Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Stevens-Johnson syndrome and toxic epidermal necrolysis
Dermatology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Epidermal necrolysis emergency
Skin pain, dusky atypical targets, blistering, detachment and erosive mucositis after medicine exposure indicate potential SJS or TEN with rapidly evolving skin failure.
Action: Stop suspected non-essential medicines immediately, admit to an experienced high-dependency environment and involve dermatology, critical care, ophthalmology and affected-mucosal specialties.
Overview
Recognise painful mucocutaneous epidermal necrolysis early, stop culprit medicines, quantify detachment, and coordinate intensive supportive and specialist care.
The early syndrome resembles influenza followed by severe skin tenderness, dusky macules or atypical flat targets and rapidly developing erosions. Bright redness can be muted in deeply pigmented skin; pain, grey-purple colour and epidermal texture are crucial. At least two mucosal sites are often involved, but morphology and biopsy matter more than a rigid count.
Estimate only detached and detachable epidermis when classifying SJS and TEN, and record total erythematous area separately. Calculate SCORTEN during the first twenty-four hours and repeat according to specialist practice, but do not use a low score to delay transfer. Histology from a fresh edge can confirm full-thickness epidermal necrosis and exclude mimics.
Clinical decisions in Stevens-Johnson syndrome and toxic epidermal necrolysis depend on trajectory and consequence. Re-examine evolving skin, repeat focused systemic assessment when the patient changes, and reconcile every result with morphology and timing; a normal early test cannot neutralise worsening pain, mucosal injury or organ dysfunction.
Key points
Aetiology
01
Medicine-triggered cytotoxicity
High-risk antimicrobials, anticonvulsants, allopurinol, some NSAIDs and other medicines trigger most cases, usually within the first weeks of exposure.
02
Infectious associations
Mycoplasma and viral illnesses can produce mucositis or erythema multiforme-like syndromes, particularly in younger people, and require careful classification.
03
Host susceptibility
Specific HLA alleles, ancestry, renal impairment and drug dose modify risk for selected culprit medicines, but universal screening is not available for every exposure.
Pathophysiology
1
Keratinocyte apoptosis
Drug-specific cytotoxic lymphocytes and soluble mediators including granulysin drive widespread programmed death of epidermal keratinocytes across affected skin and mucosa.
2
Epidermal cleavage
Confluent cell death separates epidermis from dermis, producing tender dusky skin, flaccid bullae and sheets of detachment analogous to a major burn.
3
Mucosal epithelial injury
Oral, ocular, genital and respiratory epithelia ulcerate, causing pain, fluid loss, infection exposure and long-term scarring.
4
Systemic stress
Barrier failure drives heat and fluid loss, catabolism, infection risk and multiorgan dysfunction, while underlying drug hypersensitivity may affect internal organs.
Clinical features and red flags
Pain before detachmentRed flag
Marked skin tenderness or burning out of proportion to visible change is an early warning for evolving epidermal necrosis.
Dusky atypical targets
Flat irregular targetoid macules with two poorly defined zones become confluent on face and trunk and may develop central blisters.
Multisite mucositis
Painful oral, ocular, genital or urinary erosions impair drinking, vision and voiding and require specialty-specific examination.
Epidermal shearing
Gentle pressure may displace necrotic epidermis, but repeated testing adds injury and is unnecessary once detachment is evident.
Physiological skin failureRed flag
Hypothermia, tachycardia, hypotension, oliguria and rising oxygen requirement indicate critical barrier and organ dysfunction.
01Medicine chronology and culprit assessmentFirst step
Why
Stop high-risk exposures and estimate causality from start dates, withdrawal and half-life.
Interpretation and limitations
Include recently stopped and intermittent medicines; do not re-expose to prove a suspected association.
02Two-site body-surface assessment
Why
Classify detachment and separately document the total inflamed area.
Interpretation and limitations
Use a burn chart or palm method consistently and reassess because detachment evolves; confluent erythema alone is not detached surface.
03Skin biopsy from a fresh lesion edge
Why
Confirm full-thickness epidermal necrosis and exclude key blistering mimics.
Interpretation and limitations
Send routine histology promptly and arrange separate immunofluorescence tissue if autoimmune disease remains plausible.
04SCORTEN and serial organ tests
Why
Estimate mortality risk and direct intensive monitoring.
Interpretation and limitations
Record age, malignancy, heart rate, detached surface, urea, glucose and bicarbonate at the correct time; scores support but never replace clinical escalation.
05
Differential diagnosis
01
Erythema multiforme major
Typical raised acral targets often associated with herpes differ from the truncal atypical targets, skin pain and confluent necrosis of SJS or TEN.
02
Generalised bullous fixed eruption
Recurrent sharply fixed plaques after the same medicine can blister widely, and previous site-specific pigment history helps separation.
03
Staphylococcal scalded skin syndrome
Superficial toxin-mediated cleavage usually spares mucosa and occurs in different host contexts; histology identifies the anatomical split.
04
Autoimmune blistering disease
Pemphigus and pemphigoid can cause erosions or bullae but usually differ in tempo, morphology, immunofluorescence and medicine latency.
Management
01Suspected epidermal necrolysisStop drugs and transfer earlyFirst stepSkin pain, dusky targetoid lesions, mucosal erosions or detachment appears after a plausible medicine.+
1Withdraw plausible culprit and non-essential medicines, document exact exposure dates and obtain emergency dermatology plus critical-care assessment.
