1. DERMATOLOGIC DISEASES AND DISORDERS
Suggestions for Lecturer
-1-hour lecture
-Use GNRS slides alone or to supplement own teaching materials.
-Refer to GNRS and Geriatrics At Your Fingertips for further content.
-For strength of evidence (SOE) levels, see GNRS chapter.
-Supplement lecture with handouts.
-The GNRS Teaching Slides reflect care that can be provided to older adults in all settings. The words patient, resident, and older adult have been used interchangeably, as have the words provider, clinician, and primary care provider. Given the continually ongoing changes in health care today, some of the guidelines around reimbursement may have changed since publication.

2. OBJECTIVES
Know and understand:
Normal age-related changes in skin
How to recognize and treat photoaging
The diagnosis and treatment of skin conditions common in older adults

3. TOPICS COVERED Changes in Skin with Aging and Photoaging
Common Conditions
Seborrheic Dermatitis
Rosacea
Onychomycosis
Herpes Zoster
Xerosis
Neurodermatitis
Intertrigo
Candidasis
Scabies
Louse Infections
Bullous Pemphigoid
Cherry Angiomas
Pruritus
Seborrheic Keratoses
Psoriasis
Actinic Keratoses
Stasis Dermatitis
Skin Cancers
Venous & Arterial Ulcers

4. DERMATOLOGIC CHANGES WITH AGING
Epidermal and dermal changes
Reduced lipids
Slower wound healing
Lower immune function
Reduced collagen
Hair changes

5. In youth, epidermis interdigitates with dermis
EPIDERMAL AGING
In youth, epidermis interdigitates with dermis
With aging, the interdigitations flatten, resulting in:
Reduced contact between epidermis and dermis
Decreased nutrient transfer
Increased skin fragility
Easy bruising

6. LIPIDS AND AGING
Aging is associated with decreased lipids in the top skin layer, which leads to:
Dryness and roughness
Decreased barrier function

7. IMPAIRED HEALING AND IMMUNE FUNCTION WITH AGING
Slower turnover of epidermal cells may account for slower rate of wound healing
Lower number of immune antigen-presenting cells (such as Langerhans) may cause reduced cutaneous immune surveillance

8. CHANGES IN THE AGING DERMIS
Decrease in ground substance leads to wrinkling, atrophy
Decreases in collagen and elastin cause haphazard, fragmented fiber orientation and reduced skin elasticity

9. AGING SKIN AND HAIR
Changes in follicular melanocytes cause graying hair
Shortened duration of anagen (growth phase of hair follicle) and increased duration of telogen (resting phase) results in decreased hair density

10. PHOTOAGING: The Effects of UV Exposure on Skin
Shorter wavelengths are more biologically
active (UVA and UVB)
UV light causes:
DNA damage
Decreased DNA repair
Oxidative and lysosomal damage
Altered collagen structure

11. PHOTODAMAGED SKIN
Appears wrinkled, coarse, or rough
Has mottled pigmentation, hypopigmentation, telangiectasias
Cutaneous malignancies more common

12. PREVENTING PHOTODAMAGE
Use broad-spectrum sunscreens
Avoid direct sunlight
Use protective clothing, including hats
Use sunglasses

13. TREATING PHOTODAMAGE: TOPICAL AGENTS
Only agent shown to be effective: topical tretinoin at high concentrations for long periods
Increases thickness of superficial skin layers
Reduces pigmentary changes and roughness
Increases collagen synthesis
Claims that other agents decrease photodamage are not well substantiated

14. TREATING PHOTODAMAGE: SURGERY
Procedures include chemical peeling, dermabrasion, laser resurfacing
Destroys surface populations of keratinocytes, followed by repopulation of keratinocytes from deep within sun-protected follicular structures
Controlled trials of effectiveness of surgical approaches are inconclusive and rare

