Guide to Understanding Dermatitis and Eczema

DERMATITISDERMATITIS
((EczemaEczema ))

DERMATITIS
• Definition
» Means inflammation of the skin (it is not
caused by infection), affects epidermis and
upper epidermis as a response to the external
and internal influences.
» The term “eczema” comes from Greek (? ),
describing the eruption of the skin
(blistering).

DERMATITIS
• Definition
» Eczema describes a reaction pattern of the
skin to various stimulus, some of them are
known, but most of them are unknown
» Eczema and dermatitis are both having the
same meaning and often being used for one
another.

DERMATITIS
• Classification
•
» The latest classification of eczema is not
satisfying because its not consistent.
However, it is difficult to decide a suitable
choice, because most of the eczema is
unknown.

DERMATITIS
• Classification
» Variety of eczema can be recognized in an
‘endogenous’ group (caused by internal and
constitutional factors) and ‘exogenous’
(caused by contact with the external
substances) easier (?)
» However, practically, the grouping is still not
clear and often eczema can not be classified.

DERMATITIS
• Classification
TYPE EXAMPLES
Exogenous (contact) Allergic, irritant
Photoreactive
Endogenous Atopic
Seborrheic
Nummular (discoid)
Venous (stasis ; gravitational)
Pompholyx
Unclassified Asteatotic (eczema craquele)
Lichen simplex chronicus (neurodermatitis)
Juvenile plantar dermatosis
Hard dermatitis
Lichen striatus

DERMATITIS
• GROUPING BY MORPHOLOGY OF ERUPTION
(CHRONIC AND ACUTE)
• 1.Acute Eczema
» Edema epidermal positive (spongiosis),
Terdapat epidermal edema (spongiosis),
dengan pemisahan dari keratinosit hingga
terbentuk vesikula epiderma
» Dilatation of dermis blood vessels Dilatasi
» Infiltration of inflammative cells in to
dermais and epidermis

DERMATITIS
• GROUPING BY MORPHOLOGY OF ERUPTION
(CHRONIC AND ACUTE)
• 2.Chronic Eczema
» Histopathology : thickening of ‘prickle cell’
(acanthosis) and stratum corneum
(hyperkeratosis) and retention of the core
cell of korneosit cells (parakeratosis).
» Lengthen of ‘rete ridges’, dilatation of blood
vessels (dermis) and inflammation cells in to
the skin.

HAND DERMATITIS
• Often case
• recurrent
• various lesions (acute,vesicular,
chronic with hyperkeratosis and
fissure.

HAND DERMATITIS
• Various cause and influenced by
many factors
• For children,”hand dermatitis” is
caused by atopic eczema

HAND DERMATITIS
• An atopic predisposing often leads
to “hand dermatitis” for adult,
especially because of repeated
exposure to irritant.

HAND DERMATITIS
• If allergic factor is suspected (+), do
the Patch test. Most adult with “hand
dermatitis” needs the test.

HAND DERMATITIS
• Viral infection : microscopy and
culture test (especially unilateral
“hand dermatitis”)
• Check the soles (tinea pedis can
cause “hand dermatitis” as an “id-
phenomena”)

HAND DERMATITIS
• Endogeneous recurrent “hand
dermatitis” will occur to some
patients (characterized by vesicles
on fingers, palms and sometimes
soles)

HAND DERMATITIS
• Clinical symptoms
• Hand dermatitis sometimes occurs as a
chronic eczema but also can occur as a
vesicular eruption (Pompholyx)

HAND DERMATITIS
• Vesicles can be found together in atopic
eczema or contact dermatitis ;
but Pompholyx stands alone, not together
with other disease

HAND DERMATITIS
• Can occur in young adult especially in
summer, often recurrent.
• Symptoms : microvesicles (fingers)
can extend to bulla (whole hand)
• Sensitive to nickel to some patients.

HAND DERMATITIS
• Treatment
• Acute Pompholyx needs drainage for
blisters , compression 2 times a day
• Oral antibiotic: secondary bacterial
infection +
• Steroid topical : for chronic and sub acute

CONTACT DERMATITIS
• Definition
A skin inflammation that responses to a
substance (allergen) where the skin has
come into contact.
(often chemical substances).

