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Eczema Rangeen

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  • 1. ECZEMA RANGEEN CHANDRAN R
  • 2.  Ekze, in Greek means “to boil over”. Eczema is an inflammatory condition of the skin that is characterized by erythema, papulo-vesicles, oozing & crusting in the acute stages & lichenification in the chronic stages
  • 3. CLASSIFICATIONENDOGENOUS EXOGENOUS COMBINEDSeborrheic Irritant Atopicdermatitis dermatitis dermatitisNummular Allergic Pompholyxdermatitis dermatitisLichen simplex PhotodermatitischronicusPityriasis alba Radiation dermatitisStasis Infectivedermatitis dermatitisAsteatoticeczema.
  • 4.  Exogenous eczemasMediated by external trigger factors; inherited tendenciesmay play a part. Endogenous eczemasMediated by internal factors; that is, processes originatingwithin the body. Combined EczemasSome types of eczema are precipitated by both externaland internal factors.
  • 5. CLINICAL FEATURES The inflammatory changes of eczema evolve through two stages: ◦ Acute eczematous inflammation ◦ Chronic eczematous inflammation
  • 6. ACUTE ECZEMACLINICAL FEATURES- Intense itching Intense erythema Oedema Papulovesicles Oozing
  • 7. CHRONIC ECZEMACLINICAL FEATURES Dryness of skin Excoriation Fissuring Lichenification
  • 8. COMPLICATIONSDERMATOLOGICAL PSYCHOSOCIAL Infections.  Anxiety Ide eruption  Depressions Contact dermatitis  Social complications Erythroderma  Wage loss  Debility  Social ostracism
  • 9. ITCH SCRATCH CYCLE
  • 10. DIAGNOSIS OF ECZEMAS Diagnosis in most cases, is clinical and based on a carefully taken history. Total IgE level to assess if the individual is atopic. Swabs for culture and sensitivity (Bacterial resistance) Microscopy: to rule out dermatophyte infection/ scabies
  • 11. PATCH TEST Relies on the principle of a type IV hypersensitivity reaction. Method used to determine if a specific substance causes allergic inflammation of the skin. Commonest antigen used-Nickel. TECHNIQUE- Antigens in standardised dilutions applied to the back and occluded. Patches removed after 48hrs;read after half hour. Another reading at 96hr detects delayed reaction.
  • 12. PATCH TEST
  • 13. INTERPRETATION Clinical Grading findingsNo reaction Normal skin 0Weak reaction Palpable 1+ erythema,infiltrationStrong reaction Infiltration,erythem 2+ a,papules and vesiclesExtreme reaction Intense 3+ erythema,papules and vesicles.Irritant reaction Cauterization IR
  • 14. COMBINED ECZEMAS
  • 15. ATOPIC DERMATITIS
  • 16.  Endogenous eczema triggered by exogenous agents Characterised by Pruritic,recurrent,symmetric eczematous lesions Characteristic site of involvement Personal/family historyof atopic diathesis. Increased ability to form IgE.
  • 17. ATOPIC TRIAD Atopic Dermatitis Allergic Asthma Rhinitis
  • 18. ETIOLOGY Strong genetic  Contributing factors predisposition. 1. Anxiety. Raised IgE level. 2. Temperature change. 3. Decreased humidity 4. Contact with irritants 5. Allergens 6. Microbial agents
  • 19. CLINICAL FEATURES Shows 3 distinct patterns1. Infantile phase.2. Childhood phase.3. Adult phase.
  • 20. INFANTILE PHASE 3 months-2years. Itchy papules and vesicles,becoming exudative. Begins on face;can involve rest of body. Spares diaper area.
  • 21. CHILDHOOD PHASE 2-12 years. Dry,leathery and itchy plaques. Charecteristic feature-Lichenification. Site-elbow and knee flexors. Pallor of the face is common; erythema and scaling occur around the eyes
  • 22. ADULT PHASE 12 years onwards. Lesions become more diffuse with an underlying background of erythema. Face and flexural areas are commonly involved and is dry and scaly. Xerosis is prominent. Lichenification may be present.
  • 23. Dirty neck sign
  • 24. COMPLICATIONS1. Bacterial infections-Impetigo2. Viral infections Herpes simplex,molluscum contagiosum,HPVinfection.3. Fungal infections4. Poor growth5. Side effects of steroids.
