Overview
Definition:
Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin condition characterized by pruritus, eczema, and a predisposition to other atopic diseases like asthma and allergic rhinitis
It is a complex disorder involving genetic predisposition, immune system dysregulation, and epidermal barrier dysfunction.
Epidemiology:
AD is the most common chronic skin disease in childhood, affecting 15-30% of children in developed countries, with prevalence varying geographically
Onset typically occurs in infancy or early childhood, with over 80% of cases appearing before age 5
Severe AD can significantly impact quality of life for patients and their families.
Clinical Significance:
Atopic dermatitis is a common and often debilitating condition in pediatric patients, posing significant challenges in management
Understanding evidence-based approaches to topical corticosteroid use and adjunctive therapies like dilute bleach baths is crucial for effective patient care and for success in DNB and NEET SS examinations.
Clinical Presentation
Symptoms:
Intense pruritus, often worse at night
Dry, erythematous, scaling patches or plaques
Vesicles or weeping in acute flares
Lichenification (thickened skin) in chronic lesions
Location varies by age: infants - face, scalp, extensor surfaces
older children/adults - flexural surfaces (antecubital and popliteal fossae), neck, wrists, ankles.
Signs:
Erythema, scaling, excoriations due to scratching
Possible secondary bacterial infection (e.g., Staphylococcus aureus) indicated by crusting, pustules, and increased erythema
Dennie-Morgan lines (infraorbital folds)
Hyperlinear palmar creases
Pityriasis alba (hypopigmented macules) on face/arms
Hairs can appear sparse in affected areas due to excoriation.
Diagnostic Criteria:
Diagnosis is primarily clinical, often based on the Hanifin and Rajka criteria or the UK Working Party criteria
Key elements include: 1
Pruritus
2
Chronic relapsing eczema
3
Typical morphology and distribution
4
Personal or family history of atopy (asthma, allergic rhinitis, AD)
5
Onset before age 2 years (though this is less strict)
Exclusion of other itchy dermatoses is also important.
Diagnostic Approach
History Taking:
Detailed history of pruritus duration and severity
Pattern of rash onset and evolution
Past treatments and response
Triggers (allergens, irritants, stress, infections)
Family history of atopy
History of asthma or allergic rhinitis
Presence of food allergies or other sensitivities
Red flags: rapid onset of severe widespread rash, fever, systemic symptoms suggestive of infection or drug reaction.
Physical Examination:
Thorough skin examination focusing on the morphology (erythema, scaling, lichenification, excoriations, vesicles), distribution of lesions, and presence of secondary infection
Assess for characteristic age-related patterns
Evaluate for signs of systemic illness
Examine nails for koilonychia or Beau's lines if relevant.
Investigations:
Typically, AD is a clinical diagnosis and does not require routine investigations
Allergy testing (skin prick tests, specific IgE blood tests) may be considered in select patients with suspected triggers, particularly if there is a clear association between exposure and flares, but is not mandatory for diagnosis
Culture of secondary infected lesions to identify pathogens and guide antibiotic therapy
Skin biopsy is rarely indicated.
Differential Diagnosis:
Other eczematous conditions: contact dermatitis (allergic or irritant), nummular eczema, seborrheic dermatitis
Psoriasis
Cutaneous T-cell lymphoma (mycosis fungoides in later stages)
Scabies
Pityriasis rosea
Fungal infections
Xerosis (dry skin).
Management
Initial Management:
Emollients are the cornerstone of therapy, applied liberally and frequently to restore skin barrier function
Gentle cleansing with non-soap cleansers and lukewarm water
Avoidance of triggers: harsh soaps, detergents, wool clothing, excessive heat, known allergens
Management of pruritus, especially at night, with sedating antihistamines if necessary (though evidence for efficacy is limited).
