Toxic Epidermal Necrolysis Medication

  • Author: Victor Cohen, PharmD; Chief Editor: Michael Stuart Bronze, MD   more...
 
Updated: Sep 15, 2011
 

Medication Summary

The goals of pharmacotherapy in toxic epidermal necrolysis (TEN) are to reduce morbidity and to prevent complications. No specific treatment modality has been proven effective, but agents such as crystalloids, antibiotics, antihistamines, anticoagulants, analgesics, and antiseptic agents are important for supportive care. Use of corticosteroids is controversial.

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Crystalloids

Class Summary

Fluid resuscitation is critical in TEN. In cases of acute skin failure, insensible losses may be enormous, and repletion of water loss is essential.

Isotonic sodium chloride 0.9%

 

Patients with TEN are at serious risk of dehydration, which may complicate their condition. For example, water losses in a hypercatabolic state result in hypoalbuminemia and reduced renal perfusion. This leads to acute renal failure; therefore, maintaining intravascular volume is paramount. The rate of intravenous repletion should be titrated based on urine output or central venous pressure.

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Antibiotics

Class Summary

Patients with TEN lose their epidermis, a major barrier to invading organisms. If patients become infected, morbidity is enhanced. Staphylococcus aureus is the main bacteria present during the first days, with gram-negative strains appearing later.

Case reports of Klebsiella species,[35] Escherichia coli, and Pseudomonas species recovered from patients with TEN have created concern about the possible polymicrobial nature of sepsis associated with this condition. Therefore, good gram-negative coverage may be necessary.

Nafcillin

 

Nafcillin covers most common skin organisms (eg, Staphylococcus, Streptococcus). If patient has allergy to penicillin or if methicillin-resistant S aureus (MRSA) is present on skin culture, use vancomycin.

Gentamicin

 

Gentamicin is an aminoglycoside antibiotic for gram-negative coverage. It is used in combination with both an agent against gram-positive organisms and one that covers anaerobes. Third-generation cephalosporins, such as ceftazidime, and others with good gram-negative coverage are suitable alternatives. Adjust dose based on renal insufficiency.

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Antihistamines

Class Summary

Hydroxyzine may be used when reepithelialization begins because intense pruritus may occur.

Hydroxyzine (Vistaril)

 

Hydroxyzine antagonizes H1 receptors in the periphery. It may suppress histamine activity in subcortical region of the central nervous system.

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Anticoagulants

Class Summary

Heparin is indicated for prophylaxis of thromboembolic events. Patients with TEN remain nonambulatory until skin begins to heal, and until that time, anticoagulant therapy is imperative.

Heparin

 

Heparin augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. It does not actively lyse thrombus but is able to inhibit further thrombogenesis. Heparin prevents reaccumulation of clot after spontaneous fibrinolysis. It is indicated for the prevention of thromboembolic events.

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Analgesics

Class Summary

Opiate analgesics are important to alleviate pain and anxiety associated with TEN. Much like treatment of a second-degree burn, the pain must not be ignored.

Morphine sulfate (Duramorph, Astramorph, MS Contin)

 

Morphine is the drug of choice for pain in patients with TEN. In case of allergy or intolerability, meperidine or fentanyl may be used.

Fentanyl Citrate ( Fentora, Abastral, Duragesic)

 

A synthetic opioid analgesic that is primarily a mu receptor agonist, fentanyl is 50-100 times more potent than morphine. It has short duration of action (1-2 h) and minimal cardiovascular effects, such as hypotension. Respiratory depression is uncommon, but this effect lasts longer than its analgesic effect. Fentanyl is frequently used in patient-controlled analgesia for relief of pain. Unlike morphine, fentanyl is not commonly associated with histamine release.

Meperidine (Demerol)

 

Meperidine is a synthetic opioid narcotic analgesic indicated for the relief of severe pain. This analgesic has multiple actions similar to those of morphine. However, meperidine may produce less constipation, smooth muscle spasm, and depression of cough reflex than similar analgesic doses of morphine.

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Antiseptics

Class Summary

These agents inhibit growth of gram-positive and gram-negative bacteria.

