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DR12.1-5 | Eczemas Erythroderma Drug Reactions — Practice Quiz
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A 28-year-old IT professional presents with intensely itchy, erythematous, vesicular lesions over both palms and fingers for three weeks. She reports her symptoms worsen after prolonged use of rubber gloves at work. The rest of her skin is clear. Which eczema subtype best fits this presentation?
Correct. The localized distribution confined to glove-contact skin combined with occupational rubber exposure points to allergic contact dermatitis (exogenous eczema), not pompholyx which is idiopathic and often bilateral on palms and sides of fingers without an identified contactant.
Allergic contact dermatitis is an exogenous eczema caused by a specific antigen (rubber latex/thiurams in gloves) via Type IV hypersensitivity; the occupational exposure and restricted distribution to glove-contact areas are the key diagnostic clues.
The distribution here is the key: it mirrors the glove contact area exactly. Atopic eczema typically affects flexural areas and begins in childhood. Pompholyx is idiopathic. Seborrhoeic dermatitis affects sebaceous gland-rich areas (scalp, face). Occupational rubber exposure with restricted distribution = allergic contact dermatitis.
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Irritant contact dermatitis and allergic contact dermatitis are both exogenous eczemas. Which of the following features most reliably distinguishes allergic contact dermatitis from irritant contact dermatitis?
Correct. Patch testing identifies the specific sensitizing antigen via a delayed (48-96 hour) Type IV hypersensitivity reaction and is the gold-standard investigation distinguishing allergic from irritant contact dermatitis.
Patch testing is the definitive investigation that separates Type IV (immunological) allergic contact dermatitis from non-immunological irritant contact dermatitis. Both may be restricted to contact sites and both improve on avoidance.
Both ACD and ICD can be limited to contact sites, show vesiculation, and improve on avoidance. The distinguishing test is patch testing: a positive result at 48-96 hours confirms allergic sensitization, which is absent in ICD.
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A 6-year-old boy has had recurrent itching and redness in the antecubital and popliteal fossae since age 2. His mother has allergic rhinitis and his father has asthma. Skin examination shows lichenified plaques at both elbow flexures. Which investigation is MOST useful to confirm the underlying mechanism?
Correct. Atopic eczema is associated with elevated total IgE and specific IgE to environmental/food antigens, reflecting the Th2-dominant immune environment. The flexural distribution, age of onset, and family history of atopy (rhinitis + asthma) are classic — RAST confirms the mechanism.
Atopic eczema involves a Type I IgE-mediated sensitization on a background of filaggrin barrier defect. Elevated total IgE and specific IgE/RAST confirm the atopic state. KOH is for fungal infection, patch test for ACD, biopsy is non-specific for eczema.
The classic flexural distribution since infancy, atopic family history (mother=rhinitis, father=asthma), and lichenification point strongly to atopic eczema. Serum IgE/RAST confirms IgE-mediated atopy. KOH would exclude tinea but isn't the confirmatory test here. Patch test tests contact sensitization, not atopy.
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A 55-year-old man is brought to the emergency department with generalised redness and scaling covering his entire body for 4 days. He has a long history of psoriasis. His temperature is 35.8°C, heart rate 112 bpm, and he is oedematous. What percentage of body surface area involvement defines erythroderma?
Correct. Erythroderma requires >90% BSA involvement. The hypothermia (35.8°C), tachycardia, and oedema in this patient illustrate the classic systemic complications: thermoregulatory failure (heat loss through vasodilated skin), high-output cardiac state, and hypoalbuminaemia/oedema from protein loss.
Erythroderma (exfoliative dermatitis) is defined as generalised inflammatory skin disease involving MORE THAN 90% of the body surface area. This threshold is the diagnostic criterion.
The defining threshold for erythroderma is >90% BSA. Lower cutoffs (50%, 70%, 80%) are incorrect. The systemic signs here — hypothermia, tachycardia, oedema — follow directly from loss of the skin's barrier and thermoregulatory functions when >90% is inflamed.
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The same erythrodermic patient in Q4 requires immediate primary care stabilisation before specialist referral. Which of the following is the MOST immediately life-saving intervention for this patient?
Correct. The three immediate targets in erythroderma stabilisation are: (1) thermoregulation — warm room, blankets, (2) fluid/electrolyte replacement — IV fluids, (3) barrier support — bland emollients. These address the two immediate killers: hypothermia and high-output cardiac failure. Steroids require specialist diagnosis before use.
Primary care stabilisation of erythroderma targets the immediate complications: hypothermia (warm room, blankets), fluid and electrolyte loss (IV fluids), and barrier failure (bland emollients). Systemic steroids require specialist input to confirm the underlying cause first; topical tar is irritating; antihistamines do not address the life-threatening physiology.
The immediate killers in erythroderma are hypothermia (from uncontrolled heat loss through inflamed skin) and high-output cardiac failure (from massive skin vasodilation). Correcting these — warmth + fluids + emollients — is the primary care job before specialist diagnosis guides specific therapy.
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A 35-year-old man has developed a well-demarcated, round, dark-brown hyperpigmented plaque 3 cm diameter on his right forearm. He first noticed this 2 years ago. Every time he takes ibuprofen for headaches, the lesion turns red and inflamed for 2 days, then returns to its baseline hyperpigmented state. The rest of his skin is normal. What is the diagnosis?
Correct. The pathognomonic feature is same-site recurrence: the plaque reactivates at the identical anatomical location each time ibuprofen is taken, leaving residual hyperpigmentation between episodes. This is fixed drug eruption. DRESS requires systemic involvement; SJS has widespread mucosal erosions and epidermal detachment; EM has target lesions often post-herpes.
