Eczema

Urticaria
and
Eczema
Dr. Raed Abu Serriya

URTICARIA
(Hives)
 Urticaria is a common vascular skin reaction

characterized by the appearance of wheals that are
transient and recurrent. These are erythematous, elevated
skin swelling surrounded by a halo and accompanied by
severe itching or stinging sensation.
2 Dr. Raed Abu Serriya

classificationof urticaria
according to chronisity
• Acute urticaria is more common in children
• Chronic urticaria is more common in adults
• In a lifetime, 15-20% of patients will experience urticaria
Urticaria: duration
• Acute: Lesions occur for less than 6 weeks
• Chronic: Recurrent symptoms for greater
than 6 weeks

 Urticarial lesions
• Pruritic, raised, circumscribed
• Shape varies: serpiginous, round, oval
• Lesions may have central pallo

 Pathophysiology
Dermis
 edematous
 dilated blood vessels
 mast cell degranulation

 Clinical phenotype
• Size varies: less than one centimeter to several
centimeters
• Lesions are pruritic & raised
• Can present with OR without angioedema

 Clinical phenotype
• Symptoms occur throughout the day
Often times, pruritus is most severe at night
• Transient lesions
Develop within seconds to minutes resolving within 24
hours
• Lesions are generally not painful
If lesions are painful, consider vasculitis on the
differentia

 Clinical types
 Classical urticaria
 Angioedema
 Physical urticarias
cold urticaria
solar urticaria
dermographic urticaria
aquagenic urticaria
papualr urticaria
Urticarial vasculitis
Contact urticaria
Urticarial wheals in certain skin disease
 Angio-edema
 Hereditary or aquired
 With or without classical urticaria
 Edema involves dermis and subcutaneous tissue

Management
 Identification of the cause
 Symptomatic treatment
 Spicific treatment in certain types
Acute airway abstraction and Anaphylactic shock
(adrenaline 0,5-1 mg repeat after 10 min if necessary
dermagraphism hydroxyzine
colinergic anti hist. and anticolinergic 1-2 h. befor exerc.
Hereditary angio. Danazole weak androgen, frish plasma
 Local treatment
0,5% mentol
1% campher


Classification of eczema
Endogenous eczema Exogenous eczema
•Atopic Dermatitis Contact Dermatitis

Dyshidrotic Dermatitis
Nummular Dermatitis
Stasis Dermatitis
Pityreasis alba

Contact Dermatitis
A pruritic, epidermal and dermal inflamatory

reaction caused or aggravated by items in contact
with the skin.

Contact Dermatitis
 Irritant contact dermatitis
 Allergic contact dermatitis
 Phototoxic photoallegic contact dermatitis

Irritant Contact dermatitis
 Acute
 chronic

Irritant Contact Dermatitis
 It is the most common injury of the skin

 Irritant Responses include:
 Wheals
 erythema
 Blistering
 Erosions
 Hyperkeratosis or thickening of the skin
 Pustules and skin dryness

Factors that determine the response
(Irritant Dermatitis)
 Individual factors
 Time of exposure
 Region of the skin exposed

Acute dermatitis from turpentine

Cement ulcerations

Acute bullous contact dermatitis from
a scabicide

Weak- ICD
 Prolonged contact
 Multiple exposure
 In skin that too wet or too dry
 Bleaches, cleansers, detergents, plants, soaps,
solvents, weak acids, weak alkalis

W-napkin dermatitis

Napkin dermatitis under the plastic
part of the diaper

ICD in a mechanic – caused by oil

Irritant dermatitis due to licking

Common agents that produce irritant
contact dermatitis
 Water
 Cleansers
 Alkalis
 Acids
 Oils
 Organic solvents
 Oxidants
 Plants
 Animal substances

 Most commonly located in the hands, forearms,
face and legs

 Diagnosis:
History
Examination
Laboratory investigations: patch testing

 Differential diagnosis:
Atopic eczema
Discoid eczema
Allergic contact dermatitis
Fungal infection

