REVIEW ARTICLE

Drug-related Stevens–Johnson Syndrome and Toxic Epidermal

Necrolysis: A Review
Rohini Arora1 , Rajesh K Pande2 , Shikha Panwar3 , Vivek Gupta4

A b s t r ac t
Introduction: Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are rare, life-threatening, allergic reactions affecting the skin
and mucous membranes. SJS is considered to be a milder form with less than 10% of body surface area (BSA) involvement. We report successful
management of two cases of SJS and TEN. Firstly, a case of a 24-year-old female who presented with rashes over face, chest, and upper limbs
after the oral intake of ciprofloxacin and local application of moxifloxacin eye drops. She developed high-grade fever and difficulty in breathing
requiring intubation and lung-protective mechanical ventilation and was treated with high-dose methylprednisolone, azithromycin, soframycin
skin dressings, and topical ocular antibiotics. Secondly, another case of a 16-year-old female who developed bullous eruptions over the trunk,
arms, hands, face, and sole involving 60% of BSA, after oral intake of albendazole. She was diagnosed as TEN and successfully managed with
sterile silver nitrate, soframycin dressings, and antibiotics.
Key message: Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are life-threatening, allergic reactions affecting the skin
and mucous membranes. Early identification, withdrawal of the suspected drug, and early transfer to a specialized center decrease mortality.
Keywords: Albendazole, Ciprofloxacin, Moxifloxacin, Stevens–Johnson syndrome, Toxic epidermal necrolysis.
Indian Journal of Critical Care Medicine (2021): 10.5005/jp-journals-10071-23826

Introduction 1-3
Department of Critical Care, D BL Kapur Superspeciality Hospital,
Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis New Delhi, India
(TEN) are both rare and life-threatening conditions caused by 4
Department of Pharmacology, D BL Kapur Superspeciality Hospital,
a hypersensitivity reaction involving the skin and the mucous New Delhi, India
membranes. SJS is a milder form of TEN with the involvement Corresponding Author: Rohini Arora, Department of Critical Care,
of less than 10% of body surface area (BSA), and the condition is D BL Kapur Superspeciality Hospital, New Delhi, India, Phone: +91
called TEN if the affected BSA is more than 30%. The involvement 8588806634; e-mail: drrohini8@gmail.com
of 10 to 30% of BSA is considered to be SJS‑TEN.1 We report two How to cite this article: Arora R, Pande RK, Panwar S, Gupta V.
cases—SJS by fluoroquinolones and TEN caused by albendazole. Drug-related Stevens–Johnson Syndrome and Toxic Epidermal
TEN caused by albendazole to the best of our knowledge has Necrolysis: A Review. Indian J Crit Care Med 2021;25(5):575–579.
not been reported previously. Source of support: Nil
Conflict of interest: None
Case Descriptions
Case 1
A 24-year-old female developed erythematous rashes over the glossitis and oral ulcers that was treated with local glycerin
face, chest, and upper limbs after the oral intake of ciprofloxacin application.
and local application of moxifloxacin eye drops. The patient
presented with high-grade fever and breathing difficulty Case 2
necessitating endotracheal intubation and ventilation. She was A 16-year-old female presented with bullous eruptions over
put on pressure control mode with lung-protective strategy. her face, trunk, arms, hands, genitals, and sole covering
Skin involvement was found to be approximately 10% of BSA about 60% of BSA, following oral intake of albendazole
with extensive damage to the conjunctiva and symblepharon (Figs. 1 to 3). A diagnosis of TEN was established based on
formation. A diagnosis of fluoroquinolone-induced SJS was purplish lesions over the trunk, which were more than 30%.
made based on the clinical findings. She had tachycardia that was managed with fentanyl infusion.
The patient was given high-dose methylprednisolone for The patient was managed with crystalloid and albumin infusion
3 days and azithromycin. The erosions were covered with a given through the central line, early enteral feeding with a high
sterile paraffin gauge and mometasone cream. The patient protein diet, appropriate antibiotics, and methylprednisolone.
developed hospital-acquired pneumonia and sepsis, which She developed sepsis early requiring escalation of antibiotics
were treated with appropriate antimicrobial therapy. Supportive and withdrawal of steroids. Wound care was provided with
treatment included sedatives, analgesics, and intravenous soframycin dressings (Fig. 4). and wet dressing of silver nitrate
fluids. The patient improved significantly by day 10 and was that maintains a moist wound environment. Eyes cared for with
weaned from the ventilator and shifted to ward on day 15. saline-soaked pads. The skin lesions improved by day 20 after
The patient developed symblepharon, which was released which they got converted to hyperpigmented scars, and the
successfully. She later developed painful deglutition due to patient was discharged home.

