DERMATOLOGY – 15%
Acne Vulgaris
Inflammatory skin condition assoc. with papules & pustules involving pilosebaceous units
Pathophysiology:
• 4 main factors – follicular hyperkeratinization with plugging of sebaceous ducts, increased sebum production,
Propionibacterium acnes overgrowth within follicles, & inflammatory response
• Hormonal activation of pilosebaceous glands which may cause cyclic flares that coincide with menstruation
Clinical Manifestations:
• In areas with increased sebaceous glands (face, back, chest, upper arms)
• Stage I: Comedones: small, inflammatory bumps from clogged pores
- Open comedones (blackheads): incomplete blockage
- Closed comedones (whiteheads): complete blockage
• Stage II: Inflammatory: papules or pustules surrounded by inflammation
• Stage III: Nodular or cystic acne: heals with scarring
Differential Diagnosis:
• Differentiate from rosacea which has no comedones**
• Perioral dermatitis based on perioral and periorbital location
• CS-induced acne lacks comedones and pustules are in same stage of
development
Diagnosis:
• Mild: comedones, small amounts of papules &/or pustules
• Moderate: comedones, larger amounts of papules &/or pustules
• Severe: nodular (>5mm) or cystic
Management:
• Mild: topical – azelaic acid, salicylic acid, benzoyl peroxide, retinoids, Tretinoin topical (Retin A) or topical antibiotics
[Clindamycin or Erythromycin with Benzoyl peroxide]
• Moderate: above + oral antibiotics [Minocycline 50mg PO qd or Doxycycline 100 mg PO qd], spironolactone
• Severe (refractory nodular acne): oral Isotretinoin 0.5-1.0 mg/kg/d BID x15-20 weeks
Isotretinoin: affects all 4 pathophysiologic mechanisms of acne
• Adverse effects: dry skin and lips (MC), highly teratogenic, increased triglycerides & cholesterol, hepatitis
Androgenetic Alopecia
Genetically predetermined progressive loss of terminal hairs on scalp in a distribution pattern
MC hair loss in F & M, gradual in onset & occurs after puberty; type of non-scarring alopecia
Pathophysiology:
• Key androgen leading to AA: Dihydrotestosterone (DHT) – activation of the androgen receptor shortens the androgen (growth
phase) in the normal hair growth cycle
• Pathologic specimens show decreased anagen to telogen ratio
Clinical Manifestations:
• Varying degrees of hair thinning and nonscarring hair loss
• Males: begins as bitemporal thinning of the frontal scalp then involves the vertex
• Females: thinning of the hair between the frontal and vertex of the scalp without affecting the frontal hairline
Diagnosis:
• Usually clinical
• Dermoscopy: miniaturized hair and brown perihilar casts
• In females: investigate the cause with labs such as DHEAS, testosterone levels, CBC, iron, TIBC, TSH, & vit D
Management
• Topical Minoxidil: 5% OTC, best used if recent onset alopecia involves a smaller area, requires 4-6 month trial before noticing
improvement & must be used indefinitely
- Mechanism: widens blood vessels, allows more blood oxygen & nutrients to promote growth (anagen) phase
- Adverse: pruritus & local irritation with flaking
• Oral Finasteride (Propecia): 5-alpha-reductase-type 2 inhibitor inhibts androgen (inhibits conversion of testosterone to DHT)
- Adverse: decreased libido, sexual or ejaculatory dysfunction; increased risk of high-grade prostate ca; cat X
• Hair transplant may be effective
Atopic Dermatitis (Eczema)
Rash due to defective skin barrier susceptible to drying, leading to pruritus & inflammation
Pathophysiology
• Disruption of the skin barrier (filaggrin gene mutation) and disordered immune response which manifests mostly in infancy or
almost always by age 5
• Triggers: heat, perspiration, allergens, & contact irritants (wool, nickel, food, synthetic fabrics)
,• Genetics & environmental factors play a role, + hx of atopy
- IgE, eosinophils, Langerhans cell, T helper cells all play a role in atopic dermatitis
- TH2 prominent in acute lesions, TH1 found in chronic lesions
Atopy triad: atopic dermatitis + allergic rhinitis + asthma (3 A’s)
