National Journal of Emergency Medicine
Volume 1 | Issue 3 | Year 2023

Dermatological Emergency in Emergency Medicine: A Case Series

Goutham Deivassigamany1, Nithyaraj Ramanathan2, Kirubasankaran Ezhilan3

1–3Department of Emergency Medicine, Sri Manakula Vinayagar Medical College and Hospital, Puducherry, India

Corresponding Author: Nithyaraj Ramanathan, Department of Emergency Medicine, Sri Manakula Vinayagar Medical College and Hospital, Puducherry, India, Phone: +91 9791919491, e-mail:

How to cite this article: Deivassigamany G, Ramanathan N, Ezhilan K. Dermatological Emergency in Emergency Medicine: A Case Series. Natl J Emerg Med 2023;1(3):71–76.

Source of support: Nil

Conflict of interest: None

Received on: 30 November 2023; Accepted on: 20 December 2023; Published on: 25 January 2024


Toxic epidermal necrolysis (TEN), is an acute, potentially life-threatening mucocutaneous disease often induced by drugs due to an inappropriate immune reaction. It is characterized by the widespread detachment and exfoliation of the epidermis and mucous membrane, leaving large areas of raw, exposed tissue. It is a medical emergency and requires immediate treatment. The condition might result in sepsis, a deadly complication if not treated promptly. It involves >30% of the total body surface area (TBSA), which helps to differentiate it from Stevens-Johnson syndrome (SJS) which involves 10% of TBSA. It usually occurs within a few weeks of treatment initiation, and requires a detailed medication history that plays a pivotal role in the diagnosis. The severity-of-illness score for TEN (SCORTEN) is used to estimate the prognosis. In this report, we report three cases of drug-induced severe TEN who were presented to the emergency room (ER). The presence of the characteristic skin lesions led to the diagnosis of TEN in these cases. Their TBSA was >30%, with a positive Nikolsky sign. Two of the cases had a SCORTEN of 2, and one had a SCORTEN of 6 with a significant history. Treatment was initiated with the withdrawal of the potential agent and pulse therapy with conservative treatment.

Keywords: Emergency medicine, Muco-cutaneous disease, Pulse therapy, Toxic epidermal necrolysis, Severity-of-illness score for TEN.


Toxic epidermal necrolysis (TEN), is a rare life-threatening disorder, characterized by extensive necrolysis and detachment of full-thickness epidermis, generally induced by drugs.1,2 It is a medical emergency that requires immediate treatment. The condition might result in sepsis, a deadly complication, if not treated promptly.1,2 Toxic epidermal necrolysis has a low incidence with an annual rate of 0.4–1.2 cases per million per year, but with 80% of mortality.35 Most studies reported that Asian and black patients were more susceptible to two-fold increased risk when compared with white people.3,5 As for the sex differences, the female sex predominant with men in the ratio of 1.5–1 and present between 5th and 7th decades of life.57 Toxic epidermal necrolysis involves >30% of the total body surface area (TBSA), which helps to differentiate it from Stevens-Johnson syndrome (SJS) which involves 10% of TBSA.3,4,8 It always manifests within few weeks after contact with suspicious drug.8,9 In this case series we report three cases of drug-induced severe TEN who were presented to the emergency room (EA) and their management. Their TBSA was >30% with characteristics positive Nikolsky sign. Among the cases, two case had a SCORTEN of 2 and one case had 6 with the significant history. Also, the presence of the characteristic skin lesions clicked the diagnosis of TEN in these cases. Management was done with pulse therapy and other conservative treatments. This study conformed to the provisions of the declaration of Helsinki.


Case 1

A 24-year-old male, a chronic alcoholic under rehabilitation therapy referred from a private hospital to our emergency room (ER) with complaints of discoloration and fluid-filled blisters in the trunk and hand which further spread all over the body with peeling of skin itching and touching. Followed by which patients developed fever and skin rash which gradually progressed into erythematous rash which was tender and also peeling off from body flexures (Fig. 1).

