Eczema By:- Dr. Naif Al-Shahrani Salman bin Abdazziz University
Dermatitis= Eczema =Spongiosis
Eczema Atopic Seborrheic Contact Allergic Irritant Nummular Asteatotic Stasis Neurodermatitis/Lichen Simplex Chronicus
Atopic Dermatitis 10-20% of population Primary symptom: itch Location, location, location Associated with atopic background Periorbital pallor
Clinical Manifestations & Diagnosis Must have : An itchy skin eruption. Plus 3 or more of the following: 1.History of flexural involvement (including cheeks in children under 10) 2. A history of generalized dry skin in the past year 3. Personal history of atopy (or a family history in 1st degree relative if under 4) 4. visible flexural eczema(or involving cheeks/forehead and outer limbs in children under 4) 5. Onset under 2 years of age
Assessment of severity Clear normal skin no evidence of active atopic eczema Mild areas of dry skin, frequent itching +- small areas of redness Moderate - areas of dry skin, frequent itching, redness, +- excoriation and localised thickening. Severe widespread areas of dry skin, incessant itching, redness (+- excoriation, extensive skin thickening, bleeding, oozing, cracking.
Impact on quality of life None no impact on quality of life Mild little impact on everyday activities, sleep and psychosocial well being Moderate - Moderate impact on everyday activities, psychosocial well being, frequently disturbed sleep Severe severe limitation of everyday activities and psychosocial well being, loss of sleep every night
Management Education of patient or care providers Optimal skin care Identification and avoidance of specific and non-specific trigger factors Topical treatment Systemic treatment Regular medical supervision
Management General management of patients with atopic dermatitis Topical glucocorticoids Topical calcineurin inhibitors Phototherapy of atopic dermatitis Antihistamines in atopic dermatitis Systemic immunomodulation Topical and systemic antibiotic
Common Pitfalls Misdiagnosis Scabies (intensely pruritic, burrows/vesicles, others itch) Psoriasis (elbows/knees/inflammatory arthritis/nail changes) Fungus (central sparing, well marginated, scaly border)
Eczema Herpeticum Unwell patient Severe pain Typical umbilicated, coalescing papules Herpes simplex virus (usually type 1) Urgent hospital admission
Seborrheic Eczema
Distribution Seborrheic Dermatitis Face, scalp, axillae, upper chest Chronic condition Nonsteroidal Rx Disease associations -Parkinson's disease - HIV disease
Pathogenesis Temporary Increased numbers of Pityrosporum ovale coupled with Genetic tendency.
Treatment Targeted against both P.ovale and inflammation Chronic condition therefore need for repeated periods of treatment
Anti-Pityrosporum shampoo eg Selsun, Head & Shoulders, Nizoral (contact time) Combination anti-pityrosporum and antiinflammatory cream eg Cannesten HC, Daktacort, Nizoral
Nummular Dermatitis Coin shaped patches and plaques Secondary to xerosis cutis Primary symptom itch
Asteatotic Dermatitis Extreme case of xerosis Riverbed type cracking
Stasis Dermatitis Venous hypertension Complicated by ulceration
Neurodermatitis/Lichen Simplex Sever pruritus Habitual excoriating or rubbing Skin thicken Consider underlying disease Chronicus
Acute Irritant Contact Dermatitis Commonly seen in occupational accidents(80% of OCD) Irritant reaction reaches its peak quickly, within minutes to hours after exposure Symptoms include stinging, burning, and soreness Physical signs include erythema, edema, bullae, and possibly necrosis Lesions restricted to the area where the irritant or toxicant damaged the tissue Sharply demarcated borders and asymmetry points to an exogenous cause Most frequent irritants are acids and alkaline solutions
Acute Delayed Irritant Contact Dermatitis Delayed inflammatory response characteristic of certain irritants such as anthralin, benzalkonium chloride, and ethylene oxide Visible inflammation is not seen until 8 to 24 hours after exposure Symptoms are more frequently burning rather than pruritus This form of ICD is commonly seen during diagnostic patch testing
Pathogenesis of ICD Denaturation of epidermal keratins Disruption of the permeability barrier Damage to cell membranes Direct cytotoxic effects
Allergic Contact Dermatitis Type 4 Hypersensitivity Response ACD accounts for approximately 20% of all contact dermatitis Classically well demarcated/patterned Exposure can be infrequent (once a month) Patch testing is gold standard for diagnosis Severe reactions need systemic steroids
Pathogenesis of ACD ACD is a type IV hypersensitivity response Lesions appear in acute ACD within 24 to 96 hours of exposure Requires prior sensitization to the chemical in question Subsequent re-exposure of individual leads to allergen being presented to a primed T-cell leading to release of numerous cytokines and chemotactic factors leading to the clinical picture of eczema Once sensitized a low concentration of causative chemical elicits a response
Allergic contact dermatitis to leather shoes. Mercaptobenzothiazole (MBT) is the most common cause of allergic shoe dermatitis
Allergic Contact Dermatitis Poison Ivy/Oak/Sumac
Allergic Contact Dermatitis
Patch Testing Most common site is the upper back Patients should not have a sunburn in test area, and should not apply topical corticosteroids to the patch test sites for 7 days prior to test Systemic corticosteroids should be avoided for 1 month prior to testing Patches are applied to back and reinforced with tape, patient instructed to keep back dry and patches secured until second visit at 48 hours
Patch Testing When the patient returns in 48 hours the patches need to be inspected to ensure that the testing technique is adequate As patches are removed their sites of application should be marked in order to identify the locations of particular allergens
Patch Testing Patient again asked to keep back dry until second reading, done from 48 hours from removing the patch.
Treatment of ACD Involves identification of causative allergens Clear the dermatitis with topical, or if necessary systemic corticosteroids Complete and prolonged clearing can take up to 6 weeks or more, even when allergens are being avoided