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 Stevens–Johnson Syndrome

Fig. 1: Initial skin lesions involving trunk and face (Case 2) Fig. 4: Wound care and use of barrier precautions (Case 2)

Discussion
Both SJS and TEN are rare, life-threatening acute allergic drug
reactions affecting the skin and mucous membranes. SJS affects
less than 10% of BSA, while TEN involves more than 30% of BSA,
and between 10 and 30% is SJS/TEN overlap. The mortality rate of
TEN can be up to three times higher than that of SJS because of the
extensive skin involvement and secondary complications.2
Drug reactions are the most common cause of SJS/TEN. Drugs
like antibacterial, allopurinol, sulfonamides, anticonvulsants,
and steroids are found to be associated with an increased risk
of SJS/TEN. 3 Among these drugs, sulfonamides, penicillin, and
anticonvulsants are the commonest implicating agents for
SJS/ TEN.4,5
Among nondrug infectious causes, mycoplasma pneumonia in
adults and herpes simplex virus infections in children are known
to cause SJS/TEN.6,7 A rare occurrence of TEN in a patient with
severe aplastic anemia after allogeneic hematopoietic stem cell
Fig. 2: Initial skin lesions over chest and abdomen (Case 2) transplantation has also been reported. 8 Lastly, vaccination is
also implicated as an inciting factors like human papillomavirus,
mumps, measles, rubella, hepatitis B, influenza, anthrax, and
tetanus vaccines.9
The primary cause for the development of TEN is massive
T-lymphocyte-mediated immune reaction causing destruction
of the keratinocytes-expressing foreign antigens. An increased
amount of inflammatory cytokines like tumor necrosis factor-α
(TNF-α) and interleukin-6 (IL-6) are found in blister fluid.10 They
recruit the cytotoxic T-cells to the epidermis causing cell death
by inducing apoptosis. A cascade of intracellular enzymes called
caspases is activated when cytotoxic T-lymphocytes come in
contact with target cells.
The patient may present with a prodromal phase of fever,
malaise, cough, stinging eyes, and sore throat. Other symptoms
include erythematous rash, bullae, and separation of large sheets
of epidermis from the dermis. Cutaneous lesions include diffuse
erythema with target-like lesions, blisters, and erosions. “Target
lesions”11 are less than 3 cm in diameter, round, and have three
concentric zones; a central area of dusky erythema, a middle paler
zone of edema, and an outer ring of erythema with a defined edge.
Target lesions plus involvement of at least two mucous membranes
Fig. 3: Crusting (Case 2) comprise SJS.

