Atopic Dermatitis Clinical Overview
I. The "On-Call" Snapshot
Clinical Significance in Malaysia: Atopic dermatitis (AD) is a significant burden in both primary care and paediatric departments nationwide. You will be expected to manage acute flares, identify complications like secondary infections, and provide appropriate patient education on maintenance therapy.
High-Yield Definition: A chronic, highly pruritic, inflammatory skin disease that occurs most frequently in children but also affects many adults. It is characterized by a relapsing and remitting course. (Source: Malaysian CPG on Management of Atopic Eczema, 2nd Ed., 2018).
Clinical One-Liner: It's the "itch that rashes" – a disease of a defective skin barrier and immune dysregulation, not just a simple allergy.
II. Etiology & Risk Factors
Etiology: A complex interplay between genetic predisposition (especially mutations in the filaggrin gene, FLG), immune system dysregulation (predominantly a Th2-mediated response), and environmental triggers.
Risk Factors:
Strongest: Personal or family history of atopy (the "atopic triad": AD, asthma, allergic rhinitis).
Urban environment.
Higher socioeconomic status (related to the "hygiene hypothesis").
Residence in Westernised countries.
III. Quick Pathophysiology
Think of the skin barrier as a brick wall. In AD, the "bricks" (corneocytes) and "mortar" (lipid matrix) are defective, largely due to filaggrin deficiency. This leads to:
Increased Transepidermal Water Loss (TEWL): Skin becomes pathologically dry (xerosis).
Increased Permeability: Allergens and microbes penetrate the epidermis easily.
Immune Activation: This triggers a Th2 inflammatory cascade, releasing cytokines (IL-4, IL-13, IL-31) that cause erythema and intense pruritus.
The subsequent scratching further damages the barrier, creating a vicious itch-scratch cycle.
IV. Classification
AD is primarily classified by:
Age of Onset:
Infantile: (2 months - 2 years): Typically affects the face, scalp, and extensor surfaces.
Childhood: (2 - 12 years): Predominantly affects flexural areas (antecubital and popliteal fossae).
Adolescent/Adult: Flexural areas, hands, face, and neck are common sites.
Severity:
Mild, Moderate, or Severe. This is a clinical assessment based on the extent (Body Surface Area), morphology (erythema, papulation, oozing, lichenification), and impact on quality of life (pruritus, sleep loss). Scoring systems like SCORAD or EASI exist but are mainly for research; clinical judgment is key in practice.
V. Clinical Assessment
🚩 Red Flags & Immediate Actions
Sudden widespread vesicles, punched-out erosions, fever: Suspect Eczema Herpeticum (disseminated HSV infection).
Action: Admit immediately. Take viral swabs. Start IV Acyclovir empirically. This is a medical emergency.
Extensive weeping, honey-coloured crusting, pustules, fever: Suspect widespread secondary bacterial infection (usually S. aureus).
Action: Admit. Take skin swabs for C&S. Start IV Cloxacillin or Cefazolin.
>90% body surface area erythema: Suspect Erythroderma.
Action: Admit for supportive care (fluid balance, thermoregulation) and workup. Requires senior input urgently.
History
Key Diagnostic Clues (UK Working Party Criteria - simplified): You need an itchy skin condition plus ≥3 of the following:
History of involvement of skin creases (flexures).
Personal history of asthma or allergic rhinitis (or history of atopy in a first-degree relative if <4 years old).
History of a general dry skin in the last year.
Visible flexural dermatitis.
Onset before the age of 2 years.
Symptom Breakdown:
Pruritus: This is the cardinal symptom. It is universal, often severe, and worse at night.
Xerosis (Dry Skin): Very common background feature.
Rash: Varies from ill-defined erythema with papules to weeping vesicles (acute) or thickened, hyperpigmented plaques with exaggerated skin markings (chronic lichenification).
Pertinent Negatives:
Absence of pruritus makes AD highly unlikely.
No history of contact with a specific new substance (argues against allergic contact dermatitis).
No family members or close contacts with similar severe itch (argues against scabies).
