Continuing Education Activity

Stevens-Johnson syndrome and toxic epidermal necrolysis are rare but life-threatening cutaneous adverse reactions associated with systemic inflammation, mucosal injury, epidermal detachment, and substantial short- and long-term morbidity. Prompt recognition, withdrawal of the causative drug, early supportive care, prognostic assessment, and coordinated specialty consultation are essential to reduce infection, organ failure, ocular complications, genitourinary sequelae, and mortality. Despite established classification criteria and supportive care principles, clinicians may inconsistently distinguish Stevens-Johnson syndrome and toxic epidermal necrolysis from mimicking disorders, identify high-risk medications, assess disease severity, and coordinate interprofessional treatment. This educational activity addresses that gap by reviewing clinical presentation, diagnostic evaluation, severity scoring, supportive care, emerging therapies, complication prevention, and long-term follow-up. Participants will gain actionable skills to improve diagnostic accuracy, risk stratification, treatment decisions, patient-centered supportive care, and interprofessional collaboration.

Objectives:

• Identify common medication-related, infectious, vaccine-related, malignant, and idiopathic triggers associated with Stevens-Johnson syndrome and toxic epidermal necrolysis.
• Assess clinical features that support early recognition of Stevens-Johnson syndrome and toxic epidermal necrolysis, including prodromal symptoms, cutaneous findings, mucosal involvement, and systemic complications.
• Apply severity assessment tools to estimate mortality risk and guide early treatment decisions in patients with Stevens-Johnson syndrome and toxic epidermal necrolysis.
• Collaborate with the interprofessional healthcare team to coordinate early referral, specialty consultation, complication prevention, discharge planning, and long-term follow-up.

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Introduction

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are acute, severe cutaneous adverse reactions accompanied by systemic manifestations. STS and TEN have a reported incidence of 1 to 5 cases per 1 million individuals annually, with a higher incidence in adults than in children.[1] SJS and TEN are classified as type IV hypersensitivity reactions mediated by an immunologic response to a trigger, with medications being the most common culprit.[2]

In most cases, TEN results from an immune reaction to certain drugs. However, infection, tumors, and vaccination are also potential causes. SJS shares the same pathophysiology and is considered part of the same spectrum of drug-induced epidermolysis. The main difference is the extent of skin detachment, and an important caveat is that detachable areas of the epidermis, not just detached areas, should be included in the calculation. The original classification system of 3 categories was developed in 1993. SJS affects less than 10% of the total body surface area, SJS and TEN overlap affects 10% to 30% of total body surface area, and TEN affects greater than 30% of total body surface area.[3] Results from newer studies show a mortality difference of 10% to 30% for total body surface area greater than 30%, and authors have proposed reclassifying TEN as 10% or greater.[4][5] Both SJS and TEN carry significant morbidity and mortality, with reported mortality rates as high as 34% to 50%. Furthermore, mortality correlates with the percentage of total body surface area involved. Consequently, treatment of SJS and TEN requires the expertise of several disciplines, including dermatology, allergy, immunology, burn surgery, ophthalmology, urogynecology, and psychiatry.[6]

Etiology

Stevens-Johnson syndrome and toxic epidermal necrolysis represent a severe T-cell–mediated type IV (delayed) hypersensitivity reaction. TEN can be induced by medications, infections, vaccines, or may occur idiopathically. More than 80% of cases result from medication exposure, particularly antimicrobials, antiepileptics, allopurinol, and nonsteroidal anti-inflammatory drugs.[2][7] Most cases occur 4 to 28 days after initial exposure to the drug.[7] 

Drugs that most commonly cause Stevens-Johnson syndrome/toxic epidermal necrolysis include:

• Antiepileptics: lamotrigine, carbamazepine, phenytoin, valproic acid, phenobarbital
• Allopurinol
• Antibiotics: trimethoprim-sulfamethoxazole, aminopenicillins, cephalosporins, tetracyclines
• Nevirapine (nonnucleoside reverse transcriptase inhibitor)
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Immune checkpoint inhibitors: nivolumab, pembrolizumab [2][8][9][10]

