DERMATITIS

Dermatitis

is inflammation of the skin

caused by direct exposure to the
external effect of a physical,
chemical, biological or medical
irritant.
 Classification of dermatitis

Simple contact Allergic dermatitis

(artificial)
dermatitis

Allergic Toxicodermia
соntact
dermatitis
 Dermatitis may be caused by:
 physical irritants
• high and low temperatures (burns, frostbite, chilblains)
• insolation (ultraviolet and infrared rays) -solar dermatitis
• X-ray and radioactive radiation (ionizing radiation).
• mechanical (pressure, friction)
• electricity current
 chemical irritants
• alkalis and acids, salts of same acids, disinfectants in high concentration
• synthetic texture
• disinfectants
• colors, lacquer, solvents
• Ni, Cr
 biological factors irritants
• several plants (such as white dictamnine, cow parsnip, primrose,
crowfoot plants of the cashew family and some species of redwood)
• insects, caterpillars ect.
 medical irritants
• non steroid antiinflammationary medicines
• group of antibiotics medicines
• salicylic, boric, lactatic acids, resorcini, sulfufuris, iodine
 Toxicodermia
is inflammation of the skin in which
acute inflammation of the skin
develops under the effect of

-an ingested irritant (entering t he

alimentary canal),
-administered intravenously,
subcutaneously or intramuscuarly,
or inhaled as a vapour (acting by
way of the respiratory tract)
 SIMPLE CONTACT, OR ARTIFICIAL
DERMATITIS
The characteristic features of simple (artificial)
contact dermatitis:
 exclusive occurrence at the site of action of the
unconditional irritating factor

 Appears in the place of the action of the stimulus

 simple contact dermatitis is usually acute and occurs

soon after exposure to the irritant (Disappears after the
elimination of the stimulus)
the absence of sensitization

 the absence of incubation period

subjectively: sensation of pain and burn

objectively: from erythema, hyperaemia and swelling , vesicals

and bullas with a serous or haemorrhagic content, necrosis

the border is clear

 process is focuse, asymmetrical

 the absence of tendency towards dissemination or peripheral

growth

dermatitis resolves (even without any active treatment) one or

two weeks after the action of the irritant ceases
Simple contact (artificial)
dermatitis may be caused by physical
(mechanical among others), chemical, and
biological factors.

It often develops under conditions of

production in which case it is called
occupational dermatitis (see the respective
section).
Simple dermatitis may be caused by mechanical
factors (pressure, friction)
Worn-out condition
Dry corns
The effect on the skin of high temperature
results in burns (combustio).
Four degrees of burns are distinguished.
 the first degree burn is charachterazed:
• erythema
• mild swelling on the affected skin area
• the subjective sensations are burning and pain
 the second degree of burns is:
• bullas on the hyperemic area
• swollen skin
 the third degree burn is characterized by:
• necrosis of the superficial dermal layers without the
formation of scabs
 the fourth degree of burn is characterized of :
• necrosis
• forms scab of all the dermal layers
• ulcer is revealed when the scab comes off
Burn of the
second degree
Burn of the
third degree
Chemical burn of the third
Contact
dermatitis
Exposure to low external temperature leads to
damage of the tissue by cold and is called
frostbite
four degrees of frostbite are distinguished
 the first degree of frostbite
• the affected area is congestive bluish in colour
• swollen
• the subjective sensations are prickling and itching
 the clinical picture of second degree frostbite is
• similar to that described above
• blisters with a serous or sero-haemorrhagic content
 the third degree of frostbite is marked by:
• necrosis of the affected areas
• the formation of scabs
• the subjective symptom is severe pain
 the fourth degree of frostbite
• deep necrosis of tissues
frostbite of the third degree
Simple contact dermatitis
Simple dermatitis caused chemical irritants
Tfactors, which induce simple contact dermatitis, arhe
chemical e strong acids and alkalis, salts of alkaline metals,
and mineral acids, chemical warfare substances affecting
the skin in any person
Strong solutions of the listed chemicals are obligate irritants
and induce dermatitis is acute in character
 usually takes the course of necrosis with the formation of a
scab
 leaving an ulcer when the scab drops off
Longterm exposure to weak concentrations of these
substances may induce chronic dermatitis manifested by:
 desquamation and dryness of the skin
 sometimes by the formation of painful cracks (fissures)
Chemical dermatitis may develop in children in excess
concentration of disinfectants added to their bath water.
Simple contact dermatitis
 Solar dermatitis
The short-wave of sun rays spectrum and ultraviolet
rays are mainly responsible for the occurrence of
dermatitis.
Solar dermatitis may occurs acute and chronic

