Transcript Houston NP Meeting Managing Difficult Rashes final TY handout

Managing Difficult Rashes
Debra Shelby, PhD, DNP, FNP-BC, DNC, FACDNP, FAANP
President and Founder
National Academy of Dermatology Nurse Practitioners
American College of Dermatology Nurse Practitioners
Owner, Florida Specialty Medical Services, LLC and Dermstaffing
Owner, National Institute for Dermatology
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Objectives: At the conclusion of the presentation,
participants should be able to:
 Discuss morphology and configuration of
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solitary & disseminated dermatoses.
Identify three commonly seen dermatoses.
Discuss two common diagnostic
tools/procedures used for diagnosis.
Describe three frequently used drug
classifications/ therapies used for treatment
of dermatoses.
Discuss two complications with treatment of
common dermatoses.
Conflict of Interest
 Speaker reports no conflict of interest with
this lecture
Terminology
Primary Skin Lesions
 Macule: Small spot, different in color from surrounding
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skin, that is neither elevated or depressed below skin
surface.
Papule: Small (<5mm/1cm diameter)* circumscribed
solid elevation of skin.
Plaque: Large (>5mm/1cm)* superficial lesion, often
formed by confluence of papules.
Nodule: Large (5-20mm) circumscribed solid skin
elevation.
Pustule: Small circumscribed skin elevation containing
purulent material.
Vesicle: Small (5mm/1cm)* circumscribed skin blister
containing serum.
*Textbook definitions vary from 5mm-1cm
Primary Skin Lesions Cont.
 Wheal: Irregular elevated edematous skin area, which
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often changes size and shape.
Bulla: Large (>5mm) vesicle containing free fluid
Cyst: Enclosed cavity with a membranous cavity lining,
which contain fluid or semisolid matter.
Tumor: Large nodule, which may be neoplastic
Telangiectasia: Dilated superficial blood vessel.
(Lookingbill & Marks, 2000)
(Goldstein & Goldstein (1997), pg. 3)
Secondary Morphology
 Scale: Superficial epidermal cells that are
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dead and cast off the skin.
Erosion: Superficial focal loss of part of the
epidermis; lesions usually heal without
scarring
Ulcer: Focal loss of the epidermis
extending into the dermis; lesions may heal
with scarring
Fissure: Deep skin split extending into the
dermis
Crust: Dried exudate, a “scab”
Secondary Morphology Cont.
 Erythema: Skin redness
 Excoriation: Superficial, often linear, skin erosion
caused by scratching
 Atrophy: Decreased skin thickness due to skin
thinning
 Scar: Abnormal fibrous tissue that replaces
normal tissue after skin injury
 Edema: Swelling due to accumulation of water in
tissue.
(Goldstein & Goldstein (1997) , pg. 4)
Secondary Morphology Cont.
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Hyperpigmentation: Increased skin pigmentation
Hypopigmentation: Decreased skin pigmentation
Depigmentation: Total loss of pigmentation
Lichenfication: Increased skin markings and
thickening with induration secondary to chronic
inflammation caused by scratching or other
irritation
 Hyperkeratosis: Abnormal skin thickening of the
superficial layer of the epidermis.
(Lookingbill & Marks, 2000)
(Goldstein & Goldstein (1997), pg. 4)
Asking the Right Questions
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When did it start?
What did it look like when it started?
Where did it start? Where is it located now?
What treatment have you used? What effect did
they have?
 Are there symptoms?
 Are other family members affected?
 Have they ever had the rash before?
(Goldstein & Goldstein (1997), pg. 5)
History
 Review medical history
 What are the patient’s social history
 What medications are they taking. Anything
new?
 Does the patient have any allergies?
 Is there a family history of skin diseases?
 Assess patient’s education level and
financial status
(Goldstein & Goldstein (1997), pg. 5)
Physical
 Distribution: Where are the lesions located?
 Primary features: What do they look like?
 Secondary features: Is there erythema, excoriation,
crust, or pigmentary alterations?
 Diagnosis: Is the diagnosis certain or still need to be
determined?
 Treatment: Record all treatment. Document sample
medications.
 Patient education: Give patient handouts; document
instructions given.