15. SEBORRHEIC DERMATITIS
Common chronic dermatitis
Erythema and greasy-looking scales
Typical locations: hairline, nasolabial fold, midline chest
Dandruff is often a precursor
More common in Parkinson disease
Cause unclear; normal yeast flora may cause inflammation

16. TREATMENT OF SEBORRHEIC DERMATITIS
Can be suppressed but not cured
Mild topical corticosteroids useful for acute forms (1% to 2% hydrocortisone) but not to be used chronically on face
Topical anti-yeast creams such as ketoconazole are recommended for chronic use if needed on the skin
Once controlled, maintenance with medicated shampoos that act against yeast, eg, selenium sulfide, ketoconazole, tar shampoos

17. INTRO TO ROSACEA (1 of 2)
Diffuse erythema and erythematous papules and papulopustules are seen on the cheeks, forehead, and chin
The nose shows thickening of the skin and changes consistent with an early rhinophyma

18. INTRO TO ROSACEA (2 of 2) Common in fair-skinned people
Affects all ages
Common symptom: Recurrent facial flushing from a variety of stimuli (sunlight, alcohol, caffeine, hot beverages, spice, drugs that cause vasodilation)
Chronic condition with frequent flares
Cause unknown

19. TREATMENT OF ROSACEA Avoid skin irritants, strong soaps
Reduce sun exposure; use sunscreens
For moderate to severe flares, use oral antibiotics (tetracyclines, eg, doxycycline, minocycline, or erythromycin)
For mild cases and maintenance, use topical antibiotics (erythromycin, clindamycin, metronidazole, topical sulfur preparations)

20. TREATMENT OF SEVERE ROSACEA
Severe or refractory rosacea: Oral isotretinoin
Erythema and telangiectasias:
Difficult to treat
Lasers provide option to reduce redness and improve cosmetic appearance
Rhinophyma:
Less common
Can be treated with surgical excision or electrosurgery

21. INTRO TO XEROSIS (1 of 2)
Eczema craquelé. Dry, erythematous, fissured, and cracked skin was seen on the lower legs of this patient.

22. INTRO TO XEROSIS (2 of 2) Dryness of the skin
Causes: reduced water content and reduced barrier function of aging epidermis
Exacerbated by environmental factors (decreased humidity, hot water, harsh soap)
Skin findings often more on legs; often results in pruritus
Rough itchy skin or scales; if severe, may manifest as eczema craquelé (dry, cracked appearance)

23. TREATMENT OF XEROSIS Avoid environmental triggers
Take tepid, not hot, showers
Use emollients immediately after bathing
Use moisturizing agents containing lactic acid or α-hydroxy acids to reduce roughness
Use mild topical corticosteroids episodically for irritation or inflammation

24. NEURODERMATITIS Chronic, pruritic conditions of unclear cause
Also known as lichen simplex chronicus
Lesions show signs of chronic scratching
Exclude irritant or allergic contact dermatitis
Treatment:
Potent topical corticosteroids (often under occlusion)
Emollients
Behavioral modification

25. INTERTRIGO AND CANDIDIASIS
Intertrigo and candidiasis are commonly found in the web space between the 4th and 5th toes
Moist erythema, maceration, and superficial erosion are apparent

26. INTERTRIGO
More common in older adults because of increased skin folds from decreased dermal elasticity
Often associated with secondary candidal or mixed bacterial colonization

27. TREATMENT OF INTERTRIGO
Keep area dry, open to air
Use topical antifungal powder or cream (eg, miconazole, nystatin, ketoconazole)
Use mild topical corticosteroid occasionally only to reduce inflammation; avoid use of topical steroids chronically to run risk of atrophy, etc.

