DR12.1-5 | Eczemas Erythroderma Drug Reactions — Graded Quiz

Correct. Facial skin is thin and highly absorptive. Moderate-potent steroids on the face for 6 weeks is a classic prescribing error that produces steroid rosacea, perioral dermatitis, telangiectasia, and atrophy. Only mild steroids (1% hydrocortisone) are appropriate for the face, and only briefly.

The face has thin skin with high transcutaneous absorption. Moderate-to-potent topical steroids (Group II-III) on the face cause skin atrophy, telangiectasia, perioral dermatitis, and steroid rosacea. Only mild steroids (1% hydrocortisone) should be used on the face, and only for short periods. Over-the-counter steroid-antifungal-antibiotic combination creams are a major source of facial steroid overuse in India.

The core principle violated is site-specific steroid potency selection. The face has thin, highly absorptive skin — potent steroids cause atrophy, telangiectasia, and perioral dermatitis. Only mild steroids belong on the face. This is the most common and damaging prescribing error in Indian eczema practice.

Correct. The pathophysiology is direct: >90% BSA vasodilation creates a huge radiating/convecting surface that continuously loses heat to the environment at a rate the body cannot compensate for. This is the same mechanism as a major burn losing heat — the skin's thermostat is broken in the 'open' position.

In erythroderma, >90% of the skin surface is vasodilated. The skin normally thermoregulates by varying dermal blood flow. When the entire skin surface is continuously vasodilated, convective heat loss to the environment is massively increased, overwhelming the body's ability to retain heat — causing hypothermia, especially in cool environments.

The key pathophysiology: the skin is the body's thermostat. In erythroderma, massive uncontrolled vasodilation across >90% BSA turns the skin into a heat radiator — heat loss exceeds production, causing hypothermia. This is why a warm room (not cooling) is the first stabilisation measure.

Correct. The DRESS management priority is drug cessation + urgent hospital admission. Allopurinol must be stopped immediately with a lifetime rechallenge ban. The elevated bilirubin and ALT 6× ULN indicate significant hepatitis requiring monitoring for fulminant liver failure. Outpatient management with antihistamines is dangerous here.

DRESS management: (1) Stop the culprit drug IMMEDIATELY — never rechallenge; (2) refer/admit urgently because of organ involvement risk (liver, kidneys, heart); (3) supportive care and specialist immunosuppression are hospital decisions. Outpatient management with antihistamines is inadequate for a systemic drug reaction with hepatitis and eosinophilia.

DRESS with hepatitis (ALT 6× ULN, bilirubin elevated) requires: (1) immediate drug cessation — allopurinol stopped, never rechallenge; (2) urgent hospital admission for organ monitoring. Outpatient antihistamine/topical steroid treatment is inadequate for a multi-organ drug reaction.

Correct. 35% BSA = TEN (>30%). Lamotrigine (an aromatic anticonvulsant) is a classic culprit. The burns-model management applies: IV fluids, gentle wound care with non-adhesive dressings, mucosal care, temperature control, and urgent transfer. SSSS should be in the differential but affects neonates/young children, not adults, and has superficial (subcorneal) cleavage — Nikolsky sign is also positive but SSSS does not affect mucosae.

35% BSA detachment = TEN (>30%). Lamotrigine is an aromatic anticonvulsant and a well-recognised cause of SJS/TEN. Primary care management: stop the drug immediately, initiate burns-protocol care (IV fluids via Parkland formula, non-adhesive dressings, eye care, temperature control), and arrange URGENT transfer to a burns unit. SSSS affects children and has superficial cleavage; pemphigus has IgG autoantibodies.

35% BSA detachment classifies this as TEN (not SJS/TEN overlap which is 10-30%). Burns-model care is mandatory: IV fluid resuscitation, non-adhesive wound dressings, temperature control, mucosal care. Lamotrigine must be stopped immediately. TEN in pregnancy is a dual emergency requiring specialist obstetric + burns/dermatology collaboration.

Correct. Nummular/discoid eczema: coin-shaped plaques in adults without atopy, legs are a common site, KOH negative (excludes tinea). Treatment requires a moderate-potency topical steroid (e.g., betamethasone valerate 0.1% — trunk/limbs, not face) combined with emollients to restore the barrier. Mild steroids are usually insufficient for this subtype.

Nummular (discoid) eczema presents as coin-shaped plaques, typically on extensor surfaces or legs in middle-aged adults without atopic history. KOH negative rules out tinea corporis (the critical differential in India). Treatment: moderate-potency topical steroid + emollients. Mild steroids (hydrocortisone 1%) are often insufficient for discoid eczema.

Coin-shaped (nummular/discoid) eczema in a middle-aged adult with negative KOH (tinea excluded) requires moderate-potency topical steroids on trunk/limbs. Atopic eczema starts in childhood with flexural distribution. Seborrhoeic dermatitis has greasy scales in sebaceous areas. Always do KOH scraping first to exclude tinea in India before treating eczema-like plaques.

Correct. Allopurinol started 8 weeks ago falls exactly in the DRESS latency window (2-8 weeks). In a patient with both eczema history AND a new drug, the drug history with start dates + eosinophil count + LFTs is the highest-yield initial investigation to distinguish drug-induced erythroderma (DRESS) from eczema-driven erythroderma before biopsy results are available.