576 Indian Journal of Critical Care Medicine, Volume 25 Issue 5 (May 2021)
 Stevens–Johnson Syndrome

The condition can be associated with multi-organ failure, Management

sepsis, gastrointestinal hemorrhage, and pulmonary embolism. TEN behaves like a superficial dermal burn with fluid shifts,
Ocular involvement12 of TEN occurs in 50% to 88% of cases and hypermetabolism, and high nutritional requirements. The
includes a purulent form of conjunctivitis, corneal ulceration, initial aim is the prevention of secondary infection by good
anterior uveitis, entropion, dry eye syndrome, and severe visual wound care as this is the most common cause of death. 21 Early
loss.13,14 diagnosis, early withdrawal of the suspected drug, 22 and early
Pulmonary involvement is common but usually mild in nature,15 transfer and management of these patients in a specialized unit
and only 10 to 20% requires ventilator support.16 Our first case like intensive care or burn unit 23 are associated with survival
had pulmonary involvement and developed hospital- acquired benefit. 24
pneumonia. Reported pulmonar y complications include Wound management with nonadhesive wet silver nitrate
tracheobronchial mucosal necrosis, pulmonary edema, acute dressings maintains a moist wound environment, speeds
respiratory distress syndrome, and pneumonia in 20–50% of cases. re-epithelialization, minimizes the pain, and decreases infection
Erosive and ulcerative vaginitis and vulvar bullae are seen in genital rates. 25 Wounds should be treated conservatively as much as
involvement. possible,26 as blistered skin acts as a natural biological dressing and
favors re-epithelialization. Biological or biosynthetic temporary skin
Long-term Sequelae Complications replacements27 (e.g., porcine xenografts), Biobrane (skin substitute),
Long-term complications include xerophthalmia, ectropion, and Aquacel Ag (a moisture-retentive hydrofiber dressing that
entropion, symblepharon, corneal opacity, pannus formation, releases silver within the dressing) are the latest modalities of
nasolacrimal duct obstruction, punctal stenosis, vaginal synechiae,17 skincare. Umbilical cord mesenchymal stem cell transplantation28
obliterative bronchitis or bronchiolitis, bronchiectasis, esophageal is an attractive and promising tool for skin regeneration in
stricture, recurrent cystitis, lingual ulcerations, recurrent oral patients with severe denudation due to their self-renewal capacity,
aphthae, etc.18 multilineage differentiation potential, paracrine effects, and
The presence of extensive necrolysis, idiopathic nature of immunosuppressive properties.
diseases, old age, elevated urea, creatinine and glucose levels, Pain control is a very important part of the management of
neutropenia, lymphopenia, and thrombocytopenia are linked to SJS/TEN, as these patients experience low-intensity background
a bad prognosis. SCORTEN scale19 (Table 1) has been validated pain. Longer-acting opioids and paracetamol should be given
to determine the mortality rate and is considered to be the gold for pain.
standard for prognosis. Our first patient had a SCORTEN score of 1, It is important to encourage oral feeds to avoid adhesions in
corresponding to a reported mortality of 3.2%. Our second patient the upper gastrointestinal tract, but parenteral feeding may be
had SCORTEN score of 3, with a reported mortality of 35.3%. Drug considered when the nutritional requirement cannot be met with
provocation tests20 (DPTs) are often needed when evaluating these oral intake.
patients for the correct causative agent and for the preparation of SJS/TEN patients have impaired temperature control due to
a list of drugs to be given to these patients. Since DPT may itself loss of the integument and should be cared for in rooms with
cause reactions, it has to be done under proper medical supervision. temperature and humidity control. Careful monitoring of fluid
balance with strict input and output chart is essential because
of significant insensible fluid losses, resulting in dehydration and
renal impairment.
Eye care includes 1- to 2-hourly eye lubrication and early
Table 1A: Scorten scale involvement of an ophthalmologist. Nonhealing corneal ulcers may
Risk factor 0 1 be treated with bandage contact lenses and amniotic membrane
transplantation for severe persistent corneal damage.29
Age <40 years >40 years
Associated malignancy No Yes
Specific Management
Heart rate (beats/min) <120 >120
The use of corticosteroids is debatable and remains controversial.
Serum BUN (mg/dL) <27 >27 Corticosteroids have an antiapoptotic role in the skin tissue, inhibit
Detached or compromised body
<10% >10% the initiating pathways,30 and down-regulate fas ligand (FasL) in
surface the apoptotic tissue. Studies support the early use of high-dose
Serum bicarbonate (mEq/L) >20 <20 corticosteroids30 (1–2 mg/kg/day of prednisolone for 3–5 days).
Serum glucose (mg/dL) <250 >250 Dexamethasone 8 to 16 mg/day is recommended;31 however,
the dose can be increased by 4 mg the next day if considered
necessary and the recovery is not adequate. On the other hand, the
Table 1B: Percentage of mortality opponents to corticosteroids suggest an increased risk of sepsis,
prolonged hospital stay, and increased mortality.32
No of risk factors Mortality rate (%) Other reported medical therapies for the treatment of TEN
0–1 3.2 include plasmapheresis, intravenous immunoglobulins (IVIG), and
2 12.1 cyclosporine. Literature supports early use of IVIG,33 which is a safe
3 35.3 therapy even for children with severe cutaneous drug reactions. 34
However, there are conflicting reports as well. 35
4 58.3
Cyclosporine if given early in the disease arrests the progression
5 or more >90 of the disease without increasing the risk of sepsis. 36 The mean

