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Dermatitis and
eczema
Introduction
• Inflammation of the skin
• The terms 'ECZEMA' and 'DERMATITIS' are regarded as
synonymous
• Eczema has three clinical stages of development
• Acute, Subacute, or Chronic
• Endogenous, or exogenous
Atopic
Eczema
Introduction
• Atopy (Gk. atopos = out of place) is the
general medical term for allergic conditions
such as hay fever, asthma or this type of
eczema.
• People with a tendency to suffer from allergic
conditions are said to be atopic.
Definition
• Atopic dermatitis (ie, eczema) is a
chronic pruritic skin condition due
to hereditary predisposition to react
for sensitizers usually beginning in
infancy.
Epidemiology
• Atopic eczema affects about 15 per cent of
children and up to 5 per cent of adults in
Western countries.
• The exact prevalence is not known in our
country.
• There is no predilection of sex for
occurrence however, females have a
worse prognosis.
• Approximately 60% of patients experience
their first outbreak by age 1 year and 90%
by age 5 years.
Immune Abnormalities
• Primary Defect - ?synthesis of IgE rather than IgG
Syndrome Presumed immune mechanism
Rhinitis Immediate hypersensitivity
Asthma Immediate hypersensitivity
+/- T cell involvement
Eczema ? T cell - mediated hypersensitivity
• Precise etiology is unknown, but current theories
center on a disordered immune response,
especially an imbalance of cytokines.
• The immune system of people with atopic eczema
is active in a particular way.
• Serum levels of IgE are elevated in 80% of cases.
• There is also dysregulation of the immune system
with over activity of TH2 helper cells.
• High blood level of IL-4 & IL-5 with low level of
gamma interferon is observed.
Etio-pathogenesis
• The disease also appears to have a
hereditary component; family history is
positive for atopy (i.e., asthma, allergic
rhinitis, atopic dermatitis) in two thirds of
patients.
• The exact mode of inheritance is
obscure. It is thought to be autosomal
dominance with variable penetrance.
• Defective gene is found around 11q13 for
respiratory atopy.
• Several triggers have been identified.
• Anything that could dry the skin may
exacerbate atopic dermatitis. Potential
triggers include excessive bathing, hand
washing, lip licking, sweating, or
swimming.
• Contact with solvents, detergents,
deodorants, cosmetics, and soaps can
exacerbate the disease. Loose or poorly
fitting clothing that constantly rubs the skin
also can cause problems.
• Excessive or prolonged heat may trigger a
flare-up.
• General Risk factors
– Skin infections
– Emotional stress
– Irritating clothes and chemicals
– Excessively hot or cold climate
– Food allergy in children (controversial)
– Exposure to tobacco smoke
CLINICAL PICTURE
• Although the first episode of atopic eczema
can be delayed to adulthood the majority of
people have a history that goes back to
their childhood.
• The most common presentation is that of
infants, usually younger than 6 months,
brought in by their parents for a persistent
rash
• The predominant symptom is intense
pruritus. Atopic dermatitis typically is
not associated with fever or other
constitutional symptoms.
• Distribution of lesions
–Infants: Symmetric lesions over cheeks,
forehead, scalp, trunk, and the extensor
surfaces. Lesions may extensively involve
the flexural surfaces, sparing only the
diaper area. Scalp involvement may be
severe enough to cause alopecia.
–Children:
•Symmetric lesions on wrists,
ankles, and flexor areas of the
extremities. Generalized
eruptions also may occur in this
age group.
–Adults:
•Atopic dermatitis primarily
involves the flexor areas of the
arms, legs, neck, and nipple.
•Generalization and extensor
involvement may occur.
Other manifestations
• Ichthyosis vulgaris - Observed in one
third of patients. Characterizing features
are hyperlinear palms and soles and
polygonal fishlike scales, especially on
the lower legs.
• Keratosis pilaris - Characterized by
asymptomatic horny follicular papules
on the extensor surfaces of the upper
arms, buttocks, and anterior thighs
• Hand and foot dermatitis may be the only
manifestation in adults and adolescents.
Fissuring of the palms, soles, and fingers
often occurs.
• Keratoconus is observed in severe cases. A
cone-shaped cornea (requiring corneal
transplant) may develop in the second or
third decade of life.
Associated features
• Facial erythema
• Perioral pallor
• Infraorbital fold (ie, Dennie-Morgan line)
• Dry skin
• Increased palmar linear markings
• Pityriasis alba
• Pilaris
Investigations.
