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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Severe cutaneous adverse reactions and burn-centre care

Dermatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Painful skin or mucosal loss

Skin pain, dusky atypical targets, blisters, detachment or erosions at mouth, eyes or genital mucosa after a medicine can herald SJS/TEN; shock, hypoxia, oliguria, confusion or rapidly rising organ tests signals acute skin and multiorgan failure.

Action: Stop suspected culprit medicine immediately, assess ABCDE and airway, obtain urgent dermatology and critical-care review, discuss rapid transfer to an age-appropriate Burns Centre or specialised dermatology centre co-located with intensive care, and begin warm, gentle, non-adhesive supportive care without waiting for biopsy.

Overview

Recognise SJS/TEN, DRESS and AGEP early, stop the most likely culprit safely, distinguish epidermal loss from mimics, and deliver multidisciplinary skin-failure, mucosal, ocular and organ care through the appropriate specialist centre.

SJS and TEN form a spectrum of immune-mediated keratinocyte death, usually medicine triggered. A flu-like prodrome may precede painful dusky macules, atypical flat targets and blistering. Epidermis shears with gentle lateral pressure and mucosal epithelium erodes, often at several sites. Classification uses the maximum detached or detachable body surface, not total erythematous rash. The deeper colour change can be subtle in richly pigmented skin, so pain, texture, mucosal examination and serial mapping are essential. Erythema multiforme usually has raised classic acral targets with limited detachment and is often infection associated, but diagnostic uncertainty with mucosal loss still warrants urgent review.

DRESS and AGEP are different severe reactions. DRESS has a longer latency and systemic footprint: facial oedema, fever, diffuse infiltration, nodes, eosinophilia or atypical lymphocytes and hepatitis predominate, but nephritis, pneumonitis, myocarditis, thyroiditis and other injury can emerge or relapse after drug withdrawal. AGEP develops more rapidly, particularly after antimicrobials, with pinhead sterile pustules, flexural accentuation, neutrophilia and relatively rapid resolution. Overlap exists; labels are assigned through drug chronology, clinical criteria, serial organ tests and histopathology rather than a single blood count.

Practice

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DermatologyOriginal SBA

Painful mucosal blistering

Twelve days after lamotrigine was increased, a patient develops fever, severe skin pain, dusky atypical targets, oral erosions and new epidermal blistering. What is the best immediate action?

Choose one answer, then submit
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Sources and review status5 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • PubMed record for UK adult SJS TEN guidelineCulprit withdrawal, SCORTEN, specialist setting, fluids, wounds, infection, eye and mucosal care, active-therapy uncertainty and follow-up.
  • BAD SJS TEN patient leafletCurrent patient-facing recognition, causes, hospital treatment and long-term medicine avoidance.
  • BAD highly specialised service specificationAge-specific Burns Centre or specialised dermatology centre co-located with intensive-care requirement for SJS/TEN.
  • NICE drug allergy recommendationsRecognition of SJS/TEN, DRESS and AGEP, structured documentation, information sharing and specialist referral.
  • MHRA Yellow Card schemeNational reporting route for suspected serious adverse drug reactions and device incidents.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Extensive epidermal loss resembles a superficial burn but has lower fluid requirements than a thermal injury and uniquely threatens every mucosal surface. English specialised-service standards place SJS/TEN in an age-specific Burns Centre or specialised dermatology centre co-located with age-specific intensive care. Dermatology or plastic surgery coordinates with critical care, ophthalmology, nursing, pharmacy, microbiology, pain, nutrition and oral, respiratory and urogenital specialists. The immediate determinants of outcome are rapid culprit withdrawal, specialist transfer and consistently executed supportive care; active systemic therapy remains a specialist MDT decision.