Clinical Manifestations
• Hallmark: pruritus*
• Erythematous, ill-defined blisters, papules or plaques → later the lesions dry, crust over & scale
• Older children & adults: MC in flexor creases (antecubital and popliteal folds)
• Infants: face and extensor part of extremities (from crawling & rubbing the skin)
• Nummular eczema: sharply defined discoid or coin-shaped lesions, especially on the
dorsum of the hands, feet & extensor surfaces (knees, elbows)
Diagnosis
• Clinical, can also do a skin prick test
• Increased IgE and elevated eosinophilia supports diagnosis
Acute Management
• 1st line: topical CS – avoid class I & II in children [Mometasone, Fluticasone,
Betamethasone, Triamcinolone]
• Antihistamines for pruritus, wet dressings, antibiotics if secondary infection (MC=staph aureus) develops
• Topical calcineurin inhibitors [Tacrolimus, Pimecrolimus] = steroid alternative
• Systemic: phototherapy (UVA, UVB, & narrow-band UVB) – used in children w/ mod to severe eczema, Cyclosporine,
Azathioprine, Mycophenolate mofetil, Methotrexate, Dupilumab
Chronic Management
• Maintain skin hydration: hydration & skin emollients twice daily & within 3 min of exiting a lukewarm shower
• Oral antihistamines for pruritus (Cetirizine, fexofenadine, loratadine), Hydroxyzine, Diphenhydramine
Avoid triggers (heat, low humidity), or irritants (soaps, detergents, washcloths, frequent baths)
Contact Dermatitis
Inflammation of the dermis & epidermis from direct contact between a substance & the skin surface
Irritant: MC type, causes include: chemicals (solvents, cleaners, & detergents), alcohols, or creams
Allergen: Nickel (MC worldwide), poison ivy, oak, or sumac; other metals, chemicals (fragrances, glue, hair dyes), detergents,
cleaners, acids, prolonged water exposure
Pathophysiology:
• Allergic: type IV hypersensitivity reaction (T cell lymphocyte-mediated), delayed by days
• Irritant: non-immunologic reaction (immediate)
Clinical Manifestations
• Acute: erythematous papules or vesicles (may be linear or geometric), often assoc. with localized pruritus, stinging, or burning;
may ooze, develop edema, and progress to blisters or bullae
• Chronic: lichenification fissuring and scales
Diagnosis
• Clinical diagnosis
• Patch testing: may identify potential allergens to prevent future exposures
• Histology not usually needed but will show spongiosis (intercellular edema in the epidermis)
Management
• Identification & avoidance of irritants*
• Topical corticosteroids = first-line medical treatment; use oral CS in severe/extensive reactions
• Topical calcineurin inhibitors (Tacrolimus or Pimecrolimus) are alternatives
General Measures
• Cool saline or astringent compresses, cool baths, skin emollients
• Use drying agents if oozing or weeping
• Burrow’s solution, itching can be relieved with antihistamines or calamine lotion
Burns
Degree Involvement:
• 1st degree (sunburn): erythema of involved tissue, skin blanches with pressure, skin may be tender
• Involves only epidermis
• MCC: overexposure, heals uneventfully w/ no residual scarring
• 2nd degree (partial thickness): skin is red & blistered, skin is very tender
• Involves all epidermis + some dermis, painful w/ weeping & blisters
• Superficial: blisters = expectant management
• Deep: excise & graft, heals over 4-8 weeks; if infx it can lead to full thickness burn
,• 3rd degree (full thickness): burned skin is tough & leathery, skin non-tender, painless, nonblanching
• Involves all epidermis + dermis + some fat
• Requires skin grafting & escharotomy
• 4th degree: into bone & muscle
Minor Burns: < 10% adults, < 5% children/elders, < 2% full thickness burns,
must not involve face, hands, perineum, feet, cross major joints or be
circumferential
Major burns: > 25% TBSA adults, >20% children/elders, > 10% full thickness,
or involving face, hands, perineum, feet, crossing major joints or circumferential
Treatment
