ADDITIONAL MATERIAL FOR PREPARING FOR THE LESSON

DERMATITIDES
Dermatitis is inflammation of the skin caused by direct exposure to the external
effect of a physical or chemical irritant.
The group of physical irritants includes mechanical agents (e.g. pressure, friction),
high (burns) and low (chilblain, frostbite) temperature, insolation (ultraviolet and
infrared rays), electric current, and X-ray and radioactive radiation (ionizing
radiation). Acids, alkali, the salts of some acids, disinfectants in high concentrations,
and other chemical agents are chemical irritants.
All external irritants are also divided into unconditioned and conditioned
(allergens) irritants. The unconditioned, or obligate, irritants cause dermatitis on the
exposed skin areas unfailingly and in all persons. These are strong acids and alkalis,
water of 60°G and more, etc. The conditioned irritants, or allergens, cause dermatitis
only in some people who are hypersensitive to these agents.
Dermatitides occurring under the effect of unconditioned irritants are simple, or
artificial dermatitides, whereas those caused by conditioned, facultative irritants, i.e.
allergens, are known as allergic dermatitides.
Toxicodermias in which acute inflammation of the skin develops under the effect of
an ingested irritant (entering the alimentary canal), administered intravenously,
subcutaneously or intramuscularly, or inhaled as a vapour (acting by way of the
respiratory tract) are a special type of dermatitis. Inflammation of the skin occurs if
the patient's body possesses individual intolerance of these substances.
Drug dermatitides (dermatitides medicamentosa) are also distinguished. They may
be simple (effect on the skin of high concentrations of drugs, e.g. resorcinol, salicylic
acid, etc.) or allergic (in medical personnel who work with streptomycin,
chlorpromazine and other drugs; in such cases it is said that the person is suffering from
occupational drug dermatitis). Drug dermatitis is often of a fixed character, i.e.
medication with the drug always produces lesions on the same skin areas. Drug
dermatitides are usually induced by penicillin, streptomycin, streptocid
(sulphanilamide), procaine and less frequently by amidopyrine, mepacrine, bromine,
iodine, mercury, phenobarbital, etc.
The length of time during which the irritant exerts its effect and its strength
(concentration) and properties determine whether the acute or the chronic form of
dermatitis will develop. Acute dermatitis may be manifested by erythema, swelling,
vesicular and bullous eruptions or tissue necrosis with the formation of an ulcer which
leaves a scar or cicatricial atrophy. Chronic dermatitis is characterized by mild
hyperaemia, infiltration, lichenization, and hyperkeratosis.

