Dermatitis Flashcards
Atopic Eczema/Dermatitis
- Common allergic skin disease
- Comes and goes over time, usually starts in childhood
- Primary symptom is itchy skin
Epidemiology of Atopic Eczema/Dermatitis
Atopic eczema affects 5-20% children worldwide
- 11% in the US
- Slight F > M predominance
- Majority of cases have an onset before age 5
- 60% of cases occur in the 1st year of life
- 85% by 5 years of age
- May persist into adulthood for up to half of those diagnosed during childhood
Characteristics of Atopic Eczema/Dermatitis
•Chronic, non-contagious, inflammatory skin disease
•Disruption of the skin barrier:
o Filaggrin(FLG) gene mutation
o Allergens or other triggers
•Type I hypersensitivity reaction (IgE mediated)
•Viscous cycle of pruritis and disruption of the skin surface; “the itch that rashes”
•Begins early in life, with chronic exacerbations and remissions.
Contributing Factors of Atopic Eczema/Dermatitis
•Genetic defects/family history (70%)
•Environment
-foods, dust mites, molds, pollens, animal dander, season (winter/low humidity), clothing, emotional stress
Atopic triad:
•atopic dermatitis
•allergic rhinitis (hay fever)
•asthma
Clinical Presentation of Atopic Eczema/Dermatitis
- Ranges from ill-defined, erythematous, scaling patches to edematous papules and vesicles
- Cheeks, scalp & extensor surfaces common in infants
- Flexural surfaces, hand/foot (older children/adults)
Acute - pruritic, erythematous papulovesicular lesions; serous exudate
Chronic - lichenification, papules, and excoriation
Distribution of Atopic Eczema/Dermatitis by Age
Babies - Concentrated near or around the face
Toddler & Children - Concentrated in areas with folds and creases, such as elbows and knees
Adults - Concentrated on the hands, feet, as well as head and neck region.
Features to Consider in the Diagnosis of Atopic Dermatitis
Essential Features: Required •Pruritus •Eczema (acute, subacute, chronic) •Typical morphology and age-specific patterns •Chronic or relapsing history
Important Features: Observed in majority of cases; adds support to diagnosis: •Early age of onset •Atopy •Personal and/or FH •IgE reactivity •Xerosis
Complications of Atopic Eczema/Dermatitis
- Excoriations
- Lichenification
- Thickened, dry, irritated skin due to chronic scratching
- Skin lines are accentuated
- Fissures (palms, fingers, soles) –can be very painful
- Secondary cellulitis
- Skin is often highly colonized with Staph aureus •Eczema Herpeticum –disseminated viral infection, typically primary infection of HSV 1
Atopic Eczema/Dermatitis Treatment
Optimal management includes:
•Patient education
•Avoid exacerbating factors (allergens/irritants)
•Hydrate the skin & restore the skin barrier function
•Pharmacologic treatment of skin inflammation
•Topical/oral steroids
•Calcineurin Inhibitors
•+/-Antihistamines/antibiotics
Topical Corticosteroid Use for Atopic Eczema/Dermatitis
- Mild disease: low potency, applied 1-2x daily for 2-4 weeks
- Moderate disease: medium to high potency
- Acute flares: intermediate to super high potency preparations may be used for up to 2 weeks, then replaced with a lower potency until lesions resolve.
•IMPORTANT:Use extreme caution when using topical corticosteroids on thinned-skin areas (face, neck, and skin folds). Higher absorption and risk of adverse effects!
Absorption of Topical Corticosteroids
Regional differences in percutaneous absorption (percent of the total dose absorbed across the body) are as follows: •Sole of foot –0.14 % •Palm –0.83 % •Forearm –1.0 % •Scalp –3.5 % •Forehead –6.0 % •Mandible –13 % •Genitalia –42 %
Adverse Effects of Coricosteroid Use
Skin atrophy Acneiform or rosacea-like eruptions Striae Bruising Telangiectasias Hypertrichosis
Topical Calcineurin Inhibitors
Pimecrolimus (Elidel) cream and Tacrolimus (Protopic) ointment:
•Steroid-sparing, anti-inflammatory agents
Efficacious for acute flares and maintenance therapy in adults and children ≥ 2 years old
•0.1% formulation for adults
•0.03% formulation for patients 2-15 years old
MOA –inhibits calcineurin-dependent T cell activation, impeding production of pro-inflammatory cytokines
•Applied twice daily for mild to moderate eczema of the face, eyelids, neck and skin folds.