Medical Management:
Topical corticosteroids (TCS) are the mainstay of anti-inflammatory treatment for flares
Potency and vehicle selection depend on age, location, and severity of lesions: low potency (hydrocortisone) for face/intertriginous areas, medium potency (triamcinolone) for trunk/limbs
Apply thinly once or twice daily for short durations
Long-term, intermittent use for maintenance is often necessary
Topical calcineurin inhibitors (TCIs - tacrolimus, pimecrolimus) are steroid-sparing alternatives for sensitive areas or long-term control, especially for facial or intertriginous eczema
Antiseptics/antibiotics for secondary infections: topical or oral antibiotics (e.g., cephalexin, dicloxacillin for Staph
aureus) if signs of infection
Dilute bleach baths (0.005% sodium hypochlorite solution, typically 1/2 cup bleach per 40 gallons of water) can reduce bacterial colonization and inflammation
use 1-2 times weekly for 5-10 minutes, followed by rinsing and immediate emollient application.
Steroid Stewardship:
Crucial for minimizing side effects of topical corticosteroids
Use the lowest effective potency for the shortest duration
Educate patients on proper application technique (thin layer, specific areas)
Avoid prolonged use on sensitive areas (face, groin)
Monitor for local side effects (skin thinning, striae, telangiectasias) and systemic effects (rare with appropriate topical use but possible with extensive application of superpotent steroids)
Consider TCIs as steroid-sparing options
Emphasize continuous emollient use to reduce need for TCS.
Adjunctive Therapies:
Wet wrap therapy can be effective for severe, refractory flares, involving applying emollients and/or TCS under damp bandages, followed by dry bandages
Phototherapy (UVB) may be considered for older children and adolescents with severe disease not responding to topical treatments
Systemic immunosuppressants (e.g., cyclosporine, methotrexate, azathioprine) or biologics (e.g., dupilumab) are reserved for severe, recalcitrant AD in adolescents and adults under specialist care.
Complications
Early Complications:
Secondary bacterial infections (Staphylococcus aureus, Streptococcus pyogenes) leading to impetiginization, cellulitis, or eczema herpeticum (disseminated herpes simplex virus infection)
Viral infections (molluscum contagiosum, warts).
Late Complications:
Lichenification and thickening of skin from chronic scratching
Cosmetic disfigurement and impact on self-esteem
Sleep disturbances
Increased susceptibility to skin cancers in severely immunosuppressed individuals or with long-term intense topical steroid use (rare).
Prevention Strategies:
Strict adherence to emollient regimen to maintain skin barrier
Prompt treatment of secondary infections
Dilute bleach baths to reduce bacterial load
Education on trigger avoidance
Judicious use of topical corticosteroids and consideration of steroid-sparing agents
Regular follow-up with a dermatologist.
Prognosis
Factors Affecting Prognosis:
Severity of AD, age of onset, presence of other atopic comorbidities, adherence to treatment, and response to initial therapies
Early and consistent management can lead to better long-term outcomes.
Outcomes:
Many children experience significant improvement or remission of AD by adolescence or early adulthood
However, some individuals have chronic, fluctuating disease throughout their lives
The goal of management is to control symptoms, prevent flares, and improve quality of life.
Follow Up:
Regular follow-up is essential, especially for patients with moderate to severe AD
Frequency of visits depends on disease severity and response to treatment
Education of patients and caregivers is ongoing, empowering them to manage the condition effectively at home
Monitoring for complications and adherence to the treatment plan.
Key Points
Exam Focus:
Remember the diagnostic criteria for AD
Differentiate AD from other eczematous conditions
Understand the role of emollients, topical corticosteroids (potency, vehicle, application), and topical calcineurin inhibitors
Know the indications and mechanism of dilute bleach baths for AD
Recognize signs of secondary infection.
Clinical Pearls:
Emollients are not just moisturizers
they are a critical part of treatment to repair the epidermal barrier
Apply emollients generously, at least twice daily, and immediately after bathing
Dilute bleach baths should be used 1-2 times per week, never daily, and followed by immediate rinsing and emollient application
Educate parents that steroids are safe and effective when used correctly, and that steroid-sparing agents are also important
Always assess for secondary infection when flares are recalcitrant.
Common Mistakes:
Underestimating the importance of emollients
Overusing potent topical steroids for prolonged periods or on sensitive areas
Not recognizing and treating secondary bacterial infections promptly
Relying solely on topical steroids without addressing skin barrier function
Failing to educate patients on proper application techniques and trigger avoidance.