Systemic Corticosteroids in Toxic Epidermal Necrolysis
Systemic corticosteroids are NOT routinely recommended for toxic epidermal necrolysis due to conflicting evidence on efficacy and significant concerns about increased infection risk, though early high-dose methylprednisolone (within 72 hours) may be considered in select cases. 1, 2
Evidence-Based Recommendation
The 2016 UK guidelines from the British Journal of Dermatology explicitly recommend against routine use of IV steroids in TEN, emphasizing that insufficient evidence supports their use and that infection risk is a major concern. 2 This represents the highest-quality guideline evidence available and should guide clinical decision-making.
Why Corticosteroids Are Controversial
No randomized controlled trials exist – all available evidence comes from retrospective case series with significant methodological limitations that cannot establish causation. 2, 3
Infection risk is the primary concern in patients who already have compromised skin barrier function from extensive epidermal loss, and corticosteroids may blunt the febrile response making infection detection more difficult. 2
Conflicting mortality data: Retrospective EuroSCAR analysis showed lower mortality in German patients treated with corticosteroids compared to supportive care alone, but this benefit was NOT seen in French patients, highlighting geographic and methodological inconsistencies. 2
Using systemic corticosteroids as sole therapy is not supported by current evidence. 3
If Corticosteroids Are Used Despite Guidelines
When clinicians choose to use corticosteroids (recognizing this deviates from guideline recommendations), the following approach minimizes harm:
Dosing Protocol
Intravenous methylprednisolone 0.5–1 mg/kg initiated within 72 hours of disease onset, followed by conversion to oral corticosteroids with a taper lasting at least 4 weeks. 4
Alternative approach: Methylprednisolone 40-80 mg daily (approximately 0.8-1.5 mg/kg/day for average adult) with rapid tapering over 7-10 days once disease progression arrests. 2
Dexamethasone pulse therapy (100 mg once daily for 3 days) has been studied but showed inferior outcomes compared to cyclosporine. 2, 5
Critical Timing
Must be initiated within 72 hours of disease onset to have any potential benefit – delayed administration is unlikely to help and increases infection risk. 4, 2
The reaction should be controlled within 24-48 hours, and corticosteroids should be withdrawn within 7-10 days to minimize infection complications. 6
Superior Alternative: Cyclosporine
Cyclosporine has stronger evidence than corticosteroids and should be considered first-line immunomodulatory therapy when supportive care alone is insufficient. 1, 2
Dosing: Cyclosporine 3 mg/kg daily for 10 days, then tapered over 1 month. 1, 2
Evidence: Multiple studies show reduced mortality compared to SCORTEN-predicted rates, with one study showing 0 deaths despite predicted mortality of 2.75/29 patients. 1, 2
Mechanism: Targets T-cell-mediated pathology without the broad immunosuppression and infection risk of corticosteroids. 1
Immune Checkpoint Inhibitor-Induced TEN: The Exception
For immune checkpoint inhibitor-induced SJS/TEN, corticosteroids ARE recommended because the pathology is driven by T-cell immune toxicity. 4
- Grade 3 disease: Methylprednisolone 0.5–1 mg/kg. 4
- Grade 4 disease: Methylprednisolone 1–2 mg/kg. 4
- Permanent discontinuation of the checkpoint inhibitor is mandatory. 4
What SHOULD Be Done: Prioritize Supportive Care
High-quality multidisciplinary supportive care in a specialized burn center or ICU is the most universally accepted and evidence-based intervention. 1, 2, 3
Immediate Actions
Discontinue all suspected culprit drugs immediately – this is the single most critical intervention. 1, 4
Transfer patients with >10% body surface area involvement to a specialized burn center or ICU within hours – delayed transfer significantly increases mortality. 1, 4, 2
Calculate SCORTEN within 24 hours to predict mortality (scores 0-7 correspond to 1-99% mortality). 1, 4, 2
Infection Prevention (More Important Than Steroids)
Do NOT use prophylactic systemic antibiotics – they increase colonization with resistant organisms, particularly Candida, without improving outcomes. 1, 4, 2
Monitor closely for infection signs: confusion, hypotension, oliguria, desaturation, increased skin pain, rising C-reactive protein, neutrophilia. 4, 2
Use targeted antimicrobial therapy only when clinical infection signs are present. 1, 4, 2
Common Pitfalls to Avoid
Do not use corticosteroids as monotherapy without considering alternatives like cyclosporine, given the infection risk and lack of proven benefit. 2, 3
Do not delay transfer to specialized care while debating immunomodulatory therapy – supportive care in the right setting saves more lives than any specific drug. 1, 4, 2
Do not use prophylactic antibiotics even when using corticosteroids – this compounds infection risk. 1, 4, 2
If corticosteroids are initiated, use the shortest possible duration with rapid tapering once disease progression arrests (typically 7-10 days total). 2, 6
Thalidomide increases mortality and should never be used. 4
Nuanced Clinical Context
While older case series from 1996 reported success with high-dose corticosteroids followed by rapid withdrawal 6, and some retrospective data suggest potential benefit 2, the 2016 UK guidelines represent the most comprehensive systematic review of available evidence and explicitly recommend against routine use. 1, 2 The conflicting evidence reflects the lack of randomized trials and the difficulty of controlling for confounders in retrospective studies. When mortality is already 30% and infection is the leading cause of death, adding broad immunosuppression without clear evidence of benefit violates the principle of "first, do no harm." 7
The evidence hierarchy clearly favors cyclosporine over corticosteroids when immunomodulation beyond supportive care is deemed necessary. 1, 2