Eczema (Atopic Dermatitis)

Eczema (Atopic Dermatitis) – High‑Yield Study Guide for Medical Students

Definition

Eczema is a broad clinical term describing a group of pruritic, inflammatory skin disorders characterized by erythema, edema, vesiculation, oozing, crusting, and later lichenification and scaling. In most medical exam and textbook contexts, “eczema” is often used synonymously with atopic dermatitis (AD), a chronic, relapsing inflammatory dermatosis associated with a personal or family history of atopy (asthma, allergic rhinitis, food allergy).

For exam purposes, when a vignette uses the term “eczema” in a child with flexural dermatitis and atopic history, you should think atopic dermatitis as the key diagnosis.

Epidemiology

Eczema (atopic dermatitis) is one of the most common chronic skin diseases worldwide, particularly in children.

• Prevalence: Affects up to 15–20% of children and 2–10% of adults globally, with highest prevalence in industrialized nations.
• Age of onset: Usually begins in early childhood; ~60% present in the first year of life and >80% by age 5. A subset persists into or begins in adulthood.
• Sex: Slight female predominance in many cohorts, though differences are modest.
• Ethnicity and geography: Higher prevalence in urban environments and developed countries; significant burden in African, Asian, and Western populations.
• Atopic associations: Strongly associated with other atopic diseases (allergic rhinitis, asthma, food allergy). Many patients follow an “atopic march” from AD to allergic rhinitis or asthma.

Pathophysiology

Eczema results from a complex interaction between skin barrier dysfunction, immune dysregulation, environmental factors, and genetic predisposition.

Genetic and skin barrier abnormalities

• Filaggrin (FLG) mutations: Loss-of-function mutations in the filaggrin gene are strongly associated with atopic dermatitis. Filaggrin is crucial for epidermal barrier integrity and hydration. Defects lead to increased transepidermal water loss and enhanced penetration of irritants and allergens.
• Abnormal stratum corneum: Reduced ceramides and altered lipid composition impair barrier function, promoting xerosis and increased susceptibility to inflammation and infection.
• pH changes: Higher skin surface pH can activate proteases that further disrupt the barrier and promote inflammation.

Immune dysregulation

• Th2-skewed response: Acute AD lesions show a predominant Th2 immune profile (IL‑4, IL‑13, IL‑5, IL‑31), promoting IgE production, eosinophilia, and pruritus.
• Chronic lesions: Over time, there is a mixed Th1/Th2/Th17/Th22 cytokine profile, contributing to lichenification and chronic inflammation.
• IgE and sensitization: Many patients exhibit elevated serum IgE and sensitization to aeroallergens and food allergens, although elevated IgE is not required for diagnosis.

Environmental and microbial factors

• Irritants and allergens: Soaps, detergents, wool, fragrances, and aeroallergens (dust mites, pollens, animal dander) aggravate disease by penetrating the impaired barrier.
• Climate: Low humidity, cold weather, and high water exposure promote xerosis and flares.
• Staphylococcus aureus: Frequent colonization of eczematous skin with S. aureus; bacterial superantigens and toxins can exacerbate inflammation and drive flares.
• Psychological stress: Stress can worsen pruritus and scratching behavior, perpetuating the itch–scratch cycle.

Clinical Presentation

Eczema is characterized by intense pruritus, chronic or relapsing course, and age-specific lesion distribution. The classic triad is pruritus, typical morphology and distribution, and chronic/relapsing history.

General features

• Pruritus: Hallmark symptom. Often severe, leading to scratching, sleep disturbance, and impaired quality of life.
• Primary lesions: Erythematous papules and plaques, often poorly defined; may be associated with vesicles, oozing, and crusting in acute flares.
• Chronic lesions: Lichenification (thickened skin with accentuated skin markings), xerosis, and excoriations.
• Secondary changes: Post-inflammatory hypo- or hyperpigmentation, especially in darker skin types; impetiginization with honey-colored crusting when secondarily infected.

Age-specific distribution

• Infantile phase (0–2 years):
  • Onset typically between 2–6 months.
  • Lesions predominantly on cheeks, scalp, forehead, and extensor surfaces of limbs.
  • Diaper area usually spared due to moisture barrier.
  • Acute lesions are often exudative, crusted, and erythematous.
• Childhood phase (2–12 years):
  • Distribution shifts to flexural areas: antecubital fossae, popliteal fossae, neck, wrists, ankles.
  • Chronic lichenified plaques and excoriations common.
  • Denni–Morgan infraorbital folds, periorbital darkening, and pityriasis alba (hypopigmented patches) may be seen.
• Adolescent/Adult phase:
  • Flexural involvement persists in many.
  • Hands (hand eczema), eyelids, neck, upper trunk, and nipple dermatitis may be prominent.
  • Chronic prurigo nodularis–like lesions may develop.