• Serum IgE level
• Biopsy
The UK refinement of Hanifin and
Rajka's diagnostic criteria.
Scabies should be excluded.
• In order to qualify as a case of atopic
dermatitis with the UK diagnostic
criteria, the child must have:
– An itchy skin condition (or parental report
of scratching or rubbing in a child)
• Plus three or more of the following
1) Onset below age 2 years (not used if child is
under 4 years)
2) History of skin crease involvement (including
cheeks in children under 10 years)
3) History of a generally dry skin
4) Personal history of other atopic disease (or
history of any atopic disease in a first degree
relative in children under 4 years)
5) Visible flexural dermatitis (or dermatitis of
cheeks/forehead and outer limbs in children
under 4 years)
TREATMENT
• General principles
–Development of partnership
–Individualization
• Objectives
–Healing the skin conditions
–Preventing flares
First line treatment
• General advice
– Enthusiastic social relationship
– Advice on prognosis, available treatments,
triggers, complications etc.
• Reduction of triggers
– Avoid irritants
– Cool the room
– (Dietary manipulation)
– Avoid stress.
• Topical Therapy:
1. Emollients
2. Emollients
3. Emollients
4. Emollients
5. Emollients
6. Emollients
8. Topical Corticosteroids
9. Ichthammol and coal tar
10.Antihistamines
11.Antibiotics
Second line treatment
• Intensive topical treatment
• Wet-wrap technique
• Allergy management
• UV radiation
Third line treatment
• Topical immunomodulators
–Tacrolimus, Ascomycin
• Systemic treatment
–Cyclosporin
–Methotrexate
–Prednisolone
• Desensitization
Contact Dermatitis
–Acute or chronic inflammatory reactions to
substances that come in contact with the skin.
–Two forms of CD exist
• Irritant Contact Dermatitis
• Allergic Contact Dermatitis
Contact Dermatitis
ICDlesions are confinedto the area of exposure and
previous exposure is not the prerequisite
ACDoccurs in previously sensitizedindividuals and
eczematous pruriticlesions occur even apart from the
contact site
The agent causing ACDcan be identified using patch
testing
Contact Dermatitis
Avoid the agent,
Topical steroids and if severe systemic
for a short time,
Antipruritics
Treat the complications.
Lichen Simplex Chronicus
Thickening of the skin with variable scaling that
arises secondary to repetitive scratching or
rubbing. It is not a primary process.
occurs mainly at the nuchal area.
Hyperpigmentation and lichenific-ation is the
feature.
Lichen Simplex Chronicus
Break the itch-scratch-itch cycle with
antihistamines, potent topical steroids and treat
lichenificatin by keratolytics
Advice patients not to scratch the area
Discoid Eczema
A chronic, pruritic, inflammatory dermatitis
occurring in the form of coin-shaped plaques.
Unknown cause.
Unrelated to atopic diathesis
IgE levels are normal
Commonly seen in the lower leg
Discoid Eczema
Coin shaped plaques formed by confluent
papules and vesicles are seen mainly on the
extremities.
Pruritis is common
Discoid Eczema
Skin hydration and application of potent steroid
with or without antihistamines.
Usually recurs
Seborrhoeic Dermatitis
Very common chronic dermatosis characterized
by redness and scaling occurring in regions
where the sebaceous glands are most active
Called dandruff in the scalp
Affects 4 – 5 % of the population
Seborrhoeic Dermatitis
Cause not fully inderstood
Associated factors:
Genetics
Immunosupression
Pityrosporumovale
Seborrhoeic Dermatitis
 Has two pick ages of onset: Infancy, and
Puberty.
 The infantile type commonly presents as
“cradle cap”.
 Yellowish red, often greasy, or white dry
scaling macules and papules of varying
size (5 to 20 mm), rather sharply
marginated occurs.
 The seborrhoeic areas are primarily
affected.
