eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Toxic Epidermal Necrolysis: Treatment & Medication

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
Coauthor(s): Samantha P Jellinek, PharmD, BCPS, Clinical Coordinator of Pharmacy Practice Residency Program, Manager of Medication Reconciliation and Safety, Maimonides Medical Center; Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Contributor Information and Disclosures

Updated: Feb 12, 2009

Treatment

Medical Care

Management of toxic epidermal necrolysis (TEN) requires prompt detection, withdrawal of all potential causative agents, evaluation, and largely supportive care. Early transfer of patients with toxic epidermal necrolysis to a burn or intensive care unit has been shown to reduce the risk of infection, mortality rate, and length of hospitalization. No controlled prospective treatment studies or generally accepted guidelines exist. In 1991, Avakian and colleagues published the University of Florida treatment protocol for toxic epidermal necrolysis.10 In 2007, these guidelines were revised by Fromowitz and colleagues.11 The guidelines are as follows:

  • Monitor fluids and electrolytes. Administer fluids and titrate based on central venous pressure and urine output. On average, 3-4 L are needed in patients with 50% of the body surface area affected. Parenteral nutrition or nutrition provided enterally via a soft-fine bore nasogastric tube is usually needed. Start total parenteral nutrition in patients unable to take nourishment. Early and continuous enteral nutrition reduces the risk of stress ulcers, reduces bacterial translocation and enterogenic infection, and allows earlier discontinuation of venous lines.
  • Nonpharmacological measures and therapies include the following:
    • Withdraw all unnecessary medications.
    • Withdraw the offending agent as soon as possible. One observational study showed a reduction in mortality from 26% to 5% when the implicated drugs with short elimination half-lives were withdrawn no later than the day the blisters or erosions first developed.
    • Provide daily physical therapy for range-of-motion exercises.
    • Place a central or intravenous line in areas of uninvolved skin.
    • Consider the use of plasmapheresis, if available, daily for 3 days. Plasmapheresis may enhance elimination of the drug or offending agent or inflammatory mediators such as cytokines and should be considered.12
    • Under general anesthesia, necrotic and desquamation areas are débrided within a few hours of admission.
    • Apply porcine xenografts to involved areas.
    • Irrigate the eyes every hour.
    • Provide hydrotherapy (whirlpool) twice a day. Repair and replace porcine xenografts.
    • Apply Kerlix dressings soaked in silver nitrate 0.5% to involved areas after each whirlpool session.
    • Administer Peridex mouthwash 4 times a day and white petrolatum to lips.
    • Rinse the patient’s mouth frequently and apply a topical anesthetic or spray for buccal pain. Cyclophosphamide and cyclosporine have been used with some success, but no randomized controlled studies have been performed.
    • Place the patient in a heated environment to enhance reepithelialization. However, this may enhance water losses, and appropriate hydration must be maintained. Institute a bed warmer.
    • Place a Foley catheter and nasogastric tube only when needed.
    • Consider blood transfusions when hematological complications, such as marked anemia, are evident.
  • Pharmacological therapies include the following:
    • Start systemic antibiotics for documented infection or signs of sepsis.
    • Emergence of resistance precludes the use of prophylactic antibiotics. Empiric antimicrobial therapy should include broad-spectrum antimicrobials that cover gram-negative, gram-positive, and anaerobic organisms. If staphylococcal infection is involved, administer an appropriate antistaphylococcal agent (ie, nafcillin/oxacillin for methicillin-sensitive organisms or vancomycin for methicillin-resistant organisms).
    • Provide pain relief with patient controlled analgesia (PCA). Opiate analgesics for skin pain and anxiety are essential for comforting patients.
    • Hydroxyzine may be used when reepithelialization begins because intense pruritus may occur.
    • Corticosteroids are commonly used to cease progression, but this is highly controversial. In some studies, corticosteroids have increased the incidence of mortality.
    • Patients remain nonambulatory until skin begins to heal. Until that time, anticoagulant therapy is imperative. Heparin is indicated for prophylaxis of thromboembolic events.
    • Saline applied to skin hourly is important, and then emollients are smeared.
    • Chlorhexidine solution is used to bathe the patient's skin.
    • Apply chloramphenicol ointment to prevent infection. Avoid use of silver sulfadiazine cream. Silvadene cream is a sulfa medication, a category of drugs often implicated as a cause of toxic epidermal necrolysis.
    • If within 48-72 hours of bulla onset, use sucrose-depleted intravenous immunoglobulin 1 g/kg/d (infused over 4 h) for 3 days. If more than 72 hours have elapsed since the onset of bulla but the patient is still actively progressing with new lesions, intravenous immunoglobulin may still be useful.

