39.1 Atopic Dermatitis, Contact Dermatitis & Eczematous Flares

Pathophysiology & Etiology of Atopic Dermatitis

Atopic dermatitis (AD, eczema) is a chronic, relapsing, highly pruritic inflammatory dermatosis that affects up to 15% to 20% of children and 3% to 10% of adults worldwide. It represents the initial cutaneous manifestation of the classic "atopic march", a predictable developmental sequence progressing from atopic dermatitis in infancy to food allergies, allergic rhinitis, and asthma in childhood and adolescence.

                    PATHOPHYSIOLOGY OF ATOPIC DERMATITIS

   Epidermal Barrier Defect                Immune Dysregulation (Th2-Skewed)
   ┌─────────────────────────────┐        ┌─────────────────────────────┐
   │ • FLG (Filaggrin) Mutation  │        │ • Allergen / Microbial Entry│
   │ • Decreased Ceramides       │───────>│ • Th2 Cytokines: IL-4, IL-13 │
   │ • Increased TEWL (Water Loss)│        │ • IL-31 ("Itch Cytokine")   │
   │ • Defective Stratum Corneum │        │ • Elevated Serum IgE        │
   └─────────────────────────────┘        └─────────────────────────────┘
                 │                                       │
                 ▼                                       ▼
   ┌───────────────────────────────────────────────────────────────────┐
   │                       THE ITCH-SCRATCH CYCLE                      │
   │ Severe Pruritus ──> Excoriation ──> Barrier Breakdown ──> Flares  │
   │ Superinfection Risk: Staphylococcus aureus (>90%) & HSV-1 (EH)    │
   └───────────────────────────────────────────────────────────────────┘

1. Epidermal Skin Barrier Dysfunction

• Filaggrin (FLG) Gene Mutations: Loss-of-function mutations in the FLG gene (located on chromosome 1q21 within the epidermal differentiation complex) represent the strongest known genetic risk factor for atopic dermatitis. Profilaggrin is cleaved into filaggrin monomers that aggregate keratin filaments, flattening keratinocytes into the rigid stratum corneum "bricks".
• Natural Moisturizing Factor (NMF): Filaggrin breakdown products (amino acids, pyrrolidone carboxylic acid, urocanic acid) constitute NMF, which maintains stratum corneum hydration, skin plasticity, and an acidic cutaneous mantle (pH 4.5-5.5). In FLG deficiency, transepidermal water loss (TEWL) rises dramatically, and cutaneous pH increases, which activates endogenous serine proteases (kallikreins) and degrades lipid-processing enzymes.
• Lipid Abnormalities: Deficiencies in intercellular ceramides, sphingosines, and free fatty acids disrupt the extracellular lipid "mortar", leading to microscopic cracking, xerosis, and increased susceptibility to irritants, environmental allergens, and microbes.

2. Th2-Skewed Immune Dysregulation

• Epithelial Cytokines: Damaged keratinocytes release alarmins—thymic stromal lymphopoietin (TSLP), interleukin-25 (IL-25), and IL-33—which activate dermal dendritic cells and group 2 innate lymphoid cells (ILC2s).
• Th2 Cytokine Cascades: Activated CD4+ T helper 2 (Th2) cells secrete IL-4 and IL-13, which drive B-cell class-switching to produce immunoglobulin E (IgE) and directly downregulate filaggrin and loricrin expression, creating a vicious cycle of further barrier breakdown.
• The "Itch Cytokine" (IL-31): IL-31 binds directly to the IL-31 receptor A on cutaneous unmyelinated C-fibers, triggering severe, intractable pruritus. Pruritus promotes scratching, which releases additional inflammatory mediators—the quintessential itch-scratch cycle.

3. Environmental Triggers & Colonization

• Staphylococcal Colonization: Over 90% of patients with atopic dermatitis exhibit dense cutaneous colonization with Staphylococcus aureus on lesional skin (compared to <5-10% of healthy controls). S. aureus produces enterotoxins (superantigens) that stimulate polyclonal T-cell activation and corticosteroid resistance.
• Exogenous Triggers: Low ambient humidity, cold dry winter air, excessive hot water exposure, harsh detergents, wool fabrics, emotional stress, and aeroallergens (dust mites, pet dander).

---

Clinical Phenotypes & Age-Specific Distribution

The clinical presentation and anatomical distribution of atopic dermatitis evolve characteristically across three distinct life stages. Recognizing these age-dependent patterns is a cornerstone of primary care clinical assessment and board examinations.

