Dermatology DDX Deck E-Book

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It's DDx To Go! The unique format of the Dermatology DDX Deck gives you a completely portable, uniquely convenient diagnostic tool to compare potential diagnoses visually, side by side, without the need to flip back and forth between different pages. Each laminated card includes full-color images and information about a particular diagnosis, as well as cross references (DDx-refs) to other potential diagnoses. Bound at one corner and small enough to fit in a pocket, this is the perfect reference for those on the front line of dermatological diagnosis!

  • Gain reliable, practical, and efficient guidance regarding the diagnoses and treatment of 160 of the most common dermatologic disorders, along with clinical tips presented by the experts.
  • Quickly access all the information you need to make the most accurate diagnoses, educate patients in the exam room, or prepare for the board review exam.
  • Take an in-depth approach to patients with skin of color, and cover all the fundamentals of acne, eczema, and psoriasis.

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Published 04 April 2013
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EAN13 9781455737758
Language English
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nd2 Edition Dermatology DDx Deck

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
A ssociate Professor of S urgery and Pediatrics (D ermatology) D epartment of S urgery
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
Table of Contents
Cover image
Title page
Copyright
Section 1: TOPICAL THERAPY
1. Basic principles of treatment
Maintaining The Skin Barrier
Skin Cleansing
Skin Moisturization
Topical Formulations
Topical Application And Dosing
Wet Dressings
2. Topical corticosteroids
Description
General Facts And Guidelines
Methods Of Application
Steroid−Antibiotic Mixtures
Potential Side Effects Of Topical Corticosteroids
Section 2: ECZEMA
3. Acute eczematous inflammation
Description
History
Physical Findings
Further Evaluation
Treatment
4. Rhus dermatitis (poison ivy, poison oak, poison sumac)
Description
History
Physical Findings
Treatment
5. Subacute eczematous inflammation
Description
History
Physical Findings
Treatment
6. Chronic eczematous inflammation
Description
History
Physical Findings
Treatment
7. Lichen simplex chronicus
DescriptionHistory
Physical Findings
Treatment
8. Hand eczema
Description
History
Physical Findings
Treatment
9. Asteatotic eczema
Description
History
Physical Findings
Treatment
10. Chapped, fissured feet
Description
History
Physical Findings
Treatment
11. Allergic contact dermatitis
Description
History
Physical Findings
Treatment
12. Irritant contact dermatitis
Description
History
Physical Findings
Treatment
13. Fingertip eczema
Description
History
Physical Findings
Treatment
14. Keratolysis exfoliativa
Description
History
Physical Findings
Treatment
15. Nummular eczema
Description
History
Physical Findings
Treatment
16. Pompholyx
Description
History
Physical Findings
Treatment
17. Prurigo nodularis
Description
History
Physical FindingsTreatment
18. Stasis dermatitis
Description
History
Physical Findings
Treatment
19. Venous leg ulcers
Description
History
Physical Findings
Treatment
20. Atopic dermatitis
Description
History
Physical Findings
Treatment
21. Autosomal dominant ichthyosis vulgaris
Description
History
Physical Findings
Treatment
22. Keratosis pilaris
Description
History
Physical Findings
Treatment
23. Pityriasis alba
Description
History
Physical Findings
Treatment
Section 3: URTICARIA
24. Acute urticaria
Description
History
Physical Findings
Treatment
25. Chronic urticaria
Description
History
Physical Findings
Treatment
26. Physical urticaria
Description
History
Physical Findings
Treatment
27. Angioedema
Description
History
Physical FindingsTreatment
28. Mastocytosis (urticaria pigmentosa)
Description
History
Physical Findings
Treatment
