DERMATOLOGY

DERMATITIS
 DERMATITIS

• The terms ‘eczema’ and ‘dermatitis’ may

be used interchangeably
• Describe the same clinical and histological
entity.
• Eczema is an itchy erythematous (red)
eruption consisting of ill-defined
erythematous patches or papules.
• The skin surface is usually scaly and as
time progresses, constant scratching leads
to thickened, ‘lichenified’ skin.
 DERMATITIS
Two common forms are: irritant and allergic contact dermatitis (ICD and
ACD)
ACD
ICD
• First requires sensitization to
• Type of irritant, occur → specific cell-
concentration, quantity mediated sensitization
and length of exposure • Re-exposure to the allergen
will affect severity of triggers memory T-cells to
reaction initiate inflammatory
• Eg strong acids and response within 24-48 hours
alkalines produce • Reaction not limited to site of
ulceration on a single exposure
exposure • Risk of sensitization depends
on individual’s susceptibility,
allergen concentration and
quantity
DERMATITIS – CLINICAL PRESENTATION
• Dermatitis clinical features is
divided into acute & chronic phase
In acute phase characteristic are :
➢ Erythema
➢ Vasiculation
• Red hot, swollen & itch skin, papules & tiny blisters, sometimes
coalescing to form large blisters, exudation & crusting , scaling
DERMATITIS – CHRONIC PHASE
PRESENTATION
➢ Dryness
➢ Lichenification & fissuring
• Non infective , inflammatory condition
• Drier skin, becoming more scaly, Lichenification, painful
fissure
DERMATITIS – causes
DERMATITIS – Social & Psychological
Effects of CHRONIC ECZEMA
DERMATITIS – CLASSIFICATION

Polymorphous light eruption

– sun exposure
 ATOPIC ECZEMA
• particularly common in children, but
occurs at all ages.
• appearing as areas of red and scaly skin
which may become lichenified.
• associated with intense itching and,
consequently, the prevention of scratching
is a major problem.
• Atopic hand eczema is a common
manifestation of adult atopic dermatitis.
 NUMMULAR/DISCOID ECZEMA

• most commonly occurs in middle age.

• The itchy coin-like lesions are red and
are usually 1-5 cm across.
• Lesions characteristically occur on the
limbs, but may be widespread.
 PATHOGENESIS

• Similar in all types involving similar

Inflammatory mediators (prostaglandins,
leukotriens, cytokines)

• Helper T cells sometimes activated by

superantigens from Staph. aureus

• Epidermal cytokines help to produce spongiosis &

that their secretion by keratinocytes elicited by T
lymphocytes, irritants, bacterial products, & other
stimuli
 HISTOLOGY
Acute stage:
• intercellular oedema within the epidermis (spongiosis).
• Initially, there is a widening of intercellular spaces
between keratinocytes and elongation of the intercellular
bridges.
• Further accumulation of fluid leads to the formation
of intraepidermal vesicles.
Chronic stage:
• less spongiosis & vesication
acanthosis
• hyperkeratosis , parakeratosis and irregular acanthosis are
observed
These changes accompanied by various degree of vasodilatation &
lymphocyte infiltration
 CLINICAL APPEARANCE
Acute dermatitis: Chronic dermatitis:
weeping & crusting less vesicular & exudation
more scaly, pigmented,
blistering with vesicles
thickened lichenification
redness, papules,
swelling scaling fissures
 DIAGNOSIS
• Examining skin and reviewing any medical
history.
• Location and appearance of lesions
• Patch testing
= help diagnose specific types of allergies causing your
dermatitis. small amounts of different substances are applied to
your skin and then covered. The doctor looks at your skin
during visits over the next few days to look for signs of a
reaction.
• Skin biopsy
 GOAL of treatment