                   AGE-SPECIFIC ECZEMA DISTRIBUTION

     INFANCY (<2 Years)        CHILDHOOD (2-12 Yr)          ADULTHOOD (>12 Yr)
    ┌────────────────────┐    ┌────────────────────┐    ┌────────────────────┐
    │ • Cheeks, Forehead │    │ • Flexural Creases │    │ • Lichenification  │
    │ • Scalp            │    │   - Antecubital    │    │ • Antecubital/Pop. │
    │ • Extensor Limbs   │    │   - Popliteal      │    │ • Hand Dermatitis  │
    │ • Weeping / Crusts │    │ • Wrists / Ankles  │    │ • Periocular/Neck  │
    │ • SPARES DIAPER!   │    │ • Dry & Excoriated │    │ • Chronic Relapsing│
    └────────────────────┘    └────────────────────┘    └────────────────────┘

1. Infancy Stage (Birth to 2 Years)

• Onset: Typically presents between 2 and 6 months of age.
• Lesion Morphology: Acute, intensely pruritic, erythematous papules and patches with microvesicles, exudative weeping, and serous yellow crusting.
• Distribution: Cheeks, forehead, scalp, and extensor surfaces of the extremities (knees, elbows, shins) as crawling infants rub their limbs against carpets and bedding.
• Board Exam High-Yield Pearl: Strict sparing of the diaper area! The occlusive, high-humidity microenvironment under diapers prevents cutaneous xerosis and epidermal barrier desiccation. If an infant presents with an inflammatory, beefy red rash involving the diaper area with satellite pustules, suspect Candida diaper dermatitis; if confluent erythema involves the groin creases, consider irritant contact diaper dermatitis or seborrheic dermatitis, not atopic dermatitis.

2. Childhood Stage (2 Years to Puberty)

• Lesion Morphology: Subacute to chronic dry, erythematous, excoriated papules and plaques with marked lichenification (thickening of the epidermis with accentuation of normal skin markings secondary to chronic repetitive scratching).
• Distribution: Classic flexural predilection: antecubital and popliteal fossae, volar wrists, anterior ankles, posterior neck, and infra-auricular creases.
• Associated Physical Findings:
  • Dennie-Morgan Folds: Prominent, symmetric infraorbital skin folds caused by persistent ocular rubbing and spasm of the underlying orbicularis oculi muscle;
  • Allergic Shiners: Dark, violaceous periorbital discoloration secondary to venous stasis;
  • Pityriasis Alba: Ill-defined, hypopigmented, finely scaly, non-pruritic macules and patches on the cheeks and upper arms, representing post-inflammatory hypopigmentation and mild eczematous dermatitis, commonly noticed after sun exposure;
  • Keratosis Pilaris: Folliculocentric hyperkeratotic papules ("chicken skin") on the lateral aspects of the upper arms, thighs, and buttocks;
  • Hyperlinear Palms: Accentuation of palmar skin markings strongly correlated with heterozygous FLG gene mutations.

3. Adolescent & Adult Stage (>12 Years)

• Lesion Morphology: Chronic, heavily lichenified, dry, thickened plaques, fissuring, and post-inflammatory hyper- or hypopigmentation.
• Distribution: Flexural creases, dorsal hands and wrists (chronic occupational or irritant hand dermatitis), periocular and perioral skin, upper trunk, and nape of neck.
• Adult Complications: Sleep fragmentation, severe anxiety, depression, recurrent skin soft-tissue infections, and occupational disability.

---

Long-Term Barrier Restoration & Flare Prevention

The foundation of atopic dermatitis management is continuous, proactive barrier repair and elimination of cutaneous irritants. Pharmacologic therapies fail if underlying barrier dysfunction is neglected.

The "Soak and Seal" Regimen

• Bathing Technique: Patients should take once-daily lukewarm baths or showers lasting 5 to 10 minutes. Avoid hot water, which leaches intercellular lipids and triggers mast cell histamine release.
• Soap Substitutes: Strictly avoid traditional alkaline bar soaps (pH 9.0-10.0), which elevate skin surface pH and activate degradative proteases. Recommend mild, synthetic detergent-based liquid cleansers (syndets) with an acidic or neutral pH (pH 5.5-7.0), applied sparingly to the axillae and groin only.
• The 3-Minute Rule ("Soak and Seal"): Within 3 minutes of exiting the bath, while the stratum corneum is fully hydrated, pat the skin gently with a soft towel (leaving it slightly damp) and immediately apply a generous layer of emollient to the entire body to lock in moisture.