CONTACT DERMATITIS
• Definition
There are alot of subtances in our
surroundings that can damage our skin when
it came in to contact or be exposed to the
skin.
(solid, liquid, dust in the air)

CONTACT DERMATITIS
• Definition
• Hot temperature
• high humidity skin disorder
• Pressure (easier)
• occlusion

CONTACT DERMATITIS
• Definition
• The substances work as irritant or allergen.
Divided in to :
» Irritant contact dermatitis
» Allergic contact dermatitis
» Photo contact dermatitis

CONTACT DERMATITIS
• Irritant Contact Dermatitis
» 80 % from all contact dermatitis cases.
» Caused by irritant that exposed the skin and
shows a non allergic reaction
» Not neccessary being exposed from the same
substance before ; although being exposed
for the first time, can cause dermatitis

CONTACT DERMATITIS
• Irritant substance classification
» Strong irritant
Can cause an acute irritan that occurs very
quick (ex : strong acids, strong base)
» Weak irritant
Needs time and contact more than once to
occur chronic irritant dermatitis , (ex soap,
detergent, antiseptic liquid)

CONTACT DERMATITIS
• Irritant substances can cause skin disorders
by
» dissolving skin surface,
» drying,
» damaging keratin layer,
» precipitating skin protein,
» stimulate the process of keratin
(keratinization).

CONTACT DERMATITIS
• Skin disorders caused by
» irritant substances
» concentration
» length of contact
» skin condition
» age

CONTACT DERMATITIS
• Acute irritant dermatitis caused by
strong irritant ; for example strong acid,
strong base, or plant rubber or some certain
fruits.
• Most of people will face the same prolem if
exposed by this substances.

CONTACT DERMATITIS
» Usually appears quick and clear border.
» The lowest skin disorder is erythema.
In heavy condition, bulla and epidermolysis
can be found.
» Patients’ complaints usually ; pain, sharp or
warm.
» Reaction will stop if causing substance is put
away.

CONTACT DERMATITIS
» Chronic irritant dermatitis caused by weak
irritant, for example, soap, detergent,
cleansing liquid, desinfectant, etc.
» Chronic irritant dermatitis needs repetead
contact and some period of time.

CONTACT DERMATITIS
» Factors : high level of humidity, high
temperature, pressure, rubbing and oclusion
can speed the skin disorder to appear.
» Border is not clear, dry skin, thickening skin,
squame (scales), fissure +.

CONTACT DERMATITIS
» An example for this, washer’s hand caused by
soap or detergent. (often occur to maid’s
hand).
» At one moment, because of repeated contact
to weak irritants, the skin will be resistant to
the effect of irritation, called hardening skin.

CONTACT DERMATITIS
• ALLERGIC CONTACT DERMATITIS
• Definition
» ACD can occur because of the skin being
exposed to sensitizer substance (allergen).
» Different from irritant dermatitis, ACD only
limited to the people that is very sensitive,
and so the number is less, about 20 % from
all contact dermatitis cases.

CONTACT DERMATITIS
• Pathophysiology
» ACD appears on the sensitized skin and
contact to a specific allergenic substance.
» ACD is grouped in to immunologic reaction
type IV, a slow hypersensitivity.
» There are 2 phases ;
sensitization (induction) phase
elicitation phase.

CONTACT DERMATITIS
• Sensitization phase
» This phase started when a chemical
substance called hapten joined with the skin
protein through a covalent boundary.
» Hapten is a low molecule chemical substance
(500), characteristic an uncomplete antigen.
But after joining new protein becomes a
complete antigen.

CONTACT DERMATITIS
• Sensitization phase
» The component will be served by langerhans cell in
T cell. In lymph gland, complex regional that has
been formed, will stimulated limphocyt T in
paracontex area to replicate and differentiate in
to T cell effector and memory cell.
» It formed T cell memory that will immigrate to
the skin, peripher, etc.
» Sensitization process usually takes 14 – 21 days,
fastest is 4 days.

CONTACT DERMATITIS
• Elicitation phase
» After sensitization then T cell effector goes
through blood circulation to skin.
» At this point, this person has already in risk
to get ACD.

CONTACT DERMATITIS
» If there is another similar antigen contacts
the skin of this person, then in 2 – 4 days
later, it will create a skin disorder such as
erythem, edema, vesicles.
Usually occur in the skin area that contacted
the antigen and will be itchy.
» Skin disorders sometimes may appear after
12 hours.

CONTACT DERMATITIS
» The chronology is the same with sensitization
phase ; starts with hapten joining the protein
in langerhans cell membrane (macrophage).
But the presence of this antigen recognized
by T cell effector that activates lymphocyte
to duplicate and release lymphochine.
» Lymphochine can cause various skin disorders;
erythem, edema, vesicles, papules.