•Maintenance -apply 2-3x per week to recurrent sites of involvement to reduce relapse.
•Side effects: burning, stinging and pruritis (most common during 1st week)
Other Pharmacologic Treatments for Atopic Eczema/Dermatitis
- Oral antihistamines prn pruritus (to break the itch-scratch-itch cycle)
- Antibiotics if secondary infection
- Oral steroids reserved for severe cases
Lichen Simplex Chronicus
- Aka “Neurodermatitis”
- Affects F>M, age 30-50 years old
- Secondary skin condition; lichenified plaque caused by excessive scratching or rubbing
- Exaggerated skin markings, dry, leathery appearance, pigmentation
- Common areas: scalp, back of neck, wrists, forearms, lower legs and genitals
Causes of Lichen Simplex Chronicus
- Atopic Dermatitis
- Contact Dermatitis
- Psoriasis
- Lichen Planus
- Fungal Infection
- Insect Bite
- Neuropathy (DM)
- Anxiety/stress
Lichen Simplex Chronicus Treatment
Treatment is to stop rubbing!
- High potency topical steroids
- Moisturizers
- Antidepressants: SSRIs –Paroxetine (Paxil), Sertraline (Zoloft) or tricyclic antidepressants
- 1st generation antihistamine, Hydroxyzine (Vistaril), or tricyclic antidepressant (Doxepin) can be used for nocturnal pruritus.
Dyshidrotic Eczema
- Aka “dyshidrosis” or “pompholyx”
- NOT a problem with the sweat glands
- Deep seated vesicles with “tapioca-like” appearance
- Vesicles coalesce and rupture
- Location: hands (80%), sides of fingers, palms and soles
- INTENSELY PRURITIC
- Emotional stress & hot weather precipitating factors, also found in those with nickel allergy
- Episodes usually weeks to months apart, spontaneous remission after 2-3 weeks
- Management-reassurance, wet dressings (Burow’ssoaks, aka Domeborosolution), topical steroids
Keratosis Pilaris
- Disorder of keratinization
- Forms horny plugs in hair follicles
- Rough, raised papules (flesh, red or brownish)
- Usually worse in winter months
- Outer upper arms, thighs, cheeks, upper back
- Improves with age
- Can try creams, exfoliating scrubs, topical retinoids (avoid in children), urea, salicylic acid, alpha-hydroxy acids
Classification of Contact Dermatitis
•Allergic Contact Dermatitis - a delayed-type hypersensitivity reaction
- Poison ivy (genus Toxicodendron), nickel, etc.
•Irritant Contact Dermatitis –80% of all contact dermatitis
- Household duties: hands in water, detergents, solvents, etc.
- The most common occupational skin disease
- Healthcare workers, chemical industry workers,
hairdressers, construction workers, etc.
Allergic Contact Dermatitis
- Dominant symptom is itch
- Localized to skin areas that came in contact with the allergen
- Hands, face and eyelids common
- Erythematous, papular dermatitis with indistinct margins; often blisters and edema
- Can take 1-2 days to appear
- Poision ivy, oak, and sumac (urushiol oil)
- Nickel, rubber; latex, preservatives, cosmetics, Neomycin (in topical creams/ointments)
Irritant Contact Dermatitis
- Burning, stinging pain
- Hands are most common
- Erythema, chapped skin, dryness and fissuring
- More immediate onset (minutes to hours)
Contact Dermatitis - Treatment
- Discontinue exposure to allergen or irritant.
- Decrease frequency of hand-washing if that is playing a role; use mild soap.
- Wear gloves or protective clothing.
- Apply bland emollient (Vaseline, Aquaphor, etc.)
- Topical steroids 1-2x daily for 7-14 days
- Consider an oral corticosteroid for ACD involving face or >20% BSA.
- Prednisone 0.5-1mg/kg/day (max 60mg/day) for 7 days
Drug Hypersensitivity
Immune-mediated response to a drug in a sensitized patient
Drug Allergy
Type I immune reaction mediated by IgE (urticaria, angioedema, bronchospasm, pruritis, V/D, anaphylaxis)
Adverse Cutaneous Drug Reactions
- Aka “Drug Eruptions” occur in ~2% of patients
- 90-95% are drug-induced exanthems (Type IV)
- Often described as “morbilliform” or “rubelliform” because pattern resembles a viral exanthem.
