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 sub-
stances.
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 bul- lous eruptions or tissue necrosis with the
formation of an ulcer which leaves a scar or cicatricial atrophy. Chronic dermatitis is charac terized 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 to -
wards 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 lichen ization 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 con-
gestive-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 in sensible. 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 ofchronic 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 scratch-
ing, 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 pre scribed 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 der-
matitis 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 chil dren, 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, nysta-tin, 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, ten dency 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 identified 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 pre scription of sedatives, antihistaminics,
steroid hormones, and vitamins. 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 aliment ary
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 properties. 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 en zymatic systems by the drug, toxic
damage to the tissues and vessels (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 purulent 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 pur-
gatives 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 mono-valent 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 development 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 simulta neously
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 tis sues with
cracks sometimes form on the palms and soles in protract ed 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 gradually 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 se -
borrhoeic 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 de posits 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 se vere 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, strepto- lysin 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 sen- sitization to
streptococci and staphylococci in patients with microbial eczema. Neuroendocrine disorders and changes
in metabolic processes and immunological states favour the development of sen-sitization 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. Exacer -
bations 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 dor sal
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 erup tions 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 locali zed 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 polya- mide and flannel fabrics,
contact with which induces a recurrence of the disease.
There is no unanimity of opinion to date in regard to the classi fication of seborrhoeic eczema. Some
authors relate it to chronic seborrhoeic dermatitides. Others claim that it is a peculiar infec tious disease
caused by particular micro-organisms (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 infec tion, 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 dermato sis. Seborrhoeic eczema, for
instance, occurs in infancy, but is almost never encountered in the period between infancy and puberty;
like seborrhoea it usually develops after puberty (the role of hyper-androgenia and hypo-oestrogenia).
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, aller gic 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, ke ratitis 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 in fantile eczema may have macular seborrhoeic
eruptions (erythema-tous-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
para-keratotic 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, leo-norus, tranquillizers and neuroleptics
(Elenium syn. chlordiaze-poxide, Oxylidin, syn. benzoclidine hydrochloride, Amizyl syn. benactyzine, Diazepam,
Teralen syn. Alimemazine, levomeproma-zine, Oxazepam, Thioridazine, etc.).
Corticosteroids (prednisolone, methylprednisolone, dexamethaso-ne, 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 Reta-bolil 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, B x, 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 licheni-fication.
Of no small importance is the treatment of focal infection, epi-dermophytosis which sensitizes the body,
diseases of the gastrointestinal tract, liver and pancreas, endocrine disorders, and hel-minthiasis.
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 ec-
zema. 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.

NEURODERMATOSES
The group of neurodermatoses comprises diseases which begin with very severe itching and often with
neurotic disorders continuing throughout the disease. They include prurigo, skin pruritus, urticaria,
angioneurotic oedema and various forms of neurodermitis.
The term 'neurodermitis' was introduced in 1891 by Brocq and Jacquet who regarded these diseases as skin
neuroses with characteristic intense itching and subsequent development of licheni neat ion of the skin.
In the Anglo-American literature, diffuse neurodermitis is usually designated 'atopic dermatitis'
emphasizing the congenital nature of the disease. The term 'neurodermitis 1, however, most aptly reflects
contemporary views on the aetiology and pathogenesis of this agonizing and persistent dermatosis.
The following classification of neurodermatoses is accepted in the Soviet literature: (1) skin pruritus,
localized, generalized; (2) neurodermitis, localized, diffuse; (3) prurigo, infantile, adult, nodular; (4) urticaria
(chronic).
Skin Pruritus (Pruritus Cutaneus)
Skin pruritus is an independent disease manifested by severe persistent itching and scratches. There is no
ultimate opinion to date as to the specificity of the receptors perceiving itching. It is presumed that this is
accomplished by the free nerve endings, which perceive pain, or by the endings of non-medullated fibres. All sen-
sory apparatus of the skin may participate in the origin of the sensation of itching. Impulses inducing the sensation
of itching are conducted to the subcortical and cortical centres along the non-medullated С fibres.
