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DR. Pranami Kashyap
SRD, Deptt of Dermatology
NEIGRIHMS.
ECZEMA ANDDERMATITIS
ECZEMA
⚫'Ekze', in Greek means “toboil over” but it seems that theskin is
“Boiling out” or “Oozing out” in eczema.
Erythema, papulo-vesicles, oozing &crusting, lichenification
⚫All eczemas are dermatitis, but not all dermatitis are eczemas.
THE“ITCH/ SCRATCH” CYCLE
The sensation of itch and subsequent scratching is hallmark of most eczemas
itch
scratch
itch
scratch
CLASSIFICATION
Etiology Pattern/morphology Chronicity
Endogenous Discoid Acute
Exogenous Hyperkeratotic Chronic
Combined Lichenified
Seborrheic
ETIOLOGICAL CLASSIFICATION
Eczema
Exogenous Endogenous
•Irritant Contact Derma.
•Allergic Contact Derma.
•Photo dermatitis
•Infective dermatitis
•Atopic dermatitis
•Seborrheic dermatitis
•Nummular eczema
•Stasis Dermatitis
•Asteatotic eczema
•Pompholyx
CLASSIFICATIONONTHEBASISOFCHRONICITY
Acute eczematous Sub acute eczematous Chronic eczematous
⚫Intense itching
⚫Intense erythema
⚫Oedema
⚫Papulovesicles
⚫Oozing
⚫Erythema (lesser than
in acute stage)
⚫Crusting and scaling
⚫Fissuring
⚫Slight to moderate
itching
⚫Stinging and burning
sensation
⚫Dryness of skin
⚫Excoriation
⚫Fissuring
⚫Lichenification
CLINICALFEATURES
 AcuteEczema:
• Erythematous&edematousplaque,whichisill-defined &surmountedby
papules, vesicles, pustules &exudates that dries to form crusts
• scales
 Chronic Eczema :
• Lichenification – Triad of hyperpigmentation, thickening &increased
markings of skin
• Less vesicular &exudative
• Morescaly
• Flexural lesions may develop fissures
COMPLICATIONS:
1. Dermatological :
 Infection
 Ide eruption
 Contact dermatitis
 Erythroderma
2. Psychosocial :
 Anxiety
 Depression
 Social complications
 Wage loss
 Debility
 Social ostracism
TREATMENT
 General measures:
• Removetriggers
• Hydration&useof Emollients
ACUTEPHASE:
1. Topical treatment
 AcuteEczemaofhands&feet: Soaksofpotassiumpermanganate0.01%,followedby
applicationof steroidlotionor creamis best
 Larger areas : compresses followed by soothing agents like calaminelotion
2. Systemic treatment
 Systemic steroids : used in extensivelesions &whenIde eruption develop
 Immunosuppressive: Azathioprine
 Antibiotics : usedfor infectedlesions
 Antihistamines: for itching
CHRONICPHASE
1. Steroids :
 Topicalsteroids: forlocalizedlesions– t/t ofchoice,for
lichenified lesions, topical steroids may be combined with
keratolytic agents like salicyclic acid &urea
 Systemic steroids : for extensive lesions like in airborne contact
dermatitis
2. Antibiotics : for bacterial infection – topical or systemic
3. Topical immunomodulators : for their steroid sparing action
ATOPICDERMATITIS
It is a chronic or relapsing dermatitis usually beginning in childhood
characterized by marked pruritus and rash
⚫Seen in 3% of all infant
⚫Increased between 3-6 months of age
⚫Increased worldwide incidence because of
 Pollutants
 Indoor allergen (house dust mite )
 Decline in breast feeding
ETIOPATHOGENESIS:
• Exact cause of atopic dermatitis is unknown
• It is genetic predisposition ( due to excessive I.e. hypersensitivity)
• Increased histamine release from basophils maylead to persistent
pruritus
• Produce IL-4and IL-13, which promote IgEproduction by Bcells
Triggeringfactors
⚫Anxiety; emotional stress
⚫Temperaturechange and sweating
⚫Decreased humidity
⚫Excessive washing
⚫Contact with irritants
⚫Allergens
⚫Foods
⚫Microbial agents
CLINICALFEATURES
1. Itching : Due to - contact
- trauma
- Temperaturechanges
- Psychic stress
2. Chronic thickening of skin
3. Dry skin
4. Hyperlinear palm
Oozing, crusted, erythematous,
scaly plaques on the scalp and
face, sparing the diaper area.
