Toxic Epidermal Necrolysis (TEN)

Toxic epidermal necrolysis is a life-threatening, delayed-type hypersensitivity reaction characterized by ≥30% body surface area (BSA) epidermal detachment, widespread mucosal erosions, and systemic toxicity, with mortality rates of 25–50%. [1-3] It represents the most severe end of the SJS/TEN spectrum and is a true dermatologic emergency requiring immediate recognition, drug withdrawal, and transfer to a burn/ICU center. [4-5]

The following figure illustrates the clinical spectrum from SJS to TEN based on extent of epidermal detachment:

1. History

• Medication exposure within 4–28 days is the single most critical HPI element — obtain a complete drug list including new prescriptions, OTCs, and supplements [2][7]
• Prodromal phase: 1–3 days of fever, malaise, myalgias, sore throat, cough ("flu-like" symptoms) preceding skin findings [1][7]
• Skin pain often described as burning, disproportionate to visible findings early on
• Mucosal symptoms: odynophagia, dysuria, eye pain/photophobia, genital pain [7]
• Progression: erythematous macules → atypical targetoid lesions → confluent blisters → sheet-like epidermal sloughing [7]
• Ask about prior episodes of SJS/TEN, known drug allergies, and any recent infections (especially Mycoplasma pneumoniae) [8-9]

2. Alarm Features

• Rapidly progressive skin detachment (>10% BSA and expanding)
• Positive Nikolsky sign (epidermis sloughs with lateral pressure on erythematous skin) [2][10]
• Mucosal involvement of ≥2 sites (oral, ocular, genital) [7]
• Respiratory distress — suggests bronchial epithelial involvement or aspiration [7]
• Hemodynamic instability, high-output fluid losses
• Signs of sepsis (leading cause of death in TEN) [1][7]
• Altered mental status, oliguria, or DIC [11]

3. Medications

High-risk culprit drugs (onset typically 4–28 days after initiation): [1][8][12]

• Anticonvulsants: carbamazepine, phenytoin, lamotrigine, phenobarbital
• Allopurinol
• Sulfonamide antibiotics: TMP-SMX
• NSAIDs (oxicam type especially)
• Antibiotics: β-lactams, fluoroquinolones, cephalosporins
• Others: nevirapine, immune checkpoint inhibitors [13]

Contraindicated: Thalidomide — an RCT was stopped early due to increased mortality in TEN. [14] Prophylactic systemic antibiotics are not recommended without evidence of infection. [5]

Systemic therapies (controversial, no consensus): [14-15]

• Cyclosporine 3–5 mg/kg/day (some evidence of mortality benefit vs. IVIG) [7][15]
• Systemic corticosteroids (pulse methylprednisolone 1–2 mg/kg/day) [7][13]
• IVIG 2 g/kg over 2–5 days [13][16]
• Etanercept (single dose 25–50 mg SC) — emerging data showing possible benefit [7][15][17]

4. Diet

• NPO initially if significant oral mucosal involvement or airway concerns
• Early enteral nutrition via NG/NJ tube if unable to tolerate PO — critical for wound healing and metabolic demands [5]
• High-calorie, high-protein diet (similar to burn nutrition protocols) [5]
• Aggressive IV fluid resuscitation — use burn-like fluid calculations but typically less than equivalent BSA burns (Parkland formula adjusted to ~2/3 of burn estimates) [5]
• Gastric ulcer prophylaxis recommended [5]

5. Review of Systems

• Skin: rash distribution, blistering, pain, peeling
• Eyes: redness, tearing, photophobia, blurred vision, discharge (ocular involvement in 40–84% of cases) [18]
• Oral: odynophagia, oral erosions, inability to eat/drink
• GU: dysuria, genital erosions, urinary retention
• Respiratory: cough, dyspnea, stridor (bronchial epithelial sloughing)
• GI: diarrhea, abdominal pain (GI mucosal involvement)
• Constitutional: fever, malaise, weight loss
• Psychiatric: anxiety, fear (PTSD develops in ~30–50% of survivors) [7][19]