 Treatment:
- Removal of the offending contact
- Restore a protective lipid layer
- Topical steroid may be necessary

Allergic contact dermatitis
 It is a form of cell-mediated, antigen-antibody
immune reaction ( Type IV hypersensitivity).
 Sensitization phase (1 week or longer)
 Elicitation phase (follows)
 affect few workers
 many skin sensitizers are also irritants (chromates,
nickel salts, and epoxy resin hardeners)
 cross-sensitivity

Allergic Contact Dermatitis
 Presentation: erythematous and edematous or
vesicular skin in the pattern of contact
 Mechanism: cell-mediated immune response to
antigens (contact allergens)

Contact Allergens
 poison ivy, poison oak
 Nickel sulfate
 Rubber
 Formaldehyde and related preservatives
 Para-phenylenediamine
 Fragrance
 Neomycin

Poison Ivy/Oak Dermatitis
 Presentation: acute pruritic dermatitis

with linear grouping of vesicles
 Confirmation: history of exposure

Nickel Dermatitis
 Presentation: areas in contact with jewelry or
metal clothing fasteners
 Confirmation: skin patch testing

Nickel dermatitis from brassiere clasps

Nickel dermatitis from spectacle frames

Rubber Dermatitis
 Presentation: sites of exposure to…
shoes (adhesive), elastic in clothing,
surgical gloves, etc.
 Confirmation: patch test to
accelerators and antioxidants

Chromate dermatitis from leather in work
shoes

Allergic contact dermatitis from
thiuram in latex gloves

fragrance in a cosmetic

Allergic contact dermatitis from glue
in sticking plaster

plants in the compositae

toluenesulfonyl urea in nail varnish

toluenesulfonyl urea in nail varnish

Allergic contact dermatitis caused by
garlic

Allergic contact stomatitis caused by the mercury
in amalgam dental fillings in a mercury-sensitive
person

Phototoxic contact dermatitis
 Striped and bullous
dermatitis of the legs after
exposure
to plant juices on a sunny
day

 Bullous dermatitis caused by
squeezing lime on a sunny
day

 Diagnosis:
History
Examination
Laboratory investigations: patch testing

A positive patch test to the perfume-mixture

Identification of Contact Allergens
Atopic Dermatitis

What is the Cause?
 nobody has identified a single “cause”

 atopic dermatitis is a genetic disorder
 atopic children or their relatives may also have
 asthma
 allergic rhinoconjunctivitis
 food allergies
 urticaria

Atopic Dermatitis

Environmental Suspects???
 urbanization
 outdoor pollution
 indoor pollution/insulated homes
 fewer infections/infestations
 changes in food processing
 NOBODY KNOWS FOR SURE

Pathophysiology
 specific gene abnormality not yet identified
 may be more than one disease
 down regulation of TH1 lymphocytes (TH1 cells
activate IFN- which inhibits IgE synthesis)
 upregulation of TH2 lymphocytes (TH2 cells
activate IL-4 which inhibits IFN-)

Is it a Food Allergy?
 no conclusive evidence that eczema is “a food

allergy”
 atopic children have a higher incidence of
urticaria or anaphylaxis to peanuts, eggs, fish,
milk
 certain foods cause contact irritation and
erythema eg. tomato sauce

What about milk?
 breast-feeding does not protect against atopic

dermatitis
 “allergen-free” diets in lactating women can
compromise nutrition of the baby and mother
 Effect of cow’s milk formula or soy formula in
infants with eczema difficult to evaluate

What about Allergy Testing?
 negative tests may be helpful

 80% of atopic children have positive prick and RAST
tests
 often leads to unnecessary food and lifestyle
restrictions with consequences for child’s emotional
and nutritional well-being
 parents must be told that positive tests are <
20% predictive of clinical allergy