When baby begins to crawl, the
extensor extremities become
more involved.
INFANTILE ATOPIC DERMATITIS (2m—2y)
CHILDHOOD ATOPIC DERMATITIS: (2-12 yrs.)
 Lesions become prominent on the hands, posterior
neck, antecubital and popliteal fossae
ADULT PHASE (12 YEARS ONWARDS)
Commonly involves flexural areas.
⚫The disease may be diffuse
or patchy.
⚫Dermatitis
of
theupper eyelids
and blepharitis
CRITERIAFORDIAGNOSIS(HANIFINANDRAJKA)
1. Major criteria :
 Pruritus
 Typical morphology and distribution
 Facial and ext. involvement in infant.
 Flexural lichenification in adults and children.
 Chronic and chronically relapsing dermatitis
 Personal or family H/o atopy
2. Minor criteria :
 Cataract
 Cheilitis
 Ichthyosis
 Xerosis
 Orbital darkening
 Wool intolerance
 P
. alba
 Dennie- Morgan fold
 Palmer hyperlinearity
 Itching when sweating
MANAGEMENTOFATOPICDERMATITIS
INVESTIGATIONS
1. Patch test : ( TypeIV hypersensitivity)
2. Prick test : ( TypeI hypersensitivity )
3. Bacteria &viral swabs for microscopy &culture.
TREATMENT
1. First-linetreatment
General measures -
⚫Avoidscratching
⚫Avoidfrequent useof soap, contact woollen clothes
⚫Measuretoavoidhousedust mite
T
opical treatments-
◦ Moisturizer ; Emollients; Humectants
◦ Corticosteroids
◦ Calcineurin inhibitors: Pimecrolimus; tacrolimus
 Oral treatment -
◦ Antihistamines
🞄 Sedative antihistamines preferred
🞄 Promethazine; trimeprazine; hydroxyzine
◦ Antibiotics
◦ Systemic steroids (in severe cases)
2. Second-line treatment
⚫Intensive topical therapy
⚫Wet wraptechnique
3. Third-line treatment
⚫Phototherapy
⚫Oral
immunosuppresants
◦ Cyclosporine
◦ Azathrioprine
◦ Thymopentin
◦ α- Interferon
CONTACT DERMATITIS
–Acuteorchronicinflammatoryreactions
to
substancesthatcomeincontactwithth
e skin.
–TwoformsofCDexist
• IritantContactDermatitis(ICD)
• AlergicContactDermatitis(ACD)
• Common allergen-containing products
include
• cosmetics
• Soaps
• dyes and
• jewellery.
• The most frequent sensitizers are
• fragrance
• nickel, neomycin
• formaldehyde, lanolin, and
• a host of other common environmental chemicals.
Contact Dermatitis
26
27
28
29
TREATMENT OF CONTACT DERMATITIS
▪ Avoid the agent.
▪ Topical steroids and if severe
systemic steroids can be considered
for a short time.
▪ Antipruritics
▪ Treat the complications.
DISCOID ECZEMA
▪ Nummular or Microbial eczema
▪ A chronic,pruritic,inflammatory
dermatitis occuring in the form of coin-
shaped plaques.
▪ Unknown cause.
▪ Unrelated to atopic diathesis
▪ IgE levels are normal
▪ Commonly seen in the lower limbs
32
33
TREATMENT OF DISCOID ECZEMA
▪ S kin hydration and application of
potent steroids with o r with o u t
antihistamines.
▪ Usualy recurs.
SEBORRHOEIC DERMATITIS
▪ V ery common chronic dermatosis characterized by redness
and scaling.
▪ O c c u r s i n r e g i o n s w h e r e t h e sebaceous glands are
most active.
