Stevens-Johnson syndrome (SJS) is a severe mucocutaneous reaction triggered by drugs that causes painful erythema and blistering of the skin and mucosal tissues. It is classified by the extent of body surface area involvement, from less than 10% for SJS to greater than 30% for toxic epidermal necrolysis. Common causes include certain medications, infections, and autoimmune diseases. Treatment focuses on discontinuing the triggering factor, high-dose steroids, intensive supportive care, preventing infections, and maintaining fluid and nutritional needs.
Stevens-Johnson syndrome (SJS) is a severe mucocutaneous reaction triggered by drugs that causes painful erythema and blistering of the skin and mucosal tissues. It is classified by the extent of body surface area involvement, from less than 10% for SJS to greater than 30% for toxic epidermal necrolysis. Common causes include certain medications, infections, and autoimmune diseases. Treatment focuses on discontinuing the triggering factor, high-dose steroids, intensive supportive care, preventing infections, and maintaining fluid and nutritional needs.
Stevens-Johnson syndrome (SJS) is a severe mucocutaneous reaction triggered by drugs that causes painful erythema and blistering of the skin and mucosal tissues. It is classified by the extent of body surface area involvement, from less than 10% for SJS to greater than 30% for toxic epidermal necrolysis. Common causes include certain medications, infections, and autoimmune diseases. Treatment focuses on discontinuing the triggering factor, high-dose steroids, intensive supportive care, preventing infections, and maintaining fluid and nutritional needs.
equent severe mucocutaneous eruption tri- ggerd most frequently by drugs. Stevens-Johnson syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are terms that most believe describe the same drug induced disorder. SJS describes pts with < 10% BSA involvement, SJS – TEN complex describe pts 10 to 30% BSA involvement, and TEN describes pts with > 30% BSA involvement. ETIOLOGY Drug induced epidermal apoptosis: - Anticonvulsants - Chemotherapeutic agents - NSAID, etc. Infections: - Bacteria – Mycoplasma pneumonia - Viral -- Hepatitis A virus - Fungal – Histoplasmosis
Others eg, - SLE,
- Graft vs host reaction - Lymphoreticular malignancy - Idiopathic Clinical features: - Sudden onset usually - Appears as painful, diffuse erythema with crinkled surface
- Initially may be target lesion-like or not,
but rapidly coalesce into large sheets of dusky erythema. - Some form flaccid blisters, sometimes haemorrhagic blisters.
- Eventually, large areas of skin get denuded,
exposing red oozing dermis, resembling second degree burns. - Mucosal involvement is invariable and often severe: - oral mucosa - 100% - Eye - 90% - Genital and anal mucosa – 50%
- GIT and Respiratory truct involvement
connotes grave prognosis. Stevens – Johnson syndrome STENENS – JOHNSON SYNDROM Toxic epidermal necrolysis COMPLICATIPONS - Electrolyte and fluid inbalance - Infections - Temperature dysregulation - Protein loss MANAGEMENT 1. Early diagnosis and immediate discontinuat- ion of any suspected drug or other etiology.
2. Short cource, high dose systemic steroid in
the acute phase, usually relieves the const- itutional symptoms. 3. Supportive treatment usually in burns or intensive care unit. - Correction of fluid and electrolyte imbalance. - Broadspectrum antibiotics against secondary skin infections.