Indian Journal of Critical Care Medicine, Volume 25 Issue 5 (May 2021) 577
 Stevens–Johnson Syndrome

duration of re-epithelialization and duration of hospital stay were 7. Forman R, Koren G, Shear NH. Erythema multiforme, Stevens-
significantly lower in patients receiving cyclosporine in comparison Johnson syndrome and toxic epidermal necrolysis in children:
to those patients who were managed using supportive treatment a review of 10 years’ experience. Drug Saf 2002;25(13):965–972.
DOI: 10.2165/00002018-200225130-00006.
only, without increasing mortality.37,38
8. Zakrzewski JL, Lentini G, Such U, Duerr A, Tran V, Guenzelmann S, et al.
Plasmapheresis therapy39 to remove drug metabolites and Toxic epidermal necrolysis: differential diagnosis of an epidermolytic
cytokines from circulation remains controversial. dermopathy in a hematopoietic stem cell transplant recipient. Bone
Although beneficial effect of cyclophosphamide 40 and Marrow Transplant 2002;30(5):331–333. DOI: 10.1038/sj.bmt.1703624.
tacrolimus 41 is suggested by some authors, larger studies are 9. Katoulis AC, Liakou A, Bozi E, Theodorakis M, Alevizou A,
needed to clarify these results. Zafeiraki A, et al. Erythema multiforme following vaccination
Other treatments that have been tried include chimeric anti- for human papillomavirus. Dermatology 2010;220(1):60–62.
TNF-α antibody (infliximab)42,43 and thalidomide (TNF-alpha inhibitor) DOI: 10.1159/000254898.
10. Abe R. Immunological response in Stevens-Johnson syndrome
as cytokines such as IL-6 and TNF-alpha are found in higher quantities
and toxic epidermal necrolysis. J Dermatol 2015;42(1):42–48.
in the skin of patients of TEN. Recombinant granulocyte colony- DOI: 10.1111/1346-8138.12674.
stimulating factor in a dose of 5 μg/kg/day for 5 days leads to rapid 11. Teraki Y, Shibuya M, Izaki S. Stevens-Johnson syndrome and toxic
re-epithelialization of skin as reported in some case reports. But still epidermal necrolysis due to anticonvulsants share certain clinical and
their use remains controversial, and more robust data are required laboratory features with drug-induced hypersensitivity syndrome,
to make these treatments as a standard of care. despite differences in cutaneous presentations. Clin Exp Dermatol
There are still gaps in our understanding of the pathophysiology 2010;35(7):723–728. DOI: 10.1111/j.1365-2230.2009.03718.x.
of SJS/TEN and the available treatment options. Good quality 12. López-García JS, Rivas Jara L, García-Lozano CI, Conesa E, de Juan IE,
multicenter studies are needed to understand the disease better Murube del Castillo J. Ocular features and histopathologic changes
during follow-up of toxic epidermal necrolysis. Ophthalmology
and explore the treatment options further.
2011;118(2):265–271. DOI: 10.1016/j.ophtha.2010.06.035.
13. Sotozono C, Ueta M, Koizumi N, Inatomi T, Shirakata Y, Ikezawa Z,
C o n c lu s i o n et al. Diagnosis and treatment of Stevens-Johnson syndrome and
Life-threatening SJS and TEN present a challenge in early detection toxic epidermal necrolysis with ocular complications. Ophthalmology
and subsequent management. Evidence-based practice related to 2009;116(4):685–690. DOI: 10.1016/j.ophtha.2008.12.048.
the care of patients with SJS is still evolving. Management includes 14. Gueudry J, Roujeau JC, Binaghi M, Soubrane G, Muraine M.
Risk factors for the development of ocular complications of
early identification, withdrawal of the suspected drug, and early
Stevens- Johnson syndrome and toxic epidermal necrolysis. Arch
transfer to a specialized center. Further research and clinical
Dermatol 2009;145(2):157–162. DOI: 10.1001/archdermatol.2009.540.
evidence are needed to develop appropriate and cost-effective 15. Hwang SH, Kim DH, Kim JH, Son BK, Lim DH. Chronic pulmonary
