Eczema

ECZEMA

•

Eczema, a term derived from the Greek word meaning ‘to boil’, is a clinical and histological pattern of inflammation of the skin seen in a variety of dermatoses with widely diverse aetiologies.

•

Clinically, eczematous dermatoses are characterized by variable intensity of itching and soreness, and, in variable degrees, a range of signs including dryness, erythema, excoriation, exudation, fissuring, hyperkeratosis, lichenification, papulation, scaling and vesiculation.

The terms ‘dermatitis’ and ‘eczema’ are generally regarded as synonymous, although some authors still use the term ‘dermatitis’ to include all types of cutaneous inflammation, so that all eczema is dermatitis, but not all dermatitis is eczema.

CLASSIFICATION Exogenous eczemas: •

Irritant eczema.

•

Allergic contact eczema.

•

Photoallergic contact eczema

•

Eczematous polymorphic light eruption

•

Infective eczema

•

Dermatophytide

•

Post-traumatic eczema

Endogenous eczemas: •

Atopic eczema

•

Seborrhoeic eczema

•

Asteatotic eczema

•

Discoid eczema

•

Eyelid eczema

•

Exudative discoid and lichenoid chronic dermatosis

•

Chronic superficial scaly dermatitis

•

Pityriasis alba

•

Hand eczema

•

Venous eczema

•

Juvenile plantar dermatosis

•

Metabolic eczema or eczema associated with systemic disease

•

Eczematous drug eruptions

ACUTE VS CHRONIC ACUTE ECZEMA

CHRONIC ECZEMA

Seen when disease is flaring

more longstanding

lesions are papular, edematous, different morphology, predominant exudative especially on hands and features are dryness, hyperkeratosis feet , vesicobullous and lichenification eg: pompholyx, acute episodes of contact allergic eczema, phytophotodermatitis

eg: lichen simplex nodular prurigo

PATHOGENESIS •

The interaction of trigger factors, keratinocytes and T lymphocytes seems important in most eczema types.

SENSITIZATION PHASE •

Most environmental allergens are small, lipophilic molecules with a low molecular weight (<500 Daltons).

•

The unprocessed allergen is more correctly referred to as a hapten.

hapten penetrates the skin, it binds with epidermal carrier proteins to form a hapten–protein complex, which produces a complete antigen.

the antigen presenting cells (APC) of the skin (Langerhans cells and

•

The antigen-presenting cell then migrates via the lymphatics to regional lymph nodes

•

presents the HLA-DR–antigen complex to naive antigenspecific T cells that express both a CD4 molecule that recognizes the HLA-DR and T-cell receptor CD3 complex that recognizes the processed antigen.

•

antigen can also be presented in the context of the MHC class I molecules, it would be recognized by CD8 cells.

The naive T cells are primed and differentiate into memory (also referred

which undergo clonal expansion, acquire skin-specific homing antigens,

clones of CD4+ Th1 and CD8+ type 1 cytotoxic T cells act as effectors on

The sensitization phase generally lasts 10–15 days and is often asymptomatic.

Sub- sequent exposure to the antigen

leads to an elicitation phase

Such rechallenge can occur via multiple routes, including transepid

Elicitation phase APCs and the keratinocytes can present antigen and lead to recruitment of haptenspecific T cells. T cells release cytokines, including IFN-γ and TNF-α, which, in turn, recruit other inflammatory cells while stimulating macrophages and keratinocytes to release more cytokines

inflammatory response occurs as monocytes migrate into the affected area, mature into macrophages, and attract more T cells.

This localized proinflammatory state results in the classical clinical picture of spongiotic inflammation (redness, edema, papules and vesicles, and warmth)

NEW DEVELOPMENTS

HISTOPATHOLOGY ACUTE STAGE : dominated by spongiosis, an intercellular epidermal oedema which leads to stretching and eventual rupture of the intercellular attachments, with the formation of vesicles.

Increased epidermal mitotic activity leads to acanthosis, but if spongiosis is intense, disintegration of the suprapapillary epidermis may cause clefts to form

Loosening and disruption of the individual cells occur, and some intracellular vacuolation may be found Loose, shrunken epidermal cells may resemble histiocytes. Vesicles and the oedematous epidermis may be permeated by mononuclear cells, chiefly monocytes.