SIMPLE CONTACT, OR ARTIFICIAL DERMATITIS

The characteristic features of simple (artificial) contact dermatitis are as follows:
exclusive occurrence at the site of action of the irritating factor and the absence of
sensitization and tendency towards dissemination or peripheral growth. Moreover,
such dermatitis resolves (even without any active treatment) one or two weeks after the
action of the irritant ceases. Simple contact dermatitis is usually acute and occurs
soon after exposure to the irritant.
Simple 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).
Pressure, that of a long duration in particular, and friction are among the
mechanical factors, which may induce dermatitis. Their action leads to the development
of sore skin (e.g. on the feet when the footwear is tight and does not fit; on the palms
from pressure of instruments in heavy physical exertion; in the folds, particularly in
infants, as the result of friction of touching surfaces with the development of
maceration). Sore skin is attended with hyperaemia and swelling and in some cases by
blisters (bullae) with a serous or haemorrhagic content. When the blisters rupture from
continued traumatization, eroded surfaces form, which correspond in size to that of
the traumatized area. The patients experience pain and a sensation of burning. Under
chronic pressure and friction of relatively small force the affected skin areas harden and
undergo lichenization because of infiltration of the skin, thickening of the epidermis,
and hyperkeratosis.
One of the forms of dermatitis in children is called intertrigo. It develops from
irritation of the skin by the folds of diapers and clothes and is manifested by
hyperaemia, epidermal maceration, in some cases by oozing (when erosions form), a
sensation of burning, and pain.
Accompanying pyogenic or yeast infections alter the clinical picture of sore skin or
intertrigo, sustain the inflammatory process, and lead to a more persistent course.
Other forms of simple contact dermatitis caused by physical agents are those occurring from
exposure to high and low temperatures (burns, frostbite, chilblains), ultraviolet rays (solar
dermatitis, dermatitis caused by irradiation with a mercury-vapour lamp), and X-ray and
radioactive radiation (radiation dermatitides develop under the effect of ionizing
radiation).
The effect on the skin of high temperature results in burns (combustio). Children acquire
dermatitides under the effect of high temperatures when they are bathed in water over 40°G.
Four degrees of burns are distinguished. In the first degree burn erythema and mild
swelling form on the affected skin area (the subjective sensations are burning and pain). In
second degree burns bullae form on the hyperaemic and swollen skin. A third degree burn
is characterized by necrosis of the superficial dermal layers without the formation of scabs.
In fourth degree burn all the dermal layers undergo necrosis and a scab forms; an ulcer is
revealed when the scab comes off. The prognosis is determined not only by the degree of the
burn, the condition of the patient's organism, and the attendant secondary infection, but
particularly by the size of the burnt area. Exposure to low external temperature leads to
damage of the tissue by cold and is called frostbite (congelatio), four degrees of which are
distinguished. In first degree frostbite, the affected area is congestive-bluish in colour and
swollen (the subjective sensations are prickling and itching). The clinical picture of second
degree frostbite is similar to that described above, but blisters with a serous or
serohaemorrhagic content form on the affected skin areas. A third degree frostbite is marked
by necrosis of the affected areas with the formation of scabs (the subjective symptom is
severe pain). Deep necrosis of tissues (even to the very bones) occurs in fourth degree
frostbite. The manifestations of frostbite are preceded by a latent period during which the
affected area becomes cold, pale, and insensible. Frostbite commonly occurs on exposed
areas and distal parts of the body (fingers, toes, the skin on the nose and cheeks, ears).
Factors conducive to frostbite are increased humidity of air, wind, tight footwear and
reduced resistance of some tissues (a history of frostbite, increased perspiration, injury,
etc.) and the body as a whole (physical fatigue, stress, lack of vitamins, weakening of
the body after acute or chronic infectious diseases, copious blood loss, alcoholic intoxication,
etc.). These conditions of the body may lead to frostbite even if the temperature is above
zero (5 to 8°C). Under the effect of long-term exposure to cold in combination with dampness,
asthenic individuals and those with lack of vitamins С and A (mostly children and
adolescents) develop a peculiar skin lesion called chilblain (perniones). Increased
sensitivity to cold leads to frequent recurrences of the disease in these individuals, especially
in the autumn; a remission occurs in summer. A tendency to develop acrocyanosis of the limbs
and damp, poorly heated quarters for living and working are conducive to the development
of the disease. A somewhat thickened or soft swelling with indistinct contours forms on the
affected skin areas; it is cyanotic-reddish on the distal and middle phalanges of the fingers
and toes and on the joints or pale-red with a bluish hue on the cheeks.
In warming, the sensations of itching and burning grow and tenderness appears on
palpation. Chilblains do not necessarily develop only at temperatures below 0°C.
Exposure of the skin to sun rays may lead to the development of acute or chronic solar
dermatitis (dermatitis Solaris). Of the entire spectrum of sun rays, it is the short-wave and
ultraviolet rays that are mainly responsible for the occurrence of dermatitis. Individuals who
are unused to long exposure to the sun, those with delicate, hardly pigmented skin (mostly
among the fair-haired) may develop acute solar dermatitis manifested by redness and
swelling of the skin and sometimes by vesicles and blisters, which appear a few hours after
irradiation. The process is attended with a sensation of burning and pain. General phenomena
(headache, vomiting, elevated body temperature) occur when large skin areas are involved.
The disease terminates in scaling and pigmentation in a few days. Chronic solar dermatitis
manifested by infiltration, pigmentation, and dryness of the skin is encountered in fishermen,
seamen, and individuals exposed to the sun when they work (in the fields, at construction sites,
etc.), i.e. individuals whose occupation makes them subject to insolation for lengthy
periods of time.
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 manifestation
of radiation dermatitis is determined by the dosage and penetrating capacity of radiation, the
size of the area exposed, and individual sensitivity.
Depending on the factors listed above, acute radiation dermatitis may be manifested by
erythema (with a peculiar violet or light-blue tinge), temporary loss of hair, a bullous reaction
developing against the background of intensive hyperaemia and swelling (in which cases the
process terminates in atrophy of the skin, permanent alopecia, the formation of telangiectasia,
and disorders of pigmentation known as 'motley' or 'X-ray' skin); a necrotic reaction occurs
the manifestations of which are similar to those of bullous dermatitis but are more pronounced
(with tissue necrosis) and attended with severe general phenomena.
Multiple exposure of the skin to relatively small doses of 'soft' X-rays and to radioactive
substances causes the development of chronic radiation dermatitis. The last may also he
consequent upon acute radiation dermatitis. The process is characterized by poikiloderma
(variegated skin). The skin is dry, thinned out, and lacks elasticity; there are telangiectasia,
hyperpigmented and depigmented areas, onychodystrophy and itching. Chronic radiation
damage to the skin is conducive to the formation on the affected areas of papillomas,
hyperkeratosis, and warts which may undergo malignant degeneration.
Late radiation dermatitides, among which late radiation trophic ulcer and radiation
carcinoma deserve special attention, may develop at the site of persistent radiation
dermatitides.
The chemical factors, which induce simple contact dermatitis, are strong acids and
alkalis, salts of alkaline metals, and mineral acids, chemical warfare substances affecting
the skin, and many others. With the development of chemical industry the number of
chemicals that may cause dermatitis is constantly growing. Strong solutions of the listed
chemicals are obligate irritants and induce dermatitis in any person. Such dermatitis
develops suddenly, is acute in character, and usually takes the course of necrosis with the
formation of a scab leaving an ulcer when it drops off. Long-term exposure to weak
concentrations of these substances may induce chronic dermatitis manifested by
desquamation and dryness of the skin and sometimes by the formation of painful cracks.
Chemical dermatitis may develop in children in excess concentration of disinfectants
added to their bath water.
The group of biological factors which may cause simple contact dermatitis (phytodermatitis)
includes several plants, such as white dictamnine, cow parsnip, primrose, crowfoot, plants of
the cashew family and some species of redwood (among workers of the furniture manufacturing
industry). The disease may develop when walking through dew-covered grass, resting in
meadows (particularly after a swim), and during hay-making. Such dermatitides can
develop on a mass scale, for example, in children's summer camps. They are localized on
skin areas which come in contact with the plants (usually the skin of the hands, feet, abdomen,
thighs and knees). Erythema and blisters with a serous content develop; the blisters resolve
within a week leaving pigmentation. Pavlov believes that ether oils and chlorophyll contained
in plants and possessing a photosensitizing effect play a role in the development of
phytodermatitides.
Phytodermatitis induced by primrose that possesses a marked allergenic effect is the most
commonly encountered variant. The chemical composition of the allergen is not known, but
it preserves its properties even when the plant has been dried. The disease develops a few
hours or days after contact with the plant. A bright oedomatous erythema appears in the
zone of contact (usually on the hands) and urticarial, less frequently microvesicular eruptions,
form on the adjacent skin areas (forearm, arm, face, etc.) which are often hyperaemic. The
patient is troubled by itching and a burning sensation. In tropical countries a severe
phytodermatitis induced by the plant Excoeraria agalloche develops at the site of contact
with its leaves within minutes and is manifested by erythematous spots and urticaria, which
coalesce and form extensive plaque foci. In localization on the face, oedema is particularly
pronounced; the conjunctiva and iris may be involved in the process as a result of which loss
of vision and even complete blindness may occur.
Caterpillar dermatitis may develop on contact of human skin with various caterpillars
as the result of the effect of substances excreted by their gland cells. The dermatitis develops
a few minutes after contact in the form of a swollen pink urticarial line, stretching on the skin
along the path of the caterpillar's movement. On scratching, the caterpillar's hair may be
transferred to other skin areas on which erythema and urticaria also form.
Treatment. The therapeutic measures for simple contact dermatitis are determined by the
severity of the inflammatory phenomena. In mild hyperaemia, prescriptions may be limited to
powders and corticosteroid ointments. In cases with marked hyperaemia and swelling, lotions
or aqueous shake solutions are first used and then corticosteroid ointments. In cases with
blisters, the surrounding skin areas are first cleaned with 70 per cent ethyl alcohol and 1 per
cent boric acid, after which the blisters are then punctured and the affected area painted with
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 warm baths and emollient ointments (diachylon
ointment, ointment containing 2-3 per cent salicylic acid), corticosteroid and then with
keratoelastic (containing naphthalan, tar) ointments.
First degree burns are treated with corticosteroid ointments but first cotton or gauze
moistened in 70 per cent ethyl alcohol and 1 per cent boric acid is applied to the surface of
the burn to relieve pain. Skin involved in second and third degree burns is bathed with
hydrogen peroxide, the top of the blister is cut and dressings with disinfectant solutions are
applied (for several days). Corticosteroid ointments with antibiotics (Lorinden C, Dermosolone,
Hyo-xiSone), Vishnevsky's ointment, 5 per cent sulphanilamide or 5 per cent boric acid-
naphthalan ointment are prescribed after the acute inflammatory phenomena subside.
Antibiotics are prescribed in second-third degree burn to prevent coccal infection. Extensive
burns of all degrees, fourth degree burns, as well as third and fourth degree frostbites, are treated
by surgeons (as indicated). In acute solar dermatitis, the affected areas are smeared with
cooled Unna's cream or shake lotions after the large blisters had been punctured. Emollient
or corticosteroid ointments are prescribed in chronic solar dermatitis. Photoprotective
ointments such as quinine, salol, methyluracil or protective creams containing pa-га-
aminobenzoic acid are recommended for the prevention of solar dermatitis, particularly for
persons hypersensitive to sun rays.
 Severe radiation maladies are treated in specialized in-patient clinics (mainly in those
where patients are treated for haematological diseases). The principal means of treatment in
such cases are stimulating measures (blood transfusions, biological stimulators, sera, blood
plasma, etc.), a diet rich in proteins, and vitamin therapy. The management of skin radiation
lesions depends on their severity. In early radiation skin reaction and radiation alopecia,
for instance, external treatment is not applied. In erythomatous radiation dermatitis anti-
inflammatory lotions, pastes and ointments (corticosteroid among others) are prescribed.
Bullous radiation dermatitis is treated in the same manner, but the contents of the blisters are
first removed. Preparations of calcium and antihistaminics are prescribed orally. Disinfectant
ointments and antibiotics are used in attendant pyogenic infections. Emollient ointments
and creams with a small content of keratolytic agents and steroid preparations are prescribed
in chronic radiation dermatitis. Papillomas and warts are removed by
diathermocoagulation.
The principles of contact dermatitis management described above are also applied in the
treatment of dermatitides caused by chemical agents, with the only difference that an attempt
should be made to neutralize the effect of the obligate irritant as soon as it gets on the skin
by holding the affected part under a stream of tap water.
In plant-induced dermatitides the blisters are punctured and their tops painted with
2 per cent solutions of aniline dyes.
Miliaria (seu sudamina) develops in infants and young children, especially in those
who are overnourished and in those suffering from exudative diathesis. Overheating when the
external temperature is high or a rise in body temperature in acute infections lead to rapid and
marked increase of perspiration and thus contributes to the development of the disease.
Miliaria is manifested by multiple diffuse or grouped papules or vesicles. The following
forms are distinguished: (1) miliaria crystalline, an eruption of numerous vesicles the size of a
millet, found mostly on the trunk, with no hyperaemic ring on their periphery; there is no
itching; (2) miliaria alba marked by tiny white purulent pustules on the apex of the papules;
this form often develops into miliaria rubra, when the pustules acquire an inflammatory-red
colour as the result of the macerating effect of the sweat on the skin and accompanying
pyococcal infection; the child is troubled by severe itching when these lesions occur in the
skin folds; (3) miliaria flava is a condition, in which the advancing coccal infection leads to
the formation of yellow intraepidermal pustules.
Treatment. External treatment consists in rubbing the skin with a 1 per cent boric or
salicylic acid solution prepared on 40 per cent ethyl alcohol or Alibur's solution, and powdering
with powders containing 1-2 per cent boric acid or 1 per cent Vioform (Clioquinol) and
neomycin. Oletetrin, tetracycline, and other antibiotics are prescribed in doses corresponding
to the child's body weight and age for one week in order to suppress secondary pyococcal
infection. Oral medication with Belloid and Bellaspon reduces the increased sweat production.
Measures aimed at avoiding overheating of the child and reducing abnormally high sweat
production prevent the development of miliaria.

ALLERGIC CONTACT DERMATITIS

Allergic dermatitis occurs in patients with heightened sensitivity to a definite substance,
the allergen. Hypersensitivity may be congenital, in which case the condition is called
idiosyncrasy (e.g. to eggs, citrus fruit, strawberries, etc.). Much more frequently increased
sensitivity develops in repeated contact with the allergen, which results in monovalent
sensitization of the body. The underlying factor of such sensitization is a delayed allergic
reaction attended with the formation of an antigen-antibody complex in the epidermal cells. The
general condition of the body (the state of the nervous and endocrine systems in particular) is
of importance in the occurrence of this reaction.
The number of substances that may cause allergic dermatitis is tremendous and still
growing with the development of industry, chemical among others. For example, chemical
substances (salts of chromium and nickel, synthetic resin), dyes (Ursol), some plants and
flowers may be allergens. Various drugs form a large group of allergens; these are: penicillin,
streptomycin, erythromycin, nystatin, griseofulvin, synthomycin and sulphanilamide
emulsions, sul-phacil-sodium, acetarsol, procaine hydrochloride, amidopyrine, me-thenamine,
formalin, mercury preparations, resorcinol, salicylic acid, Psoriasin, and many other drugs
used for external application.
Though the allergen comes in contact with a limited skin area, the whole body is
nevertheless sensitized. Monovalent sensitization occurs at first. In recurrences of allergic
dermatitis, however, group, or less frequently, polyvalent sensitization may develop,
which is one of the signs of the transformation of allergic dermatitis to eczema.
Besides the clinical manifestations characteristic of contact dermatitis, signs typical of
eczema occur in patients with allergic dermatitis but they are less pronounced
(vesiculation, weeping, tendency to recur).
In contact allergic dermatitis erythema, swelling, and the pa pular and vesicular
lesions are localized on areas, which had been exposed to the allergen (commonly the
back of the hand, the face, cheeks, and neck, less frequently the lower limbs, forearms and
arms) but in some patients the process tends to spread to the covered skin areas (Fig.
19). Repeated contact with the allergen facilitates the transformation of allergic
dermatitis to eczema. The main feature distinguishing eczema from allergic dermatitis
is the resolution of the latter following removal of the aetiological factor, which is iden-
tified by means of positive skin tests (see the section dealing with occupational skin
diseases).
Treatment. First of all the cause of allergic dermatitis must be identified and
removed. External anti-inflammatory treatment, which depends on the morphological
features of the eruption, is supplemented without fail by hyposensitization treatment,
the prescription of sedatives, antihistaminics, steroid hormones, and vi tamins. The
management of patients with allergic dermatitis is therefore planned on the same
principles as the treatment of eczema patients (see the respective section), but before
all else the effect of the stimulating and sensitizing factors is removed.