Other potential etiologies include infections such as Mycoplasma pneumoniae, hepatitis A, and human herpesvirus 7; malignant neoplasms such as hepatocellular carcinoma and lung cancer; and vaccination, especially with the meningococcal vaccine.[11][12][13] TEN has been reported in patients with COVID-19 due to either the viral infection or the medications used during treatment.[14][15]

Epidemiology

Stevens-Johnson syndrome and toxic epidermal necrolysis have a reported incidence of 1 to 5 cases per 1 million individuals annually. SJS and TEN have a higher incidence in adults than in children, likely due to increased exposure to potential triggers.[1][6] Incidence also varies by country due to differences in the use of medications associated with SJS and TEN, such as antitubercular or anti-HIV medications, along with differences in genetic background.[2] In 1996, a German study estimated the yearly prevalence per 1 million individuals of both SJS and TEN at approximately 1.9 cases.[16] The reported figure for both SJS and TEN cases in the United Kingdom between 1995 and 2013 was 5.76 cases per 1 million inhabitants per year.[17] In Japan, TEN affects approximately 1 patient per million adults per year.[18]

Results from many recent studies have highlighted the association between specific human leukocyte antigen (HLA) alleles and the development of TEN, particularly in Southeast Asian populations.[19][20] For example, the HLA-B*1502 allele found in the Han Chinese population is highly associated with carbamazepine-induced Stevens-Johnson syndrome and toxic epidermal necrolysis.[1][2] Asian, Black, and White patients have differing susceptibility to SJS and TEN. Findings from one study suggested that Asian and Black patients had a 2-fold to 3-fold increased risk compared with White patients.[21] Moreover a clear predilection in women exists, with a female to male ratio of 1.5:1.[22] Most patients with TEN are between the fifth and seventh decades of life. However, TEN can affect people of any age. In general, adult cases are mainly drug-induced, whereas infections are the main cause in children.[21] 

Pathophysiology

Stevens-Johnson syndrome and toxic epidermal necrolysis are traditionally regarded as T-cell–mediated type IV (delayed) hypersensitivity reactions. T-cell receptors expressed on CD8+ cytotoxic T cells are activated by covalent binding of drugs presented by the major histocompatibility complex on an antigen-presenting cell. This theory is known as the hapten-prohapten model. However, several drugs can bind noncovalently to the human HLA complex and T-cell receptors via the pharmacological interaction concept.

The activated CD8+ T cells then trigger downstream production of cytokines and chemokines, as well as apoptosis of epidermal keratinocytes, through various pathways, including the Fas/Fas ligand (FasL) pathway, the perforin/granzyme pathway, and granulysin. Increased granulysin levels are detected in SJS and TEN blisters, and the severity of skin symptoms correlates with serum granulysin levels. However, granulysin levels are not a specific biomarker for SJS or TEN because serum granulysin can also be elevated in other cutaneous drug reactions.[4][10] Recent research suggests that exosomes and necroptosis may also be involved in the pathogenesis of SJS and TEN.[10] 

Results from a study by Zang et al revealed elevated expression of microRNA (miRNA) miR-375-3p in plasma exosomes from patients with SJS and TEN. This miRNA promotes epidermal apoptosis induction by downregulating the expression of the X-linked inhibitor of apoptosis (XIAP).[23] Results from a study by Saito et al showed that necroptosis, a form of programmed cell death induced by the interaction between annexin A1 and formyl peptide receptor 1 (FPR1), also contributes to keratinocyte death in SJS and TEN.[24]

