A. Acute vesiculobullous lesions

B. Chronic vesiculobullous lesions

A. Predominantly vesicular

B. Predominantly bullous

i. HSV infection

ii. Varicella infection

iii. Herpangina

iv. Hand, foot and mouth disease

v. Pemphigus

vi. Familial benign chronic pemphigus

vii. Epidermolysis bullosa

viii. Erythema multiforme (mucosal)

i. Bullous pemphigoid

ii. Cicatricial pemphigoid

iii. Epidermolysis Bullosa

iv. Dermatitis herpetiformis

i. Herpes simplex infections

ii. Varicella infections

iii. Herpangina

iv. Hand, foot and mouth disease

i. Pemphigus

ii. Bullous pemphigoid

iii. Cicatricial pemphigoid

iv. Erythema multiforme

v. Dermatitis herpetiformis

• Erythema multiforme is an acute self-limiting, inflammatory dermatological disorder that involves skin, mucus membrane and sometimes, internal organs.

i. Infectious agents: Mycoplasma pneumonia, herpes simplex, etc.

ii. Drug hypersensitivity: Oxicam NSAIDs, anticonvulsants like carbamazepine, phenobarbital, etc., sulpha drugs, salicylates, allopurinol and penicillin.

iii. Hyperimmune reaction: It is an immune-mediated disease initiated by the deposition of immune complexes in the superficial microvasculature of skin and mucosa or cell mediated immunity.

a. EM minor or erythema multiforme minor: It represents the localized eruptions of skin with mild or no mucosal involvement.

b. EM major or erythema multiforme major or Stevens–Johnson syndrome (SJS): It is more severe mucosal and skin disease and is potentially life-threatening disorder.

• Occurs chiefly in children and young adults between the age of 15–40 years and males are more commonly affected than females.

• Characterized by the occurrence of asymptomatic vividly erythematous discrete macules, papules or occasionally vesicles and bullae that appear symmetrically distributed over hands and arms, legs and feet, face and neck.

• It is a self-limiting form of disease.

• The classical dermal lesions of erythema multiforme, which often appear on extremities are concentric ring like resulting from varying shades of erythema giving rise to terms ‘target’, ‘iris’, or ‘Bull’s eye’ lesions.

• The palms of the hands will show target-like lesions more than any other skin surface.

• The vesicles of mucosal surface develop rapidly and are short lived and become eroded or ulcerated and bleed profusely.

• Recurrence is common, patient also develops tracheobronchial ulceration and pneumonia.

• Erythema multiforme major or SJS is a variant of erythema multiforme that represents a life-threatening and debilitating hypersensitivity.

• Patients were described as having ‘ocular-genital lesions’. Skin lesions involve necrosis of scrotal skin, penile skin or vulval and labial surfaces.

• The ocular component is epithelial necrosis of the cornea and conjunctiva, which develop prominent ulceration and necrosis, often leading to blindness directly or to visual loss caused by secondary infection.

• Oral lesions are severely painful large, haemorrhagic, crusting ulcers, especially of the lips and labial mucosa.

• The pain prevents oral intake of fluids or solids.

• The oral lesions will secondarily produce drooling, resulting in excesses fluid and electrolyte loss and leads to secondary infection, ultimately resulting in cervical lymphadenitis.

• The progression from the initial emergence of lesions to a full debilitating clinical picture with skin and mucous membrane necrosis often occurs within 24 hours.

• Oral lesions tend to be haemorrhagic ulcers that crust and may be seen on any portion of the oral mucosa, with predilection for lip vermilion.

• Oral lesions will occur in only 50% of cases with skin lesions and will emerge concurrently.

• Oral lesions suggestive of erythema multiforme without concomitant skin lesions probably do not represent true erythema multiforme, they often represent a lichenoid drug eruption or an immune-based disease.

• The microscopic appearance of erythema multiforme is not diagnostic as it depends in part on the stage of the lesion and the area of the biopsy.

• It usually consists of changes such as intercellular or intracellular oedema and necrosis of epithelium.

• Necrosis of prickle cells is a significant finding. Epithelial necrosis is also very prominent within the centre of ‘iris’ lesions.

• Vesicles may form within epithelium or at epithelial–connective tissue junction.

• Subepithelial connective tissue shows oedema and perivascular infiltration of lymphocytes and macrophages.

• Both types of erythema multiforme are clinical diagnoses.

• A mucosa or skin biopsy is recommended to rule out identifiable immune-based and viral diseases.

• The main differential lesion is toxic epidermal necrolysis

• Severe cases of pemphigus or cutaneous pemphigoid may also mimic erythema multiforme major, but the progression of signs and symptoms is not nearly as rapid.

• Cause should be identified and withdrawn.

• Erythema multiforme minor usually requires no treatment. It is self-limiting, will improve after 5–8 days, and will completely resolve within 2–4 weeks.

• In some cases, antibiotics are required to treat secondary skin or oral infections appropriately.

• For all the forms of erythema multiforme, symptomatic treatment including oral antihistamines, analgesics, local skin care and soothing mouthwashes is of great importance.

• The necrosed skin is treated as a burn with topical antimicrobial creams (1% silver sulphadiazine; Silvadene, Aventis), and the eyes are irrigated and patched.

• Erythema multiforme major (SJS), however, requires systemic corticosteroids.

• Topical steroid therapy coupled with antibiotics may be considered whereas systemic steroid therapy is controversial.

• Once the intensity of the disease resolves and no new skin lesions are developing, corticosteroids are discontinued.

A. Acute vesiculobullous lesions

B. Chronic vesiculobullous lesions

A. Predominantly vesicular

B. Predominantly bullous

i. HSV infection

ii. Varicella infection

iii. Herpangina

iv. Hand, foot and mouth disease

v. Pemphigus

vi. Familial benign chronic pemphigus

vii. Epidermolysis bullosa

viii. Erythema multiforme (mucosal)

i. Bullous pemphigoid

ii. Cicatricial pemphigoid

iii. Epidermolysis bullosa

iv. Dermatitis herpetiformis

i. Herpes simplex infections

ii. Varicella infections

iii. Herpangina

iv. Hand, foot and mouth disease

i. Pemphigus

ii. Bullous pemphigoid

iii. Cicatricial pemphigoid

iv. Erythema multiforme

v. Dermatitis herpetiformis

• Aphthous ulcers are also commonly known as ‘canker sores’.

• According to their clinical characteristics, aphthous ulcers are divided into two types:

a. Recurrent aphthous minor

The lesions emerge in four stages:

b. Recurrent aphthous major

• The pathogenesis of aphthous stomatitis is unknown.

• The current concept is that RAS is a clinical syndrome with several possible causes the major factors identified are heredity, haematologic deficiencies, immunologic abnormalities and nutritional deficiencies.

• Other factors include trauma, psychological stress, anxiety and allergy to foods such as milk, cheese, wheatflour and detergent present in toothpaste, that is sodium lauryl sulphate (SLS).

• Histologic examination is not usually indicated for aphthous ulcers, although it is sometimes helpful for difficult clinical cases. The findings are rather nonspecific.

• No specific diagnosis is required. It is a clinical-recognition diagnosis.