The epithelium of the trachea, bronchi, or gastrointestinal tract may be involved in SJS and TEN. Ocular symptoms are the most common complication in TEN, experienced by 20–79% of those with TEN, even by those who do not experience immediate ocular manifestations. These can include dry eyes, photophobia, symblepharon, corneal scarring or xerosis, subconjunctival fibrosis, trichiasis, decreased visual acuity, and blindness. Cause
Drug reactions have been reported to cause 80–95% of TEN cases.The drugs most often implicated in TEN are:

antibiotics
sulfonamides (sulfamethoxazole, sulfadiazine, sulfapyridine)
beta-lactams (cephalosporins, penicillins, carbapenems)
nonsteroidal anti-inflammatory drugs
allopurinol
antimetabolites (methotrexate)
antiretroviral drugs (nevirapine)
corticosteroids
anxiolytics (chlormezanone)
anticonvulsants (phenobarbital, phenytoin, carbamazepine, lamotrigine, and valproic acid).TEN has also been reported to result from infection with Mycoplasma pneumoniae or dengue virus. Contrast agents used in imaging studies as well as transplantation of bone marrow or organs have also been linked to TEN development. HIV
HIV-positive individuals have 1000 times the risk of developing SJS/TEN compared to the general population. The reason for this increased risk is not clear. Genetics
Certain genetic factors are associated with increased risk of TEN. For example, certain HLA-types such as, HLA-B*1502, HLA-A*3101, HLA-B*5801, and HLA‐B*57:01 have been seen to be linked with TEN development when exposed to specific drugs. Pathogenesis
The immune systems role in the precise pathogenesis of TEN remains unclear. It appears that a certain type of immune cell (cytotoxic CD8+ T cell) is primarily responsible for keratinocyte death and subsequent skin detachment. Keratinocytes are the cells found lower in the epidermis and specialize in holding the surrounding skin cells together.
Differential diagnosis
Staphylococcal scalded skin syndrome
Drug-induced linear immunoglobulin A dermatosis
Acute graft versus host disease
Acute generalized exanthematous pustulosis
Erythroderma
Drug reaction with eosinophilia and systemic symptoms aka DRESS
A generalized morbilliform eruption

Treatment
The primary treatment of TEN is discontinuation of the causative factor(s), usually an offending drug, early referral and management in burn units or intensive care units, supportive management, and nutritional support.Current literature does not convincingly support use of any adjuvant systemic therapy. Initial interest in Intravenous immunoglobulin (IVIG) came from research showing that IVIG could inhibit Fas-FasL mediated keratinocyte apoptosis in vitro. Unfortunately, research studies reveal conflicting support for use of IVIG in treatment of TEN. Ability to draw more generalized conclusions from research to date has been limited by lack of controlled trials, and inconsistency in study design in terms of disease severity, IVIG dose, and timing of IVIG administration. Larger, high quality trials are needed to assess the actual benefit of IVIG in TEN. Numerous other adjuvant therapies have been tried in TEN including, corticosteroids, ciclosporin, cyclophosphamide, plasmapheresis, pentoxifylline, acetylcysteine, ulinastatin, infliximab, and granulocyte colony-stimulating factors (if TEN associated-leukopenia exists). There is mixed evidence for use of corticosteroids and scant evidence for the other therapies. A meta-analysis from 2002 concluded that there is no reliable evidence for the treatment of TEN. Thalidomide did not show any benefit and was associated with increased mortality compared with placebo. Prognosis
The mortality for toxic epidermal necrolysis is 25–30%. People with SJS or TEN caused by a medication have a better prognosis the earlier the causative medication is withdrawn.