Histopathology

Histologic findings in drug-induced SJS include full-thickness epidermal necrosis, subepidermal bullae, keratinocyte necrosis, and dense dermal infiltrates containing numerous eosinophils or neutrophils. Unlike SJS, TEN is characteristically pauci-inflammatory, with little dermal or epidermal inflammation. Histology of TEN is characterized by extensive full-thickness epidermal necrosis with subsequent epidermal detachment.[25]

Toxicokinetics

The drugs implicated in SJS/TEN share key toxicokinetic properties:

• Long half-life: Drugs with longer half-lives tend to increase the risk of SJS and TEN because they persist longer in the body and allow prolonged immune activation.
• Systemic administration: Nearly all drugs that cause SJS or TEN are administered systemically, ensuring widespread exposure to keratinocytes.
• Latency period: Symptoms can develop within a few days to 8 weeks after starting a new drug, and subsequent exposure can result in symptoms within hours due to immune memory.[10]

History and Physical

A thorough history is important to identify the causative agent because symptoms typically present within 8 weeks of beginning therapy, with most cases appearing between 4 days and 4 weeks after drug initiation.[9] Approximately 5% of reported cases show no history of recent drug use.[26] Most patients report a prodrome of influenza-like symptoms, such as malaise, fever, myalgias, and upper respiratory tract symptoms, preceding the rash by 1 to 21 days.[27][28] 

Cutaneous manifestations of SJS and TEN include erythematous, targetoid, annular, or purpuric macules; flaccid bullae; and large, painful erosions that occur predominantly on the face and trunk, often spreading to the extremities (see Image. Stevens-Johnson Syndrome of the Lower Extremities). These macular lesions become confluent, progress to vesicles and bullae, and eventually develop into full-thickness necrosis, detachment, and skin sloughing, which often causes severe pain (see Image. Toxic Epidermal Necrolysis).[2] Skin lesions typically exhibit a positive Nikolsky sign, characterized by epidermal detachment with gentle lateral pressure or traction. The scalp is spared in almost all patients.

The hallmark feature of SJS or TEN is mucosal involvement. Mucosal involvement, including erythema and erosion, occurs in 90% of patients and generally precedes skin eruption by 1 to 3 days. The oropharynx, eye, and genitalia are the most frequently affected mucosal membranes. However, other areas have also been reported, including the respiratory and gastrointestinal tracts.[29][30] Respiratory involvement may lead to serious pulmonary disease even with normal chest radiography findings. Initial ocular involvement is common and can range from acute conjunctivitis, eyelid edema, and erythema to more severe forms, including corneal ulceration.[31][32] The release of massive cytokine levels may lead to major metabolic disturbances, including sepsis, multiorgan failure, and gastrointestinal tract hemorrhage. These complications contribute to the high mortality rate of 30% associated with TEN.[33] In patients with suspected SJS or TEN, clinicians should conduct a thorough skin examination to evaluate the extent of cutaneous involvement. Ophthalmology, urology, and gynecology specialists should also evaluate patients for mucosal involvement.[2] 

Evaluation

Toxic epidermal necrolysis is a clinical diagnosis that is confirmed by early histological analysis of the affected skin. Early skin biopsy confirms the diagnosis and guides the treatment plan. A frozen section may help expedite the diagnosis. Histological evaluation of the skin biopsy should include immunofluorescent analysis to differentiate TEN from other dermatological diseases.

No specific blood tests diagnose TEN. However, a basic screening evaluation, including a complete blood count, erythrocyte sedimentation rate, coagulation studies, urea and electrolytes, and liver function tests, is essential for planning supportive treatment, detecting organ failure, and assessing the overall prognosis. Anemia and lymphopenia are common. Notably, neutropenia is an unfavorable prognostic factor.[33]

The coagulation profile and blood count should be kept within reference ranges, especially in patients with extensive mucosal involvement, as this may increase the risk of severe bleeding, particularly from the gastrointestinal tract. Transfusion of blood or blood products may be considered in some cases.[18] Imaging studies are not essential for the diagnosis of TEN. However, imaging can be used to assess complications, such as chest radiography for pulmonary involvement. Another useful test is the patch test, which may help identify the causative agent in approximately 50% of patients.[34]

