Eczema & Related Dermatoses CB EDIT

What diagnostic clue is indicative of Rhus dermatitis?

"Black lacquer" Urushiol oil can oxidize, leaving black spots on the leaves, but sometimes on the skin

Infant Seborrheic Dermatitis

"Cradle Cap" ‣Appears a week after birth & last several months ‣Scalp, face, neck, trunk, and folds ‣More inflamed & redder than adults ‣Secondary Candida infection possible ‣Minimal Sx → content & feed well

Differential dx for infant seborrheic dermatitis?

"seb derm" ‣Atopic dermatitis ‣ICD ‣Candidiasis ‣Tinea capitis

Classic chronolonigcla scheme of eczema

Acute eczema: vesiculation, exudation, no time for scale to develop yet Subacute eczema: juicy papules, starting to get scaly and dry Chronic eczema: lichenification Exact presentation depends on location, etiology, and timing

PV presentation

Almost all pts have mucosal involvement; may precede widespread skin involvement or remain mucosal Skin lesions manifest as flaccid, thin walled bullae that rupture easily Very painful but minimal pruritis (BP is pruritic) Epidermal cleaveage makes skin fragile, easily blisters

Bullous pemphigoid vs pemphigus vulgaris

BP better tolerated, PV fatal within 2-5 years

Differential dx for Stasis Dermatitis?

Bilateral lower extremity cellulitis is rare! ‣Contact Dermatitis ‣Infection

REMEMBER WITH STASIS

Bilateral lower extremtiy cellultis is rare

AD pathogenesis

Epidermal barrier dysfunction Immune dysregulation Microbial colonization Epicutaneous (and systemic?) sensitization

Treatment for Pompholyx?

First Line: ‣Trigger avoidance ‣Topical Steroids ‣Cold compresses ‣Oral corticosteroids (severe) Alternatives ‣Topical Calcineurin inhibitors ‣Light therapy ‣Hyperhidrosis therapy - neurotoxin, anticholinergics, iontophoresis Severe/Recalcitrant Disease: ‣Systemic immunosuppressants

Treatment for Mild to moderate Atopic Dermatitis?

For mild to moderate AD ‣Emollients and behavior may be enough ‣Topical corticosteroids ‣Topical steroid-sparing agents for children, face, and intertriginous areas

Treatment for moderate to severe Atopic Dermatitis?

For moderate to severe AD ‣Everything for mild-to-moderate, plus: ‣Phototherapy ‣Systemic immunosuppressive agents: Systemic corticosteroids ‣Biologic agent(s): IL-4 and IL-13 blockade ‣JAK pathway inhibitors

Epidermal Barrier Dysfunction

Genetic; but worsened by environment and behavior ‣Filaggrin mutation

Epicutaneous sensitization

More easily to form allergies

Pemphigus vulgaris

More macerated blisters, no shiny, balloon like look, not taut

Pemphigus Vulgaris

autoimmune bullous dz with a chronic course Less common then BP, may start a bit earlier Untreated=poor prognosis

Frequent clinical context for stasis derm

varicose veins, thrombophlebtis

Childhood Atopic Dermatitis

(2-12 years) ‣Exudative lesions → lichenification and xerosis ‣Locations: Flexural extremities, Periorificial, Neck, Hands/wrists and feet/ankles Sleep disturbance still common, starts to have social effects

Infantile Atopic Dermatitis

(<2 years) ‣Distribution: Cheeks, Scalp, Neck, Trunk, Extensor extremities ‣Lesions → edematous and exudative Sleep disturbance common

Adolescent/Adult Atopic Dermatitis

(>12 years) ‣Increasing trend toward lichenification "senile eczema" ‣Involvement of flexural folds continues Trouble areas may be more prominent (chronic hand dermatits, chronic facial dermatitis) As patient becomes older, there is more marxed xerosis, less lichenificaition

