重症多形红斑与中毒性表皮坏死松解症的临床分析

目的探讨重症多形红斑(SJS)与中毒性表皮坏死松解症(TEN)的致病因素、发生规律、临床特点和治疗措施。方法对42例SJS和20例TEN住院患者的临床资料进行回顾性分析。结果 SJS组和TEN组患者中,药物为最常见病因。致敏药物中排在前三位的分别是抗癫痫药(29.03%)、别嘌呤醇(16.13%)及抗生素(16.13%)。SJS与TEN的黏膜损害率均为100%,TEN组的皮损范围、损害程度、黏膜病变均较SJS组更广泛、更严重,TEN的日、最大糖皮质激素用量均高于SJS。结论药物是SJS和TEN发病最主要的原因。TEN患者较SJS患者病变广泛且严重。别嘌呤醇与卡马西平应用需谨慎,激素联合免疫球蛋白IVIG治疗有效。     

糖皮质激素联合人免疫球蛋白治疗Stevens-Johnson综合征和中毒性表皮松解症

  目的  探讨Stevens-Johnson综合征(Stevens-Johnson syndrome, SJS)和中毒性表皮松解症(toxic epidermal necrolysis, TEN)的临床特征及治疗方法, 以提高对SJS/TEN的认识。  方法  回顾性分析北京协和医院7例SJS/TEN患者的临床表现、疾病严重程度、眼部受累程度、致敏药物、治疗方案及临床结局。  结果  患者年龄26~81岁, 均伴有黏膜损害, 致敏药物以非甾体类抗炎药、抗惊厥药及别嘌醇为主, 7例均使用大剂量糖皮质激素联合人免疫球蛋白治疗, 治愈6例, 死亡1例。  结论  SJS/TEN是一组累及全身皮肤黏膜严重威胁患者生命的疾病, 病死率高, 早期足量使用大剂量糖皮质激素联合人免疫球蛋白为主要的治疗手段, 伴有系统疾病的患者预后较差。眼部损伤与疾病严重程度具有不同步性, 需及早给予针对性治疗。     

Morbidity and mortality of mucocutaneous diseases in the pediatric population at a tertiary care center.

Toxic epidermal necrolysis (TEN) is a life threatening desquamating disease that is often an adverse reaction to drugs. Because mortality is so high, up to 30% nationally, and the morbidity significant, these cases are managed in burn centers. This study was conducted to evaluate what drugs were given to children who developed exfoliating skin disease and to identify the complications that these patients suffered. Thirty-two pediatric cases of erythema multiforme, Stevens-Johnson syndrome (SJS), and TEN were identified during a period of 8 years in which the average number of admissions to the burn center was 200 per year. Age, sex, drug history before admission, drug treatment during hospital stay, and clinical outcomes were noted. Several drugs were identified as probable causative agents. The most common cause of exfoliating disease was a combination of azithromycin and ibuprofen, followed by ibuprofen alone. Notably, the combination of ibuprofen and another drug was responsible for four additional cases, making the total percentage of pediatric cases involving ibuprofen 47%. Although no children died, several children with TEN and SJS suffered severe ocular involvement, sepsis, pneumonia, and genitourinary complications. All of the children who experienced complications had received ibuprofen. Chi-square analysis showed the correlation between ibuprofen and complications to be statistically significant (<0.05). This association was not observed with any other drug administered. Not only is ibuprofen a potential etiologic agent of exfoliating skin disease in children, it also may contribute to the development of complications in pediatric patients with the disease. Although this association does not prove that ibuprofen is the definitive cause of complications in these cases, caution is advised when giving this drug to children with suspected erythema multiforme, SJS, and TEN.     

Phenotype standardization for immune-mediated drug-induced skin injury

Advances in genetic research and molecular biology techniques have made it possible to begin to characterize the underlying genetic factors that predispose patients to serious forms of drug-induced skin injury (DISI). To facilitate research in this area, we have set out standardized phenotypic definitions for (i) Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), (ii) acute generalized exanthematous pustulosis (AGEP), and (iii) hypersensitivity syndrome (HSS; also known as drug reaction with eosinophilia and systemic symptoms (DRESS) and drug-induced hypersensitivity syndrome (DIHS)). A DISI Expert Working Group comprising participants with varied expertise reviewed and debated current terminology and diagnostic criteria for DISI and agreed on the minimum phenotypic criteria for selected forms of DISI (SJS/TEN, AGEP, and HSS). In addition, an algorithm has been developed to aid appropriate clinical categorization of patients with DISI. These standardized criteria will be important in facilitating adequate and accurate patient recruitment in order to advance research in pharmacogenomic, immunological, mechanistic, and epidemiological studies.     

