2. Group Members
• HUMAIRA MUSHTAQ
• ROOFIA MUJTABA KHAN
• SABAAMANULLAH
• SAMEERAAHMED
• SARA SHAH
• SANIA SOHAIL
• SYEDA RAMEESHA RIZVI
• WAJIHA DILSHAD
• YUSRA SHUJA
• ZOHA HABIB
• ZOHA KHALID
3. INTRODUCTION
■ A condition where patches of skin become inflamed,
itchy, red, cracked and rough.
■ Interchangeable terms ‘eczema’ and ‘dermatitis’.
■ “Eczema” meaning ‘to boil’ describes the characteristic
tiny bubble like blisters of the condition.
‘Dermatitis’ means ‘inflammation of the skin’.
■ A common convention is to describe as:
‘eczema’ those that are endogenous or
constitutional.
‘dermatitis’ those that are exogenous or due to
contact.
4. PATHOPHYSIOLOGYAND CLINICAL
FEATURES
■ The histological features of eczema/dermatitis are similar, regardless of cause and
differ in the acute and chronic phases.
■ In acute stage, fluid escapes from dilated dermal blood vessels to produce edema, or
swelling in the epidermis.
■ This collects into vesicles or tiny blisters, particularly where the skin is thick, as on the
palms and soles causing exudation and crusting.
■ The chronic stage shows less edema and vesiculation and more thickening of the
epidermis and horny layers.
■ These layers produced by prolonged rubbing and scratching by the sufferer.
5. TYPES OF ECZEMA
1. ACUTE ECZEMA/DERMATITIS:
– Red, hot, swollen and itchy skin.
– Papules and tiny blisters, sometimes coalesce
to form large ones.
– Exudation and crusting.
– Scaling.
6. TYPES OF ECZEMA
2. CHRONIC ECZEMA/DERMATITIS:
– Drier skin, becoming more scaly.
– Lichenification ( dry, thickened, leathery skin
with exaggerated skin markings, due to
rubbing and scratching).
– Painful fissures.
7. CLINICALTYPES
1. ATOPIC ECZEMA:
– Common skin disorder of childhood.
– Term ‘atopy’ describes an exaggerated susceptibility to form
IgE to allergen.
– Etiology genetic, environmental and immunological
factors.
– Epidermal Langerhans cell have high-affinity IgE receptors
through which theT-helper cells release cytokinin and
produce skin inflammation.
– Mostly affects the face and flexures like front of elbows and
wrist.Also affects the back of knees.
– Detected by radio-allergosorbent test.
8. CLINICALTYPES
– Epidermal Langerhans cell have high-affinity IgE
receptors through which theT-helper cells release
cytokinin and produce skin inflammation.
– Mostly affects the face and flexures like front of
elbows and wrist. Also affects the back of knees.
– Detected by radio-allergosorbent test.
10. CLINICALTYPES
2. CONTACT DERMATITIS
There are 2 types of contact dermatitis:
Contact Dermatitis
Allergic (cell mediated
immune or type IV
reaction
Primary irritant (wear and
tear or irritation)
11. CLINICALTYPES
Allergic contact dermatitis
■ Usually hands.
■ Burning, pruritus, pain.
■ Dry and fissured skin.
Irritant contact dermatitis
■ Usually exposed areas of skin.
■ Pruritus is dominant symptom.
■ Vesicles and bullae.
12. CLINICALTYPES
a) ALLERGIC CONTACT DERMATITIS:
CAUSES:
Metal e.g. nickel
Topical medicaments (antibiotics, antihistamines and local
anesthetics); creams, ointment bases and preservatives
Dyes
Plants
Rubber compounds
In industry: resins, plastics and cement frequently cause
problems.
13. CLINICALTYPES
DIAGNOSIS:
First and most important step is:
• Detailed history
• Note the pattern and distribution of rash
Common patterns include:
• Metal fastenings in clothes such as zips and jeans studs (nickel allergy)
• Gloves
• Rash around eyes indicate airborne allergens from plants, nail varnish or strike
anywhere matches (which release phosphorous sesquisulfide vapor)
• Allergens in local application of medicaments
14. CLINICALTYPES
If confirmation or further investigation is required, patch testing is useful.