Emollient Selection Hierarchy

1. Ointments (First-Line / Most Effective): Anhydrous, petrolatum-based formulations (e.g., white petrolatum, Aquaphor). They provide superior lipid barrier occlusion and minimal water evaporation. Because they contain no water, they require no chemical preservatives, minimizing allergic contact sensitization.
2. Creams (Second-Line): Water-in-oil emulsions with moderate lipid content. Cosmetically acceptable for daytime use or warmer climates, but require chemical preservatives that may cause transient stinging on inflamed skin.
3. Lotions (Contraindicated / Avoid in Eczema): High water and alcohol content with low lipid content. Lotions evaporate rapidly, worsening cutaneous xerosis through evaporative water loss, and contain fragrances and preservatives that provoke contact sensitization.

Dilute Bleach Baths (Sodium Hypochlorite)

• For patients with recurrent, frequent bacterial superinfections, dilute sodium hypochlorite baths reduce S. aureus skin bioburden and suppress cutaneous NF-kB-mediated inflammation.
• Recipe: Add 1/2 cup (120 mL) of standard 6% household bleach to a full 40-gallon bathtub of lukewarm water (achieving an approximate concentration of 0.005%), soaking for 10 minutes 2 to 3 times weekly, followed by clean water rinsing and immediate emollient sealing.

---

Topical Pharmacotherapy & Corticosteroid Hierarchy

When non-pharmacologic barrier restoration is insufficient, topical anti-inflammatory pharmacotherapy is indicated for acute flares and proactive maintenance.

Topical Corticosteroid (TCS) Potency Hierarchy

Topical corticosteroids are categorized into 7 potency classes based on cutaneous vasoconstrictor assays (Class 1 = superpotent; Class 7 = lowest potency).

Cutaneous & Systemic Adverse Effects of TCS

• Local Adverse Effects: Epidermal and dermal atrophy, irreversible striae distensae (especially in axillae and groin), telangiectasias, purpura, perioral dermatitis, rosacea-like rebound flares, and hypopigmentation.
• Ocular Complications: Long-term application of medium- or high-potency corticosteroids to the periorbital skin can cause increased intraocular pressure, open-angle glaucoma, and posterior subcapsular cataracts.
• Systemic Absorption: Extensive application of high-potency steroids over large body surface areas (especially under occlusion or in infants with high surface-area-to-body-mass ratios) can lead to hypothalamic-pituitary-adrenal (HPA) axis suppression, iatrogenic Cushing syndrome, and pediatric growth impairment.

Topical Calcineurin Inhibitors (TCIs): The Steroid-Sparing Gold Standard

• Mechanism of Action: Tacrolimus (0.03% ointment for children 2-15 years; 0.1% ointment for adults) and Pimecrolimus (1% cream) bind to intracellular immunophilin FKBP-12, forming a complex that inhibits calcineurin phosphatase. This prevents dephosphorylation of the nuclear factor of activated T-cells (NFAT), blocking transcription of proinflammatory cytokines (IL-2, IL-3, IL-4, IFN-gamma) and downregulating T-cell activation.
• Clinical Indications:
  • First-line steroid-sparing therapy for sensitive, thin-skinned anatomic sites: face, eyelids, periocular skin, neck, and intertriginous folds.
  • Proactive maintenance therapy: applied twice weekly to previously affected sites to prevent recurrent flares.
• Safety Advantages: TCIs do NOT inhibit collagen synthesis and therefore cause zero cutaneous atrophy, striae, or telangiectasias, and do not increase intraocular pressure when applied to eyelids.
• Patient Counseling: Clinicians must warn patients that TCIs frequently cause localized transient burning, warmth, and stinging during the first 3 to 5 days of application. This burning sensation resolves as cutaneous inflammation improves. Storing the tube in the refrigerator prior to application minimizes stinging.
• FDA Boxed Warning Pearl: Although TCIs carry an FDA boxed warning regarding theoretical risk of lymphoma and skin malignancies, extensive 10-year post-marketing registry data (APPLES study) have confirmed no increased incidence of malignancy compared to the general population.