(Goldstein & Goldstein (1997), pg. 5)
Diagnosing
 Lesions may be differentiated by their
morphologic characteristics
 Lesions may be differentiated by their
characteristic distribution
 Lesions are often seen in a particular age
(Goldstein & Goldstein (1997), pg. 7)
(Lookingbill & Marks, 2000)
Classic Distribution of Common
Skin Disorders
 Atopic Dermatitis: Extensor surfaces in infants;
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flexural areas in young children and adults
Hand and Foot Eczema: Palms, soles
Psoriasis: Extensor surfaces, posterior scalp,
sacral area and intertriginous areas.
Scabies: Finger webs, wrists, axilla, waist, groin,
and feet
Seborrhea: Scalp, ears, central face, chest, and
groin
(Goldstein & Goldstein, 1997)
(Lookingbill & Marks (2000), pg. 7)
Diagnostic Tests
 Potassium /hydroxide Prep (KOH):
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- Used to identify fungus or yeast from
epidermal scrapings
Fungal Cultures: Useful in hair or nail infections.
Can be used for skin.
Bacterial Cultures
Scabies test
Tzanck Smear: Herpes infections
Wood’s Lamp Examination: Tinea, dyschromia,
erythrasma
PAS: Periodic acid-Schiff
Dermatologic Therapies
Most Common Drug Therapies
 Topical Glucocorticosteriods
 Antibiotics
 Antifungals
 Immunomodulators
 Biologics
Don’t forget: With some rashes, effective
emollients are as important as drug therapies.
Dermatologic Therapies
 Ointments: Consists of mainly water suspended in oil.
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Generally the most potent vehicle because of their occlusive
effect.
Creams: Semisolid emulsions of oil in 20% to 50% water.
Most cosmetically appealing
Lotions: Powder-in-water preparations. Least potent, but are
useful in hairy areas and conditions with large surface areas.
Solutions: Consist of water mixed with various medications
or substances. Used for soaks and open, wet dressings
Gels: Oil-in-water emulsions with alcohol in the base.
Combines the best therapeutic advantages of ointments with
the best cosmetic advantages of creams
Foams: Alcohol based, great for large areas and hairy
locations
(Goldstein & Goldstein (1997), pg. 11)
Topical Glucocorticosteroids
 Class I: Superpotent
Examples: Clobetasol proprionate ointment, cream 0.5%
Betamethasone diproprionate gel and ointment 0.05%
Class II: High Potency
Examples: Betamethasone diproprionate AF cream 0.05%,
Fluocinonide gel, ointment and cream 0.05%
Class III: High Potency
Examples: Triamcinolone acetonide cream 0.5%
Betamethasone valerate ointment 0.1%
(Bolognia,Jorizzo, & Rapini (2003), p. 1882)
Topical Glucocorticosteroids cont.
 Class 4: Medium Potency
Examples: Fluticasone proprionate cream 0.05%,
Triamcinolone acetonide (Kenolog)cream 0.1%
Class 5: Medium Potency
Examples: Hydrocortisone butyrate cream 0.1%
Triamcinolone acetonide lotion
Class 6: Low Potency
Examples: Desonide cream 0.05%
Fluocinolone acetonide cream 0.01%
(Bolognia, Jorizzo & Rapini (2003), p. 1882)
Topical Gluticocorticosteroids cont.