Figs 1A to C: Case 1: (A) At the time of admission in ED-day 1 with extensive peeling of the skin with discoloration of the skin. SCORTEN score-2; TBSA->50% (consent obtained); (B) Patient on follow-up shows the regression of the lesions after the treatment initiation; (C) Patient after discharge and complete regression of the lesions

On detailed history taking, he was a chronic alcoholic and smoker, for which he was undergoing rehabilitation therapy. During the therapy he had seizures and was diagnosed with alcohol withdrawal syndrome with seizure episodes, for which he was initiated on the antiepileptic tablet phenytoin 100 mg thrice a day (TDS) for five days. On the seventh day, he started to develop the symptoms mentioned above and on the 10th day it started to peel skin on its own. His last meal intake was only a liquid diet.

Upon arrival at the ED, the initial examination was done, patent airway, breathing was spontaneous, with respiratory rate (RR) 24 breaths per min, SpO2 at room air (oxygen saturation) was 94%, blood pressure (BP) was 80/not recordable mm Hg, pulse rate (PR) was 123 per minute, capillary refilling time (CRT) was >5 seconds, Glasgow coma scale (GCS) was 15/15 (E4, V5, M6), capillary blood glucose (CBG)101 mg/dL, Jugular venous pressure (JVP) not raised, and the temperature was 100.6° Fahrenheit (F). Laboratory investigations were done and presented in Table 1.

Table 1: Laboratory investigations done in all cases at the time of admission
Laboratory investigation Case 1 Case 2 Case 3 Normal range Units
Random blood sugar (RBS) 245 323 213 70–100 mg/dL
Hemoglobulin (Hb) 10 7.4 12 13–17 gm/dL
White blood cells (WBC) 13,500 13,500 10,000 4,000–11,000 cells/mm3
Platelet count 2.09 9.21 2.21 1.50–4.50 lakhs/mm3
Serum urea 30 56 16 15–45 mg/dL
Creatinine 0.9 0.8 0.4 0.6–1.2 mg/dL
Bilirubin total 0.9 0.9 0.1 0.2–1 mg/dL
Bilirubin direct 0.3 0.3 0.2 Up to 0.2 mg/dL
Albumin 3.9 2.1 3.8 3.7–5.3 mg/dL

His cutaneous examination revealed lesions that were erythematous to violaceous and purpuric macules which initially involved the trunk and spread distally to the limbs. Subsequently, blackish discoloration of the skin was seen. Lesions also involved the right cornea and lips. Nikolsky sign was found to be positive. Total body surface area was >50% with a severity-of-illness score for TEN (SCORTEN) score of 2 on examination. Without further delay, a central line was inserted in the right internal jugular vein (IJV) and stated on the intravenous (IV) injection Paracetamol (1 g IV) for fever, injection fentanyl (50 μg IV) for the pain management, injection Rantac (50 mg IV). The diastolic BP (DBP) was not detectable in this patient and to further prevent hypovolemic shock, IV fluids (IVF) of Normal saline (NS) 1 liter was given, followed which the BP was improved to 100/70 mm Hg. Then, NS was changed to IVF ringer lactate (RL) 500 mL at 125 mL/hour and BP was checked hourly. Wound dressing with nanosilver was done. Then finally, pulse therapy with injection dexamethasone (1.5 mg/kg) was administered. After the emergency management, the patient was immediately transferred to the Dermatology department for further consultation and management.

Case 2

A 45-year-old female brought to our ER with complaints of fluid-filled blisters developed in multiple raw areas. Pus discharge was present over the scalp, face, chest, and axilla for 30 days. Initially patient sounded the fluid-filled blister over the scalp and face so she self-diagnosed chicken pox and bought over-the-counter medication tablet acyclovir 400 mg TDS for five days and consumed over a period of 10 days. Subsequently, she developed blisters on the skin that progressed to ulcers over the scalp, face, eyes, neck, truck, and even in the oral cavity with odynophagia (painful swallowing), which led to poor oral intake and cachexia (Fig. 2). She is not allergic to any other food or other medication, previously. Known case of type 2 diabetes and systemic hypertension, for which she was on regular medication with no significant past and no allergic history.

Figs 2A and B: Case 2: (A) At the time of admission in ED-Day 1-shows extensive exfoliation of the skin in trunk, with oral mucosa and eye involvement (consent was obtained); (B) Patient during the follow-up started regression of the lesions after treatment initiation

Upon admission to the ER, the patient was conscious. Her systemic examination showed that the patient’s airway was patent and spontaneous breathing. RR: 23 breaths/min; SpO2 at room air was 96%, BP was 70/not recordable mm Hg, PR was 121/min, and CRT was >5 seconds. The GCS was found to be 15/15 (E4 V5 M6), JVP was not raised, and CBG was 316 mg/dL. The temperature was 102.4° F at the time of admission. Laboratory investigations are presented in Table 1.

