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ECZEMA

    RANGEEN CHANDRAN R
 '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
CLASSIFICATION
ENDOGENOUS EXOGENOUS                COMBINED


Seborrheic        Irritant          Atopic
dermatitis        dermatitis        dermatitis
Nummular          Allergic          Pompholyx
dermatitis        dermatitis
Lichen simplex    Photodermatitis
chronicus
Pityriasis alba   Radiation
                  dermatitis
Stasis            Infective
dermatitis        dermatitis
Asteatotic
eczema.
 Exogenous eczemas
Mediated by external trigger factors; inherited tendencies
may play a part.


 Endogenous eczemas
Mediated by internal factors; that is, processes originating
within the body.


 Combined Eczemas
Some types of eczema are precipitated by both external
and internal factors.
CLINICAL FEATURES


 The inflammatory changes of eczema
  evolve through two stages:
 ◦ Acute eczematous inflammation
 ◦ Chronic eczematous inflammation
ACUTE ECZEMA

CLINICAL FEATURES-
   Intense itching
   Intense erythema
   Oedema
   Papulovesicles
   Oozing
CHRONIC ECZEMA


CLINICAL FEATURES
   Dryness of skin
   Excoriation
   Fissuring
   Lichenification
COMPLICATIONS


DERMATOLOGICAL         PSYCHOSOCIAL
 Infections.           Anxiety
 Ide eruption          Depressions
 Contact dermatitis    Social complications
 Erythroderma          Wage loss
                        Debility
                        Social ostracism
ITCH SCRATCH CYCLE
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
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.
PATCH TEST
INTERPRETATION

                    Clinical                Grading
                    findings
No reaction         Normal skin             0

Weak reaction       Palpable                1+
                    erythema,infiltration
Strong reaction     Infiltration,erythem    2+
                    a,papules and
                    vesicles
Extreme reaction    Intense                 3+
                    erythema,papules
                    and vesicles.
Irritant reaction   Cauterization           IR
COMBINED ECZEMAS
ATOPIC DERMATITIS
 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.
ATOPIC TRIAD

         Atopic
        Dermatitis




                     Allergic
   Asthma
                     Rhinitis
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
CLINICAL FEATURES



 Shows 3 distinct patterns
1. Infantile phase.
2. Childhood phase.
3. Adult phase.
INFANTILE PHASE



 3 months-2years.
 Itchy papules and vesicles,becoming exudative.
 Begins on face;can involve rest of body.
 Spares diaper area.
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
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.
Dirty neck sign
COMPLICATIONS

1. Bacterial infections-Impetigo
2. Viral infections
    Herpes simplex,molluscum contagiosum,HPV
infection.
3. Fungal infections
4. Poor growth
5. Side effects of steroids.
Atopic dermatitis




Management
 First-line treatment
 Second-line treatment
 Third-line treatment
 Counselling; occupational advice
Management of Atopic
dermatitis



First-line treatment
 Identify and control „flare factors‟
 Topical treatments
 ◦ Bathing; Emollients; Humectants
 ◦   Corticosteroids
 ◦   Calcineurin inhibitors: Pimecrolimus; tacrolimus
 ◦   Icthamol and tar
Management of Atopic
dermatitis



First-line treatment
 Oral treatment
  1. Antihistamines
   Sedative antihistamines preferred
   Promethazine; trimeperazine; hydroxyzine
 2. Antibiotics
 3. Systemic steriods (in severe cases)
Management of Atopic
dermatitis


Second-line treatment
 Intensive topical therapy
 Wet wrap technique
 Allergy management
  ◦ Food
  ◦ Inhalants
  ◦ Contact allergy
Management of Atopic
dermatitis

Third-line treatment
 Phototherapy
 Oral immunosuppresants
  ◦ Cyclosporine
  ◦ Azathriopine
  ◦ Thymopentine
 ◦ α- Interferon
 Desensitization
POMPHOLYX



 Dyshydrotic eczema/acute vesiculobullous hand
  eczema
 It is a skin condition that is characterized by
  small blisters on the hands or feet.
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.
TREATMENT



 Saline soaks followed by topical steroids.
 Antibiotics in bacterial infection.
Sole dyshydrosis
Advanced stage of dyshidrosis on
the palm showing cracked and
peeling skin
EXOGENOUS
DERMATITIS
CONTACT DERMATITIS
CONTACT DERMATITIS


Reaction of skin to contactants.
2 types-
 IRRITANT CONTACT DERMATITIS
 ALLERGIC CONTACT DERMATITIS.
IRRITANT CONTACT
        DERMATITIS
ETIOLOGY
 Occupational/recreational exposure.