Stevens-Johnson syndrome and toxic epidermal necrolysis: oncologic considerations

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are severe skin toxicities that may occur in patients with cancer. They are caused by infection or a drug reaction and can result in sepsis, severe ocular complications, and even death. Skin lesions usually are preceded by prodromal flulike symptoms. A rash with subsequent blistering and denudation follows. Diagnosis is made by skin biopsy, and classification is based on body surface area and visceral organ involvement. Because many of the drugs associated with SJS and TEN are used to treat cancer, early recognition and intervention are critical to achieving a favorable outcome. Interventions include stopping the suspected offending agent. The use of steroids is controversial. Healthcare professionals always should consider an early transfer to a burn unit for patients with a comorbid condition such as cancer because this action is associated with improved outcomes. Implications for oncology nurses and a case study are presented in this article.     

Warfarin‐induced Stevens–Johnson syndrome with severe liver injury

Stevens–Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) is a life-threatening mucocutaneous disease that is predominantly drug-induced. Warfarin is the most commonly used drug for long-term anti-coagulant therapy; however, warfarin-induced SJS/TEN is seldom reported. In this study, we presented the case of a 61-year-old man who developed SJS after receiving multiple-drug therapy following aortic valve replacement surgery. The patient was diagnosed with drug-induced liver injury (DILI) based on significantly abnormal liver function test results. Warfarin was identified as the culprit drug using the algorithm of drug causality for epidermal necrolysis (ALDEN) score, enzyme-linked immunospot (ELISPOT) assay, and Roussel Uclaf Causality Assessment Method (RUCAM). After warfarin discontinuation and corticosteroid therapy, the lesions and liver function test findings improved. Human leukocyte antigen typing was conducted to detect the risk allele. To our knowledge, this is the first reported case of warfarin-induced SJS/TEN with DILI. This case suggests that commonly used and safe pharmaceutical agents such as warfarin can potentially cause serious adverse events, including SJS/TEN and DILI. The application of ALDEN, the ELISPOT assay, and RUCAM could be useful in identifying culprit drugs.     

HLA‐B*1502 Strongly Predicts Carbamazepine‐Induced Stevens–Johnson Syndrome and Toxic Epidermal Necrolysis in Thai Patients with Neuropathic Pain

Background: Carbamazepine (CBZ) is one of the standard pharmacological treatments for neuropathic pain. However, its serious adverse drug reactions include Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Recently, HLA‐B*1502 allele was implicated as a genetic marker of CBZ‐induced SJS/TEN in some Asian epilepsy populations. Methods: This is a case control study to describe the clinical characteristics of SJS/TEN in Thai patients with neuropathic pain who were treated with CBZ, and to determine the association of HLA‐B*1502 in these patients, comparing with those who exposed to CBZ for at least 6 months without any cutaneous reactions. Results: Thirty‐four SJS/TEN patients and 40 control patients were included in this study. Mean age of SJS/TEN patients was 47 years. SJS/TEN was developed in 10.8 ± 1.4 days after initiation of CBZ. HLA‐B*1502 allele was found in 32 of 34 SJS/TEN patients (94.1%) but it was found only in 7 of 40 control patients (17.5%). The association was very strong with an odds ratio of 75.4. Sensitivity and specificity of this HLA‐B*1502 genotype test were 94.1% and 82.5%, respectively, while the positive predictive value and negative predictive value were 1.43% and 99.98%, respectively. Positive and negative likelihood ratios were 5.37 and 0.07, respectively. Conclusions: HLA‐B*1502 is a strong genetic marker for CBZ‐induced SJS/TEN in Thai patients with neuropathic pain. The screening for this marker should be performed prior to initiation of CBZ treatment to assess the risk of this serious side effect.     