Seborrhoeic Dermatitis
Seleniumsulfide shampoo
Ketoconazole shampoo
Topical steroids
Systemic azoles
UV radiation
Recurrences and remissions are common
Pityriasis Alba
A common disfiguring hypomelanosis of the face
presenting as white area (alba) with scaling
(pityriasis)
Cause is not known
Atopic state may be present
Asympromatic or mildly pruritic
Pityriasis Alba
Hydrocortisone cream or ointment 1%, is
effective
Avoid frequent washing with soap
Self limiting conditionsthat disappears with age

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14Dermatitis and Eczema.ppt

  • 2. Introduction • Inflammation of the skin • The terms 'ECZEMA' and 'DERMATITIS' are regarded as synonymous • Eczema has three clinical stages of development • Acute, Subacute, or Chronic • Endogenous, or exogenous
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  • 7. Introduction • Atopy (Gk. atopos = out of place) is the general medical term for allergic conditions such as hay fever, asthma or this type of eczema. • People with a tendency to suffer from allergic conditions are said to be atopic.
  • 8. Definition • Atopic dermatitis (ie, eczema) is a chronic pruritic skin condition due to hereditary predisposition to react for sensitizers usually beginning in infancy.
  • 9. Epidemiology • Atopic eczema affects about 15 per cent of children and up to 5 per cent of adults in Western countries. • The exact prevalence is not known in our country. • There is no predilection of sex for occurrence however, females have a worse prognosis. • Approximately 60% of patients experience their first outbreak by age 1 year and 90% by age 5 years.
  • 10. Immune Abnormalities • Primary Defect - ?synthesis of IgE rather than IgG Syndrome Presumed immune mechanism Rhinitis Immediate hypersensitivity Asthma Immediate hypersensitivity +/- T cell involvement Eczema ? T cell - mediated hypersensitivity
  • 11. • Precise etiology is unknown, but current theories center on a disordered immune response, especially an imbalance of cytokines. • The immune system of people with atopic eczema is active in a particular way. • Serum levels of IgE are elevated in 80% of cases. • There is also dysregulation of the immune system with over activity of TH2 helper cells. • High blood level of IL-4 & IL-5 with low level of gamma interferon is observed. Etio-pathogenesis
  • 12. • The disease also appears to have a hereditary component; family history is positive for atopy (i.e., asthma, allergic rhinitis, atopic dermatitis) in two thirds of patients. • The exact mode of inheritance is obscure. It is thought to be autosomal dominance with variable penetrance. • Defective gene is found around 11q13 for respiratory atopy.
  • 13. • Several triggers have been identified. • Anything that could dry the skin may exacerbate atopic dermatitis. Potential triggers include excessive bathing, hand washing, lip licking, sweating, or swimming. • Contact with solvents, detergents, deodorants, cosmetics, and soaps can exacerbate the disease. Loose or poorly fitting clothing that constantly rubs the skin also can cause problems.
  • 14. • Excessive or prolonged heat may trigger a flare-up. • General Risk factors – Skin infections – Emotional stress – Irritating clothes and chemicals – Excessively hot or cold climate – Food allergy in children (controversial) – Exposure to tobacco smoke
  • 15. CLINICAL PICTURE • Although the first episode of atopic eczema can be delayed to adulthood the majority of people have a history that goes back to their childhood. • The most common presentation is that of infants, usually younger than 6 months, brought in by their parents for a persistent rash
  • 16. • The predominant symptom is intense pruritus. Atopic dermatitis typically is not associated with fever or other constitutional symptoms. • Distribution of lesions –Infants: Symmetric lesions over cheeks, forehead, scalp, trunk, and the extensor surfaces. Lesions may extensively involve the flexural surfaces, sparing only the diaper area. Scalp involvement may be severe enough to cause alopecia.
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  • 21. –Children: •Symmetric lesions on wrists, ankles, and flexor areas of the extremities. Generalized eruptions also may occur in this age group.
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  • 25. –Adults: •Atopic dermatitis primarily involves the flexor areas of the arms, legs, neck, and nipple. •Generalization and extensor involvement may occur.
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  • 31. Other manifestations • Ichthyosis vulgaris - Observed in one third of patients. Characterizing features are hyperlinear palms and soles and polygonal fishlike scales, especially on the lower legs. • Keratosis pilaris - Characterized by asymptomatic horny follicular papules on the extensor surfaces of the upper arms, buttocks, and anterior thighs
  • 32. • Hand and foot dermatitis may be the only manifestation in adults and adolescents. Fissuring of the palms, soles, and fingers often occurs. • Keratoconus is observed in severe cases. A cone-shaped cornea (requiring corneal transplant) may develop in the second or third decade of life.