TOXICODERMIA
Toxicodermia, or toxico-allergic dermatitis, is acute inflammation of the skin and,
sometimes, the mucous membranes, which is caused by an irritant acting by way of the
respiratory tract or the alimentary canal or one that was introduced into the vein,
under the skin or into the muscle. These are usually cases of drug toxicodermia.
Drug toxicodermia is a manifestation of the sensitizing effect of the medicine. A
combination of allergic and toxic components in different proportions is often
responsible for its pathogenesis and causes the development of various lesions of the
skin, mucous membranes, the nervous and vascular system, and the internal organs,
which are typical of drug disease. Drug toxicodermia may occur as the result of long-
term medication with some agent. In some patients it is a manifestation of a para-allergic
reaction. In such cases preceding diseases (rheumatism, tonsillitis, epidermophytosis,
etc.) prepare the organism for drug intolerance. Drug toxicodermia occurs in some
patients as the result of drug idiosyncrasy. Besides the drugs mentioned in the section on
allergic dermatitis, chlortetracycline, chloramphenicol, preparations of organic arsenic
(neoarsphenamine) and iodine, vaccines and sera, vitamins B l5 Be, and Bla,
chlorpromazine hydrochloride, antipyrine, AGTH, angiotrophine, chloro-quine
phosphate, guingamine (chloroquine diphosphate) and others possess allergic propert ies.
Antibiotics, sulphonamides and quinine compounds have particularly marked allergic
properties.
On entering the cells of the skin and other tissues, the allergen binds with the
functional cytoplasmic structures (nucleoproteins, mitochondria) and then enters the
blood plasma. Affection of the skin and other organs may also result from suppression
of the enzymatic systems by the drug, toxic damage to the tissues and ves sels
(especially in overdosage), and change in body reactivity.
The clinical picture of drug toxicodermia is characterized by ery-thematous, papular,
vesicular or papulovesicular eruptions. Diffuse papular or vesicular (bullous) eruption
is often found on the skin and mucous membranes, diffuse erythematous foci or
erythrodermia are rarer. One and the same drug may cause a morphologically different
form of toxicodermia in different individuals.
At the same time, some drugs produce a clinical picture of toxi-codermia typical precisely
of them. Iodine or bromine toxicoder-mia occurring in medication with iodine or bromine
salts and alcohol iodine solutions, for instance, is characterized by the development of an
acneiform eruption ('bromine' or 'iodine' acne) or tuberous bromoderma (iododerma), which
is manifested by succulent soft plaques elevated above the skin surface and covered with pu-
rulent crusts. On removal of the crusts, a vegetating surface of a pus secreting infiltrate is
exposed. In toxicodermia induced by sul-phonaxnides, erythematous reddish-brown with a
lilac tinge foci develop which are demarcated and have rounded outlines. Sulpho-namide
toxicodermia is manifested particularly often in the form of fixated erythema which appears
at one and the same place a few hours after medication with a sulphonamide drug and after
disappearing (in a few days) leaves a slate-brown pigmentation intensifying after each
recurrence.
Bullae sometimes form on the plaques. The favoured localization of sulphonamide
erythema are the hands, lips, oral mucosa and the region of the genitals.
Among the general symptoms, which may be encountered, are 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) attended with general
indisposition, a feeling of jadedness, 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). The subjective
symptoms in most cases come down to a sensation of itching, burning, tension and
tenderness of the skin on the affected area.
Providing that the allergen drug is discontinued in good time, drug toxicodermia is
usually short-lived. In cases with involvement of the cardiovascular system and the internal
organs, however, the prognosis may be unfavourable.
In some cases the skin manifestations of drug toxicodermia may resemble those of lichen
rubrum planus, erythema exudativum multiforme, eczema, pityriasis rosea, etc.
The presence of symptoms of involvement of the internal organs, nervous system and vessels
in drug toxicodermia is important in making the differential diagnosis. The aetiological role
of drugs may be authentically confirmed by means of allergological examination (skin tests,
leucocyte agglomeration test, basophil degranu-lation test, etc.). In some cases with suspected
sulphonamide erythema, 0.15-0.3 g of the same sulphonamide drug, which the patient had been
given most frequently, may be prescribed in the clear period (provocation method). If the drug
had been chosen correctly, the process exacerbates. A similar test is performed with antipy-
rine and barbiturates.
Treatment is based on removing the causes or discontinuing the drug which had caused the
disease. After that, hyposensitization therapy is conducted, antihistaminics, vitamin C,
vitamins of the В complex, rutoside, diuretics (theobromine and sodium salicylate,
hydrochlorothiazide, furocemide, mullein decoction) and purgatives are prescribed. External
agents that cause an anti-inflammatory effect and relieve itching and burning (powders,
aqueous and oil shake lotions) are prescribed.
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, extensive 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 (see below).
Treatment follows the principles of toxicodermia therapy (see above). Without the use of
steroid hormones, a therapeutic effect cannot be achieved in many instances. Moreover,
abundant drinking, intravenous infusions of a 30 per cent sodium hyposulphite solution in a
single dose of 2-10 ml, and external application of steroid creams are recommended.

