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ECZEMA.pptx
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- 2. • Eczema (Greekword) - to boil • Clinical and histological pattern of inflammation seen in variety of dermatoses with diverse aetiologies. • Clinically - itching and soreness, - dryness, erythema, excoriation, exudation, fissuring, hyperkeratosis, lichenification, papulation, scal-ing and vesiculation.
- 4. Incidence and prevalence •Survey in US on over 20,000 people - point prevalence of all forms of eczema - 18 / 1000, 7 of whom had atopic eczema. • Hand eczema, dyshidrotic eczema , nummular eczema – 2 / 1000. • In UK, eczema consultations - 10% of total dermatology caseload • A tertiary referral centre in Singapore – b/w 1989 and 1990 – 25 448 new cases - 67% of eczema cases – endogenous and 13.7% - CD. • Exfoliative dermatitis - 0.5% of . There was inc in endo eczema 1989– 90 compared 1973.
- 5. • According toan Indian study, out of 300 patients aged up to 17 years, 24% had eczema. • In another Indian study, 37% of 300 patients aged above 60 years had an eczema.
- 6. Age • In theNational Health and Nutrition Examin-ation Survey (NHANES) epidemiological survey in USA, atopic eczema - most common form found up to age of 11 years; with Perioral eczema - MC • Several patterns - found in children- juvenile plantar dermatosis and napkin dermatitis. • Nummular dermatitis, asteatotic eczema of legs - elderly males in winter. • In older factory workers - irritant hand eczema although ACD becomes less common with age.
- 7. • Ethnicity reportedin all ethnic groups • Associated diseases Atopic eczema is associated with some forms of non‐atopic eczematous dermatoses, in particular hand eczema
- 8. Pathophysiology • The interactionof trigger factors, keratinocytes and T lymphocytes - imp in most eczema types. • In ICD- 3 processes - disturbed barrier function, epidermal cell change and release of inflammatory mediators and cytokines. • Certain irritants - chronic reaction in which effect on epidermal cell turnover predominates – lichenification • whereas in acute irritant reactions, inflammatory mediator and cytokine release ~ acute allergic CD.
- 9. • After activationof immune pathway - accumulation of inflammatory cells progresses - morphological changes. • Histological changes of primary ID ~ ACD, but proceed quickly, depending on conc. of irritant. • At 3 – 6 h - epidermal Intracellular & intercellular oedema. • within 24 h - epidermal necrosis, with cellular vacuolation and nuclear pyknosis occurs. • In severe forms - to subepidermal blister formation.
- 10. • Genetic studies– filaggrin binds and condenses the keratin cytoskeleton, - squame formation. • Loss‐of‐ function mutations of fillaggrin gene – Impaired skin barrier function - atopic eczema and some subtypes of non‐atopic eczema.
- 12. Clinical features • History- hallmark of eczema - pruritus - disturb sleep and quality of life. • When taking history, imp - occupation and recreational activi-ties - relevant in irritant and allergen exposures. • Presentation - Acute eczema - oedematous vesicular and may be exudative. • Chronic eczema - erythema, scaling, excoriation and lichenification.
- 13. Secondary dissemination • Tendencyto spread far from point of origin and to become generalized - autoeczematization. • Spread likely when primary site - legs / feet. • Secondary eruption - small oedematous papules - eczematous and confluent in small plaques. • Symmetrical. • Generalized secondary eruption can evolve into erythroderma, which may become self‐perpetuating.
- 14. • The disseminationmechanism • ACD may spread. eg in allergy to lanolin applied to leg that may involve hand used to apply it. o Topical medicament sensitivity is very common in stasis dermatitis. • Ingestion / injection of allergen in already sensitized person - • Focus on highly irritated skin causes generalized irritability • Allergic response to microorganisms and bacterial hypersensitivity to their metabolic products
- 15. Conditioned hyperirritability. • Phenomenonwhere area of inflamed skin on one part of body results in generalized hyperirritability of skin at distant sites. • Eg. tendency for pts suffering from eczema have a higher proportion of false + ‘irritant’ reactions to patch tests. • ‘angry back’syndrome, in which strongly positive patch test response can increase % of false + rxns on back at same time, is an example of this.
- 16. • Mechanisms underlyingdissemination and conditioned hyperirritability. • Circulating activated T lymphocytes - increased in no. • Peripheral blood mononuclear cells - increased proliferation • Suggests that an abnormal CMI response against autologous skin antigens could be occurring.