Fixed drug eruption is defined by recurrence at exactly the SAME site every time the culprit drug is ingested; the hallmark is post-inflammatory hyperpigmentation between episodes. NSAIDs (ibuprofen) and co-trimoxazole are classic culprits.
Same-site recurrence at the exact same anatomical location every time a drug is taken is the defining feature of fixed drug eruption. The residual dusky hyperpigmentation between episodes is also characteristic. DRESS has systemic organ involvement and occurs weeks after starting a drug. SJS/TEN involves widespread epidermal detachment.
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A 30-year-old woman started carbamazepine 5 weeks ago for epilepsy. She now presents with facial oedema, generalised morbilliform rash, fever 38.5°C, and tender cervical lymphadenopathy. Blood tests show: total eosinophils 1,800/µL (normal <500), ALT 180 U/L (normal <40). What is the most likely diagnosis?
Correct. DRESS criteria are met: 5-week latency (2-8 week window), facial oedema, generalised rash, fever, lymphadenopathy, eosinophilia (1,800/µL — significantly elevated), and hepatitis (ALT 180, 4.5× ULN). Carbamazepine is one of the most common culprits. SJS/TEN would show epidermal detachment and mucosal erosions, not eosinophilia with hepatitis.
DRESS is diagnosed by: (1) latency of 2-8 weeks after starting the drug, (2) facial oedema (distinctive), (3) morbilliform rash with possible erythroderma, (4) lymphadenopathy, (5) eosinophilia (>1,500/µL), and (6) internal organ involvement (typically hepatitis — elevated ALT). Carbamazepine is a classic culprit aromatic anticonvulsant.
The DRESS triad to remember: (1) LONG latency (2-8 weeks — longer than SJS/TEN), (2) FACIAL OEDEMA (distinctive), (3) ORGAN involvement (liver is commonest). Eosinophilia (>1,500/µL) is the haematological hallmark. Carbamazepine, phenytoin, and allopurinol are classic culprits.
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A 45-year-old HIV-positive man on co-trimoxazole develops painful erosions on his lips and oral mucosa, bilateral conjunctival injection, and a blistering rash over his trunk with Nikolsky sign positive. Skin detachment involves approximately 12% of his body surface area. What is the correct classification of this reaction?
Correct. 12% BSA detachment falls in the SJS/TEN overlap category (10-30%). SJS is <10%, TEN is >30%. Co-trimoxazole is the single most common culprit drug for SJS/TEN, and HIV-positive patients have a markedly higher risk.
The BSA cutoffs: SJS = <10% detachment, SJS/TEN overlap = 10-30%, TEN = >30%. At 12%, this is the overlap zone. The defining features common to the spectrum are: mucosal erosions (oral, ocular, genital), positive Nikolsky sign (epidermal shearing), and a culprit drug (co-trimoxazole is the most common trigger, especially in HIV patients).
The BSA threshold for classification: SJS < 10%, overlap 10-30%, TEN > 30%. At 12% detachment, this patient is in the SJS/TEN overlap zone. Co-trimoxazole + HIV is the highest-risk combination for SJS/TEN.
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You are the primary care doctor managing the patient from Q8 (SJS/TEN overlap, 12% BSA). What is the SINGLE most important immediate step in primary care before transfer to a burns unit?
Correct. Stop the culprit drug IMMEDIATELY — this is the single most important step at every tier of drug reaction severity, and is especially critical in SJS/TEN. The primary care doctor can and MUST do this before transfer. IVIG and immunomodulators are specialist hospital interventions.
Stopping the culprit drug is the SINGLE most important intervention in any cutaneous adverse drug reaction, and is most critical in SJS/TEN where continued drug exposure directly drives epidermal death. IVIG and cyclosporin are specialist hospital treatments. Silver sulfadiazine (a sulfonamide) is CONTRAINDICATED in sulfonamide-induced TEN. Steroids are controversial and hospital-only.
In any cutaneous adverse drug reaction, stopping the culprit drug is ALWAYS the first and most important step — regardless of setting or resources. This is especially critical in SJS/TEN: each additional dose continues driving T-cell-mediated epidermal death. Note: silver sulfadiazine is a sulfonamide and is CONTRAINDICATED when co-trimoxazole (a sulfonamide) is the culprit.
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A 40-year-old woman is referred to your clinic with a chronic symmetrical eczema of both lower legs for 18 months. On examination, there is brown-black hyperpigmentation, varicose veins, slight oedema, and a healing ulcer near the right medial malleolus. What is the most likely diagnosis?
Correct. Stasis eczema is caused by chronic venous insufficiency and is clinically recognised by the triad of varicose veins + haemosiderin pigmentation + bilateral lower-leg distribution, with medial malleolar ulceration in advanced cases. It is an endogenous eczema (arising from internal physiology, not a contactant).
Stasis eczema (gravitational/varicose eczema) is an endogenous eczema caused by chronic venous insufficiency. The hallmarks are: bilateral lower-leg distribution, varicose veins, haemosiderin-brown pigmentation, oedema, and medial malleolar ulceration — all resulting from chronic venous hypertension.
The bilateral lower-leg location, varicose veins, brown haemosiderin pigmentation, oedema, and medial malleolar ulcer together form the classic picture of stasis (gravitational) eczema — an endogenous eczema driven by chronic venous hypertension. Atopic eczema affects flexures; nummular eczema forms discrete coin-shaped plaques; seborrhoeic dermatitis affects sebaceous areas.
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