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Derm CasesDermatology / Emergency Medicine / Allergy

Derm Cases · Dermatology / Emergency Medicine / Allergy

OSCE — severe cutaneous adverse drug reactions: SJS/TEN, DRESS, AGEP recognition and first response

An 8-minute OSCE station on recognising SJS/TEN, DRESS and AGEP, immediate culprit-drug cessation, SCORTEN-guided TEN severity thinking, HLA risk associations, and initial supportive/emergency care.

8 minosce2 min readVerification in progress

Target exams

NEET-PGINICETUSMLEPLABMRCP
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Target exams

NEET-PGINICETUSMLEPLABMRCP
Prompt
An 8-minute OSCE station on recognising SJS/TEN, DRESS and AGEP, immediate culprit-drug cessation, SCORTEN-guided TEN severity thinking, HLA risk associations, and initial supportive/emergency care.

Brief (to candidate)

A 40-year-old started allopurinol and an antibiotic 3 weeks ago. Now febrile with facial oedema, morbilliform rash, lymphadenopathy and ALT rise. A second vignette shows dusky macules, mucosal erosions and skin pain after a sulphonamide. You have 8 minutes to classify SCARs, stop culprits, and initiate emergency management.

Candidate instructions

  1. Differentiate morbilliform drug rash, SJS/TEN, DRESS/DIHS, AGEP, and fixed drug eruption.
  2. Immediate action: stop culprit(s) and triage severity.
  3. Apply SCORTEN concepts for TEN prognosis.
  4. Recall key HLA associations (e.g. B5801 allopurinol; B1502 carbamazepine in some Asian populations).
  5. Outline supportive care and specialist pathways.
[6]

Examiner checklist (mark each domain / 10)

DomainKey actions expected
SJS/TENPainful dusky macules, epidermal necrosis, ≥2 mucosal sites often; SJS <10% BSA, TEN ≥30%, overlap 10–30%; stop drug, burn-unit/ICU supportive care; SCORTEN risk score[2][15]
DRESSLatency often 2–8 weeks; fever, facial oedema, morbilliform → exfoliative, lymphadenopathy, haematologic abnormalities, hepatitis or other organ involvement; RegiSCAR criteria conceptually; long steroid taper often needed under specialist care[7][9][13]
AGEPAcute sterile pustules on erythema, often fever and neutrophilia, shorter latency after drug (commonly antibiotics); usually resolves after withdrawal ± supportive care[8]
First responseImmediate withdrawal of high-risk culprits (allopurinol, aromatic anticonvulsants, sulphonamides, oxicams, etc.); ABC/fluids, wound care, ophthalmology for ocular mucosa, avoid re-exposure
GeneticsHLA-B*5801 and allopurinol SCAR risk; HLA-B*1502 and carbamazepine SJS/TEN in some Southeast Asian ancestry — screen where guidelines recommend before certain drugs[5][6]
Mimics / otherViral exanthem, staphylococcal scalded skin (usually kids, no mucosa like TEN), autoimmune blistering — history of new drugs is pivotal
DocumentationAllergy record, medic-alert, report to pharmacovigilance

Model key actions

  • Recognise DRESS (delayed, facial oedema, organ involvement) vs SJS/TEN (necrosis + mucosa) vs AGEP (pustular).[2][9][8]
  • Stop allopurinol/anticonvulsant/sulphonamide culprits immediately and escalate TEN to intensive supportive care.[2][15]
  • Mention HLA risk alleles where relevant for prevention/counselling.[5][6]

Common errors

  • Continuing the culprit antibiotic/allopurinol “to finish the course.”
  • Treating TEN on a general ward without supportive critical care pathway.
  • Missing internal organ involvement in DRESS.
  • Labelling everything “viral rash” despite new high-risk drug.
  • No allergy documentation / future avoidance plan.
[2]
References9ShowHide
  1. [1]Del Pozzo-Magaña BR, Liy-Wong C. Drugs and the skin: A concise review of cutaneous adverse drug reactions. British Journal of Clinical Pharmacology, 2024.PMID 35974692
  2. [2]Shah H, Parisi R, Mukherjee E, et al. Update on Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: Diagnosis and Management. American Journal of Clinical Dermatology, 2024.PMID 39278968
  3. [5]Chung WH, Hung SI, Hong HS, et al. Medical genetics: a marker for Stevens-Johnson syndrome. Nature, 2004.PMID 15057820
  4. [6]Hung SI, Chung WH, Liou LB, et al. HLA-B*5801 allele as a genetic marker for severe cutaneous adverse reactions caused by allopurinol. Proceedings of the National Academy of Sciences USA, 2005.PMID 15743917
  5. [7]Kardaun SH, Sidoroff A, Valeyrie-Allanore L, et al. Variability in the clinical pattern of cutaneous side-effects of drugs with systemic symptoms: does a DRESS syndrome really exist? British Journal of Dermatology, 2007.PMID 17300272
  6. [8]Sidoroff A, Dunant A, Viboud C, et al. Risk factors for acute generalized exanthematous pustulosis (AGEP) — results of a multinational case-control study (EuroSCAR). British Journal of Dermatology, 2007.PMID 17854366
  7. [9]Mizukawa Y, Shiohara T. Recent advances in the diagnosis and treatment of DIHS/DRESS in 2025. Allergology International, 2025.PMID 40251070
  8. [13]Cacoub P, Musette P, Descamps V, et al. The DRESS syndrome: a literature review. American Journal of Medicine, 2011.PMID 21592453
  9. [15]Sekula P, Dunant A, Mockenhaupt M, et al. Evaluation of SCORTEN on a cohort of patients with Stevens-Johnson syndrome and toxic epidermal necrolysis included in the RegiSCAR study. Journal of Burn Care and Research, 2011.PMID 21228709
PreviousOSCE — seborrhoeic-like scalp and diaper rash: LCH staging, CD1a, BRAF pathwayDermatology / Paediatrics / Haematology-oncologyNextOSCE — skin as a window: map cutaneous signs to systemic diseaseDermatology / Internal medicine / Oncology