• Monitor ABC’s, fluid replacement, topical antibiotic – cleanse w/ mild soap
& water, no ice, irrigate chemical burns w/ running water x20 min, topical
Bacitracin applied to superficial burns, wrap finger & toes individually to
prevent maceration & gauze between, give antibiotics: silver sulfadiazine
• >10 % in children or >15% adults: formal fluid resuscitation w/ Lactated Ringers IV x 24 hours [1/2 in 1 st 8 hours, with ½ in
remaining 16 hours]
• Parkland Formula to determine how much LR: 4mL x %BSA x weight (kg)
Diaper Dermatitis – Irritant Dermatitis – Perioral
Pathophysiology Pathophysiology
• Irritant contact dermatitis d/t overhydration of the skin, maceration, • MC in young woman w/ hx of prior topical steroid
prolonged contact with urine/feces use in area
Clinical Manifestations Clinical Manifestations
• Erythematous, scaly diaper area with papulovesicular or bullous • Papulopustules on erythematous base → confluent
lesions, fissures & erosions plaques, and scales around the mouth
• Genitocrural folds are spared in irritant dermatitis • May see satellite lesions, & vermillion border spared
Diagnosis Diagnosis
• Clinical, may use KOH prep • Clinical
Management • Culture to rule out staphylococcal infection
• Zinc oxide ointment or Vitamin A/D ointment & leave area open to Management
air or cover w/ topical emollient • Topical metronidazole; can also use erythromycin or
Diaper Dermatitis – Candidal Pimecrolimus
Pathophysiology • If no clearance: systemic tx w/ minocycline,
• Infection occurs 48-72 hours after, MC in immunocompromised doxycycline or tetracycline
Clinical Manifestations General Measures
• Isolated to perineal area & involves genitocrural folds • Avoid topical steroids! C/I d/t → flare of lesions
• Satellite lesions may be visible – tiny, red papules & papulovesicles
Diagnosis
• Clinical, may use KOH prep
Management
• Hydrocortisone 1% BID + antifungal (Nystatin cream)
• Avoid high strength topical CS
Drug Eruptions
• Medication-induced changes in the skin & mucous membrane, most are hypersensitivity reactions
• Most cutaneous drug reactions are self-limited if offending drug is discontinued
• Triggers: Antigen from foods, insect bites, drugs, environmental, exercise-induced, & infections
Pathophysiology
• Type I: IgE mediated, immediate – urticaria & angioedema
• Type II: cytotoxic, antibody-mediated (drugs in combo w/ cytotoxic antibodies → cell lysis)
• Type III: immune antibody-antigen complex – drug-mediated vasculitis & serum sickness
• Type IV: delayed [cell-mediated] morbilliform reaction – Erythema Multiform
• Non-immunologic: cutaneous drug rxns d/t genetic incapability to detoxify certain meds (sulfa, anticonvulsants)
Drug Eruption: Exanthematous Drug Eruption
Morbilliform or maculopapular drug eruption characterized by macules/small papules after the initiation of drug treatment
Pathophysiology
, • Type IV delated hypersensitivity reaction that most commonly occurs 5-14 days
after initiation of offending medication or within 1-2 days in previously sensitized
individuals
• Any drug can cause it but Penicillin, sulfa-containing meds, NSAIDs, & Allopurinol
are common causes
Clinical Manifestations
• Generalized distribution of bright red macules & papules that coalesce to form
plaques, primarily involving trunk & proximal extremities
• Systemic symptoms include low-grade fever & pruritus
Management
• Prompt withdrawal = mainstay of treatment
• Symptomatic treatment: oral antihistamines (H1 blockers) – second or first-generation
• Oral corticosteroids are reserved for severe cutaneous reactions
Drug Eruption: Angioedema
Self-limited localized subcutaneous (or submucosal) swelling resulting from extravasation of
fluid into interstitium
• Affects mucosal tissues of the face, lips, tongue, larynx, hands, feet & genitalia
• Onset in minutes to hours with spontaneous resolution in hours to a few days
Types
• Mast-cell (histamine) mediated – allergic reactions
• Angioedema that may be accompanied w/ other allergic reaction symptoms (urticaria,