     Water
     Detergents
     Solvents
     Abrasive dusts
     Alkalis
     Cutting oils
PREDISPOSING
FACTORS
 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
SITES



 Skin of face.
 Scrotum
 Back of hands.
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.
PATHOGENESIS



 Chemical directly injures skin without involving
  immunologic pathway.
 Develops in patients exposed to chemicals and
  develop with 1st exposure itself.
MANAGEMENT

PROPHYLAXIS
 Complete avoidance
 Relative avoidance-
  Gloves and clothing.

TREATMENT
 Topical steroids ointments
 Emollients.
ALLERGIC CONTACT
DERMATITIS

 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.
ETIOLOGY

PLANTS      Parthenium
METALS      Nickel
            Chromates
Cosmetics   Paraphenylenediamine
            Formaldehyde
            Parabens
MEDICINES   Neomycine
            Benzocaine
RUBBER      Mercapto mix
            Thiuram mix
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)
CLINICAL FEATURES

MORPHOLOGY
   ACUTE ECZEMA

o Progress from erythema to edema to
  papulovesiculation.
o Manifest as edema in eyelids and genitalia.
   CHRONIC ECZEMA
o Itchy lichenified plaques.
quaternium-15   hair dying
PHOTOCONTACT
DERMATITIS
 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. Phototoxic
2. Photoallergic
PHOTOTOXIC         PHOTOALLERGIC
    Common            Less Common
Non immunological        TYPE IV
                     Hypersensitivity
    Sunburn            Eczematous
Phototoxic reactions:
Inducing agents
Topical
   Perfumes
   Dyes
   Psoralens
   Tars
   Plants (lime, celery)

 Systemic
 Psoralen
 Tetracycline
 Phenothiazine
Photoallergic reactions:
      Inducing agents
   Perfumes (soaps, aftershave)
   Sunscreens (PABA)
   Neomycin
   Halogenated compounds
   Parthenium (congress grass)

 Systemic
 NSAIDS
 Phenothiazine
 Thiazides
Papules that largely have become confluent to form
plaques
INFECTIOUS
             ECZEMATOID
             DERMATITIS


 Form of dermatitis caused by the spreading of purulent
  material that exudes from the site of an infection.
ETIOLOGY



 Bacterial/Viral infection-Primary event
 Eczema-Seconadary event
CLINICAL FEATURES


 Seen around discharging wounds and ulcers
 Presents as an area of advancing erythema
  sometimes with microvesicles at the edge around
  the lesion
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.
Dermatophytid caused by
Trichophyton rubrum
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.
ENDOGENOUS DERMATITIS
SEBORRHEIC
DERMATITIS
 Seborrheic dermatitis is a papulosquamous
  disorder patterned on the sebum-rich areas of the
  scalp, face, and trunk.
 SITES-
   Scalp,eyebrows,nasolabial folds,retroauricular
area presternal and interscapular regions.
 EPIDEMIOLOGY-
 Age-
  Onset at puberty;peaks at 40yrs.
 Gender-
  Common in males
ETIOLOGY


 Microbial-
     Overgrowth of Malassezia furfur
 Genetic Predisposition
 Immunodeficiency
 Associated with psoriasis and Parkinson‟s disease.
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.
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.
TREATMENT
 Topical therapy             Systemic Therapy
1. Topical antifungals        In extensive lesions and
                               HIV+ve patients.
 Topical
  ketoconazole,selenium       Include antibiotics and
  sulphide and ciclopirox.     antifungal
                               agents(fluconazole/itraco
2. Topical steroids            nazole)
 Combined with
  antifungal agents in
  flexural and exudative
  lesions.
 Combined with salicylic
  acid in recalcitrant
  lesions of scalp.
LICHEN SIMPLEX
CHRONICUS


 Neurodermatitis.
 Skin disorder characterized by chronic itching and
  scratching
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.
ETIOLOGY