Associated features

• Atopic stigmata: Xerosis, keratosis pilaris, ichthyosis vulgaris, hyperlinear palms, allergic shiners, Dennie–Morgan folds.
• Atopic comorbidities: Asthma, allergic rhinitis, food allergy, eosinophilic esophagitis in some patients.
• Sleep and psychosocial impact: Chronic itching and visible lesions can cause sleep disturbance, anxiety, depression, and impaired school/work performance.

Diagnosis

The diagnosis of eczema (atopic dermatitis) is clinical, based on characteristic morphology, distribution, and chronic relapsing course, along with a history of atopy. No single lab test is diagnostic.

Diagnostic criteria (conceptual)

Several diagnostic criteria exist (e.g., Hanifin and Rajka, UK Working Party). The essential features commonly include:

• Essential features (must be present):
  • Pruritus.
  • Chronic or relapsing dermatitis.
  • Typical age-specific morphology and distribution (facial/extensor in infants; flexural in children/adults).
• Important features (support diagnosis):
  • Personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis).
  • Early age of onset.
  • Xerosis.
  • Atopic stigmata (e.g., Dennie–Morgan folds, hyperlinear palms).

Investigations

• Routine labs: Generally not required for typical cases.
• Serum IgE: Often elevated but nonspecific and not required for diagnosis.
• Allergy testing: Skin prick tests or specific IgE testing only in selected patients (e.g., suspected food allergy, severe refractory disease, or planning immunotherapy).
• Patch testing: Consider in adults with chronic hand eczema or suspicion of allergic contact dermatitis component.
• Skin biopsy: Rarely needed; may be used when diagnosis is unclear or to exclude other dermatoses (psoriasis, cutaneous T-cell lymphoma).

Differential diagnosis

• Psoriasis: Sharply demarcated plaques, silvery scale, typical involvement of extensor surfaces, scalp, and nails; less pruritic in many cases.
• Seborrheic dermatitis: Greasy yellow scale on scalp, face, and intertriginous areas; less intense pruritus; in infants, “cradle cap.”
• Contact dermatitis: Irritant or allergic; history of exposure; lesions confined to contact sites.
• Scabies: Intense nocturnal pruritus, burrows in web spaces, involvement of family members or close contacts.
• Nummular dermatitis: Coin-shaped eczematous plaques, often on extremities; may overlap with atopic dermatitis.
• Tinea corporis: Annular lesions with central clearing and active scaly border; positive KOH for dermatophytes.

Management

Management of eczema centers on restoring the skin barrier, controlling inflammation and pruritus, preventing and treating infections, and avoiding triggers. Treatment is escalated stepwise based on severity (mild, moderate, severe).

General skin care and trigger avoidance (foundation of all therapy)

• Emollients:
  • Cornerstone of therapy; used daily, liberally, and frequently, even when skin appears normal.
  • Prefer thick creams or ointments (e.g., petrolatum-based) over lotions.
  • Apply immediately after bathing (“soak and seal”) to lock in moisture.
• Bathing practices:
  • Short, lukewarm baths or showers (5–10 minutes), once daily or every other day.
  • Avoid hot water and harsh soaps; use mild, fragrance-free cleansers.
• Trigger avoidance:
  • Avoid wool, rough fabrics, and occlusive, non-breathable clothing; use soft cotton layers.
  • Use fragrance-free detergents; avoid fabric softeners and dryer sheets.
  • Minimize exposure to dust mites, pollens, pet dander where relevant.
• Anti-scratch measures:
  • Keep nails short; use cotton gloves or pajamas in young children at night.
  • Behavioral strategies to reduce scratching, especially in older children and adults.

Topical anti-inflammatory therapy

Topical therapy is first-line for most patients.

