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Drug-Induced Bullous Disorders Treatment & Management

  • Author: David F Butler, MD; Chief Editor: William D James, MD  more...
Updated: Mar 29, 2016

Medical Care

Withdrawal of the offending medication is the most important aspect of treatment of bullous drug reactions. Most reactions are self-limited. Conservative treatment of these disorders involves using wet compresses of Burrow solution and the application of moderate- to high-potency topical corticosteroids. More severe reactions may require the use of systemic corticosteroids.

The use of corticosteroids in the treatment of SJS and TEN is controversial. Patients with SJS and TEN are usually managed as inpatients in the intensive care or burn units. Fluid hydration, electrolyte balance, and nutritional support are the cornerstones of therapy. Rigorously guard against infection. Intravenous gamma globulin (IVIG) shows promise in the treatment of TEN. The IVIG reduces apoptosis by blocking CD95 on T cells.[33] In TEN, early withdrawal of precipitating drugs may reduce mortality if the drug has a short half-life.[34]



Limited forms of EM can be managed on an outpatient basis; however, careful consideration should be given to patients with SJS and TEN regarding an early referral to an intensive care unit or preferably a burn unit. Eye involvement that can occur in EM, SJS, and TEN requires an ophthalmologic evaluation.



Avoid use of the offending drug.

Contributor Information and Disclosures

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Specialty Editor Board

Michael J Wells, MD, FAAD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD, FAAD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, Texas Medical Association

Disclosure: Nothing to disclose.

Lester F Libow, MD Dermatopathologist, South Texas Dermatopathology Laboratory

Lester F Libow, MD is a member of the following medical societies: American Academy of Dermatology, American Society of Dermatopathology, Texas Medical Association

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Ponciano D Cruz, Jr, MD Professor and Vice-Chair, Paul R Bergstresser Chair, Department of Dermatology, University of Texas Southwestern Medical Center

Ponciano D Cruz, Jr, MD is a member of the following medical societies: Texas Medical Association

Disclosure: Received consulting fee from RCTS for independent contractor; Received honoraria from Mary Kay Cosmetics for consulting; Received grant/research funds from Galderma for principal investigator.

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Small pustules on erythematous patch (acute generalized exanthematous pustulosis).
Annular hyperpigmented patch (fixed drug eruption).
Target or iris lesions on palm (erythema multiforme).
Coalescing eroded patches (Stevens-Johnson syndrome).
Stevens-Johnson syndrome.
Crusted erosions on scalp (drug-induced pemphigus).
Small vesicle at edge of urticarial plaque (drug-induced pemphigoid).
Tense vesicles in annular array (linear immunoglobulin A dermatosis).
Erosions, scars, milia, and vesicle (pseudoporphyria).
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