 Scratching in predisposed individuals.
 Atopy.
TREATMENT



 Topical steroids and keratolytic agents-to break itch-
  scratch cycle.
 Antihistamines.
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)
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 white
siderotic plaques with dilated capillary loops.
COMPLICATIONS

1. Ulceration
2. Bacterial infection-resulting in
   cellulitis,lymphangitis
3. Allergic contact dermatitis
4. Deformity-”inverted champagne” bottle
   appearance.
5. Malignant change
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.
NUMMULAR ECZEMA


 Discoid eczema.
 Name comes from the Latin word “nummus,"
  which means "coin.“
 Characterized by round or oval-shaped itchy
  lesions
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
CLINICAL FEATURES

 AGE/GENDER
Middle aged males.
 SITES:
Extremities(distal parts)
 MORPHOLOGY
Extremely itchy,multiple,sharply demarcated coin
shaped vesicular/crusted plaques.
TREATMENT


 SYMPTOMATIC:
      Antihistamines
 LOCALIZED LESIONS
     Topical steroid+br.spectrum antibiotics
 EXTENSIVE LESIONS:
     PUVA sol/narrow band UVB
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.
ETIOLOGY



 Unknown.
 Public swimming pools could be a factor.
 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
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.
TREATMENT

Management
 Self-limiting condition; hypopigmentation is not due
  to vitiligo.
 Emollients to control scaling.
 Sunscreens.
 Short course of a topical steroid for actively
  inflammed lesions.
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.
ETIOLOGY



 Old age.
 Dry skin
 Low humidity
 Hypothyroidism
 Malignancy
CLINICAL FEATURES



 Extremely itchy.
 Skin is dry with fine reticulate red supericial
  fissures
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.
DIFFERENTIAL
 DIAGNOSIS
PSORIASIS                     ECZEMA

Moderately itchy.Scratching   Very itchy.Scratching results
results in bleeding           in oozing.

Well defined indurated        Not so well defined and not
plaques.                      indurated.

Surmounted with silvery       Scale-crust.
scales.

Nail changes-Typical          Variable.

Auspitz sign-Positive         Negative
SCABIES IN INFANTS             INFANTILE ECZEMA



Burrows                        Papulovesicles



On palms and soles;genitalia   Spares palms and soles



Family history-positive        Positive for atopic diathesis
DERMATOPHYTIC                ECZEMA
INFECTIONS


Annular lesions(center       Discoid lesions
relatively clear)


Exudation-Minimal/crusting   Exudation/crusting/
                             lichenification