• Topical corticosteroids (TCS):
  • Mainstay for acute flares and ongoing control.
  • Choose potency based on patient age, site, and severity:
    • Low-potency (e.g., hydrocortisone 1–2.5%): face, intertriginous areas, infants.
    • Medium-potency (e.g., triamcinolone 0.1%): trunk and extremities in children/adults.
    • High-potency (e.g., clobetasol 0.05%): short courses for lichenified, thick plaques in adults (avoid on face and flexures).
  • Apply once or twice daily during flares; taper frequency or potency as improvement occurs.
  • Adverse effects: skin atrophy, striae, telangiectasias, perioral dermatitis, HPA axis suppression with prolonged high-potency use, especially under occlusion.
• Topical calcineurin inhibitors (TCI):
  • Examples: tacrolimus ointment, pimecrolimus cream.
  • Useful for steroid-sparing therapy, particularly on face, neck, and intertriginous areas.
  • Can be used for maintenance (“proactive therapy”) a few times per week to prevent flares.
  • Adverse effects: transient burning or stinging; theoretical malignancy risk is discussed, but data remain limited.
• Topical PDE-4 inhibitors:
  • Crisaborole ointment in some regions; used for mild to moderate disease as a steroid-sparing agent.

Antipruritic therapy

• Oral antihistamines:
  • Non-sedating antihistamines have limited direct effect on pruritus in AD but may help with associated urticaria or allergic rhinitis.
  • Sedating antihistamines (e.g., hydroxyzine, diphenhydramine) may help sleep in selected patients; use cautiously.
• Topical agents:
  • Cooling lotions, menthol-based preparations, or pramoxine-containing formulations may provide adjunctive relief in some patients.

Infection prevention and management

• Bacterial infection:
  • Look for weeping, crusting, pustules, or sudden exacerbations suggestive of S. aureus or Streptococcus superinfection.
  • Use topical antibiotics (e.g., mupirocin) for localized infection; systemic antibiotics for more extensive disease or systemic signs.
• Bleach baths:
  • Dilute bleach baths (e.g., 1/4–1/2 cup of 6% household bleach in a full bathtub of water, 1–2 times per week) can reduce bacterial colonization and flares in moderate to severe AD.
• Viral infections:
  • Be vigilant for eczema herpeticum (widespread painful vesiculopustules, punched-out erosions, systemic symptoms) and molluscum contagiosum; these may require antiviral or specific therapy.

Systemic and advanced therapies

Reserved for moderate to severe eczema not adequately controlled with optimized topical therapy and good skin care.

• Phototherapy:
  • Narrowband UVB or UVA1 can be effective for chronic, widespread AD.
  • Requires access to specialized centers; monitor for photoaging and skin cancer risk with long-term use.
• Biologic therapy:
  • Agents targeting type 2 inflammation (e.g., monoclonal antibodies against IL‑4/IL‑13 pathways) have transformed management of moderate to severe AD in many guidelines.
  • Consider in patients with severe disease, recurrent infections from topical/systemic steroids, or significant quality-of-life impairment.
• Systemic immunosuppressants (off-label in many regions):
  • Agents such as cyclosporine, methotrexate, azathioprine, or mycophenolate may be used in refractory cases under specialist supervision.
  • Require careful monitoring for organ toxicity and infection.
• Short-course systemic corticosteroids:
  • Not first-line for chronic management due to rebound flares and adverse effect profile.
  • May be used short-term in severe flares when other options are not immediately available, ideally as a bridge to safer long-term therapy.

Education and long-term care

• Patient and caregiver education is crucial for adherence: explaining chronic nature, correct use of topical steroids, and importance of daily emollients.
• Action plans with step-up/step-down therapy can guide management of flares versus maintenance.
• Address psychological comorbidities (anxiety, depression) and social impacts where relevant.

Key Clinical Pearls for Exams and Practice

• Pruritus is essential: If it doesn’t itch, think twice about the diagnosis.
• Age-related distribution is high-yield:
  • Infants: face and extensor surfaces.
  • Children/adults: flexural surfaces.
• Xerosis and barrier dysfunction underlie disease; emollients are foundational therapy and should be continued even when inflammation is controlled.
• Topical corticosteroids are first-line for flares; choose potency based on site and severity and use for limited durations to minimize adverse effects.
• Topical calcineurin inhibitors are especially useful for steroid-sensitive areas (face, eyelids, skin folds) and for long-term maintenance.
• Always consider and treat secondary infection in suddenly worsening eczema, particularly with crusting or systemic symptoms.
• Think of the atopic march: children with severe early AD are at increased risk for food allergy, asthma, and allergic rhinitis.
• Differentials to keep in mind: psoriasis, seborrheic dermatitis, contact dermatitis, scabies, and tinea corporis; clinical distribution and morphology help differentiate.
• Long-term control requires a combination of trigger avoidance, regular emollients, appropriate topical anti-inflammatory therapy, and patient education.