- 5% are drug-induced urticarial (Type I)
- Rarely, severe non-allergic hypersensitivity cutaneous reactions occur (EM major, SJS/TEN and DIHS)
Drug-Induced Exanthems
- Account for 90% of all adverse cutaneous drug reactions•Develops within 5-14d of exposure
- Morbilliform rash -erythematous macules, papules (rarely pustules/bullae)
- Involves trunk and proximal extremities; mucosal involvement is absent
- PCNs and sulfonamides common
Urticaria
“hives”
Intensely pruritic, circumscribed, raised, erythematous eruption with central pallor
Angioedema
Swelling deeper in dermis and subQ tissue (face/lips)
- Tongue swelling, laryngeal edema -> Airway
obstruction
Treatment of Common Cutaneous Drug Reactions
- Discontinue the offending drug!
- Supportive and/or symptomatic care•Systemic corticosteroids
- Topical steroids or antihistamines prn pruritus
- Resolution is typically within 5-14 days
- Post-inflammatory hyperpigmentation may occur
- Counsel regarding avoidance and cross-reacting drugs in the future
Severe Cutaneous Drug Reactions
Drug-Inducing Hypersensitivity Syndrome (DIHS)
Steven-Johnson Syndrome / Toxic Epidermal Necrolysis (SJS/TEN)
Drug-induced Hypersensitivity Syndrome
A serious drug-induced reaction characterized by: •Fever (100.4-104°F) •Facial edema •Rash (morbilliform eruption) •Lymphadenopathy •Blood abnormalities •Visceral involvement
Causes: antiepileptic agents, allopurinol, sulfonamides, minocycline, vancomycin and dapsone
Morbidity is 5-10%
Stevens-Johnson Syndrome & Toxic Epidermal Necrolysis
•Rare, acute, potentially LIFE THREATENING mucocutaneous reactions!
- Nearly always caused by medications
- Epidermal necrosis and sloughing of the mucous membranes and skin; Fas/Fasligand-induced apoptosis
SJS/TEN – Epidemiology & Etiology
- Affects all age groups and races
- Incidence is 100-fold higher in HIV-infected individuals
- Malignancy, genetic factors (HLA type) and SLE are also risk factors
- Overall mortality ranges from 10-30%
- Commonly implicated medications:
- Allopurinol
- Anticonvulsants (phenobarbital, phenytoin, carbamazepine, and lamotrigine*)
- Sulfonamides*
- NSAIDs
- Other causes: Mycoplasma pneumoniae*
*Most common causes in pediatrics
SJS/TEN – Clinical Presentation
- Prodrome: fever often >39C (102.2F) and flu-like sxs 1-3 days before lesions develop
- Skin lesions: tender erythematous, purpuric macules, vesicles/bullae form, skin sloughing
- Denudation: skin detachment
- SJS < 10% TBSA
- TEN >30% TBSA
•Nikolsky Sign: the elicitation of skin blistering as a result of gentle mechanical pressure on the skin.
Mucosal involvement (90%)
•Erythema and edema of lips
•Intraoral bullae; ruptured bullae, painful friable raw surfaces and hemorrhagic crusts
•Oral, genital, and/or ocular involvement (conjunctival itching, burning, pain, corneal ulceration and photophobia)
SJS/TEN - Diagnosis
Clinical initially; skin biopsy and cultures (blood, wound, mucosal lesions)
SJS/TEN - Treatment
- Discontinue offending medication
- Hospital admission -if extensive skin denudation, ICU/burn unit
- Supportive care:
- Nutritional and fluid replacement (via IV and NG tubes)
- Temperature maintenance
- Pain relief
- Ocular management
- Wound care/sterile handling
Complications of SJS/TEN
Acute Phase (lasts 8-12 days) •Fatal complications •Dehydration and acute malnutrition •Infection: skin, mucous membranes, lungs (pneumonia), and septicemia(S. aureus and P. aeruginosa) •GI ulceration and perforation •Acute respiratory distress syndrome •Shock and multiple organ failure •Thromboembolism
Long-term sequelae
•Cutaneous, mucosal, ocular, and pulmonary complications
