Recent lecture at Salt

• 45% of all adverse drug reactions are in the skin
• Cutaneous drug reactions occur in 2 to 3% of all hospitalized patients

• Allopurinol
• Anticonvulsants
• NSAIDs
• Sulfa drugs
• Bumetanide
• Captopril
• Furosemide
• Penicillamine
• Piroxicam
• Thiazide diuretics

• Digoxin
• Diphenhydramine hydrochloride
• Aspirin
• Aminophylline
• Prochlorperazine
• Ferrous sulfate
• Prednisone
• Codeine
• Tetracycline
• Morphine
• Regular insulin
• Warfarin
• Serotonin-specific reuptake inhibitors (SSRIs)

• Amoxicillin - 5.1%
• Trimethoprim sulfamethoxazole - 4.7%
• Ampicillin - 4.2%
• Semisynthetic penicillin - 2.9%
• Blood (whole human) - 2.8%
• Penicillin G - 1.6%
• Cephalosporins - 1.3%
• Quinidine - 1.2%
• Gentamicin sulfate - 1.0%

• The first step is to review the patient's complete medication list, including over-the-counter supplements.
• Document any history of previous adverse reactions to drugs or foods. Consider alternative etiologies, especially viral exanthems and bacterial infections.
• Note any concurrent infections, metabolic disorders, or immunocompromise (eg, due to HIV infection, cancer, chemotherapy) because these increase the risk of drug eruptions.

• All prescription and over-the-counter drugs including topical agents, vitamins, and herbal and homeopathic remedies
• The interval between the introduction of a drug and onset of the eruption
• Route, dose, duration, and frequency of drug administration
• Parenterally administered drugs, which are more likely than oral agents to cause anaphylaxis
• Topically applied drugs, which are more likely than other drugs to induce delayed-type hypersensitivity reactions
• Multiple courses of therapy and prolonged administration of a drug, which can cause allergic sensitization
• Any improvement after drug withdrawal and any reaction with readministration

• Evaluate for features of TEN or hypersensitivity syndrome.
• Mucous membrane erosions
• Blisters (Blisters herald a severe drug eruption.)
• Nikolsky sign (epidermis sloughs off with lateral pressure)
• Confluent erythema
• Angioedema and tongue swelling
• Palpable purpura
• Skin necrosis
• Lymphadenopathy
• High fever, dyspnea, or hypotension

• .

• Purpura
• Pityriasis rosea-like
• Psoriasiform
• Exfoliative dermatitis
• Exanthematic (maculopapular)
• Anaphylactoid reactions
• Urticaria
• Serum sickness
• Erythema multiforme
• Stevens-Johnson syndrome
• Toxic epidermal necrolysis
• Fixed eruptions
• Lichenoid eruptions

• Drug eruptions can mimic a wide range of dermatoses.
• The morphologies
• morbilliform
• urticarial
• papulosquamous
• pustular & bullous.
• Medications can also cause pruritus and dysesthesia without an obvious eruption.
• Considered in any patient who suddenly develops a symmetric cutaneous eruption.
• Divided into immunological and nonimmunological reactions.

• exanthems (46%) (maculopapular, morbilliform, or erythematous)
• urticaria (23%)
• fixed drug eruptions (10%)
• erythema multiforme (5.4%)
• all other forms (less than 5%)

• Bilateral and symmetric
• Typically begin on the trunk or on pressure areas of bedridden patients. Viral rashes may start on the face and progress to involve the trunk, and are more often accompanied by conjunctivitis, lymphadenopathy
• Mucosal involvement varies.
• Usually occur within a week of drug therapy, but may occur as late as 2 weeks after therapy has ended. They often last 1 to 2 weeks and have a benign course.
• May be accompanied by fever, pruritus, eosinophilia
• Scarlatiniform, rubelliform or mobilliform
• Less common are eruptions with large macules, polycylic and gyrate erythem
• Usually, but not always, recur on rechallenge

• Within 36h ( rechallenge minutes)
• Angioedema less than 1%
• May progress to systemic anaphylaxis
• Reaction can be immediate or delayed for days
• Often with pruritus
• Individual lesions typically last less than 24 hours
• When the drug is discontinued, the lesions resolve rapidly.
• IgE mediated are frequently caused by antibiotics, especially penicillin, radiographic contrast media, and anaesthetics.
• Angiotensin-converting enzyme inhibitors, NSAIDS, opiates, and curare can produce urticaria and angioedema that are not IgE mediated.

• Cutaneous vasculitis typically begins as erythematous macules and papules on dependent areas, such as the lower extremities or back/buttocks or supine patients which become tender and purpuric.
• Bullae and necrosis can occur.
• Often have fever, myalgias, arthralgias, and fatigue
• immune complex disease, but the exact mechanism is unknown.
• Allopurinol, cimetidine, furosemide, penicillins, sulfonamides, hydantoins, and thiazide diuretics.

• Single or several erythematous, eczematous, or bullous plaques. 30min to 8h after drug
• Pruritus is rare, but burning and discomfort are possible.
• The face and genitalia are common sites of involvement
• Recur in the same location with repeated drug administration
• Followed by postinflammatory hyperpigmentation
• Penicillins, tetracycline, sulfonamides, barbiturates, phenolphthalein, and gold salts.

• Severe life-threatening drug reaction that affects the skin and mucous membranes
• Confluent bullae and sheet-like epidermal shedding
• Fever and pain are common.
• Disease spreads quickly (within 2 to 3 days)
• Mortality can approach 30%.
• Nikolsky's sign, defined as epidermal detachment by lateral pressure, is positive over involved areas. The etiologic agents for toxic epidermal necrolysis are the same as those for erythema multiforme and Stevens-Johnson syndrome

• 1 in 10,000 mostly obese women
• painful red plaques on the breasts, hips, and buttocks 3 to 5 days after therapy initiation.
• Hemorrhagic bullae and necrosis follow
• Individuals with protein C deficiency are at high risk Prompt recognition and treatment of warfarin necrosis can minimize fatalities.
• Heparin necrosis is typically a localized reaction at injection sites and usually appears as purpuric plaques
• Necrosis is triggered by thrombosis via platelet aggregation and the formation of fibrin thrombi. Thrombocytopenia is common, but fibrinogen and fibrin split products are normal. The reaction is probably immune mediated.

• Sulfasalazine - 20%
• Trimethoprim-sulfamethoxazole - 14.9%
• Dapsone - 3.1%
• Aminopenicillins - 9.3%
• Penicillins - 3.8%
• Anticonvulsants - 3.4%
• Penicillinase-resistant penicillins - 2.9%
• Cephalosporins - 2.7%
• Quinolones - 2.1%
• Ketoconazole - 2.0%
• Clindamycin - 1.8%
• Tetracycline - 1.2%

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