Dermatitis or eczema

DR. Ali El-ethawi Specialist Dermatologist M.B.CH.B , F.I.C.M.S, C.A.B.D

5th class lecture

Dermatitis or eczema

• The terms eczema and dermatitis• are used interchangeably, • denoting a polymorphic inflammatory reaction

pattern involving the epidermis and dermis.

• There are many etiologies and a wide range of clinical findings.

chronic eczema/dermatitis,is characterized by pruritus, xerosis, lichenification; (leathery thickened

state ,with increase skin markings ) hyperkeratosis, ± fissuring .

Acute eczema/dermatitis ; is characterized by; pruritus, Weeping &crusting erythema; (redness of the skin usually

with ill define border) vesiculation.

Classification

Exogenous dermatitis Irritant contact dermatitis Allergic contact dermatitis photodermatitis

endogenous dermatitis Atopic dermatitis seborrheic dermatitis discoid dermatitis asteatotic dermatitis Gravitational dermatitis (stasis, venous)

complications

• Eczema can interfere with work , sportingActivities , job can be lost • All sever forms of eczema have a huge

effect on quality of life

• Heavy bacterial colonization is common all types of eczema.

• Local superimposed allergic reactions to medications can provoked dissemination .

Investigation • Exogenous eczema ; patch test; standardized non irritating substances concentration of

common allergens are applied to the normal skin of the back. ( see –eczema- 48-96h)

• Endogenous eczema in atopic dermatitis Pricking test ; prepared diluted antigens and a control are palced as

single drops on marked area on forearm then prick the skin gently (see –wheal-10 min )

Serum IgEScraping for microscopical exam. &culture

Contact Dermatitis (CD)

• As the skin primary interface with the environment, it expose to exogenous chemicals and physical agents.

• CD, is either acute or chronic inflammatory reactions to substances that come in contact with the skin.

• CD is either 1. Irritant contact dermatitis (ICD) is caused by a

irritant chemicals; 2.allergic contact dermatitis (ACD) by an antigen

(allergen).

Irritant contact dermatitis (ICD)

ICD is the most common form of occupational skin disease.

resulting from repeated workplace exposure of the hands to

chemicals that are capable of irritating the skin, acutely or chronically • It is accounts for >80% of all cases of CD• Occur in ; housekeeping; hairdressing; medical, dental, and veterinary services; cleaning services; agriculture; food preparation; printing; painting; metal work; mechanical engineering; car maintenance; construction; fishing.

• Etiologic Agents;Abrasives, cleaning agents, oxidizing agents (e.g., sodium hypochlorite); reducing agents (e.g., phenols, hydrazine, aldehydes,

thiophosphates), plants (e.g., spurge, Boracinaceae, Ranunculaceae),

animal enzymes, secretions; dessicant powders, dust, soils; excessive exposure to water.

Irritant CD Symptoms ; Acute ; Stinging, smarting itching ⇛Chronic ; Itching/pain 

Lesions; Skin Findings: May occur minutes after exposure or may be delayed up to 24 h. The spectrum of changes ranges from erythema to vesiculation and caustic

burn with necrosisDependent on concentration of agent and state of skin barrier; occurs only

above threshold level .(strong irritants –acute reaction after brief contact while weak irritants ---need

long time& prolong exposure)

Edge;Acute; Sharp, strictly confined to site of exposure 

Chronic; ill-defined Distribution ;

localized to one region (The hands are the most commonly affected area) or generalized (plant dermatitis).

Incidence;  May occur in practically everyone  

Duration; Days, weeks , depending on tissue damage.Patch Tests; These are negative in ICD.

Treatment

• AcuteIdentify and remove the etiologic agent. Wet dressings with gauze soaked in Burow's solution. Topical glucocorticoid preparations. systemic glucocorticoids in severe cases, may be indicated. • Subacute and ChronicIdentify and remove etiologic/pathogenic agent.Use a potent topical glucocorticoid preparation, and provide adequate

lubrication. As healing occurs, continue with lubricating/protective creams or

ointments.Topical calcineurin inhibitors ; newer topical anti-inflammatory

agents (pimecrolimus and tacrolimus) are being evaluated.