  • 25. Atopic dermatitisManagement First-line treatment Second-line treatment Third-line treatment Counselling; occupational advice
  • 26. Management of AtopicdermatitisFirst-line treatment Identify and control „flare factors‟ Topical treatments ◦ Bathing; Emollients; Humectants ◦ Corticosteroids ◦ Calcineurin inhibitors: Pimecrolimus; tacrolimus ◦ Icthamol and tar
  • 27. Management of AtopicdermatitisFirst-line treatment Oral treatment 1. Antihistamines  Sedative antihistamines preferred  Promethazine; trimeperazine; hydroxyzine 2. Antibiotics 3. Systemic steriods (in severe cases)
  • 28. Management of AtopicdermatitisSecond-line treatment Intensive topical therapy Wet wrap technique Allergy management ◦ Food ◦ Inhalants ◦ Contact allergy
  • 29. Management of AtopicdermatitisThird-line treatment Phototherapy Oral immunosuppresants ◦ Cyclosporine ◦ Azathriopine ◦ Thymopentine ◦ α- Interferon Desensitization
  • 30. POMPHOLYX Dyshydrotic eczema/acute vesiculobullous hand eczema It is a skin condition that is characterized by small blisters on the hands or feet.
  • 31. CLINICAL FEATURES Summer aggravation. Recurrent episode of deep seated,bland looking vesicles(blisters) Vesicles resolve gradually in 3 to 4 weeks, and may be followed by chronic eczematous changes. Sites-fingers,palms and soles.
  • 32. TREATMENT Saline soaks followed by topical steroids. Antibiotics in bacterial infection.
  • 33. Sole dyshydrosis
  • 34. Advanced stage of dyshidrosis onthe palm showing cracked andpeeling skin
  • 35. EXOGENOUSDERMATITIS
  • 36. CONTACT DERMATITIS
  • 37. CONTACT DERMATITISReaction of skin to contactants.2 types- IRRITANT CONTACT DERMATITIS ALLERGIC CONTACT DERMATITIS.
  • 38. IRRITANT CONTACT DERMATITISETIOLOGY Occupational/recreational exposure. Water Detergents Solvents Abrasive dusts Alkalis Cutting oils
  • 39. PREDISPOSINGFACTORS PATIENT FACTORS  ENVIRONMENTAL FACTORS Dry skin  Persons in occupations Atopic individuals of : ◦ Hairdressing ◦ Medical, dental, veterinary ◦ Food preparation, catering, fishing ◦ Printing and painting, metal work ◦ Construction
  • 40. SITES Skin of face. Scrotum Back of hands.
  • 41. CLINICAL FEATURES Spectrum of features ranging from dryness,redness or chapping to an acute caustic burn. Acute Exudative Lesions- Exposure to a strong irritant. Dry Dermatic Lesions- Chronic repeated exposure to a weak irritant.
  • 42. PATHOGENESIS Chemical directly injures skin without involving immunologic pathway. Develops in patients exposed to chemicals and develop with 1st exposure itself.
  • 43. MANAGEMENTPROPHYLAXIS Complete avoidance Relative avoidance- Gloves and clothing.TREATMENT Topical steroids ointments Emollients.
  • 44. ALLERGIC CONTACTDERMATITIS Allergic contact dermatitis (ACD) is a delayed type of induced sensitivity (allergy) resulting from cutaneous contact with a specific allergen to which the patient has developed a specific sensitivity. This allergic reaction causes inflammation of the skin manifested by varying degrees of erythema, edema, and vesiculation.
  • 45. ETIOLOGYPLANTS PartheniumMETALS Nickel ChromatesCosmetics Paraphenylenediamine Formaldehyde ParabensMEDICINES Neomycine BenzocaineRUBBER Mercapto mix Thiuram mix
  • 46. PATHOGENESIS Type IV hypersensitivity reaction to exogenous antigens. Antigen Processed by antigen presenting cells Processed antigen+Sensitised lymphocytes Multiplication of lymphocytes Release cytokines Skin injury(inflammation,itching and rashes)
  • 47. CLINICAL FEATURESMORPHOLOGY ACUTE ECZEMAo Progress from erythema to edema to papulovesiculation.o Manifest as edema in eyelids and genitalia. CHRONIC ECZEMAo Itchy lichenified plaques.