  • 33. Associated features • Facial erythema • Perioral pallor • Infraorbital fold (ie, Dennie-Morgan line) • Dry skin • Increased palmar linear markings • Pityriasis alba • Pilaris
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  • 41. Investigations. • Serum IgE level • Biopsy
  • 42. The UK refinement of Hanifin and Rajka's diagnostic criteria. Scabies should be excluded. • In order to qualify as a case of atopic dermatitis with the UK diagnostic criteria, the child must have: – An itchy skin condition (or parental report of scratching or rubbing in a child)
  • 43. • Plus three or more of the following 1) Onset below age 2 years (not used if child is under 4 years) 2) History of skin crease involvement (including cheeks in children under 10 years) 3) History of a generally dry skin 4) Personal history of other atopic disease (or history of any atopic disease in a first degree relative in children under 4 years) 5) Visible flexural dermatitis (or dermatitis of cheeks/forehead and outer limbs in children under 4 years)
  • 44. TREATMENT • General principles –Development of partnership –Individualization • Objectives –Healing the skin conditions –Preventing flares
  • 45. First line treatment • General advice – Enthusiastic social relationship – Advice on prognosis, available treatments, triggers, complications etc. • Reduction of triggers – Avoid irritants – Cool the room – (Dietary manipulation) – Avoid stress.
  • 46. • Topical Therapy: 1. Emollients 2. Emollients 3. Emollients 4. Emollients 5. Emollients 6. Emollients
  • 47. 8. Topical Corticosteroids 9. Ichthammol and coal tar 10.Antihistamines 11.Antibiotics
  • 48. Second line treatment • Intensive topical treatment • Wet-wrap technique • Allergy management • UV radiation
  • 49. Third line treatment • Topical immunomodulators –Tacrolimus, Ascomycin • Systemic treatment –Cyclosporin –Methotrexate –Prednisolone • Desensitization
  • 50. Contact Dermatitis –Acute or chronic inflammatory reactions to substances that come in contact with the skin. –Two forms of CD exist • Irritant Contact Dermatitis • Allergic Contact Dermatitis
  • 51. Contact Dermatitis ICDlesions are confinedto the area of exposure and previous exposure is not the prerequisite ACDoccurs in previously sensitizedindividuals and eczematous pruriticlesions occur even apart from the contact site The agent causing ACDcan be identified using patch testing
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  • 65. Contact Dermatitis Avoid the agent, Topical steroids and if severe systemic for a short time, Antipruritics Treat the complications.
  • 66. Lichen Simplex Chronicus Thickening of the skin with variable scaling that arises secondary to repetitive scratching or rubbing. It is not a primary process. occurs mainly at the nuchal area. Hyperpigmentation and lichenific-ation is the feature.
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  • 73. Lichen Simplex Chronicus Break the itch-scratch-itch cycle with antihistamines, potent topical steroids and treat lichenificatin by keratolytics Advice patients not to scratch the area
  • 74. Discoid Eczema A chronic, pruritic, inflammatory dermatitis occurring in the form of coin-shaped plaques. Unknown cause. Unrelated to atopic diathesis IgE levels are normal Commonly seen in the lower leg
  • 75. Discoid Eczema Coin shaped plaques formed by confluent papules and vesicles are seen mainly on the extremities. Pruritis is common
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  • 78. Discoid Eczema Skin hydration and application of potent steroid with or without antihistamines. Usually recurs
  • 79. Seborrhoeic Dermatitis Very common chronic dermatosis characterized by redness and scaling occurring in regions where the sebaceous glands are most active Called dandruff in the scalp Affects 4 – 5 % of the population
  • 80. Seborrhoeic Dermatitis Cause not fully inderstood Associated factors: Genetics Immunosupression Pityrosporumovale
  • 81. Seborrhoeic Dermatitis  Has two pick ages of onset: Infancy, and Puberty.  The infantile type commonly presents as “cradle cap”.  Yellowish red, often greasy, or white dry scaling macules and papules of varying size (5 to 20 mm), rather sharply marginated occurs.  The seborrhoeic areas are primarily affected.
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  • 87. Seborrhoeic Dermatitis Seleniumsulfide shampoo Ketoconazole shampoo Topical steroids Systemic azoles UV radiation Recurrences and remissions are common
  • 88. Pityriasis Alba A common disfiguring hypomelanosis of the face presenting as white area (alba) with scaling (pityriasis) Cause is not known Atopic state may be present Asympromatic or mildly pruritic
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  • 92. Pityriasis Alba Hydrocortisone cream or ointment 1%, is effective Avoid frequent washing with soap Self limiting conditionsthat disappears with age