CONTACT DERMATITIS
• Immunoregulation
» As mentioned above, after hapten joined the
specific membrane protein,can stimulate T cell
effector and memory cell.
» But if the chemical substance molecule doesnt
have enough time to stick on the skin and
penetrating the skin quickly and circulate to other
organs, for example ,lymph.
» In this area, it will stimulate T cell supresor and
will cause the patient become tolerant.

CONTACT DERMATITIS
• Immunoregulation
» This situation also occurs if the substance is being
taken orally or through intravenous injection or
being put on the skin that lack of langerhans cell
or damaged becauseof UVA,UVB,Puva.
» So, in one person can occur 2 types of process at
one time ; sensitization and supression process
(tolerant), depend on entrance way of hapten.

CONTACT DERMATITIS
• Clinical Appearance
» ACD disorder is difficult to differ from irritant
dermatitis.
» Usually started with erythema, then papule,
vesicle and exudate.
» On palms, foot and fingers, early symptom as deep
vesicle, grouped and itchy.

CONTACT DERMATITIS
» Lesion can be extended to surrounding ofold
lesion, join together, and the border becomes
unclear.
» New lesion can also appear quite far from the old
lesion.
» In chronic ACD, the disorder is dry skin,
thickening, fissure appears, squame,
lichenification, papule.

PHOTOCONTACT DERMATITIS
• Can be toxic dermatitis or allergic,
depends on the type of substance that
contact the skin.
• After contacted with certain substance,
lighted with UVA, skin becomes inflamed
with eczema manifestation for example skin
contacts with kumarin and being lighted by
UVA can cause phototoxic.

• Meanwhile,Photo allergic occurs based on immunologic
reaction and this reaction appears only in a small
number of patients that has been sentisized before
with photosensitize substance and then exposed by
the sun light.
• Photosensitize substance example : phenotiazine,
sulfonamide, non steroid topical substance, anti
inflammation, britionole, sunblock (PABA), eosin,
guinidin, parfume, coloring substance, etc.

• Clinical Manifestation
» Phototoxic dermatitis seems similar with
burned skin by ultraviolet.
» Erythema appears, edema and becomes
bulla.
» Localized based on contacted area.
» Diffuse, if exposed by an evaporating
substance, through the air

» Phototoxic dermatitis often leaves
hyperpigmentation lesion that can stay for
few months.
» Photoallergic dermatitis also can look
similar with sun burned skin.
» Usually papule and vesicle +

» Localized on the sun exposed area, for
example, face, ear, collar’s border,
extensor part of the arm, dorsal of the
hand.
» In chronic condition, squame (scales) and
lichenification can be found.

• Diagnosis
» Anamnesis about the history of disease, is
important to diagnose a ACD.
» In chronic ACD, skin disorder appears slow,so
patient often dont recognise when, how and
what substance that they have contacted with.
» Moreover, there is a possibility to have a cross
reaction with another chemical substance.

• Diagnosis
» From anamnesis, may be found the cause
of dermatitis (irritant or alergy).
» Lesion examination and localization are also
important to help determine diagnosis.
» To prove that dermatitis was caused by
allergic contact ; it is necessary to do
Patch Test.

• Treatment
» Avoid causing factor.
If causing factor is put away and no
complication, it will heal without medication
after 1- 2 weeks.
» Topical Corticosteroid.
» Systemic corticosteroid can be given in
heavy condition.
» Anti histamine as anti pruritus.

ATOPIC DERMATITIS
• Definition
• Recurrent skin inflammation
• chronic and itchy
• Occurs to baby, children and adult
• often occur together with atopic stigma
as asthma, allergic rhinitis, conjunctivitis,
atopic eczema (patient or patient’s family)

ATOPIC DERMATITIS
• Etiology dan Pathogenesis
» The cause of atopic dermatitis is still
unknown.
» Many factors influences this disease for
example ; immunological factor, genetic,
physiological and pharmacological.

ATOPIC DERMATITIS
• Some theories came up to discuss the
etiology of atopic dermatitis, 2 of the
most known theories :
» Immunology deficiency that based on Ig E
increase and disturbance of T cell.
» Beta adrenergic receptor blockade on the
skin

ATOPIC DERMATITIS
» But this theory can not explain well about
all the aspects that appears in this disease
» Most of the scientists take the increase of
Ig E for atopic dermatitis patient as a non
specific sign.
» Further research is necessary to find the
possibility of Ig E that is bounded in the
system.