Key points

  • SJS/TEN typically causes prodrome, disproportionate skin pain, dusky macules or atypical targets, flaccid blisters, epidermal detachment and prominent ocular, oral or genital erosions.
  • Classify by detached or detachable surface: SJS below 10%, overlap 10% to 30%, and TEN above 30%; extent can evolve after presentation and must be remapped.
  • DRESS usually emerges two to eight weeks after starting a culprit with fever, widespread eruption, facial oedema, nodes, eosinophilia or atypical lymphocytes and liver, kidney, lung or cardiac injury.
  • Build a calendar of every medicine started, increased, intermittently taken or stopped in the previous two months, including antimicrobials, anticonvulsants, allopurinol, analgesics and non-prescription products.
  • Withdraw likely culprit treatment immediately but do not create avoidable harm by indiscriminately stopping physiological corticosteroid, antiseizure cover or another essential medicine without a safe substitute.
  • SJS/TEN care prioritises culprit withdrawal and meticulous multidisciplinary support; no single systemic immunomodulator has conclusive superiority over high-quality conservative care in the UK guideline.
  • Early ophthalmology, daily eye, mouth and urogenital review, respiratory surveillance, individualised fluids, enteral nutrition, pain control and non-traumatic wound care prevent lifelong disability as well as death.

Aetiology

01

High-risk medicines

Anticonvulsants, allopurinol, sulfonamide antimicrobials, some NSAIDs, antiretrovirals and other agents can trigger delayed T-cell reactions, with risk shaped by exposure timing and host genetics.

02

Infection-associated mimic or trigger

Mycoplasma or viral mucositis and erythema multiforme may resemble SJS, while acute infection can also complicate drug-induced epidermal loss and alter treatment.

03

Uncertain or multiple exposure

Polypharmacy, intermittent dosing and medicines stopped before eruption obscure attribution; a structured latency calendar prevents the newest or most familiar drug being blamed reflexively.

Pathophysiology

  1. 1
    Drug-specific T cells activate

    A drug, metabolite or pharmacological interaction with immune receptors activates cytotoxic T cells in susceptible individuals after a characteristic sensitisation period.

  2. 2
    Keratinocytes undergo death

    Cytotoxic mediators including granulysin and death-receptor signalling cause widespread full-thickness epidermal necrosis, separation and mucosal epithelial loss in SJS/TEN.

  3. 3
    Barrier loss drives physiology

    Denuded dermis loses fluid, heat and protein, permits microbial invasion and produces high metabolic demand, haemodynamic instability and severe nociceptive pain.

  4. 4
    DRESS inflammation enters organs

    A prolonged drug-specific immune response, sometimes accompanied by herpesvirus reactivation, recruits eosinophils and lymphocytes into liver, kidney, lung, heart and endocrine tissue.

  5. 5
    AGEP recruits neutrophils

    Drug-driven cytokines attract neutrophils rapidly into superficial epidermis, creating many sterile pustules with fever and leukocytosis but less full-thickness necrosis than TEN.

Clinical features and red flags

SJS or TEN

Severe skin pain, dusky macules or atypical targets, flaccid blisters, sheet-like detachment and acute erosive mucositis after a high-risk medicine define the core syndrome.

Ocular involvement

Grit, photophobia, red eye, discharge, lid-margin ulceration or reduced vision may progress quickly to conjunctival scarring, dry eye and irreversible corneal damage.

Airway involvement

Hoarseness, cough, dyspnoea, hypoxia, increased secretions or haemoptysis can reflect sloughing respiratory epithelium and predict a need for rapid critical-care intervention.

DRESS pattern

Delayed fever, diffuse infiltrated eruption, prominent facial oedema, lymphadenopathy, eosinophilia or atypical lymphocytes with liver, renal, lung or cardiac injury supports DRESS.

AGEP pattern

Abrupt sheets of tiny sterile non-follicular pustules beginning in folds, with fever and neutrophilia shortly after a medicine, suggests acute generalised exanthematous pustulosis.

Hidden skin-tone change

Grey, purple-brown or minimally red tender skin may already be necrotic; examine reflected light, texture, blisters and mucosae and compare with the patient's baseline.

Acute skin failureRed flag

Hypothermia, tachycardia, hypotension, oliguria, confusion, severe pain, expanding detachment or hypoxia indicates barrier and organ failure regardless of the named SCAR.