ACUTE SOLAR DERMATITIS manifested by rush, which

appear a few hours after irradiation
 redness and swelling of the skin
 sometimes by vesicles and blisters
 sensation of burning and pain
 general phenomena occur when large skin areas
are involved (headache, vomiting, elevated body
temperature)
 the disease terminates in scaling and pigmentation
in a few days
Solar dermatitis
Photodermatitis
Photodermatitis
Photodermatiti
s
Photodermatitis
 Simple dermatitis caused chemical irritants
Various types of ionizing radiation (X-ray radiation, alpha-, beta-
and gamma- rays, neutron radiation) may induce acute or
chronic radiation dermatitides.
The degree of the radiation dermatitis manifestation is determined
by:
 the dosage
 penetrating capacity of radiation
 the size of the area exposed
 individual sensitivity
X-ray ulcer
X-ray dermatitis
 Biological dermatitis Simple dermatitis caused
biological factors
The group of biological factors may cause simple
contact dermatitis (phytodermatitis)
The disease may develop when walking through
dew-covered grass, resting in meadows
(particularly after a swim), and during hay-making,
in children's summer camps
 the lesions localized on skin areas which come in
contact with the plants (on the hands, feet,
abdomen, thighs and knees)
 erythema and blisters with a serous content
develop
 the blisters resolve within a week leaving
pigmentation
phytodermatitis
Simple dermatitis caused
electricity current
Electricity effect
The treatment of simple
contact dermatitis is
determined by:
 remove of irritant, allergen
 the condition of the patient's organism
 the attendant secondary infection
 particularly by the size of the pathologic area
External Treatment
 on mild hyperaemia can using powders and
corticosteroid ointments, on hyperaemia and swelling
solution for application or aqueous shake solutions,
corticosteroid cream, aerosol “Pantenol”, “Alosolum”,
losions “Pantenol”, “Bepanten” and etc.
 on erosions area can using Castellani's paint or
aqueous alcohol solutions of aniline dyes which also
cause a favourable effect in concomitant secondary
infection
 chronic dermatitides - are treated by corticosteroid
and then with keratoplastic (containing naphthalan,
tar) ointments
 corticosteroid ointments with antibiotics - Lorinden C,
Dermosolone, HyoxiSone, Belogent and etc.
 ALLERGIC CONTACT
DERMATITIS

Etiology:
is caused by facultative
(conditioned) stimuli after the
preliminary sensitization of
the organism
 Clinical signs of contact allergic
dermatitis:

 Process is focused
 Precipitations are asymmetric
in the place of contact with
the allergen
 Boundaries of centers are
clear
 Rash is polymorphous (spots,
papules, blisters, bubbles and
the pustules)
Contact allergic
dermatitis of the
face
Contact allergic dermatitis
Contact allergic
dermatitis of the
face
Contact nickel dermatitis
Contact allergic dermatitis of feet
 Treatment.
Systemic:
 hyposensitization treatment
 sedatives
 antihistamines
 steroid hormones
 vitamins
External anti-inflammatory treatment depends on the
morphological features of the eruption
The management of patients with allergic dermatitis is
there fore planned on the same principles as the
treatment of eczema patients, but before all else the
effect of the stimulating and sensitizing factors is
removed
Systemic Treatment
 antihistamines – suprastin, klaridol, klaritin, arius
and etc.
 desensebilsation medicine - (intravenous infusion
of calcium chloride , calcium gluconate 10% or
sodium hyposulphate 30%solutions)
 sedaive medicine – extractus valeriane, persen,
novo-passte and etc.
 enterosorbents – enteros gel, polifepan, polisorb
and etc
External Treatment
 on mild hyperaemia can using powders and
corticosteroid ointments, cream, on hyperaemia and
swelling solution for application or aqueous shake
solutions, corticosteroid ointment, cream, aerosol
“Pantenol”, “Alosolum”, losions “Pantenol”,
“Bepanten” and etc.
 on erosions area can using Castellani's paint or
aqueous alcohol solutions of aniline dyes which also
cause a favourable effect in concomitant secondary
infection
 chronic dermatitides - are treated by corticosteroid
and then with keratoplastic (containing naphthalan,
tar) ointments
 corticosteroid ointments with antibiotics - Lorinden C,
Dermosolone, HyoxiSone, Belogent and etc.
 Toxicodermia, or toxico-allergic
dermatitis
, is acute inflammation of the skin and,
sometimes, the mucous membranes