Erythroderma has four major causes: psoriasis, eczema, drug reaction, and cutaneous lymphoma. When a new drug (allopurinol, 8 weeks) has been started in the critical window alongside a pre-existing eczema history, the clinical work-up must first integrate the drug history (start dates, timing relative to erythroderma onset) with eosinophil count and LFTs to differentiate drug-induced DRESS/exanthematous reaction from eczema flare. Biopsy may follow but is not the first-line distinguishing investigation.

When erythroderma occurs and a new drug was started in the relevant time window, drug history with start dates + eosinophil count + LFTs is the first investigation priority. Allopurinol at 8 weeks is squarely in the DRESS window. Biopsy gives histological clues (spongiosis for eczema, lichenoid changes for drug) but takes days and does not immediately guide drug cessation.

Correct. The primary care action for fixed drug eruption: identify the culprit drug (ask the patient to bring or describe the tablet — NSAIDs, co-trimoxazole, metronidazole are most common), counsel permanent avoidance, and document the drug allergy. Burns unit referral is inappropriate — FDE is a benign, self-limiting reaction. Patch testing is not the investigation for FDE.

Fixed drug eruption management: (1) identify the causative drug — ask the patient to bring the tablet or identify it; common culprits include NSAIDs (ibuprofen), co-trimoxazole, metronidazole, and tetracyclines; (2) permanently counsel to avoid the drug; (3) document in the case record and give a written alert; (4) topical steroids and urgent referral are not required for FDE. Rechallenge confirms the diagnosis but is not recommended routinely.

Fixed drug eruption management in primary care: identify the culprit drug and advise permanent avoidance. FDE is benign and self-limiting — the hyperpigmentation between episodes is post-inflammatory and does not need treatment. Patch testing is used for ACD, not FDE (a photopatch or oral provocation test under specialist supervision can confirm FDE, but is not primary care practice).

Correct. TCIs (tacrolimus 0.03% in children, tacrolimus 0.1% in adults; pimecrolimus 1%) are the preferred step-up for facial eczema because they are effective without causing atrophy or telangiectasia. They are especially appropriate here because: (1) face/neck site, (2) parental steroid concern, (3) moderate eczema not controlled by mild steroids.

Topical calcineurin inhibitors (TCIs — tacrolimus 0.03% for children 2-15 years, pimecrolimus 1%) are the step-up treatment of choice for facial/periocular eczema because they do not cause skin atrophy, making them specifically preferred over potent steroids in thin-skinned areas. For children 2-15 years, tacrolimus 0.03% ointment is the approved dose. Systemic therapies (prednisolone, methotrexate) are not the next step for moderate eczema.

The face requires non-atrophogenic options when stepping up beyond mild steroids. Topical calcineurin inhibitors (tacrolimus 0.03% for children 2-15 years, pimecrolimus for milder/younger cases) are the correct step-up for facial eczema — they do not cause atrophy. Betamethasone valerate 0.1% on a child's face would cause significant atrophy and steroid side effects.

Correct. The drug history is the highest-yield transfer note item for erythroderma. In psoriasis, triggers such as lithium, antimalarials, NSAIDs, and — critically — sudden steroid withdrawal can precipitate erythroderma. The specialist needs to know what drugs to stop (or whether any drug is the primary cause rather than psoriasis flare) before starting systemic therapy.

For the receiving specialist planning definitive therapy for erythroderma, the most critical information is the complete drug history (including all recent additions and OTC drugs). In psoriatic erythroderma, drugs that precipitate the flare (lithium, antimalarials, sudden systemic steroid withdrawal, NSAIDs) or cause independent drug-induced erythroderma must be identified — because stopping them is a therapeutic intervention independent of psoriasis management. IgE, ANA, and calcium are not relevant to erythroderma cause or definitive management.

The most actionable single piece of information for the receiving specialist in erythroderma is the complete drug history. Erythroderma causes include drug reactions, and even in known psoriasis patients, a new drug may be the trigger. Identifying and stopping the culprit drug is the highest-priority intervention alongside psoriasis-specific therapy.

Correct. Irritant contact dermatitis from repeated wet work: 20-30 handwashes per shift strips stratum corneum lipids and disrupts the brick-and-mortar barrier via direct physical damage — no immunological sensitisation required. Negative patch test excludes ACD. Healthcare workers are the highest-risk group for occupational ICD.

Irritant contact dermatitis (ICD) is the commonest occupational skin disease. Repeated wet work and detergent exposure strips the stratum corneum lipids and disrupts the skin barrier — a direct physical/chemical (non-immunological) process. Negative patch testing excludes ACD. No atopic history excludes atopic eczema. ICD is the default diagnosis when patch testing is negative in an occupationally exposed worker.

Repeated handwashing in healthcare workers is the textbook cause of occupational irritant contact dermatitis. The mechanism is physical/chemical — detergent and repeated water exposure strips barrier lipids and disrupts corneocyte cohesion without immunological sensitisation. Negative patch test confirms this is not ACD.