The Severity of Illness Score for Toxic Epidermal Necrolysis (SCORTEN) is a tool used to assess disease severity and predict mortality. SCORTEN comprises 7 independent variables assessed within the first 24 hours after hospital presentation, and the score estimates mortality risk (see Table 1). Variables include age older than 40 years, heart rate of 120 beats/min or greater, presence of cancer or hematologic malignant neoplasm, affected body surface area of 10% or greater within the first day, serum blood urea nitrogen (BUN) level greater than 28 mg/dL, serum bicarbonate level less than 20 mEq/L, and serum glucose level greater than 252 mg/dL. According to these risk factors, a patient's mortality score can range from 3.2% if only 1 risk factor is present to greater than 90% if 5 or more risk factors are present.[27]

 Tests and the corresponding results that are useful in the diagnosis of SJS/TEN include:

• Urgent frozen sections of skin biopsy: full-thickness skin necrosis
• Punch biopsy sent for direct immunofluorescence: negative results
• Complete blood count: anemia, lymphopenia, neutropenia, eosinophilia, atypical lymphocytosis
• Liver function tests: elevated transaminase levels, hypoalbuminemia
• Renal function: microalbuminuria, renal tubular enzymes in urine, reduced glomerular filtration rate, rising creatinine and urea levels, hyponatremia
• Pulmonary function: bronchial mucosal sloughing on bronchoscopy, interstitial infiltrates on chest radiography
• Cardiac function: abnormal electrocardiogram and imaging findings

SCORTEN estimates mortality risk in patients with SJS or TEN, with higher scores correlating with increased mortality risk (see Table 2).[12]  SCORTEN should be assessed within the first 24 hours of admission and reevaluated on day 3.  

Table

Table 1. Severity of Illness Score for Toxic Epidermal Necrolysis (SCORTEN) Risk Factors.

 Abbreviations: BUN, blood urea nitrogen

Table

Table 2. Mortality Rate of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis According to Risk Factors.

The Clinical Risk Score for TEN (CRISTEN) predicts early-stage mortality using only clinical information, without requiring laboratory data, and may be beneficial as an adjunct to SCORTEN for early prognostication.[4][5] This tool is useful due to its simplicity, versatility, and predictive accuracy.[4] The score is calculated by summing the values for each risk factor, with a higher score indicating a higher mortality risk (see Table 3).

 Table 3. The Clinical Risk Score for Toxic Epidermal Necrolysis (CRISTEN)

Table

Parameter  Score 

Abbreviations: BSA, body surface area; CRISTEN, Clinical Risk Score for Toxic Epidermal Necrolysis; SJS/TEN, Stevens-Johnson syndrome and toxic epidermal necrolysis; TEN, toxic epidermal necrolysis; UTI, urinary tract infection.

To determine the causative drug, drug rechallenge is the most reliable approach. However, drug rechallenge is contraindicated in SJS and TEN due to the risk of life-threatening consequences. In delayed-type hypersensitivity reactions such as SJS or TEN mediated by drug-specific T cells, patch testing is a useful adjunct.[35] 

Treatment / Management

The mainstay of treatment of toxic epidermal necrolysis is supportive care until reepithelialization of the affected skin. Supportive measures include fluid resuscitation, pain control, wound care, and nutritional support. Early treatment of patients with TEN in the emergency department should focus primarily on 2 measures: discontinuation of the offending drug and early referral to a burn unit or intensive care unit experienced in treating such patients. When implemented in the first 24 hours of blister formation, these 2 measures decrease the infection rate and hospital length of stay and improve overall survival.[36]