ECZEMA
General Information
Eczema (Gk. eczema to erupt, to boil) is a universally encountered, mostly acute, less
frequently chronic, recurrent skin disease, characterized by pleomorphism of the
morphological lesions; it occurs at any age. 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.
The term 'eczema' has been used for many centuries (two centuries В. С.) but to designate
various rapidly developing dermatoses. It was only in the first half of the 18th century that
Willan (1808), Bateman (1813), Rayer (1823) and other authors set eczema apart as a
nosological form.
In various stages of the study of eczema, the principal role in its aetiology and
pathogenesis was attributed to the nervous system (neurogenic theory), the endocrine glands,
the allergic state of the body (allergic theory), hereditary factors, and other causes. It should
be admitted that the aetiology and even the pathogenesis of eczema are extremely
complicated, not always identical, and are still unknown in many of their aspects.
It is now accepted (Skripkin, Shakhtmeister and others) that the eczema process
develops as the result of the effect of a complex of neuroallergic, endocrine, metabolic and
exogenic factors. The exogenic irritants include chemical and biological agents, bacterial
allergens, physical factors, drugs, foodstuffs, cosmetics, etc.
At the onset of the disease allergic reactivity sometimes is monovalent in character.
With the advancement of the dermatosis the sick organism begins reacting differently in
both quality and quantity to numerous irritants and allergens, which testifies to the de-
velopment of polyvalent sensitization characteristic of eczemas. The eczematous reaction
is a delayed allergic reaction. In some patients, however, immediate-delayed reactions
(anaphylactoid reaction) may develop with the use of drugs (penicillin, procaine hydro-
chloride, vitamins of the В complex, etc.).
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 and distinguish as
independent forms also seborrhoeic (eczema seborrhoeicum), infantile (eczema infantum),
varicose (eczema varicosum) eczemas. Pavlov, Sha-poshnikov and others distinguish true,
microbial and occupational eczemas. We shall mainly discuss true (idiopathic), microbial,
infantile, seborrhoeic, and occupational eczemas. Each of these forms may be acute,
subacute or chronic. We shall also take note of the less frequently encountered forms of
eczema
True (Idiopathic) Eczema
Erythema (eczema erythematosum) appears at the onset against the background of which
micro vesicles (to the size of a pin head), papules (mostly exudative), and pustules form
(eczema vesiculosum, papulovesieulosum, papulosum, and pustulosum). The micro vesicles
in the centre of the focus rupture, the serous exudate seeps onto the skin surface and produces
oozing areas with a macerated and scaling horny layer (eczema madidans). Careful
examination of the focus will reveal numerous 'point' erosions from which small drops of
serous exudate emerge (serous wells).
The clinical picture is characterized by clear-cut pleomorphism and variegated
eruptions. Erythematous spots, micro vesicles, papules, pustules, erosions, and numerous
scratches may be simultaneously encountered at the peak of the inflammatory process.
True and false (evolutional) pleomorphism, 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 foci of
affection, and the alternation of the affected skin areas with healthy areas ('archipelago'
pattern) are extremely characteristic of the eczematous process. The eruptions are
symmetric and tend to spread to the skin on the upper and lower limbs and trunk. The
patients are troubled by itching of various intensity, which is conducive to the
development of neurotic disturbances with insomnia. With the gradual abatement of the
inflammatory phenomena, typical of an eczematous process, the oozing is replaced
by the formation of crusts and scales and the appearance of peeling (eczema crustosum,
eczema squamosum) and secondary pigmento-vascular or depigmented spots which
resolve gradually. Foci of dry and peeling skin with the formation of cracks in the horny
layer (eczema craquele) may arise. Callous hyperkeratotic tissues with cracks
sometimes form on the palms and soles in protracted chronic eczema (eczema tyloticum).
The course of eczema is often aggravated by accompanying pyogenic infection; pustules
and purulent crusts form in such cases (eczema impetiginosum).
Despite the marked pleomorphism that is typical of eczema, one type of the
morphological lesions may sometimes be prevalent, in which case it is possible to
diagnose the forms of true eczema mentioned above. It should be emphasized that the
transformation of acute weeping eczema to the chronic form usually occurs graduall y
and is attended with increasing tissue infiltration and the change of active hyperaemia
to passive hyperaemia. A chronic eczematous process often exacerbates with the
reappearance of active hyperaemia, microvesicles, and oozing and intensification of
itching.
In children idiopathic eczema occurs in the second or third months of life and is
manifested by symmetrical erythematous-squamous and exudative-papular eruptions
with unclearly defined outlines and microvesicles on the face and upper or lower limbs
and is marked by severe itching. Eczema in children, however, is usually characterized
by a combination of signs of the true, microbial, and seborrhoeic forms.
The following varieties of true eczema are known.
Pruriginous eczema. This form is characterized by eruption of small, the size
of a millet, papulovesicular lesions on an indurated base; they neither rupture nor form
erosions. The foci of affection are localized on the face, the flexor surfaces of the elbows
and knees, in the inguinal region, and on the extensor surfaces of the limbs; the lesions
recur often and the disease takes a chronic course. As the result of the protracted
course, scratches, excoriations, and deposits of cellular infiltrate, the skin on the
affected areas becomes rough, pigmented, dry, chapped, and undergoes
lichenification, though less markedly than in neurodermitis. Attacks of itching and
severe neurotic reactions with insomnia are very characteristic of this dermatosis. The
disease usually exacerbates in the winter and a remission occurs in the summer. This
disease is as if an intermediate form between true eczema and priirigo.
In children, pruriginous eczema usually develops at the age of 4 to 6 months (in
contrast to seborrhoeic and true eczema which sets in in the first weeks and months of
life) and is marked by stable dermatographia alba, which reflects the prevalence of
the tonus of the sympathetic part of the vegetative nervous system. The areas of
affection described above are usually arranged in children against an oedematous,
erythematous background and are often attended with bronchial asthma.
Dyshidrotic eczema (eczema dyshidroticum) 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. Large multiloculate bullae are
encountered less frequently. Lying in the epidermis, the vesicles are seen through it and
resemble boiled rice. The patients are often troubled by severe itching. The vesicles
may rupture and turn into excoriations or they dry up and form flat yellowish crusts.
Sharply demarcated foci of affection form later and have a marked inflammatory colour,
which distinguishes dyshidrotic eczema from true dyshidrosis (dyshidrosis vera) and
epidermophytids of the palms (in dyshidrotic epidermophytosis mycelial threads of the
epidermophyton fungus are found on the covers of the vesicles on the arch of the
foot).
Microbial Eczema
The aetiology and pathogenesis of microbial (paratraumatic, localized around the
wound) eczema, in distinction from those of true eczema, have been studied sufficiently.
It is considered established that the antigenic properties of pyococcal flora and
pathogenic fungi, yeasts included, are capable of sensitizing the skin to these allergens.
The increased titres of strepto- and staphylokinase, streptolysin 0 and staphylolysin,
the positive cutaneous-allergic reactions with speci fie antigens, and the detection of
serum antibodies against tissue antigens confirm the existence of an allergic state with
sensitization to streptococci and staphylococci in patients with micro bial eczema.
Neuroendocrine disorders and changes in metabolic processes and immunological states
favour the development of sensitization to the microbial antigen. We have revealed an
obvious dependence between the diminution of immunogenesis activity and the
intensification of the allergic condition, both in children ai \d in adults.
These causes are responsible for the development of the peculiar clinical picture of
microbial eczema, which differs considerably from that of the other forms of eczema.
Microbial eczema usually begins as an asymmetric process on the legs, the back of the
hands, and the scalp. There is a characteristic sharply demarcated focus of affection
(Plate I) often with a fringe of separating epidermal horny layer on the periphery
and a weakly pronounced tendency of the dermatosis to disseminate. The borders of
the foci (acute inflammatory erythema, exudative papules, micro vesicles, pustules) are
often curved and there are accumulations of greenish-yellaw seropurulent and
sanguineous crusts and erosions on their surface.
On areas free of crusts the affected surface is red or congestive-red and bleeds
easily. Punctate weeping (serous or eczematous wells) which is characteristic of eczema
are seen here and there. Exacerbations of the disease occurring from time to time lead
to intensification of itching.
Microbial eczema often sets in with pustules, acute inflammatory erythema and
exudative papules, which appear on the periphery of a trophic ulcer on the leg, in the
region of a postoperative stump, around a fistula; it may also develop as the result of
improper application of a plaster cast, inadequate treatment of the skin around a
wound with iodine tincture, and other factors. In such cases mi-crobiai eczema is called
paratraumatic or eczema arising around a wound. Several varieties of microbial eczema
are known.
Nummular eczema. This form is characterized by mildly elevated and sharply
demarcated foci of affection with regular round contours and a diameter of 1-2 cm and
more; there are oedema, erythema, exudative papules and pronounced drip weeping.
It is a variety of microbial eczema. The process tends to spread to the skin on the trunk
and the limbs, although its favourite localization is the dorsal surface of the hands.
The disease tends to recur and is highly resistant to treatment.
In children microbial eczema is usually combined with ioci of chronic infection
(otitis, rhinitis, highmoritis, frontitis, chronic tonsillitis, conjunctivitis) and other
streptostaphylococcal diseases.
The frequent appearance of secondary allergic eruptions, the morphologically
pleomorphic microbids, during exacerbation of the process is also characteristic of
microbial eczema. These are usually erythematous scaling spots or papular and
papulovesicular eruptions which are 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 ^nd punctate erosions with drip weeping
(serous or eczematous wells).
Varicose eczema. The varicose complex of symptoms in the lower limb
facilitates the development of this disease. It is localized in the region of the
varicosity, around the varicose ulcers, and in the areas of sclerosed skin. Factors
favouring the development of the disease are injuries, hypersensitivity to drugs used in
the treatment of varicose ulcers, and maceration of the skin in application of dressing.
The clinical picture is characterized by pleomorphic lesions, sharply circumscribed
boundaries of the foci, and moderate itching, which makes varicose eczema similar to
microbial and paratraumatic forms in clinical manifestations.
Sycosiform eczema. This form may be encountered in individuals suffering from
sycosis complicated by eczematization. Follicular pustules pierced through the middle
by a hair shaft develop on inflamed skin and recur from time to time; these are
symptoms of sycosis. Sycosiform eczema is characterized by extension of the process
beyond the hirsute areas, the presence of eczematous wells, weeping and severe itching.
Lichenification of the skin occurs and follicles appear incessantly. The favoured
localization of the process is the upper lip, the beard, the axillae and the pubis.
Eczema of the nipples and the areola of the breast in females. The characteristic
lesions are crimson foci covered in places with layers of crusts and crusty scales and
marked by weeping and cracks. The process is sharply circumscribed and very
persistent. Eczema of the nipples is often a consequence of injuries inflicted during
breast-feeding or results from complicated scabies.
Seborrhoeic Eczema
Seborrhoeic eczema is localized on the scalp, face, chest and between the shoulder
blades, i.e. in places where seborrhoea often occurs. Vesiculation and weeping are very
rare in these patients. The presence of seborrhoeids (rounded yellowish-pink
erythematous spots covered with greasy yellowish scales) is a characteristic symptom.
Copious stratified yellowish crusts and scales form on the scalp, the hairs on the
affected areas are shiny and sometimes stuck together in bundles (pityriasis
amiantacea), and seropurulent exudation is often found in the fold behind the ears.
In some cases, severely itching grouped follicular papular eruptions localized mainly
on the lower limbs (eczema folliculorum) gain prominence. The patient complains of
itching (sometimes very intensive), which may precede the clinical manifestations. The
patient is hypersensitive to polyamide and flannel fabrics, contact with which induces
a recurrence of the disease.
There is no unanimity of opinion to date in regard to the classification of seborrhoeic
eczema. Some authors relate it to chronic seborrhoeic dermatitides. Others claim that
it is a peculiar infectious disease caused by particular microorganisms (morococci) or
streptostaphylococci. It is also contended that it would be more correct to diagnose
the condition as chronic diffuse streptoderma rather than as seborrhoeic eczema. We
think that the term 'seborrhoeic eczema' is more correct because it reflects the essence
and morphology of the pathological process. As to the microbial infection, it may play
the role of an antigen in such patients. There is no room for doubt that disturbances
in the neuroendocrine system and body reactivity are of pathogenic importance in
this dermatosis. Seborrhoeic eczema, for instance, occurs in infancy, but is al most
never encountered in the period between infancy and puberty; like seborrhoea it usually
develops after puberty (the role of hyperandrogenia and hypooestrogenia).
Infantile Eczema
In children the eczematous process usually develops against the background of
exudative diathesis, often as a result of hereditary altered immunological reactivity.
Most parents or close relatives of infants with eczema had manifestations of allergy
on the skin, mucous membranes or in the internal organs in the past. It has been reported
that if one of the parents (mainly the mother) has an allergic disease (bronchial asthma,
allergic rhinitis, eczema, neurodermitis, etc.), the child has a 40 per cent chance of
becoming ill, whereas if both parents are sick, the extent of the risk increases to 50 -
60 per cent. Children with exudative diathesis often have torpid foci of focal chronic
infection, bronchial asthma, hay fever, acute respiratory infections, conjunctivitis,
keratitis and gastro-intestinal disorders, and, according to the latest data reported by
Shakhtmeister, dysfunction of the liver and pancreas.
Children suffering from eczema often develop against the background of diminished
immunobiological body resistance manifestations of alimentary allergy (to casein of
mother's or cow's milk) and infectious allergic reactions which are often induced
by foci of chronic infections and then by hypersensitivity to drugs and other chemicals.
The disease begins in infancy. 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 form on it; in places they are covered
with massive brownish crusts which leave weeping eroded surfaces. Signs of
intertriginous eczema may be found in the region of the gluteal and inguinofemoral folds.
Besides the weeping foci described above, children with infantile eczema may have
macular seborrhoeic eruptions (erythematous-squamous spots, seborrhoeids) on the
face, trunk, and limbs. Infantile eczema is therefore characterized in most cases by the
simultaneous presence of the signs of true, microbial, and seborrhoeic forms of eczema. The
children are usually overfed, oedematous, they sleep badly and are excited. The lymph nodes
are enlarged. Eosinophilia is a frequent finding. Infantile eczema occurs usually to the age
of 3 years after which the process transforms to persistent diffuse or disseminated
neurodermitis.
Histopathology. The presence of foci of spongiosis in the epidermal Malpighian layer is
typical of the acute period of eczema. The spongiosis is characterized by oedema mainly of
the prickle-cell layer, separation and tearing off of the cells of this layer, and the formation of
small often multilobate cavities directly under the horny layer. Parakeratosis is seen in the
horny layer. The papillary layer of the dermis is marked by dilation of vessels, the formation
of a lymphocytic-histiocytic infiltrate around them, and oedema of the connective tissue.
The infiltrate in microbial eczema contains polymorphonuclear leucocytes. Acanthosis, the
formation of parakeratotic scales and crusts, and a more pronounced infiltrate of the dermis are
characteristic of chronic eczema.
The findings in seborrhoeic eczema include moderately thickened epidermis, parakeratosis,
marked acanthosis, absence of the granular layer, poorly pronounced vacuolar degeneration
and spongiosis. A mild peri vascular lymphocytic and neutrophilic infiltrate is found in the
dermis. Munro's microabscesses may be seen here and there in the epidermis.
Degenerating exudative cells are detected in the foci of affection in vaccination
(complication of eczema by virus infection after smallpox vaccination of a child Suffering from
the dermatosis or after his contact with children who had received the smallpox vaccine).