Red flags requiring action

Investigations

  1. 01
    Medicine chronology and causality assessmentFirst step
    Why
    Identify the likely culprit quickly enough to reduce ongoing injury.
    Interpretation and limitations
    Plot exact start, dose change, intermittent exposure and stop dates over at least 8 weeks, compare known latency and notoriety, and include medicines already stopped before the rash.
  2. 02
    Full skin and mucosal surface map
    Why
    Classify SJS/TEN and detect evolving eye, oral, genital and airway disease.
    Interpretation and limitations
    Record total rash and detached or detachable surface separately on a body chart, photograph with consent, and repeat daily because SJS can evolve into overlap or TEN.
  3. 03
    Skin biopsies
    Why
    Confirm epidermal necrosis and exclude immunobullous or other mimicking disease.
    Interpretation and limitations
    Send lesional skin in formalin for routine histology and a separate perilesional specimen in the correct medium for direct immunofluorescence; treatment and transfer do not await results.
  4. 04
    Full blood count and film
    Why
    Detect eosinophilia, atypical lymphocytes, neutrophilia, cytopenia and prognostic abnormalities.
    Interpretation and limitations
    Eosinophilia can appear late in DRESS and also occur in AGEP; neutropenia increases infection risk, while any blood pattern must be integrated with organs, timing and biopsy.

Differential diagnosis

01

Erythema multiforme major

Raised typical three-zone acral targets, an infectious trigger and limited detachment favour erythema multiforme, although severe mucositis still needs specialist assessment.

02

Generalised bullous fixed drug eruption

Sharply demarcated recurrent dusky plaques at previous sites, shorter re-exposure latency and islands of unaffected skin suggest bullous fixed drug eruption.

03

Autoimmune blistering disease

Pemphigus, bullous pemphigoid, linear IgA disease and paraneoplastic pemphigus are separated by morphology, histology and perilesional direct immunofluorescence.

04

Staphylococcal scalded skin

Superficial toxin-mediated cleavage, periorificial fissuring and absent mucosal erosions, particularly in children or renal failure, contrast with full-thickness SJS/TEN necrosis.

05

GPP or AGEP

Pustules, psoriasis history, drug latency, eosinophilia, flexural distribution, histology and time to resolution distinguish generalised pustular psoriasis from acute drug pustulosis.

Management

01First-line emergency sequenceStop culprit and transfer earlyFirst stepFirst linePainful blistering, epidermal loss or severe mucositis raises SJS/TEN or another SCAR.+
  1. 1Stop the likely culprit immediately, preserve essential treatment with safe alternatives, assess ABCDE and airway, weigh the patient and map skin and every mucosal site.
  2. 2Contact dermatology, critical care and the regional specialised service early; arrange care in an age-specific Burns Centre or dermatology centre co-located with intensive care.
  3. 3Obtain histology and immunofluorescence biopsies, FBC, metabolic and organ profiles, cultures and imaging without delaying transfer or supportive treatment.
  4. 4Calculate SCORTEN within 24 hours, record causality reasoning and notify ophthalmology immediately so the first formal eye examination occurs within 24 hours.
02Gold-standard supportive careProtect every failing surface

Complications

01

Sepsis and multiorgan failure

Colonised denuded dermis can seed bloodstream infection, while fluid loss and inflammation contribute to shock, renal injury, respiratory failure and death.

02

Ocular surface destruction

Acute conjunctival epithelial loss forms adhesions and scars, leading to severe dry eye, trichiasis, corneal opacity, infection and permanent visual impairment.

03

Mucosal stenosis

Oral, genital, urinary and gastrointestinal erosions can heal with adhesions, painful intercourse, urinary obstruction, swallowing difficulty and chronic mucosal dryness.

04

Respiratory epithelial loss

Bronchial sloughing can obstruct airways, cause atelectasis and require ventilation; later bronchiolitis obliterans or chronic functional impairment may persist.

05

Delayed DRESS sequelae

Hepatitis, nephritis or myocarditis can relapse during taper, while thyroid disease and other autoimmune complications may arise months after apparent cutaneous recovery.