Topical PDE-4 & JAK Inhibitors

• Crisaborole 2% Ointment: A boron-based topical phosphodiesterase-4 (PDE-4) inhibitor approved for mild-to-moderate atopic dermatitis in patients >=3 months of age. PDE-4 inhibition elevates intracellular cyclic AMP (cAMP), suppressing NF-kB and downregulating proinflammatory cytokine release.
• Ruxolitinib 1.5% Cream: A topical Janus kinase (JAK1/JAK2) inhibitor approved for short-term and non-continuous chronic treatment of mild-to-moderate AD in non-immunocompromised patients >=12 years. Provides rapid antipruritic relief within 24 to 48 hours.

---

Advanced Systemic Biologics & Emerging Therapies

For patients with moderate-to-severe atopic dermatitis whose disease remains uncontrolled despite optimized topical barrier repair and topical pharmacotherapies, systemic targeted biologic therapy is the standard of care.

Dupilumab (Anti-IL-4R-alpha)

• Mechanism: A fully human IgG4 monoclonal antibody that binds specifically to the shared IL-4 receptor alpha (IL-4R-alpha) subunit, simultaneously inhibiting signaling of both IL-4 and IL-13 through the Type I and Type II receptor complexes.
• Indications: Approved for moderate-to-severe atopic dermatitis in adults and pediatric patients down to 6 months of age.
• Dosing (Adults): Initial loading dose of 600 mg subcutaneously (two 300 mg injections), followed by 300 mg subcutaneously every 2 weeks.
• Efficacy: Produces rapid, dramatic reductions in pruritus, marked improvement in Eczema Area and Severity Index (EASI-75) scores, and substantial restoration of the epidermal barrier without organ toxicity.
• Adverse Effects: Injection site reactions, transient blood eosinophilia, and conjunctivitis / blepharitis (occurs in 10% to 20% of eczema patients on dupilumab, responsive to lubricating eye drops, fluorometholone ophthalmic drops, or tacrolimus 0.03% ophthalmic ointment).

Other Biologics & Oral JAK Inhibitors

• Tralokinumab: Monoclonal antibody neutralizing IL-13 specifically, approved for moderate-to-severe AD in adults.
• Oral JAK Inhibitors (Upadacitinib, Abrocitinib): Highly effective oral small-molecule inhibitors of JAK1 offering rapid disease clearance, but carrying class boxed warnings (major adverse cardiovascular events, thrombosis, serious infections, malignancies) requiring baseline laboratory screening.

---

Infectious Complications: Superinfections & Eczema Herpeticum

Compromised physical barriers, decreased antimicrobial peptides (cathelicidins and beta-defensins), and intense scratching predispose atopic individuals to secondary cutaneous infections.

                    ECZEMA INFECTIOUS COMPLICATIONS

    BACTERIAL (Staphylococcus aureus)       VIRAL: ECZEMA HERPETICUM (HSV-1)
   ┌────────────────────────────────┐      ┌────────────────────────────────┐
   │ • Honey-colored crusts         │      │ • DERMATOLOGIC EMERGENCY!      │
   │ • Pustules, purulent exudate   │      │ • Monomorphic umbilicated      │
   │ • Impetiginization of eczema   │      │   vesicles / punched-out sores │
   │ • Rx: Topical Mupirocin OR     │      │ • Fever, chills, adenopathy    │
   │   Oral Cephalexin / TMP-SMX    │      │ • Emergency IV/Oral Acyclovir! │
   └────────────────────────────────┘      └────────────────────────────────┘

1. Bacterial Superinfection (Secondary Impetiginization)

• Microbiology: Staphylococcus aureus (methicillin-sensitive or MRSA) and Streptococcus pyogenes (Group A Strep).
• Clinical Presentation: Sudden worsening of baseline eczema, accompanied by honey-colored (meliceric) crusting, painful follicular pustules, weeping purulent exudate, and regional lymphadenopathy.
• Management:
  • Localized superficial crusting: Topical Mupirocin 2% ointment three times daily for 5 to 7 days.
  • Widespread or systemic involvement: Oral systemic antibiotics with anti-staphylococcal coverage: Cephalexin 500 mg QID (or dicloxacillin) for MSSA; Trimethoprim-Sulfamethoxazole (TMP-SMX 1-2 DS tabs BID) or Doxycycline 100 mg BID for suspected community-acquired MRSA.

