Dermatology - Toxic epidermal necrolysis (TEN)
Stevens Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are both severe and sometimes fatal responses of the skin and mucous membranes. They are characterized by widespread death and separation of the outer layer of the skin. Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are different forms of the same disease, which can occur spontaneously or as a result of medication. The main distinction between them is in the extent of the body surface area affected. The interval between initial drug exposure and the appearance of symptoms is typically 1-3 weeks, however this is more frequently observed when the drug is administered again. A premonitory phase characterized by fever, general discomfort, and joint pain frequently takes place 1-3 days before the appearance of a rash. Altered nutrition, sensitivity to light, uncomfortable urination, and feelings of unease may manifest. The individual experiences a mild to moderate sensitivity of the skin, along with a sensation of burning or itching in the conjunctiva. This is followed by discomfort, a burning feeling, soreness, and abnormal sensations in the skin known as paresthesia. Mouth lesions are unpleasant, sensitive. The prodromal rash is morbilliform and might be targetoid with or without purpura. The lesions quickly merge together; alternatively, there may be no distinct lesions, but instead a widespread redness and absence of a rash. As the rash develops further, it undergoes necrosis and forms crinkled macules that grow in size and merge together. Subsequently, there is a detachment of the outer layer of skin and the appearance of soft, raised blisters that extend when pressure is applied to reddened areas (known as the Nikolsky sign). In cases of trauma, the skin's top layer is completely detached, revealing the underlying dermis which appears red and is seeping, similar to a second-degree burn caused by heat. The involvement of lips, buccal mucosa, conjunctiva, genital, and anal skin is constant and unavoidable. The eyes exhibit conjunctival diseases characterized by hyperemia, the production of pseudomembranes, keratitis, corneal erosions, and subsequent adhesions between the eyelids and the bulbar conjunctiva. The potential causes for the condition include drug eruptions, erythema multiforme, scarlet fever, phototoxic eruptions, toxic shock syndrome, graft-versus-host disease, thermal burns, phototoxic reactions, staphylococcal scalded-skin syndrome (more common in young children and rare in adults), fixed drug eruption, and exfoliative dermatitis. Prompt identification and cessation of potentially implicated medication(s) are of utmost significance. Patients receive optimal care in an intermediate or intensive care unit. Administer IV fluids and electrolytes as necessary for a patient with a severe third-degree thermal burn. However, a smaller amount of fluid is typically necessary for a thermal burn of same magnitude. Administering systemic glucocorticoids at the onset of the disease and in large quantities can effectively decrease the incidence of illness or death. During the advanced stages of the condition, they should not be used. Early administration of high-dose intravenous immunoglobulins effectively prevents illness development. It is advised against undergoing surgical debridement. Early treatment of ocular lesions with erythromycin ointment is recommended.
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