The airway should be evaluated frequently, and supplemental oxygen via a face mask should be administered if needed. If respiratory distress occurs, endotracheal intubation should be performed. Fluid resuscitation using crystalloids should be guided by a standard burn resuscitation protocol (eg, the Parkland formula). The target of resuscitation should be to maintain adequate tissue perfusion by achieving a mean arterial pressure greater than 65 mm Hg, a central venous pressure of 8 to 12 mm Hg, and a urine output of 0.5 to 1 mL/kg/h.[18][37] Pain control is extremely important to decrease patient distress. Opiates or patient-controlled analgesia can be used. Nonadhesive sterile dressings should be used to cover areas of skin erosions, and care should be taken to prevent hypothermia, especially in the prehospital setting.[36]

Nutritional support is crucial for patients with TEN due to the disease's hypercatabolic nature. Enteral feeding is superior to parenteral feeding because it decreases the risk of bacterial translocation. If the oral mucosa is significantly affected, a nasogastric tube may be used. Energy requirements and nutritional support must be carefully calculated, with a target of 20 to 25 kcal/kg/d.[38][39] Stevens-Johnson syndrome and toxic epidermal necrolysis require the expertise of multiple disciplines: wound care, intensivists, dermatology, clinical pharmacology, burn surgery, ophthalmology, urogynecology, psychiatry, pulmonology, respiratory therapy, physical and occupational therapy, and registered dietitians.[6]

Wound Care

Aseptic wound care is important to prevent secondary infection until reepithelialization. Skin lesions usually heal within 2 weeks, whereas mucosal lesions may take longer. No standard approach to wound care exists. Strong evidence does not support early, late, or no debridement of the affected skin. If wound debridement is performed, it should be done under general anesthesia. The involved area can be dressed with several options, including biological dressings, such as allografts, xenografts, and homografts; biosynthetic dressings, such as Biobrane (Smith and Nephew); or silver-impregnated dressings. Good wound care also reduces analgesic requirements.[40][41][42]

Infection is common and may be lethal. Staphylococcal infection is the most common, followed by pseudomonal infection, which occurs after prolonged hospitalization.[43] Prophylactic antibiotics are not recommended because they do not change survival rates.[44] However, microbiological assessment of skin lesions should be performed on the day of presentation and every 48 hours to detect and treat early infection. Indications for antibiotic treatment include evidence of infection in skin swabs, rapid deterioration of the patient's condition, or a sudden drop in the patient's temperature. Empiric antibiotics should cover gram-positive and gram-negative organisms, as well as anaerobes.[36]

Pharmacotherapy

No proven effective treatment modality exists, including systemic corticosteroids, plasmapheresis, cyclosporine, anti–tumor necrosis factor α therapy (TNF-α), or intravenous immunoglobulin (IVIG).[45][46] All reported clinical data regarding these medications are anecdotal and mainly based on observational studies. The rarity of TEN cases makes high-quality randomized controlled clinical trials to test the efficacy of these treatment modalities extremely challenging. Systemic corticosteroids are commonly used to halt the progression of TEN. However, results from some studies linked corticosteroids to increased mortality incidence.

Results from a 2020 study using SCORTEN to predict mortality found that high-dose corticosteroid therapy produced the greatest reduction in mortality, followed by corticosteroid pulse therapy.[17] Recently, results from a study showed that TNF-α inhibitor and corticosteroid combination therapy was more effective and safer than corticosteroid monotherapy for SJS and TEN; therefore, this combination therapy may be considered an alternative for patients with SJS or TEN who respond poorly to conventional corticosteroid therapy.[47]. Results from a systematic review and network meta-analysis published in 2021 showed that combination treatment with corticosteroids and IVIG may reduce the risk of mortality in patients with TEN.[48]

Complications

Ocular complications are common and sometimes serious. Early ophthalmology consultation is vital, and treatment usually consists of topical lubricants, antibiotics, or corticosteroid drops. Genitourinary complications are also common. Topical estrogen is used to promote mucosal healing. In severe cases, menstrual suppression may be helpful to minimize the potential risk of vaginal adenosis. According to the clinical presentation, further input may be needed from other specialists, including urology, otolaryngology, and respiratory medicine. Furthermore, all patients with TEN should be assessed for the need for postdischarge psychological support.[36]