Ways irritant acting through:

 the respiratory tract or
 the alimentary canal
 introduces into the vein
 introduces into the muscle
 under the skin

These are usually cases of drug toxicodermia.

 Clinical signs of toxicoderma:

 Process bears the diffuse nature

 Precipitations are symmetric
 Boundaries are illegible
 Rash is polymorphous
Toxicoderma
Toxicoderma
 Clinical picture
The causes of toxicodermia as a rule are drugs and foods
Toxicodermia can manifeste like diffuse and local (fixed) process
Diffuse toxicodermia:
 often found on the skin, lips and mucous membranes
 the clinical picture of toxicodermia is characterized by
polymorphic eruptions (papules, wheal, erythema, spots,
papulo - vesicales)
 diffuse erythematous foci or erythrodermia develop are rarer
 the general symptoms - functional disorders of the nervous
system (irritability, which is replaced by a state of depression,
insomnia, emotional lability, etc.), elevated body temperature
(in some patients) transient arthralgia, symptoms of involvement
of the cardiovascular system (including the small vessels, which
causes the development of the haemorrhagic component), as
well as the liver and kidneys (drug disease)
 subjective symptoms: sensation of itching and sometimes
burning sensation
 leucocytosis, eosinophilia, anemia,
Fixed toxicodermia:
Fixed drug
erythema
 Stiven-Johnson
syndrome
Аcute severe allergic reaction characterized by
extensive lesions of the skin and mucous membranes
induced by medication.
Most often, Stevens — Johnson syndrome
develops when taking medications, but in some
cases, the cause of the disease can not be found
out. Among medicinal drugs, which upon receipt
often develops Stevens— Johnson syndrome, there
are: sulfonamides, allopurinol, phenytoin,
carbamazepine, fenilbutazon, piroxicam, and
chlormezanone, penicillins.
In Stevens — Johnson syndrome,
there is a lesion of the mucous
membranes of at least two organs,
the lesion area reaches no more than
10% of the entire skin.
Stevens — Johnson syndrome develops
acute, skin and mucosal lesions are
accompanied by severe General disorders:
high body temperature (38... 40 °C),
headache, comatose state, dyspeptic
phenomena
Rashes are localized mainly on the skin of
the face and trunk. Th e c linical pi cture i s c
h aracterized b y t h e a p pearance o f m
ultiple polymorphic rashes in the form of
purplish - red s pots w ith a b luish t inge, p
apules, v esicles, and target- shaped foci.
Very quickly (within a few hours), blisters form
in these places up to the size of an adult's
palm or larger; when they merge, they can
reach gigantic sizes. Bubble tires are relatively
easy to destroy ( a positive symptom of
Nikolsky ), forming extensive bright red eroded
wet surfaces, bordered by fragments of bubble
tires ("epidermal collar"). Sometimes on the
skin of the palms and feet appear rounded
dark red spots with a hemorrhagic component.
The most severe lesion is observed on the mucous
membranes of the mouth, nose, genitals, the red
border of the lips and in the perianal area, where
blisters appear, which quickly open, exposing
extensive, sharply painful erosions covered with a
grayish fibrinous plaque. Thick brown-brown
hemorrhagic crusts are often formed on the red
border of the lips. When the eyes are affected,
blepharoconjunctivitis is observed, there is a risk of
developing corneal ulcers and uveitis. Patients
refuse to eat, complain of pain, burning,
hypersensitivity when swallowing, paresthesia,
photophobia, painful urination.
Lyell's toxicoallergic bullous epidermal
necrolysis
is a peculiar form of drug toxicodermia. Extensive brownish-
red foci occur suddenly and acutely on the skin and mucous
membranes and flabby bullae form against their background.
When the bullae rupture and the superficial epidermal layers
are peeled off, exten¬sive eroded oozing surfaces form.
Nikolsky's sign is positive. The patient's general condition is
grave. There are septic fever (up to 39-40°C), disorders of
cardiac activity, neutrophilia, increased ESR and the
appearance of red blood cells, protein and casts in the urine.
The condition must be differentiated from exfoliative dermatitis,
toxicosis of pregnancy, acute pemphigus, severe form of
erythema exudativum multiforme, and the Stevens-Johnson
syndrome.
Layell`s
syndrome
Nikolsky symptom
Layell`s syndrome
Layell`s syndrome
Layell`s
syndrome
Systemic therapy
 is based on removing the causes or discontinuing the
drug which had caused the disease
 diet
 hyposensitization therapy
 antihistaminis
 vitamin C, P, В complex
 Ca
 diuretics
 enterosorbents
 antipyretics
 hormones therapy (prednisolon, dexometason etc.)
 Systemic therapy
 1. Systemic corticosteroid medications:
 ■ prednisone 90-150 mg per day intramuscularly or
intravenously
 ■ dexamethasone 12-20 mg per day intramuscularly or
intravenously
 2. Infusion therapy (alternation of different schemes is
allowed): ■ potassium chloride + sodium chloride +
magnesium chloride 400.0 ml intravenous drip, for a
course of 5-10 infusions, or ■ sodium chloride 0.9% 400 ml
intravenous drip for a course of 5-10 infusions,Skin disease
Five hundred sixty sixor ■ calcium gluconate 10% 10 ml 1
time per day intramuscularly for 8-10 days; ■ sodium
thiosulfate 30% 10 ml 1 time per day intravenously for a
course of 8-10 infusions.
External Treatment
We should get the anti-inflammatory effect and
relieve itching and burning
 shake solutions (lotions) with menthol, anesthesin
etc.
 hormonal cream (celestoderm, beloderm, elocom
etc.)
 lotions for application
 aniline solutions on erosions
Eczema
it’s a polyvalentic, chronic recurrent diseases
of allergic genesis and characterized by
polymorphic itching eruption.

