•ekzein-to boil out;to effervesce

•All eczema are dermatitis but not all dermatitis are eczema

•Def-Eczema is an inflammatory skin reaction

characterized
•Clinically- itching, redness, scaling and clustered papulo-
vesicles.

• Histologically -by spongiosis, acanthosis, and a superficial

perivascular lympho-histiocytic infiltrate.
Classification:
 Exogenous eczemas – due to external trigger
factors
 inherited tendencies play a minor role.
 Endogenous eczema - not due to exogenous or
external environmental factors.
Exogenous:
 Irritant contact dermatitis.
 Allergic contact dermatitis
 Polymorphous light eruption
 Infective dermatitis

Endogenous:
 Atopic dermatitis
 Hand eczema
 Seborrhoiec dermatitis
 Stasis eczema
 Asteatotic eczema
 Discoid eczema
 Pityriasis alba
ACUTE ECZEMA:
 Intense itchy vesicles ,blisters, redness.
 Cold compresses, Condys, Burrows, NS,
 Steroid lotion, sedative antihistamine. &
systemic treament
SUBACUTE ECZEMA:
 moderate-itching, redness
scaling, fissuring, parched, scalded
CHRONIC:
 moderate-itching- thickened skin, lichenification
 Steroid ointment, under occlusion , intralesional
 tacrolimus, doxepin
Atopic dermatitis-
 chronically relapsing, pruritc, condition occurring in
infants and children
 Nearly always begins in childhood. 2-3mths
 Remitting and fluctuating
 Complex interplay b/w environmental, immunologic,
genetic, factors.

Pathogenisis:
 IgE is increased
 Reduced CMI
 aeroallergens
 AEC is increased
DIAGNOSTIC FEATURES OF ATOPIC
DERMATITIS

Major features (3 of 4 present):

 Pruritus
 Typical morphology and distribution of skin lesions
 Chronic or chronically relapsing dermatitis
 Personal or family history of atopy
Minor features (3 of 23 present):
 Xerosis
 Ichthyosis/palmar hyperlinearity/keratosis pilaris
 Immediate (type I) skin test reactivity
 Elevated serum IgE
 Early age of onset
 Tendency towards cutaneous infections/impaired cell-
mediated immunity
 Tendency towards non-specific hand or foot dermatitis
 Nipple eczema
 Cheilitis
 Recurrent conjunctivitis
 Dennie–Morgan infraorbital fold
 Keratoconus
 Anterior subcapsular cataract
 Orbital darkening
 Facial pallor/erythema
 Pityriasis alba
 Anterior neck folds
 Pruritus when sweating
 Intolerance to wool and lipid solvents
 Perifollicular accentuation
 Food intolerance
 Course influenced by environmental/emotional factors
 White dermographism/delayed blanch
Distribution varies :

 Infantile phase: Face,scalp, extensors of

extremities

 Childhood phase: 18-24mths- flexural

involvement- neck, antecubital & popliteal fossae,
wrist, ankles .

 Adult phase:

Lichenification over flexures

Treatment:
 Elimination of inflammation and infection-
topical/systemic steroids, tacrolimus, antibotics,
antihistamine
 Emollients-Preserving&restoring stratum corneum
 Controlling exacerbating factors

Dont’s:
 avoid frequent bathing, hand washing, wool, perfumes,
sweating, overdressing
SEBORRHOEIC DERMATITIS:
 Dandruff-visible desquamation from the scalp surface,
precursor of seborrhoeic dermatitis
 Yeast Malassezia ovale (Malassezia furfur)
 SD occurs in first months of life, rare before puberty
peaks between 18 and 40 years of age.

Occurs in patients with Parkinsonism, myocardial

ischaemia, malabsorption, epilepsy, obesity and
alcoholism, alcoholic pancreatitis, HIV
 Dull or yellowish red in colour and covered with
itchy, greasy scales.
 Perifollicular redness and scaling
 Sharply marginated patches extend beyond the
frontal hairline as the 'corona seborrhoeica
 Scalp,medial part of the eyebrows, the glabella,
and the nasolabial fold, presternal areas.
 Trunk- petaloid form, pityriasiform
 Infantile- adherent scaling of the scalp during
infancy on the vertex, during the first few weeks
[cradle cap]
Treatment:Regular use of medicated shampoos

 selenium sulphide, ketoconazole,tar, salicylic acid,

1% terbinafine, ciclopiroxalamine, 1%metronidazole

 face and trunk- mild steroid ointments-

Hydrocortisone ointment (0.5%) , Ketoconazole
cream 2% or combination.

 generalised SD-systemic steroids(prednisolone),

itraconazole 100 od for 21 days.
DISCOID (NUMMULAR) ECZEMA:

 Discrete, one or more coin shaped czematous

plaques 1-5 cm

 Symmetrically over extensors of limbs,

dorsa of the hands and feet

 Acute, subacute, chronic stage

HAND ECZEMA

 Pompholyx

 Hyperkeratotic palmar eczema

 Ring eczema

 Wear and tear' dermatitis

 Fingertip eczema
Hand eczema
Pompholyx:
 sudden onset of crops of itchy clear deep seated
vesicles over palms and soles.
 Recurrent Usually symmetrical
 Resolves after 3-4wks.
 Etiology:orally ingested metal
compounds(Ni,Chr,Co)+hypohidrosis
 Dermatophytid
 Contact dermatitis
 drugs
Pompholyx
Pityriasis alba
 occurs predominantly in children between the ages
of 3 and 16 years.
 rounded, oval or irregular plaque
 pink or skin-coloured, and has fine lamellar or
branny scaling.
 Erythema subsides leaving persistent fine scaling
and depigmentation
 Face(around the mouth),chin,cheek
 Manifestation of atopy dermatitis
 Emollients and mild steroids- 1%
hydrocortisone,tacrolimus
Stasis eczema:
 Venous insufficiency
 stasis hypoxia poor nutrition for tissue -
dermatitis,
 release of proteolytic enzymes by sequestrated
WBC.
 Acute,subacute,chronic dermatitis
 Brownish black pigmentation, varicosity of the
superficial veins, oedema, purpura,
haemosiderosis, ulceration, or small patches of
atrophy ('atrophie blanche').
Asteatotic eczema
 Decrease in skin surface lipid. Senile eczema and
asteatotic eczema
 eczéma craquelé
 on the legs, arms and hands.
 Dry ,scaly skin.finger pulp-dry cracked and parchment
 Shins-pavement pattern
 Hemorrhagic fissures ,erythema,eczematous change
 Asso-zinc def,myxoedema,malignancy
 Warm room,emollients containing urea, Bath oils or
oatmeal packs
 mild topical corticosteroids
Lichen simplex chronicus:
 Lichenification is a cutaneous response to repeated
rubbing or scratching.
 One or more intensly pruritic lichenified plaques,
 Sites accesible for scratching –
occipital,nuchal,wrist,legs,perineum,scrotum,vulva
 Priritus-may not relieve unless pain/burning
produced by self inflicted injury
 Anxiety ,stress. psychological history
 sedative antihistamine ,potent steroid cream under
occlusion
(…..contd.)
 dermal infiltration with triamcinolone (10mg/ml),
 occlusive band-age which prevents spsychological
historcratching.
 5% doxepin cream
PRURIGO NODULARIS
• Localised LSC
• grouped, and numerous, hard globular nodule, 1-3cm
in diameter, with a raised, warty surface
• Crust and scale may cover recently excoriated lesions.
• extensor surfaces of limbs.
• Trigger may be insect bite,trauma,
• intralesional steroid , Thalidomide
• UVA, benoxaprofen, cyclosporin, azathioprine, topical
capsaicin
Lichen striatus-
 Self-limiting, inflammatory, linear dermatitis of
unknown origin
 5-15yrs
 Linear band of hypopigmented lichenoid papules
 Distributed in the lines of Blaschko
 Resolve in 2wks -4mths
 Topical and I/L steroids
INFECTIVE DERMATITIS-
 Dermatitis around the discharging ulcers ,moist
skin lesion
 Caused by microorg,&their products.
 Clears when org .is eradicated
 Steroid+antibiotic,wet compresses
Polymorphic light eruption(PMLE):
 common photodermatosis
 Erythemaous,itchy papules,plaques,vessicle,on
exposed skin.
 Photoprotection,steroids.
Contact dermatitis
 Dermatitis casused by exposure to substance in
environment

Irritant contact dermatitis:

 Most common contact dermatitis
 Non-immunological reaction
 No prior sensitization required
 Lesions remain localised to the site of contact.
Irritant contact dermatitis
 c/f-Varies depending on the conc. of irritant from
mild xerosis to erythema/chapping,severe
ulcerations.
Acute: vesicles and bullae (savlon,)
Chronic: hyperkeratosis, fissuring and scaling.
Common irritants-alkalis, dye, ammonia containing
products
Treatment: barrier creams, gloves, mild steroid.
Irritant contact dermatitis
Allergic contact dermatitis
 Delayed hypersensitivity-sensitization
phase,rechallenge phase,elicitation phase

 Prior sensitization required

 Eczematous lesion may spread beyond the site of

contact and cause systemic symptoms.

 Common cause-
plants,nickel.chromate,paraphenylene di amine(dye),
rubber,fragrances,preservatives
Allergic contact dermatitis
 Patch test –diagnostic .(application of substance in
nonirritating concentration)

 MC plant allergen-parthenium hysterophorus

 MC metal causing ACD-nickel.

 Treatment:avoidance of allergen,emollients,moderate
to potent steroids.
ACD
PATCH TEST