2Biopsy a fresh representative edge when safe, measure detached and detachable surface and initiate physiological monitoring without awaiting pathology.
3Transfer early to the locally designated experienced setting because transport becomes harder after extensive skin failure develops.
02Intensive supportive careProtect organs and denuded surfacesSJS, overlap or TEN is confirmed or remains the leading diagnosis during progression.+
1Use a warm environment, carefully titrated fluid, enteral nutrition where possible, multimodal analgesia and atraumatic non-adherent wound care.
Complications
01
Sepsis and organ failure
Loss of barrier, invasive devices and critical illness increase bacterial infection, shock, renal injury, respiratory failure and death.
02
Ocular scarring
Acute conjunctival epithelial loss can lead to symblepharon, dry eye, corneal damage and sight loss without early specialist care.
03
Genitourinary adhesions
Erosive genital and urinary involvement can heal with stenosis, adhesions, dyspareunia and obstructive symptoms unless actively managed.
04
Psychological and medicine harm
Trauma, chronic pain, visible scarring and fear of future prescribing persist, while imprecise culprit records may deny necessary unrelated treatments.
Monitoring and follow-up
During acute SJS or TEN, record fluid balance, temperature, pain, nutrition, respiratory status, detachment and infection indicators at least daily.
Repeat ocular and genital examination through the acute phase because new epithelial injury may develop after admission.
After discharge, monitor vision, dry eye, oral intake, urinary and sexual function, scarring, pigment change and psychological recovery.
At every review of Stevens-Johnson syndrome and toxic epidermal necrolysis, record lesion evolution, new mucosal or systemic features, medicine changes, treatment adherence and adverse effects.
Give a named route for urgent reassessment if breathing, circulation, fever, skin pain, blistering, facial swelling, reduced urine output or other organ symptoms develop during Stevens-Johnson syndrome and toxic epidermal necrolysis.
Special situations
Detached area is not all redness
Classification counts detached or easily detachable epidermis; the wider inflamed field should be documented separately.
Eyes cannot wait
Early ophthalmic intervention can reduce permanent ocular surface scarring even when the patient reports little initial discomfort.
Pain is an early biomarker
Severe tenderness may precede visible blistering and is more concerning than itch in a drug eruption.
Antibiotics are evidence-led
Denuded skin becomes colonised, but prophylactic systemic antibiotics can select resistance without preventing all sepsis.
Recovery involves every mucosa
Skin closure does not end care for ocular dryness, genital adhesion, oral stenosis or airway sequelae.
Common pitfalls
01
Waiting for more than ten percent detachment before acting on an early painful mucocutaneous syndrome.
02
Counting every erythematous area as detached surface and misclassifying severity.
03
Using systemic antibiotic prophylaxis automatically in the absence of clinical infection.
04
Delaying ophthalmology until corneal symptoms become severe.
05
Recording suspected penicillin allergy only when several simultaneous high-risk medicines have not been causally ranked.
Practice
Two practice questions
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Question 1 of 2
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DermatologyOriginal SBA
Painful mucocutaneous eruption
A patient has fever, severe skin tenderness, dusky truncal macules and painful mouth and eye erosions twelve days after starting a high-risk medicine. What is the immediate management priority?
Sources and review status3 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Apply principles in context and verify current guidance when a decision affects care. Source check completed 27 Aug 2026; clinical approval remains outstanding.
Painful skin, fever and mucosal erosion often precede obvious detachment; do not wait for large blisters to suspect SJS or TEN.
SJS involves under ten percent detached or detachable body surface, overlap ten to thirty percent, and TEN more than thirty percent.
Stop likely culprit and non-essential medicines immediately, using a dated timeline because latency and drug half-life influence causality.
Transfer to an experienced intensive, burns or specialist dermatology environment according to local pathways before avoidable deterioration.
Support temperature, fluid, nutrition, pain, wounds and thrombosis prevention; avoid routine prophylactic systemic antibiotics without infection evidence.
Obtain ophthalmology review within the acute phase even when eye symptoms initially appear mild, and assess oral, genital and urinary mucosa.
Stevens-Johnson syndrome and toxic epidermal necrolysis must be assessed by lesion duration, onset, distribution, symptoms, mucosal findings, systemic physiology and the full medicine timeline rather than by colour alone.
For Stevens-Johnson syndrome and toxic epidermal necrolysis, document the working diagnosis, excluded emergencies, uncertain culprit or trigger, treatment response and the exact safety-net given.
Microbiology guided by infection evidence
Why
Identify sepsis in a high-risk barrier-failure patient.
Interpretation and limitations
Take cultures from clinically indicated sites before antibiotics when safe; routine surveillance growth from skin does not alone prove invasive infection.
2
Assess daily for infection and thrombosis risk, avoiding routine systemic antibiotic prophylaxis while treating proven or strongly suspected sepsis promptly.
3Coordinate acute ophthalmology, oral, gynaecology or urology care and respiratory review according to involved mucosal surfaces.
03Recovery and future safetyPrevent scarring and re-exposureRe-epithelialisation has begun and the patient is leaving critical or inpatient care.+
1Continue eye, genital, oral, skin and psychological follow-up because functional scarring can emerge after apparent surface healing.
2Provide a precise culprit assessment and written avoidance plan, including cross-reactive medicines only when evidence supports that relationship.
3Explain residual pigment, nail shedding, fatigue and trauma symptoms and give direct access for late ocular or urinary deterioration.