28. INTRO TO BULLOUS PEMPHIGOID (1 of 2)
Tense, fluid-filled, and hemorrhagic bullae on an erythematous base were seen on the trunk and extremities
Some of the bullae have ruptured and left a scab with crusting

29. INTRO TO BULLOUS PEMPHIGOID (2 of 2)
An autoimmune blistering disorder
Occurs most often in adults in 60s and 70s
Blisters are usually large and tense, on normal or erythematous skin; may be filled with clear or hemorrhagic fluid
Diagnosis by biopsy and immunofluorescence
Condition may last from months to years, but often is self-limited

30. BULLOUS PEMPHIGOID: PATHOPHYSIOLOGY IS UNCLEAR
Antigens develop in the hemidesmosomes
Antibodies bind to bullous pemphigoid antigen, activating the complement cascade
Attracted leukocytes and degraded mast cells cause separation of epidermis from basement membrane

31. TREATMENT OF BULLOUS PEMPHIGOID
For localized disease, use topical corticosteroid, calcineurin inhibitors, and nicotinamide with tetracycline
For more extensive disease:
Systemic corticosteroid
Other immunosuppressant (azathioprine or cyclophosphamide)
Tetracycline and niacinamide combination therapy
IV immunoglobulin and rituximab (off-label)

32. PRURITUS
In older adults can be very severe and compromise QOL
Extensive differential diagnosis: xerosis; scabies; allergic, irritant, or atopic dermatitis; bullous pemphigoid; renal disease; liver disease; thyroid disease; anemia; occult malignancies; drugs

33. TREATMENT OF PRURITUS
Treat the underlying cause if possible
For symptom relief, use topical corticosteroids, emollients, menthol in calamine, capsaicin (off-label), pramoxine
Use oral antihistamines with caution
UVB phototherapy has been used for severe, refractory cases

34. INTRO TO PSORIASIS (1 of 2)
Characteristic well-demarcated beefy red plaques with overlying silvery-white scales are evident on the back of this patient

35. INTRO TO PSORIASIS (2 of 2)
Affects 2% of the population, with bimodal incidence (mid-20s, 50s and 60s)
Genetic predisposition; multigene mode of inheritance
Environmental factors may trigger
Other triggers include physical trauma, infections, stress, medications (oral corticosteroids, lithium, β-blockers, ACE inhibitors, NSAIDs)
5%8% also have psoriatic arthritis with pain, swelling, and stiffness in small joints

36. TREATMENT OF PSORIASIS (1 of 2)
Advise patient to eat a healthful diet, lose weight, and exercise (metabolic syndrome)
Topical treatment:
May control mild disease but may be irritating or messy
Include corticosteroids, vitamin D derivatives (calcipotriene), topical retinoids (tazarotene), salicylic acid, tar compounds
Long-term use of topical corticosteroids is limited by cutaneous atrophy

37. TREATMENT OF PSORIASIS (2 of 2)
Systemic treatment
If no response to topicals
Phototherapy
Immunosuppressive agents (cyclosporine, methotrexate)
Oral retinoids, anti-TNF agents
Biologic agents
UV therapy
Can be used with topical therapy
PUVA (psoralen with UVA light) and UVB

38. STASIS DERMATITIS
An early sign of chronic venous insufficiency of legs triggered by chronic venous hypertension and incompetent valves
Typically seen in medial supramalleolar areas and associated with pruritus
Risk of ulceration
Treatment
Compression bandages or stockings
Leg elevation at rest
Emollients and cautious topical corticosteroids

39. VENOUS AND ARTERIAL ULCERS
Lower-extremity ulcers are most often caused by vascular disease or neuropathy
72% venous disease
22% mixed arterial and venous cause
6% pure arterial disease

40. CHARACTERISTICS OF VENOUS AND ARTERIAL ULCERS
Venous disease
Arterial disease
Signs and symptoms
Limb heaviness, aching and swelling that is associated with standing and is worse at end of day, brawny skin changes
Claudication (pain in leg with walking), ankle-brachial index < 0.9, loss of hair, cool extremities
Risk factors
Advanced age, obesity, history of deep-vein thrombosis or phlebitis
Age >40, cigarette smoking, DM, HTN, hyperlipidemia, male gender, sedentary lifestyle
Location of ulcers
Along the course of the long saphenous vein, between the lower medial calf to just below the medial malleolus
Over bony prominences