Her cutaneous examination showed multiple large eroded and crusted lesions that were distributed craniocaudally. It involved the chest, abdomen, and trunk, both oral and conjunctive. Extensive ulcerative lesions over an erythematous base with crusting and serosanguineous fluid were present with positive Nikolsky sign. SCORTEN score was six and TBSA was >40%. As for the management, the central line was inserted in the right femoral vein and administered injection Paracetamol (1 g IV), injection Fentanyl (50 μg IV) and injection Rantac (50 mg IV) for the symptomatic management of fever and pain. Since DBP was not detected in this patient also, hence IVF NS was given (1 liter), and BP was improved. For this patient, injection noradrenaline double strength (5 μg/mL/hour IV) was given. Then, the IVF NS was changed to RL 500 mL with a flow of 125 mL/hour. Wound dressing was done with nano silver. For this patient also, pulse therapy of injection dexamethasone (1.5 mg/kg) was given. Then, we sought a dermatologist’s consent, and the patient was transferred to the dermatology ward for further management and follow-up.

Case 3

A 50-year-old male was admitted to ER with the complaints of fever and sudden pealing of skin over the trunk, back, and genitalia for three days. Initially, it started over the chest and further progressed all over the trunk and back. He had a history of fever for five days for which he visited the nearby private clinic and was prescribed antipyretics and antibiotics. He had tablet paracetamol (650 mg TDS) and tablet ciprofloxacin 500 mg BD (twice daily) for five days was given. After intake of the medicine, on the sixth day he developed the symptoms of skin peeling. He had no history of any allergic reaction to any food or medication previously. His past history was not significant to the present complaints (Fig. 3).

Fig. 3: Case 3 at the time of admission in ER-Day 1 shows discoloration and peeling of skin (consent was obtained)

The patient was conscious and oriented. On initial examination his airway was patent with spontaneous breathing. RR was 19 breaths/min, SpO2 98% at room air, BP was 130/70 mm Hg, PR was 101 beats/min, CRT <5 sec, CBG was 162 mg/dL, not raised JVP, and his GCS scoring was 15/15 (E4 V5 M6). The temperature was 98°F initially. Laboratory investigations are presented in Table 1. The cutaneous examination showed superficially cutaneous lesions that involved the trunk with fluid discharge. Lesions are also present in the genitalia region. Nikolsky sign was found to be positive with a TBSA of >30% and a SCORTEN score of 2 on examination. Peripheral line was secured immediately for the management and injection Paracetamol (1 g IV), injection Morphine (3 mg IV), injection Rantac (50 mg IV) was given to reduce the pain and fever. Then IVF with 1 liter of NS, followed with 500 mL of RL in the flow of 125 mL/hour was administered. Nano silver dressing was done and inj. dexamethasone of 1.5 mg/kg was given as the pulse therapy. Then, the patient was transferred to dermatology department for further management.


Allergic reactions induced by drugs were the most common presentation in the emergency room. Among the dermatological conditions, SJS and TEN were common emergency presentations which are life-threatening with severe muco-cutaneous reactions characterized by blistering and denudation of the skin.1,5,10 When compared to SJS, TEN was more severe and might result in a poor prognosis. It was initially described by Alan Lyell in 1956 as “an eruption resembling scalding of the skin”.11

Etiology of the TEN depicts that it was induced by certain medications, infections, vaccines, or even idiopathy.1 According to EuroSCAR study done in 2008 by Mockenhaupt et al., showed that various drugs result in TEN (Table 2).12 Added to that, infections such as mycoplasma pneumoniae, hepatitis A, herpes virus, malignancies such as hepatocellular carcinoma, lung cancer, vaccinations especially the meningococcal vaccine.13,14 In our case series, we found that phenytoin, acyclovir, and ciprofloxacin were the drugs that were taken by the patient, followed which TEN occurs, that were in concordance with the previous studies.