6. Collateral History and Family History

• Confirm exact medication names, doses, and start dates from pharmacy records
• Prior drug allergies or adverse drug reactions — previous drug allergy is a significant risk factor (OR 5.21) [12]
• Family history of SJS/TEN or drug hypersensitivity reactions
• Ethnic background — relevant for HLA-associated risk:
  • HLA-B15:02: carbamazepine-induced SJS/TEN (Southeast Asian/Han Chinese ancestry) [7][20]
  • HLA-B58:01: allopurinol-induced SJS/TEN (higher prevalence in Black and Asian populations) [21]
  • HLA-A31:01: carbamazepine-induced SCARs (Northern European, Japanese) [7][20]
• HIV status (increased SJS/TEN risk) [6]

7. Risk Factors

• New medication within past 4–28 days (most important risk factor) [2]
• HIV/AIDS (100-fold increased incidence) [3]
• Active malignancy [12][22]
• Autoimmune disease: SLE (OR 17.41), psoriasis (OR 10.28) [12]
• Prior drug allergies (OR 5.21) [12]
• Epilepsy (OR 4.92 — likely confounded by anticonvulsant use) [12]
• Diabetes mellitus, history of CVA [12]
• Genetic susceptibility (HLA alleles as above) [7]
• Slow acetylator phenotype [3]
• Concurrent radiation therapy

8. Differential Diagnosis

• Staphylococcal scalded skin syndrome (SSSS): superficial (subcorneal) cleavage plane vs. full-thickness necrosis in TEN; no mucosal involvement; more common in infants; Nikolsky sign positive but biopsy distinguishes [23-24]
• Erythema multiforme major: typical target lesions with 3 concentric rings, acral distribution, often HSV-related [6-7]
• Generalized bullous fixed drug eruption (GBFDE): well-demarcated round plaques, eosinophils on biopsy, dermal melanophages [23]
• Acute graft-versus-host disease: requires transplant history; satellite cell necrosis on biopsy [23]
• Linear IgA bullous dermatosis: positive direct immunofluorescence (linear IgA at BMZ) [7][23]
• Paraneoplastic pemphigus: positive DIF distinguishes [24]
• AGEP: subcorneal pustules, less mucosal involvement [24]
• Autoimmune blistering diseases (pemphigus vulgaris, bullous pemphigoid): DIF positive [3]
• Drug hypersensitivity syndrome/DRESS: eosinophilia, organ involvement, less epidermal detachment [10]

9. Past Medical History

• Prior SJS/TEN episodes (absolute contraindication to re-exposure to culprit drug)
• Autoimmune conditions (SLE, psoriasis)
• Malignancy (especially if on chemotherapy or immunotherapy)
• HIV/immunosuppression
• Chronic kidney disease (affects drug clearance and prognosis)
• Epilepsy and current anticonvulsant regimen
• Gout and allopurinol use
• Prior HLA testing results

10. Physical Exam

Vital signs: Fever (often >38.5°C), tachycardia, hypotension in severe cases

Skin:

• Dusky erythematous or violaceous macules, often starting on face/trunk [7]
• Atypical targetoid lesions (flat, irregular, dusky center — NOT classic EM targets) [2]
• Flaccid bullae, confluent epidermal detachment in sheets
• Nikolsky sign: positive on erythematous areas [7][10]
• Asboe-Hansen sign: lateral extension of blister with pressure
• Estimate %BSA detachment (TEN = ≥30%) [1][8]

Mucosal exam (involved in ~80% of cases): [7]

• Oral: hemorrhagic erosions, pseudomembranes, crusted lips
• Ocular: conjunctival hyperemia, pseudomembranes, chemosis, corneal erosions [7][18]
• Genital/urethral: erosions, dysuria
• Nasal/pharyngeal: erosions