No systemic symptoms like fever or weight loss in a standard flare.
Physical Examination (OSCE Approach)
General Inspection: Look for signs of chronic disease and atopy:
Allergic shiners (dark circles under eyes).
Dennie-Morgan folds (infraorbital creases).
"Atopic salute" (transverse nasal crease from rubbing).
Hertoghe's sign (thinning of the lateral third of the eyebrows).
Vitals: Should be normal. Fever suggests secondary infection.
Disease-Specific Examination (Skin):
Look (Morphology & Distribution):
Acute: Erythema, papules, vesicles, oozing, crusting.
Chronic: Lichenification (thickened skin with accentuated lines), excoriations, fissuring, xerosis.
Distribution: Check the typical age-specific areas mentioned in Section IV. Don't forget hands, eyelids, and nipples in adults.
Pertinent Negatives:
Absence of well-demarcated, silvery-scaled plaques (psoriasis).
Absence of greasy, yellow scales in the nasolabial folds or scalp (seborrhoeic dermatitis).
Absence of burrows in web spaces (scabies).
Differentiating Disease Stage:
Mild: Few areas of dry skin, infrequent itching, minimal impact on daily activities.
Moderate: Areas of dry skin, frequent itching, erythema, and some impact on daily activities and sleep.
Severe: Widespread dry skin, incessant itching, erythema, possibly with exudation, fissuring, and lichenification. Severe limitation of daily activities and nightly sleep loss.
Clinical Pearl: Always check the flexures. Even in a patient with a facial flare, the presence of subclinical lichenification in the popliteal fossae points towards an underlying atopic diathesis.
VI. Diagnostic Workflow
Differential Diagnosis:
Seborrhoeic Dermatitis:
Points For: Erythema, rash can appear on face/scalp in infants ("cradle cap").
Points Against: Greasy yellow scale, less pruritic, typically involves scalp, nasolabial folds, and chest.
How to Differentiate: Location and character of the scale.
Scabies:
Points For: Intensely pruritic rash.
Points Against: Pruritus is classically worse at night. Look for burrows (web spaces, wrists), papules on genitalia. History of affected contacts is key.
How to Differentiate: Presence of burrows and contact history. A therapeutic trial of antiscabietics can be diagnostic.
Psoriasis:
Points For: Chronic inflammatory rash.
Points Against: Well-demarcated, erythematous plaques with a classic silvery scale. Auspitz sign. Nail pitting. Typically affects extensors (knees, elbows) and scalp.
How to Differentiate: The well-demarcated nature and silvery scale are characteristic.
Investigations Plan:
The diagnosis is clinical. No routine laboratory tests are needed for diagnosis.
Bedside / Initial: None required for a standard flare.
First-Line (only if indicated):
Skin Swab (Bacterial/Viral): If you suspect secondary infection or eczema herpeticum. Send for C&S and viral PCR.
Adjunctive (for specific clinical questions):
IgE levels / Skin Prick Test: Not for diagnosis. Only useful if a specific food or aeroallergen trigger for flares is suspected in moderate-severe disease, to guide avoidance strategies. Do not order this routinely.
VII. Staging & Severity Assessment
As mentioned, severity is graded as Mild, Moderate, or Severe. This assessment directly dictates your management plan. The goal is to match the potency of your anti-inflammatory agent (usually a topical steroid) to the severity of the flare. Using a potent steroid for mild eczema is overkill; using hydrocortisone for a severe flare is useless.
VIII. Management Plan
A. Principle of Management:
Restore the skin barrier: Aggressive use of emollients.
Reduce inflammation & pruritus: Topical anti-inflammatory agents.
Identify and avoid triggers: Patient education.
Treat secondary infections: Antibiotics/antivirals when present.
B. Immediate Stabilisation (The ABCDE Plan):
The ABCDE approach is not relevant for a standard AD flare. It is reserved for complications like anaphylaxis (if a food trigger is involved) or sepsis from secondary infection.