29. Pruritic urticarial papules and plaques of pregnancy
Description
History
Physical Findings
Treatment
Section 4: ACNE, ROSACEA, AND RELATED DISORDERS
30. Comedonal acne
Description
History
Physical Findings
Treatment
31. Pustular acne
Description
History
Physical Findings
Treatment
32. Cystic acne
Description
History
Physical Findings
Treatment
33. Perioral dermatitis
Description
History
Physical Findings
Treatment
34. Rosacea (acne rosacea)
Description
History
Physical Findings
Treatment
35. Hidradenitis suppurativa
Description
History
Physical Findings
Treatment
Section 5: PSORIASIS AND OTHER PAPULOSQUAMOUS DISEASES
36. Psoriasis: hands and feet
Description
History
Physical Findings
Treatment
37. Psoriasis: lesionsDescription
History
Physical Findings
Treatment
38. Psoriasis: nails
Description
History
Physical Findings
Treatment
39. Psoriasis: special forms
Description
History
Physical Findings
Treatment
40. Seborrheic dermatitis
Description
History
Physical Findings
Treatment
41. Grover disease (transient acantholytic dermatosis)
Description
History
Physical Findings
Treatment
42. Pityriasis rosea
Description
History
Physical Findings
Treatment
43. Lichen planus
Description
History
Physical Findings
Treatment
44. Lichen sclerosus
Description
History
Physical Findings
Treatment
45. Pityriasis lichenoides et varioliformis acuta
Description
History
Physical Findings
Treatment
Section 6: BACTERIAL INFECTIONS
46. Impetigo
Description
History
Physical Findings
Treatment
47. CellulitisDescription
History
Physical Findings
Treatment
48. Folliculitis
Description
History
Physical Findings
Treatment
49. Pseudofolliculitis barbae
Description
History
Physical Findings
Treatment
50. Furuncles and carbuncles
Description
History
Physical Findings
Treatment
51. P s e u d o m o n a s folliculitis
Description
History
Physical Findings
Treatment
52. Otitis externa
Description
History
Physical Findings
Treatment
Section 7: SEXUALLY TRANSMITTED INFECTIONS
53. Syphilis
Description
History
Physical Findings
Treatment
54. Chancroid
Description
History
Discussion
Physical Findings
Treatment
55. Genital warts
Description
History
Physical Findings
Treatment
56. Genital herpes simplex
Description
History
Physical Findings
Treatment57. Pubic lice
Description
History
Physical Findings
Treatment
58. Molluscum contagiosum
Treatment
Section 8: VIRAL INFECTIONS
59. Warts (verruca vulgaris)
Description
History
Physical Findings
Treatment
60. Flat warts
Description
History
Physical Findings
Treatment
61. Plantar warts
Description
History
Physical Findings
Treatment
62. Molluscum contagiosum
Description
History
Physical Findings
Treatment
63. Herpes simplex (cold sores, fever blisters)
Description
History
Physical Findings
Treatment
64. Varicella (chickenpox)
Description
History
Physical Findings
Treatment
65. Herpes zoster (shingles)
Description
History
Physical Findings
Ophthalmic Zoster
Treatment
66. Hand, foot, and mouth disease
Description
History
Physical Findings
TreatmentSection 9: FUNGAL INFECTIONS
67. Candidiasis (moniliasis)
Description
History
Physical Findings
Treatment
68. Candidal balanitis
Description
History
Physical Findings
Treatment
69. Candidiasis (diaper dermatitis)
Description
History
Physical Findings
Treatment
70. Candidiasis of large skin folds (candidal intertrigo)
Description
History
Physical Findings
Treatment
71. Tinea versicolor
Description
History
Physical Findings
Treatment
72. Tinea of the nails
Description
History
Physical Findings
Treatment
73. Angular cheilitis
Description
History
Physical Findings
Treatment
74. Cutaneous fungal infections (tinea)
Description
History
Physical Findings
Treatment
75. Tinea of the foot
Description
History
Physical Findings
Treatment
76. Tinea of the groin
Description
History
Physical Findings
Treatment77. Tinea of the body
Description
History
Physical Findings
Treatment
78. Tinea of the hand
Description
History
Physical Findings
Treatment
79. Tinea incognito
Description
History
Physical Findings
Treatment