 Class 7: Low Potency
 Topicals with hydrocortisone,
dexamethasone and prednisolone
Remember:
 Brand names may be higher potency than generic
 Vehicle can affect potency
 Many topical medications have the same name, but different
strength that can change class potency. Make sure you check
strength
(Bolognia, Jorizzo, & Rapini (2003), pg 1882)
Papulosquamous
Diseases
Eczema
 Eczema is a broad term to describe an array of
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inflammatory skin disorders
Classified by several classification schemes:
Cause, location, degree of involvement, or a
generalized condition
Acute: severe, with edema, vesicles, and bullae
Subacute: Scaling plaques
Chronic: Thickened accentuated skin markings
called lichenfication
(Lookingbill & Marks, 2000)
(Goldstein & Golstein (1997), pg. 157)
Atopic Dermatitis
 Very pruritic skin disorder involving cutaneous
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hypersensitivity
Usually begins in early infancy after 6 weeks of age
Variable symptoms
Associated with decreased cellular immunity
Often becomes colonized with Staph. aureus
Extensor surfaces and face of children
Flexural areas in children and adults
Plaques, papules, erythema, scale, excoriations,
fissures, crust, and lichenfication
(Lookingbill & Marks, 2000)
(Goldstein & Golstein (1997), pg. 157)
Contact Dermatitis
 Pruritic, reactionary skin disorder that results when
a particular substance comes in contact with the
skin
 Second most common cause of occupational
disability
 Contact dermatitis occurs when an allergen or
related compound causes a delayed type of
hypersensitivity reaction on re-exposure (poison ivy)
(Lookingbill & Marks, 2000)
(Goldstein & Golstein (1997), pg. 162)
Treatments
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Find source of allergy
Corticosteroids (careful with vehicle selection)
Pimecrolimus (Elidel)
Tacrolimus (Protopic)
Lactic acid (avoid in inflamed skin)
Hydration: Emollients, protective barriers, hyaluronic
acid, and petrolatum. (careful with vehicle selection
and ingredients)
-Vanicream, Vanicream lite lotion, Vanicream bar,
Vanicream ointment.
 Mild cleansers, laundry soap, no fabric softner
 Narrow band UVB
 Treat secondary bacterial or fungal infections
Irritant Dermatitis
 Irritant dermatitis occurs secondary to any
non-allergic skin irritation resulting from
exposure to an offending agent, either with
initial or repeated exposures (hand
washing, bleach, moisture, friction)
Irritant Dermatitis Treatment
 Find source of irritation or friction
 Intertriginous: Make sure you biopsy to rule out Inverse
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psoriasis
Good hygiene
Control moisture: Knitted polyester fabric
With or without silver (InterDry Ag, Maxorb Ag)
Control friction
Treat fungal and bacterial infections
Corticosteroids (careful with vehicle selection and
potency)
Pimecrolimus (Elidel)
Tacrolimus (Protopic)
Skin barriers
Stasis Dermatitis
 Chronic eczematous process resulting from suboptimal
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lower extremity circulation and chronic venous insufficiency
More common in people over 50
Higher incidence in women than men
Predisposing conditions: Varicose veins,
cardiac failure, surgery, trauma, thrombophlebitis, and
hypoalbuminemia.
Early signs include hyperpigmentation caused by leakage of
blood into the dermis and its subsequent breakdown into
hemosiderin.
(Golstein & Goldstein (1997), p. 169
Treatments
This is a collaborative team effort! PCP, derm, wound care, and
vascular surgeon
 Compression: support hose, elastic wraps, unna boot (after
DVT ruled out!)
 Diuretics (with the presence of pitting edema)
 Elevate legs
 Corticosteroids
 Emollients: Careful selection
 Pharmacology: Antibiotics, prednisone, Diosmin and
Pentoxifylline
 Low salt diet
 Restrict sitting and standing for long periods
 Vascular Surgeon
Psoriasis
 Chronic, recurrent, hyperproliferative
inflammatory disorder of unknown cause
 Affects 3-5 million people in the U.S.
 Initially appears most commonly in people
younger than 20 years old, peak incidence
occurs around 22.5 years, but can occur at any
age, even after age 60
 Characterized by erythematous plaques with
thick, adherent, silvery scales.
( Wolff & Johnson, 2005)
(Lookingbill & Marks, 2000)
(Goldstein & Golstein. 1997)
Psoriasis cont.
 Auspitz sign: Punctate bleeding points
from capillaries close to the top layer of
skin after one peels off the scale
 Distribution: Extensor surfaces, typically
sparing the face.
(Goldstein & Golstein. 1997)
Treatments
 Topical Corticosteroids
 NO PREDNISONE: REBOUND
 Calcipotriene (Dovonex cream, ointment,
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scalp solution)
Immunomodulators
Biologics
Tar
PUVA, narrow band UVB
Methotrexate, Soriatane
Inverse Psoriasis
 Skin folds: Axilla, breasts, genitals, groin
and buttocks
 Biopsy to confirm when other treatments
are ineffective.
 Control moisture: Knitted polyester fabric
(InterDry, Maxorb), Castellani’s Paint
 Treatment same as psoriasis. Careful with
topical steroids in intertriginous areas.