treatment guidelines for optimal care of these patients. complications due to toxic epidermal necrolysis. Allergy Asthma
Respir Dis 2013;1(4):391–394. DOI: 10.4168/aard.2013.1.4.391.
Orcid 16. Kamada N, Kinoshita K, Togawa Y, Kobayashi T, Matsubara H, Kohno
Rajesh K Pande https://orcid.org/0000-0002-0149-727X M, et al. Chronic pulmonary complications associated with toxic
epidermal necrolysis: report of a severe case with anti-Ro/SS-A and
Rohini Arora https://orcid.org/0000-0003-3322-4185 a review of the published work. J Dermatol 2006;33(9):616–622.
Shikha Panwar https://orcid.org/0000-0002-0669-4731 DOI: 10.1111/j.1346-8138.2006.00142.x.
Vivek Gupta https://orcid.org/0000-0002-8719-5677 17. Kaser DJ, Reichman DE, Laufer MR. Prevention of vulvovaginal
sequelae in Stevens-Johnson syndrome and toxic epidermal
necrolysis. Rev Obstet Gynecol 2011;4(2):81–85. DOI: 10.3909/
References riog0152.
1. Bastuji-Garin S, Rzany B, Stern RS, Shear NH, Naldi L, Roujeau 18. Oplatek A, Brown K, Sen S, Halerz M, Supple K, Gamelli RL. Long-term
JC. Clinical classification of cases of toxic epidermal necrolysis, follow-up of patients treated for toxic epidermal necrolysis. J Burn
Stevens- Johnson syndrome and erythema multiforme. Arch Care Res 2006;27(1):26–33. DOI: 10.1097/01.bcr.0000194268.01514.f8.
Dermatol 1993;129(1):92–96. DOI: 10.1001/archderme. 19. Guégan S, Bastuji-Garin S, Poszepczynska-Guigné E, Roujeau JC,
2. Barvaliya M, Sanmukhani J, Patel T, Paliwal N, Shah H, Tripathi C. Drug- Revuz J. Performance of the SCORTEN during the first 5 days of
induced Stevens-Johnson syndrome (SJS), toxic epidermal necrolysis hospitalization to predict the prognosis of epidermal necrolysis.
(TEN), and SJS-TEN overlap: a multicentric retrospective study. J Invest Dermatol 2006;126(2):272–276. DOI: 10.1038/sj.jid.5700068.
J Postgrad Med 2011;57(2):115–119. DOI: 10.4103/0022-3859.81865. 20. Ramam M, Kumar U, Bhat R, Sharma VK. Oral drug provocation test
3. Roujeau JC, Kelly JP, Naldi L, Rzany B, Stern RS, Anderson T, et al. to generate a list of safe drugs: experience with 100 patients. Indian
Medication use and the risk of Stevens-Johnson syndrome or toxic J Dermatol Venereol Leprol 2012;78(5):595–598. DOI: 10.4103/0378-
epidermal necrolysis. N Engl J Med 1995;333(24):1600–1607. DOI: 6323.100563.
10.1056/NEJM199512143332404. 21. Roujeau JC, Chosidow O, Saiag P, Guillaume JC. Toxic epidermal
4. Sethuraman G, Sharma VK, Pahwa P, Khetan P. Causative drugs and necrolysis (Lyell syndrome). J Am Acad Dermatol 1990;23(6 Pt 1):1039–
clinical outcome in Stevens Johnson Syndrome (SJS), Toxic Epidermal 1058. DOI: 10.1016/0190-9622(90)70333-d.
Necrolysis (TEN), and SJS-TEN overlap in children. Indian J Dermatol 22. Garcia-Doval I, LeCleach L, Bocquet H, Otero XL, Roujeau JC. Toxic
2012;57(3):199–200. DOI: 10.4103/0019-5154.96192. epidermal necrolysis and Stevens-Johnson syndrome: does early
5. Mockenhaupt M, Viboud C, Dunant A, Naldi L, Halevy S, Bouwes withdrawal of causative drugs decrease the risk of death? Arch
Bavinck JN, et al. Stevens-Johnson syndrome and toxic epidermal Dermatol 2000;136(3):323–327. DOI: 10.1001/archderm.136.3.323.
necrolysis: assessment of medication risks with emphasis on 23. McGee T, Munster A. Toxic epidermal necrolysis syndrome: mortality
recently marketed drugs. The EuroSCAR-study. J Invest Dermatol rate reduced with early referral to regional burn center. Plast Reconstr
2008;128(1):35–44. DOI: 10.1038/sj.jid.5701033. Surg 1998;102(4):1018–1022. DOI: 10.1097/00006534-199809040-
6. Mulvey JM, Padowitz A, Lindley-Jones M, Nickels R. Mycoplasma 00014.
pneumoniae associated with Stevens Johnson syndrome. Anaesth 24. Palmieri TL, Greenhalgh DG, Saffle JR, Spence RJ, Peck MD, Jeng JC,
Intensive Care 2007;35(3):414–417. DOI: 10.1177/0310057X0703500317. et al. A multicenter review of toxic epidermal necrolysis treated in