Acute eczema. The epidermis shows distinct vesicle formation. The vesicle contains serum, and a moderate number of inflammatory cells.

SUBACUTE STAGE In the subacute stage, spongiosis and vesiculation diminish

increasing acanthosis is associated with formation of a parakeratotic horny layer.

This often contains layers of coagulated plasma and pyknotic nuclei of inflammatory cells.

Subacute eczema. There is irregular acanthosis and patchy spongiosis, with the formation of incipient microvesicles. A few lymphocytes are migrating up from the dermis into the epidermis

CHRONIC STAGE hyperkeratosis gradually replaces parakeratosis.

Acanthosis is more prominent than spongiosis.

Inflammatory cells are less evident in the epidermis, but dermal changes become more prominent.

The rete ridges become elongated and broadened. The changes are then those of lichenification.

Chronic lichenified eczema. There is compact hyperkeratosis, some patchy parake

Mild spongiosis is seen throughout much of the epidermis, and there is a lymphocy

• • • • •

Vascular dilatation in the dermis is marked in all stages. The papillary vessels are involved, and in lichenification they may become tortuous. eosinophils are particularly common in eczematous drug eruptions. In the presence of infection, polymorphs may invade the epidermis. In grossly lichenified eczema, prurigo and exfoliative dermatitis, the infiltrate is mixed, and may be so dense that it simulates a granuloma.

Asteatotic eczema Synonyms • Winter

eczema • Eczéma craquelé

Definition:

It is a type of eczema occurring due to excess water loss from the epidermis resulting in dehydration of the stratum corneum.

Aetiology •

Excess water loss from the epidermis results in dehydration

•

Significant decrease in free fatty acids in the stratum corneum.

•

Stratum corneum lipids act as water modulators

•

cutaneous loss of these lipids can increase transepidermal water loss to 75 times that of healthy skin.

•

Elderly persons with decreased sebaceous and sweat gland activity

•

patients on antiandrogen therapy

•

people using degreasing agents

•

people bathing without replacing natural skin emollients lost to bath water

•

Malnutrition, particularly zinc deficiency.

•

Diuretics can affect the hydration of the skin

stratum corneum loses water

cells shrink

decreased cellular volume can stress the skin’s elasticity, crea

• Fissures

rupture dermal capillaries,

causing clinical bleeding

C/Fs •

Elderly patients complain of pruritus

•

predominantly occurs on the legs, usually on the extensors.

•

Finger pulps are dry, cracked, and parchment like, and a depression is created by prolonged pressure on the pulp.

•

The shins have a pavement stone appearance (crazy pavement pattern—eczema craquelé).

•

Secondary lesions like eczematous changes and excoriations often complicate the lesions.

•

Hemorrhagic fissures with erythema and eczematous changes finally develop

Principles of Management of Asteatotic Eczema

•

Protect from the cold and winds

•

Avoid direct contact of woolens with the skin

•

Take short baths with lukewarm water

•

Use soap sparingly on the involved areas

•

Avoid harsh detergents or drying soaps

•

Pat the skin dry after bathing

•

Apply an emollient immediately after bathing, and as frequently as required to moisturize the skin

•

Apply topical steroid ointments with or without polyethylene occlusion.

•

Antihistamines and many treatment modalities have been used to relieve chronic persistent pruritus in the elderly like topical doxepin; oral doxepin, amitriptyline, mirtazapine, ondansetron, gabapentin and naloxone and UVB therapy

Discoid eczema Synonym : • Nummular eczema • Discoid

eczema is characterized by a single, nonspecific morphological feature, namely circular or oval plaques of eczema with a clearly demarcated edge.

ETIOLOGY •

It frequently occurs in those with xerotic skin.

•

Xerotic skin permits various aeroallergens to enter the skin and induce nummular eczema.

•

Round eczematous oozing or dry scaly round lesions occur in AD.

•

Though increased bacterial colonization is known in the affected skin, its etiologic role is not proved; neither is the role of an internal focus of infection.

•

One recent study identified neurogenic contributors to inflammation

•

substance P and calcitonin gene-related peptide positive nerve fibers were more frequent in lesions than in nonlesional papillary dermis.