C. Definitive Treatment (The Ward Round Plan): A Stepwise Approach
Foundation for ALL severities (Maintenance Therapy):
Emollients: Apply liberally, frequently (at least 2-3 times a day), and all over the body, not just on affected areas. Ointment-based (e.g., aqueous cream, white soft paraffin) are generally more effective than lotions. Apply immediately after bathing ("soak and seal").
Education: Explain the chronic nature of the disease, the importance of adherence, and trigger avoidance (e.g., harsh soaps, heat, wool clothing).
Mild Disease (Active Treatment):
Topical Corticosteroids (TCS): Mild potency (e.g., Hydrocortisone 1%) applied once or twice daily to inflamed areas until the flare resolves.
Moderate Disease (Active Treatment):
TCS: Moderate potency (e.g., Betamethasone valerate 0.025%/0.1%, Mometasone furoate 0.1%) applied once daily.
Topical Calcineurin Inhibitors (TCI): Tacrolimus 0.03%/0.1% or Pimecrolimus 1%. Excellent as second-line or steroid-sparing agents, especially for sensitive areas like the face and flexures.
Severe Disease (Active Treatment):
TCS: Potent (e.g., Betamethasone dipropionate 0.05%) for short-term use.
Wet Wraps: Can be very effective for rapid control of severe flares, especially in children. Requires inpatient admission.
Phototherapy (UVB): An option for chronic, widespread disease refractory to topicals.
Systemic Therapy: For refractory, severe cases under specialist care. Options include oral corticosteroids (short-term rescue only), Ciclosporin, Azathioprine, or biologics like Dupilumab.
Managing Pruritus:
Sedating Antihistamines: (e.g., Chlorpheniramine, Hydroxyzine) at night can help break the itch-scratch cycle by promoting sleep, not through their antihistaminergic effect on the skin.
D. Long-Term & Discharge Plan:
Provide a written management plan.
Prescribe adequate quantities of emollients and topical steroids.
Stress proactive therapy: using TCS 1-2 times a week on previously affected areas can prevent flares.
Arrange follow-up in the clinic to review treatment efficacy and adherence.
IX. Complications
Immediate/Short-Term:
Bacterial Superinfection (S. aureus): Most common complication. Manage with topical or oral antibiotics.
Eczema Herpeticum: A medical emergency. Requires IV Acyclovir.
Long-Term:
Lichenification & Scarring: Permanent skin changes from chronic scratching.
Psychological Impact: Sleep disturbance, anxiety, depression, poor self-esteem. Do not underestimate this.
X. Prognosis
Generally good. ~60% of children will outgrow their AD by adolescence.
Factors for persistence into adulthood:
Severe disease in childhood.
Strong family history of atopy.
Coexisting asthma or allergic rhinitis.
Early age of onset.
XI. How to Present to Your Senior
Use the SBAR format.
(S)ituation: "Dr, I'm calling about patient [Name] in [Location], a [Age]-year-old with a flare of known atopic dermatitis."
(B)ackground: "He has a history of AD since infancy, normally controlled with emollients and mild topical steroids. He has no other medical issues."
(A)ssessment: "On examination, there are erythematous, weeping plaques over both antecubital and popliteal fossae, with some honey-coloured crusting. Vitals are stable. My impression is a moderate-to-severe flare with suspected secondary bacterial infection."
(R)ecommendation: "I plan to take a skin swab for C&S, start him on a moderate-potency topical steroid like betamethasone, and prescribe a course of oral cloxacillin. I would like to confirm the plan with you."
XII. Summary & Further Reading
Top 3 Takeaways:
AD is a clinical diagnosis. Don't order unnecessary tests.
Emollients are the absolute foundation of management for all severities. Prescribe them generously.
Use a stepwise approach for anti-inflammatory agents, matching the potency of the topical steroid to the severity of the flare.
Key Resources:
Malaysian CPG: CPG Management of Atopic Eczema, 2nd Edition (2018)
UpToDate: Search for "Atopic dermatitis (eczema): Pathogenesis, clinical manifestations, and diagnosis".
Amboss: Search for "Atopic dermatitis".