Allergic Contact Dermatitis

One of the most frequent, and costly skin problems. An eczematous (papules, vesicles, pruritic) dermatitis due to re-exposure to a substance

to which the individual is sensitized.

Epidemiology ;Frequent disease . Over 3700 allergens have been reported to cause ACD in humans

Age of Onset ; is uncommon in young children and in individuals older than 70 years.Occupation ;One of the most important causes of disability in industry. Pathogenesis ; is a classic, delayed, cell-mediated hypersensitivity

It has the following features;Pervious contact is needed to induce the allergy.Its specific to one chemical or its relatives. After the allergy has been established, all areas of skin will react to the allergen.Sensitization persists indefinitely. desensitization is seldom possible.

clinically present may as acute eczematous dermatitis after allergen exposure and initial sensitization or after elicitation in a previously sensitized individual reaction.

The severity of condition is relatively independent of amount applied, usually very low concentrations sufficient but depends on degree of sensitization.

• The original site of the eruption gives a clue to the likely allergen

but secondary spread may later obscure this. Easily recognizable patterns are exist ;nickel allergy ,for

example --- give rise to eczema under jewelry & jean stud • The likely sites for ACD are ;hands, feet, eyelids, and lips, which

commonly come in contact with the environment.

The acute phase --- erythematous, indurated, scaly plaques,

The chronic phase; which is usually marked by lichenified erythematous plaques

• History; The eruption starts in a sensitized individual 48 h or days after contact with the allergen.

• Symptoms; Itching pain⇛  • Lesion; 

Acute ;Erythema  papules  vesicles erosions crust scaling⇛ ⇛ ⇛ ⇛ ⇛

Chronic; Papules, plaques, scaling, crusts

• edge& site; Acute; Sharp, confined to site of exposure but spreading in the

periphery; usually tiny papules; may become generalized  Chronic; Ill-defined, more spreads 

• Patch Tests• positive ------ shows erythema and papules, as well as

possibly vesicles confined to the test site. • In ACD sensitization is present on every part of the skin; • application of the allergen to any area of normal skin

provokes an eczematous reaction.• Differential Diagnosis• By history and clinical findings including evaluation of site

and distribution. • Histopathology may be helpful; verification of offending

agent (allergen) by patch test.• Exclude ICD ;atopic dermatitis, seborrheic dermatitis (face),

psoriasis (palms and soles), dermatophytosis

Management of ACD

• Termination of Exposure• Identify and remove the etiologic agent.• Topical Therapy;• Topical glucocorticoid ointments/gels are

effective for early nonbullous lesions. • Systemic Therapy• Glucocorticoids are indicated if severe for

exudative lesions..

Atopic dermatitis (AD) • is a pruritic, chronic relapsing skin disease of unknown origin that occurs

most commonly during early infancy and childhood (an adult-onset variant is

recognized).

It is frequently associated with abnormalities in skin barrier function and allergen sensitization.

Atopic dermatitis (AD)

• A chronic or chronically relapsing disorder with major features of: 1. Pruritus 2. Eczematous dermatitis (acute, subacute, or chronic) with

typical morphology and age-specific patterns 3. Facial and extensor involvement in infancy 4. Flexural eczema/lichenification in children and adults.

• Commonly associated with: Personal or family history of atopy (allergic rhinitis, asthma,

urticaria, acute allergic reactions to foods). Xerosis/skin barrier dysfunction IgE reactivity.

• Age of Onset ; 60% of patients between 2 months -1yr. 30% are seen for the first time by age 5, 10% develop AD between 6 and 20 years of age. Rarely AD has an adult onset.

• Gender ;Slightly more common in males than females.