•

Mast cells were also found to have increased in number in the lesional skin.

•

Allergic contact dermatitis is relatively common in persistent discoid eczema.

•

The most common allergens implicated are rubber chemicals, formaldehyde, neomycin, chromium, nitrofurazone, colophony, fragrance mix, cobalt and nickel.

HISTOPATHOLOGY •

Epidermal changes observed in lesional skin include focal spongiosis and intraepidermal vesiculations.

•

Papillary dermis shows edema and perivascular lymphohistiocytic infiltrate.

•

In some dry lesions, psoriasiform pattern characterized by alternating para and orthokeratosis is seen.

C/Fs •

Pruritus

•

erythematous, edematous papules or vesicles that coalesce to form round eczematous lesions, one to several centimeters in diameter.

•

symmetrically distributed on the dorsal aspects of the hands and feet, extensors of the arms and legs, and occasionally on the thighs or the trunk.

•

Lesions evolve from acute to subacute eczemas.

•

The borders of the lesions are well defined.

•

Central clearing and peripheral extension make the lesions ring-shaped or annular.

•

Hyperpigmentation is commonly seen.

•

Discoid eczema is a chronic, relapsing condition that generally exacerbates in winter.

D/Ds •

AD

•

Allergic contact dermatitis

•

Irritant contact dermatitis

•

Polymorphous light eruption

•

Psoriasis

•

Tinea corporis

•

Autoeczematization

•

Mycosis fungoides

•

Small plaque parapsoriasis

•

A personal or family history of atopy and other features of AD help to differentiate.

•

Irritant contact dermatitis sometimes produces round lesions, but history of an irritant contact is helpful.

•

Allergic contact dermatitis lesions are usually not round and are asymmetrical.

•

Patch testing may be carried out if allergic contact dermatitis is suspected, particularly when the patient’s occupation suggests it.

•

Psoriatic lesions are round and dry, but scaling is characteristic.

•

Itching is generally minimal or absent.

•

Tinea corporis lesions are annular and active peripherally.

Treatment •

compressors for oozy lesions.

•

Topical steroids are the most commonly used treatment for nummular eczema.

•

Generally moderately potent topical steroids are sufficient.

•

In acute, oozing disease, topical steroid under wet wrap gives rapid relief.

•

In the case of relapsing disease, long-term treatment with topical calcineurin inhibitors or weekly topical steroid therapy can be pursued.

•

A course of antibiotics with anti staphylococcal activity such as cloxacillin or a cephalosporin may be given in the presence of secondary infection.

•

Antipruritic sedative antihistamines such as hydroxyzine may be required.

•

If the lesions are multiple, involving extensive areas, prednisolone should be given in the dose of 40 mg/day to start with, and tapered over 3 weeks.

•

continuous use of an emollient cream is required for prevention of recurrence.

HAND ECZEMA

•

The term hand eczema implies that the dermatitis is largely confined to the hands, with only minor involvement of other areas.

CLASSIFICATION Classification is based partly on • •

Aetiology Morphology

Hand eczema: aetiological possibilities to be considered.

Exogenous : • Contact

irritants Chemical (e.g. soap, detergents, solvents) Physical (e.g. friction, minor trauma, cold dry air) • Contact allergens Delayed hypersensitivity (type IV) (e.g. chromium, rubber) Immediate hypersensitivity (type I) (e.g. seafood) • Ingested allergens (e.g. drugs, possibly nickel, chromium) • Infection (e.g. following bacterial infection of hand wounds) • Secondary dissemination (e.g. dermatophytide reaction to tinea pedis)

Endogenous: • Idiopathic (e.g. discoid, hyperkeratotic palmar eczema) • Immunological or metabolic defect (e.g. atopic) • Psychosomatic: stress aggravates, but may not be causative • Dyshidrosis: increased sweating aggravates, but may not be causative

Morphological patterns of hand eczema. •

Apron eczema

•

Chronic acral dermatitis

•

Discoid eczema

•

Fingertip eczema

•

‘Gut’ eczema

•

Hyperkeratotic palmar eczema

•

Pompholyx

•

Recurrent focal palmar peeling

•

Ring eczema

•

‘Wear and tear’ dermatitis (dry palmar eczema)

•

Other patterns (e.g. patchy vesiculosquamous)

Histopathology •

differences between the various forms of hand eczema are clinical rather than histological

•

thickened horny layer and the presence of numerous sweat glands modify the histological features of eczema on the hands.