KOH mount-+ve for fungus     -ve
Eczema Rangeen

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Eczema Rangeen

  • 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. CLASSIFICATION ENDOGENOUS EXOGENOUS COMBINED Seborrheic Irritant Atopic dermatitis dermatitis dermatitis Nummular Allergic Pompholyx dermatitis dermatitis Lichen simplex Photodermatitis chronicus Pityriasis alba Radiation dermatitis Stasis Infective dermatitis dermatitis Asteatotic eczema.
  • 4.  Exogenous eczemas Mediated by external trigger factors; inherited tendencies may play a part.  Endogenous eczemas Mediated by internal factors; that is, processes originating within the body.  Combined Eczemas Some types of eczema are precipitated by both external and internal factors.
  • 5. CLINICAL FEATURES  The inflammatory changes of eczema evolve through two stages: ◦ Acute eczematous inflammation ◦ Chronic eczematous inflammation
  • 6. ACUTE ECZEMA CLINICAL FEATURES-  Intense itching  Intense erythema  Oedema  Papulovesicles  Oozing
  • 7. CHRONIC ECZEMA CLINICAL FEATURES  Dryness of skin  Excoriation  Fissuring  Lichenification
  • 8. COMPLICATIONS DERMATOLOGICAL PSYCHOSOCIAL  Infections.  Anxiety  Ide eruption  Depressions  Contact dermatitis  Social complications  Erythroderma  Wage loss  Debility  Social ostracism
  • 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.
  • 13. INTERPRETATION Clinical Grading findings No reaction Normal skin 0 Weak reaction Palpable 1+ erythema,infiltration Strong reaction Infiltration,erythem 2+ a,papules and vesicles Extreme reaction Intense 3+ erythema,papules and vesicles. Irritant reaction Cauterization IR
  • 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 patterns 1. 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.
  • 22.
  • 23. 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
  • 24.
  • 25. 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.
  • 27.
  • 28. COMPLICATIONS 1. Bacterial infections-Impetigo 2. Viral infections Herpes simplex,molluscum contagiosum,HPV infection. 3. Fungal infections 4. Poor growth 5. Side effects of steroids.
  • 29. Atopic dermatitis Management  First-line treatment  Second-line treatment  Third-line treatment  Counselling; occupational advice
  • 30. Management of Atopic dermatitis First-line treatment  Identify and control „flare factors‟  Topical treatments ◦ Bathing; Emollients; Humectants ◦ Corticosteroids ◦ Calcineurin inhibitors: Pimecrolimus; tacrolimus ◦ Icthamol and tar
  • 31. Management of Atopic dermatitis First-line treatment  Oral treatment 1. Antihistamines  Sedative antihistamines preferred  Promethazine; trimeperazine; hydroxyzine 2. Antibiotics 3. Systemic steriods (in severe cases)
  • 32. Management of Atopic dermatitis Second-line treatment  Intensive topical therapy  Wet wrap technique  Allergy management ◦ Food ◦ Inhalants ◦ Contact allergy
  • 33. Management of Atopic dermatitis Third-line treatment  Phototherapy  Oral immunosuppresants ◦ Cyclosporine ◦ Azathriopine ◦ Thymopentine ◦ α- Interferon  Desensitization
  • 34. POMPHOLYX  Dyshydrotic eczema/acute vesiculobullous hand eczema  It is a skin condition that is characterized by small blisters on the hands or feet.
  • 35.
  • 36. 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.
  • 37. TREATMENT  Saline soaks followed by topical steroids.  Antibiotics in bacterial infection.
  • 39. Advanced stage of dyshidrosis on the palm showing cracked and peeling skin
  • 42. CONTACT DERMATITIS Reaction of skin to contactants. 2 types-  IRRITANT CONTACT DERMATITIS  ALLERGIC CONTACT DERMATITIS.
  • 43. IRRITANT CONTACT DERMATITIS ETIOLOGY  Occupational/recreational exposure. Water Detergents Solvents Abrasive dusts Alkalis Cutting oils
  • 44. PREDISPOSING FACTORS  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
  • 45. SITES  Skin of face.  Scrotum  Back of hands.
  • 46.
  • 47.
  • 48. 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.
  • 49. PATHOGENESIS  Chemical directly injures skin without involving immunologic pathway.  Develops in patients exposed to chemicals and develop with 1st exposure itself.
  • 50. MANAGEMENT PROPHYLAXIS  Complete avoidance  Relative avoidance- Gloves and clothing. TREATMENT  Topical steroids ointments  Emollients.
  • 51. ALLERGIC CONTACT DERMATITIS  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.
  • 52. ETIOLOGY PLANTS Parthenium METALS Nickel Chromates Cosmetics Paraphenylenediamine Formaldehyde Parabens MEDICINES Neomycine Benzocaine RUBBER Mercapto mix Thiuram mix
  • 53.
  • 54.
  • 55. 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)
  • 56. CLINICAL FEATURES MORPHOLOGY  ACUTE ECZEMA o Progress from erythema to edema to papulovesiculation. o Manifest as edema in eyelids and genitalia.  CHRONIC ECZEMA o Itchy lichenified plaques.
  • 57. quaternium-15 hair dying