80. Tinea of the scalp
Description
History
Physical Findings
Treatment
81. Tinea of the beard
Description
History
Physical Findings
Treatment
Section 10: EXANTHEMS AND DRUG REACTIONS
82. Non-specific viral rash
Description
History
Physical Findings
Treatment
83. Erythema infectiosum
Description
History
Physical Findings
Treatment
84. Cutaneous drug eruptions
Description
History
Physical Findings
Treatment
Section 11: HYPERSENSITIVITY SYNDROMES AND VASCULITIS
85. Erythema multiforme
Description
History
Physical Findings
Treatment
86. Stevens–Johnson syndrome
DescriptionHistory
Physical Findings
Treatment
87. Erythema nodosum
Description
History
Physical Findings
Treatment
88. Cutaneous small vessel vasculitis (hypersensitivity vasculitis)
Description
History
Physical Findings
Treatment
89. Henoch–Schönlein purpura
Description
History
Physical Findings
Treatment
90. Schamberg disease (Schamberg purpura)
Description
History
Physical Findings
Treatment
91. Sweet syndrome
Description
History
Physical Findings
Treatment
Section 12: INFESTATIONS AND BITES
92. Scabies
Description
History
Physical Findings
Treatment
93. Head lice (pediculosis)
Description
History
Physical Findings
Treatment
94. Bee and wasp stings
Description
History
Physical Findings
Treatment
95. Lyme disease
Description
History
Physical Findings
Treatment
96. Rocky Mountain spotted fever
DescriptionHistory
Physical Findings
Treatment
97. Flea bites
Description And History
Physical Findings
Treatment
98. Cutaneous larva migrans
Description
History
Physical Findings
Treatment
Section 13: VESICULAR AND BULLOUS DISEASES
99. Dermatitis herpetiformis
Description
History
Physical Findings
Treatment
100. Pemphigus vulgaris
Description
History
Physical Findings
Treatment
101. Pemphigus foliaceus
Description
History
Physical Findings
Treatment
102. Bullous pemphigoid
Description
History
Physical Findings
Treatment
Section 14: CONNECTIVE TISSUE DISEASES
103. Chronic cutaneous lupus
Description
History
Physical Findings
Treatment
104. Acute cutaneous lupus erythematosus
Description
History
Physical Findings
Treatment
105. Dermatomyositis
Description
History
Physical Findings
Treatment106. Scleroderma
Description
History
Physical Findings
Treatment
107. Morphea
Description
History
Physical Findings
Treatment
Section 15: LIGHT-RELATED DISEASES AND DISORDERS OF PIGMENTATION
108. Sun-damaged skin, photoaging
Description
History
Physical Findings
Treatment
109. Polymorphous light eruption
Description
History
Physical Findings
Treatment
110. Porphyria cutanea tarda
Description
History
Physical Findings
Treatment
111. Vitiligo
Description
History
Physical Findings
Treatment
112. Idiopathic guttate hypomelanosis
Description
History
Physical Findings
Treatment
113. Lentigo, juvenile lentigo, solar lentigo
Description
History
Physical Findings
Treatment
114. Melasma (chloasma, mask of pregnancy)
Description
History
Physical Findings
Treatment
Section 16: BENIGN SKIN TUMORS
115. Seborrheic keratosis
DescriptionHistory
Physical Findings
Treatment
116. Skin tags
Description
History
Physical Findings
Treatment
117. Dermatofibroma
Description
History
Physical Findings
Treatment
118. Keloids and hypertrophic scars
Description
Physical Findings
Treatment
119. Keratoacanthoma
Description
History
Physical Findings
Treatment
120. Nevus sebaceus
Description
History
Physical Findings
Treatment
121. Chondrodermatitis nodularis helicis
Description
History
Physical Findings
Treatment
122. Epidermal cyst
Description
History
Physical Findings
Treatment
123. Pilar cyst
Description
History
Physical Findings
Treatment
124. Sebaceous hyperplasia
Description
History
Physical Findings
Treatment
125. Syringomas
Description
History
Physical Findings
TreatmentSection 17: PREMALIGNANT AND MALIGNANT NON-MELANOMA SKIN
TUMORS
126. Basal cell carcinoma
Description
History
Physical Findings
Treatment
127. Actinic keratosis
Description
History
Physical Findings
Treatment
128. Squamous cell carcinoma
Description
History