Eczema – Psychological Issues
 How does it affect sleep?
 How does it impact on the patient’s behavior and
family life?
 Is the patint’s diet or lifestyle restricted?
 Are there psychosocial factors that cause anxiety
eg. At home, at school

Clinical picture
 Infantile phase
 Lesions mostly start on the face
 Itchy erythematous discrete or confluent edematous papules, it
may become exudative and crusted
 Childhood phase
 Mostly involved the elbows and knee flexures, side of the neck,
wrists and ankles and hands.
 Itchy erythematous papules which tend to be lichenificated,
often in discoid patches
 Adulthood phase
 Lichenification of flexures and hands

Atopic Dermatitis
 There is no “cure”
 Eczema can be
controlled
 60% of children
“outgrow” eczema by
11 years of age
 Treatment better than
searching for the
“cause”

Treatment
 Skin care and emollients
 Treatment of infection
 Topical anti-inflammatory agents
 STEROIDS
 NEW NON-STEROID TOPICAL
IMMUNOMODULATORS
 Antihistamines

Is the eczema infected?
 most cases of eczema are colonized by Staphylococcus
Aureus - staphylococcal superantigens may play a
pathogenetic role
 consider antistaphylococcal antibiotic therapy in all cases of
weeping, crusted or very excoriated eczema
 also consider
 STREPTOCOCCUS, HERPES SIMPLEX

Treatment
Antibiotics, topical steroids, baths and

emollients are safe and effective therapy
Eczema Checklist 1
 do parents have a basic
understanding of the
disease
 what have they been told by
other health care
professionals, pharmacists,
naturopaths, family and
friends
 do they have realistic
expectations

Eczema – Checklist 2
 is skin care adequate
 Baths and emollients
 is topical therapy optimal
 Topical steroids/steroid-
free agents
 is the eczema infected
 Antibiotics oral/topical

Eczema Checklist 3
 Are other measures necessary?
 Wet wraps
 Higher potency topical steroids for short periods
 Phototherapy
 Psychological evaluation/counselling for child, parents,
parent/child interaction
 Cyclosporin, Azathioprine

Quality of Life

Atopic Dermatitis
 Aim of treatment is to
improve the child’s
quality of life and that of
the family

“Patients aren’t as concerned about how
much you know until they know how much
you care”
“Compassion without competence is

dangerous”

Nummular eczema
(Discoid eczema)
Dr. Majdy Naim
History
 Nummular eczema is a name

given to a stubborn, itchy rash
that forms coin-shaped patches
on the skin

 The lesions as they get older may
clear in the center or become scaly
and then resemble fungus or
psoriasis.
 The condition tends to be chronic,

with periods when it gets much
better or worse.
Physiology
 The cause is unknown.
 Ithas recently been considered a

form of adult onset atopic
dermatitis.

 Onset
has been associated with
medications.
 More common in the winter.

 Frequently associated with dry
skin.
 Wool, soaps and frequent bathing
(more than once a day) often
worsen the condition.

Physiology
 People with eczema often have skin
that is dry and easily irritated by
soap, detergents, and rough
clothing.
 Hot and cold weather often
aggravates eczema.

 Theprevalence of nummular
dermatitis is 2 cases per 1000
people
 Nummulardermatitis is more
common in males than in females

2 peaks of age distribution.
 The most common is in the
sixth to seventh decade of life.
This is most often seen in males.
 A smaller peak occurs in the
second to third decade of life,
which is most often seen in
Distribution
 Most commonly located on the
extremities, particularly the legs, but
they may occur on the trunk, hands,
or feet.
 It does not involve the face and
scalp.
 Lesions are often symmetrically
91distributed Dr. Raed Abu Serriya
o The lesions flatten to macules,
usually with brown
postinflammatory
hyperpigmentation that gradually
lightens.
o The pigment may never
92
completely fade, particularly when
Treatment
 Unfortunately, there is no cure.