41. INTRO TO ONYCHOMYCOSIS (1 of 2)
Nails infected by fungi are often yellow, thickened, and friable, with yellow-brown debris under the nail plate

42. INTRO TO ONYCHOMYCOSIS (2 of 2)
Affects about one third of older adults
 incidence in older adults with obesity, DM, PAD, immunodeficiency, chronic tinea pedis, or psoriasis
Causes: dermatophytes (80% of infections), yeasts, and saprophytes
Causes thickening of the nail plate and can create pain
In pts with neuropathy, can be a source of nail bed ulcerations
In pts with DM, the break in the epidermal barrier can serve as a route for bacterial infections

43. TREATMENT OF ONYCHOMYCOSIS
For cosmetic concerns, comorbidities (diabetes), or pain
No topical antifungal agent is effective
Topical ciclopirox painted on nail daily for 1 year <12% effective
Oral terbinafine, fluconazole and itraconazole
Effective, but duration of treatment, adverse event profile, and high potential for drug interactions warrant caution in older adults
Treatment may take 3 to 4 months
Relapse rate is high

44. INTRO TO HERPES ZOSTER (1 of 2)
This patient had clusters of vesicles and pustules on an erythematous base involving a thoracic dermatome

45. INTRO TO HERPES ZOSTER (2 of 2)
More than 2/3 of cases occur in people 50
Lifetime risk 20% in healthy adults and 50% in immunocompromised individuals
Most important reason for varicella zoster virus (VZV) reactivation is senescence of the cellular immune response to VZV with increasing age
Reactivation also associated with HIV, malignancy, use of immunosuppressive drugs
Usually self-limited if immunity is intact

46. COMPLICATIONS OF HERPES ZOSTER (1 of 2)
Involvement of ophthalmic branch of trigeminal nerve
Requires careful ophthalmic monitoring
Hutchinson’s sign: vesicles on the tip of the nose; represents involvement of nasociliary branch
Ramsay-Hunt syndrome (involvement of facial or auditory nerves)
Presents as herpes zoster of external ear or tympanic membrane
Leads to facial palsy with or without tinnitus, vertigo, and deafness

47. COMPLICATIONS OF HERPES ZOSTER (2 of 2)
Pain can precede, co-exist, or persist after rash
Post-herpetic neuralgia: pain that persists or appears after rash has healed, or 30 days after onset of rash
Occurs in 70% of people ≥70 years
Often difficult to treat

48. DIAGNOSIS OF HERPES ZOSTER
Characteristic physical exam findings (ie, dermatomal distribution)
Tzanck smear from base of vesicle shows multinucleated giant cells and epithelial cells containing intranuclear inclusion bodies
Smear can be sent for direct fluorescent antibody staining
Definitive diagnosis by viral culture

49. TREATMENT OF HERPES ZOSTER
Should start within 72 hours of rash
Acyclovir, valacyclovir, or famciclovir
Early treatment halts progression of disease, increases rate of clearance of virus from vesicles, decreases incidence of visceral and cutaneous dissemination, decreases ocular complications when eye is involved, may decrease pain and incidence of post-herpetic neuralgia
Wet compresses/topical antibiotics can treat secondary bacterial infection

50. TREATMENT OF POST-HERPETIC NEURALGIA
No definitive therapy
Tricyclic antidepressants (off-label), opioids, topical capsaicin, gabapentin, topical lidocaine, pregabalin, tramadol
Zoster vaccination recommended for adults > 60 years

51. CANDIDIASIS (1 of 2)
At risk: older people with decreased mobility, increased skin moisture or friction, poor hygiene, diabetes mellitus
Rash may resemble intertrigo but have peripheral satellite pustules
Oral thrush may develop in those on corticosteroid inhalers, antibiotics, or immunosuppressants, and those with concomitant diabetes