ATOPIC DERMATITIS
» In human being, mast cell, macrophage and T
cell have receptor for Ig E.
» If there is Ig E and specific antigen, then T
cell can release supressor factor and Ig E
induction, and macrophage can release
leucotriene.
» Immunological theory on atopic dermatitis
actually was inspired from observation result
that 75 % of patients have history of another
atopic disease, the patient or the family.

ATOPIC DERMATITIS
» Atopic dermatitis patients often show
wheal reaction to antigen such as food or
inhalant from their surrounding.
» From the investigation by RAJKA to 1200
atopic dermatitis patients,it is found that
80 % from the patients had sudden skin
reaction as a response to one or more
antigen.

ATOPIC DERMATITIS
• Immunity Disturbance
» 80 % of atopic dermatitis patients going
through a cellular immunity decrease and so
it is easy to get infected by herpes virus
simplex, vaccinia, coxsackie,chronic
dermatophytosis, sensitivity of a specific
contact allergen is decreased, response to
clinical test for candida, streptococcus and
staphylococcus are decreased.

ATOPIC DERMATITIS
» This immunity effect can be a rhyme or
not with the level of disease.
» Because the cellular immunity relates to T
cell so number of T cell in atopic
dermatitis patient’s circulation also
decreased.

ATOPIC DERMATITIS
» The skin of atopic dermatitis patients are
being occupied by staphylococcus in the
highest number of colony, whether in lesion
area and also in the area that seems
normal. Meanwhile, in normal skin,
staphylococcus aureus only be found less
than 5 %.

ATOPIC DERMATITIS
» Until now, the function of Ig E and
allergen in atopic dermatitis are still
speculative. The highest amount of Ig E in
serum occurs when atopic dermatitis appear
together with asthma or rhinitis allergica.

ATOPIC DERMATITIS
• VASCULAR REACTION
» The most wellknown disturbance of vascular
reaction is white dermagraphys. That is a white
line that appears after the scratch on the skin
with something blunt, when in normal condition
should create a red line, epicutan absorption,
esther, nicotinyt acid creates a pale reaction to
many atopic dermatitis patients when came up
as erythema in normal people.
» In atopic dermatitis patient, it causes
paleness around the urtika.

ATOPIC DERMATITIS
• PRURITUS
» The atopic dermatitis patients’ complaint
mainly is about the skin becomes extremely
itchy
» Itchiness could be localized (one area) or
generalized
» Some of the areas that is more sensitive
to itchiness, for example, ears, scalp,
neck, elbow fold, knee and arm wrist, foot
wrist, and the back of foot.

ATOPIC DERMATITIS
• PRURITUS
• It is common to scratch often in the afternoon
and evening to sleep, can also scratching while
sleeping.
• The etiology of pruritus hasn’t been clearly known.
• 2 types of pruritus (RAJKA)
» itchiness came from immunologic stimulation by
releasing mediator
» intrinsic factor where the stimulation border
limit toward itchiness is decreased

ATOPIC DERMATITIS
• PRURITUS
» The factor that can cause exacerbation of
pruritus ; allergen, decreasement of air
humidity, too much sweating, and irritant
substances (wool, soap, detergent, etc).

ATOPIC DERMATITIS
• Clinical appearance and Pathogenesis
» Skin disorder in atopic dermatitis ; papule,
folicular, lichenification, vesicle, dry skin
and unshiny skin,
hyperpigmentation/hypopigmentation.
» Other skin disorder in atopic dermatitis ;
infra opital pit (morgan’s line), numerous
skin creases on the palms (tenar or
hypotenar), cataract (heavy case),
geographys’ tongue.

ATOPIC DERMATITIS
3 PHASES OF ATOPIC DERMATITIS
• I. ATOPIC DERMATITIS FOR INFANT
» Usually appears in the age of 6 – 8 weeks,
but can also appears at 2 – 3 weeks age.
The lesion starts appear as papule in
follicle called eximfollicular.
» Lesions are on the face, nect and upper
body. Beside papule, there is also light
erythem.

ATOPIC DERMATITIS
» If the baby has already been able to scratch,
erosion can occur, exudation and crust on the
face, ears, upper chest, the back of foot and
hand that extend to scalp, extensor
extremities, butt, body, thigh, and anogenital,
rare to happen on the nose. Sometimes can
extend to be exofoliative.