Monitoring and follow-up

  • Map detached and detachable surface, new lesions, skin pain and re-epithelialisation daily with standardised photographs and consent; record rash area separately from epidermal loss.
  • Monitor temperature, pulse, blood pressure, oxygen saturation, mental state, weight, fluid input, urine, pain and nutrition frequently and respond to trends before shock develops.
  • Perform and document daily ophthalmic, oral and urogenital review throughout the acute phase; any new respiratory symptom or hypoxia triggers immediate intensivist and airway discussion.
  • Trend FBC, renal, liver, bicarbonate, glucose, magnesium, phosphate, albumin and CRP, adding cardiac or lung markers when DRESS or respiratory epithelial disease is possible.
  • Sample suspicious skin and blood for infection and look for increased pain, a dominant organism, hypotension, oliguria, confusion or hypoxia; fever alone is not specific in SJS/TEN.
  • Reconcile allergy entries across care records and verify the patient can name the culprit, cross-reacting risks and safe alternatives before discharge.

Special situations

Pain precedes detachment

Disproportionate tenderness on dusky skin can announce keratinocyte necrosis before obvious blistering, making palpation and mucosal examination decisive early tests.

A low score cannot defer care

SCORTEN estimates mortality after the emergency is recognised; it neither excludes evolving disease nor substitutes for early specialist transfer and surveillance.

Burn care is not burn arithmetic

The environment, nursing and wound expertise are valuable, but epidermal necrolysis usually requires less fluid than Parkland calculations predict for thermal injury.

Eosinophilia can arrive late

An initially normal eosinophil count does not exclude DRESS when latency, facial oedema and organ injury fit, so serial blood counts matter.

Active therapy remains unsettled

IVIg, systemic corticosteroids and ciclosporin have advocates, but the UK guideline found no conclusive superior intervention and prioritises specialist-governed supportive care.

Healing skin is not full recovery

Ocular scarring, genital stenosis, respiratory disease, pigment change, chronic pain, fatigue and psychological trauma may emerge after re-epithelialisation.

Common pitfalls

  1. 01

    Calling a painful mucosal eruption erythema multiforme without mapping detachable epidermis and reviewing high-risk medicines.

  2. 02

    Waiting for biopsy or a positive Nikolsky sign before stopping the probable culprit and arranging specialist transfer.

  3. 03

    Under-recognising necrosis because early inflammation is grey or violaceous rather than bright red in darker skin.

  4. 04

    Counting the whole erythematous rash as detached surface and misclassifying SJS/TEN severity.

  5. 05

    Using a Parkland formula unchanged and causing pulmonary, intestinal or cutaneous oedema through over-resuscitation.

  6. 06

    Giving prophylactic systemic antibiotics for colonised skin without clinical infection.

  7. 07

    Using one normal eosinophil count to exclude DRESS despite evolving hepatitis and facial oedema.

  8. 08

    Starting unproven systemic immune therapy outside the specialist skin-failure MDT while supportive tasks are incomplete.

  9. 09

    Recording allergy as antibiotics or rash instead of the exact culprit, phenotype, date, severity and safe alternatives.