TREATMENT OF ECZEMAS
The application of a complex of hypnosuggestive therapy, electric sleep, sedatives,
antihistaminics, and (in cases of a torpid eczematous process) low doses of corticosteroids is
most expedient and pathogenetically substantiated in the management of patients with eczema.
In simultaneous use of these methods, an effect is produced both on the central parts of the
nervous system and on the mechanisms which determine the development of allergic
inflammatory reactions.
Hyposensitization therapy also includes medication with calcium preparations and sodium
hyposulphite (2 to 10 ml of a 10 per cent calcium chloride or 30 per cent sodium hyposulphite
solution is infused intravenously every other day; a total of 20 infusions) in combination with
antihistaminics (0.025 g of suprastin given three times a day or 1.0 ml of a 2.5 per cent solution
injected subcutaneous ly; 0.1 g of mebhydrolin napadisylate, 0.001 g of clemastinfume-rat,
Q.05 g of diphenhydramine hydrochloride or 0.025 g of prome-thazine hydrochloride given two
or three times a day in the afternoon and evening).
Diuretics (hydrochlorothiazide, furocemide, mullein decoction, theobromine and sodium
salicylate) are taken in the morning the first four or five days to reduce tissue oedema.
Intramuscular injections of a 25 per cent solution of magnesium sulphate (4-6-8 and then 10
ml is injected every other day to a total of 10 to 15 injections) prove very beneficial in
individuals with a tendency to hypertension. Magnesium sulphate causes a hyposensitizing,
sedative and hypotensive effect, reduces tissue oedema and inflammatory potential, and
improves the filtration function of the kidney.
Histaglobulin therapy produces positive results. Intracutaneous injection of the preparation
by the 'lemon peel' method is extremely effective; it is injected in gradually increasing doses of
0.05-0.1 ml and then in doses of 0.25-0.4-0.6-Q.8-1.0 and so on to a dose of 2.0 ml at intervals
of two or three days. The injections are made at eight points (four on the lateral surface of the
right, and four points on the lateral surface of the left arm). No more than 0.25 ml is injected
at each point.
Sedatives are prescribed: preparations of bromine, Valerian, leonorus, tranquillizers and
neuroleptics (Elenium syn. chlordiazepoxide, Oxylidin, syn. benzoclidine hydrochloride,
Amizyl syn. benactyzine, Diazepam, Teralen syn. Alimemazine, levomeproma-zine,
Oxazepam, Thioridazine, etc.).
Corticosteroids (prednisolone, methylprednisolone, dexamethasone, triamcinolone, 1
tablet taken three or four times a day for six to eight days) are prescribed to cause an effect
on the allergic and inflammatory phases in severe forms of the disease if there are no
contraindications and when other measures prove ineffective.
With abatement of the inflammatory and allergic signs, the dose is gradually reduced to
half a tablet given two or three times a day (at first daily, and then every other day) and then
corticosteroids are discontinued.
Anabolic steroid hormones are given simultaneously with corticosteroids. These are
methandrostenolone, or Nerobolil, and Retabolil syn. nandrolone decanoate, which contribute
to normalization of protein metabolism and an increase in the body's resistance to infections.
Whenever indicated, vitamins are prescribed (A, Bx, B2, Be, B12, B16, E, K, and C, folic,
nicotinic, orotic acids, calcium pangamate and pantothenate).
Intramuscular injections of 5 per cent vitamin Bx (1 ml injected daily, a total of 20-30
injections) and vitamin B12 (200-500 ug given daily or every other day) are prescribed in true
eczema. Oral medication with riboflavin, pyridoxin (10-50 mg of vitamin Be) and vitamin B16
jn a dose of 0.05 g to be taken two or three times a day is indicated in seborrhoeic eczema.
Antibiotic therapy produces a good effect in microbial eczema and when pyogenic infection
develops in other forms of eczema.
Pyrogenic agents (pyrogenal, prodigiosan) are indicated in persistent chronic eczema with
marked infiltration and deep lichenification.
Of no small importance is the treatment of focal infection, epidermophytosis which
sensitizes the body, diseases of the gastrointestinal tract, liver and pancreas, endocrine disorders,
and helminthiasis.
Treatment of eczema in children begins with the arrangement of a diet regimen because
the alimentary factors play an important role in the origin and development of eczemas in them.
Breast milk and cow's milk is replaced by yoghourt. The amount of liquids, table salt, and
carbohydrates is reduced by 10-20 per cent because they contribute to the retention of water in
the tissues and therefore intensify the degree of skin inflammatory reaction. Proper artificial
feeding of infants and regular meals for the nursing mother are important.
Rational nutrition and diet play an essential role in the management of eczema in adults
and children: extractive substances, citrous fruits, mushrooms, meat broth, and spicy foods
are restricted or completely removed from the diet. Milk and vegetables produce good results.
Spa therapy is advisable after abatement of the acute stage. Treatment at hydrogen-sulphide
health resorts, sea bathing, and heliotherapy are indicated.
Acupuncture is prescribed in eczema marked by severe itching. Bucky's rays may be
recommended in chronic eczema with limited foci of affection. Applications of ozocerite,
paraffin, and therapeutic muds are recommended in severe infiltration with lichenification.
Radiotherapy is indicated only in persisting recurrent eczema attended with pronounced
infiltration when all other therapeutic measures have been tried.
The external treatment of eczema depends on the degree of the inflammatory process. The
scales and crusts should be first removed from the foci. For this purpose dressings with sterile
gauze soaked in vegetable oil are applied to the lesions. The application of oilcloth (without
cotton) facilitates cleansing of the focus. The bandage is left for 12 to 24 hours. The weeping
stages of eczema respond well to treatment with cooled lotions containing 2 per cent boric
acid, 0.25 per cent silver nitrate, 0.5 per cent resorcinol, 0.25 per cent amidopyrin, etc. It is
not advisable to treat infants with lotions containing resorcinol and boric acid, otherwise
toxicosis may develop. After weeping ceases, corticosteroid ointments are used (0.5 per cent
prednisolone, 0.25 per cent Depersolone, Locacorten, Flucinar, Ftorokort, Ultralan,
Celestoderm). Bearing in mind that the hormones might be absorbed by the skin, particularly
by areas exposed as the result of the eczematous process, steroids should be applied to
limited skin areas in children, or they should be mixed with Unna's cream. Steroid ointments
may be replaced by various pastes or aqueous shake mixtures to which are added 1-2 per
cent of anaesthesin and naphthalan which intensify the antipruritic effect.
With the gradual abatement and elimination of acute inflammation, stronger keratoplastic
agents are applied: ointments containing 5-10-20 per cent naphthalan, 1-2 per cent tar which
resolve the infiltrate, 2-5 per cent sulphur, 2-3-5 per cent ichthammol, etc.
In treating seborrhoeic eczema of the scalp, oil compresses are prescribed first (to remove
the crusts), after which a good effect is produced by Lokasalen, Hyoxisone, 5 per cent sulphuric,
2 per cent salicylic acid ointments or 1 per cent ammoniated mercury ointment containing 0.5-
0.75 per cent salicylic acid.
Naphthalan or one third-one fourth of Wilkinson's ointment with two thirds-three fourths
zinc ointment or zinc paste may be prescribed in microbial (para traumatic) varicose eczema.
Antiparasitic external disinfectants have a very good effect in microbial eczema, but may
induce an exacerbation of the process in other forms of eczema. Aniline dyes and Gastellani's
paint produce a good result in microbial eczema.
Dressings with diachylon ointment, which may be applied under oilcloths but without
cotton, have a favourable effect in hyperkeratotic stratifications (e.g. keratotic eczema).
Prognosis. In acute eczema the prognosis is more favourable. Microbial and seborrhoeic
eczemas may be completely cured. Idio-pathic, sycosiform and pruriginous eczemas respond
to treatment less readily. Recurrences may occur in any form of eczema. The prognosis is much
poorer if eczema develops in oedematous and asthenic infants, in elderly individuals, and in
persons weakened by infection or toxicosis.
Prevention. Observance of hygienic habits is important in all forms of eczema.
Moreover, this contributes to the prevention of secondary infection, which aggravates the
course of the main process. Small lesions in mild folliculitis should be painted with Castellani's
paint or 1-2 per cent aqueous or alcohol solutions of aniline dyes. In extensive skin lesions
the patient is not permitted to take baths or showers for some time. In some patients,
however, baths with a chamomile decoction, for instance, and in treating children, a decoction
of bran, oak bark, etc. produce a therapeutic effect. Overheating of the body must be avoided.
Patients with eGzema are recommended a diet of dairy and vegetable foods, boiled meat,
cereals, carrot and apple juices, stewed prunes, vegetables, fruits. Citrous fruits may induce
violet exacerbation in some patients. Liquids and easily assimilated carbohydrates should be
limited and extractive substances avoided. Alcoholic beverages, salty and spicy foods, canned
food and pickles are prohibited. Children must neither be overfed nor undernourished.
Much importance is attached to normal activity of the gastrointestinal tract and treatment
of intercurrent diseases.
In patients with the varicose complex of symptoms, elastic stockings or bandaging the legs
with therapeutic rubber bandages is a measure for the prevention of varicose eczema. To
prevent such eczema, varicosity, ulcers, fissures, fistulas and wounds are treated (jointly with
a surgeon). Improper treatment of a burn or frostbite may also lead to the development of
eczema.
Nursing mothers with eczema of the nipples must strain their milk. Individuals with
eczema of the hands should avoid using water that is either too hot or too cold, and should not
use detergents in laundering. Contact with presumable allergens in everyday activities and
during work should be excluded as much and as long as possible.
To prevent Kaposi's varicelliform eruption and eczema vaccinatum, individuals who had
suffered from lichen pemphigoides or those who had undergone smallpox vaccination should
not be allowed to take care of children with eczema for ten to fifteen days.
Treatment of infestation twith helminths and treatment of foci of chronic or acute
infection in the future mothers and a rational diet are very important in the prevention of
eczema in infants, because the allergens circulating in the mother's blood-stream penetrate the
placenta and sensitize the infant while it is still in the period of intrauterine development. In
such cases exogenic allergens entering with the mother's milk after the birth of the child thrive
on prepared ground. Pregnant women, particularly those known to have had allergic
parentage, should abstain from eating a lot of eggs and sweets and drinking much milk.
Their diet should be rich in vitamins and must include a variety of vegetables, boiled meat,
yoghourt and cottage cheese, as well as fruits (oranges, tangerines, apricots, peaches,
strawberries, raspberries should be limited). It is expedient to prescribe some vitamins in
addition to the diet (vitamin A concentrate in drops, the vitamin В complex in pills, ascorutin
in tablets).
It is not advisable for patients suffering from eczema to wear synthetic, flannel or woolen
underwear. These patients should be kept under dispensary surveillance and examined by the
dermatologist regularly for control and prescription of treatment in conformity with the
condition of the skin and the body as a whole.