Prevalence •

hand eczema are very common

•

commoner in females

•

particularly housewives, and the main causative factors were vegetables such as garlic and onion, followed by soaps and detergents.

•

building construction workers, medical and paramedical workers, and teachers; 53% were sensitive to metals (nickel, cobalt, and chromate), 41% to medicaments, 20% to rubber, and 20% to vegetables.

•

beauticians, including hairdressers, had hand dermatitis; 69% were patch test positive for Para-phenylenediamine, rubber, nickel, shampoos, ammonium thioglycollate, ammonium persulfate, henna mixture, and detergent.

Morphological patterns of hand eczema.

Apron eczema: • involves the proximal palmar aspect of two or more adjacent fingers and the contiguous palmar skin over the metacarpophalangeal joints, thus resembling an apron. • This pattern of hand eczema can be irritant or allergic, but is often considered endogenous.

Chronic acral dermatitis: affects patients in middle age. • A chronic, hyperkeratotic, papulovesicular eczema of the hands and feet, intensely pruritic, is associated with grossly elevated IgE levels in subjects with no personal or family history of atopy. • The condition responds to oral corticosteroids, but the response to topical therapy is poor •

FINGER TIP ECZEMA •

characteristic pattern, involving the palmar surface of the tips of some or all the fingers.

•

skin is dry, cracked and breaks down into painful fissures.

•

it may occasionally extend along the palmar surfaces of the fingers to merge with palmar eczema

Two patterns may be distinguished: • The first pattern involves most or all of the fingers, mainly those of the dominant hand, and particularly the thumb and forefinger. • usually

worse in the winter and generally improves on holiday.

• it

is a cumulative irritant dermatitis in which degreasing agents combine with trauma as causative factors.

•

The second pattern involves the thumb, forefinger and third finger of one hand.

•

This is usually occupational (whether in factory, market garden or house).

•

It may be either irritant (e.g. in newspaper-delivery employees) or allergic (e.g. to colophony in polish, or to tulip bulbs or stems.

•

The condition usually involves the dominant hand

•

In these cases, patch testing (and 20-min contact tests) may be rewarding.

GUT ECZEMA Synonym

Slaughterhouse eczema

•

Workers who eviscerate and clean pig carcasses are at risk of developing vesicular eczema which starts in the finger-webs and spreads to the sides of the fingers.

•

This is a mild, self-limiting condition, which clears in a week or two, even if the patient remains at work, but it can recur at intervals.

•

Workers in Danish bacon factories call this ‘fat eczema’.

•

The pathogenesis is unknown, but some slaughter- men have developed contact urticaria from exposure to animal blood

Hyperkeratotic palmar eczema (SYN:TYLOTIC ECZEMA)

•

characterized by highly irritable, scaly, fissured, hyperkeratotic patches on the palms and palmar surfaces of the fingers.

•

The aetiology is unknown.

•

It is most frequent in men of middle age or over, and is extremely refractory to treatment, although PUVA may be helpful.

•

Steroid ointments, crude coal tar, salicylic acid and Grenz rays may be tried.

•

Oral retinoid tablets such as alitretinoin and etretinate may be helpful

RING ECZEMA •

An itchy patch of eczema appears beneath a finger ring and may spread to the adjacent finger or adjoining palmar area.

•

Collection of a soap film under the ring and pressure of the ring on the skin are the main causes.

•

This explains the age of onset, which is after marriage or childbirth, after which contacts with soaps, detergents, and cleansers increase considerably.

•

Patch testing may reveal nickel, chromium, and cobalt sensitivity

MANAGEMENT GENERAL •

Efforts to avoid allergens and irritants are very important.

•

Patch testing may help in identifying allergens.

•

Barrier creams cannot be relied upon for prevention.

•

Rubber gloves may provide protection, but are uncomfortable to wear in a tropical climate for more than a short period owing to sweating.

•

The use of cloth gloves below the rubber gloves may be tolerable.