ATOPIC DERMATITIS
» The lesion on the head often covered by thick
crust and difficult to differ from sebhoroic
dermatitis.

ATOPIC DERMATITIS
» Characterized lesions on the folds usually
start to appear after the baby is more than
one year old age, as follicular papul or
lichinification.

ATOPIC DERMATITIS
» Most symptom to atopic dermatitis patients
infant type is dissapear at the end of the
year or before that.
» Some of the types of the food may cause
exacerbation, usually in 1 year old age ; for
example , white egg, wheat, milk and orange.

ATOPIC DERMATITIS
• II. ATOPIC DERMATITIS FOR CHILDREN
» Appears at 2 – 10 years old age.
» Skin disorders : erythem, papule,
lichenification, excoriation
» Location : elbow fold, knee fold, arm wrist,
eye lid, face, neck.

ATOPIC DERMATITIS
» Extreme itchiness cause patient to do
scratch and the scratch cause the skin
thicking and secondary changing that cause
more itchiness, so it goes on a circle ;itch-
scratch cycle.

ATOPIC DERMATITIS
» Usually while the sensitivity of the children
to eggs, wheat and milk are decreased, in
other hand, the sensitivity of the children
to wool, cat’s hair, dog’s hair and flowers
are increased.

ATOPIC DERMATITIS
• III. ATOPIC DERMATITIS FOR TEENAGAGER AND ADULT
» Skin disorder : skin thickening,
lichenification, squame (scales) and light
erythem.
» Location : elbow fold, knee fold, front
neck, side forehead, around the eyes,
arm and wrist.

ATOPIC DERMATITIS
» For teenager/adult ; populovesicle
eruption on the hand and foot with
lichenification. Can also occur
generalized eruption, most heavy is in
the folds especially lichenification.
» Usually skin is dry and thickening

ATOPIC DERMATITIS
» Patients’ complaint : itchy (pruritus) that
gets worse with emotional disturbance.
» Retention of sweat creates more
itchiness.
» Other predisposition factor : dry skin,
iritation, certain food, tension,nervous.

ATOPIC DERMATITIS
» Nervous tension seems to be an
important predisposing factor in atopic
dermatitis especially for adults.
» When the patient gets older, atopic
dermatitis level is decreased and usually
is healed in the 4th decade.

ATOPIC DERMATITIS
• Complication
– Bacterial infection, especially with
staphylococcus aureus, often cause
exacerbation. The type of skin infection :
» Impetigo bullosa and staphylococcus
scalded skin syndrome
» Folliculitis
» Furunkel, carbuncle,abcess,erysipelas

ATOPIC DERMATITIS
• Complication
– Viral infection
» Can increase insidence of veruca molluscum
contagiousum, eczema herpetikum, and
eczema vaccinatum.
– Fungal infection : fungal infection occurs 3
times more in atopic dermatitis patients.

ATOPIC DERMATITIS
• Complication
– Pityrosporum infection
» In atopic patient, pityrosporum ovale colony
on the skin cause sensitization trough Ig E
can cause atopic dermatitis.

ATOPIC DERMATITIS
• Complication
– Parasite infection
» Children with atopic dermatitis that is
infected by scabies insect, will have extreme
itchy with eczema exacerbation and
secondary skin infection will stay although
the insect already treated.
» Scabies infection in atopic dermatitis patient
is more dangerous than the non atopic.

ATOPIC DERMATITIS
• Complication
– Contact Dermatitis
» The skin of atopic dermatitis patient has an
abnormal stratum corneum that can not hold
out the water.
» This causes the structure of the skin
becomes fragile and creates fissure, so
irritant and allergen are easy to get into
epidermal or dermal cell and become contact
dermatitis.

ATOPIC DERMATITIS
• Complication
– Complication (eyes)
» Blepharo conjunctivitis
» Keratokonus and cataract
» Conjunctivitis vernalis

ATOPIC DERMATITIS
• Complication
– Erythroderma Exfolliative
» This condition can occur when
corticosteroid (that uses to control a
heavey disease)stops suddenly,
superinfection that extends and extreme
irritant contact reaction.

ATOPIC DERMATITIS
• Complication
– Growth Disturbance
» This occurs because of several possibilities
» Corticosteroid for medication (topical and
systemic)
» Atopic dermatitis occurs together with
asthma bronchiale, gastrointestinal disorder
; malabsorbtion or strict diet and leads to
malnutrition.