Chlorhexidine gluconate (PerioGard, Peridex, Hibiclens, Avagard)

 

Chlorhexidine binds to negatively charged bacterial cell walls and extramicrobial complexes. It has bacteriostatic and bactericidal effects.

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Topical Anesthetics

Class Summary

Topical anesthetics can be applied to mucous membranes, especially buccal, to relieve pain.

Benzocaine (Americaine, Anbesol, Chiggerex Plus)

 

Benzocaine inhibits neuronal membrane depolarization, blocking nerve impulses. It provides oral or mucosal anesthesia, thereby controlling pain.

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Corticosteroids

Class Summary

While corticosteroids may be used, their use is highly controversial. Although high-dose corticosteroids used early in the course of TEN (within 24-48 hours of onset) may halt the progression of the reaction, many experts believe that corticosteroids should not be used because they predispose patients to infection, mask early signs of sepsis, encourage GI bleeding, and impair or delay wound healing.

If corticosteroids are used, the initial high dose is titrated down as quickly as possible and tapered off, usually over 7-10 days.

Dexamethasone (Baycadron)

 

Dexamethasone decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reducing capillary permeability. Other corticosteroids, such as methylprednisolone, prednisone, and hydrocortisone, also may be used.

Methylprednisolone (Solu-Medrol, Medrol, A-Methapred)

 

Methylprednisolone is a highly potent synthetic glucocorticoid that causes diverse metabolic effects and modifies the body's immune responses to various stimuli.

Prednisone

 

Prednisone, a synthetic glucocorticoid analog, acts as a potent immunosuppressant. It May inhibit cyclooxygenase, which, in turn, inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.

Hydrocortisone (A-Hydrocort, Solu-Cortef, Cortef)

 

Hydrocortisone elicits anti-inflammatory properties and causes profound and varied metabolic effects. This agent modifies the body's immune response to diverse stimuli.

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Contributor Information and Disclosures
Author

Victor Cohen, PharmD  Clinical Pharmacy Manager, Department of Emergency Medicine, Maimonides Medical Center, Assistant Professor, Division of Pharmacy Practice, Arnold and Marie Schwartz College of Pharmacy and Health Sciences, Long Island University

Victor Cohen, PharmD is a member of the following medical societies: American Association of Colleges of Pharmacy, American College of Clinical Pharmacy, American Society of Health-System Pharmacists, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Samantha P Jellinek, PharmD, BCPS  Clinical Coordinator of Pharmacy Practice Residency Program, Manager of Medication Reconciliation and Safety, Maimonides Medical Center

Samantha P Jellinek, PharmD, BCPS is a member of the following medical societies: American College of Clinical Pharmacy and American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD  Professor, Stewart G Wolf Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

Additional Contributors

Theodore J Gaeta, DO, MPH, FACEP Clinical Associate Professor, Department of Emergency Medicine, Joan and Sanford Weill Medical College at Cornell University; Vice Chairman and Program Director of Emergency Medicine Residency Program, Department of Emergency Medicine, New York Methodist Hospital; Academic Chair, Adjunct Professor, Department of Emergency Medicine, St George's University School of Medicine

Theodore J Gaeta, DO, MPH, FACEP is a member of the following medical societies: Alliance for Clinical Education, American College of Emergency Physicians, Clerkship Directors in Emergency Medicine, Council of Emergency Medicine Residency Directors, New York Academy of Medicine, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Gregory P Garra, DO Clinical Assistant Professor, Department of Emergency Medicine, Stony Brook University School of Medicine; Residency Program Director, Department of Emergency Medicine, Stony Brook University Hospital

Gregory P Garra, DO is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Mark L Plaster, MD, JD Executive Editor, Emergency Physicians Monthly

Mark L Plaster, MD, JD is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: M L Plaster Publishing Co LLC Ownership interest Management position

Jennifer Stellke, DO Resident Physician, Department of Emergency Medicine, Stony Brook University Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, American GeriatricsSociety, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, Infectious Diseases Societyof America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Baxter International and Johnson & Johnson Royalty Other

References
  1. Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau JC. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermatol. Jan 1993;129(1):92-6. [Medline].