flushing, generalized pruritus, bronchospasm, stridor, throat tightness, & hypotension)
• Bradykinin-mediated: ACE inhibitor-induced or hereditary (d/t C1 esterase inhibitor
deficiency)
• Angioedema without allergic reaction symptoms
Diagnosis
• No information to suggest an external cause & the patient has isolated angioedema without
pruritus or urticaria
• ? Obtain C4 levels & C1 inhibitor antigenic level
Management
• Immediate assessment & ongoing airway protection – epinephrine if severe
• Mast-cell (histamine) mediated – epinephrine (if severe), glucocorticoids, and antihistamines
• Bradykinin-mediated:
• C1 inhibitor concentrate, Ecallantide (kallikrein inhibitor), Icatibant (bradykinin-beta2 receptor antagonist), FFP if other
therapies aren’t available
• Danazol @ lowest dose may be needed for long-term management in hereditary causes
Erythema Multiform
Type IV hypersensitivity reaction assoc. w/ certain infections, medications (sulfa drugs), & other various triggers
Risk factors:
• MC: HSV, Mycoplasma in children, S. pneumoniae
• Meds: sulfa drugs, beta-lactams, Phenytoin, Phenobarbital, Allopurinol
• Malignancy, autoimmune, idiopathic
Clinical Manifestations
• Target lesions w/ 3 components on trunk & extremities: (1) dusky, central
area or blister + (2) dark red inflammatory zone surrounded by pale ring of
edema + (3) erythematous halo on extreme periphery of lesion
• (-) Nikolsky sign = no epidermal detachment, often febrile
• Minor: target lesions distributed acrally w/ no mucosal membrane
involvement
• Major: target lesions acrally progressing centrally + mucosal membrane involvement (oral, genital, or ocular) & no epidermal
detachment
Diagnosis
• Clinical, bx if dx not clear
Management
• Symptomatic: d/c offending drug, give antihistamines, analgesics, skin case
• Oral lesions: Corticosteroid + Lidocaine + Diphenhydramine mouthwash
• Severe: systemic corticosteroids
• Mycoplasma related: antibiotics
• HSV related: Acyclovir
Acne Vulgaris
Inflammatory skin condition assoc. with papules & pustules involving pilosebaceous units
Pathophysiology:
• 4 main factors – follicular hyperkeratinization with plugging of sebaceous ducts, increased sebum production,
Propionibacterium acnes overgrowth within follicles, & inflammatory response
• Hormonal activation of pilosebaceous glands which may cause cyclic flares that coincide with menstruation
Clinical Manifestations:
• In areas with increased sebaceous glands (face, back, chest, upper arms)
• Stage I: Comedones: small, inflammatory bumps from clogged pores
- Open comedones (blackheads): incomplete blockage
- Closed comedones (whiteheads): complete blockage
• Stage II: Inflammatory: papules or pustules surrounded by inflammation
• Stage III: Nodular or cystic acne: heals with scarring
Differential Diagnosis:
• Differentiate from rosacea which has no comedones**
• Perioral dermatitis based on perioral and periorbital location
• CS-induced acne lacks comedones and pustules are in same stage of
development
Diagnosis:
• Mild: comedones, small amounts of papules &/or pustules
• Moderate: comedones, larger amounts of papules &/or pustules
• Severe: nodular (>5mm) or cystic
Management:
• Mild: topical – azelaic acid, salicylic acid, benzoyl peroxide, retinoids, Tretinoin topical (Retin A) or topical antibiotics
[Clindamycin or Erythromycin with Benzoyl peroxide]
• Moderate: above + oral antibiotics [Minocycline 50mg PO qd or Doxycycline 100 mg PO qd], spironolactone
• Severe (refractory nodular acne): oral Isotretinoin 0.5-1.0 mg/kg/d BID x15-20 weeks
Isotretinoin: affects all 4 pathophysiologic mechanisms of acne
• Adverse effects: dry skin and lips (MC), highly teratogenic, increased triglycerides & cholesterol, hepatitis
Androgenetic Alopecia
Genetically predetermined progressive loss of terminal hairs on scalp in a distribution pattern
MC hair loss in F & M, gradual in onset & occurs after puberty; type of non-scarring alopecia