Systemic: Lung auscultation (crackles suggest bronchial involvement), abdominal exam

11. Lab Studies

• CBC: lymphopenia is characteristic and predictive of SJS/TEN; neutrophilia may indicate secondary infection [10]
• BMP/CMP: BUN/creatinine (renal function — SCORTEN parameter), glucose >252 mg/dL (SCORTEN), bicarbonate <20 mmol/L (SCORTEN/ABCD-10) [25-26]
• LFTs: transaminases often elevated (hepatic involvement)
• Coagulation studies: PT/INR, fibrinogen, D-dimer (DIC screening) [11]
• Blood cultures: if sepsis suspected
• Lactate: sepsis workup
• Serum albumin: marker of severity and nutritional status
• Procalcitonin: may help distinguish infection from sterile inflammation
• Mycoplasma pneumoniae serology/PCR: especially in children or cases without drug trigger [8]

12. Imaging

• Chest X-ray: baseline and if respiratory symptoms present — evaluate for pneumonia, ARDS, bronchial epithelial sloughing [27]
• CT chest if concern for pulmonary complications not seen on CXR
• Imaging is NOT diagnostic for TEN — diagnosis is clinical [4]
• Imaging is primarily used to identify complications (pneumonia, effusions)

13. Special Tests

Diagnostic:

• Skin biopsy: full-thickness epidermal necrosis with subepidermal cleavage; sparse dermal inflammatory infiltrate [3][7]
• Direct immunofluorescence (DIF): negative — essential to rule out autoimmune blistering diseases [7]
• Frozen section biopsy: can provide rapid confirmation in the ED/ICU setting

Scoring systems:

• SCORTEN (Score of Toxic Epidermal Necrolysis): 7 parameters assessed within 24 hours of admission — predicts in-hospital mortality [8][25][28]
  • Age >40, malignancy, HR >120, initial BSA detachment >10%, BUN >28 mg/dL, glucose >252 mg/dL, bicarbonate <20 mmol/L
  • Score 0–1: 3.2% mortality; Score ≥5: 90% mortality [1][14]
• ABCD-10: alternative scoring (age, bicarbonate, cancer, dialysis, 10% BSA) [25-26]
• ALDEN score: algorithm to identify the most likely culprit drug when multiple drugs are involved [2]

Pharmacogenomic testing (pre-prescription screening): [20]

• HLA-B15:02 before carbamazepine in patients of Southeast Asian descent (FDA-recommended) [20]
• HLA-B58:01 before allopurinol (ACR-recommended in high-risk populations) [21]

14. ECG

• ECG is indicated to evaluate for tachycardia (SCORTEN parameter: HR >120 bpm) and to screen for cardiac complications [22]
• Myocardial involvement is uncommon acutely but case reports describe myocardial infarction during acute TEN [11]
• SJS/TEN survivors have elevated long-term cardiovascular morbidity and mortality persisting 4–7 years post-event, attributed to sustained proinflammatory and hypermetabolic states [11]
• Monitor for DIC-related cardiac complications [11]

15. Assessment

TEN is classified by ≥30% BSA epidermal detachment (SJS <10%, overlap 10–30%). [1][8] It is a delayed-type (Type IV) hypersensitivity reaction mediated by drug-specific cytotoxic T cells and NK cells, with granulysin as the key effector molecule causing keratinocyte apoptosis. [1][25]

Severity stratification: SCORTEN should be calculated within 24 hours and repeated at day 3. [25][28] Mortality ranges from 3.2% (SCORTEN 0–1) to 90% (SCORTEN ≥5). [1] Recent data suggest SCORTEN may overestimate mortality in contemporary cohorts due to improvements in supportive care. [25][28]

Complications to anticipate: sepsis (leading cause of death), ARDS, acute renal failure, DIC, GI hemorrhage, electrolyte derangements, and multiorgan failure. [1][7] Long-term sequelae affect >80% of survivors — cutaneous (82%), ocular (59%), oral (48%), and psychological (depression 49%, anxiety 47%, PTSD 37%). [19]

