The lecture has been given on Oct. 24th, 2010 by Dr. Ali El-Ethawi.

1. 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

2. 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.

3. 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.

4. Classification
Exogenous dermatitis
Irritant contact dermatitis
Allergic contact dermatitis
photodermatitis
endogenous dermatitis
Atopic dermatitis
seborrheic dermatitis
discoid dermatitis
asteatotic dermatitis
Gravitational dermatitis (stasis, venous)

5. complications
• Eczema can interfere with work , sporting
Activities , 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 .

6. 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 IgE
Scraping for microscopical exam. &culture

7. 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).

8. 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.

9. • 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.

10. 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 necrosis
Dependent 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)

11. 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.

12. Treatment
• Acute
Identify 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 Chronic
Identify 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.

13. 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.

14. 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.

16. The acute phase --- erythematous, indurated, scaly plaques,
The chronic phase; which is usually marked by lichenified erythematous
plaques

17. • 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

18. • 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

19. 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..

20. 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.

21. 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.

22. • 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

23. 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 .

24. 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 )

25. • 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
Immunodeficiency
Relative zinc deficiency
Lichen Simplex Chronicus
Seborrheic Dermatitis
Mycosis fungoides
Tinea Corporis

26. Laboratory Examinations
Blood 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

27. 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.

28. 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.

30. • 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.

31. Management
Skin Hydration
"Moisturize" involved skin after bath or shower with hydrated
petrolatum or other moisturizing cream.
Topical Preparations
Glucocorticoids ;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/mL
Systemic Therapy
Systemic antibiotics if S. aureus is present.
Phototherapy; PUVA or UVB 311-nm Therapy .Very effective.

32. 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

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

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

35. Adult forms SD ;
Trunk
Petaloid
Follicular

36. 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)

37. • 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.

38. • 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

39. 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

40. • 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

41. 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.

42. • 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.