• The skin is examined for an eczematous reaction under the test patches at 48 hours
and 96 hours, which indicates delayed hypersensitivity.
• Once the allergy is confirmed,
– Must avoid the allergen
– Since this type of allergy is lifelong
– And dermatitis persists as long as contact continues.
15. CLINICALTYPES
b) PRIMARY IRRITANT DERMATITIS
CAUSES:
Common cause of hand eczema,
particularly seen in housewives,
nurses, hairdressers, caterers and
those who work with oils and greases
in industry.
It occurs due to contact with anything
that dehydrates the skin and removes
the natural protective oils from the
skin, allowing evaporation of water
and penetration of irritants.
16. CLINICALTYPES
DIAGNOSIS:
No allergy is involved in this type and therefore patch testing is not usually indicated
unless a co-existing allergy is suspected.
17. OTHER ECZEMAS
1. SEBORRHOEIC ECZEMA:
• This involves areas of the body with a high density
of sebaceous glands.
• Areas it involves are face, scalp and upper trunk.
• It occurs after puberty when these glands become
active.
• It is due to an overgrowth pityrosporum , a yeast
that is normal commensal on the skin.
• The skin is red with greasy yellow scales and the
scalp shows severe dandruff.
18. OTHER ECZEMAS
2. DISCOID ECZEMA:
• As the name suggests, this occurs in
circular patches.
• These characteristically occur on the
forearms and lower legs and are intensely
itchy.
• They are frequently excoriated and
become secondarily infected.
19. OTHER ECZEMAS
3. STASIS ECZEMA:
• This is usually the result of varicose veins, venous
stasis and edema in the lower leg.
• It is particularly around the ankle and may
progress to varicose ulceration.
• The patient with varicose eczema is particularly
at risk of developing allergic contact dermatitis to
topical medicaments such as antibiotics and
vehicles.
20. OTHER ECZEMAS
4. ASTEATOSIS ECZEMA:
• This means “lacking in oil”.
• It is typically found in elderly in whom the skin becomes over dry, perhaps
aggravated by the use of soap.
21. TREATMENT
The same basic principles of treatment apply regardless of
the type of eczema.
1. EMOLLIENTS:
• The mainstay of eczema treatment is the use of
liberal quantities of moisturizers as, in all types.
• Adequate use of emollients will reduce the
requirement of typical steroid, both in quantity
and potency.
• A soap substitute such as emollient cream should
be applied before, during and after bathing.
22. TREATMENT
2. TOPICAL CORTICOSTEROIDS:
• Eczema is an inflammatory and
immunological condition. So treatmemts
must be anti inflammatory and directed at
modifying the immune response, which in
many case means corticosteroids mostly
topical
• Topical steroids developed over the past 50
years have revolutionised the treatment of
inflammatory dermatitis but, it is apparent
that with great potency greater will be the
chances of adverse effects.
23. TREATMENT
• For e.g.: Epidermal Atrophy ( thinning), telangiectasia ( prominent surface blood
vessels ), striae ( stretch marks), and premature aging due to collagen loss.
Reduce growth rates in children after prolonged use have been reported.
• As a result primary care doctors and their patients are now only too well aware of
the potential hazards of steroid usage.
• The aim of topical steroid therapy is to control the eczema using a potent
application if necessary, under close supervision, and then to maintain control
using a drug of lowest effective potency.
24. TREATMENT
3. OTHERTOPICAL IMMUNOMODULATORS:
• Two calcineurin inhibitors have been introduced
for the treatment of atopic eczema.
• Calcineurin is a cytotoxic enzyme involved in
activation ofT-lymphocytes.
• Macrolide antibiotics, tacrolimus, pimecrolimus
are of low molecular weight to penetrate the
stratum corneum of the skin, particularly when its
barrier function is impaired in eczema.
25. TREATMENT
a)TACROLIMUS:
It is comparable in efficacy to potent topical steroids.
It is available only as an ointment.
It may produce a burning sensation in the skin at the beginning of the treatment.
Systemic absorption is negligible.
26. TREATMENT
b) PIMECROLIMUS:
It is less potent then tacrolimus but penetrate stratum corneum more efficiently.