52. CANDIDIASIS (2 of 2)
Diagnosis: KOH preparation reveals spores and pseudohyphae
Treatment:
Keep skin dry
Improve hygiene
Use topical or oral anticandidal agents (nystatin, ketoconazole)

53. SCABIES (1 of 2) Infestation of mite Sarcoptes scabiei
Common in institutionalized older people; epidemics can occur in long-term-care facilities
Spread by person-to-person contact
Eradication can be difficult
Signs and symptoms include severe pruritus (esp. of hands, axillae, genitalia, and peri-umbilical region), erythematous papules, and linear burrows

54. SCABIES (2 of 2)
Diagnosis: scraping of suspected lesion (mite excreta, eggs, or mite may be seen)
Treatment:
Often initiated when suspicion of infestation is strong
Topical permethrin 5% or oral ivermectin (200 mc/kg)
Re-treat in 1 week if itching and lesions persist
Launder bed linens and clothing in hot water and dry in high heat, or leave in closed bag for 10 days
Pruritus may persist for weeks to months
Treat caregivers

55. LOUSE INFESTATIONS
Lice can infest the body (pediculosis corporis), scalp (pediculosis capitis), or pubic hair (pediculosis pubis)
Treatment:
Pyrethrin or derivatives (permethrin) topically
Treat caregivers and close contacts
Combs, brushes, hats, clothing, bedding, and towels must be washed in hot water

56. SEBORRHEIC KERATOSES
Benign growths common in adults > 40 years old
Tan, gray, black, waxy or warty papules and plaques with stuck-on appearance
Can be removed for cosmetic purposes
Occasionally confused with melanoma 7

57. CHERRY ANGIOMAS Most common acquired cutaneous vascular proliferations
Round to oval, bright red, dome-shaped papules
Benign and composed of dilated congested capillaries and postcapillary venules
Remove with excision, electrodessication or laser ablation

58. ACTINIC KERATOSES (1 of 2)
Rough, scaly, red-brown macules on sun-exposed skin
Also known as solar keratoses; result from chronic UV radiation exposure
Poorly circumscribed, occasionally scaly erythematous macules and papules in sun-exposed areas

59. ACTINIC KERATOSES (2 of 2)
Considered premalignant, but may resolve without treatment
Up to 20% progress to squamous cell cancer
Treatment:
Cryotherapy with liquid nitrogen
Photodynamic therapy
Topical acids
Topical 5-fluorouracil or imiquimod (off-label)
Excision

60. SQUAMOUS CELL CARCINOMA
Second most common form of skin cancer
Affects people in mid- to late life
Occurs most commonly in chronically sun-exposed areas
Propensity to occur in longstanding nonhealing wounds and in burn and radiation scars
Presentation: chronic erythematous papules, plaques, or nodules with scaling, crusting, or ulceration

61. TREATMENT OF SQUAMOUS CELL CARCINOMA
Surgical excision
Mohs’ micrographic surgery in cosmetically important areas
Cryotherapy or local radiation for patients unable to tolerate surgery

62. INTRO TO BASAL CELL CARCINOMA (1 of 2)
This is a pearly papule that is ulcerated in the center and has a characteristic rolled border
Basal cell carcinoma, ulcerated

63. INTRO TO BASAL CELL CARCINOMA (2 of 2)
Most common cancer in US
Risk factors: fair skin, chronic sun exposure
Treatment: surgical excision
Mohs’ micrographic surgery may be needed to ensure adequate excision and tissue sparing
When surgery is not feasible, can be treated with ablative methods such as cryosurgery, radiation, curettage with electrodesiccation and topical imiquimod