ATOPIC DERMATITIS
• Complication
– Skin Amyloidosis
» Extreme itchiness in atopic dermatitis can
cause chronic iritation to the skin because
of scratch and can lead to create amyloid on
the skin to people that has the tendency.

ATOPIC DERMATITIS
• Treatment
• GENERAL
» Inform the patient about the disease, assure
them that the prognosis is good
» Children should wear cotton clothes ; wool can
iritate the skin
» Avoid hot weather
» Cut the nails

ATOPIC DERMATITIS
• Treatment
• GENERAL
» Cats, dogs that can cause exacerbation to
some patients should be put away
» Avoid insects, dust at home
» Job that relates to water
» Job in industry that possible to be exposed
by oil that contains irritant that should be
avoided.

ATOPIC DERMATITIS
• Treatment
• SPECIFIC
TERAPHY INDICATION
Emolien Mostly eczema, ikhtiosis
Topical steroid Mostly eczema
Oral antihistamine Pruritus
Ter preparate Lichenification/Excoriated
eczema
Oral antibiotic Superinfection
Evening primrose Special cases, eczema light -
heavy
Oil Eczema
Food management Food allergy/resistent eczema
PUVA Highly resistent eczema

ATOPIC DERMATITIS
• Topical Therapy
• Emolien
» Emolien such as “aqueous cream” and
emulsifying ointment should be taken
regulerly on the skin and also as a soap
replacement.
» Emolien causes the dry skin becomes humid,
decrease the scratches, decrease the need
of topical steroid.

ATOPIC DERMATITIS
• Topical Therapy
• Topical steroid
» Children : 1 % hydrocortison 2 times a day
• antibiotic or topical antiseptic
» For eczema with infection, can be used
together with steroid.

ATOPIC DERMATITIS
• Topical Therapy
• “Coal far” or “ichthammol” paste is useful
for eczema lichenification.
• Short period compress for exudative
eczema.

ATOPIC DERMATITIS
• Systemic therapy
• Antihistamine for itchiness
• Linoleic acid and linoleic gamma for pruritus
• Erythromicyn for cases with infection
• Herpeticum eczema : “acyclovir”
• For patients with heavy and resistent atopic
eczema

CIRCUMSCRIPT NEURODERMATITIS
(LICHEN SIMPLEX CHRONICUS)
• Skin disorder occurs because of
scratches or rubbing repeatedly.
• Lichenification is the main lesion for
circumscript neurodermatitis.

• Lesions : lichenification, papule, squame
(scale) and hyperpigmentation. Scratches
cause erosion, excoriation can leave scars.
• Location : areas that are easy to reach by
hand
• For women, mostly on the neck area, for
men, usually in anogenital area.

» Other places ; face, wrist, lower arm
(extensor) near the elbow,upper thigh,
lateral foot, dorsum pedis, scrotum, vulva
and also in scalp.
» Clinical variation, placate with clear border
or unclear ; grouped papule,hard and dry
with rough surface.

» Large papule ,nodul like ; prurigo nodularis
» Subjective complaint : itchy (on and off)
» Often occur to old people that the skin has
become dry

• Histopathology
• Epidermis becomes hyperkeratosis, partly
parakeratosis, hypergranulosis in some
places, irreguler acanthosis, lengthen
retridges.

• Treatment
• Avoid scratching
• Topical medicine : high potent
corticosteroid (ointment)
• If not succeed ; intra lesion injection with
triamsinolon acetonid.

SEBORRHEIC DERMATITIS
• DEFINITION
• Seborrheic dermatitis is a chronic skin
inflammation in the area that contains alot
of sebacea glands especially scalp, eye brow,
and face.

• ETIOLOGY
• Etiology of seborrheic dermatitis is still
unknown
• Over activities of sebacea glands
• Incidence for new born baby is the same
with the size and activity of early ages
sebacea glands

• ETIOLOGY
• It is known that new born baby has a large
sebacea gland and high caebum secretion level
• Other research shows that pityrosporum ovale, a
lipofilic fungus increasing in number in seborrheic
dermatitis patients
• Other suspected factors : climate, genetic,
environment, hormon and neurologic.