  • 48. quaternium-15 hair dying
  • 49. PHOTOCONTACTDERMATITIS Eczematous condition triggered by an interaction between an unharmful or less harmful substance on the skin and ultraviolet light. Distribution typically on the light exposed areas of the skin. Two types:1. Phototoxic2. Photoallergic
  • 50. PHOTOTOXIC PHOTOALLERGIC Common Less CommonNon immunological TYPE IV Hypersensitivity Sunburn Eczematous
  • 51. Phototoxic reactions:Inducing agentsTopical Perfumes Dyes Psoralens Tars Plants (lime, celery) Systemic Psoralen Tetracycline Phenothiazine
  • 52. Photoallergic reactions: Inducing agents Perfumes (soaps, aftershave) Sunscreens (PABA) Neomycin Halogenated compounds Parthenium (congress grass) Systemic NSAIDS Phenothiazine Thiazides
  • 53. Papules that largely have become confluent to formplaques
  • 54. INFECTIOUS ECZEMATOID DERMATITIS Form of dermatitis caused by the spreading of purulent material that exudes from the site of an infection.
  • 55. ETIOLOGY Bacterial/Viral infection-Primary event Eczema-Seconadary event
  • 56. CLINICAL FEATURES Seen around discharging wounds and ulcers Presents as an area of advancing erythema sometimes with microvesicles at the edge around the lesion
  • 57. DERMATOPHYTID Eczematous reaction that occurs as an allergic response to a dermatophyte infection elsewhere on the skin Most common dermatophytid is an inflammation in the hands resulting from a fungus infection of the feet.
  • 58. Dermatophytid caused byTrichophyton rubrum
  • 59. Diagnostic criteria A proven focus of dermatophyte infection. A positive skin test to a group-specific trichophytin antigen. Absence of fungi in the dermatophytid lesion. Clearing of the dermatophytid after the eradication of the primary fungal infection.
  • 60. ENDOGENOUS DERMATITIS
  • 61. SEBORRHEICDERMATITIS
  • 62.  Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. SITES- Scalp,eyebrows,nasolabial folds,retroauriculararea presternal and interscapular regions. EPIDEMIOLOGY- Age- Onset at puberty;peaks at 40yrs. Gender- Common in males
  • 63. ETIOLOGY Microbial- Overgrowth of Malassezia furfur Genetic Predisposition Immunodeficiency Associated with psoriasis and Parkinson‟s disease.
  • 64. CLINICAL FEATURES INFANTILE SEBORRHEIC DERMATITIS Commonly affects within first 3 months of life; affects both sexes equally. Begins as cradle cap. Lesions comprise tiny papules covered with yellow, greasy scales; and redness in the diaper area and axillae.
  • 65. CLINICAL FEATURES ADULTS Affects hairy areas; mostly men (30 to 60 years). Scalp: Earliest sign is dandruff; later followed by greasy scales and retroauricular fissuring. Face: Scaling; erythema of eyebrows, nasolabial folds; and squamous blepharitis may occur. Trunk: Papules, greasy scales, petaloid pattern. Flexural areas: Marginated erythema, greasy scaling and secondary infection.
  • 66. TREATMENT Topical therapy  Systemic Therapy1. Topical antifungals  In extensive lesions and HIV+ve patients. Topical ketoconazole,selenium  Include antibiotics and sulphide and ciclopirox. antifungal agents(fluconazole/itraco2. Topical steroids nazole) Combined with antifungal agents in flexural and exudative lesions. Combined with salicylic acid in recalcitrant lesions of scalp.
  • 67. LICHEN SIMPLEXCHRONICUS Neurodermatitis. Skin disorder characterized by chronic itching and scratching
  • 68. CLINICAL FEATURES Symptoms-extremely itchy MORPHOLOGY-Single/multiple lichenified plaques Lesion reappear after treatment is stopped Commonly affects adults (30 to 50 years); often in atopics SITES-Nape of neck in women,legs in men,anogenital area in both.
  • 69. ETIOLOGY Scratching in predisposed individuals. Atopy.
  • 70. TREATMENT Topical steroids and keratolytic agents-to break itch- scratch cycle. Antihistamines.