▪ Affects 4 – 5 % of the population
M i l d e r f o r m s i n t h e s c a l p r e f e r r e d t o a s
d a n d r u f f o r p i t y r i a s i s
s i c c a . 71
SEBORRHOEIC DERMATITIS
▪ Cause not understood
▪ Associatedfactors:
▪ Genetics
▪ Immunosupresion
▪ Pityrosporum ovale(
Malassezia furfur)
38
39
TREATMENT OF SEBORRHOEIC DERMATITIS
▪ S e l e n i u m sulfide shampoo
▪ Ketoconazole shampoo
▪ Topical steroids
▪ Systemic azoles
▪ UV radiation
▪ Recurrences and remissions are
common
ECZEMA AND DERMATITIS for dematology.pptx

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ECZEMA AND DERMATITIS for dematology.pptx

  • 1. DR. Pranami Kashyap SRD, Deptt of Dermatology NEIGRIHMS. ECZEMA ANDDERMATITIS
  • 2. ECZEMA ⚫'Ekze', in Greek means “toboil over” but it seems that theskin is “Boiling out” or “Oozing out” in eczema. Erythema, papulo-vesicles, oozing &crusting, lichenification ⚫All eczemas are dermatitis, but not all dermatitis are eczemas.
  • 3. THE“ITCH/ SCRATCH” CYCLE The sensation of itch and subsequent scratching is hallmark of most eczemas itch scratch itch scratch
  • 4. CLASSIFICATION Etiology Pattern/morphology Chronicity Endogenous Discoid Acute Exogenous Hyperkeratotic Chronic Combined Lichenified Seborrheic
  • 5. ETIOLOGICAL CLASSIFICATION Eczema Exogenous Endogenous •Irritant Contact Derma. •Allergic Contact Derma. •Photo dermatitis •Infective dermatitis •Atopic dermatitis •Seborrheic dermatitis •Nummular eczema •Stasis Dermatitis •Asteatotic eczema •Pompholyx
  • 6. CLASSIFICATIONONTHEBASISOFCHRONICITY Acute eczematous Sub acute eczematous Chronic eczematous ⚫Intense itching ⚫Intense erythema ⚫Oedema ⚫Papulovesicles ⚫Oozing ⚫Erythema (lesser than in acute stage) ⚫Crusting and scaling ⚫Fissuring ⚫Slight to moderate itching ⚫Stinging and burning sensation ⚫Dryness of skin ⚫Excoriation ⚫Fissuring ⚫Lichenification
  • 7. CLINICALFEATURES  AcuteEczema: • Erythematous&edematousplaque,whichisill-defined &surmountedby papules, vesicles, pustules &exudates that dries to form crusts • scales  Chronic Eczema : • Lichenification – Triad of hyperpigmentation, thickening &increased markings of skin • Less vesicular &exudative • Morescaly • Flexural lesions may develop fissures
  • 8. COMPLICATIONS: 1. Dermatological :  Infection  Ide eruption  Contact dermatitis  Erythroderma 2. Psychosocial :  Anxiety  Depression  Social complications  Wage loss  Debility  Social ostracism
  • 9. TREATMENT  General measures: • Removetriggers • Hydration&useof Emollients ACUTEPHASE: 1. Topical treatment  AcuteEczemaofhands&feet: Soaksofpotassiumpermanganate0.01%,followedby applicationof steroidlotionor creamis best  Larger areas : compresses followed by soothing agents like calaminelotion 2. Systemic treatment  Systemic steroids : used in extensivelesions &whenIde eruption develop  Immunosuppressive: Azathioprine  Antibiotics : usedfor infectedlesions  Antihistamines: for itching
  • 10. CHRONICPHASE 1. Steroids :  Topicalsteroids: forlocalizedlesions– t/t ofchoice,for lichenified lesions, topical steroids may be combined with keratolytic agents like salicyclic acid &urea  Systemic steroids : for extensive lesions like in airborne contact dermatitis 2. Antibiotics : for bacterial infection – topical or systemic 3. Topical immunomodulators : for their steroid sparing action
  • 11. ATOPICDERMATITIS It is a chronic or relapsing dermatitis usually beginning in childhood characterized by marked pruritus and rash ⚫Seen in 3% of all infant ⚫Increased between 3-6 months of age ⚫Increased worldwide incidence because of  Pollutants  Indoor allergen (house dust mite )  Decline in breast feeding
  • 12. ETIOPATHOGENESIS: • Exact cause of atopic dermatitis is unknown • It is genetic predisposition ( due to excessive I.e. hypersensitivity) • Increased histamine release from basophils maylead to persistent pruritus • Produce IL-4and IL-13, which promote IgEproduction by Bcells