2. Eczema Herpeticum (Kaposi Varicelliform Eruption)

• Pathophysiology: A potentially life-threatening dermatologic emergency resulting from the acute, widespread dissemination of Herpes Simplex Virus (predominantly HSV-1, rarely HSV-2) across damaged, barrier-deficient eczematous skin.
• Clinical Presentation:
  • Rapid eruption of crops of monomorphic, dome-shaped, umbilicated vesicles clustered over active or quiescent eczematous areas (most frequently the head, neck, and upper trunk);
  • The vesicles rapidly evolve into punched-out, circular, hemorrhagic erosions with scalloped borders that coalesce into large, denuded, oozing areas;
  • Systemic Symptoms: High fever, rigors, malaise, irritability, and painful regional lymphadenopathy.
• Complications: Secondary bacterial sepsis (S. aureus), viremic dissemination to the brain, liver, and lungs, and herpes keratoconjunctivitis (corneal ulceration, scarring, and permanent visual loss if periorbital skin is involved).
• Diagnostic Confirmation: Clinical diagnosis confirmed by viral PCR swab of vesicular fluid (gold standard) or Tzanck smear demonstrating multinucleated giant cells and Cowdry A inclusion bodies.
• Emergency Treatment:
  • Immediate Antiviral Therapy: Delaying treatment can be catastrophic.
    • Mild, early outpatient disease: Oral Valacyclovir 1,000 mg TID (or oral acyclovir 400 mg 5 times daily) for 10 to 14 days.
    • Moderate-to-severe, extensive, toxic, or pediatric disease: Hospital admission and Intravenous Acyclovir 5 to 10 mg/kg every 8 hours until clinical improvement, then transition to oral.
  • Urgent Ophthalmology Consultation: Mandatory whenever lesions approach the periorbital zone, forehead, or nose to evaluate for dendritic keratitis with fluorescein slit-lamp examination.
  • Pitfall to Avoid: Never apply topical corticosteroids or calcineurin inhibitors to active eczema herpeticum! Immunosuppressants exacerbate viral replication and fatal systemic dissemination.

---

Contact Dermatitis: Irritant vs. Allergic

Contact dermatitis comprises acute or chronic inflammatory skin reactions provoked by cutaneous exposure to exogenous chemical, physical, or biological substances. It is divided into two fundamentally distinct mechanisms: Irritant Contact Dermatitis (ICD) and Allergic Contact Dermatitis (ACD).

| Diagnostic Feature | Irritant Contact Dermatitis (ICD) | Allergic Contact Dermatitis (ACD) | | :--- | :--- | :--- | :--- | | Incidence | 80% of all contact dermatitis | ~20% of all contact dermatitis | | Mechanism | Non-immunologic direct chemical or physical cytotoxicity to stratum corneum | Type IV delayed-type hypersensitivity (cell-mediated, T-cell driven) | | Prior Sensitization | Not required; occurs on first exposure if concentration/irritant is strong | Strictly required (sensitization phase: 10-14 days; elicitation: 24-72 hours) | | Predominant Symptom | Burning, stinging, smarting, or pain > pruritus | Intense, severe pruritus > pain/burning | | Lesion Morphology | Dryness, erythema, scaling, cracking, fissuring, glazed or chapped appearance | Erythema, edema, grouped vesicles/bullae, weeping, crusting, lichenification | | Distribution & Margins | Strictly confined to the precise boundaries of contact ("decrescendo" pattern) | Extends beyond the contact zone; geographic, artificial, or linear patterns | | Common Culprits | Frequent handwashing (water/wet work), soaps, harsh detergents, alkalis, solvents, acids | Urushiol (poison ivy), nickel, neomycin, fragrance mix, PPD, acrylates | | Diagnostic Gold Standard | Clinical diagnosis of exclusion | Diagnostic epicutaneous patch testing |

---

Common Contact Allergens & Diagnostic Patch Testing

High-Yield Board Allergens

1. Urushiol (Toxicodendron genus: Poison Ivy, Poison Oak, Poison Sumac): The most common cause of ACD in North America. Produces pathognomonic linear arrays of pruritic papules and tense vesicles where plant leaves brushed against exposed skin.
2. Nickel Sulfate: The most prevalent contact allergen worldwide. Manifests as well-circumscribed eczematous plaques beneath earrings (earlobes), jean button snaps (periumbilical "belt buckle" dermatitis), wristwatches, or metal eyeglass frames.
3. Neomycin & Bacitracin: Common components of over-the-counter "triple antibiotic" ointments. Sensitization frequently develops when patients apply ointment to chronic stasis ulcers, surgical wounds, or lacerations, producing an intense flare misdiagnosed as "worsening wound infection."
4. Paraphenylenediamine (PPD): Oxidizing chemical found in permanent hair dyes and "black henna" temporary tattoos. Sensitization causes severe scalp and facial edema or acute vesicular eruptions.
5. Fragrance Mix & Preservatives: Methylisothiazolinone (MI/MCI) in wet wipes and cosmetics; formaldehyde releasers in lotions.