578 Indian Journal of Critical Care Medicine, Volume 25 Issue 5 (May 2021)
 Stevens–Johnson Syndrome

U.S. burn centers at the end of the twentieth century. J Burn Care management and future directions. Br J Dermatol 2005;153(2):241–
Rehabil 2002;23(2):87–96. DOI: 10.1097/00004630-200203000-00004. 253. DOI: 10.1111/j.1365-2133.2005.06721.x.
25. Worswick S, Cotliar J. Stevens–Johnson syndrome and toxic 37. Singh GK, Chatterjee M, Verma R. Cyclosporine in Stevens Johnson
epidermal necrolysis: a review of treatment options. Dermatol Ther syndrome and toxic epidermal necrolysis and retrospective
2011;24(2):207–218. DOI: 10.1111/j.1529-8019.2011.01396.x. comparison with systemic corticosteroid. Indian J Dermatol Venereol
26. Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson Leprol 2013;79(5):686–692. DOI: 10.4103/0378-6323.116738.
syndrome. Orphanet J Rare Dis 2010;5:39. DOI: 10.1186/1750-1172- 38. Kirchhof MG, Miliszewski MA, Sikora S, Papp A, Dutz JP. Retrospective
5- 39. review of Stevens-Johnson syndrome/toxic epidermal necrolysis
27. Ramakrishnan KM, Sankar J, Venkatraman J. Role of biological treatment comparing intravenous immunoglobulin with
membranes in the management of Stevens Johnson syndrome – cyclosporine. J Am Acad Dermatol 2014;71(5):941–947. DOI: 10.1016/
Indian experience. Burns 2007;33(1):109–111. DOI: 10.1016/j. j.jaad.2014.07.016.
burns.2006.04.029. 39. Giudice G, Maggio G, Bufano L, Memeo G, Vestita M. Management
28. Li X, Wang D, Lu Z, Chen J, Zhang H, Sun L. Umbilical cord of toxic epidermal necrolysis with plasmapheresis and cyclosporine
mesenchymal stem cell transplantation in drug-induced Stevens- A: our 10 years’ experience. Plast Reconstr Surg Glob Open
Johnson syndrome. J Eur Acad Dermatol Venereol 2013;27(5):659– 2017;5(2):e1221. DOI: 10.1097/GOX.0000000000001221.
661. DOI: 10.1111/j.1468-3083.2012.04572.x. 40. Heng MC, Allen SG. Efficacy of cyclophosphamide in toxic
29. Sharma N, Thenarasun SA, Kaur M, Pushker N, Khanna N, Agarwal T, epidermal necrolysis. Clinical and pathophysiologic aspects.
et al. Adjuvant role of amniotic membrane transplantation in acute J Am Acad Dermatol 1991;25(5 Pt 1):778–786. DOI: 10.1016/s0190-
ocular Stevens-Johnson syndrome: a randomized control trial. Ophthal­ 9622(08)80969-3.
mology 2016;123(3):484–491. DOI: 10.1016/j.ophtha.2015.10.027. 41. Dogra PM, Chatterjee M, Neema S. Tacrolimus for treatment of
30. O’Donoghue JM, Céspedes YP, Rockley PF, Nigra TP. Skin biopsies to toxic epidermal necrolysis. Indian J Dermatol Venereol Leprol
assess response to systemic corticosteroid therapy in early-stage TEN: 2015;81(6):642–644. DOI: 10.4103/0378-6323.168328.
case report and review of the literature. Cutis 2009;84(3):138–140. 42. Hunger RE, Hunziker T, Buettiker U, Braathen LR, Yawalkar N.