Fungal Infections
Fungal Infections
 Dermatophyte v. yeast
 Hyphae v. hyphae and spores
 Look for erythematous plaques with scale,
central clearing, and well-demarcated
borders.
 Use topical antifungals
 Lamisil (Terbinafine), Sporonox
(Itraconazole) and Ketoconazole
(Lookingbill & Marks, 2000)
(Goldstein & Golstein. 1997)
Avoid Pitfalls
 Biopsy and get fungal cultures
 Make sure you treat with right antifungal
medication
 Past history of steroids?
 Majocchi’s granuloma: Deep follicular
fungal infection
 Remember: Topical only reach so far into
the dermis. Deep tissue needs systemic
antifungals.
Tinea Cruris
 Dermatophyte infection of the groin
 Scrotum most often spared
 Characterized by pruritus or burning
sensations
 Erythema, scale, central clearing, and
well defined borders
 KOH, antifungals
(Lookingbill & Marks, 2000)
(Goldstein & Golstein. 1997)
Tinea Manus
 Dermatophyte infection of hand and nails
 Usually unilateral, but is virtually always
associated with bilateral involvement of
the hands
 Plaques, scale, erythema, desquamation
 KOH
 Antifungals and oral agents
(Lookingbill & Marks, 2000)
(Goldstein & Golstein. 1997)
Tinea Pedis
 Dermatophyte infection of the feet.
 Erythema, scale, maceration, and
vesicles
 KOH
 Antifungals, topical, and oral
 Treat secondary bacterial infections
Tinea Versicolor
 Yeast infection caused by pitysporum
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orbiculare
Hyphae and spores
Produces azelaic acid which inhibits
pigment transfer to keratinocytes
Predisposing factors include hot, humid
weather
Selenium sulfide, Nizoral (Ketoconazole)
(Lookingbill & Marks, 2000)
(Goldstein & Golstein (1997), pg. 107)
Candidiasis
 Seen with intertrigo (irritant derm)
 Caused by candida
 Skin folds, under breasts, abdominal folds,
groin, rectum, axillae, and fingerwebs.
Scrotum is involved
 Beefy red lesions with satellite erythematous
papules and/or pustules
 KOH negative (pseudohyphae and spores)
 Selenium sulfide, Nizoral (Ketoconazole),
econazole
(Lookingbill & Marks, 2000) (Goldstein & Golstein (1997), pg. 107)
Bacterial Infections
Erythrasma
 Superficial infection of any intertriginous
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area
Caused by Corynebacterium minutissimun
Common in hot humid climates
Well-defined, brown patches with scale
Pruritus
Wood’s lamp reveals coral-red
fluorescence
(Golstein & Goldstein (1997), pg. 302)
Treatments
 Topical antibiotics: Benzoyl peroxide,
erythromycin, clindamycin, mupirocin
ointment or cream
 Oral antibiotics: Erythromycin,
Doxycycline, or Clarithromycin
 Good hygiene
Folliculitis
 Array of pustular infections that involve the hair
follicle
 Superficial or deep
 Staph aureus most common, but can be caused
by pseudomonas and pitysporum
 Deep:
- Furuncle- deep inflammatory nodule
- Carbuncle- aggregation of furuncles
(Lookingbill & Marks, 2000)
(Goldstein & Golstein. 1997)
Other Causes
 Herpes: Herpes Simplex shaving near cold
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sore
Gram negative
Lupus
Pseudo folliculitis
Immune
-Eosinophilic Pustular: associated with HIV
-Eosinophilic folliculitis: rare autoimmune
Oil folliculitis
Treatment
 Antibiotics (oral and topical):
Doxycycline, minocycline.
Clindamycin, erythromycin
 Benzoyl peroxide
 Dapsone gel
 Retinoids
 Antifungals
 Isotretinoin
A word on MRSA
 Drain lesions and irrigate
 Culture and Sensitivity
 Treat nares: Mupirocin ointment and
gentamicin ointment
 Systemic and topical
 Washes: Hibiclens; caution ototoxic
Avoid face, head and genitals! Give very clear
written instructions to patient. Be aware of
allergic reactions and avoid on inflammatory
dermatoses.
Thank You
Questions?