•

Polyvinyl chloride gloves may be used in rubber-sensitive persons.

•

Soap substitutes may be tried.

Topical Therapy •

Frequent use of moisturizers is needed.

•

Mid-to-high potency topical corticosteroids may be needed for a short period.

•

Later, mild steroids along with an emollient may be adequate.

•

In resistant cases, high-potency steroid under occlusion may be required.

•

A combination of a topical steroid with tar and salicylic acid may be tried in hyperkeratotic and chronic eczemas.

•

A new nonsteroid immunomodulator, topical tacrolimus ointment 0.1% has been found useful.

•

Topical and systemic antibacterials may have to be used in the presence of secondary infection.

Oral Therapy •

Sedative antihistamines may be needed for itching.

•

Acitretin is effective in chronic hyperkeratotic hand eczema.

•

Cyclosporine has been tried in difficult cases.

•

Ranitidine is useful as an adjuvant to a topical steroid in atopic hand eczema.

•

One study found good results with disulfiram, an oral chelating agent, 200 mg/day for 8 weeks when metal allergy due to a dietary item was suspected to be the cause.

Phototherapy and Photochemotherapy: •

In resistant and persistent cases, oral PUVA or UVB therapy should be tried.

•

It is useful in several types of hand eczema, including allergic contact dermatitis, hyperkeratotic hand eczema, and dyshidrotic eczema.

•

In a study, 28 patients with chronic palmar eczema were treated by soaking the hands (and feet when affected) in warm water containing 1 mg/L 8-methoxypsoralen for 15 minutes, immediately followed by exposure to increasing doses of PUVA, starting with 0.5 J/cm2.

•

The treatment was given four times per week up to 25 treatments.

•

Excellent to good response was obtained in 93% of 14 patients having pompholyx and 86% of 14 patients with hyperkeratotic hand eczema.

•

Shortwave UVB has been used with success in chronic hand eczema.

•

MEL delivery system has been used in the treatment of chronic hand eczema.

•

There was a mean improvement in 46% of chronic nonatopic and 54% in atopic hand eczema.

POMPHOLYX (SYN. DYSHIDROTIC ECZEMA) •

This disease is characterized by palmoplantar vesiculation.

•

When it involves the palms it is called cheiropompholyx and when on the soles, podopompholyx.

•

dyshidrotic eczema is a misnomer as pompholyx has no causal relationship with the sweat glands or sweating.

ETIOLOGY •

The cause remains obscure.

•

hereditary predisposition may be important

•

The role of the sweat glands has been disputed.

•

eczematous changes have been both induced and relieved by sympathectomy reducing hyperhidrosis.

•

A thorough examination of serial sections of pompholyx vesicles showed that sweat ducts were often pushed aside by the tense vesicles or passed between them.

•

The contents and pH of the vesicular fluid suggested that vesicles ruptured the sweat ducts rather than the reverse.

•

The role of atopy is also difficult to assess, a family or personal history of atopy was obtained in 54 out of 131 patients with pompholyx.

•

Primary irritants can cause pompholyx, for example in metal workers exposed to soluble oils.

•

Direct-contact allergens may sometimes evoke a palmar vesicular reaction instead of the more common dorsal pattern.

•

Responsible allergens include primin, isopropyl paraphenylenediamine, benzoisothiazolones and dichromates.

•

Perfumes, fragrances and balsam ingredients must also be considered as potential allergens.

•

Patch tests of nickel sulphate applied to the palms or fingers of nickel-sensitive subjects may produce a vesicular pompholyx-like reaction.

•

The role of ingested metals in provoking exacerbations of vesicular palmar hand eczema has been studied.(Eg.oral nickel sulphate)

•

Chromium and cobalt allergy may also occasionally be implicated.

•

Oral neomycin provoked pompholyx.

•

•

•

•

Fungal infection can provoke eczema of the palms. In the past this pompholyx dermatophytide was diagnosed more frequently than it is now, and it has been regarded as a rare association in other studies Irritant or allergic dermatitis resulting from treatment of a fungal infection of the foot may also precipitate a palmar pompholyx. Primary allergic contact dermatitis of the feet, for example from rubber shoe chemicals, may induce a sympathetic palmar eruption.