Physical Findings
Treatment
129. Bowen disease
Description
History
Physical Findings
Treatment
130. Leukoplakia
Description
History
Physical Findings
Treatment
131. Cutaneous T-cell lymphoma
Description
History
Physical Findings
Treatment
132. Paget disease of the breast
Description
History
Physical Findings
Treatment
133. Extramammary Paget disease
Description
History
Physical Findings
Treatment
134. Cutaneous metastasis
Description
Physical Findings
Section 18: NEVI AND MALIGNANT MELANOMA
135. Nevi, melanocytic nevi, moles
Description
History
Physical FindingsTreatment
136. Atypical mole syndrome (dysplastic nevus syndrome)
Description
History
Physical Findings
Treatment
137. Malignant melanoma, lentigo maligna
Description
History
Physical Findings
Treatment
138. Melanoma mimics
Description
History
Physical Findings
Treatment
139. Congenital melanocytic nevi
Description
History
Physical Findings
Treatment
Section 19: VASCULAR TUMORS AND MALFORMATIONS
140. Hemangiomas of infancy
Description
History
Physical Findings
Treatment
141. Vascular malformations
Description
History
Physical Findings
Treatment
142. Cherry angioma
Description
History
Physical Findings
Treatment
143. Angiokeratoma
Description
History
Physical Findings
Treatment
144. Venous lake
Description
History
Physical Findings
Treatment
145. Pyogenic granuloma
Description
History
Physical FindingsTreatment
146. Kaposi sarcoma
Description
History
Physical Findings
Treatment
147. Telangiectasias
Description
History
Physical Findings
Treatment
148. Spider angioma (nevus araneus)
Description
History
Physical Findings
Treatment
Section 20: HAIR AND NAIL DISEASES
149. Androgenic alopecia (male pattern baldness)
Description
History
Physical Findings
Treatment
150. Androgenic alopecia in women (female pattern hair loss)
Description
History
Physical Findings
Treatment
151. Alopecia areata
Description
History
Physical Findings
Treatment
152. Trichotillomania
Description
History
Physical Findings
Treatment
153. Fungal nail infections
Description
History
Physical Findings
Treatment
154a. Nail diseases: Psoriasis
Description
History
Physical Findings
Treatment
154b. Nail diseases: Paronychia, P s e u d o m a s infection, white spots or bands
Acute Paronychia
Chronic Paronychia
P s e u d o m o n a s InfectionWhite Spots Or Bands
154c. Nail diseases: Ridging and beading, habit tic deformity, onycholysis
Ridging And Beading
Habit Tic Deformity
Onycholysis
Distal Plate Splitting
154d. Nail diseases: Digital mucous cyst, nevi and melanoma, hematoma
Digital Mucous Cysts
Nevi And Melanoma
Subungual Hematoma
Section 21: NEONATAL DISEASE
155. Erythema toxicum neonatorum
Description
History
Physical Findings
Treatment
156. Miliaria
Description
History
Physical Findings
Treatment
157. Cutis marmorata
Description
History
Physical Findings
Treatment
Section 22: CUTANEOUS MANIFESTATIONS OF INTERNAL DISEASE
158. Acquired cutaneous paraneoplastic syndromes
Pruritus
Sign Of Leser–Trélat
Dermatomyositis
Sweet Syndrome
Paraneoplastic Pemphigus
Carcinoid Syndrome
Glucagonoma Syndrome
159. Inherited cutaneous paraneoplastic syndromes
Cowden Syndrome
Gardner Syndrome
Muir–Torre Syndrome
160. Acanthosis nigricans
Description
History
Physical Findings
Treatment
161. Neurofibromatosis
Description
History
Physical Findings
Treatment162. Tuberous sclerosis
Description
History
Physical Findings
Treatment
163. Granuloma annulare
Description
History
Physical Findings
Treatment
164. Necrobiosis lipoidica
Description
History
Physical Findings
Treatment
165. Pyoderma gangrenosum
Description
History
Physical Findings
Treatment
166. Lasers in dermatology
Introduction
Use Of Lasers In Dermatology
Complications And Limitations
167. Leshmaniasis
Description
History
Physical Findings
Skin Findings
Treatment
168. Leprosy (Hansen disease)
Description
History
Physical Findings
TreatmentCopyright
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Potencies of topical steroids (many available as generic drugs)