• Seborrheic dermatitis has a predilection in
the hairy areas, because those areas have
many sebacea glands ; scalp, back of ear,
ear’s hole, face, eye lid, nosolabial fold,
beard, chest, back, around umbilicus, arm
pit, thigh fold,pubic, anogenital, mamae fold
(women)

• Distribution of lesion tendent to bilateral or
symetris although often found only in one or
several areas

• Seborrheic dermatitis lesion usually is an
oily scale, yellowish, and red in the bottm
(erythem)
• Border is not clear, itchiness is on and off
• Lowest seborrheic type : dandruff , usually
found on the head, scale is white.

• In scalp : dandruff, and also can be found
other form of seborrheic dermatitis ; an oily
scale called pityriasis steatoides with
erythema and thick crust.
• Can also occur to the baby, the scalp is
covered by yellow scales or brown mixed
with epitel , look similar to a cap, called
Cradel cap.

• A heavy seborrheic can attack eyebrow,
forehead, nose, sulcus nasolabialis, back of
the ear, presternal area and the area
between scapula.
• Blefaritis can occur, often to young adult
men and women.

– 3 types of seborrheic based on location
of lesion :
• 1. Head Seborrheic
» Oily scales are found in hairy area
» Sometimes crusts are found, called pityriasis
steatoides
» Extension can reach the back of ear (retro
auricularis) and can extend to forehead,
called corona seborrheic

– 3 types of seborrheic based on
location of lesion :
• 2. Face Seborrheic
» Mouth area, palpebra,sulcus nasolabial, chin,
macula erythem with yellowish oily scales on
the top.
» If it comes to palpebra, blefaritis can occur
» If it comes to hairy area, for example to
chin and above the lips, folicullitis can occur

– 3 types of seborrheic based on
location of lesion :
• 3. seborrheic dermatitis (body and ... )
» this type attacks pre-sternal area, lesion :
dry eczema and yellowish oily scales.
» In arm pit area, pubic, area below the
breast with wet intertrigo lesion that
secondary is being occupied by candida
albicans. Can be found in old people.

• HISTOPATHOLOGY
• Histopathology appearance is not specific,
vary to the level of the disease.
• In acute and subacute stage, epidermis
becomes ortokeratosis and parakeratosis
and spongiosis

• HISTOPATHOLOGY
• In the edge of hair follicle that extends
and reach keratin mass, parakeratosis
that contains neutrofil can be found 
this is a characterized disorder for
seborrheic dermatitis
• Upper epidermis ; limphohistiocyt
perivascular

• HISTOPATHOLOGY
• Chronic : histopathology is difficult to
differ from psoriasis
• Epidermis becomes ortokeratosis,
parakeratosis,acanthosis (psoriasis like) ;
spongiosis may be found
• Lengthen of papil (papilomatosis), upper
epidermis vessel extends with inflammation
cell around it.

• TREATMENT
• General
» Patient needs to know that this disease is
often recurrent and chronic
» Avoid the causing factors ; tired, sleepless,
tension / stress, fatty food and
carbohydrate, alcohol
» It is important to maintain general health and
to keep the skin clean

• TREATMENT
• Systemic
» Sedative or antihistamine ; to less itchness
in acute and heavy level
» Corticosteroid systemic : short period to
overcome the inflammation
» Antibiotic : secondary infection +
» B complex and B6 vitamin are also useful

• TREATMENT
– Topical Therapy
• Infant  clean the crusts on head by
acidium salisicum 3- 5 % in olive oil, and
rub with acid cream or hidrocortison lotion
for few days

• TREATMENT
– Topical Therapy
• Adult  shampoo contains :
– Selenium sulfida 2 %,2 – 3 times a week for
10 mins
– Zink pynithione1-2% or ter or acidium
salisicum
– Ketokonazole 1 – 2%

• TREATMENT
– Topical Therapy
• Then can also be rubbed with hydrocortison cream
or lotion
• Acid salicyl 2 % ointment, sulfur 4 % and 2 % ter
and ketokonazole cream
• Folds area often together with candidiasia 
gentian violet 0,5 % solution
• Corticosteroid topical ; for example 1 %
hydrocortison in other area

STASIS DERMATITIS
• Definition
• Stasis dermatitis occurs when the lower
leg’s blood vessels (vena) is disturbed.
• Disturbance of vena’s valve, especially
connecting vena or deep vena for example ;
pasca trombphlebitis

STASIS DERMATITIS
• Definition
• Capilary pressure will increase, causes
edema that will dissapear if the patient
lays down ; red blood cell extravasasion
because of the damage of capiler ; so
then blood vessels in papil will become
irreversibel stasis, lengthen and curved
also can become trombosis.