Urticaria

Urticaria is a disease of allergic and toxic genesis characterized by urticarial eruptions on

the skin and less frequently on the mucous membranes. Exogenic (physical, thermal,
mechanical, chemical agents, drugs, antibiotics in particular, sera and foods) and endo-genic
(pathological processes in the viscera, e.g. gastro-intestinal tract, liver, disturbed activity of
the nervous system) causes of urticaria are distinguished. The pathogenic mechanism of its
development in all cases has many links in common. The aetiological (auto-genic and exogenic)
factors promote the development of immediate-delayed hypersensitivity and thus cause the
accumulation of chemically active substances of the type of histamine. Histamine, which forms
from the amino acid histidine under the effect of the enzyme histidine decarboxylase, induces
dilation of the capillaries and increases the permeability of the vascular walls, as a consequence
of which acute oedema of the dermal papillary layer develops and causes the appearance of
blisters on the skin. Mast cells and basophils are the reservoir of histamine, in which it is
bound with the intracellular tissue proteins by peptide bonds and may be freed by
proteases. The proteases (trypsin) are activated in the antigen-antibody reaction (binding of
the antigen with the antibodies attached on the mast cell). The secretion of serotonin,
acetylcholine, bradykinin, slow action substance which potentiate the effect of histamine
is also activated as the result of the antigen-antibody reaction.
Incompletely split protein products, which have still retained specificity, may play the role
of an allergen. They enter the blood stream and induce the production of antibodies to a definite
food. Toxins (spoiled or incompletely assimilated foodstuffs) and toxic substances, which form
in the colon in colitis and in deficient renal fuaction, may also be allergens. Bacterial
allergy may be in duced by staphylococci, streptococci and other micro-organisms usually
from foci of chronic infection. Functional disorders of the nervous system play an important
part in the pathogenesis of urticaria, which particularly applies to the vegetative nervous
system with its regulating centre, the hypothalamus, where the nerve impulses are switched
to humoral because of the presence of cholin-ergic and adrenergic centres in it. In particular,
cholinergic urticaria developing in nervous excitation is caused by the production of
acetylcholine in the tissues under the effect of irritation of the cholinergic (parasympathetic)
system. Acetylcholine induces a vascular reaction similar to the reaction to histamine.
Autosensitiza-tion to acetylcholine with the development of an auto-antigen-auto-antibody
reaction may also occur. In bites of bloodsucking insects (mosquitoes, fleas, midges, mits)
chemically active agents of the type of histamine enter the skin with their saliva. Invasion
by helminths plays a tremendous role in the development of urticaria!
The clinical picture of urticaria has a great variety, in view of which several types are
distinguished: acute, including Quincke's acute circumscribed oedema (angioneurotic
oedema), chronic recurrent and stable chronic papular urticaria.
Acute urticaria is characterized by an abrupt onset: the appearance of severe itching and
abundant urticarial lesions of various size elevated above the skin surface. They are pinkish-
red with a mat hue in the centre and a pink fringe with uneven contours on the periphery. The
wheals are usually round, less frequently elongated and irregular in shape. The lesions may
coalesce into extensive zones and the general condition of the body may be disturbed (elevated
body temperature, gastro-intestinal disorders, indisposition, chill, i.e. 'urticarial fever'). The
wheals are mainly localized on the trunk, hands, buttocks and less frequently on other skin
areas. Eruptions may occur on the mucous membranes of the lips, tongue, soft palate,
nasopharynx and larynx, in which event the oedema makes respiration and swallowing difficult.
The wheal eruptions are ephemeral, i.e., the lesions are short-lived and usually disappear in one
or two hours. Acute urticaria lasts several days. Drug or food allergy (parenteral
administration of therapeutic sera, vaccines, transfusion of blood, etc.) is usually
encountered. Artificial urticaria is an atypical variety of acute urticaria. It is characterized
by the formation of wheals, usually linear, in response to mechanical irritation, i.e. in
demonstrating dermatographia. In distinction from common urticaria, there is no itching.
Acute circumscribed oedema (syn. giant urticaria, angioneurotic oedema, Quincke's disease)
is characterized by sudden development of circumscribed oedema of the skin (mucous
membrane) and subcutaneous fat of the face (lips, cheeks, eyelids, etc.) or the genitals.
The skin is hard-elastic to the touch and white or less frequently pink. There are usually
no subjective sensations though in rare cases burning and itching may be experienced. The
oedema subsides in a few hours or in one or two days, but recurrences are possible. An-
gioneurotic oedema is sometimes combined with ordinary urticaria. In oedema of the larynx,
stenosis and asphyxia may occur. In localization of oedema in the region of the orbits, the
eyeballs may be displaced medially and acuity of vision is reduced.
Differential diagnosis is made with lymphostasis, recurrent erysipelas, and the Melkersson-
Rosenthal syndrome from which angioneurotic oedema is distinguished by an abrupt onset
and shortlived existence of the lesions that resolve without a trace.
Chronic recurrent urticaria is distinguished by less abundant eruptions, but occurs in
attacks for several months or years and usually develops against the background of long-term
sensitization caused by foci of chronic infection (tonsillitis, adnexitis, etc.), disturbed activity
of the gastro-intestinal tract, liver, etc. Recurrences of the disease characterized by the
appearance of urticaria on different skin areas are replaced by remissions of various duration.
Headache, weakness, elevated body temperature and arthralgia may develop during eruption
of the urticarial lesions, while nausea, vomiting and diarrhoea may occur in oedema of the
gastro-intestinal mucosa. Agonizing itching may be attended with insomnia and neurotic
disorders. The blood is marked by eosinophilia and thrombocytopenia.
Stable papular urticaria develops when persistent stable urticarial lesions transform into
papules as the result of the development of cellular infiltration (composed mainly of
lymphocytes) in the derm is as well as hyperkeratosis and acanthosis, in addition to the stable
circumscribed oedema. The papules are reddish-brown and are mostly localized on the
extensor surfaces of the limbs. The disease is usually encountered among females. Many
authors claim that stable papular urticaria should be considered a variety of prurigo.
Solar urticaria is a variety of photodermatosis which develops in individuals suffering
from diseases of the liver and disturbed porphyrin metabolism in marked sensitization to
ultra-violet rays. It is mostly encountered among females. The disease is characterized by
the appearance of urticarial eruptions on exposed skin areas (face, upper limbs, etc.). It is
of seasonal character (spring and summer). In long-term exposure to the sun, the eruptions
may be attended with a general body reaction in the form of disorders of respiration and
cardiac activity; shock may occur.
The histological picture in chronic urticaria is marked by acute inflammatory changes in
the foci of affection. Mild intercellular oedema is found in the epidermal Malpighian layer.
There is con the connective-tissue fibres are loosened and swollen and mild eosinophilic,
lymphocytic and histiocytic infiltrate is seen around the vessels.
The diagnosis presents no difficulties. Differential diagnosis with strophulus is based on the
presence of urticarial lesions alone in chronic urticaria, which are localized at random
without involvement of the favoured sites of strophulus. It is more difficult to differentiate
urticaria from the bites of insects (mosquitoes, fleas, bedbugs, etc.) because typical urticarial
eruptions often appear at the sites of the bite. It is very important to take into account the
seasonal character of the eruption and its localization, and the sanitary conditions in the family
or children's establishment. In Duhring's disease, in addition to wheals, there are bullae and
vesicles with eosinophilia as well as hypersensitivity to iodine preparations.
Treatment. In acute and chronic urticaria it is essential to identify and remove all possible
pathogenic factors contributing to the development of the disease. Special attention should be
paid to the diet, regimen, condition of the nervous system and gastro-intestinal tract and
detection and treatment of foci of chronic infection. It is highly advisable for the patient to
consult a neurologist and otorhinolaryngologist and to examine the patient for helminths and,
whenever necessary, carry out dehelminthization, to treat foci of chronic infection and to
remove alimentary and drug allergens. A salt purgative, a diet of dairy products and
vegetables, sedatives, hypersensitizing agents (calcium preparations, infusion of sodium
hyposulphite, injections of magnesium sulphate), and antihistaminics are prescribed.
Preparations of bromide and valerian, Nanophyn, Dimedrol, Peritol, Tavegil (Glemastine
fumarate), Diazolin (Mebhydrolin Napadisy-late), Stugeron (Ginnarizine), Alfadryl
(Moxastine), Suprastin (chlo-ropyramine), Diprazine (promethazine hydrochloride), Seduksen
(Diazepam), as well as drugs containing ephedrine and belladonna and their derivatives are
used. To reduce vascular permeability, calcium chloride, calcium gluconate or calcium lactate
are prescribed simultaneously orally or intramuscularly together with vita min G and
rutin. Purgatives, cleansing enema, and in some patients diuretics (furosemid, theobromine and
sodium salicylate) may prove valuable in acute urticaria. Iron preparations, salicylates,
 vitamins Bla and Be, sodium hyposulphite, Salol and Atophan (Cinchophen) are recommended
in chronic urticaria for correcting metabolic processes. In severe forms of the disease AGTH and
corticos-teroid hormones are given, followed by histaglobin therapy. External therapy is of no
essential importance. Aqueous-zinc pastes, ointments with corticosteroid hormones and baths
with a decoction of bur-marigold, chamomile, starch or bran are prescribed.
The prognosis is usually favourable. Attention should be focused at identifying and
removing the allergenic factors. Regular treatment combined with rational organization of the
diet regimen and care may result in clinical recovery.
The prevention of urticaria consists of treatment of gastro-intestinal disorders, diseases of
the liver, and foci of infection, removal of the allergenic factors, and prescription of a
rational dietary regimen.