www.elsevierhealth.com






Recommended shelving classification:
Dermatology

SECT ION 1: TOPICAL T HERAPY

1
Basic principles of
treatment

DDx Ref 70 • 79 • 108
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).
MAINTAINING THE SKIN BARRIER
• Functions of the skin: fluid homeostasis; protection 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 fragranced 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
exfoliating 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 petroleum 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
G ently 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. S kin location affects ease of medication
penetration. The following anatomic locations are organized in increasing
difficulty of medication 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. •
I mmerse 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. tepidwater, Burow’s solution). • G ently 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.
2
Topical corticosteroids

DDx Ref 15 • 20 • 37
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.
DESCRIPTION
• Topical corticosteroids: used to treat inflammatory dermatoses; safe and
effective with proper use. • Corticosteroid potency: organized into seven groups
based on their anti-inflammatory activity; group I (strongest) to group VI I
(weakest).
GENERAL FACTS AND GUIDELINES
I mportant 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. S teroid concentrations reflect relative strength for a particular
corticosteroid (triamcinolone 0.025%, 0.05%, 0.1%) and cannot be used to
compare strengths between corticosteroids. Fluorinated 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 VI I topical
corticosteroids (hydrocortisone) for more difficult rashes; eyelid dermatitis and
intertriginous 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
O cclusive dressings (e.g. S aran Wrap) hydrate the stratum corneum and allow
enhanced corticosteroid absorption; allow for use of lower-strength
corticosteroids. O cclusive dressings can be used during the day for periods up to
2 h, or 8 h during sleep. S imple 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 dressings:
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, irritation, dryness (largely due to
the vehicle), hypertrichosis, hypopigmentation, miliaria and folliculitis, skin
breakdown, glaucoma, cataracts, rebound phenomenon (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 incognito, impetigo
incognito, scabies incognito. • I nfants are at increased risk for systemic
absorption.
SECT ION 2: ECZEMA

3
Acute eczematous
inflammation

DDx Ref 11 • 16 • 75
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.
DESCRIPTION
Acute eczematous inflammation is characterized clinically by erythema, edema,
and vesiculation. Weeping and oozing of acute lesions is typical. Pruritus is often
severe.
HISTORY
• Multiple causes, including allergic contact hypersensitivity 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. I rritant
dermatitis is common after repeated water, solvent, or detergent exposure. • I n
an ‘id reaction’, acute eczema with vesicles occurs at a distant site (e.g. hands)
from an active fungal infection (e.g. feet). • S tasis dermatitis, scabies, irritant
reactions, and dyshidrotic and atopic eczema may present as acute eczema. • I f
provoking factors can be avoided, eruption 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. I nflammation
moderate to intense. Tiny, clear, fluid-filled vesicles. Bullae may develop.
FURTHER EVALUATION
• Consider patch testing for delayed-type hypersensitivity 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 preparation 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 allergens with specific allergen trays.
TREATMENT
• Cool, wet dressings and topical steroid creams suppress inflammation and
itching. S oak 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
I I I ), rub in well. • Reserve oral corticosteroids for severe or generalized acuteeczema. Approximately 1 mg/kg q.d. initially, tapering over 3 weeks. Too short a
course may result in recurrence and rebound. • O ral antihistamines such as
diphenhydramine (Benadryl) and hydroxyzine (Atarax) can relieve itching;
sedative effect promotes sleep. • I f secondary infection suspected, culture,
review sensitivity, and use an appropriate oral antibiotic for 10–14 days. •
Remove all patient’s topicals (lotions, topical over-the-counter medicaments,
antiitch preparations); treat with topical steroids only or bland emollients such as
plain Vaseline. Keep skin care and exposures minimal and simple.
4
Rhus dermatitis (poison ivy, poison
oak, poison sumac)

DDx Ref 11 • 47 • 75
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.6
6
Dried urushiol on the skin may leave behind a telltale black ink-like mark.
DESCRIPTION
Poison ivy, oak, and sumac (Anacardiaceae family, T o x i c o d e n d r o n genus) are the
most common causes of allergic contact dermatitis in the US A; they are rare in
Europe. Related plants grow in S outh-East Asia, and Central and S outh America.
The plant oleoresin (lipid-soluble portion) contains highly allergenic catechol
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 sensitization can result from plant
exposure. After sensitization, 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, pa ern of contact, individual
susceptibility. • Pruritic, edematous, linear erythematous streaks, usually with
vesicles and large bullae on exposed skin. • Airborne particulate ma er from
burning plant can cause intense facial erythema and marked edema; eyelids can
be dramatically swollen. • O ne 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. • S hort, cool tub baths, with or without colloidal oatmeal (Aveeno),
are soothing. • Calamine lotion helps control itching. • O ral antihistamines
(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 I I –V) is generously applied after wet dressing. I f periorbital
skin involved, a weaker topical steroid (group VI –VI I ) is advised for limited
duration (twice daily for 7 days). • For severe, widespread inflammation, oral
prednisone 0.75–1 mg/kg q.d. every morning, slowly tapered over 3 weeks. • I vy
Block barrier cream can prevent or lessen dermatitis, but must be applied beforeplant contact.
5
Subacute eczematous
inflammation