When to question if something might NOT be AD

-When onset is sudden (chronic usually) - Pruritis is absetn (AD usually itchy) - Distribution is atypical (AD is usually symetrical)

Dx for bullous pemphigoid

Biopsy with direct immunofluoerscene is gold standard! Two biopsies, H&E, punch from blister edge Dif: punch from perilesional skin

Pemphigus vulgaris dx

Biopsy with direct immunofluoerscene is gold standard! Two biopsies, H&E, punch from blister edge Dif: punch from perilesional skin Serum ELISA testing increasingly common

Vesiculobullous Disease

Bullous Pemphigoid Pemphigus Vulgaris

Seborrheic dermatisis

Chronic, superficial inflammatory disease that is usually mild in severity Very common, affects all age groups but worst in infancy and after puberty due to sebaccous gland activity

Seb derm dx

Clinical dx, labs and biopsy often not helpful

ICD vs ACD

IDC: Contactant is directly toxic Affects anyone Onset time is minutes to hours Dose dependant Burning, stinging, sore symptoms ACD: immune phenomen contactant is allergenic; response is immunologically mediated (T4 rxn) Only affects those who are already sensitized Time to onset is greater than 1 day Very small doses are sufficient for rxn Prutic symptoms

Seb Derm special pops

Increased incidnece and seveirty with neurological disease, esp in Parkinsons Increased incidence and severity with HIV/AIDS New and dramatic presentation in at-risk patients should prompt testing

PV pathogenesis

Intraepidermal blister formation; proteins are between the keratinocytes and the epidermis "melts" BP is subdermal

Nummular eczema

Less common form of dermatitis Coin shaped lesions (nummulus) Unclear pathogenesis Usually on extremeties, tend to be better defined, well demarcted INTENSE PRURITIS Morphology ranges from acute weeoping to dry and lichenefied, but without thick psoriasiform scale Course may be chronic but usually responds well to treatment

Treatment for Lichen Simplex Chronicus?

Local therapy: ‣Corticosteroids ‣Antipruritics: doxepin, capsaicin (not so helpful) Systemic therapy: ‣Antihistamines ‣Anxiolytics in select cases Referral to Psychiatry

Bullous pemphigoid presentation

May be polymorphic depending on stage Early stage: pruritis is common, often non bullous, may be nonspecific, may mimic urticaria Bullous phase: vesicle and bullae appear over normal or erythemaous tissue blisters are TENSE Nikolsjy sign is absent (skin does not slough w pressure) Common areas: groin, axillae, flexural areas; 30% of patients have oral involvement

Nummular dermatitis w/u

No specific workup, assess for other forms of eczema that may be noncomitant Culture and patch if diagnosis is in doubt

Bullous Pemphigoid

autoimmune, blistering disease NOT eczematous dermatoses Can be very itchy but NOT an eczematous dermatosis Autoimmune bullous disease with chronic course Rare, but most common AIBD Primarily a dz of older adults Attacks structural layer between epidermis/dermis, leading to subdermal blister formation

Nummular managnment

can sometimes be resistant to treatment and decrease quality of life Topical corticosteroids and calcinuerin inhibtors Some patient req light therapy or systemic treatment for widespread, refractory dz

Contact dermatitis

cutanteous inflammatory reaction caused by contact with an exogenous substance Clinically: erythema, scaling, edema, vesiculatipn, erosions, lichenification, fissuring

BP management

generally has a reasonable prognosis but can have signifcant negative imapact on QOL Mortality increases w age May resolve spontaneously after months to years Mild disease: super potent topical steroids, calcineruine inhibitors Extensive/severe dz: oral corticosteroids, maybe systemic immunosuppresents

Seb derm etioligy

not completetly clear but clearly sebaceous gland function is contributory, based on distribution and affected ages Suspected mechanism: lipophilic yeast Malassezia furfur which produces inflammatory free fatty acids

Pemphigus vulgaris managnment

without treatment PV generally fatal within 2-5 years With treatment, morbidity and mortality are greatly reduced although still sig In treated patients, SE of therapy are most common cause of death Systemic corticosteroids are 1st line to gain control Rituzimab being used Additional theraputic considerations include pain, nutrition, wound care and secondary infection

Labs/Diagnostics for Pompholyx?