•

bacterial foci can play a role

•

The role of stress, patients with pompholyx are unduly susceptible to stress.

•

Pompholyx may rarely follow a drug eruption.

•

Aspirin ingestion, oral contraceptives and cigarette smoking also increase the risk of pompholyx

HISTOPATHOLOGY •

•

Fully formed lesions show the changes of acute eczema modified by the thick, overlying epidermis. The subsequent course is that of a subsiding eczema, with hyperkeratosis and epidermal shedding

C/Fs •

common before the age of 40 years.

•

Onset before 10 years is unusual.

•

sudden onset of crops of clear vesicles, which appear deeply seated and ‘sago-like’.

•

but a sensation of heat and prickling of the palms may precede attacks.

•

Vesicles may become confluent and present as large bullae, especially on the feet.

•

Itching may be severe, preceding the eruption of vesicles.

•

The attack subsides spontaneously, and resolution with desquamation occurs in 2–3 weeks

•

In mild cases, only the sides of the fingers may be affected, but in a typical case the vesicles develop symmetrically on the palms and/or soles.

•

Unilateral or asymmetrical patterns occur, but this should alert the dermatologist to look for contact causes of the eruption.

•

In 80% of patients only the hands are involved.

•

feet alone each account for about 10% of patients.

•

Secondary infection with pustule formation and lymphangitis is not uncommon

•

Rubbing and inappropriate treatment may produce secondary eczematous changes extending beyond the volar surfaces.

•

After recurrent attacks spreading to the dorsa of the fingers, the nails may develop dystrophic changes, irregular transverse ridging and pitting, thickening and discoloration.

•

They may occur at intervals of 3 or 4 weeks for months or years, or at long irregular intervals.

DIAGNOSIS •

Chronic, recurrent vesiculation without periods of remission may be termed chronic vesicular dermatitis.

•

A circumscribed and asymmetrical area of scaling and vesiculation of the palm or sole should suggest the possibility of dermatophytosis, and scrapings should be examined for fungus.

•

If the erythema is limited to one or two interdigital clefts, or is asymmetrical, or involves the dorsal skin to any extent, the possibility of a contact dermatitis must be considered, and excluded by a careful history and by patch testing.

•

In pustular psoriasis of the palms and soles there are usually no clear vesicles. The pustules are sterile on culture, and leave characteristic brown marks as they resolve.

•

Occasionally, secondary bacterial infection of pompholyx may occur, with pustule formation, but in these cases the lesions tend to be painful, with surrounding erythema, and culture of the pus yields the causative organism.

•

A pustular bacteride secondary to bacterial infection elsewhere in the body may also lead to confusion.

•

Repeated attacks of pompholyx may produce hyperkeratotic lesions that mimic psoriasis vulgaris.

•

Pemphigoid, linear IgA disease and pemphigoid gestationis occasionally present with blisters on the palms that mimic pompholyx.

TREATMENT •

Any obvious cause of the eruption should be eliminated

•

In the acute phase, rest and bland applications are indicated.

•

Involvement of the feet may require the patient to be treated in bed.

•

The hands or feet should be soaked three or four times a day in either Burow’s solution (aluminium acetate 1%) or potassium permanganate solution (diluted 1:8000).

•

Large bullae may be aspirated using a sterile syringe.

•

Systemic antibiotics will be required if secondary bacterial infection develops.

•

This is most likely to be staphylococcal, and flucloxacillin is usually effective.

•

As the eruption subsides the soaks should be discontinued, and zinc cream or oily calamine lotion can be substituted.

•

Topical steroids are useful in the subacute and chronic phases.

•

In a few severe cases - oral steroids.

•

For chronic pompholyx which has entered the hyperkeratotic phase, tar preparations such as 2–5% crude coal tar may be used, or a steroid preparation may be combined with a coal-tar solution.

•

Low-dose methotrexate and radiation therapy have both been used with success in refractory cases

other treatments : •

Local photochemotherapy (PUVA) and UVA1 phototherapy.

•

Intradermal botulinum toxin (BTXA) and tap water iontophoresis when associated with hyperhidrosis or aggravated in summer.

•

In resistant cases radiation therapy has been tried with good results.

