10.2 Eczema, Dermatitis & Skin Infections
Key Takeaways
- Atopic dermatitis is a chronic pruritic disease driven by filaggrin mutations; flares are treated with topical corticosteroids of appropriate potency, while maintenance focuses on emollients and trigger avoidance.
- Allergic contact dermatitis is a T-cell mediated Type IV hypersensitivity reaction confirmed by patch testing, whereas irritant contact dermatitis is a non-immunologic physical or chemical barrier injury.
- Cellulitis is a deep dermis infection presenting as poorly demarcated, spreading erythema, requiring systemic beta-lactam antibiotics targeting streptococci and staphylococci.
- Impetigo is a highly contagious superficial infection with honey-colored crusts; localized cases are treated with topical mupirocin, while widespread infections require oral cephalexin.
- Superficial tinea fungal infections present as annular plaques with active scaling borders, diagnosed by KOH prep showing septate hyphae, and managed with topical azoles (or oral antifungals for capitis/unguium).
Atopic Dermatitis (Eczema): Pathogenesis and Management
Atopic dermatitis (AD) is a chronic, pruritic, inflammatory skin disease that typically begins in childhood and follows a relapsing course.
- Pathogenesis: Driven by a combination of genetic predisposition (e.g., loss-of-function mutations in the filaggrin gene [FLG], which encodes a key structural protein in the stratum corneum), epidermal barrier dysfunction (leading to increased transepidermal water loss and allergen penetration), immune dysregulation (predominantly Th2-mediated helper T-cell response), and environmental triggers.
- Clinical Presentation: The hallmark is severe pruritus ("the itch that rashes"). Lesion morphology and distribution are age-dependent:
- Infants (<2 years): Pruritic, erythematous, edematous papules and plaques with oozing and crusting on the cheeks, scalp, and extensor surfaces of limbs. The diaper area is classically spared.
- Children and Adults: Chronic, lichenified plaques localized primarily to flexural folds (antecubital and popliteal fossae, volar wrists, ankles, and neck).
- Triggers: Low humidity, heat, sweating, irritants (soaps, detergents, wool), stress, and secondary infections (especially Staphylococcus aureus colonization).
- Management:
- Skin Barrier Restoration: Daily bathing in lukewarm water for 5-10 minutes, followed immediately (within 3 minutes) by the application of thick emollients (ointments or creams rather than lotions) to lock in moisture.
- Topical Corticosteroids (TCS): The first-line therapy for active flares. Use the lowest effective potency. Mild potency (e.g., Hydrocortisone 1-2.5%) for face and skin folds; medium-to-high potency (e.g., Triamcinolone acetonide 0.1%, Betamethasone valerate) for the trunk and extremities.
- Steroid-Sparing Agents: Topical calcineurin inhibitors (Tacrolimus 0.03% or 0.1% ointment, Pimecrolimus 1% cream) or topical phosphodiesterase-4 (PDE-4) inhibitors (Crisaborole 2%) are used for sensitive areas (face, eyelids, intertriginous zones) to prevent steroid-induced atrophy.
- Pruritus Control: Sedating oral antihistamines (e.g., Hydroxyzine, Diphenhydramine) at bedtime can help patients sleep by reducing night-time scratching. Non-sedating antihistamines are generally ineffective.
Contact Dermatitis: Irritant vs. Allergic
Contact dermatitis is an inflammatory skin reaction caused by direct exposure to an exogenous substance. It is categorized into two main types:
| Feature | Irritant Contact Dermatitis (ICD) | Allergic Contact Dermatitis (ACD) |
|---|---|---|
| Pathophysiology | Non-immunologic direct chemical or physical damage to the skin barrier. | Type IV (delayed-type) T-cell mediated hypersensitivity reaction. |
| Exposure | Occurs after single or repeated exposure to an irritant (e.g., soap, acid, wet work). | Occurs in sensitized individuals upon re-exposure to an allergen. |
| Clinical Features | Dry, scaly, cracked skin, erythematous patches; burning/stinging pain is more prominent than itch. | Erythematous, vesicular, intensely pruritic plaques; may exhibit linear patterns (e.g., poison ivy). |
| Localization | Strictly limited to the area of contact with the offending agent. | May spread beyond the borders of direct contact. |
| Diagnosis | Clinical diagnosis based on history of exposure. | Confirmed via patch testing (standard series applied to the back for 48 hours). |
- Management: The primary intervention is identifying and avoiding the offending substance. In the acute phase, mid-to-high potency topical corticosteroids are used. For severe, widespread cases (>20% body surface area or severe facial involvement), a systemic corticosteroid taper (e.g., oral Prednisone starting at 0.5-1.0 mg/kg/day and tapered over 2-3 weeks) is indicated.