The following figure shows the frequency of long-term sequelae in SJS/TEN survivors:

16. Treatment Plan

Immediate stabilization (ED):

• Discontinue ALL suspected culprit drugs immediately — this is the single most impactful intervention [1][4][8]
• Airway assessment — early intubation if oropharyngeal/laryngeal involvement or respiratory distress [4]
• IV fluid resuscitation (crystalloid, burn-like protocols at ~2/3 Parkland formula) [5]
• Pain management (IV opioids often required; avoid NSAIDs if suspected culprit)
• Temperature regulation (warm environment, 28–32°C) [5]

Wound care:

• Nonadherent dressings; avoid debridement of intact blisters [5]
• Gentle handling — minimize shear forces
• Topical antiseptics; silver-based dressings may be used [17]

Mucosal care:

• Eyes: urgent ophthalmology consult; preservative-free lubricants, topical corticosteroid drops (0.1% betamethasone within 4 days of onset reduces sequelae), consider amniotic membrane transplantation [18][29]
• Oral: mouthwashes, topical anesthetics, soft diet
• GU: Foley catheter if urethral involvement; gynecology/urology consult [13]

Systemic immunomodulatory therapy (no consensus; institution-dependent): [14-15]

• Cyclosporine 3–5 mg/kg/day for 7–14 days — meta-analysis suggests mortality benefit vs. IVIG (RR 0.18) [15]
• Systemic corticosteroids: methylprednisolone 1–2 mg/kg/day — controversial but widely used [7][13]
• IVIG 2 g/kg over 2–5 days — evidence mixed; may be beneficial combined with corticosteroids [15-16]
• Etanercept 25–50 mg SC single dose — emerging evidence of benefit (RR 0.32 vs. supportive care) [7][15][17]
• Thalidomide is contraindicated (increased mortality) [14]

Supportive measures: DVT prophylaxis, stress ulcer prophylaxis, nutritional support, infection surveillance [5]

The following figure shows the distribution of culprit drugs and treatment approaches across European centers:

17. Disposition

• All patients with suspected TEN require admission — ideally to a burn unit or ICU with multidisciplinary access (burn surgery, dermatology, ophthalmology, critical care) [4-5]
• Transfer to a burn center if not available at presenting facility [4]
• SCORTEN ≥3 or BSA >10% detachment warrants ICU-level care [25]
• No patient with TEN should be discharged from the ED

Specialist consultations (all urgent): [4][13]

• Dermatology
• Ophthalmology
• Burn surgery
• Critical care/ICU
• Urology/gynecology (if GU involvement)
• Pulmonology (if respiratory involvement)

18. Follow Up / Return Precautions

Post-discharge follow-up (multidisciplinary, prolonged): [7][30]

• Dermatology: 2–4 weeks, then every 3–6 months for 1–2 years — monitor for cutaneous sequelae (dyspigmentation, scarring, nail dystrophy)
• Ophthalmology: within 1–2 weeks post-discharge and regularly for years — up to 65% develop chronic ocular complications (dry eye, symblepharon, corneal scarring, visual impairment) [7][18][31]
• Psychiatry/psychology: screen for PTSD, depression, anxiety — affects ~50% of survivors [19]
• Allergy/immunology: formal drug causality assessment (ALDEN score), documentation of culprit drug, MedicAlert bracelet [2]

Return precautions:

• Fever, new rash, worsening skin pain, eye redness/vision changes, difficulty breathing, signs of infection at wound sites
• Expected re-epithelialization: begins ~1 week after disease onset, completes in 2–3 weeks [7]

Lifelong precautions:

• Absolute avoidance of the culprit drug and structurally related compounds
• Pharmacogenomic testing and documentation in medical records
• Patient education regarding OTC medications (especially NSAIDs, cold medications) [32]
• Awareness of increased long-term cardiovascular risk [11]

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