PITYRIASIS ALBA •

This is a pattern of dermatitis in which hypopigmentation is the most conspicuous feature.

•

Some erythema and scaling usually precede the development of hypopigmentation but these are often relatively mild.

AETIOLOGY •

Pityriasis alba is often a manifestation of atopic dermatitis but it is not confined to atopic individuals.

C/Fs Pityriasis alba occurs predominantly in children between the ages of 3 and 16 years. • The sexes are equally susceptible. •

•

The individual lesion is a rounded, oval or irregular hypopigmented patch which is usually not well marginated.

•

Lesions are often slightly erythematous and have fine scaling.

•

Initially, the erythema may be conspicuous and there may even be minimal serous crusting.

•

Later, the erythema subsides completely, and at the stage at which the lesions are commonly seen by a physician they show only persistent fine scaling and hypopigmentation.

•

There are usually several patches ranging from 0.5 to 2 cm in diameter, but they may be larger, especially on the trunk.

•

In children the lesions are often confined to the face, cheeks ,mouth and chin.

•

In 20% of affected children the neck, arms and shoulders are involved as well as the face.

•

Most cases persist for some months, and some may still show hypopigmentation for a year or more after all scaling subsides.

•

Recurrent crops of new lesions may develop at intervals. The average duration of the common facial form in childhood is a year or more.

•

DIAGNOSIS •

Theage, incidence, the fine scaling and the distribution of the lesions usually suggest the diagnosis.

•

Conspicuous hypopigmentation may lead to a misdiagnosis of vitiligo.

•

Naevus depigmentosus most commonly presents at birth or before 3 years of age, and most often causes single, wellmarginated lesions on the trunk.

•

this condition may be difficult to distinguish from pityriasis alba when it occurs on the face and in cases of later onset.

•

Discoid eczema in an atopic child is intensely pruritic, and the lesions are larger and more oedematous.

•

In older children and adults, the lesions on the trunk, during their early erythematous phase, may be mistaken for psoriasis but the distribution and the relatively mild scaling should exclude this diagnosis.

•

Mycosis fungoides, although relatively rare, may present with lesions clinically resembling pityriasis alba.

•

This condition may also be difficult to distinguish histologically, so follow-up and repeat biopsy are sometimes required.

TREATMENT •

pigmentation takes a long time to recover.

•

The scaling may be reduced by a bland emollient cream

•

for chronic lesions on the trunk a mild tar paste may be helpful.

•

Mild topical corticosteroids are helpful if inflammation persists.

•

Topical tacrolimus and pimecrolimus likely to prove helpful in pityriasis alba

VENOUS ECZEMA (SYN: GRAVITATIONAL ECZEMA) Definition: Eczema secondary to venous hypertension. • This condition is also called stasis eczema or varicose eczema. • It is increased venous pressure rather than stasis which seems to be the prerequisite. • Although it is often associated with varicose veins these are not always present.

PATHOGENESIS • Chronic

venous insufficiency (CVI) of the lower extremities is the cause of stasis syndrome. • The venous flow up from the feet against gravity is made possible, physiologically by the action of the calf muscles and competence of valves in the veins. • This mechanism is defective in CVI because of damage to the veins by thrombophlebitis or due to structural weakness of the veins in the form of an incompetent valvular system.

Because of incompetent valves

there is blood reflux from the deep to the superficia

causing venous hypertension

•

Recent theories of CVI are related to the abnormal microcirculation leading to an inflammatory response.

•

This commonly occurs in those who have to work in a stationary position for hours.

•

Other causes are related to the obstruction of one of the major veins, particularly the ileofemoral, due to external pressure caused by neoplastic invasion, hemangioma, or arteriovenous fistula.

It is believed that fibrinogen molecules escape through a porous endothelium into interstitial fluid

•

•

where they form a fibrin sheath around the capillaries.

•

This acts as a barrier to the diffusion of oxygen and other nut

•

stasis leads to hypoxia and poor nutrition of tissues, promoting tissue damage and resulting in dermatitis.

•

Another explanation for cutaneous inflammation is the release of proteolytic enzymes and free radicals from sequestrated white blood cells in venules (due to venous hypertension),

•

which produces tissue damage.

