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    1. No mucosa involment
    2. < 10% body surface involvement
    1. SJS = upto 10%
    2. b.SJS – TEN overlap = 10 - 30% body surface involvement
    3. TEN > 30% body surface involvement

Erythema Multiforme Exudativum Or Bullosum

  1. Erythema Multiforme Exudativum Or Bullosum
    1. An inflammatory eruption characterized by symmetric erythematous, edematous, or bullous lesions of the skin or mucous membranes.
    2. Most other cases are due to infectious diseases (eg, herpes simplex [probably most common], hepatitis C, coxsackieviruses and echoviruses, Mycoplasma pneumoniae, psittacosis, histoplasmosis) or drug therapy. drug cause erythema multiforme; penicillin, sulfonamides, barbiturates. Vaccinia, (BCG), and poliomyelitis vaccines.
    3. The mechanism by which infectious agents, drugs, or vaccines cause erythema multiforme is unknown, but it is generally considered a hypersensitivity reaction.
Symptoms, Signs, and Diagnosis
  1. Onset is usually sudden, with erythematous macules, papules, wheals, vesicles, and sometimes bullae appearing mainly on the distal portion of the extremities (palms, soles) and on the face; hemorrhagic lesions of the lips and oral mucosa can also occur . 
  2. The skin lesions (target or iris lesions) are symmetric in distribution and often annular, with concentric rings, central purpura, and grayish discoloration of the epidermis or vesicle). Itching is variable. 
  3. Systemic symptoms vary; malaise, arthralgia, and fever are frequent. Attacks sometimes last 2 to 4 wk and recur in the fall and spring for several years.

​Erythema Multiforme Sub Types

  1. Erythema multiforme minor: Skin lesions without involvement of mucous membranes
  2. Erythema multiforme major: Skin lesions with involvement of mucous membranes
  3. Herpes associated erythema multiforme
  4. Mucosal erythema multiforme (Fuchs syndrome, ectodermosis pluriorificialis): mucous membrane lesions without cutaneous involvement.

Epidermal Necrolysis (SJS & TEN)

  1. Stevens-Johnson syndrome
    1. Characterized by bullae on the oral mucosa, pharynx, anogenital region, and conjunctiva; target-like lesions; and fever. 
    2. The patient may be unable to eat or properly close the mouth. 
    3. The eyes may become very painful; purulent conjunctivitis may make it impossible for the patient to open them. 
    4. Symblepharon production, keratitis with corneal ulceration, iritis, and uveitis may occur. 
    5. The conjunctival lesions may leave resistant corneal opacity and synechia. The condition is occasionally fatal.
    6. The skin lesions of erythema multiforme must be distinguished from bullous pemphigoid, urticaria, and dermatitis herpetiformis; the oral lesions, from aphthous stomatitis, pemphigus, and herpetic stomatitis. Hand, foot, and mouth disease produced by coxsackieviruses A5, A10, and A16 must also be considered.
  2. Treatment
    1. The cause, if found, should be treated, eliminated, or avoided. 
    2. Simple erythema often needs no treatment. Erythema multiforme associated with mycoplasmal pneumonia should be treated with tetracycline. 
    3. Local treatment depends on the type of lesion. 
      • Vesicles and bullous or erosive lesions can be treated with intermittent Burow's solution, saline, or tap-water compresses. 
      • Cheilitis and stomatitis of erythema multiforme may require special care. 
      • Use of systemic corticosteroids is controversial; some patients, especially those with severe mouth and throat lesions, seem to succumb more readily to fatal respiratory infections if treated with systemic corticosteroids. However, these drugs have been beneficial in severe erythema multiforme (if used early) and in chronic erythema multiforme. 
      • Systemic antibiotics (as indicated by culture and sensitivity) and fluid and electrolyte replacement may be lifesaving in patients with extensive mucous membrane lesions. 
      • If frequent or severe erythema multiforme is preceded by herpes simplex, acyclovir 200 mg five times daily may prevent attacks.

Toxic Epidermal Necrolysis (Lyell’s Syndrome)

A life-threatening skin disease in which the epidermis peels off in sheets, leaving widespread denuded areas. Toxic epidermal necrolysis (TEN) most often occurs in adults. 
Sulfonamides, barbiturates, NSAIDs, phenytoin, allopurinol, and penicillin, SJS – 5-12%
TEN is one of the few true dermatologic emergencies; the mortality rate is 30 - 35%.


  1. TEN typically begins with painful localized erythema that disseminates rapidly. 
  2. At the sites of erythema, flaccid blisters occur or the epidermis peels off in large sheets with gentle touching or pulling (Nikolsky's sign). Malaise, chills, myalgias, and fever accompany the denudation. 
  3. Widespread areas of erosion, including all mucous membranes (eyes, mouth, genitalia), occur within 24 to 72 h, and the patient may become gravely ill. Affected areas of skin often resemble second-degree burns. 
  4. Death is caused by fluid and electrolyte imbalance and multiorgan sequelae (eg, pneumonia, GI bleeding, glomerulonephritis, hepatitis, infection).


  1. Rapid diagnosis is important so that a possibly offending drug can be stopped. 
  2. Before widespread erythema and epidermal denudation occur, it may be difficult to distinguish TEN from morbilliform drug eruptions or erythema multiforme minor and the Stevens-Johnson syndrome (erythema multiforme major). TEN is often thought to be a continuum of the latter two diseases. 
  3. Although TEN closely resembles staphylococcal scalded skin syndrome, these disorders can be differentiated by the patient's age, the clinical setting, and the level of the epidermal split seen on biopsy.
    SCORTEN – Prognostic scoring system.


  1. Patients should be hospitalized;. Suspected drugs should be stopped immediately. 
  2. Patients should be isolated to minimize exogenous infection and treated as are those with severe burns by protecting the skin and denuded areas from trauma and infection and by replacing fluid and electrolyte losses.
  3. Although controversial, systemic corticosteroid use has been successful when initiated early in the course of disease. The idea is to stop further immunologic injury to the skin, but systemic corticosteroids will not breathe life into dead keratinocytes or reverse programmed death of skin. Corticosteroids often seem to enhance the propensity to gram-negative or other sepsis and increase the mortality rate; thus, if these drugs are used, a short course is safer. 
  4. IVIG (Intravenous immunoglobulin
  5. Septicemia, the most common cause of death, often occurs with pulmonary infections and must be recognized and treated promptly. 
  6. Ophthalmologic consultation is often required because there may be considerable crusting of the conjunctiva.
  7. To prevent phimosis, urologic consultation may be necessary

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