• Manage the itch

• Avoid irritants
• Maintain skin integrity

Pharmacological Non-pharmacological
 PHARMACOLOGICAL
Topical corticosteroid
•Mainstay of anti-inflammatory therapy
•Used after failure of lesions to respond to good skin care and
regular use of moisturizers alone.
•Intermediate & high-potency: for acute control of AD
• BD application until lesions significantly improved and less
thick, for up to several weeks at a time.
•Low-potency: maintenance therapy
• Proactive, intermittent use; once- to twice-weekly on
commonly flaring areas - to prevent relapses
✓ The choice of TCS in AE depends on the:
a) age of the patient
b) site of skin lesions
c) chronicity of skin lesions
d) severity of skin inflammation
 PHARMACOLOGICAL
Topical Calcineurin Inhibitors (Tacrolimus; pimecrolimus)

•Steroid-sparing, anti-inflammatory agents

•Approved to be used only for age 2 years and above
•Efficacious in
•acute flares (BD application)
•maintenance therapy (intermittent application twice
daily or 2–3 times per week)
•Cause skin burning and pruritus when applied
to acutely inflamed skin. Consider initial
treatment with topical corticosteroids to
minimize TCI application site reactions
 PHARMACOLOGICAL
Antimicrobial agent
•Aetiology: S. aureus
•Atopic individuals are predisposed to skin infections due to a
compromised physical barrier, diminished immune recognition and
impaired antimicrobial peptide production.
•Topical antimicrobial agents (ie. Mupirocin): should be limited to the
management of active bacterial skin infections
•In cases of active secondary infection, topical or systemic antibiotics
are often needed.
•Bleach bath used as antiseptic bath to reduce colonisation of bacteria
including MRSA.
•Other antiseptic baths (e.g. potassium permanganate, triclosan,
chlorhexidine) may be helpful in reducing bacterial colonisation of the
skin.
 PHARMACOLOGICAL
DUPIXENT (DUPILUMAB)
• New FDA approved - injection to treat adults with
moderate-to-severe eczema (atopic dermatitis).
intended for patients whose eczema is not
controlled adequately by topical therapies, or those
for whom topical therapies are not advisable.
• can be used with or without topical corticosteroids.

binds to a protein [interleukin-4 (IL-4) receptor

alpha subunit (IL-4Ra)], that causes
inflammation. By binding to this protein,
Dupixent is able to inhibit the inflammatory
response that plays a role in the development of
atopic dermatitis
 NON - PHARMACOLOGICAL
Bathing practices

• Soak in warm water (>10 minutes)

• followed by application of moisturizers
• critical to maintain adequate cutaneous hydration
• avoidance of damaging, drying, and irritating soaps with alkaline
pH
 NON - PHARMACOLOGICAL
Wet Wrap Therapy

•Consists of two layers of tubular bandage or garments with inner wet and
outer dry layers, applied over moisturiser alone or in combination with TCS
•Used in the setting of significant flares - Quickly reduce AD severity,
•wrap is worn from several hours to 24 hours at a time, depending on
patient tolerance
•Help by occluding the topical agent for increased penetration, decreasing
water loss, as well as providing a physical barrier against scratching.
 NON - PHARMACOLOGICAL
Moisturizers
• Cornerstone of AD treatment
• indicated as primary therapy for mild AD
• As adjunctive therapy for moderate-to-severe AD
• For treatment of active disease, maintenance, and prevention of
flares.
• Improve skin barrier function and reduce transepidermal water
loss - thereby increasing skin hydration
 NON - PHARMACOLOGICAL
Moisturizers are formulated with varying
amounts of different active ingredients
Emollients
◦ e.g. glycol and glyceryl stearate, soy sterols, ceramides and
linoleic acid
◦ lubricate and soften the skin
Occlusive agents
◦ e.g. petrolatum, dimethicone, mineral oil
◦ form a layer to retard evaporation of water,
Humectants
◦ e.g. glycerine, lactic acid, urea
◦ attract and hold water.
 PHOTOTHERAPY

