Eczema Rangeen

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Eczema Rangeen

  1. 1. ECZEMA RANGEEN CHANDRAN R
  2. 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. 3. CLASSIFICATIONENDOGENOUS EXOGENOUS COMBINEDSeborrheic Irritant Atopicdermatitis dermatitis dermatitisNummular Allergic Pompholyxdermatitis dermatitisLichen simplex PhotodermatitischronicusPityriasis alba Radiation dermatitisStasis Infectivedermatitis dermatitisAsteatoticeczema.
  4. 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. 5. CLINICAL FEATURES The inflammatory changes of eczema evolve through two stages: ◦ Acute eczematous inflammation ◦ Chronic eczematous inflammation
  6. 6. ACUTE ECZEMACLINICAL FEATURES- Intense itching Intense erythema Oedema Papulovesicles Oozing
  7. 7. CHRONIC ECZEMACLINICAL FEATURES Dryness of skin Excoriation Fissuring Lichenification
  8. 8. COMPLICATIONSDERMATOLOGICAL PSYCHOSOCIAL Infections.  Anxiety Ide eruption  Depressions Contact dermatitis  Social complications Erythroderma  Wage loss  Debility  Social ostracism
  9. 9. ITCH SCRATCH CYCLE
  10. 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. 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. 12. PATCH TEST
  13. 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. 14. COMBINED ECZEMAS
  15. 15. ATOPIC DERMATITIS
  16. 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. 17. ATOPIC TRIAD Atopic Dermatitis Allergic Asthma Rhinitis
  18. 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. 19. CLINICAL FEATURES Shows 3 distinct patterns1. Infantile phase.2. Childhood phase.3. Adult phase.
  20. 20. INFANTILE PHASE 3 months-2years. Itchy papules and vesicles,becoming exudative. Begins on face;can involve rest of body. Spares diaper area.
  21. 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. 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. 23. Dirty neck sign
  24. 24. COMPLICATIONS1. Bacterial infections-Impetigo2. Viral infections Herpes simplex,molluscum contagiosum,HPVinfection.3. Fungal infections4. Poor growth5. Side effects of steroids.
  25. 25. Atopic dermatitisManagement First-line treatment Second-line treatment Third-line treatment Counselling; occupational advice
  26. 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. 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. 28. Management of AtopicdermatitisSecond-line treatment Intensive topical therapy Wet wrap technique Allergy management ◦ Food ◦ Inhalants ◦ Contact allergy
  29. 29. Management of AtopicdermatitisThird-line treatment Phototherapy Oral immunosuppresants ◦ Cyclosporine ◦ Azathriopine ◦ Thymopentine ◦ α- Interferon Desensitization
  30. 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. 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. 32. TREATMENT Saline soaks followed by topical steroids. Antibiotics in bacterial infection.
  33. 33. Sole dyshydrosis
  34. 34. Advanced stage of dyshidrosis onthe palm showing cracked andpeeling skin
  35. 35. EXOGENOUSDERMATITIS
  36. 36. CONTACT DERMATITIS
  37. 37. CONTACT DERMATITISReaction of skin to contactants.2 types- IRRITANT CONTACT DERMATITIS ALLERGIC CONTACT DERMATITIS.
  38. 38. IRRITANT CONTACT DERMATITISETIOLOGY Occupational/recreational exposure. Water Detergents Solvents Abrasive dusts Alkalis Cutting oils
  39. 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. 40. SITES Skin of face. Scrotum Back of hands.
  41. 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. 42. PATHOGENESIS Chemical directly injures skin without involving immunologic pathway. Develops in patients exposed to chemicals and develop with 1st exposure itself.
  43. 43. MANAGEMENTPROPHYLAXIS Complete avoidance Relative avoidance- Gloves and clothing.TREATMENT Topical steroids ointments Emollients.
  44. 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. 45. ETIOLOGYPLANTS PartheniumMETALS Nickel ChromatesCosmetics Paraphenylenediamine Formaldehyde ParabensMEDICINES Neomycine BenzocaineRUBBER Mercapto mix Thiuram mix
  46. 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. 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. 48. quaternium-15 hair dying
  49. 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. 50. PHOTOTOXIC PHOTOALLERGIC Common Less CommonNon immunological TYPE IV Hypersensitivity Sunburn Eczematous
  51. 51. Phototoxic reactions:Inducing agentsTopical Perfumes Dyes Psoralens Tars Plants (lime, celery) Systemic Psoralen Tetracycline Phenothiazine
  52. 52. Photoallergic reactions: Inducing agents Perfumes (soaps, aftershave) Sunscreens (PABA) Neomycin Halogenated compounds Parthenium (congress grass) Systemic NSAIDS Phenothiazine Thiazides
  53. 53. Papules that largely have become confluent to formplaques
  54. 54. INFECTIOUS ECZEMATOID DERMATITIS Form of dermatitis caused by the spreading of purulent material that exudes from the site of an infection.
  55. 55. ETIOLOGY Bacterial/Viral infection-Primary event Eczema-Seconadary event
  56. 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. 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. 58. Dermatophytid caused byTrichophyton rubrum
  59. 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. 60. ENDOGENOUS DERMATITIS
  61. 61. SEBORRHEICDERMATITIS
  62. 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. 63. ETIOLOGY Microbial- Overgrowth of Malassezia furfur Genetic Predisposition Immunodeficiency Associated with psoriasis and Parkinson‟s disease.
  64. 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. 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. 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. 67. LICHEN SIMPLEXCHRONICUS Neurodermatitis. Skin disorder characterized by chronic itching and scratching
  68. 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. 69. ETIOLOGY Scratching in predisposed individuals. Atopy.
  70. 70. TREATMENT Topical steroids and keratolytic agents-to break itch- scratch cycle. Antihistamines.
  71. 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. 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. 73. COMPLICATIONS1. Ulceration2. Bacterial infection-resulting in cellulitis,lymphangitis3. Allergic contact dermatitis4. Deformity-”inverted champagne” bottle appearance.5. Malignant change
  74. 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. 75. NUMMULAR ECZEMA Discoid eczema. Name comes from the Latin word “nummus," which means "coin.“ Characterized by round or oval-shaped itchy lesions
  76. 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. 77. CLINICAL FEATURES AGE/GENDERMiddle aged males. SITES:Extremities(distal parts) MORPHOLOGYExtremely itchy,multiple,sharply demarcated coinshaped vesicular/crusted plaques.
  78. 78. TREATMENT SYMPTOMATIC: Antihistamines LOCALIZED LESIONS Topical steroid+br.spectrum antibiotics EXTENSIVE LESIONS: PUVA sol/narrow band UVB
  79. 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. 80. ETIOLOGY Unknown. Public swimming pools could be a factor.
  81. 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. 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. 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. 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. 85. ETIOLOGY Old age. Dry skin Low humidity Hypothyroidism Malignancy
  86. 86. CLINICAL FEATURES Extremely itchy. Skin is dry with fine reticulate red supericial fissures
  87. 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. 88. DIFFERENTIAL DIAGNOSIS
  89. 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. 90. SCABIES IN INFANTS INFANTILE ECZEMABurrows PapulovesiclesOn palms and soles;genitalia Spares palms and solesFamily history-positive Positive for atopic diathesis
  91. 91. DERMATOPHYTIC ECZEMAINFECTIONSAnnular lesions(center Discoid lesionsrelatively clear)Exudation-Minimal/crusting Exudation/crusting/ lichenificationKOH mount-+ve for fungus -ve

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