DERMATITIS
Classification of dermatitis
Dermatitis may be caused by:
 physical irritants
• high and low temperatures (burns, frostbite, chilblains)
• ultraviolet rays (solar dermatitis)
• X-ray and radioactive radiation
• mechanical (pressure, friction)
• electricit y
 chemical irritants
• alkalis and acids, salts of same acids
• 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

Classification of dermatitis according to the irritants

 Physical dermatitis
 Chemical dermatitis
 Biological dermatitis
 Medical dermatitis

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
 simple contact dermatitis is usually acute and occurs soon after exposure to the irritant
 the absence of sensitization
 the absence of incubation period
 subjectively: sensation of pain and burn
 objectively: from erythema and bullas to necrosis, asymmetrical process, the border is clear
 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

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

The prognosis of burns is determined by:

 the degree of the burn
 the condition of the patient's organism
 the attendant secondary infection
 particularly by the size of the burnt area

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
The manifestations of frostbite are preceded by a latent period during which the affected area
becomes cold, pale, and insensible and occurs on exposed areas and distal parts of the body
(fingers, toes, the skin on the nose and cheeks, ears).
Factors conducive to frostbite are:
 increased humidity of air
 wind
 tight footwear
 reduced resistance of some tissues (a history of frostbite, increased perspiration, injury, etc.)
 reduced resistance of the body as a whole (physical fatigue, stress, lack of vitamins,
weakening of the body after acute or chronic infectious diseases, copious blood loss, alcoholic
intoxication, etc.).

Chilblain
 A peculiar skin lesion called develop under the effect of longterm exposure to cold in
combination with dampness, asthenic individuals and those with lack of vitamins С and A
(mostly children and adolescents).
Factors conducive to chilblain are:
 a tendency to develop acrocyanosis of the limbs
 damp
 poorly heated quarters for living and working
Chilblain is characterized by:
 a thickened or soft swelling with indistinct contours forms on the affected skin areas
 has cyanotic-reddish color on the distal and middle phalanges of the fingers and toes and on the
joints
 bluish hue of swelling on the cheeks
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

CHRONIC SOLAR DERMATITIS

Individuals whose occupation makes them subject to insolation for lengthy periods of time
CHRONIC SOLAR DERMATITIS manifested by:
 infiltration
 pigmentation
 dryness of the skin
Is encountered in fishermen, seamen, and individuals exposed to the sun when they work (in the
fields, at construction sites, etc.)
Radiation dermatitis
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

Depending on the factors listed above, acute radiation dermatitis may be manifested by:
 erythema (with a peculiar violet or light-blue tinge),
 temporary loss of hair
 bullous reaction developing against the background of intensive hyperemia and swelling
 in which cases the process terminates in atrophy of the skin, permanent alopecia, the formation
of telangiectasia, and disorders of pigmentation known as 'motley' or 'X-ray' skin
 a necrotic reaction occurs the manifestations of which are similar to those of bullous dermatitis
but are more pronounced (with tissue necrosis) and attended with severe general phenomena

 Multiple exposure of the skin to relatively small doses of 'soft' X-rays and to radioactive
substances causes the development of chronic radiation dermatitis.
 The last may also he consequent upon acute radiation dermatitis.
 the process of chronic radiation dermatitis is characterized by:
 poikiloderma (variegated skin)
 the skin is dry
 thinned out
 lacks elasticity
 telangiectasia
 hyperpigmented and depigmented areas
 onychodystrophy and
 itching

 Chronic radiation damage to the skin is conducive to the formation on the affected areas of
papillomas, hyperkeratosis, and warts which may undergo malignant degeneration
 Late radiation dermatitides, among which late radiation trophic ulcer and radiation carcinoma
deserve special attention, may develop at the site of persistent radiation dermatitides.

Chemical dermatitis
The chemical factors, which induce simple contact dermatitis, are 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.
Biological dermatitis
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

Miliaria
Miliaria develops in infants and young children, especially in those who are overnourished and in
those suffering from exudative diathesis.
Factor of risk:
The external temperature is high or a rise in body temperature in acute infections lead to rapid and
marked increase of perspiration and thus contributes to the development of the disease.
The following forms are distinguished of miliaria:
 miliaria crystalline characterazed by:
• vesicles the size of a millet,localazed in horny layer of epidermis
• with no hyperaemic ring on their periphery
• localized mostly on the trunk
• there is no itching
 miliaria rubra characterazed by:
• appearances of red papules
• with hyperaemic ring on their periphery
• In center of papules appear small vesicles with cloudy content
• localized mostly on the trunk, neck, in the skin folds
• severe itching
 miliaria alba characterazed by
• white purulent pustules on the apex of the papules
• accompanying pyococcal infection
 miliaria flava is a condition, in which the advancing coccal infection leads to the formation of
yellow intraepidermal pustules

The treatment of simple contact dermatitis is determined by:

 remove of irritant
 the condition of the patient's organism
 the attendant secondary infection
 particularly by the size of the pathologic area

Systemic Treatment
 antihistamines – suprastin, klaridol, klaritin, arius and etc.
 desensebilsation medicine - (intravenous infusion of calcium chloride, calcium gluconate or
sodium hyposulphate solutions)
 sedaive medicine – extractus valeriane, persen, novo-passte and etc.
 enterosorbents – enteros gel, polifepan and etc

External Treatment
 on mild hyperaemia can using powders and corticosteroid ointments, on hyperaemia and
swelling solution for application or aqueous shake solutions, corticosteroid ointment, saerosol
“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.

Clinical picture of allergic contact dermatitis

 occurs in patients with heightened sensitivity to a definite substance, the allergen
 hypersensitivity may be congenital, in which case the condition is called idiosyncrasy (e.g. to
eggs, citrus fruit, strawberries, etc.)
 much more frequently increased sensitivity develops in repeated contact with the allergen,
which results in monovalent sensitization of the body
 allergen penetrated to organism through the skin
 has incubation period
 rush is localized on areas, which had been exposed to the allergen, but in some patients the
process tends to spread to the covered skin areas
 objectively: asymmetrical process, the border is not clear, polimorphic eruption (erythema,
swelling, papules and vesicular lesions)
 resolution of the lesions after removal the action of the aetiological factor, that is the main sign
distinguishing eczema from allergic dermatitis
 positive skin allergic tests (application test, intracutaneus test, scarification test)
 repeated contact with the allergen facilitates the transformation of allergic dermatitis to eczema

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

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
TOXICODERMIA
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.

Factor of risk of toxicodermia development :

 genetic (drug toxicodermia occurs in some patients as the result of drug idiosyncrasy)
 allergic disease
 diseases of GIT, lien, bile cyst and ether internal organs
 contraceptive content Cu, Ag
 allergic foods
 useful of medicine - iodine, vaccines and sera, vitamins B1 B6, and B12,, antipyrine,
angiotrophine, analgetics, barbiturates, Novocain and particularly antibiotics, sulphonamides
 manifestation of a paraallergic reaction (in such cases preceding diseases (rheumatism,
tonsillitis, epidermophytosis, etc.) prepare the organism for drug intolerance
 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:
 localized as a rule on the mucous membrane of oral cavity and on the genital organs
 the clinical picture fixed toxicodermia is characterized by polymorphic eruptions (erythema,
spots, vesicles, bullas)
 subjective symptoms: sensation of itching and sometimes burning sensation

One and the same drug may cause a morphologically different form of toxicodermia in different
individuals

Providing that the allergen drug is discontinued in good time, drug toxicodermia is usually
shortlived.
In cases with involvement of the cardiovascular system and the internal organs, however, the
prognosis may be unfavourable.