For moderate-to-severe disease refractory to topical therapy

◦ Narrowband UVB
◦ administered 2 to 3 times per week.
◦ Potential adverse effects: erythema and burns, photo aging and
increased skin cancer risk
 SYSTEMIC THERAPY
Antihistamine
• Antihistamines should not be used as monotherapy or to
substitute topical therapy in atopic eczema (AE).
• Sedating antihistamines may be considered as a short-term
measure at bedtime in AE patients with sleep disturbance
Immunomodulating Agents
• Systemic corticosteroids may be considered for short-term
control of severe acute exacerbation of atopic eczema (AE)
• Azathioprine, cyclosporin A, methotrexate or mycophenolate
may be used in the treatment of severe AE after optimisation
of topical treatment.
• Severe AD refractory to topical regimens and phototherapy or
when quality of life is severely affected
To determine the severity of atopic
dermatitis
 Patient COUNSELLING
1)Select clothing made of soft cotton fabrics, not polyester.
2) Identify and remove irritants and allergens
3)Importance of not using topical corticosteroids as emollients
4)Amount of topical corticosteroid to apply?
5)Corticosteroids should not be applied for at least half
an hour after emollient application to avoid Dilution of
the corticosteroid or its spread to unaffected areas.
7)Consider using antihistamines at bedtime to reduce
scratching at night.
8)Keep the child cool; avoid situations in which
overheating occurs.
9)Avoid triggering factors
 SCALP DERMATITIS
• Is also known as Seborrheic dermatitis

• chronic inflammatory dermatologic condition that usually appears on

areas of the body with a large density of sebaceous glands, such as the
scalp, face

• skin changes is cause by inflammatory response to a common skin

organism, Malassezia yeast – a fungal microorganism
SCALP DERMATITIS – predisposing factors
SCALP DERMATITIS – pATHOPHYSIOLOGY
 SCALP DERMATITIS VS SCALP PSORIASIS

➢ an autoimmune disease.
➢ Psoriasis is long-lasting while
dandruff may come and go.
➢ scalp psoriasis looks like scaly,
silvery, or powdery patches
➢ It may spread. Psoriasis patches
can creep

➢ Itchy
➢ Flakes
➢ Hair fall off
 SCALP DERMATITIS - MANAGEMENT

Mild seborrheic dermatitis = selenium sulfide, zinc pyrithione, or

coal tar can control symptoms
➢ Tea tree oil shampoo may also decrease symptoms.

Selenium sulfide = slowing the growth of the yeast that causes the infection
Zinc pyrithione = inhibit the antifungal activity by disrupting the membrane
Coal tar = reduce the mitotic activity in the epidermis
Salicylic acid = reduce inflammation, reduce flakes & itchiness
 SCALP DERMATITIS - MANAGEMENT

• For long-term control, antifungal shampoos containing ketoconazole

2% (Nizoral) or ciclopirox 1% (Loprox) can be used daily or at least
two or three times per week for several weeks, until remission is
achieved.

• Once-weekly use of these medicated shampoos can prevent relapse.

• These shampoos should remain on the hair for at least five minutes to
guarantee adequate exposure to the scalp.
 SCALP DERMATITIS - MANAGEMENT

• Severe scalp inflammation = topical corticosteroids can be

beneficial
• Help to reduce itching and inflammation.
• Use with ketoconazole shampoo

Exm = clobetasol 0.05% shampoo (Clobex) twice weekly

alternating with ketoconazole 2% shampoo twice weekly can
reduce acute symptoms more quickly and maintain control longer
after discontinuing use, compared with ketoconazole alone.
 references

• Gupta AK, Bluhm R, Cooper EA, et al. Seborrheic dermatitis. Dermatol

Clin. 2003;21:401–112.

• Clark GW, Pope SM, Jaboori KA. Diagnosis and treatment of seborrheic
dermatitis. Am Fam Physician. 2015 Feb 1;91(3):185-90. PMID: 25822272.

• Hay RJ. Malassezia, dandruff and seborrhoeic dermatitis: an overview. Br J

Dermatol. 2011;165(Suppl 2):2–8.

• British Association of Dermatologists. Management of serborrheic dermatitis.