It is available as a cream.
It appears to inhibit flares of atopic eczema.
27. TREATMENT
4. ANTIBIOTICS:
• Swabs should be taken from infected patient before starting oral antibiotics.
• Choice of antibiotics to cover Staphylococcus aureus is erythromycin or
flucloxacillin, should be given for 10 days.
• Chronic infection require long term treatment.
• Herpes simplex virus should be treated with acyclovir.
28. TREATMENT
5. DRYINGAGENTS:
• In vesicular or weeping eczema the blister and oozing
areas are dried using potassium permanganate baths,
soaks or wet compresses.
• Crystals or tablets are added to warm water to produce
purplish-pink color.
• Skin soaked for at least 15 minutes.
• This appears to have astringent and antiseptic defect.
29. TREATMENT
6. ANTI HISTAMINES:
• Pruritus is one of the distressing feature of
eczema which can be treated from the
short term use of sedative anti-histamine
at night.
30. TREATMENT
7. COAL FOR PREPARATIONS:
• Tar is an effective antipruritic.
• Tar creams and ointments are useful in treatment of discoid eczema.
31. TREATMENT
8. BANDAGING:
• In atopic eczema, bandages can be used to
prevent scratching and to keep ointments and
creams in contact with the skin.
• A wet wrapping bandage is also a technique
made up of emollient and steroids and used to
keep inner layer of skin moist and gives
soothing effect.
• To control varicose eczema, compression
bandaging or graduated support stockings are
probably used.
32. TREATMENT
9. TOPICAL IMIDAZOLES:
• Many imidazole drugs are used to treat eczema.
• Ketoconazole is most widely used to reduce the population of pityrosporum
ovale and controls seborrhoeic eczema and dandruff. It is available in shampoo or
creams.
33. TREATMENT
10. SYSTEMICTHERAPIES:
a) Systemic steroids:
Oral corticosteroids are used as a short term treatment in acute eczema which is now
very rare.
This type of management is required in conditions like acute exacerbation eczema, acute
allergic contact dermatitis and erythrodermic eczema. of atopic
34. TREATMENT
b) Cyclosporine:
It is an immunosuppressant drug extremely effective in the
treatment of chronic eczema mainly used in adult patients and also
in children.
ItsTherapeutic range is 2.5-5mg/kg.
When the drug is stopped, eczema may tends to relapse and to
avoid such cases intermittent courses can be very useful.
Its adverse reactions include hypertension and renal impairment.
There are number of drugs that interact with cyclosporine and must
be used with caution.
Topical preparation of cyclosporine cannot be used to treat eczema
due to poor skin penetration.
35. TREATMENT
c) Azathioprine:
It is an antimitotic drug used as steroid sparing agent to
treat severe resistant eczema at a dose of 50-150mg per
day.
It acts more slowly than cyclosporine but widely used for
long term treatment.
It suppresses bone marrow and proper monitoring
should be done with regular blood tests.
36. TREATMENT
d) Other immune modulators:
Interferon-gamma has been used in cases of severe refractory eczema and includes
unpleasant flu like side effects.
Methotrexate has also been used in unresponsive adult atopic eczema but has never
been evaluated in clinical trials.
37. TREATMENT
e) Evening primrose oil:
It is used to treat resistant eczema
especially where extreme dryness is
the major problem.
38. TREATMENT
11. PHOTOTHERAPY:-
• PUVA - for atopic patients.
• UVB - in dry stage.
• Narrow band UVB therapy is effective ans safer
than PUVA.
• Side effects:- burning, premature ageing and
increase risk of cancer.
39. TREATMENT
12. OTHERTHERAPIES:-
• DIET: under supervision of a dietitian.
• CHINESE HERBAL MEDICINE:
According to patients conditions.
• ALTERNATIVETHERAPIES:
hypnotherapy, yoga, psychotherapy.
40. PATIENT CARE
■ Effect on life of patients - appearance, loss of
sleep.
■ Advice.
■ Cool cotton clothing - suitable for eczema.
■ House dust mite precautions.
■ Emollient application.
■ Exposure to water, detergents, oils, greases,
degreaser may result in recurrence.