Pathophysiology:
• Key androgen leading to AA: Dihydrotestosterone (DHT) – activation of the androgen receptor shortens the androgen (growth
phase) in the normal hair growth cycle
• Pathologic specimens show decreased anagen to telogen ratio
Clinical Manifestations:
• Varying degrees of hair thinning and nonscarring hair loss
• Males: begins as bitemporal thinning of the frontal scalp then involves the vertex
• Females: thinning of the hair between the frontal and vertex of the scalp without affecting the frontal hairline
Diagnosis:
• Usually clinical
• Dermoscopy: miniaturized hair and brown perihilar casts
• In females: investigate the cause with labs such as DHEAS, testosterone levels, CBC, iron, TIBC, TSH, & vit D
Management
• Topical Minoxidil: 5% OTC, best used if recent onset alopecia involves a smaller area, requires 4-6 month trial before noticing
improvement & must be used indefinitely
- Mechanism: widens blood vessels, allows more blood oxygen & nutrients to promote growth (anagen) phase
- Adverse: pruritus & local irritation with flaking
• Oral Finasteride (Propecia): 5-alpha-reductase-type 2 inhibitor inhibts androgen (inhibits conversion of testosterone to DHT)
- Adverse: decreased libido, sexual or ejaculatory dysfunction; increased risk of high-grade prostate ca; cat X
• Hair transplant may be effective
Atopic Dermatitis (Eczema)
Rash due to defective skin barrier susceptible to drying, leading to pruritus & inflammation
Pathophysiology
• Disruption of the skin barrier (filaggrin gene mutation) and disordered immune response which manifests mostly in infancy or
almost always by age 5
• Triggers: heat, perspiration, allergens, & contact irritants (wool, nickel, food, synthetic fabrics)
,• Genetics & environmental factors play a role, + hx of atopy
- IgE, eosinophils, Langerhans cell, T helper cells all play a role in atopic dermatitis
- TH2 prominent in acute lesions, TH1 found in chronic lesions
Atopy triad: atopic dermatitis + allergic rhinitis + asthma (3 A’s)
Clinical Manifestations
• Hallmark: pruritus*
• Erythematous, ill-defined blisters, papules or plaques → later the lesions dry, crust over & scale
• Older children & adults: MC in flexor creases (antecubital and popliteal folds)
• Infants: face and extensor part of extremities (from crawling & rubbing the skin)
• Nummular eczema: sharply defined discoid or coin-shaped lesions, especially on the
dorsum of the hands, feet & extensor surfaces (knees, elbows)
Diagnosis
• Clinical, can also do a skin prick test
• Increased IgE and elevated eosinophilia supports diagnosis
Acute Management
• 1st line: topical CS – avoid class I & II in children [Mometasone, Fluticasone,
Betamethasone, Triamcinolone]
• Antihistamines for pruritus, wet dressings, antibiotics if secondary infection (MC=staph aureus) develops
• Topical calcineurin inhibitors [Tacrolimus, Pimecrolimus] = steroid alternative
• Systemic: phototherapy (UVA, UVB, & narrow-band UVB) – used in children w/ mod to severe eczema, Cyclosporine,
Azathioprine, Mycophenolate mofetil, Methotrexate, Dupilumab
Chronic Management
• Maintain skin hydration: hydration & skin emollients twice daily & within 3 min of exiting a lukewarm shower
• Oral antihistamines for pruritus (Cetirizine, fexofenadine, loratadine), Hydroxyzine, Diphenhydramine
Avoid triggers (heat, low humidity), or irritants (soaps, detergents, washcloths, frequent baths)
Contact Dermatitis
Inflammation of the dermis & epidermis from direct contact between a substance & the skin surface
Irritant: MC type, causes include: chemicals (solvents, cleaners, & detergents), alcohols, or creams
Allergen: Nickel (MC worldwide), poison ivy, oak, or sumac; other metals, chemicals (fragrances, glue, hair dyes), detergents,
cleaners, acids, prolonged water exposure
Pathophysiology:
• Allergic: type IV hypersensitivity reaction (T cell lymphocyte-mediated), delayed by days
• Irritant: non-immunologic reaction (immediate)
Clinical Manifestations