Table 2: Drugs that cause TEN
Antibiotics-sulphonamides, chloramphenicol, penicillin, and quinolones Antiepileptics-barbiturate, carbamazepine, phenytoin, valproate, and lamotrigine Nonsteroidal anti-inflammatory drugs (NSAID)-oxybutazone and piroxicam
Antiviral drugs-oseltamivir and abacavir Allopurinol  


One of the theories proposed was oxidative stress and keratinocyte apoptosis. In keratinocytes, the biomarker for oxidative stress is Glutathione S-Transferase-p (GST-p), which has been detected at higher levels in patients with TEN with 10- to 20-fold increased levels when compared with other cutaneous drug reactions.1517 The drug that interferes with the detoxification pathways results in the accumulation of reactive oxygen special (ROS) which is the major cause of oxidative stress and triggers programmed cell death.15,16

Another pathology involved is Fas-Fas ligand or granulysin-mediated apoptosis.18 The causative drug may cause keratinocytes to express Fas constitutively, upregulating Fas-L in the process of activating a death receptor-mediated apoptotic cascade.2,18 Drug-specific CD8+ cytotoxic T cells may assemble inside epidermal blisters because of the medication’s interaction with cells that express the major histocompatibility complex class I, releasing perforin and granzyme B that can kill keratinocytes.1,2,7,18 Drug-activated monocytes release annexin A1, which causes keratinocytes to undergo necroptosis. Additionally, the medication may cause CD8+ T cells, NK (Natural killer) cells, and NK T-cells to become activated and produce granulysin, which can cause keratinocyte death without cell interaction.1,2,5,7,18

Clinical Presentation

To date, no markers were available for the early diagnosis of TEN, as it depends on the clinical examination only. In drug-induced TEN, usually occurs within 1–3 weeks of the initiation of the treatment.1 The clinical presentation begins with prodromal flu-like symptoms, followed by a muco-cutaneous morbilliform rash, located at the acral areas, later spread quickly over the body.5,19 They are characterized as ill-defined dusky erythematous macular rash and bullae, which then coalesce to form sheet-like blisters, subsequently slough out leaving moist denuded dermis.1,11,13 Blisters that are flaccid occur and burst quickly causing larger areas of denudation.

Nikolsky sign which is the denudation of blister formation at the pressure site as the skin is extremely fragile.1,2,7,9 The positive Nikolsky sign is considered as the pathognomonic features of the TEN.1,2,4,5,9 This at times leads to multiorgan failure due to sepsis and predisposes to death in around 30% of patients.10,19 Examination of the early lesions shows apoptotic keratinocytes scattered in the basal layer of the epidermis and in established lesions full thickness of epidermal necrosis and subepidermal bullae presents.1,20 All our patients in this case series were presented with the above-mentioned skin lesion and with the positive Nikolsky sign, which ultimately led to a diagnosis of TEN.

Various literature, found that patients were also presented with major mucosal involvement with painful erosion at oral (70–100%), genital region (40–63%), and ocular (50–78%) involvement.5,10,19 These are in concordance with our patients results, as two patients had mucosal involvement. Furthermore, in patients with severe TEN, it might lead to systematic involvement and result in acute renal failure (5%), respiratory distress syndrome, bronchiolitis obliterans, leukopenia, hepatitis, and anemia.5,10,19 In our case series, one patient present with diabetes mellitus was aggravated by the systemic treatment with corticosteroids and also increased the blood glucose level without control.

Since there is no standard guideline for the treatment, prompt recognition and abandonment of the suspected drug with rapid intervention will help in a satisfactory prognosis.7 The SCORTEN was a recognized and validated measure to assess the disease severity and the prognosis was developed by Bastuji-Garin et al., and included seven clinical criteria.21 This scale is also used to predict the mortality rate (Table 3).21 In our case series, two patients had a SCORTEN of score 2 with the risk of mortality was 12.1% and one patient’s score was 6, indicating a high risk of mortality (90%).

Table 3: Severity-of-Illness for TEN (SCORTEN) scoring system21
SCORTEN parameter Individual score SCORTEN sum Predicted mortality rate (%)
Yes (1) No (0)
Age >40 years <40 years 0–1 3.2
Presence of cancer Yes No 2 12.1
Heart rate >120 bpm <120 bpm 3 35.8
TBSA involved at day 1 >10% <10% 4 58.3
Serum urea level >10 mmol/L <10 mmol/L >5 90
Plasma glucose level >14 mmol/L <14 mmol/L    
Bicarbonate level <20 mmol/L >20 mmol/L    
Bpm, beats per minute; mmol/L, millimole per liter