DDx Ref 12 • 18 • 77
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.
DESCRIPTION
S ubacute 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. • I tching variable; can be moderate to severe,
or rather mild. • Resolves without scarring when provoking or contributing
aggravating factors are removed. May require treatment to resolve. • Excoriation
and repeated exposure to aggravating conditions (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 dermatoses that may present as subacute eczema. • A ention 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 pa ed dry following bathing. • Emollients with simple
formulations lacking the most common allergy-associated ingredients (e.g.
Aveeno, Cetaphil, DML, Acid Mantle) are be er than lotions. Plain petroleum
jelly is an excellent emollient. • I nfrequent washing with bar-type mild soap (e.g.
Dove, Cetaphil, Keri, Purpose, Basis) is also helpful. • G roup I I –V steroid creams
twice a day with or without plastic occlusion. O cclusion hastens resolution while
increasing absorption. Duration of occlusion should be specified, limited, and
supervised. • Alternative is steroid ointment applied twice a day without
occlusion. • Non-steroid topical immune modulators tacrolimus (Protopic
ointment 0.1, 0.03%) and pimecrolimus (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 management of subacute eczema in
atopic patients. • Tar ointments and creams (many over-the-counter
preparations) 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
sensitivity should be checked). • Ask about occupation, duties at home, and
hobbies, as these may contribute to ongoing skin irritation or allergy. G loves 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
rubberrelated 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.
6
Chronic eczematous
inflammation

DDx Ref 7 • 15 • 20
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.
DESCRIPTION
Affected skin is inflamed, red, scaling, and thickened (lichenified).
HISTORY
• There is moderate to intense, prolonged itching. • S cratching and rubbing
become habitual and may be done subconsciously. • The disease becomes
selfperpetuating. • S cratching 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
• I ntense itching can lead to excoriations. • I nflamed, itchy skin thickens, and
surface skin markings become more prominent. • Thick plaques with deep
parallel skin markings appear (lichenification). • S ites commonly involved are
those easily reached or creased areas. • Common locations are the back of the
neck, popliteal fossae, ankles, eyelids, anogenital skin, palms, soles and legs in
stasis dermatitis. • Hyperpigmentation or hypopigmentation can occur on
affected skin.
TREATMENT
• O intments penetrate lichenified skin well and are generally more effective
than creams on lichenified skin. • Consider and evaluate for contact irritants and
allergens. S implify 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
nigh1 ime itch urge. • G roup I or I I creams or ointments applied twice a day can
be effective (not for face location). • G roup I I –V steroids are used with plastic
occlusion for 2–8 h. • I ntralesional injections (e.g. triamcinolone (Kenalog)
10 mg/mL) are very effective; resistant plaques are reinjected at 3- to 4-week
intervals. • S teroid-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.
7
Lichen simplex chronicus

DDx Ref 18 • 20 • 37
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.
DESCRIPTION
Localized plaque of chronic eczematous inflammation 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 li le tendency to enlarge. O nce 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 sca ered
randomly on the scalp, occur in patients who frequently pick at the scalp. •
Areas most commonly affected are conveniently reached, commonly the outer
portion of lower legs, wrists, ankles, posterior neck, scalp, eyelids, fold behind the
ear, scrotum, vulva, and anal skin. • I nfection can mimic lichen simplex
chronicus; consider potassium hydroxide examination. • Contact allergy may
cause, lead to, or complicate. Patch testing can be helpful.
TREATMENT
• S tress 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. • S cratching 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 I I steroid gel such as
fluocinonide (Lidex) or a solution such as clobetasol (Cormax scalp solution)
twice each day for 2 weeks. • Moist, secondarily infected areas respond to oral
antibiotics and topical steroid lotion. • Nigh ime itching can be diminished with
oral antihistamines such as diphenhydramine (Benadryl) or hydroxyzine
(Atarax). • G renz 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.
8
Hand eczema

DDx Ref 20 • 37 • 47
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.1
Erythema, yellow scaling, and fissuring characterize this more
psoriasislike dermatitis on the fingers.
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
chemicals 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 additives). • 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; occasionally, contact urticaria
(type 1 allergy) is culprit. • Recurrent, intensely pruritic vesicles on lateral
fingers and palms: suspect pompholyx. • Fingertip eczema (dryness, spli ing,
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, solvents. I f hand sanitizer can be
used in place of washing hands, it is less irritating and should be recommended.
Chronic frictional trauma also an irritant. • Take protective measures (e.g. vinyl
gloves for wet or chemical work). • Medium- to high-potency (groups I I –I V)
topical steroids twice daily. O intments preferred. Most effective when used
intermi3 ently. • For severe dermatitis, a superpotent topical corticosteroid
applied after wet dressings containing Burow’s solution, twice a day for 3–5 days,