- 17. Investigations • A thoroughclinical examination . • Laboratory test - in case of secondary infections. • Skin biopsy - limited role • Patch testing not routinely necessary • Useful when- involves the face, hands, feet or in a case of atypical, asymmetrical dermatitis. • Study – 50 pts - clinically suspected discoid eczema were patch- tested • Patch test analysis - out of 50, 28 reacted to allergens. Potassium dichromate was MC allergen (20%), followed by nickel (16%), cobalt chloride, and fragrance (12%) .
- 18. Treatment • Mainstay -Properhydration, avoidance of triggers • Stress-induced exacerbations - psychosomatic counseling recommendable. • 308 nm excimer light (MEL) in chronic localized hand dermatoses - 46% impr atopic and 54% in nonatopic • Mtx (5 mg/week) - recalcitrant eczema in five elderly patients - dramatic improvement in 3 weeks
- 19. • Phototherapy andimmunosuppressives (e.g., azathioprine, chlorambucil, and methotrexate) are also used
- 20. • Study thatincluded 39 randomised controlled trials involving 2599 randomised participants – showed Probiotics probably make little or no difference in participant‐ or parent‐rated symptoms of eczema.
- 21. • Also dailyemollient during infancy in a multicentre RCT found no evidence that daily emollient during first year of life prevents eczema in high risk children
- 22. Management • Moderateor potenttopical CS at least for a few days, speed resolution of acute episodes. • Tacrolimus ointment 0.1% is ~ in potency to potent topical CS, while pimecrolimus has a lower potency . • Wet wrapping tech-nique, - layer of wet tubular bandage is covered with a dry layer, can be particularly useful. Hazards - risk of hypothermia, although, in moderation, cool-ing effect is benefi cial. Emollients and other medications can be applied under the bandaging as required. • When secondary infection is present, oral antibiotics may be required. • antiseptics + steroids - when indication, in order to avoid unecessary exposure to the risks of sensitization and emergenceof bacterial resistance.
- 23. • Subacute eczema- If acute eczema fail to clear in 3–4weeks, consider perpetuating factors • Dermatology day unit review or admission to hospital can be helpful.. • Paste bandages - ensure they are firm but not tight. • CS under polythene occlusion - helpful reduce pruritus.
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- 25. Nummular dermatitis (discoid eczema) •Circular/oval plaques of eczema with clearly demarcated edge. • Chronic problem – undergoes relapses & remissions. • Affects women in early adulthood, in men - older age groups. • Some authors - high incidence of atopy, but others have not and levels of IgE - within normal range • Histology - subacute dermatitis
- 26. • Organisms -Colonization of lesions by staphy - increase severity. • Genetics - indirect link via atopy • Environmental factors - clinically relevant underlying allergic CD in about 1/3 of patients. In one case series, 8 of 13 pts reported impr as result of avoidance of allergens identified by patch testing . • Dry skin - associated, particularly in the elderly • Association with excessive alcohol intake reported. • Sensitivity to aloe, depilating creams , mercury , methyldopa, oral gold therapy in some +nt.
- 27. Clinical features • coin‐shapedplaque of closely set vesicles on erythematous base. • In acute phase - dull red, very exudative and highly pruritic less - less vesicular , scaly, with central clearing- annular lesions. • As fade - leave dry, scaly patches. • After period of b/w 10 days and several months - secondary lesions occur - in a mirror‐image confi guration on opposite side of body. • Dormant patches may become active again, if Rx is discontinued prematurely.
- 28. • Clinical variants •Nummular dermatitis: exudative type. • Nummular dermatitis: dry type. • Nummular dermatitis of the hands. • Exudative discoid and lichenoid chronic dermatosis • All forms of nummular dermatitis are chronic, with partial remis-sion during which plaques tend to clear in centres • Most are worse during colder months of year.
- 30. Management • General considerations- avoidance of irritants. • Bed rest , removal from a stressful envirnment. • Correct ambient conditions of low humidity. • Emollients and topical CS - useful. • Topical antiseptic or antibiotic - considered. • Broad‐spectrum oral antibiotic are often helpful in severe exudative cases.