Consultations

  • Most patients with toxic epidermal necrolysis require specialized care under the direction of physicians with experience in handling this disorder. Burn-unit care represents an option worthy of serious consideration.
  • A dermatologist is consulted to identify and to confirm toxic epidermal necrolysis.
  • A plastic surgeon is consulted to débride areas of skin necrosis, as indicated.
  • An ophthalmologist is consulted to prevent conjunctival-corneal adhesions, especially if vision is threatened. Ophthalmological complications are common and may require long-term treatment with corticosteroids.
  • An internal medicine specialist is consulted to assist in patient treatment.
  • Consultation with a respiratory medicine specialist may be important, since respiratory mucosa may slough. Establishment of pulmonary toilet may be advisable.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Crystalloids

This is used as an initial imperative medication in toxic epidermal necrolysis (TEN) for supportive care. 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 toxic epidermal necrolysis are at serious risk of dehydration, which may complicate matters. 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. Intravenous rate of repletion should be titrated based on urine output or central venous pressure.

Adult

In a case report, 3-4 L IV were needed daily to replete a patient with 50% of body surface area affected; this was anecdotal, and titration of fluids must be specific to the patient

Pediatric

Titration is specific to the patient

Edema in brain or lungs; pulmonary edema

Pregnancy

A - Fetal risk not revealed in controlled studies in humans

Precautions

May induce pulmonary edema; monitor urine output and electrolytes

Corticosteroids

While corticosteroids may be used, their use is highly controversial. In one study, a reduction of mortality by 50% was attributed solely to not using corticosteroids. Many 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.

However, in some published literature, high-dose corticosteroids have been used early in the onset of toxic epidermal necrolysis (within 24-48 h) and have demonstrated a halt in the progression of the reaction.

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

For many, corticosteroids are still the anchor of therapy in patients with toxic epidermal necrolysis. Withholding corticosteroids may prolong reaction and delay healing, increasing damage. However, corticosteroids have also been reported to increase morbidity and mortality, and some experts have not recommended their use.


Dexamethasone (Decadron, Dexasone)

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

Adult

Initial: 16 mg IV; increase based on surface area involvement if no adverse effects noted; once progression has ceased, may switch to PO and taper by 50%
Average dosing: 4-100 mg IV

Pediatric

Not established

None reported for acute treatment

Documented hypersensitivity; signs of sepsis or fungal infection; peptic ulcer disease; pulmonary edema

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Predisposes patients to sepsis; if no improvements in healing of skin lesions are observed, may need higher doses; monitor patients closely; GI bleeding and pulmonary edema (due to fluid retention caused by corticosteroids) may occur

Antibiotics

Patients with toxic epidermal necrolysis lose their epidermis, a major barrier to invading organisms. If patients become infected, morbidity is enhanced. Bacterial sampling of skin lesions should be performed the first day and every 48 hours. Indicators for antibiotic treatment include increased number of bacteria cultured from the skin with selection of a single strain, sudden decrease in temperature, or deterioration of the patient's condition. S aureus is the main bacteria present during the first days, with gram-negative strains appearing later.

Aspiration pneumonia is a major complication of toxic epidermal necrolysis and results in an increased risk of mortality. Therefore, empiric antimicrobial therapy is essential to treat patients with signs and symptoms suggestive of sepsis. Case reports of Klebsiella species,13 Escherichia coli, and Pseudomonas species recovered from patients with toxic epidermal necrolysis have created concern about the possible polymicrobial nature of sepsis associated with this condition. Therefore, good gram-negative coverage may be necessary.


Nafcillin (Unipen)

Covers most common skin organisms such as Staphylococcus and Streptococcus. If patient has allergy to penicillin or if MRSA is present on skin culture, use vancomycin.

Adult

1-2 g IV q4h

Pediatric

Neonates: 10 mg/kg IV tid/qid
Children: 50 mg/kg IV divided qid

Nafcillin may inactivate aminoglycosides; high doses of penicillin may cause hemostatic defects

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Superinfections, resistance, thrombophlebitis, and electrolyte imbalance (with high doses) may occur


Gentamicin (Gentacidin, Garamycin)

Third-generation cephalosporins, such as ceftazidime, and others with good gram-negative coverage are suitable alternatives. Adjust dose based on renal insufficiency.