Erosive cheilitis as an early manifestation in DRESS syndrome

Drug reaction with eosinophilia and systemic symptoms (DRESS) is a distinct part of severe cutaneous adverse reactions (SCARs). It is characterized by fever, rash, hematologic abnormalities, lymphadenopathy, or/and different degrees of visceral organ involvement. Its diagnosis is particularly challenging due to the variability of its clinical presentations and its long latency period (2–6 weeks). Allopurinol, an uric acid‐lowering drug, has been incriminated in several cases of allopurinol‐induced DRESS syndrome. Through this paper, we present a case of allopurinol‐induced DRESS syndrome with initial oral mucosal involvement. A 69‐year‐old female patient presented with an erosive cheilitis that started 1 week prior to his presentation. The cheilitis was associated with maculopapular rash and fever. She started taking allopurinol, as treatment of Gout, 6 weeks before hospitalization. The histologic findings obtained from skin biopsy were consistent with a toxic drug reaction. A complete blood count (CBC) showed a moderate eosinophilia. Alteration of renal function was also noted, and the diagnosis of allopurinol‐induced DRESS syndrome was made. Systemic corticosteroid therapy was therefore started. The patient completely recovered and had been healthy for 3 years before developing a recurrence after re‐challenge with allopurinol.     

Norfloxacin-induced toxic epidermal necrolysis

OBJECTIVE: To report a case of toxic epidermal necrolysis (TEN) in a man who was treated with oral norfloxacin for prostatitis. CASE SUMMARY: A 40-year-old man presented with a severe skin reaction, which was diagnosed as TEN. He had received norfloxacin 800 mg/day over a 14-day period for prostatitis and, 10 days after finishing the treatment regimen, he developed cutaneous and mucous lesions typical of TEN. After a prolonged hospitalization and treatment with oral prednisolone therapy, fluid resuscitation, and wound dressing, the man recovered. DISCUSSION: TEN is an infrequent, yet often fatal, severe systemic and cutaneous disease that is most often an adverse drug reaction. There are few case reports of TEN induced by fluoroquinolones. A MEDLINE search (1966-February 2005) revealed no reports of toxic epidermal necrolysis, but one incidence of Stevens-Johnson syndrome due to norfloxacin therapy. An objective causality assessment suggests that TEN was probably related to norfloxacin in this patient. CONCLUSIONS: To our knowledge, this is the first case of TEN associated with the use of oral norfloxacin. We hope that this case report creates awareness that norfloxacin-induced TEN is possible.     

Clinical, Etiologic, and Histopathologic Features of Stevens-Johnson Syndrome During an 8-Year Period at Mayo Clinic

OBJECTIVE: To examine clinical, etiologic, and histologic features of Stevens-Johnson syndrome and to identify possible correlates of clinical disease severity related to etiologic and histopathologic findings.PATIENTS AND METHODS: This is a retrospective review of patients seen at Mayo Clinic between January 1, 2000, and December 31, 2007.RESULTS: Of 27 patients (mean age, 28.1 years), 22 (81%) had involvement of 2 or more mucous membranes, and 19 (70%) had ocular involvement. Medications, most commonly antibiotics and anticonvulsants, were causative in 20 patients. Mycoplasma pneumoniae infection caused 6 of the 27 cases. Corticosteroids were the most common systemic therapy. No patients with mycoplasma-induced Stevens-Johnson syndrome had internal organ involvement or required treatment in the intensive care unit, in contrast to 4 patients each in the drug-induced group. Three patients had chronic ocular sequelae, and 1 died of complications. Biopsy specimens from 13 patients (48%) showed epidermal necrosis (8 patients), basal vacuolar change (10 patients), and subepidermal bullae (10 patients). Biopsy specimens from 11 patients displayed moderate or dense dermal infiltrate. Histologic features in drug-induced cases included individual necrotic keratinocytes, dense dermal infiltrate, red blood cell extravasation, pigment incontinence, parakeratosis, and substantial eosinophils or neutrophils.CONCLUSION: Our clinical and etiologic findings corroborate those in previous reports. M pneumoniae—induced Stevens-Johnson syndrome manifested less severely than its drug-induced counterpart. The limited number of biopsies precludes unequivocal demonstration of histopathologic differences between drug-induced and M pneumoniae—induced Stevens-Johnson syndrome.EM = erythema multiforme; EuroSCAR = European Study of Severe Cutaneous Adverse Reactions; SJS = Stevens-Johnson syndrome; TEN = toxic epidermal necrolysisStevens-Johnson syndrome (SJS) is a rare, severe, immune-mediated cutaneous reaction usually secondary to an idiosyncratic reaction to medication, although infection with Mycoplasma pneumoniae is also a well-documented cause.¹ In 1922, Stevens and Johnson² described a strikingly distinct disease in 2 children as an “extraordinary, generalized eruption with continued fever, inflamed buccal mucosa and severe purulent conjunctivitis.” In ensuing years, controversy existed as to whether SJS indeed was a separate entity or merely a severe form of erythema multiforme (EM).³ More recent evidence suggests that EM with mucous membrane involvement and SJS are 2 different diseases with distinct causes.⁴ Although various classification systems exist, the most widely accepted consensus definition was proposed by Bastuji-Garin et al⁵ in 1993: SJS consists of epidermal “detachment below 10% of the body surface area plus widespread macules or flat atypical targets.” Other studies have described histopathologic correlates in patients with EM, SJS, and toxic epidermal necrolysis (TEN).^6-9 The aim of the current study was to retrospectively examine clinical, etiologic, and histopathologic data from patients with SJS to identify possible correlates of clinical disease severity related to specific etiologic and histopathologic findings.     