- 31. Asteatotic eczema (Eczémacraqueléé • Winter eczema ) • Develops in very dry skin, usually in elderly. • Sites : legs, arms and hands • Characteristic - crazy‐paving pattern on legs .(eczéma craquelé). • Flare during winter. • Recent study of elderly Japanese care home residents – prevalence of 16.4% for those in rehabilitation, 41.2% - in long‐term residential care. • May be presenting sign of myxoedema, Zn def.
- 32. • Predisposing factors •Dry skin. • Reduction in lipid with age , illness, malnutrition or hormonal decline • Increased transpiration relative to envirnmental water content • loss of integrity of water reservoir of horny layer; • Chapping by industrial / domestic. • Low environmental humidity, dry,cold winds • Repeated minor trauma. • Percutaneous absorption thru damaged epidermis is increased, contact irritants may further damage skin.
- 33. • Exact pathogenesisof skin changes is obscure. • Amino acid content of skin is lower in more severe cases • A decrease in keratohyaline‐derived natural moisturizers • Ederly persons with decreased sebaceous and sweat gland activity, patients on antiandrogen therapy • Diuretics - impo contributory factor in elderly people. • Cimetidine has also been reported to cause asteatotic dermatitis , as have topical corticosteroids.
- 34. Clinical features • HistoryIrritation - intense, and worse with changes of temperature, particularly on undressing at night. • Presentation - legs, arms and hands. • Surface of backs of hands - criss‐cross fashion. • Finger pulps - dry and cracked, producing distorted prints and retaining prolonged depression after pressure (‘parchment pulps’). • Legs - superficial markings more marked and deeper . • Fissures - may become haemorrhagic.
- 35. • Clinical variants: Generalized forms involving trunk as well as legs rare - but should raise suspicion of malignancy. • Association with malignant lymphoma, angioimmunoblastic lymphadenopathy, anaplastic gastric adenocarcinoma and spheroidal cell carcinoma of thebreast • Complications and co‐morbidities - secondary infection . • Nummular dermatitis can occur with asteatotic eczema, although relationship uncertain. • Disease course and prognosis Without Rx – chronic, relapsing each winter , clearing in summer, eventually becoming permanent.
- 36. • Investigations -in generalized form. • Management Humidify central heating where possible, abrupt temperature changes should be avoided. • Wool - poorly tolerated . • Baths – best restricted , should not be hot. • Emollients - use after bathing and during day. • Prescribe soap substitutes • Weak topical CS , those in urea base - appropriate as urea encourages hydration. Among the older , ichthammol is of value.
- 37. Dermatitis and eczemaoff the handds • hand eczema implies that the dermatitis is largely confined to the hands, with only minor involvement of other areas.
- 39. Epidemiology • Crude incidenceof self‐reported hand eczema - 5.5 /r 1000 person‐years in retrospective study from Sweden. • Age : In women, peaks in young adults , decline with increasing age. • Sex : 2F > M • Associated diseases: history of atopic eczema elsewhere
- 40. Pathophysiology • Predisposing factors:Atopy, naturally dry skin, or superadded contact allergic or irritant dermatitis. • The common link - filaggrin gene mutations - more likely to develop digital fissures • Role of stress - difficult to evaluate, disease itself is very stressful. • Preport of exacerbations with acute anxiety present. • Occasionally, - history of premenstrual exacerbation, or deterioration during pregnancy +nt.
- 41. • Pathology :differences between various forms - clinical rather than histological. • Environmental factors : Contact irritants - commonest exogenous cause • Contact allergens eg. chromate, epoxy glues and rubber also imp. • Occupations - hairdressers, fish industry workers, farmers, construction workers, dental and medical personnel, metal workers and caterers etc
- 42. • Type 1allergic rxns to certain proteins - hand eczema eg. those who prepare seafood. • Amongst HCWs , rxns to natural rubber latex protein in latex gloves – problem - contact urticaria to rhinitis, asthma and anaphylaxis • Oral ingestion of allergens (nickel, chromium or balsam of Peru) - aggravate hand eczema in sensitized subjects • Cold dry air play some part.
- 43. • Clinical features •Particular attention to patient’s occupational and recreational activities – potential contact allergies. • Severe impact on QOL - due to pruritus, painful fissuring, loss of dexterity and impairment of social functioning. • Median DLQI scores - 7.0 and 8.0 in males and females, respectively.