64. MAJOR CLINICAL PATTERNS OF BASAL CELL CARCINOMA
Description
Nodular
Most common variant; waxy, translucent papule with overlying telangiectasias
Morpheaform
Scar-like appearance; can look atrophic
Superficial
Erythematous macule or papule with fine scale or superficial erosion
Note: Some lesions appear as superficial ulcers with characteristic rolled borders; others are pigmented and may be confused with melanomas

65. INTRO TO MELANOMA (1 of 2)
Incidence is increasing; affects adults of all ages
Risk factors: fair skin, family history, dysplastic or numerous nevi, sunlight exposure
Regular skin examinations and early recognition are key for favorable prognosis
Treatment: surgical excision, possibly lymph node dissection or adjuvant therapy (immunotherapy, chemotherapy)

66. INTRO TO MELANOMA (2 of 2)
Irregular variegation in pigment (shades of brown and blue-black) and irregular borders suggest melanoma

67. TYPES OF MELANOMA Clinical pattern Description Lentigo maligna
Seen most commonly on atrophic, sun-damaged skin; an irregularly shaped tan or brown macule that slowly enlarges
Superficial spreading
Irregularly shaped macule, papule, or plaque with varied color
Nodular
Rapidly growing papule or nodule, often black or gray
Acral lentiginous
Palms, soles, or nail beds; all skin types; dark brown or black patch; highest incidence in those 65 and older

68. ACRAL LENTIGINOUS MELANOMA
Type of melanoma
Presents as a dark macular growth with irregular borders on volar surfaces of palms, soles (as in this case), and nails

69. The incidence of skin disease increases with aging and sun exposure
SUMMARY
The incidence of skin disease increases with aging and sun exposure
Dermatologic care of older people requires:
Knowledge of cutaneous changes of aging and effects of cumulative UV radiation exposure
Knowledge of common tumors, inflammatory diseases, and infections commonly seen in older adults

70. CASE 1 (1 of 3)
A 66-year-old white woman comes to the office because she is concerned about her appearance: her face and neck have fine wrinkles and mottled hyperpigmentation.
She states that her skin burns easily. She had significant sun exposure when she was young but now uses sunscreen most of the time she goes outside.
She does not smoke.
She wants to know which skin product is most effective for her wrinkles and hyperpigmentation. You counsel her to have consistent protection from the sun, including wearing a hat that shades her face and neck, and to use a broad-spectrum sunscreen with SPF 15 or above.

71. CASE 1 (2 of 3)
Which of the following topical agents has the most evidence on effectiveness in decreasing mottled hyperpigmentation and wrinkles due to photoaging?
Antioxidants
Retinoids
Peptides
Fluorouracil
Hydroxy acids

72. CASE 1 (3 of 3)
Which of the following topical agents has the most evidence on effectiveness in decreasing mottled hyperpigmentation and wrinkles due to photoaging?
Antioxidants
Retinoids
Peptides
Fluorouracil
Hydroxy acids
ANSWER: B
The prescription topical retinoids tretinoin and tazarotene are approved by the FDA for palliation of skin changes due to photodamage in patients who have a comprehensive skin care plan and avoid sunlight. Tretinoin has the most evidence for its effectiveness in palliating photoaging. According to the manufacturers, the safety and efficacy have not been established beyond 48 weeks for tretinoin and beyond 52 weeks for tazarotene when used for photoaging. Both drugs can cause erythema, scaling, dryness, burning, stinging, and irritation, especially at the beginning of treatment.
Retinoids found in OTC cosmetic preparations are less irritating, but the data on their efficacy are more limited. Topical retinol (vitamin A) is unstable and is degraded to inactive forms once exposed to sun or air. According to a 2010 review, topical products containing retinaldehyde have the most evidence of effectiveness for aging skin. Patients should avoid exposure to UV light while using retinoids, because these agents may cause photosensitivity.
There are limited data on topical antioxidants, and peptides have not been rigorously studied in randomized trials. The idea of using topical 5% fluorouracil for photoaging emerged when patients who used it for actinic keratosis (AK) reported skin smoothing and softening. In a nonrandomized, open-label study of 21 patients with AK and photodamage, fluorouracil improved wrinkles and pigmentations as well as AK. As expected, it also caused significant skin irritation. Fluorouracil is not approved by the FDA for palliation of photoaging, and it should not be used for patients with photoaging who do not have AK.
Hydroxy acids are exfoliants and moisturizers present in OTC creams and lotions. In several randomized trials, they improved roughness and mottled pigmentation, without improvement in wrinkles.