Bacterial Skin Infections: Cellulitis & Impetigo
Cellulitis
Cellulitis is a bacterial infection of the deep dermis and subcutaneous tissue.
- Pathogens: Most commonly Streptococcus pyogenes (Group A Streptococcus) and Staphylococcus aureus.
- Clinical Presentation: Poorly demarcated, spreading erythema, warmth, edema, and tenderness, typically unilateral and most commonly affecting the lower extremity. Systemic signs (fever, chills, leukocytosis) may occur. A portal of entry (e.g., trauma, interdigital tinea pedis, venous ulcers) is often present.
- Management:
- Non-purulent Cellulitis (Streptococcal suspect): Oral Cephalexin (500 mg four times daily) or Dicloxacillin.
- Purulent Cellulitis/MRSA Suspected: Trimethoprim-sulfamethoxazole (TMP-SMX) or Doxycycline.
- IV Antibiotics (Cefazolin, Vancomycin): Indicated for patients with systemic toxicity, rapid progression, immunocompromised state, or failure to respond to oral agents.
Impetigo
Impetigo is a highly contagious superficial bacterial skin infection.
- Non-bullous Impetigo (70%): Presents as papules and vesicles that rupture, leaving behind pathognomonic honey-colored crusts on an erythematous base, usually around the nose and mouth. Caused by S. aureus and S. pyogenes.
- Bullous Impetigo: Characterized by fragile, flactid bullae containing clear yellow fluid, caused by exfoliative toxins produced by S. aureus.
- Management:
- Localized Disease: Topical Mupirocin 2% ointment applied three times daily for 5-7 days.
- Widespread or Bullous Disease: Oral Cephalexin or Dicloxacillin.
Superficial Tinea Fungal Infections
Superficial dermatophytoses are fungal infections of keratinized tissues (skin, hair, nails) caused by Trichophyton, Microsporum, or Epidermophyton species.
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Tinea Corporis (Ringworm): Characterized by an annular, erythematous, scaling plaque with an active, elevated border and central clearing.
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Tinea Cruris (Jock Itch): Erythematous plaques with scaling borders in the groin, typically sparing the scrotum.
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Tinea Pedis (Athlete's Foot): Scaling and maceration of the interdigital spaces, or a hyperkeratotic "moccasin" pattern.
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Tinea Capitis (Scalp Fungal Infection): Scaly patches, alopecia, and broken hairs ("black dots"). May present as a kerion (a boggy, inflammatory mass). Requires oral antifungal therapy (e.g., oral Griseofulvin or Terbinafine) because topical agents cannot penetrate the hair follicle.
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Tinea Unguium (Onychomycosis): Thickened, yellowed, dystrophic nails. Requires oral Terbinafine after confirming the diagnosis with KOH preparation, culture, or PCR.
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Diagnosis: Skin scraping from the active scaling border, examined under light microscopy with potassium hydroxide (KOH) prep, demonstrating septate, branching hyphae.
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Treatment: Localized skin infections are treated with topical azoles (e.g., Clotrimazole, Ketoconazole) or allylamines (e.g., Terbinafine) for 2-4 weeks. Oral ketoconazole should be avoided due to hepatotoxicity. Combination steroid-antifungal creams should be avoided to prevent tinea incognito and skin atrophy.
A 6-year-old boy presents with severe itching and dry skin. On examination, he has erythematous, lichenified plaques in both his antecubital and popliteal fossae. His mother notes that his symptoms flare during the winter. What is the most appropriate first-line pharmacotherapy for this patient's active flares?
A 42-year-old construction worker presents with a painful, erythematous, swollen rash on his left lower leg that has been spreading over the past 48 hours. On examination, the area is warm to the touch, tender, and has poorly demarcated borders. A small fissure is noted in the web space between his fourth and fifth toes. There is no fluctuance or purulent drainage. Which of the following is the most appropriate initial empiric oral antibiotic?
An 8-year-old girl presents with a scaly, pruritic patch on her scalp associated with localized hair loss and several broken hairs that appear as 'black dots.' A KOH preparation of a hair shaft confirms the presence of dermatophyte spores. What is the most appropriate treatment for this patient?