Diagnostic Patch Testing (Epicutaneous Testing)

• Clinical Role: The gold standard for identifying the specific causative allergen in persistent, unexplained, or occupational contact dermatitis.
• Procedure: Standardized allergen panels (e.g., T.R.U.E. Test) are applied to unaffected skin on the upper back in hypoallergenic chambers.
• Timing of Interpretations:
  • Patches are left in place for 48 hours, then removed for the initial reading (identifies early reactions);
  • A second delayed reading is performed at 72 to 96 hours (and occasionally at 7 days). The delayed reading is essential because Type IV cell-mediated reactions require 3 to 4 days to manifest fully.
• Critical Test Distinction: Patch testing evaluates Type IV delayed hypersensitivity. In contrast, skin prick testing (prick/puncture) evaluates Type I immediate IgE-mediated hypersensitivity (used for allergic rhinoconjunctivitis, food allergies, and venom anaphylaxis).

---

Management of Rhus Dermatitis & The 21-Day Oral Steroid Rule

Rhus dermatitis (Toxicodendron / poison ivy dermatitis) accounts for countless primary care visits every spring and summer. Family physicians must recognize the pharmacokinetics of urushiol to prevent undertreatment.

                   RHUS DERMATITIS (POISON IVY) TRIAGE

                         Assess Severity & BSA Involved
                                       │
            ┌──────────────────────────┴──────────────────────────┐
            ▼                                                     ▼
   LOCALIZED DISEASE (<20% BSA)                  EXTENSIVE / SEVERE DISEASE
   • Spares face, eyes, genitalia                • >20% BSA involvement OR
   • High-Potency Topical Steroid:               • Face, eyelids, neck, genitalia OR
     Clobetasol 0.05% BID x 10-14 days           • Severe blistering & functional deficit
   • Cool compresses, calamine lotion                             │
   • Oral antihistamines for sleep                                ▼
                                                 ORAL PREDNISONE TAPER OVER 14-21 DAYS!
                                                 • Initial: 0.5 - 1.0 mg/kg/day (40-60 mg)
                                                 • Taper gradually over 2 to 3 weeks
                                                 • NEVER GIVE A 6-DAY MEDROL PACK!
                                                 • Prevents Severe Rebound Flares

The Pathophysiology of Urushiol Persistence

• Urushiol is an extremely lipophilic, non-volatile oleoresin. Once absorbed into the stratum corneum and sebaceous lipids, it remains bound to epidermal cell membranes for 2 to 3 weeks, continuously stimulating allergen-specific CD4+ and CD8+ memory T cells.
• Contact with plant sap initiates sensitization; washing thoroughly with soap and water within 10 to 15 minutes of exposure can remove unabsorbed resin, but washing after 30 to 60 minutes is ineffective.

The 21-Day Oral Corticosteroid Rule: The Ultimate Board Trap

[!CAUTION] THE FATAL BOARD MISTAKE: NEVER PRESCRIBE A SHORT 5- TO 6-DAY MEDROL DOSEPACK FOR POISON IVY! A classic board scenario presents a patient with severe, widespread poison ivy dermatitis involving the face, arms, and legs. Prescribing a standard 6-day methylprednisolone "dose pack" (which tapers from 24 mg down to 0 mg over 6 days) is incorrect medical practice! While the patient improves dramatically during the first 4 to 5 days, the steroid is discontinued while active urushiol antigen is still bound in the skin. This invariably triggers an explosive, severe rebound dermatitis that is often worse than the original presentation. Correct Guideline Regimen: When systemic therapy is indicated, prescribe Oral Prednisone starting at 0.5 to 1.0 mg/kg/day (typically 40 to 60 mg daily), tapered slowly and steadily over a minimum of 14 to 21 days (2 to 3 full weeks) (e.g., 60 mg daily for 5 days, 40 mg daily for 5 days, 20 mg daily for 5 days, and 10 mg daily for 5 days).