• Prevalence ;Between 7 and 15% reported in population studies

in Scandinavia and Germany. • Etiology& Pathogenesis; • AD results from complex interactions between genetic susceptibility

resulting in a defective skin barrier, defects in the innate immune system, and heightened immunologic responses to allergens and microbial antigens

age -specific and morphology patterns

1. Infant --- usually facial lesions + patchy lesions else where

( AD tends to be acute eczema )

2.Older child ----lesions settling into elbow &knee flexures also on wrists &ankles .

3. Mid teens ----

AD may clear or persist or change the pattern;i.e; Options; • Clear • localized hand eczema • generalized low grade eczema• eczema remain stays

confined to limb flexures ( AD tends to be chronic eczema )

• Diagnosis; History in infancy, clinical findings (typical distribution sites,

morphology of lesions, white dermatographism• Differential Diagnosis Allergic Contact Dermatitis, Irritant Contact Dermatitis,

Nummular Dermatitis Scabies Psoriasis, Plaque

ImmunodeficiencyRelative zinc deficiencyLichen Simplex Chronicus

Seborrheic DermatitisMycosis fungoidesTinea Corporis

Laboratory ExaminationsBlood Studies; Increased IgE in serum, eosinophilia

Course and Prognosis• Untreated involved sites persist for months or years.• Spontaneous, more or less complete remission during childhood occurs in >40% with

occasional, more severe recurrences during adolescence

Management; Acute dermatitis

– 1. Wet dressings and topical glucocorticoids; topical antibiotics (mupirocin ointment) when indicated.

– 2. Oral H1 antihistamines are useful in reducing itching. eg;Hydroxyzine – 3. Oral antibiotics (dicloxacillin, erythromycin) to eliminate S. aureus

Subacute and Chronic

– 1. Hydration (oilated baths or baths with oatmeal powder) followed by application of emollients (e.g., hydrated petrolatum) form the basic daily treatment needed to prevent xerosis.

– 2. Topical anti-inflammatory agents such as glucocorticoids, hydroxyquinoline preparations, and tar are the mainstays of treatment. Of these, glucocorticoids are the most effective.

– 3. Topical calcineurin inhibitors. Topical tacrolimus and pimecrolimus have been developed as nonsteroidal immunomodulators . They potently suppress itching and inflammation and do not lead to skin atrophy.

– 4. Oral H1 antihistamines are useful in reducing itching.

– 5. Systemic glucocorticoids should be avoided, except in rare instances in adults for only short courses .

– 6. UVA-UVB phototherapy ,Narrow band UVB (311 nm), and PUVA photochemotherapy also effective.

– 7. In severe cases of adult AD and in normotensive healthy persons without renal disease cyclosporin.

– 8. Patients should learn and use stress management techniques.

discoid eczema (NUMMULAR ECZEMA)

• A chronic disorder of unknown etiology.

• It characterized by papules and papulovesicles

coalesce to form nummular plaques with oozing,

crust, and scale.

• Most common sites of involvement are

upper extremities, including the dorsal hands in women,

and the lower extremities in men.

• Pathology may show acute, subacute, or chronic eczema.

• Distribution • Regional clusters of lesions (e.g., on legs or trunk) or generalized, scattered. Lower legs (older men), trunk, hands and fingers (younger females).• Differential Diagnosis dermatophytosis, ICD or ACD, psoriasis, early stages of mycosis fungoides, impetigo,

familial pemphigus.Course and Prognosis• Chronic. Lesions last from weeks to months. • Often difficult to control even with potent topical glucocorticoid preparations.

Management

Skin Hydration "Moisturize" involved skin after bath or shower with hydrated

petrolatum or other moisturizing cream.Topical PreparationsGlucocorticoids ;applied bid until lesions have resolved. Steroid

impregnated tape. Crude Coal Tar ;2 to 5% crude coal tar ointment daily. May be combined with glucocorticoid preparation. Tar baths are useful in patients with refractory lesions. Intralesional triamcinolone, 3 mg/mLSystemic TherapySystemic antibiotics if S. aureus is present.Phototherapy; PUVA or UVB 311-nm Therapy .Very effective.