  2. LYELL A. Toxic epidermal necrolysis: an eruption resembling scalding of the skin. Br J Dermatol. Nov 1956;68(11):355-61. [Medline].

  3. LANG R, WALKER J. An unusual bullous eruption. S Afr Med J. Feb 4 1956;30(5):97-8. [Medline].

  4. Debre R, Lemy M, Lamotte M. L'erythrodermie bulleuses avec epidermolyse. Bull Soc Pediatr (Paris). 1939;37:231-238.

  5. Lyell A. Toxic epidermal necrolysis (the scalded skin syndrome): a reappraisal. Br J Dermatol. Jan 1979;100(1):69-86. [Medline].

  6. Pereira FA, Mudgil AV, Rosmarin DM. Toxic epidermal necrolysis. J Am Acad Dermatol. Feb 2007;56(2):181-200. [Medline].

  7. Nagy N, McGrath JA. Blistering skin diseases: a bridge between dermatopathology and molecular biology. Histopathology. Jan 2010;56(1):91-9. [Medline].

  8. Abe R, Shimizu T, Shibaki A, Nakamura H, Watanabe H, Shimizu H. Toxic epidermal necrolysis and Stevens-Johnson syndrome are induced by soluble Fas ligand. Am J Pathol. May 2003;162(5):1515-20. [Medline]. [Full Text].

  9. Posadas SJ, Padial A, Torres MJ, Mayorga C, Leyva L, Sanchez E, et al. Delayed reactions to drugs show levels of perforin, granzyme B, and Fas-L to be related to disease severity. J Allergy Clin Immunol. Jan 2002;109(1):155-61. [Medline].

  10. Paul C, Wolkenstein P, Adle H, Wechsler J, Garchon HJ, Revuz J, et al. Apoptosis as a mechanism of keratinocyte death in toxic epidermal necrolysis. Br J Dermatol. Apr 1996;134(4):710-4. [Medline].

  11. Nassif A, Moslehi H, Le Gouvello S, Bagot M, Lyonnet L, Michel L, et al. Evaluation of the potential role of cytokines in toxic epidermal necrolysis. J Invest Dermatol. Nov 2004;123(5):850-5. [Medline].

  12. Chung WH, Hung SI, Yang JY, Su SC, Huang SP, Wei CY, et al. Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis. Nat Med. Dec 2008;14(12):1343-50. [Medline].

  13. Roujeau JC, Kelly JP, Naldi L, Rzany B, Stern RS, Anderson T, et al. Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med. Dec 14 1995;333(24):1600-7. [Medline].

  14. Moshfeghi M, Mandler HD. Ciprofloxacin-induced toxic epidermal necrolysis. Ann Pharmacother. Dec 1993;27(12):1467-9. [Medline].

  15. Ernst ME, Ernst EJ, Klepser ME. Levofloxacin and trovafloxacin: the next generation of fluoroquinolones?. Am J Health Syst Pharm. Nov 15 1997;54(22):2569-84. [Medline].

  16. Creamer JD, Whittaker SJ, Kerr-Muir M, Smith NP. Phenytoin-induced toxic epidermal necrolysis: a case report. Clin Exp Dermatol. Mar 1996;21(2):116-20. [Medline].

  17. Lissia M, Mulas P, Bulla A, Rubino C. Toxic epidermal necrolysis (Lyell's disease). Burns. Mar 2010;36(2):152-63. [Medline].

  18. Abood GJ, Nickoloff BJ, Gamelli RL. Treatment strategies in toxic epidermal necrolysis syndrome: where are we at?. J Burn Care Res. Jan-Feb 2008;29(1):269-76. [Medline].

  19. Chung WH, Hung SI, Hong HS, Hsih MS, Yang LC, Ho HC, et al. Medical genetics: a marker for Stevens-Johnson syndrome. Nature. Apr 1 2004;428(6982):486. [Medline].

  20. Ferrell PB Jr, McLeod HL. Carbamazepine, HLA-B*1502 and risk of Stevens-Johnson syndrome and toxic epidermal necrolysis: US FDA recommendations. Pharmacogenomics. Oct 2008;9(10):1543-6. [Medline]. [Full Text].