- 44. Clinical variants • Hyperkeratoticpalmar eczema - highly irritable, scaly, fissured, hyperkeratotic patches on palms and palmar surfaces of the fingers • Common, 2–5% of all applications for permanent disability pensions in some western European countries .
- 45. • Pompholyx. oedemafluid accumulates to form visible vesicles or bullae. • Because of thick epidermis, blisters become relatively large before bursting. • 5–20% of cases of hand eczema. • Chronic, recurrent vesiculation without periods of remission -chronic vesicular dermatitis.
- 46. • Apron eczema- involves proximal palmar aspect of two or > adjacent fingers and contiguous palmar skin over MCP joints - resembling apron • Chronic acral dermatitis - distinctive syndrome - middle age. • Chronic, intensely pruritic, hyperkeratotic, papulovesicular eczema with elevated IgE levels with no history of atopy. • Responds to oral CS, response to topical therapy is poor. • Nummular dermatitis
- 47. • Fingertip eczema- involves palmar surface of tips of fingers. • Skin - dry, cracked, sometimes breaks down into painful fissures • Two patterns – 1st MC involves most / all fingers- dominant hand (thumb and forefinger). • Worse in winter , improves on holiday. • A cumulative irritant dermatitis; patch tests are negative • 2nd pattern - thumb, forefinger and third finger of one hand. • Occupational and may be either irritant or allergic • patch testing (and 20 min contact tests) may be rewarding.
- 48. • Gut’/slaughterhouse eczema-Workers who eviscerate and clean pig carcasses - vesicular eczema which starts in finger webs and spreads to sides • Mild, self limiting condition • Workers in Danish bacon factories call this ‘fat eczema’, • Patchy vesiculosquamous eczema. amixture of irregular, patchy, vesiculosquamous lesions on both hands, usually asymmetrical. • In contrast to discoid hand eczema, degree of activity and distribution of the lesions vary. • Nail changes - common if the nail folds areaffected.
- 49. • Recurrent focalpalmar peeling - desquamation enaires, keratolysis exfoliativa , ringed keratolysis of the palms. • During summers , superficial, white desquamation develop on the sides of the fingers and on palms or feet • Appear abruptly, expand before peeling off. • Little / no irritation. •
- 50. • Ring eczemayoung women, rarely men. • Irritable patch of eczema begins under ring – usually broad wedding ring – and typically spreads • Nickel, cobalt and even chromium sensitivity - commonly found on patch testing • Probably due to concentrations of soap beneath rings, microtrauma, also play a role.
- 51. Differentials • Psoriasis • Tineamanuum • Lichen planus • Palmoplantar pustulosis • Pemphigoid, linear IgA disease and pemphigoid gestationis
- 53. • Alitretinoin –vitamin A derivative. • According to the Cochrane review, alitretinoin 30 mg achieved investigator-rated control in 432 compared with 157 participants per 1000 with placebo. • In study, 28 patients with chronic palmar eczema were treated by soaking hands - water containing 1 mg/L 8-MOP for 15 minutes, immediately followed by exposure to increasing doses of PUVA, starting with 0.5 J/cm2. • Rx - four times per week up to 25 treatments. • Excellent to good response - 93% of 14 patients having pompholyx and 86% of 14 patients with hyperkeratotic hand eczema. High doses of UVB give comparable results. Shortwave UVB has been used with success in chronic hand eczema.
- 54. • Acitretin -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.
- 55. • In anobservational prospective study, 47 adult patients with hand eczema and atopic dermatitis – dupilumab at a 600 mg loading dose, followed by 300 mg every 2 weeks. • Primary outcome was a minimum improvement of 75% on the hand eczema severity index after 16 weeks (HECSI-75). HECSI- 75 was achieved by 28 (60%) • JAK inhibitors. - small molecules, may penetrate the epidermal barrier thus being of potential not only for systemic, but also for topical use in hand eczema. • Delgocitinib pan-JAK inhibitor specific for JAK1, JAK2, JAK3 and TYK2 kinases. - suitable therapeutic agent for topical use in hand eczema.
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Editor's Notes
- #14 If primary lesion is acutely inflamed, the eruption increases in severity If local lesion settles , eruption will subside, will recur very readily if local lesion relapses.
- #15 It is believed that eczema patients have a lower threshold for irritation. A mild irritant sets up a severe irritation on their skin with subsequent dissemination.1