At the same time, some drugs produce a clinical picture of toxicodermia typical precisely of
them

Iodine or bromine toxicodermia

 occurring in medication with iodine or bromine salts and alcohol iodine solutions, for
instance,
 is characterized by the development of an acneiform eruption ('bromine' or 'iodine' acne) or
tuberous bromoderma (iododerma),
 is manifested by succulent soft plaques elevated above the skin surface and covered with
purulent crusts
 On removal of the crusts, a vegetating surface of a pus secreting infiltrate is exposed

Toxicodermia induced by sulphonaxnides,

 the favoured localization of sulphonamide erythema are the hands, lips, oral mucosa and the
region of the genitals
 erythematous reddish-brown with a lilac tinge foci develop which are demarcated and have
rounded outlines
 is manifested particularly often in the form of fixated erythema which appears at one and the
same place a few hours after medication with a sulphonamide drug
 disappearing (in a few days) leaves a slate-brown pigmentation intensifying after each
recurrence.
 bullae sometimes form on the plaques

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.)

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
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.

Etiology
It is now accepted (Skripkin, Shakhtmeister and others) that the eczema process develops as the
result of the effect of a complex of:
 neuroallergic
 endocrine
 metabolic
 exogenic factors (chemical and biological agents, bacterial allergens, physical factors, drugs,
foodstuffs, cosmetics, etc)
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
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.

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

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

Sycosiform eczema
This form may be encountered in individuals suffering from sycosis complicated by
eczematization.
is characterized by:
 the typical localization on the upper lip, the beard, the axillae and the pubis
 follicular pustules pierced through the middle by a hair shaft develop on inflamed skin
 these are symptoms of sycosis
 extension of the process beyond the hirsute areas
 the presence of eczematous wells
 the presence of weeping
 sensation of severe itching
 lichenification of the skin

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, hyperpigmentation
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).

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
In children the eczematous process usually develops :
 against the background of exudative diathesis, often as a result of hereditary altered
immunological reactivity
 most parents or close relatives of infants with eczema had manifestations of allergy on the
skin, mucous membranes or in the internal organs in the past.
 when one of the parents (mainly the mother) has an allergic disease (bronchial asthma,
allergic rhinitis, eczema, neurodermitis, etc.),
 children with exudative diathesis often have torpid foci of focal chronic infection, bronchial
asthma, hay fever, acute respiratory infections, conjunctivitis, keratitis and gastro-intestinal
disorders, and dysfunction of the liver and pancreas
 infectious allergic reactions which are often induced by hypersensitivity to drugs and other
chemicals.
Clinical picture of 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.

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 or
sodium hyposulphate solutions)
 enterosorbents – enteros gel, polifepan and etc
 corticosteroid therapy
 vitamin and microelements – B2, B15,B 6, sulfur
 antibiotics
 antifungal drugs

External therapy
 application – sol. ac. boric 2%, sol. 0.25 per cent silver nitrate, 0.5 per cent resorcinol, 0.25
per cent amidopyrin, sol. rivanoli 1:1000 etc
 shake solution – (oily, watery, hydro-alcoholy) which are added 1-2 per cent of anaesthesin
and naphthalan which intensify the antipruritic effect
 corticosteroid ointments - 0.5 per cent prednisolone, 0.25 per cent Depersolone, Locacorten,
Flucinar, Ftorokort, Ultralan, Celestoderm etc
 keratoplastic agents - ointments containing 5-10-20 per cent naphthalan, 1-2 per cent tar
which resolve the infiltrate, 2-5 per cent sulphur, 2-3-5 per cent ichthammol, etc.
 aniline solution- Castellani's, brilliant grin
 aerosol – oxycort, polcortolon etc

Educational, methodical and informational support of the discipline

Main literature

1. Goodheart's Photoguide to Common Pediatric and Adult Skin Disorders [electronic resource] /
Goodheart, Herbert P.; Gonzalez, Mercedes E. Edition: Fourth edition. Philadelphia : Wolters
Kluwer Health. 2016. URL:
http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1473155&lang=ru&si
te=ehost-live&ebv=EK&ppid=Page-__-1

2. Encyclopedia of Dermatology : (6 Volume Set) [electronic resource] /Pratt, Meghan. Series:

Dermatology--laboratory and Clinical Research. New York : Nova Science Publishers,
Inc. 2016. URL:
http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1164792&lang=ru&si
te=ehost-live&ebv=EB&ppid=pp_Cover

Additional literature

1. Habif, Thomas P. Clinical Dermatology : a color guide to diagnosis and therapy / Thomas P.
Habif. - 6nd ed. - [S. l.] : Elsevier, 2016. - 1008 p. : il. (30)

2. Tropical Dermatology / ed.: S. K. Tyring, O. Lupi, U. R. Hengge. - 2nd ed. - Edinburch [etc.] :
Elsevier Science, 2017. - 491 p. : il. (30)

3. Lichen Planus: Epidemiology, Symptoms and Treatment [electronic resource] / Summers,

Yvonne L. Series: Dermatology--laboratory and Clinical Research Series. New York : Nova
Science Publishers, Inc. 2015. URL:
http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1084536&lang=ru&si
te=ehost-live&ebv=EB&ppid=pp_Cover

4. Pemphigus Vulgaris : Autoimmune Bullous Disease [electronic resource] / Švecová, Danka.

Series: Dermatology Laboratory and Clinical Research. New York : Nova Science Publishers,
Inc. 2015. URL:
http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=979565&lang=ru&sit
e=ehost-live&ebv=EB&ppid=pp_Cover

5. Lever's Histopathology of the Skin [electronic resource] / Elder, David E. Edition: Eleventh
edition. [Philadelphia] : Wolters Kluwer Health. 2015. URL:

http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1473038&lang=ru&si
te=ehost-live&ebv=EK&ppid=Page-__-1

6. Pediatric Dermatology : A Quick Reference Skin [electronic resource] / Krowchuk, Daniel P.;
American Academy of Pediatrics; Mancini, Anthony J. Edition: 3rd edition. Elk Grove Village,
IL : American Academy of Pediatrics. 2016. URL:

http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1270469&lang=ru&si
te=ehost-live&ebv=EB&ppid=pp_Front_Cover

7. Succinct Pediatrics: Evaluation and Management for Infectious Diseases and Dermatologic
Disorders [electronic resource] / Feld, Leonard G.; American Academy of Pediatrics; Mahan,
John D. Elk Grove Village, IL : American Academy of Pediatrics. 2017. URL:

http://search.ebscohost.com/login.aspx?direct=true&db=e600xww&AN=1461380&lang=ru&si
te=ehost-live&ebv=EB&ppid=pp_516

Periodicals

1. Russian journal of skin and venereal diseases

2. Clinical dermatology and venereology

Electronic information support and professional databases

 Official website of the Ministry of Health of the Russian Federation. Electronic
rubricator of clinical recommendations URL: http://cr.rosminzdrav.ru/#!/
 Official website of the Ministry of health of the Russian Federation. Primary
health care standards. URL:
https://www.rosminzdrav.ru/ministry/61/22/stranitsa-979/stranitsa-983/1-
standarty-pervichnoy-mediko-sanitarnoy-pomoschi
 Official website of the Ministry of health of the Russian Federation. Standards of
specialized medical care. URL:
https://www.rosminzdrav.ru/ministry/61/22/stranitsa-979/stranitsa-983/2-
standarty-spetsializirovannoy-meditsinskoy-pomoschi
 Official website of the Ministry of health of the Russian Federation. Standards of
emergency medical care. URL:
https://www.rosminzdrav.ru/ministry/61/22/stranitsa-979/stranitsa-983/3-
standarty-skoroy-meditsinskoy-pomoschi
 Official website of the Ministry of health of the Russian Federation. URL:
https://www.rosminzdrav.ru/ministry/61/4/stranitsa-857/poryadki-okazaniya-
meditsinskoy-pomoschi-naseleniyu-rossiyskoy-federatsii
 Official website of the World Health Organization.URL: http://www.who.int/ru/
 Consultant Plus. URL:
https://kurskmed.com/department/library/page/Consultant_Plus
 The official website of the scientific electronic library eLIBRARY.RU. URL:
https://elibrary.ru/
 Official website of the National Electronic Library (NEB).URL: http://нэб.рф/
 Federal electron medical library URL: http://193.232.7.109/feml
Database of international scientific citation index «Web of science». URL:
http://www.webofscience.com/

 Full-text database «Medline Complete». URL: http://search.ebscohost.com/

 The official website of the scientific electronic library «КиберЛенинка». URL:
https://cyberleninka.ru/
 Database of the international science citation index "Scopus". URL:
https://www.scopus.com
 Full-text database «Polpred.com Обзор СМИ». URL: http://polpred.com/
 PubMed. URL: https://www.ncbi.nlm.nih.gov/pubmed/
 BioMed Central (BMC). URL: http://www.biomedcentral.com/
 Electronic library system "Student Consultant" URL: http://www.studentlibrary.ru
 Official website of the Russian society of dermatovenerologists and
cosmetologists. Federal clinical recommendations (protocols) on
dermatovenerology. URL: http://www.cnikvi.ru/docs/clinic_recs/klinicheskie-
rekomendatsii-2017/
 Orders Of The Ministry Of Health of the Russian Federation.
http://dermatology.my1.ru/load/prikazy/30