Adult

1 mg/kg IV q8h
High-dose aminoglycosides also may be initiated, such as 4-7 mg/kg IV for 1 dose, then a random sample after 6-14 h must be performed (ie, once daily aminoglycoside therapy)

Pediatric

Not established

Coadministration with vancomycin, other aminoglycosides, cephalosporins, penicillins, and amphotericin B may increase nephrotoxicity; aminoglycosides enhance effects of neuromuscular blocking agents, thus prolonged respiratory depression may occur; coadministration with loop diuretics may increase auditory toxicity of aminoglycosides; possible irreversible hearing loss of varying degrees may occur (monitor regularly)

Documented hypersensitivity; non–dialysis-dependent renal insufficiency

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Narrow therapeutic index (not intended for long-term therapy); caution in renal failure (not on dialysis), myasthenia gravis, hypocalcemia, and conditions that depress neuromuscular transmission; adjust dose in renal impairment; audiology examinations; watch for superinfection

Antihistamines

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


Hydroxyzine (Anxanil, Atarax, Atozine, Durrax, Vistaril)

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

Adult

25 mg IM/PO tid/qid

Pediatric

<6 years: 50 mg/d IM in divided doses
>6 years: 50-100 mg/d IM in divided doses

CNS depression may increase with alcohol or other CNS depressants; start with 50% of dose if using concomitant CNS depressants

Documented hypersensitivity; IV administration (hemolysis may occur); early pregnancy

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Associated with clinical exacerbations of porphyria (may not be safe for patients who are porphyric); ECG abnormalities (alterations in T waves) may occur; may cause drowsiness; inject IM well within body of relatively large muscle

Anticoagulants

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


Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents reaccumulation of clot after spontaneous fibrinolysis. Indicated in prophylaxis of formation of thromboembolic event.

Adult

5000 U SC q12h

Pediatric

Initial dose: 50 U/kg IV
Maintenance infusion: 15-25 U/kg/h IV
Increase dose by 2-4 U/kg/h IV q6-8h prn using aPTT results

High-dose penicillin may induce bleeding; heparin may antagonize effects of corticosteroids; antihistamines may counteract effect of heparin; digoxin, nicotine, and tetracycline may decrease effects; NSAIDs, ASA, dextran, dipyridamole, and hydroxychloroquine may increase heparin toxicity

Documented hypersensitivity; severe thrombocytopenia; uncontrollable bleeding, except when due to DIC

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic disease, patients who are elderly, and patients with indwelling catheters; may develop hyperkalemia because of hypoaldosteronism

Analgesics

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


Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC, but, in case of allergy or intolerability, meperidine or fentanyl may be used.

Adult

2-15 mg/70 kg IV

Pediatric

Infants and children: 0.1-0.2 mg/kg/dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose

Phenothiazines may antagonize analgesic effects of opiate agonists; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects of morphine with coadministration

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult; MAOI use within last 2 wk

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Vagolytic effects may increase ventricular rate; upper airway disease may occur; caution in patients who are elderly and debilitated; patients with hypoxic or hypercapnic conditions; avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Antiseptics

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


Chlorhexidine gluconate (PerioGard, Peridex, Hibiclens)

Binds to negatively charged bacterial cell walls and extramicrobial complex, causing bacteriostatic and bactericidal effects.

Adult

Apply after rinsing skin with water, then apply enough to cover surface and rinse again

Pediatric

Administer as in adults

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May stain tooth surfaces, restorations, and the dorsum of the tongue; avoid contact with eyes and ears; for topical use only

Local topical anesthetics

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


Benzocaine (Americaine, Anbesol)

Inhibits neuronal membrane depolarization, blocking nerve impulses. For oral or mucosal anesthesia. Used to control pain.

Adult

Apply to affected area prn

Pediatric

Administer as in adults

Hyaluronidase and sulfonamides may alter activity

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Topical anesthetic can produce reactions similar to parenteral anesthetics; administer minimal effective dose to avoid adverse drug reactions; dose commensurate with patient's age and acute illness and children's age, size, and physical condition; caution in severely irritated mucosa or sepsis; if rash occurs, discontinue; methemoglobinemia and dermatitis may occur

More on Toxic Epidermal Necrolysis

Overview: Toxic Epidermal Necrolysis
Differential Diagnoses & Workup: Toxic Epidermal Necrolysis
Treatment & Medication: Toxic Epidermal Necrolysis
Follow-up: Toxic Epidermal Necrolysis
Multimedia: Toxic Epidermal Necrolysis
References
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Further Reading

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Keywords

toxic epidermal necrolysis, TEN, toxic epidermal necrosis, acute disseminated epidermal necrosis, acute skin failure, Lyell syndrome, Lyell’s syndrome, Stevens-Johnson syndrome, SJS-TEN

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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, UMDNJ-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.

Medical Editor

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.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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 Geriatrics Society, 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 Society of 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: Nothing to disclose.

CME Editor

Eleftherios Mylonakis, MD, Clinical and Research Fellow, Department of Internal Medicine, Division of Infectious Diseases, Massachusetts General Hospital
Eleftherios Mylonakis, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American Society for Microbiology, and Infectious Diseases Society of America
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 Physician Executives, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Federation for Clinical Research, American Medical Association, American Society for Microbiology, Association of Professors of Medicine, Association of Program Directors in Internal Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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