•

Increased endothelial contact and adhesion of white blood cells can be due to an increased expression of adhesion molecules ICAM-1 and VCAM-1 on the vascular endothelium in the affected skin.

•

hemodynamic forces such as venous hypertension, circulatory stasis, and modified conditions of shear and stress play an important role in inflammatory reaction accompanied by leukocyte activation.

•

The leukocyte activation is accompanied by the expression of integrins and synthesis and release of many inflammatory molecules, including proteolytic enzymes, leukotrienes, prostaglandin, bradykinin, free oxygen radicals, cytokines, and other inflammatory mediators.

•

The inflammatory reaction eventually leads to venous dermatitis, venous ulceration, and ultimately to liposclerotic skin

C/Fs •

Venous eczema is an erythematous, scaly and often exudative eruption usually seen around the ankle and lower leg.

•

similar changes occur at other sites of venous hypertension such as the pendulous skin over an obese abdomen or in association with an ateriovenous fistula in the upper limb.

•

The eczema may develop suddenly or insidiously.

•

The patients are usually middle-aged or elderly and most often female.

•

The increased incidence in females is presumably due to hormonal effects and the tendency for venous thrombosis to occur during pregnancy.

•

The eczema is often accompanied by other manifestations of venous hypertension, including dilatation or varicosity of the superficial veins, oedema, purpura, haemosiderosis, ulceration, orsmall patches of white, atrophic, telangiectatic scarring (‘atrophie blanche’).

•

Leashes of dilated venules around the dorsum of the foot or the ankle are particularly common.

•

There may be a subepidermal vascular proliferation producing purple papules around the ankle, which may resemble Kaposi’s sarcoma.

•

Secondary patches of eczema may develop on the other leg, even when it is not affected by obvious venous insufficiency.

•

Generalized secondary dissemination may occur, and occasionally this can progress to erythroderma.

•

These changes are often modified by secondary contact dermatitis, infection and rubbing.

•

Allergic contact dermatitis is a common complication of gravitational eczema, possibly because of the large number of antigen-presenting cells in the inflamed skin.

STASIS ECZEMA

D/Ds •

Atopic dermatitis may manifest as lichenified patches around the ankle or behind the knees.

•

Allergic contact dermatitis of the lower legs is usually due to topical medicaments.

•

Patch testing is often indicated.

•

An infected ulcer may be complicated by infective eczema spreading from the edge of the ulcer, with response to appropriate antibiotic therapy.

•

Discoid eczema is common on the lower leg, usually on the anterior or anterolateral aspect.

•

Asteatotic eczema commonly affects the legs of elderly patients.

•

Psoriasis may present as a single, irritable plaque on the leg, but is usually more scaly and clearly marginated.

•

Hypertrophic lichen planus of the lower leg may occasionally be mistaken for eczema if there are no characteristic lesions elsewhere.

•

Dermatophyte infection may present as diffuse erythema and scaling and may be difficult to recognize, particularly if it has been treated with topical steroids.

Profuse actinic keratoses may cause red irritable patches on the lower legs in sunny climates. • In the late stage of borreliosis the leg can feel heavy, with thick cyanotic itchy skin which may mimic the changes of venous hypertension •

TREATMENT •

The underlying venous hypertension should be controlled.

•

Obese patients should be urged to lose weight.

•

Well-fitted support stockings or firm bandages can be helpful if worn reguarly and care is taken to avoid the formation of a band at the top of the leg.

•

The legs should be elevated as effectively as possible.

•

Mild topical steroids may be used to relieve irritation,

•

use of potent steroids should be limited to short periods of a few days as they may cause cutaneous atrophy and increase the risk of ulceration.

•

Topical tacrolimus has been reported to be effective

•

Bacterial infection must be treated where appropriate

•

If trauma is thought to be playing a part, and the patient cannot resist scratching, a paste bandage may be helpful.

To reduce venous hypertension: Firm elastic bandage or appropriate elastic stockings Stasis dermatitis : •

Mild topical corticosteroids may be used

•

Oral antibiotics for secondary infection

•

Sedative antihistamines to relieve itching

Adjuvant therapy: •

Pentoxifylline 400 mg three times a day

•

Calcium dobesilate 500 mg twice a day

THANK YOU