However, there are effective
ways of controlling it.

Treatment
 Lukewarm or cool baths or showers

reduce itching
 Application of moisturizers or
medicated topical preparations to
seal the water in the skin.

 Steroids are the most commonly
used therapy to reduce
inflammation.
 Ointments are usually more
effective than creams because they
are more occlusive, form a barrier
between the skin and the
95 environment, and more effectively
 Oral,intramuscular, or parenteral
steroids may be required in cases
of severe, generalized eruptions

Treatment
 Tar preparations are helpful to
decrease inflammation, particularly in
older, thickened, scaly plaques.
 When eruptions are generalized and
prolonged, phototherapy (generally
UVB) may be helpful. ]

 Oral antihistamines or sedatives
may help reduce itching and
improve sleep.
 Oral antibiotics, such as
dicloxacillin, cephalexin, or
erythromycin, should be used in
98
cases of secondary infection.
DYSHIDROTIC ECZEMA

 Dyshidrotic eczema is a recurrent
or chronic relapsing form of
vesicular palmoplantar dermatitis
of unknown etiology (also
termed pompholyx

Etiology
 The etiology of dyshidrotic

eczema is unresolved and is
believed to be multifactorial

Pathophysiology
 Thehypothesis of sweat gland
dysfunction has been disputed
because vesicular lesions have
not been shown to be
associated with sweat ducts.
However, hyperhidrosis is an
aggravating factor in 40% of
patients with dyshidrotic
eczema.
 Sex
 The male-to-female ratio is 1:1.
 Age
 4-76years; the mean age is 38 years.
 After middle age, the frequency of
episodes tends to decrease.

History
 pruritus of hands and feet with a

sudden onset of vesicles.
 Dyshidrotic eczema episodes vary
in frequency from once per month
to once per year.

factors that possibly are related to
eruptions
 Emotional stress
 Personal or familial atopic

diathesis (eg, asthma, hay fever,
sinusitis)
 Certainwork exposures (eg, cobalt)

and/or recreational exposures
 Recent exposure to contact allergens
(eg, nickel, balsams, chromate,
before condition flares
 Exposure to contact irritants before

condition flares

 Recent exposure to costume
jewelry (patients with palmar
pompholyx and allergic to
nickel)
 Recent treatment with

intravenous immunoglobulin
Clinic
 Symmetric crops of clear vesicles
and/or bullae on the palms and
lateral aspects of fingers
characterize dyshidrotic eczema
 Feet, soles, and the lateral aspects
of toes also may be affected.

Laboratory Studies
 Diagnosis is usually made

clinically.
 Bacterial culture and sensitivity
exclude secondary infection.

 Blood tests are not usually
ordered; however,
immunoglobulin E levels are
commonly elevated.
 Patch testing to exclude allergic
contact dermatitis.
 Some mildly affected patients
experience spontaneous
resolution within 2-3 weeks.
 Compresses with a 1:10.000

solution of potassium
permanganate are also effective.
 Drain large bullae with a sterile
syringe, and leave the roof intact.
 Prescribe systemic antibiotics
that cover Staphylococcus aureus
and group A streptococci.

 Topical corticosteroids are the
mainstay of treatment.
 Topical antipruritics with
pramoxine are useful.
 Systemic corticosteroids can also
be used
 Some patients may benefit from
 Bath-PUVA improves the eruption
and pruritus is an option.
 Local narrow-band UV-B has been
shown to be as effective as bath-
PUVA in patients with chronic hand
eczema of dry and dyshidrotic
types.
 Botulinum toxin A injections may
 For severe refractory pompholyx, azathioprine,
methotrexate,mycophenolate mofetil,
cyclosporine,or etanercept may be helpful.
Consider measuring thiopurine
methyltransferase levels, which may help guide
azathioprine therapy.
 Iontophoresis may be helpful as adjuvant
treatment.