‣ Usually clinical diagnosis Patch ‣Culture ‣Scraping for KOH, scabies

Pompholyx (Dyshidrosis)

‣"Tapioca-like", pruritic, vesicular erruption, variably inflamed vesicles Clinically distinct eczema of unknown cause ‣Hands, lateral fingers >> feet ‣Symmetrical ‣Very pruritic, can burn/painful ‣Attacks last weeks, relapses common Etiology: Unknown Freq affects QOL

List the important classes that cause Irritant Contact Dermatitis.

‣Acids ‣Alkalis, ‣Detergents/ Disinfectants ‣Metal Salts ‣Organic solvents ‣Water

Prevention of Rhus Dermatitis?

‣Avoid contact with the plants! ‣Wash skin with soap to remove resin, ASAP (5-10 mins) ‣Launder all clothing ‣Blocking products- IvyGuard

Labs/Diagnostics for Lichen Simplex Chronicus?

‣Clinical Dx ‣Lab Work only if clinical dx cannot be made

Treatments for Stasis Dermatitis?

‣Compression stockings, Unna booting ‣Topical steroids - Eczema & pruritus ‣Wound care- chronic ulcers ‣Vascular surgery - advance disease

List the Exogenous triggers for Pompholyx.

‣Contact dermatitis ‣Environmental/ seasonal change

List the ways atopic dermatitis can be maintained.

‣Counseling and lifestyle → promoting a good epidermal barrier ‣Frequent use of emollients ‣Short showers or baths in cool(-ish) water - hot waters strips body from oils ‣Avoidance of harsh soaps and excessive scrubbing ‣Avoidance of common allergens ‣Antimicrobial treatment with dilute bleach baths ‣Avoid itchy clothing, excessive dust, excessively dry environments

Maintenance for Lichen Simplex Chronicus?

‣DO NOT SCRATCH! If left alone, lesions will slowly improve ‣Educate about itch-scratch cycle ‣Warn about frequent chronic nature

Immune Dysregulation

‣Elevated IgE ‣Vast array of interleukins and cytokines in cascades

Stasis Dermatitis

‣Eruption on the lower extremities due to chronic venous insufficiency/venous stasis Early Stage: ‣Intermittent pitting edema at ankle ‣Bronze appearance - hemosiderin deposit ‣Itchy & red Later Stage: ‣Edema becomes permanent as adipose tissues & fascia become adherent End Stage: ‣Ulceration & lipodermatosclerosis ‣Scaly & pruritic - true stasis dermatitis Risk Factors: ‣Varicose Veins ‣Thrombophlebitis Etiology: ‣Sebaceous gland function is contributory ‣Lipophilic yeast Malassezia fufur - produces inflammatory free fatty acids

Rhus Dermatitis

‣Erythematous, pruritic rash, often with vesiculation (linearity) 12-72 hours after contact ‣Aerosolized, facial swelling is common and mimics angioedema ‣Blister fluid is not contagious ‣Etiology: Poison Oak/Ivy (Urushiol) ‣Risk Factors: Frequently seen in hikers and Gardners

List the endogenous triggers for Pompholyx.

‣Hyperhidrosis ‣Atopy ‣Emotional stress ‣Id reaction

Adult Seborrheic Dermatitis

‣Lesions: Greasy-appearing scale with inflamed base ‣Symmetric ‣Scalp, postauricular, eyebrows, eyelids, nasolabial folds, mental crease ‣Less common → chest, axillae, umbilicus, groin, gluteal cleft ‣Mild Sx→may itch or burn

What treatment is recommended for Rhus Dermatitis?