Differential Diagnosis

Stevens-Johnson syndrome and toxic epidermal necrolysis exist along a disease spectrum, with severity defined by the extent of cutaneous involvement. Epidermal detachment involving less than 10% of the total body surface area is classified as SJS. Epidermal detachment involving more than 30% of the total body surface area is classified as TEN. Overlap between SJS and TEN occurs when the affected body surface area is 10% to 29%. The main differential diagnosis is erythema multiforme major. Erythema multiforme major usually affects less than 10% of the body surface area and is characterized by a symmetric acral distribution of target lesions with or without blister formation. In contrast, SJS and TEN consist mainly of skin blisters arising on erythematous macules in a central distribution involving the face and trunk. Moreover, 2 or more mucous membranes are involved in 90% of SJS and TEN cases. Skin biopsy is also an important tool to differentiate TEN and SJS from other disorders.

Other differential diagnoses include:

• Drug-induced hypersensitivity syndrome
• Linear IgA bullous dermatosis
• TEN-like lupus erythematosus 
• Generalized bullous fixed drug eruption 
• Acute graft-versus-host disease 
• Toxic shock syndrome, which usually presents with early multiorgan failure and unique cutaneous manifestations such as macular rashes affecting the palms and soles, that later evolve to desquamation over 14 days
• Paraneoplastic pemphigus, a mucocutaneous manifestation of malignant neoplasm
• Exfoliative erythroderma, which usually affects only the skin, spares the mucous membranes and is painless in most cases
• Staphylococcal scalded skin syndrome in children, which is associated with evidence of staphylococcal infection, no history of drug intake, and usual sparing of mucous membranes [2][9][49]

Pertinent Studies and Ongoing Trials

New therapeutic strategies currently under investigation include:

• PC111, a human monoclonal antibody targeting the Fas and Fas ligand pathway
• Targeting the interaction between annexin A1 and formyl peptide receptor 1 to block necroptosis
• Janus kinase and signal transducers of activation inhibitors [4]

Prognosis

While SJS and TEN are relatively rare, both are associated with mortality rates as high as 34% to 50%, with mortality correlating with body surface area involvement.[2][45][50] Infection is the main cause of death. Other potential lethal complications include acute respiratory distress syndrome, pulmonary embolism, renal failure, cardiac failure, and gastrointestinal bleeding.[51] Other risk factors associated with increased mortality include older age, identification with racial and ethnic minority groups, chronic kidney disease, pneumonia, sepsis, and malignant neoplasm.[52] Although the hospitalization rate of SJS and TEN has gradually declined over time, the mortality rate remained stable between 2010 and 2020.[52] 

Early recognition and intervention lead to the best outcomes. As previously discussed, the SCORTEN score, formalized by Bastuji-Garin et al, is a valid method for assessing disease severity and survival rates. SCORTEN is based on 7 variables that must be evaluated within the first 24 hours after hospital admission. These variables include age, affected body surface area, heart rate, presence of a malignant neoplasm, and serum levels of urea, glucose, and bicarbonate.[27]

Complications

Several complications can occur in patients with TEN because of extensive cutaneous and mucosal membrane involvement. In the early stage, painful stomatitis may interfere with oral intake and increase the risk of dehydration. Loss of the epithelial barrier increases the risk of infection and septicemia. Septicemia may evolve into septic shock and multiorgan failure.[2][43] In the long term, the involved skin may show signs of hypopigmentation or hyperpigmentation, whereas the affected mucosal surfaces may heal with stenosis and strictures (see Image. Healing Toxic Epidermal Necrolysis). In women, vulvovaginal involvement is common and can lead to stenosis, vulvar adenosis, and dyspareunia. In men, phimosis is the most common complication.[53]