  21. Struck MF, Hilbert P, Mockenhaupt M, Reichelt B, Steen M. Severe cutaneous adverse reactions: emergency approach to non-burn epidermolytic syndromes. Intensive Care Med. Jan 2010;36(1):22-32. [Medline].

  22. Revuz J, Roujeau JC, Guillaume JC, Penso D, Touraine R. Treatment of toxic epidermal necrolysis. Créteil's experience. Arch Dermatol. Sep 1987;123(9):1156-8. [Medline].

  23. Koh MJ, Tay YK. An update on Stevens-Johnson syndrome and toxic epidermal necrolysis in children. Curr Opin Pediatr. Aug 2009;21(4):505-10. [Medline].

  24. Bastuji-Garin S, Fouchard N, Bertocchi M, Roujeau JC, Revuz J, Wolkenstein P. SCORTEN: a severity-of-illness score for toxic epidermal necrolysis. J Invest Dermatol. Aug 2000;115(2):149-53. [Medline].

  25. Magina S, Lisboa C, Leal V, Palmares J, Mesquita-Guimarães J. Dermatological and ophthalmological sequels in toxic epidermal necrolysis. Dermatology. 2003;207(1):33-6. [Medline].

  26. Power WJ, Ghoraishi M, Merayo-Lloves J, Neves RA, Foster CS. Analysis of the acute ophthalmic manifestations of the erythema multiforme/Stevens-Johnson syndrome/toxic epidermal necrolysis disease spectrum. Ophthalmology. Nov 1995;102(11):1669-76. [Medline].

  27. Barrera JE, Meyers AD, Hartford EC. Hypopharyngeal stenosis and dysphagia complicating toxic epidermal necrolysis. Arch Otolaryngol Head Neck Surg. Dec 1998;124(12):1375-6. [Medline].

  28. Bachot N, Roujeau JC. Differential diagnosis of severe cutaneous drug eruptions. Am J Clin Dermatol. 2003;4(8):561-72. [Medline].

  29. Avakian R, Flowers FP, Araujo OE, Ramos-Caro FA. Toxic epidermal necrolysis: a review. J Am Acad Dermatol. Jul 1991;25(1 Pt 1):69-79. [Medline].

  30. Fromowitz JS, Ramos-Caro FA, Flowers FP. Practical guidelines for the management of toxic epidermal necrolysis and Stevens-Johnson syndrome. Int J Dermatol. Oct 2007;46(10):1092-4. [Medline].

  31. Endorf FW, Cancio LC, Gibran NS. Toxic epidermal necrolysis clinical guidelines. J Burn Care Res. Sep-Oct 2008;29(5):706-12. [Medline].

  32. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic epidermal necrolysis and Stevens-Johnson syndrome: does early withdrawal of causative drugs decrease the risk of death?. Arch Dermatol. Mar 2000;136(3):323-7. [Medline].

  33. Palmieri TL, Greenhalgh DG, Saffle JR, Spence RJ, Peck MD, Jeng JC, et al. A multicenter review of toxic epidermal necrolysis treated in U.S. burn centers at the end of the twentieth century. J Burn Care Rehabil. Mar-Apr 2002;23(2):87-96. [Medline].

  34. Chaidemenos GC, Chrysomallis F, Sombolos K, Mourellou O, Ioannides D, Papakonstantinou M. Plasmapheresis in toxic epidermal necrolysis. Int J Dermatol. Mar 1997;36(3):218-21. [Medline].

  35. Picard E, Gillis D, Klapholz L, Schreiber L, Engelhard D. Toxic epidermal necrolysis associated with Klebsiella pneumoniae sepsis. Pediatr Dermatol. Dec 1994;11(4):331-4. [Medline].

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Toxic epidermal necrolysis (TEN) ulcer in great toe (initial infection).
Hemorrhagic crusting of mucous membranes in toxic epidermal necrolysis (TEN).
Maculopapular rash in toxic epidermal necrolysis (TEN).
Diffuse maculopapular rash in toxic epidermal necrolysis (TEN).
Toxic epidermal necrolysis (TEN) blister on the index finger.
Epidermal sloughing in toxic epidermal necrolysis (TEN).
 
 
 
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