‣Mild cases - topical steroids, antipruritics (calamine, Sarna lotion), cool baths ‣Moderate to severe - The above, plus oral prednisone up to 1 mg/kg, tapered over 3 weeks BE AWARE OF REBOUND WHEN TREATMENT COURSE IS TOO SHORT

Risk factors for Seborrheic Dermatitis?

‣Neurologic Disease (Parkinsons) ‣HIV/AIDS

Irritant Contact Dermatitis

‣Painful: Burning, stinging, sore ‣Erythema, scaling, edema, vesiculation, erosions, lichenification, fissuring "lip-licker's dermatitis" ‣Risk Factors: Anyone ‣Mechanism: Directly Toxic

What labs/diagnostics are used for suspected allergic contact dermatitis?

‣Patch testing → determining causative agent ‣T.R.U.E: checks for most common allergens (provocative test) ‣Applied to patient's back in-office, and rechecked 2 and 4 days later

Allergic Contact Dermatitis

‣Pruritic ‣More eczema characteristics ‣Erythema, scaling, edema, vesiculation, erosions, lichenification, fissuring Can present in rectangular shape, sharply defined lines ‣Mechanism: Response is immunologically-mediated ‣Risk factors: Affects only those who are already sensitized

Differential dx for adult seborrheic dermatitis?

‣Psoriasis ‣Butterfly rash (Lupus) ‣Dermatomyositis

Lichen Simplex Chronicus

‣Reactive dermatosis as a result of rubbing/scratching →epidermal thickening Large lichenificed lesions representing epidermal hypertrophy Can happen in the context of a seperately identifiable disease or on its own ‣Erythema → in early lesions ‣One to many, large, scaly, moderately well demarcated, lichenified plaques ‣Dyspigmentation → hypo or hyper ‣Neck, wrists, ankles, hands, pretibial, genitals ‣Itch-Scratch Cycle: Lesions itch spontaneously → positive feedback loop Risk Factors: ‣Adolescents and adults

Differential dx for Pompholyx?

‣Scabies ‣Tinea ‣Psoriasis ‣Keratolysis exfoliativa

What are the stigmata of manipulation for Lichen Simplex Chronicus?

‣Scratch Marks ‣Erosion/Ulceration

Microbial colonization

‣Staphylococcus and its antigens initiate and worsen inflammation through multiple mechanisms

Atopic Dermatitis

‣The prototypical eczematous dermatitis ‣Chronic, waxing and waning inflammatory disease of the skin seen in atopic patients ‣Atopy: a tendency toward hypersensitivity reactions ‣Not sudden, distribution is symmetrical , and will experience pruritus

Treatment for adult seborrheic dermatitis?

‣Topical antifungals (ie. azoles, ciclopirox, zinc pyrithione, selenium sulfide) ‣‣Shampoo for scalp ‣‣Creams for face/body ‣Corticosteroids for flares ‣Alternatives - tar, calcineurin inhibitors, phosphodiesterase inhibitors

Lab/Diagnostics for Stasis Dermatitis?

‣Vascular imaging/Ultrasound ‣Culture ‣Biopsy - CAUTION (poor healing)

Maintenance for Stasis Dermatitis?

‣Weight management ‣Leg elevation ‣Compression hose ‣Regular exercise

Treatment for infant seborrheic dermatitis?

‣bathing and gentle dislodging of scale may be sufficient ‣Azole antifungals for more persistent cases ‣Infantile seborrheic dermatitis is generally self-limited

List the important classes that cause Allergic Contact Dermatitis.

‣preservatives ‣formaldehyde releasers ‣rubber products ‣topical antibiotics ‣textile dyes ‣adhesives ‣metals (nickel) ‣plants

Pathogenesis for Stasis Dermatitis?

‣venous hypertension, exudation of heme and serum proteins → resulting cycle of inflammation, microangiopathy, and fibrosis ‣Topical antibiotics are a common cause of allergic contact dermatitis! As disease becomes chronic, sensitization to topical therapies often becomes additional contributing factor