STASIS DERMATITIS
• Definition
• Then system will be full of liquid and
blood, and will cause edema and lysis 
hemosiderin
• Hemosiderin is collected under the skin,
causes the black dots.
• Will become anoxia and death of tissue.

STASIS DERMATITIS
• Definition
• Itchy appears
• If not treated, will become infection,
then necrosis and ulcus , called ulcus
varicosus
• Stasis dermatitis often occurs to adult
men and women .

STASIS DERMATITIS
• Clinical Symptom
• If the stasis goes on for a long time,
edema will be replaced with fibrotic cell,
so that the skin for the lower leg will be
thickened and hard.
• Slowly it can also become ulcus, called
ulcus varicosum.

STASIS DERMATITIS
• Treatment
• Acute dermatitis stasis and exudative :
nitrat Ag 0,25 – 0,5 % solution compression,
permanganas kalikus solution 1 : 10.000
• Corticosteroid systemic : heavey dermatitis
(short period)
• Antibiotic systemic : senondary infection +

STASIS DERMATITIS
• Treatment
• Topical medicine ; iktiol 2 % zinc oxida
ointment : acute dermatitis stasis
• Lay down with the legs up ; if there is edema
• After edema dissapears, use elastic bandage
that works for pressuring, and also helps
the muscle to pump blood in to the heart.

NUMULARIS DERMATITIS
• Definition
• coin – shaped patches dermatitis

• Etiology
• Causing factor is not known exactly
• Some mentioned that Numularis dermatits
may be happened as a manifestation of
atopic dermatitis , especially to infant and
children below 10 years old.

• Etiology
• Many factors influences numularis
dermatitis, wether alone or with other
people.
• Bactery, for example staphylococcus
aureus, often is found on the lower lesion
numularis dermatitis, but the function is
not know yet.

• Etiology
• Food allergy, focal infection, stress, emotion,
local trauma (physical and chemical) is suspected
to influence the appearance of numularis
dermatitis.
• Dry skin, especially to old people  ease the
appearance of disease
• Many types of materials can cause exacerbation
for example wool, soap and topical medicine.

• Insidence
• Numularis dermatitis mostly happened to
men than to women.
• Men : 20 – 30 years old & 50 – 60 years
old
• Women : 15 – 19 years old & 50 – 60
years old.

• Histophatology
• Clinical appearance depends on the stage
of the disease
• Acute stage : vesicles in epidermis and
extreme spongiosis and exocitosis
lymphocyte.

• Histophatology
• Dilatation of blood vessel in dermis with
lymphohistiocyte surrounds
• Chronic lesion : chage in epidermis 
hyperkeratosis, acanthosis,
hypergranulosis
• Dermis in the area of papil is fibrotic and
beomce inflammed perivascular.

» Lesion seems to be a coin with various size
until placate
» Skin disorder : starts with papulo vesikula
on the erythem base, appears suddenly on
the skin and seems normal, then burst and
become exudation and crust
» Eruption started with a single lesion or few
lesions
» Acute lesion : extremely itchy, sometimes
burning

• Chronic lesion : squame and lichenification
• Most numularis dermatitis, lesion becomes
crusted and spreading to other areas
including face, meanwhile spreaded
papulovesicle group will join and become
placate  it maybe because of secondary
infection
• Numularis dermatitis is a chronic
dermatitis and tendent to recurent

• Skin disorder localized on the legs, upper
extremities and body
• Forearm is the most area to be
attacked ; 5 cm or more placate lesion
then spreadto fingers and lower arm
(extensor)
• For men, lesion started from lower legs
especially to older age

• TREATMENT
• Topical steroid combined with antibiotic :
secondary infection +

XEROTIK DERMATITIS
( ASTHEATOTIC ECZEMA)
• Definition
• Dermatitis that occurs in winter and often
attack old people with predisposition

XEROTIK DERMATITIS
• Dry and smooth scales
• Skin ikthiosis
• Fissures becomes red and inflammed

XEROTIK DERMATITIS
• Location :
• Lokalisasi yang sering adalah daerah tulang
kering yang dapat meluas ke paha, tubuh dan
lengan

XEROTIK DERMATITIS

XEROTIK DERMATITIS
• Treatment
• Emolien, low topical steroid

Guide to Understanding Dermatitis and Eczema

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Guide to Understanding Dermatitis and Eczema