Trimethoprim/sulfamethoxazole-induced toxic epidermal necrolysis.

OBJECTIVE: To report a case of toxic epidermal necrolysis (TEN) associated with trimethoprim/sulfamethoxazole (TMP/SMX). CASE SUMMARY: A 34-year-old Asian woman developed a severe, desquamating mucocutaneous reaction (TEN) after six days of taking TMP/SMX to treat a presumed urinary tract infection (UTI). DISCUSSION: TMP/SMX is often recommended as first-line therapy for UTIs, sinusitis, bronchitis, and as prophylaxis and treatment for Pneumocystis carinii pneumonia. TEN is a rare, but severe condition associated with sulfonamide use. This article describes a typical case and offers an opportunity for review of this potentially serious reaction. CONCLUSIONS: Sulfonamides are often implicated in the majority of drug-induced cases of TEN. This case report illustrates the typical presentation of sulfonamide-induced TEN with a prodrome, characteristic rash, mucous membrane lesions, and systemic involvement. Practitioners should be aware of this rare adverse effect and closely observe patients for cutaneous manifestations or complaints. Any suspected drug should be discontinued if clinical evaluation leads to the suspicion of Stevens-Johnson syndrome or TEN.     

DRESS syndrome à la carbamazépine avec réactivation du cytomégalovirus

Drug-induced hypersensitivity or drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a severe skin adverse drug reaction induced by a limited number of drugs. DRESS syndrome occurs within 1 to 8 weeks of the treatment. We report a 36-year-old man who presented a DRESS syndrome associated with carbamazepine and cytomegalovirus reactivation. All symptoms resolved after drug withdrawal and treatment with corticoids and ganciclovir. The DRESS syndrome features, pathophysiology, and treatment are discussed based on the available literature.     

Cephalexin-induced Stevens-Johnson syndrome.

OBJECTIVE: To report a case of cephalexin-induced Stevens-Johnson syndrome (SJS), a devastating adverse drug reaction that involves the entire skin surface and mucosal areas of the body. DATA SOURCES: MEDLINE search (key terms cephalosporins, Stevens-Johnson syndrome, erythema multiforme, and systemic lupus erythematosus) and references identified from bibliographies of pertinent articles. DATA SYNTHESIS: Clinical presentation and manifestations of SJS include the skin, eyes, gastrointestinal tract, and pulmonary system. Infectious complications are the leading cause of mortality. Early intervention is important to prevent progression of SJS. The case described is consistent with the features of this syndrome. The patient presented with fever, arthralgias, and malaise. Skin lesions included a diffuse violet macular rash with erythema and multiple bullous lesions on her neck and abdomen. The skin biopsy was consistent with SJS. Multiple mucocutaneous ulcers were found in her mouth, but no evidence of lower gastrointestinal tract involvement was documented. She remained relatively free of pulmonary complaints except for the presenting bronchitis. CONCLUSIONS: Cephalexin should be added to the list of agents to consider as iatrogenic causes of SJS.     