• Acute: erythematous papules or vesicles (may be linear or geometric), often assoc. with localized pruritus, stinging, or burning;
may ooze, develop edema, and progress to blisters or bullae
• Chronic: lichenification fissuring and scales
Diagnosis
• Clinical diagnosis
• Patch testing: may identify potential allergens to prevent future exposures
• Histology not usually needed but will show spongiosis (intercellular edema in the epidermis)
Management
• Identification & avoidance of irritants*
• Topical corticosteroids = first-line medical treatment; use oral CS in severe/extensive reactions
• Topical calcineurin inhibitors (Tacrolimus or Pimecrolimus) are alternatives
General Measures
• Cool saline or astringent compresses, cool baths, skin emollients
• Use drying agents if oozing or weeping
• Burrow’s solution, itching can be relieved with antihistamines or calamine lotion
Burns
Degree Involvement:
• 1st degree (sunburn): erythema of involved tissue, skin blanches with pressure, skin may be tender
• Involves only epidermis
• MCC: overexposure, heals uneventfully w/ no residual scarring
• 2nd degree (partial thickness): skin is red & blistered, skin is very tender
• Involves all epidermis + some dermis, painful w/ weeping & blisters
• Superficial: blisters = expectant management
• Deep: excise & graft, heals over 4-8 weeks; if infx it can lead to full thickness burn
,• 3rd degree (full thickness): burned skin is tough & leathery, skin non-tender, painless, nonblanching
• Involves all epidermis + dermis + some fat
• Requires skin grafting & escharotomy
• 4th degree: into bone & muscle
Minor Burns: < 10% adults, < 5% children/elders, < 2% full thickness burns,
must not involve face, hands, perineum, feet, cross major joints or be
circumferential
Major burns: > 25% TBSA adults, >20% children/elders, > 10% full thickness,
or involving face, hands, perineum, feet, crossing major joints or circumferential
Treatment
• Monitor ABC’s, fluid replacement, topical antibiotic – cleanse w/ mild soap
& water, no ice, irrigate chemical burns w/ running water x20 min, topical
Bacitracin applied to superficial burns, wrap finger & toes individually to
prevent maceration & gauze between, give antibiotics: silver sulfadiazine
• >10 % in children or >15% adults: formal fluid resuscitation w/ Lactated Ringers IV x 24 hours [1/2 in 1 st 8 hours, with ½ in
remaining 16 hours]
• Parkland Formula to determine how much LR: 4mL x %BSA x weight (kg)
Diaper Dermatitis – Irritant Dermatitis – Perioral
Pathophysiology Pathophysiology
• Irritant contact dermatitis d/t overhydration of the skin, maceration, • MC in young woman w/ hx of prior topical steroid
prolonged contact with urine/feces use in area
Clinical Manifestations Clinical Manifestations
• Erythematous, scaly diaper area with papulovesicular or bullous • Papulopustules on erythematous base → confluent
lesions, fissures & erosions plaques, and scales around the mouth
• Genitocrural folds are spared in irritant dermatitis • May see satellite lesions, & vermillion border spared
Diagnosis Diagnosis
• Clinical, may use KOH prep • Clinical
Management • Culture to rule out staphylococcal infection
• Zinc oxide ointment or Vitamin A/D ointment & leave area open to Management
air or cover w/ topical emollient • Topical metronidazole; can also use erythromycin or
Diaper Dermatitis – Candidal Pimecrolimus
Pathophysiology • If no clearance: systemic tx w/ minocycline,
• Infection occurs 48-72 hours after, MC in immunocompromised doxycycline or tetracycline
Clinical Manifestations General Measures
• Isolated to perineal area & involves genitocrural folds • Avoid topical steroids! C/I d/t → flare of lesions
• Satellite lesions may be visible – tiny, red papules & papulovesicles
Diagnosis
• Clinical, may use KOH prep
Management
• Hydrocortisone 1% BID + antifungal (Nystatin cream)
• Avoid high strength topical CS
Drug Eruptions
• Medication-induced changes in the skin & mucous membrane, most are hypersensitivity reactions