  • 71. STASIS ECZEMA Gravitational eczema/Venous eczema Refers to the skin changes that occur in the leg as a result of "stasis" or blood pooling from insufficient venous return. ETIOLOGY: Secondary to venous hypertension. Late sequel of previous deep vein thrombosis. SITE-Lower third of leg(medial malleolus)
  • 72. CLINICAL FEATURES Begins with pedal edema around ankles. Over period of time,brownish pigmentation appears(punctate initially and later confluent) LIPODERMATOSCLEROSIS- Long standing case presents with ivory whitesiderotic plaques with dilated capillary loops.
  • 73. COMPLICATIONS1. Ulceration2. Bacterial infection-resulting in cellulitis,lymphangitis3. Allergic contact dermatitis4. Deformity-”inverted champagne” bottle appearance.5. Malignant change
  • 74. Management Leg elevation; weight reduction in obese patients. Compression by regular use of firm elastic bandage or well fitting stockings. Sedative antihistamines Topical steroids. Systemic antibiotics for secondary bacterial infection.
  • 75. NUMMULAR ECZEMA Discoid eczema. Name comes from the Latin word “nummus," which means "coin.“ Characterized by round or oval-shaped itchy lesions
  • 76. ETIOLOGY Unknown in many case. Frequent association with atopy Reaction to bacterial antigens has been suspected. Can also be worsened by stress and caffeine, which dehydrates the body and thus the skin
  • 77. CLINICAL FEATURES AGE/GENDERMiddle aged males. SITES:Extremities(distal parts) MORPHOLOGYExtremely itchy,multiple,sharply demarcated coinshaped vesicular/crusted plaques.
  • 78. TREATMENT SYMPTOMATIC: Antihistamines LOCALIZED LESIONS Topical steroid+br.spectrum antibiotics EXTENSIVE LESIONS: PUVA sol/narrow band UVB
  • 79. PITYRIASIS ALBA Common skin condition mostly occurring in children and usually seen as dry, fine-scaled, pale patches on the face. Characterized by asymptomatic, slightly elevated, hypopigmented, scaly patches; indistinct borders.
  • 80. ETIOLOGY Unknown. Public swimming pools could be a factor.
  • 81.  Affects children (3 to 16 years) and disappears in early adulthood; may be a manifestation of atopic dermatitis. SITES:Face, perioral area, chin and cheeks; lateral aspect of the upper arm; and thighs. Hypopigmentation appears prominent in dark skinned patients and during summer as it stands out against the tanned skin
  • 82. CLINICAL FEATURES Individual lesions develop through 3 stages and sometimes are itchy: Raised and red - although the redness is often mild and not noticed by parents Raised and pale. Smooth flat pale patches.
  • 83. TREATMENTManagement Self-limiting condition; hypopigmentation is not due to vitiligo. Emollients to control scaling. Sunscreens. Short course of a topical steroid for actively inflammed lesions.
  • 84. ASTEATOTIC ECZEMA Eczema craquelé Form of eczema that is characterized by changes that occur when skin becomes abnormally dry, itchy, and cracked. Common in old people.
  • 85. ETIOLOGY Old age. Dry skin Low humidity Hypothyroidism Malignancy
  • 86. CLINICAL FEATURES Extremely itchy. Skin is dry with fine reticulate red supericial fissures
  • 87. Management Advise to live in a warm room; avoid exposure to cold winds. Wear woollen clothing over the cottons, avoid direct contact with wool. Restrict bathing with very hot water; and use of soaps and detergents. Application of emollient, immediately after bathing frequently thereafter to keep the skin moisturized. Substituting aqueous cream for soap prevent recurrence.
  • 88. DIFFERENTIAL DIAGNOSIS
  • 89. PSORIASIS ECZEMAModerately itchy.Scratching Very itchy.Scratching resultsresults in bleeding in oozing.Well defined indurated Not so well defined and notplaques. indurated.Surmounted with silvery Scale-crust.scales.Nail changes-Typical Variable.Auspitz sign-Positive Negative
  • 90. SCABIES IN INFANTS INFANTILE ECZEMABurrows PapulovesiclesOn palms and soles;genitalia Spares palms and solesFamily history-positive Positive for atopic diathesis
  • 91. DERMATOPHYTIC ECZEMAINFECTIONSAnnular lesions(center Discoid lesionsrelatively clear)Exudation-Minimal/crusting Exudation/crusting/ lichenificationKOH mount-+ve for fungus -ve