General management of this condition includes the withdrawal of the potential drug that caused TEN followed by continuous monitoring of the patient. Based on the pathologic and immunological basis of TEN, three major drugs are used as the systemic treatment in the acute phase, including systemic corticosteroids, intravenous immunoglobulin (IVIg), and cyclosporine.5,19,22,23 Nowadays, pulse therapy is used constantly for patients with TEN.24 It is the discontinuous or intermittent IV infusion of very high doses of corticosteroids (1.5 mg/kg IV methylprednisolone or 100 mg IV dexamethasone) along with certain immunosuppressive agents over short periods to minimize the side effects of the conventional corticosteroid therapy.24 In our cases, rapid systemic corticosteroid was initiated with a central IV line (Fig. 4).

Figs 4A and B: Central IV-line placement in patients with TEN

Thus, based on the characteristics of the history and the skin lesions along with TBSA and SCORTEN made the diagnosis of the current cases easier and its management.

Emergency Room Management of TEN

Patients admitted with TEN in ER were assessed for the airway, breathing, circulation, disability, and exposure (ABCDE) procedure. Identifying the drug that caused TEN and withdrawing immediately without any delay. Followed with fluid management, where it is essential to avoid hypovolemic shock. Pain management is to be done that reduces the pain, followed by sepsis management which reduces the mortality. Since the patient’s skin was exposed, wound care was done with dressing. To improve wound healing and avoidance of the extensive peeling of the skin due to the unknown immune reaction to the drug, tacrolimus medication was given at the ER management. Pulse therapy was used.24

Complications of TEN

The major complication of TEN was sepsis. Ocular complications were common among these patients which require ophthalmic consultation. Other complications include electrolyte imbalance which requires fluid replacement, hypoalbuminemia, and dehydration.1,2 Also, due to the mucosal involvement of the oral mucosa leads to odynophagia further leads to cachexia. Moreover, all patients with TEN should be evaluated for the need for post-discharge psychological support.25


Toxic epidermal necrolysis, a drug-induced mucocutaneous disease considered as rare but extremely severe and life-threatening, needs to be recognized and assessed with prompt action. Treatment to be initiated by cessation of the drug that leads to the condition acts as a first-line management. The patients require multidisciplinary care in an intensive care unit or severe burns unit to reduce morbidity and mortality.


Goutham Deivassigamany


1. Labib AM, Milroy C. Toxic Epidermal Necrolysis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2022.Available from:

2. Stătescu L, Constantin M, Morariu HS, et al. Toxic epidermal necrolysis-A case report. J Crit Care Med Univ Med Si Farm Din Targu-Mures 2017;3(1):29–33.DOI:

3. Chaby G, Ingen-Housz-Oro S, De Prost N, et al. Idiopathic Stevens-Johnson syndrome and toxic epidermal necrolysis: Prevalence and patients’ characteristics. J Am Acad Dermatol 2019;80(5):1453–1455.DOI: 0.1016/j.jaad.2018.10.058.

4. Kim HI, Kim SW, Park GY, et al. Causes and treatment outcomes of Stevens-Johnson syndrome and toxic epidermal necrolysis in 82 adult patients. Korean J Intern Med 2012;27(2):203–210.DOI: 0.3904/kjim.2012.27.2.203.

5. Schwartz RA, McDonough PH, Lee BW. Toxic epidermal necrolysis: Part I. Introduction, history, classification, clinical features, systemic manifestations, etiology, and immunopathogenesis. J Am Acad Dermatol 2013;69(2):173.e1–e13; quiz 185–186.DOI: 0.1016/j.jaad.2013.05.003.

6. Hsu DY, Brieva J, Silverberg NB, et al. Morbidity and mortality of Stevens-Johnson syndrome and toxic epidermal necrolysis in United States adults. J Invest Dermatol 2016;136(7):1387–1397.DOI: 0.1016/j.jid.2016.03.023.

7. Poulsen VOB, Nielsen J, Poulsen TD. Rapidly developing toxic epidermal necrolysis. Case Rep Emerg Med 2013;2013:e985951.DOI: 0.1155/2013/985951.

8. Bastuji-Garin S, Rzany B, Stern RS, et al. Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme. Arch Dermatol 1993;129(1):92–96.PMID: 8420497.

9. Roujeau JC, Kelly JP, Naldi L, et al. Medication use and the risk of Stevens-Johnson syndrome or toxic epidermal necrolysis. N Engl J Med 1995;333(24):1600–1607.DOI: 0.1056/NEJM199512143332404.

