be
hypopigmented and anesthetic. Leonine facies,
saddle nose-deformity, madarosis and enlarged ear-
lobes are all part of this variant. • Borderline
leprosy: most common form. May have larger
plaques and nodules, affects the peripheral nervous
system. Unstable variant, moves toward lepromatous
or tuberculoid form. • Tuberculoid leprosy: smaller,
fewer patches or plaques on the trunk and extremi-
ties, which are less elevated, may be anesthetic and
either hypopigmented or hyperpigmented. Neural
invasions may lead to pain, muscle weakness, loss
of fingers and toes as well as blindness. • Non-skin
findings: enlarged peripheral nerves such as the
greater auricular, ulnar, radial, common peroneal and
posterior tibial. Decreased sensation to pain, tem-
perature and touch is common.
TREATMENT
• There were no effective treatments for leprosy until
dapsone, a sulfonamide, was introduced in the
1940s. • Resistance developed with monotherapy,
and combination therapy emerged in the 1960s with
clofazimine and rifampicin and dapsone. • Other
medications, such as minocycline and ofloxacin, may
be used in combinations, with the above.
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Potencies of topical steroids
(many available as generic drugs)
Brand name
CLASS 1 - SUPERPOTENT
Clobex Lotion/Spray 0.05%
Cormax Cream/Ointment/Solution 0.05%
Diprolene Gel/Ointment 0.05%
Olux Foam 0.05%
Psorcon Ointment 0.05%
Temovate Cream/Ointment/Solution 0.05%
Ultravate Cream/Ointment 0.05%
Vanos Cream 0.1%
CLASS 2 - POTENT
Cyclocort Ointment 0.1%
Diprolene Cream AF 0.05%
Diprolene Ointment 0.05%
Elocon Ointment 0.1%
Halog Ointment/Cream 0.1%
Lidex Cream/Gel/Ointment 0.05%
Psorcon Cream 0.05%
Topicort Cream/Ointment 0.25%
Topicort Gel 0.05%
CLASS 3 - UPPER MID-STRENGTH
Cutivate Ointment 0.005%
Diprosone Cream/Lotion 0.05%
Luxiq Foam 0.12%
Topicort Cream 0.05%
Valisone Ointment 0.1%
CLASS 4 - MID-STRENGTH
Cordran Ointment 0.05%
Cyclocord Cream/Lotion 0.1%
Derma-Smoothe/FS Oil 0.01%
Elocon Cream/Lotion 0.1%
Kenalog Cream/Ointment/Spray 0.1%
Synalar Ointment 0.025%
Westcort Ointment 0.2%
CLASS 5 - LOWER MID-STRENGTH
Cordran Cream/Lotion 0.05%
Cutivate Cream/Lotion 0.05%
Dermatop Cream 0.1%
DesOwen Ointment 0.05%
Diprosone Lotion 0.05%
Kenalog Lotion 0.1%
Locoid Cream/Ointment/Solution 0.1%
Synalar Cream 0.025%
Valisone Cream 0.1%
Westcort Cream 0.2%
CLASS 6 - MILD
Aclovate Cream/Ointment 0.05%
DesOwen Cream/Lotion 0.05%
Synalar Cream/Solution 0.01%
Valisone Lotion 0.1%
CLASS 7 - LEAST POTENT
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Recommended shelving classification:
Dermatology
Generic name
Clobetasol propionate
Clobetasol propionate
Betamethasone dipropionate
Clobetasol propionate
Diflorasone diacetate
Clobetasol propionate
Halobetasol propionate
Flucinonide
Amcinonide
Betamethasone dipropionate
Betamethasone dipropionate
Mometasone furoate
Halcinonide
Flucinonide
Diforasone diacetate
Desoximetasone
Desoximetasone
Fluticasone propionate
Betamethasone dipropionate
Betamethasone valerate
Desoximetasone
Betamethasone valerate
Flurandrenolide
Amcinonide
Flucinolone Acetonide
Mometasone furoate
Triamcinolone acetonide
Fluocinolone acetonide
Hydrocortisone valerate
Flurandrenolide
Fluticasone propionate
Prednicardbate
Desonide
Betamethasone dipropionate
Tramcinolone acetonide
Hydrocortisone butyrate
Fluocinolone acetonide
Betamethasone valerate
Hydrocortisone valerate
Alclometasone dipropionate
Desonide
Fluocinoloene acetonide
Betamethasone valerate
Topicals with hydrocortisone