The name of the disease focuses attention on

the important sign of acute eczema, namely,
multiple small grouped vesicles which rupture
rapidly with the formation of serous 'wells'
somewhat resembling the surface of boiling
water.
 Classification
There is no single generally accepted
classification to date. Some scientists
(Mashkilleison and others) subdivide eczema
into acute (eczema acutum), subacute
(eczema subacutum) and chronic (eczema
chronicum) forms

distinguish the next forms of eczema:

 true: idiopathic, dyshidrotic
 microbial: varicose, mycotic, paratraumatic,
nummular, sycosiform, eczema of the nipples
and the areola of the brest
 seborrhoeic
 infantile
 occupational eczemas
 Stages of development

Exudation

Vesicles Crusts

Papules Scales

Erythema Pigmentation
 True (Idiopathic) Eczema
The clinical picture is characterized by the next signs:
 clearcut polymorphism and variegated eruptions (erythematous
spots, micro vesicles, papules, pustules, erosions, and numerous
scratches)
 true and false (evolutional) polymorphism, i.e. the simultaneous
presence on the affected areas of vesicles, erythema, exudative
papules, small erosions with drop oozing, scales, crusts, and other
lesions, the interrupted character of the affection foci
 the alternation of the affected skin areas with healthy areas
('archipelago' pattern)
 formation of serous 'wells' somewhat resembling the surface of
boiling water
 border is not clear
 process is symmetrical
 itching sensation of various intensity