  • Do not give routine prophylactic systemic antibiotics; culture strategically and treat clinical infection, because indiscriminate exposure selects Candida and resistant colonisation.
  • Document the exact culprit and drugs to avoid, notify every care setting and report through MHRA Yellow Card; specialist allergy input is needed when causality remains uncertain or broad avoidance compromises care.
    • Skin pain, epidermal tenderness, dusky or blistering targets, positive shearing, any mucosal erosion, facial oedema with fever, eosinophilia or organ injury, pustules with systemic illness, hypotension, hypoxia, oliguria, confusion, rising transaminases, myocarditis symptoms or a rapidly spreading eruption requires same-day hospital and dermatology assessment.
  • 05
    Serial organ and metabolic profile
    Why
    Find DRESS involvement and quantify acute skin-failure physiology.
    Interpretation and limitations
    Repeat urea, creatinine, electrolytes, bicarbonate, glucose, magnesium, phosphate, liver tests, albumin and CRP; add troponin, ECG, echocardiography, gas or imaging to symptoms.
  • 06
    SCORTEN within 24 hours
    Why
    Estimate mortality risk and inform the intensity of SJS/TEN monitoring.
    Interpretation and limitations
    Score age over 40, malignancy, pulse over 120, detachment over 10%, urea over 10 mmol/L, glucose over 14 mmol/L and bicarbonate below 20 mmol/L; never use a low score to delay transfer.
  • 07
    Microbiology and sepsis assessment
    Why
    Detect invasive infection without treating colonisation indiscriminately.
    Interpretation and limitations
    Culture blood for sepsis and sample several sloughy or crusted skin sites serially; a newly predominant organism plus rising pain, hypotension, oliguria or hypoxia increases invasive-infection concern.
    • SJS/TEN is suspected or confirmed in specialist care.
    +
    1. 1Nurse in a warm side room with barrier precautions, minimise shear and adhesives, place lines through unaffected skin when possible and deliver background and procedural analgesia.
    2. 2Clean gently with warmed saline, cover with greasy emollient and non-adherent dressings and let the skin-failure MDT choose conservative or surgical wound management daily.
    3. 3Guide fluid by perfusion, urine, weight, electrolytes and lactate because SJS/TEN usually needs less than a Parkland thermal-burn calculation; start early enteral nutrition when oral intake fails.
    4. 4Provide daily eye, mouth and urogenital examinations, respiratory monitoring, thrombosis and pressure protection and systemic antibiotics only for clinical infection with microbiology advice.
    03DRESS organ sequenceTrack injury beyond the rashDelayed eruption with fever, facial oedema, eosinophilia, nodes or organ-test abnormality suggests DRESS.+
    1. 1Withdraw the likely culprit and seek dermatology and the relevant organ-specialist input, admitting systemic disease even when skin detachment is limited.
    2. 2Trend blood count, liver, kidney and inflammatory tests and screen heart, lung, thyroid and other organs from symptoms and culprit profile; abnormalities may evolve after withdrawal.
    3. 3Use topical therapy for skin symptoms and reserve systemic corticosteroid or another immunomodulator for specialist assessment of significant organ disease, infection risk and a slow relapse-aware taper.
    4. 4Continue post-discharge organ and thyroid surveillance, document avoidances precisely and do not perform unsupervised re-exposure or challenge.
    04Discharge safetyMake re-exposure difficultAcute skin and organ disease has stabilised enough for transfer or discharge.+
    1. 1Give a plain-language written diagnosis, exact culprit and related drugs to avoid, reaction date, uncertainties and safe alternatives; update electronic records and the GP.
    2. 2Submit an MHRA Yellow Card and arrange specialist drug-allergy or dermatology investigation when attribution is uncertain or broad avoidance compromises future care.
    3. 3Arrange early eye and dermatology or burns follow-up plus oral, genital, respiratory, psychological and organ-specific care, explaining that late scarring and DRESS relapse can occur.
    Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
    Provides a greasy non-adherent barrier that limits friction and evaporative loss while conservative re-epithelialisation proceeds.

    White soft paraffin and liquid paraffin 50:50 ointment

    Apply gently over intact and denuded epidermis after warmed cleansing and whenever the surface dries, generally at least every 4 hours during acute specialist care.

    Application can shear fragile epidermis, so use experienced nursing or aerosolised delivery when appropriate; paraffin-contaminated linen and dressings are a major fire hazard and require strict flame avoidance.

    Reduces hospital-associated venous thromboembolism during immobility, systemic inflammation and critical illness alongside mechanical and mobilisation measures when tolerated.

    Weight-adjusted LMWH thromboprophylaxis

    Give the hospital protocol's prophylactic subcutaneous dose once daily, adjusted for body weight and renal function, while mobility is substantially reduced unless contraindicated.

    Review active bleeding, severe thrombocytopenia, renal impairment and imminent procedures each day; extensive skin loss changes injection-site choice, and therapeutic anticoagulation requires a separate indication.