10. Creamer D, Walsh SA, Dziewulski P, et al. U.K. guidelines for the management of Stevens-Johnson syndrome/toxic epidermal necrolysis in adults 2016. Br J Dermatol 2016;174(6):1194–1227.DOI:

11. Lyell A. Toxic epidermal necrolysis: An eruption resembling scalding of the skin. Br J Dermatol 1956;68(11):355–361.DOI: 0.1111/j.1365-2133.1956.tb12766.x.

12. Mockenhaupt M, Viboud C, Dunant A, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis: Assessment of medication risks with emphasis on recently marketed drugs. The EuroSCAR-study. J Invest Dermatol 2008;128(1):35–44.DOI: 0.1038/sj.jid.5701033.

13. Wu J, Lee YY, Su SC, et al. Stevens-Johnson syndrome and toxic epidermal necrolysis in patients with malignancies. Br J Dermatol 2015;173(5):1224–1231.DOI: 0.1111/bjd.14052.

14. Chahal D, Aleshin M, Turegano M, et al. Vaccine-induced toxic epidermal necrolysis: A case and systematic review. Dermatol Online J 2018;24(1):13030/qt7qn5268s.PMID: 29469759.

15. Paquet P, Piérard GE. Glutathione-S-transferase pi expression in toxic epidermal necrolysis: A marker of putative oxidative stress in keratinocytes. Skin Pharmacol Physiol 2007;20(2):66–70.DOI: 0.1159/000097652.

16. Hayes JD, Pulford DJ. The glutathione S-transferase supergene family: Regulation of GST and the contribution of the isoenzymes to cancer chemoprotection and drug resistance. Crit Rev Biochem Mol Biol 1995;30(6):445–600.DOI: 0.3109/10409239509083491.

17. Chung WH, Hung SI, Yang JY, et al. Granulysin is a key mediator for disseminated keratinocyte death in Stevens-Johnson syndrome and toxic epidermal necrolysis. Nat Med 2008;14(12):1343–1350.DOI: 0.1038/nm.1884.

18. Abe R. Toxic epidermal necrolysis and Stevens-Johnson syndrome: Soluble Fas ligand involvement in the pathomechanisms of these diseases. J Dermatol Sci 2008;52(3):151–159.DOI: 0.1016/j.jdermsci.2008.06.003.

19. Sassolas B, Haddad C, Mockenhaupt M, et al. ALDEN, an algorithm for assessment of drug causality in Stevens-Johnson syndrome and toxic epidermal necrolysis: Comparison with case-control analysis. Clin Pharmacol Ther 2010;88(1):60–68.DOI: 0.1038/clpt.2009.252.

20. Harr T, French LE. Toxic epidermal necrolysis and Stevens-Johnson syndrome. Orphanet J Rare Dis 2010;5:39.DOI: 0.1186/1750-1172-5-39.

21. Fouchard N, Bertocchi M, Roujeau JC, et al. SCORTEN: A severity-of-illness score for toxic epidermal necrolysis. J Invest Dermatol 2000;115(2):149–153.DOI: 0.1046/j.1523-1747.2000.00061.x.

22. Sharma VK, Sethuraman G, Kumar B. Cutaneous adverse drug reactions: Clinical pattern and causative agents–a 6-year series from Chandigarh, India. J Postgrad Med 2001;47(2):95–99.PMID: 11832597.

23. Aihara M, Kano Y, Fujita H, et al. Efficacy of additional I.V. immunoglobulin to steroid therapy in Stevens-Johnson syndrome and toxic epidermal necrolysis. J Dermatol 2015;42(8):768–777.DOI: 0.1111/1346-8138.12925.

24. Mittal R, Sudha R, Murugan S, et al. Pulse therapy in dermatology. Sri Ramachandra J Med 2007;1(2):44–46.Available from:

25. Seminario-Vidal L, Kroshinsky D, Malachowski SJ, et al. Society of dermatology hospitalists supportive care guidelines for the management of stevens-johnson syndrome/toxic epidermal necrolysis in adults. J Am Acad Dermatol 2020;82(6):1553–1567.DOI: 0.1016/j.jaad.2020.02.066.

© The Author(s). 2023 Open Access. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (, which permits unrestricted use, distribution, and non-commercial reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.