Stevens-Johnson syndrome

Stevens-Johnson Syndrome (SJS), or erythema multiforme, is a severe, acute, adverse, cutaneous reaction to certain medications, such as phenytoin and topical nitrogen mustard. The risk of developing SJS is high when phenytoin and steroids are administered during cranial irradiation. SJS produces headache, malaise, sore throat, fever, and sloughing of the skin and mucous membranes. Prompt recognition of SJS and withdrawal of the offending medication is key to treating this disorder. Nurses play an important role in assessing patients and educating them about signs and symptoms of SJS.     

Possible cefotaxime-induced Stevens-Johnson syndrome

OBJECTIVE: To report a case of possible cefotaxime-induced Stevens-Johnson syndrome (SJS). CASE SUMMARY: A 72-year-old woman with an upper urinary tract infection developed erosions and blisters on the skin and the mucous membranes, as well as fever and prostration, soon after the administration of cefotaxime. This presentation is consistent with the features of SJS. Resolution of the clinical manifestations was observed after discontinuation of the drug; all other drugs, infections, or immunologic disorders that could have caused this syndrome were carefully excluded. An objective causality assessment revealed that SJS was possibly associated with the use of cefotaxime. DISCUSSION: Although cephalosporins have been associated with an increased risk for SJS and cefotaxime has been suspected of being associated with SJS in a previous case-control study, this is the first full report for cefotaxime-related SJS in the literature. An immunologically mediated reaction may be the underlying mechanism. CONCLUSIONS: Although cefotaxime administration seems to be the underlying cause of the SJS observed in our patient, establishment of a definite causal relationship requires additional cases and supportive data.     

Phenytoin-induced Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS) Syndrome: A Case Report from the Emergency Department

Background

Drug rash with eosinophilia and systemic symptoms (DRESS) syndrome is an uncommon but serious hypersensitivity drug reaction most frequently associated with antiepileptics. Clinical manifestations include rash, fever, and visceral organ involvement, most commonly hepatitis. The mortality rate associated with DRESS syndrome is approximately 10%, the majority due to fulminant liver failure.

Objectives

We report one case of phenytoin-induced DRESS syndrome in a patient who presented to the Emergency Department (ED). Our objectives for this case report include: 1) to learn the importance of DRESS syndrome; 2) to recognize the signs and symptoms of DRESS syndrome; 3) to know what diagnostic studies are indicated; and 4) to learn the appropriate treatment.

Case Report

We report one case of phenytoin-induced DRESS syndrome in a 34-year-old man, previously on phenytoin for seizure prophylaxis, who presented to the ED with 5 days of worsening symptoms including generalized rash, fever, tongue swelling, and dysphagia. Laboratory results revealed an eosinophilia and elevated liver enzymes. With initiation of steroids, the transaminitis improved despite increasing eosinophilia and development of an atypical lymphocytosis. Fever and angioedema resolved with improvement of the rash, and the patient was discharged on hospital day 3.

Conclusion

Given the significant mortality related to DRESS syndrome, ED staff should have a low threshold for suspecting the condition in patients who present with unusual complaints and skin findings after starting any antiepileptic drug. Early diagnosis and prompt treatment with corticosteroids is imperative.     

Stevens-Johnson syndrome: pathogenesis, diagnosis, and management

Cutaneous drug reactions are the most common type of adverse drug reaction. These reactions, ranging from simple pruritic eruptions to potentially life-threatening events, are a significant cause of iatrogenic morbidity and mortality. Stevens-Johnson syndrome (SJS) is a serious and potentially life-threatening cutaneous drug reaction. Although progress has been made in the management of SJS through early detection, prompt hospitalization, and immediate cessation of offending agents, the prevalence of permanent disabilities associated with SJS remains unchanged. Nevertheless, despite being a problem that is global in scope, government and health care agencies worldwide have yet to find a consensus on either diagnostic criteria or therapy for this disorder. Here, we provide the internist and emergency room physician with a brief review the SJS literature and summarize the latest recommended interventions with the hope of improving early recognition of this disease and prevention of permanent sequelae and mortality that frequently complicate SJS.     