Seborrheic dermatitis (SD)

is a common chronic papulosquamous dermatosis that is usually easily recognized Infantile and adult forms exist.

• Characterized by erythema and greasy scaling( The affected skin is pink, edematous, and covered with yellow-brown scales and crusts).

• Lesions favor scalp, ears, face, chest, and flexural areas.

• May be a cutaneous marker of human immunodeficiency virus infection and acquired immunodeficiency syndrome, especially when severe, atypical, and therapy resistant

Infantile forms;Scalp (cradle cap)

Trunk (including flexures and napkin area)

Adult forms ;• Scalp• Face (may include blepharitis)• ear

Adult forms SD ;

TrunkPetaloidFollicular

Clinical Patterns of Seborrheic Dermatitis

Infantile forms;• Scalp (cradle cap)• Trunk (including flexures and napkin area)

Adult forms ;• Scalp• Face (may include blepharitis)• Trunk

• Petaloid• Pityriasiform• Flexural• Eczematous plaques• Follicular

• Genitalia • Generalized (may be erythroderma)

• Age of Onset ;• Infancy (within the first months), puberty, most between 20 and 50 years or

older.• Sex ;More common in males.• Incidence ;2 to 5% of the population • The disease varies from mild to severe.• Mild scalp SD causes flaking, (i.e., dandruff).• Generalized and even erythrodermic forms may occur

• Etiology ;unknown but may be related to increased sebum secretion, abnormal sebum composition, certain drugs, or Malassezia yeasts. And Genetic Factors.

• Prognosis and Clinical Course• The disease is usually protracted over

weeks to months. • Exacerbation and, rarely, generalized

exfoliating dermatitis may occur. • The prognosis is good. • There is no indication that infants with

seborrheic dermatitis are more likely to suffer from the adult form of the disease

Management• This chronic disorder requires initial therapy followed by chronic

maintenance therapy. • adult • Frequent shampooing with shampoos containing selenium sulfide,

zinc pyrithione, are helpful. 2% ketoconazole shampoo, Tar shampoos are equally effective in many patients.

• Low-potency glucocorticoid solution, lotion, or gels. • Pimecrolimus, 1% cream, is beneficial.• Antifungals • Topical metronidazole • topical Lithium which possess antifungal properties

• Topical Calcineurin Inhibitorstacrolimus have anti-inflammatory properties also exhibits antifungal properties

• Vitamin D3 analogues (calcipotriol cream or lotion, calcitriol ointment, or tacalcitol ointment).

• Oral isotretinoin (13-cis-retinoic acid) is a useful, although not officially approved

• Infants• SCALP; removal of crusts ; proper skin

care.• body folds drying lotions ,• In cases of candidiasis ,nystatin or

amphotericin B lotion or cream .• in cases of oozing • Imidazole preparations (e.g., 2 percent ketoconazole in

soft pastes, creams, or lotions) may also be effective

Asteatotic Dermatitis       A common pruritic dermatitis that occurs especially in older persons, in the winter in temperate climates—related to the low humidity of heated houses. The sites of predilection are the legs ,arms, and hands but also the trunk. The eruption is characterized by dry, "cracked," superficially fissured skin with slight scaling.

The incessant pruritus can lead to lichenification, which can even persist when the environmental conditions have been corrected.

• Cause; • The disorder results from too frequent bathing in hot soapy baths or

showers and/or in older persons living in rooms with a high environmental temperature and low relative humidity.

• Management ;• by avoiding over bathing with soap, especially tub baths, and

increasing the ambient humidity to >50%, by using room humidifiers; • also using tepid water baths containing bath oils for hydration,• followed by immediate liberal application of emollient ointments,

such as hydrated petolatum. • If skin is inflamed, use medium-potency glucocorticoid ointments,

applied twice daily until the eczematous component has resolved.