The transformation of acute eczema to the chronic form usually

occurs gradually and is attended with increasing tissue infiltration
and the change of active hyperaemia to passive hyperaemia.
True eczema
Hyperkeratotic eczema of the palms
Nummular eczema
This form is characterized by:
 mildly elevated and sharply demarcated foci of
affection with regular round contours
 diameter of 1-3 cm and more
 the oedema, erythema, exudative papules and
pronounced drip weeping
 typical localization is the dorsal surface of the hands
but has tends to spread to the skin on the trunk and
the limbs
 tends to recur and is highly resistant to treatment
 the frequent appearance of secondary allergic
eruptions, the morphologically polymorphic microbids
 accompanied with intensive itching
In some cases (in growth of sensitization) they may
transform to true eczema with the formation of very
many rapidly rupturing microvesicles and punctate
erosions with drip weeping (serous or eczematous
wells).
Numular
eczema
Numular eczema
 Dyshidrotic eczema
is characterized by:
 the formation of small, the size of a pin head, and hard
to the touch vesicles on the sides of the fingers and
toes and sometimes on the palms and soles on the
hyperemic area
 large multicameres bullaes are encountered less
frequently
 the vesicles may rupture and turn into excoriations or
they dry up and form flat yellowish crusts
 lying in the epidermis, the vesicles are seen through it
and resemble boiled rice
 often troubled by severe itching, burn sensation
Dishydrosiformous eczema
Eczema of the nipples and the
areola of the breast in females
Eczema of the nipples is often a consequence of
injuries inflicted during breast-feeding or results from
complicated scabies.
Is characterized by:
 lesions are crimson foci covered in places with
layers of crusts
 crusty - scales
 weeping and fissures
 Infantile Eczema
 the disease begins in infancy usually to the age of 3
years
 eruptions appear on the face and then spread to
other body areas
 the skin of the face becomes red and swollen, and
copious coalescing exudative papules and small
vesicles
 in places they are covered with massive brownish
crusts which leave weeping eroded surfaces
 the children are usually overfed, oedematous, they
sleep badly and are excited
 the lymph nodes are enlarged
 eosinophilia is a frequent finding in common analysis of
blood
 after which the process transforms to persistent diffuse
or disseminated neurodermitis
Infantile eczema is therefore characterized in most cases
by the simultaneous presence of the signs of true,
microbial, and seborrhoeic forms of eczema.
Infantile eczema
Microbial eczema
Is often aggravated by accompanying pyogenic
infection, fungus, trauma and varicous symptoms
and characterized by:
 monovalent sensebilisation to infectionic agent
 localization as a rule on the limbs
 asymmetrical process
 clear border
 around or scalloped edges
 the eruption is covered with purulent crusts
 eroded surface is seen after removing the crusts
Initial stage of
venous
hypertension
Paraulcerous
microbic eczema
Seborrheic
eczema
Places of localisation
of seborrhea on the
face
Seborrheal
eczema
Seborrheal
eczema
 Varicose eczema
The varicose complex of symptoms in the lower limb
facilitates the development of this disease.
Factors of risk the development of the disease are
 injuries
 hypersensitivity to drugs used in the treatment of
varicose ulcers
 maceration of the skin in application of dressing
The clinical picture is characterized by:
 localization in the region of the varicosity, around the
varicose ulcers, and in the areas of sclerosed skin
 polymorphic eruption
 sharply circumscribed boundaries of the foci
 moderate itching, which makes varicose eczema
similar to microbial and paratraumatic forms in
clinical manifestations
Varicous disease,
hyperpigmentatio
n
 Treatment of eczema
Systemic therapy
 hypoallergic diet
 removing the causes of the diseases
 sedaive medicine – extractus valeriane, persen, novo-
passte and etc.
 antihistamines – suprastin, klaridol, klaritin, arius and etc.
 desensebilsation medicine - (intravenous Infusion of
calcium chloride, calcium gluconate 10% or sodium
hyposulphate 30% solutions)
 enterosorbents – enteros gel, polifepan and etc
 corticosteroid therapy
 vitamin and microelements – B2, B15,B 6, sulfur
 antibiotics
 antifungal drugs
 Exudation - aplication, aerosol

Vesicles - aniline
Crusts- pasta, aniline
solution
solution

Papules - shake
solution, cream, Scales - shake solution
aerosol cream, ointment, pasta

Erythema - shake
solution, cream, Pigmentation- cream,
aerosol ointment, solution