Safety profile of etifoxine: A French pharmacovigilance survey

Etifoxine chlorhydrate is a benzoxazine derivative approved for the treatment of psychosomatic manifestations of anxiety since 1979. Previously labeled adverse drug reactions (ADRs) only include drowsiness, benign cutaneous reactions, and acute hypersensitivity reactions. The objectives were to examine recent data on etifoxine‐related ADR by reviewing Individual Case Safety Reports (ICSRs) recorded in France especially unexpected ADRs. Etifoxine‐related ICSRs were extracted from the French Pharmacovigilance database from 1 January 2000 to 30 April 2012 and data from the marketing authorization holder up to 31 December 2011 were also obtained. Of the 350 cases retained for analysis, 123 (35%) were considered serious. Dermatological or acute hypersensitivity reactions were the most frequent ADRs (59%) mainly isolated cutaneous eruptions. However, there were 24 cases of severe toxidermia (DRESS in 5, erythema multiforme in 10 and Stevens–Johnson syndrome in 5) with etifoxine as the most suspected drug in 11 patients, and seven cases of vasculitis or serum sickness‐like reaction. Liver disorders were reported in 34 patients of whom 25 developed acute hepatitis with a cytolytic biological pattern in 16. Other unexpected ADRs included 16 reversible cases of metrorrhagia with positive rechallenge in 5, and three cases of biopsy‐proven microscopic colitis of which one recurred after etifoxine re‐administration. Although etifoxine has been marketed for more than 30 years, this survey identified a number of unexpected and sometimes serious ADRs, in particularly severe toxidermia and acute cytolytic hepatitis. A recent update of the French etifoxine summary of the product characteristics (SPC) was based on these findings.     

Stevens‐Johnson syndrome: Pathogenesis,diagnosis, and management

Cutaneous drug reactions are the most common type of adverse drug reaction. These reactions, ranging from simple pruritic eruptions to potentially life‐threatening events, are a significant cause of iatrogenic morbidity and mortality. Stevens‐Johnson syndrome (SJS) is a serious and potentially life‐threatening cutaneous drug reaction. Although progress has been made in the management of SJS through early detection, prompt hospitalization, and immediate cessation of offending agents, the prevalence of permanent disabilities associated with SJS remains unchanged. Nevertheless, despite being a problem that is global in scope, government and health care agencies worldwide have yet to find a consensus on either diagnostic criteria or therapy for this disorder. Here, we provide the internist and emergency room physician with a brief review the SJS literature and summarize the latest recommended interventions with the hope of improving early recognition of this disease and prevention of permanent sequelae and mortality that frequently complicate SJS.     

Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis: A Concise Review with a Comprehensive Summary of Therapeutic Interventions Emphasizing Supportive Measures

Introduction

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are two of the most severe dermatologic conditions occurring in the inpatient setting. There is a lack of consensus regarding appropriate management of SJS and TEN.

Purpose

The scientific literature pertaining to SJS and TEN (subsequently referred to as SJS/TEN) is summarized and assessed. In addition, an interventional approach for the clinician is provided.

Methods

PubMed was searched with the key words: corticosteroids, cyclosporine, etanercept, intravenous immunoglobulin, Stevens-Johnson syndrome, and toxic epidermal necrolysis. The papers generated by the search, and their references, were reviewed.

Results

Supportive care is the most universally accepted intervention for SJS/TEN. Specific guidelines differ from the care required for patients with thermal burns. Adjuvant therapies are utilized in most severe cases, but the data are thus far underwhelming and underpowered. Using systemic corticosteroids as sole therapy is not supported. A consensus regarding combined corticosteroids and intravenous immunoglobulin (IVIG) has not been reached. Data regarding IVIG, currently the standard of care for most referral centers, is conflicting. Newer studies regarding cyclosporine and tumor necrosis factor inhibitors are promising, but not powered to provide definitive evidence of efficacy. Data regarding plasmapheresis is equivocal. Thalidomide increases mortality.

Conclusion

Clinicians who manage SJS/TEN should seek to employ interventions with the greatest impact on their patients’ condition. While supportive care measures may seem an obvious aspect of SJS/TEN patient care, providers should understand that these interventions are imperative and that they differ from the care recommended for other critically ill or burn patients. While adjuvant therapies are frequently discussed and debated for hospitalized patients with SJS/TEN, a standardized management approach is not yet clear based on the current data. Therefore, until further data are available, decisions regarding such treatments should be made on a case-by-case basis.