  • 13. Triggeringfactors ⚫Anxiety; emotional stress ⚫Temperaturechange and sweating ⚫Decreased humidity ⚫Excessive washing ⚫Contact with irritants ⚫Allergens ⚫Foods ⚫Microbial agents
  • 14. CLINICALFEATURES 1. Itching : Due to - contact - trauma - Temperaturechanges - Psychic stress 2. Chronic thickening of skin 3. Dry skin 4. Hyperlinear palm
  • 15. Oozing, crusted, erythematous, scaly plaques on the scalp and face, sparing the diaper area. When baby begins to crawl, the extensor extremities become more involved. INFANTILE ATOPIC DERMATITIS (2m—2y)
  • 16. CHILDHOOD ATOPIC DERMATITIS: (2-12 yrs.)  Lesions become prominent on the hands, posterior neck, antecubital and popliteal fossae
  • 17. ADULT PHASE (12 YEARS ONWARDS) Commonly involves flexural areas. ⚫The disease may be diffuse or patchy. ⚫Dermatitis of theupper eyelids and blepharitis
  • 18. CRITERIAFORDIAGNOSIS(HANIFINANDRAJKA) 1. Major criteria :  Pruritus  Typical morphology and distribution  Facial and ext. involvement in infant.  Flexural lichenification in adults and children.  Chronic and chronically relapsing dermatitis  Personal or family H/o atopy
  • 19. 2. Minor criteria :  Cataract  Cheilitis  Ichthyosis  Xerosis  Orbital darkening  Wool intolerance  P . alba  Dennie- Morgan fold  Palmer hyperlinearity  Itching when sweating
  • 20. MANAGEMENTOFATOPICDERMATITIS INVESTIGATIONS 1. Patch test : ( TypeIV hypersensitivity) 2. Prick test : ( TypeI hypersensitivity ) 3. Bacteria &viral swabs for microscopy &culture.
  • 21. TREATMENT 1. First-linetreatment General measures - ⚫Avoidscratching ⚫Avoidfrequent useof soap, contact woollen clothes ⚫Measuretoavoidhousedust mite T opical treatments- ◦ Moisturizer ; Emollients; Humectants ◦ Corticosteroids ◦ Calcineurin inhibitors: Pimecrolimus; tacrolimus
  • 22.  Oral treatment - ◦ Antihistamines 🞄 Sedative antihistamines preferred 🞄 Promethazine; trimeprazine; hydroxyzine ◦ Antibiotics ◦ Systemic steroids (in severe cases)
  • 23. 2. Second-line treatment ⚫Intensive topical therapy ⚫Wet wraptechnique 3. Third-line treatment ⚫Phototherapy ⚫Oral immunosuppresants ◦ Cyclosporine ◦ Azathrioprine ◦ Thymopentin ◦ α- Interferon
  • 25. • Common allergen-containing products include • cosmetics • Soaps • dyes and • jewellery. • The most frequent sensitizers are • fragrance • nickel, neomycin • formaldehyde, lanolin, and • a host of other common environmental chemicals.
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  • 30. TREATMENT OF CONTACT DERMATITIS ▪ Avoid the agent. ▪ Topical steroids and if severe systemic steroids can be considered for a short time. ▪ Antipruritics ▪ Treat the complications.
  • 31. DISCOID ECZEMA ▪ Nummular or Microbial eczema ▪ A chronic,pruritic,inflammatory dermatitis occuring in the form of coin- shaped plaques. ▪ Unknown cause. ▪ Unrelated to atopic diathesis ▪ IgE levels are normal ▪ Commonly seen in the lower limbs
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  • 35. TREATMENT OF DISCOID ECZEMA ▪ S kin hydration and application of potent steroids with o r with o u t antihistamines. ▪ Usualy recurs.
  • 36. SEBORRHOEIC DERMATITIS ▪ V ery common chronic dermatosis characterized by redness and scaling. ▪ O c c u r s i n r e g i o n s w h e r e t h e sebaceous glands are most active. ▪ Affects 4 – 5 % of the population M i l d e r f o r m s i n t h e s c a l p r e f e r r e d t o a s d a n d r u f f o r p i t y r i a s i s s i c c a . 71
  • 37. SEBORRHOEIC DERMATITIS ▪ Cause not understood ▪ Associatedfactors: ▪ Genetics ▪ Immunosupresion ▪ Pityrosporum ovale( Malassezia furfur)
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  • 40. TREATMENT OF SEBORRHOEIC DERMATITIS ▪ S e l e n i u m sulfide shampoo ▪ Ketoconazole shampoo ▪ Topical steroids ▪ Systemic azoles ▪ UV radiation ▪ Recurrences and remissions are common