73. CASE 2 (1 of 4)
An 80-year-old woman is evaluated because she has erythematous lesions. Initially, the lesions were on her arms and legs; by the end of 1 week, they had spread to her trunk, and several large blisters appeared. The lesions are itchy and cause her to scratch.
History includes hypertension and dementia.
Medications include atenolol, amlodipine, donepezil, calcium, and vitamin D; she has taken each for several years.
The patient lives in a nursing home. A detailed history reveals no specific association with the onset of the rash.

74. CASE 2 (2 of 4)
On physical examination, the patient appears frail and in mild distress. She has no fever.
There are areas of erythema with tense blisters and serous exudate, occasionally blood-tinged. Some blisters have opened in oval erosions with serous exudate; the erosions do not coalesce. Some blisters are healing and covered with scabs.
There is no mucosal involvement, and the Nikolsky sign (in which the top layer of skin comes away with gentle rubbing) is negative.

75. CASE 2 (3 of 4)
Which of the following is the most likely diagnosis?
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Bullous pemphigoid
Pemphigus vulgaris
Erythema multiforme

76. Which of the following is the most likely diagnosis?
CASE 2 (4 of 4)
Which of the following is the most likely diagnosis?
Stevens-Johnson syndrome
Toxic epidermal necrolysis
Bullous pemphigoid
Pemphigus vulgaris
Erythema multiforme
ANSWER: C
The most likely diagnosis is bullous pemphigoid, because the bullae are tense—not flaccid— and do not coalesce when they break. Bullous pemphigoid is the most common autoimmune bullous disorder and occurs primarily in older adults.
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered severity variants of the same disease; they are characterized by epidermal detachment. In SJS, the skin detachment affects <30% of body surface area, while in TEN it affects >50%. When skin detachment is between 30% and 50%, the syndrome is considered SJS or TEN overlap. Often fever and mucosal involvement develop days before the rash appears. Initial lesions are macular and may form target lesions with purpuric centers. The lesions can coalesce and progress to superficial flaccid bullae. Epidermal necrosis is pathognomonic for SJS/TEN. Usually at least 2 mucous surfaces are involved. SJS and TEN are rare reactions to drugs; >200 drugs have been implicated. The most common are antibiotics, NSAIDs, allopurinol, and anticonvulsants. The patient in this case was not taking any of these medications and did not have flaccid bullae or mucosal involvement.
Erythema multiforme (EM) can present with oral involvement, a generalized eruption with flaccid bullae, and desquamation similar to that of SJS or TEN. Typically, EM follows an episode of herpes simplex outbreak, which had not occurred in this case. Pemphigus vulgaris also presents with flaccid, easily ruptured intraepidermal blisters. Oral involvement is present in 60% of cases but less common in drug-induced pemphigus. This patient’s bullae are tense and thus unlikely to be pemphigus vulgaris.
Histopathologic examination is essential for definitive diagnosis of bullous disorders.

77. Copyright © 2014 American Geriatrics Society
GNRS4 Teaching Slides Editor: Barbara Resnick, PhD, CRNP, FAAN, FAANP, AGSF GNRS4 Teaching Slides modified from GRS8 Teaching Slides based on chapter by Jane M. Grant-Kels, MD and questions by Angela Gentili, MD Managing Editor: Andrea N. Sherman, MS
Copyright © 2014 American Geriatrics Society