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DERMATITIS & ECZEMA
DIAGNOSIS
LAB RESULTS
▪ Skin biopsy, blood tests
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Chapter 2 Dermatitis & Eczema
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▫ Topical calcineurin inhibitors ▪ Maintain skin hydration
▫ Oral cyclosporine ▫ Thick, unscented creams with low water
▫ Dupilumab (IL-4 receptor antagonist) content/ointments without water
▫ Apply after bathing/hand washing
OTHER INTERVENTIONS ▫ Avoid lotions with high water/low oil
content (evaporation dries out skin,
▪ Reduce exposure to environmental
triggers outbreak)
allergens
▪ Control pruritus
▪ Avoid triggers
▫ Prevent scratching; keep fingernails
▫ Heat, low humidity
short (esp. young children)
▪ Manage stress/anxiety
CONTACT DERMATITIS
osms.it/contact-dermatitis
Allergic contact dermatitis
PATHOLOGY & CAUSES ▪ Anacardiaceae family plants
▫ Poison ivy, poison oak, poison sumac
▪ Inflammation of skin after contact exposure
to allergens/irritants ▪ Nickel, fragrances, dyes
▪ Localized ▫ Induction phase: immune system
primed for allergic response to antigen
▪ Exposure to foreign substance triggers
immune response ▫ Elicitation phase: contact allergens are
typically haptens → small, can cross
▪ Most common form: irritant contact
stratum corneum of skin to associate
dermatitis
with epidermal proteins → form
complete reactive antigen → dendritic
CAUSES cells recognise antigen → internalise
▪ Exposure to irritant (irritation may be antigen, transport to lymph nodes →
mechanical/chemical/physical) present to T lymphocytes → trigger
▫ Acute: strong irritant immune response → cell mediated
immune response (Type IV delayed
▫ Chronic: recurring exposure to weak
hypersensitivity) → memory cells
irritant
remain within skin. Future exposure
▪ Detergents, surfactants, extreme pH, → triggers memory cells → immune
organic solvents, water response (cytokines, chemokines, TNF,
▫ Altered epidermal barrier function: Fat lymphocytes, granulocytes migrate)
emulsion → defatting of dermal lipids →
cellular damage to epithelium → DNA
damage, transepidermal water loss RISK FACTORS
→ cytotoxic cell damage → cytokine ▪ Age
release from keratinocytes → activation ▫ Infants: highest risk
of innate immunity ▫ > 65 years old: lowest risk
▪ Plants with spines/irritant hairs ▪ Body site exposure
▪ Low humidity ▫ Difference in thickness of stratum
▫ Skin loses moisture more easily corneum, barrier function
▫ Face, dorsum of hands, finger webs are
prone to irritation
▪ Atopy
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DIAGNOSIS
OTHER DIAGNOSTICS
▪ History of possible exposure to irritant/
allergen
▪ Patch allergen testing
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SEBORRHOEIC DERMATITIS
osms.it/seborrhoeic-dermatitis
Distribution
PATHOLOGY & CAUSES ▪ Areas containing significant number of
sebaceous glands
▪ Sebaceous gland-centered skin
▫ External ear, center of face, upper trunk,
inflammation
areas where skin rubs together
▪ Response to fungal antigens/irritants
▪ Scalp
▪ Chronic/relapsing
▫ Infants: aka cradle cap; self-resolving
▪ Typically mild form of dermatitis
▫ Adults: aka dandruff (pityriasis sicca);
mildest form
CAUSES ▫ Fine, white scaliness without erythema
▪ Occurs in sites with greater density of +/- pruritus
sebaceous glands ▫ Severe cases: inflammation; patchy
▪ Not a disease of sebaceous glands, nor orange plaques with yellow, oily scales
increased sebum production (pityriasis steatoides); may progress
▪ Suspected connection to lipid-dependent to oozing/crusting fissures affecting
fungal genus Malassezia outer canal, concha of ear (vulnerable to
▫ Immune response to fungus superinfection)
▫ Local irritants produced by fungus ▪ Face
▪ Children ▫ Forehead, eyebrows, glabella, nasolabial
folds; may affect cheeks/malar area in
▫ Nutritional deficiencies of biotin,
butterfly distribution
pyridoxine (vitamin B6), riboflavin
(vitamin B2) ▫ Frequently affects areas of facial hair
distribution
RISK FACTORS
▪ Age (biphasic incidence: 2–12 months
of age to adolescence; adulthood: peaks
30s–40s)
▪ Hyperandrogenism
▪ Biological males > biological females
▪ HIV
▪ Parkinson’s
▪ Stress
▪ Cold, dry weather
▪ Sleep deprivation
▪ Poor general health
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▪ Periocular
▫ Blepharitis, free margin redness
TREATMENT
▫ Yellow crusting between lashes MEDICATIONS
▫ Can occur in isolation/part of larger ▪ Topical antifungals
distribution
▪ Antifungal shampoo
▪ Trunk (five distinct patterns of distribution)
▪ Topical corticosteroids
▫ Moist, skin-contact regions: axillae,
▪ Topical calcineurin inhibitors
inframammary folds, umbilicus,
genitocrural ▪ Oral antifungals
▫ Petaloid pattern: fine, scaling plaques ▪ Antiandrogens
over sternum/interscapular ▫ Reserved for individuals for whom
▫ Annular/arcuate: round, scaly plaques, feminization/male infertility is
may have hypopigmented central unproblematic
clearing ▫ Sexually-active, uterus-bearing people:
▫ Pityriasiform pattern: mimics pityriasis combine with contraception to avoid risk
rosea, 5–15mm oval, scaly lesions along to fetus
lines of skin tension
▫ Psoriasiform pattern: large, rounded OTHER INTERVENTIONS
erythematous plaques with thick scales ▪ Cradle cap
▫ Apply emollient (petroleum jelly,
vegetable oil, baby oil) to scalp overnight
DIAGNOSIS to loosen scales → remove scales with
soft toothbrush
OTHER DIAGNOSTICS ▫ Frequent shampooing with mild, non-
▪ History, appearance, distribution medicated baby shampoo → remove
scales with soft toothbrush
▫ Extensive/persistent cases → medical
therapy
▪ Topical
▫ Coal tar shampoo/ointment
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