• Most cutaneous drug reactions are self-limited if offending drug is discontinued
• Triggers: Antigen from foods, insect bites, drugs, environmental, exercise-induced, & infections
Pathophysiology
• Type I: IgE mediated, immediate – urticaria & angioedema
• Type II: cytotoxic, antibody-mediated (drugs in combo w/ cytotoxic antibodies → cell lysis)
• Type III: immune antibody-antigen complex – drug-mediated vasculitis & serum sickness
• Type IV: delayed [cell-mediated] morbilliform reaction – Erythema Multiform
• Non-immunologic: cutaneous drug rxns d/t genetic incapability to detoxify certain meds (sulfa, anticonvulsants)
Drug Eruption: Exanthematous Drug Eruption
Morbilliform or maculopapular drug eruption characterized by macules/small papules after the initiation of drug treatment
Pathophysiology
, • Type IV delated hypersensitivity reaction that most commonly occurs 5-14 days
after initiation of offending medication or within 1-2 days in previously sensitized
individuals
• Any drug can cause it but Penicillin, sulfa-containing meds, NSAIDs, & Allopurinol
are common causes
Clinical Manifestations
• Generalized distribution of bright red macules & papules that coalesce to form
plaques, primarily involving trunk & proximal extremities
• Systemic symptoms include low-grade fever & pruritus
Management
• Prompt withdrawal = mainstay of treatment
• Symptomatic treatment: oral antihistamines (H1 blockers) – second or first-generation
• Oral corticosteroids are reserved for severe cutaneous reactions
Drug Eruption: Angioedema
Self-limited localized subcutaneous (or submucosal) swelling resulting from extravasation of
fluid into interstitium
• Affects mucosal tissues of the face, lips, tongue, larynx, hands, feet & genitalia
• Onset in minutes to hours with spontaneous resolution in hours to a few days
Types
• Mast-cell (histamine) mediated – allergic reactions
• Angioedema that may be accompanied w/ other allergic reaction symptoms (urticaria,
flushing, generalized pruritus, bronchospasm, stridor, throat tightness, & hypotension)
• Bradykinin-mediated: ACE inhibitor-induced or hereditary (d/t C1 esterase inhibitor
deficiency)
• Angioedema without allergic reaction symptoms
Diagnosis
• No information to suggest an external cause & the patient has isolated angioedema without
pruritus or urticaria
• ? Obtain C4 levels & C1 inhibitor antigenic level
Management
• Immediate assessment & ongoing airway protection – epinephrine if severe
• Mast-cell (histamine) mediated – epinephrine (if severe), glucocorticoids, and antihistamines
• Bradykinin-mediated:
• C1 inhibitor concentrate, Ecallantide (kallikrein inhibitor), Icatibant (bradykinin-beta2 receptor antagonist), FFP if other
therapies aren’t available
• Danazol @ lowest dose may be needed for long-term management in hereditary causes
Erythema Multiform
Type IV hypersensitivity reaction assoc. w/ certain infections, medications (sulfa drugs), & other various triggers
Risk factors:
• MC: HSV, Mycoplasma in children, S. pneumoniae
• Meds: sulfa drugs, beta-lactams, Phenytoin, Phenobarbital, Allopurinol
• Malignancy, autoimmune, idiopathic
Clinical Manifestations
• Target lesions w/ 3 components on trunk & extremities: (1) dusky, central
area or blister + (2) dark red inflammatory zone surrounded by pale ring of
edema + (3) erythematous halo on extreme periphery of lesion
• (-) Nikolsky sign = no epidermal detachment, often febrile
• Minor: target lesions distributed acrally w/ no mucosal membrane
involvement
• Major: target lesions acrally progressing centrally + mucosal membrane involvement (oral, genital, or ocular) & no epidermal
detachment
Diagnosis
• Clinical, bx if dx not clear
Management
• Symptomatic: d/c offending drug, give antihistamines, analgesics, skin case
• Oral lesions: Corticosteroid + Lidocaine + Diphenhydramine mouthwash
• Severe: systemic corticosteroids
• Mycoplasma related: antibiotics
• HSV related: Acyclovir