‫حمية‬
‫المرضى الذين يعانون حساسية النيكل ‪ ،‬ينظر في اتباع نظام غذائي‬ ‫‪‬‬
‫منخفض النيكل لمدة ‪ 4-3‬أسابيع‪ .‬ونظام الحمية قليال ما تنجح ويصعب على‬
‫المرضى متابعتة‪ .‬النظام الغذائي يتطلب تجنب األطعمة الغنية بالنيكل ‪ ،‬مثل‬
‫األطعمة المعلبة ‪ ،‬األطعمة المطبوخة باستخدام أواني النيكل مطلي ‪،‬‬
‫والرنجة ‪ ،‬والمحار ‪ ،‬والهليون ‪ ،‬والفاصوليا ‪ ،‬والفطر والبصل والذرة ‪،‬‬
‫والسبانخ ‪ ،‬الطماطم ‪ ،‬البازالء ‪ ،‬وطحين الحبوب ‪ ،‬والكمثرى ‪ ،‬راوند ‪،‬‬
‫الشاي والكاكاو والشوكوال ‪ ،‬ومسحوق الخبز‪.‬‬
‫المرضى الذين يعانون من حساسية الكوبالت ‪ ،‬ينظر في اتباع نظام غذائي‬

‫منخفض الكوبالت مثل تجنب المشمش والفول والبيرة ‪ ،‬والبنجر ‪ ،‬والملفوف‬
‫‪ ،‬والقرنفل والكاكاو والشوكوال والقهوة والكبد والمكسرات ‪ ،‬والشاي‬
‫والطحين والحبوب بأسرها‪.‬‬
‫‪118‬‬ ‫‪Dr. Raed Abu Serriya‬‬
Seborrheic dermatitis

Seborrheic dermatitis
A papulosquamous disorder
patterned on the sebum-rich
areas of the scalp, face, and trunk
 In addition to sebum, this
dermatitis is linked to
Malassezia, immunologic
abnormalities, and activation of
 Commonly aggravated by changes
in humidity, changes in seasons,
trauma (eg, scratching), or
emotional stress.
 The severity varies from mild
dandruff to exfoliative erythroderma.

Pathophysiology
 normallevels of Malassezia but

an abnormal immune response

Age
 The usual onset occurs with

puberty.
 It peaks at age 40 years and is
less severe, but present, among
older people.
 In infants, it occurs as cradle cap
or, uncommonly, as a flexural
 Frequency :3-5 %, dandruff 15-20%
 Race: Seborrheic dermatitis occurs
in persons of all races.
 Sex: The condition is slightly worse
in males than in females.

 Scalp appearance varies from mild,
patchy scaling to widespread, thick,
adherent crusts
 Skin lesions manifest as greasy
scaling over red, inflamed skin
 Distribution follows the oily and
hair-bearing areas of the head and
the neck, such as the scalp, the
forehead, the eyebrows, the lash
line, the nasolabial folds, the beard,
Treatment
 Topicalcorticosteroids
 Dandruff responds to more frequent
shampooing
 Selenium sulfide (2.5%),
ketoconazole, and ciclopirox
shampoos may help by reducing
Malassezia yeast scalp reservoirs
Pityreasis alba

Pityriasis Alba
 A chronic eczema of unknown origin
 Usually occurs in children
 Sometimes a manifestation of atopic
darmatitis

 It appears as a rounded, erythematous or whitish fine
scaly patches mostly on the face
 The course is variable
 Treatment with emollients or weak corticosteroids

Thank you for your attention!

Eczema

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Urticaria

Dr. Raed Abu Serriya

 Urticaria is a common vascular skin reaction

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Endogenous eczema Exogenous eczema

•Atopic Dermatitis Contact Dermatitis

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A pruritic, epidermal and dermal inflamatory

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 It is the most common injury of the skin

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 Presentation: acute pruritic dermatitis

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 nobody has identified a single “cause”

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 no conclusive evidence that eczema is “a food