  • 58. PHOTOCONTACT DERMATITIS  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. Phototoxic 2. Photoallergic
  • 59. PHOTOTOXIC PHOTOALLERGIC Common Less Common Non immunological TYPE IV Hypersensitivity Sunburn Eczematous
  • 60. Phototoxic reactions: Inducing agents Topical  Perfumes  Dyes  Psoralens  Tars  Plants (lime, celery) Systemic  Psoralen  Tetracycline  Phenothiazine
  • 61. Photoallergic reactions: Inducing agents  Perfumes (soaps, aftershave)  Sunscreens (PABA)  Neomycin  Halogenated compounds  Parthenium (congress grass) Systemic  NSAIDS  Phenothiazine  Thiazides
  • 62. Papules that largely have become confluent to form plaques
  • 63. INFECTIOUS ECZEMATOID DERMATITIS  Form of dermatitis caused by the spreading of purulent material that exudes from the site of an infection.
  • 64. ETIOLOGY  Bacterial/Viral infection-Primary event  Eczema-Seconadary event
  • 65. CLINICAL FEATURES  Seen around discharging wounds and ulcers  Presents as an area of advancing erythema sometimes with microvesicles at the edge around the lesion
  • 66.
  • 67. 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.
  • 69. 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.
  • 72.  Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk.  SITES- Scalp,eyebrows,nasolabial folds,retroauricular area presternal and interscapular regions.  EPIDEMIOLOGY-  Age- Onset at puberty;peaks at 40yrs.  Gender- Common in males
  • 73. ETIOLOGY  Microbial- Overgrowth of Malassezia furfur  Genetic Predisposition  Immunodeficiency  Associated with psoriasis and Parkinson‟s disease.
  • 74. 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.
  • 75.
  • 76. 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.
  • 77.
  • 78. TREATMENT  Topical therapy  Systemic Therapy 1. Topical antifungals  In extensive lesions and HIV+ve patients.  Topical ketoconazole,selenium  Include antibiotics and sulphide and ciclopirox. antifungal agents(fluconazole/itraco 2. Topical steroids nazole)  Combined with antifungal agents in flexural and exudative lesions.  Combined with salicylic acid in recalcitrant lesions of scalp.
  • 79. LICHEN SIMPLEX CHRONICUS  Neurodermatitis.  Skin disorder characterized by chronic itching and scratching
  • 80. 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.
  • 81.
  • 82. ETIOLOGY  Scratching in predisposed individuals.  Atopy.
  • 83. TREATMENT  Topical steroids and keratolytic agents-to break itch- scratch cycle.  Antihistamines.
  • 84. 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)
  • 85. 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 white siderotic plaques with dilated capillary loops.
  • 86.
  • 87. COMPLICATIONS 1. Ulceration 2. Bacterial infection-resulting in cellulitis,lymphangitis 3. Allergic contact dermatitis 4. Deformity-”inverted champagne” bottle appearance. 5. Malignant change
  • 88. 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.
  • 89. NUMMULAR ECZEMA  Discoid eczema.  Name comes from the Latin word “nummus," which means "coin.“  Characterized by round or oval-shaped itchy lesions
  • 90. 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
  • 91. CLINICAL FEATURES  AGE/GENDER Middle aged males.  SITES: Extremities(distal parts)  MORPHOLOGY Extremely itchy,multiple,sharply demarcated coin shaped vesicular/crusted plaques.
  • 92.
  • 93. TREATMENT  SYMPTOMATIC: Antihistamines  LOCALIZED LESIONS Topical steroid+br.spectrum antibiotics  EXTENSIVE LESIONS: PUVA sol/narrow band UVB
  • 94.
  • 95. 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.
  • 96. ETIOLOGY  Unknown.  Public swimming pools could be a factor.
  • 97.  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
  • 98. 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.
  • 99.
  • 100.
  • 101. TREATMENT Management  Self-limiting condition; hypopigmentation is not due to vitiligo.  Emollients to control scaling.  Sunscreens.  Short course of a topical steroid for actively inflammed lesions.
  • 102. 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.
  • 103. ETIOLOGY  Old age.  Dry skin  Low humidity  Hypothyroidism  Malignancy
  • 104. CLINICAL FEATURES  Extremely itchy.  Skin is dry with fine reticulate red supericial fissures
  • 105. 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.
  • 106.
  • 108. PSORIASIS ECZEMA Moderately itchy.Scratching Very itchy.Scratching results results in bleeding in oozing. Well defined indurated Not so well defined and not plaques. indurated. Surmounted with silvery Scale-crust. scales. Nail changes-Typical Variable. Auspitz sign-Positive Negative
  • 109. SCABIES IN INFANTS INFANTILE ECZEMA Burrows Papulovesicles On palms and soles;genitalia Spares palms and soles Family history-positive Positive for atopic diathesis
  • 110. DERMATOPHYTIC ECZEMA INFECTIONS Annular lesions(center Discoid lesions relatively clear) Exudation-Minimal/crusting Exudation/crusting/ lichenification KOH mount-+ve for fungus -ve