Ocular complications are among the most common and serious sequelae of TEN. Therefore, early ophthalmology consultation is advisable in such cases. Corneal ulceration, xerophthalmia, meibomian gland dysfunction, panophthalmitis, and blindness are reported ocular complications.[31] Respiratory complications include pulmonary embolism, acute respiratory distress syndrome, and pneumonia.[54] Gastrointestinal tract complications include extensive bleeding from the affected mucosa, gingival synechia, and xerostomia due to involvement of the salivary glands.[55]

Long-term complications of SJS/TEN include:

• General: fatigue, malaise, sleep problems, chronic pain
• Psychiatric and psychosocial: depression, anxiety, posttraumatic stress disorder, dysthymia
• Cutaneous: scarring, dyspigmentation, development of new melanocytic nevi, pruritus, nail dystrophy, alopecia, photosensitivity
• Ocular: dry eyes, ocular hypersensitivity, pain, symblepharon, eyelid dysfunction, visual impairment, photophobia
• Oral mucous membrane: discomfort, dry mouth, periodontal disease, and gingival inflammation
• Otorhinolaryngologic: dysphonia, otalgia, tinnitus
• Pulmonary: dyspnea, cough, obstructive lung disease
• Gastrointestinal: esophageal strictures, dysphagia, intestinal ulcers, malabsorption
• Gynecologic and genitourinary: vulvar pain, dyspareunia, vulvovaginal stenosis, labial fusion, phimosis, urethral strictures [2][55][2][56]

Postoperative and Rehabilitation Care

Patients may need ongoing physical therapy due to joint contractures from excessive skin scarring.

Deterrence and Patient Education

Stevens-Johnson syndrome and toxic epidermal necrolysis are acute, severe cutaneous adverse reactions accompanied by systemic manifestations. These disease processes occur most commonly in adults after medication exposure. Because of the significant morbidity and mortality associated with SJS and TEN, patients should seek immediate medical attention to minimize acute and long-term complications associated with these disorders. Guidelines recommend that patients with SJS or TEN receive treatment in an intensive care unit or burn unit because treatment of these conditions requires the expertise of multiple disciplines, including wound care, intensivists, dermatology, clinical pharmacology, burn surgery, ophthalmology, urogynecology, psychiatry, pulmonology, respiratory therapy, physical and occupational therapy, and registered dietitians.

Enhancing Healthcare Team Outcomes

Because of the significant morbidity and mortality associated with SJS and TEN, patients require treatment from a well-rounded team of healthcare professionals. Early transfer to a burn facility or intensive care unit with staff experienced in treating complex wounds, fluid resuscitation, and mechanical ventilation improves overall survival in these patients. Dermatologists have a vital role in identifying and treating these cases. SJS and TEN require expertise from multiple disciplines, including wound care, intensive care, dermatology, allergy and immunology, clinical pharmacology, burn surgery, ophthalmology, urogynecology, and psychiatry.[6]

A plastic surgery consultation is also important for assessing the need for debridement of necrotic skin areas. Moreover, early involvement of ophthalmology is essential to decrease long-term ocular complications. Pulmonology consultation may be needed to assess the need for airway clearance in cases of pulmonary mucosal sloughing. Other specialties, such as otolaryngology and urology, may also be involved. Additionally, the involvement of registered dietitians and physical therapists is imperative for optimizing patient nutrition and mobility.[36][37][57] Patients require a multifaceted team during the acute stage of SJS and TEN, as well as appropriate long-term follow-up after discharge. Patients with SJS or TEN can experience long-term health complications and substantial psychosocial effects that are important to address.

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Disclosure: Alexandra Mathis declares no relevant financial relationships with ineligible companies.

Disclosure: Renford Cindass declares no relevant financial relationships with ineligible companies.

Disclosure: Karthik Krishnamurthy declares no relevant financial relationships with ineligible companies.