31. Kardaun SH, Jonkman MF. Dexamethasone pulse therapy for Stevens- Rapid resolution of toxic epidermal necrolysis with anti-TNF-alpha
Johnson syndrome/toxic epidermal necrolysis. Acta Derm Venereol treatment. J Allergy Clin Immunol 2005;116(4):923–924. DOI: 10.1016/
2007;87(2):144–148. DOI: 10.2340/00015555-0214. j.jaci.2005.06.029.
32. Hynes AY, Kafkala C, Daoud YJ, Foster CS. Controversy in the use 43. Meiss F, Helmbold P, Meykadeh N, Gaber G, Marsch WCh, Fischer
of high-dose systemic steroids in the acute care of patients with M. Overlap of acute generalized exanthematous pustulosis and
Stevens-Johnson syndrome. Int Ophthalmol Clin 2005;45(4):25–48. toxic epidermal necrolysis: response to antitumour necrosis
DOI: 10.1097/01.iio.0000177430.89645.6d. factor-alpha antibody infliximab: report of three cases. J Eur
33. Prins C, Kerdel FA, Padilla RS, Hunziker T, Chimenti S, Viard I, et al. Acad Dermatol Venereol 2007;21(5):717–719. DOI: 10.1111/j.1468-
Treatment of toxic epidermal necrolysis with high dose intravenous 3083.2006.02026.x.
immunoglobulins: multicenter retrospective analysis of 48 consecutive 44. Egan CA, Grant WJ, Morris SE, Saffle JR, Zone JJ. Plasmapheresis as an
cases. Arch Dermatol 2003;139(1): 26–32. DOI: 10.1001/archderm.139.1.26. adjunct treatment in toxic epidermal necrolysis. J Am Acad Dermatol
34. Barron SJ, Del Vecchio MT, Aronoff SC. Intravenous immunoglobulin 1999;40(3):458–461. DOI: 10.1016/s0190-9622(99)70497-4.
in the treatment of Stevens-Johnson syndrome and toxic epidermal 45. Furubacke A, Berlin G, Anderson C, Sjöberg F. Lack of significant
necrolysis: a meta-analysis with meta-regression of observational treatment effect of plasma exchange in the treatment of drug-induced
studies. Int J Dermatol 2015;54(1):108–115. DOI: 10.1111/ijd.12423. toxic epidermal necrolysis? Intensive Care Med 1999;25(11):1307–1310.
35. Bachot N, Revuz J, Roujeau JC. Intravenous immunoglobulin DOI: 10.1007/s001340051063.
treatment for Stevens-Johnson syndrome and toxic epidermal 46. Su SC, Chung WH. Cytotoxic proteins and therapeutic targets in severe
necrolysis: a prospective noncomparative study showing no benefit cutaneous adverse reactions. Toxins (Basel) 2014;6(1):194–210. DOI:
on mortality or progression. Arch Dermatol 2003;139(1):33–36. 10.3390/toxins6010194.
DOI: 10.1001/archderm.139.1.33. 47. Thong BY. Stevens-Johnson syndrome/toxic epidermal necrolysis:
36. Chave TA, Mor timer NJ, Sladden MJ, Hall AP, Hutchinson an Asia-Pacific perspective. Asia Pac Allergy 2013;3(4):215–223. DOI:
PE. Toxic epidermal necrolysis: current evidence, practical 10.5415/apallergy.2013.3.4.215.

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