Before making the diagnosis of skin pruritus it is necessary to rule out all diseases of the skin, blood, liver,
kidney, pancreas, metabolic disorders, etc., in which itching is among the symptoms of the malady. The diagnosis
of pruritus excludes the presence of any primary morphological lesion. As to the secondary morphological lesions,
these may be present in the form of excoriations and haemor-rhagic (punctate and linear) crusts. In some patients
the nails acquire a peculiar 'polished' sharpened appearance as a result of prolonged skin itching. The itching
usually occurs in paroxysms in the morning or at night, less frequently during the day. Its intensity varies from
mild to very severe, causing partial or total insomnia. Severe itching interferes with the patient's work.
Lichenification sometimes develops against the background of severe itching and scratching. In such cases it is said
that skin pruritus has developed into neuroder-mitis. According to its extent, itching is subdivided into universal
or generalized, and localized. Localized itching is most frequently found in the region of the genitals (vulva,
scrotum) and anus. Less frequently it develops on the medial surface of the thighs and legs and on the neck and
head. Localized skin pruritus may be caused by helminths (mainly the threadworm), inflammation of the mucous
membrane of the vulva, vagina, rectum and anus, vegetoneurosis with local disorders (increased sweating on
the itching skin areas) and by neuropsychic, neurosexual, endocrine and other disorders. The cause of
generalized itching, in addition to the functional disorders mentioned above, may be metabolic disturbances in
elderly and old individuals (senile pruritus), toxicosis (pruritus in pregnancy) and other causes which, however,
cannot always be disclosed.
Treatment. Antihistaminic agents such as mebhydroline napadisy-late (Diazolin) (0.05-0.1 g taken two or three
times a day), prome-thazine hydrochloride (Pipolphen), chloropyramine (Suprastin), fe-nethazine (Phenethazine)
(0.025 g given three times a day, preferably in the afternoon and evening), and diphenylhydramine hydrochloride
(0.03-0.05 g taken twice a day) cause a temporary symptomatic effect in pruritus. Intramuscular injections
(daily or every other day) of Suprastin or Pipolphen (1-2 ml of a 2.0-2.5 per cent solution) have a more
marked antipruritic effect.
Calcium preparations (intravenous infusion of a 10 per cent calcium chloride solution, or intramuscular
injection of a 10 per cent calcium gluconate solution) have a favourable effect in some pa tients. They should
be prescribed in predominance of the tonus of the parasympaticus (red dermatographia). In sympathicotonia
(white delayed and stable dermatographia) these agents are contraindi-cated because they stimulate the
sympathetic part of the vegetative nervous system. Some patients with persistent and excruciating itching may
be given corticosteroid hormones (see the section dealing with the treatment of diffuse neurodermitis) if there are
no contraindications. It is advisable to combine corticosteroid medication with electric sleep therapy and
hypnosis. A common horsetail decoction is recommended for patients with senile pruritus (1 table-spoonful of
horsetail brewed in three quarters of a glass of boiling water; 1.0-1.5 hours later the decoction is filtered and drunk
in gulps throughout the day, treatment lasts two to two and a half weeks).
Patients with neurotic disorders are given sedatives (bromide, if tolerated well), valerian and neuroplegics
(Seduksen syn. Diazepam, Chlordiazepoxide, Librium, Trioxazine). Among the physiothera-peutic procedures,
which produce a favourable effect in generalized pruritus, are artificial or natural (at the corresponding spa)
sulphurated hydrogen or radon baths, with decoctions of oak bark or bur-marigold, or with bran (1 kg for each bath)
and sea bathing. Among the external means of treatment, which cause a temporary effect in generalized
pruritus, are rubbing with a 1-2 per cent alcohol solution of thymol, carbolic acid, menthol, a 5 per cent chloretone
(chlorbutol) solution in 60-70 per cent ethyl alcohol, chloral hydrate and cooling shake mixtures containing
menthol. Dryness of the skin is treated by oral medication with vitamins A, B 2 and B3, and external application of
an emollient cream (lanolini, 01. Olivarum, Aq. distill, aa 30.Q).
We have suggested a method of injections around the itching skin areas in localized pruritus. The focus is first
anaesthesized by irrigation with ethyl chloride (or no anaesthesia is produced) and then an intramuscular
injection of 0.15-0.25 per cent methyl blue solution with bencain in a mixture with a prolongator is made:
Rp: Sol. Methyleni coerulei medicinalis 0.25% 100.0
Bencaini 4.0
MDS. For injections
Immediately before the injection, 10-15 ml of this solution is mixed with an equal amount of an agent
which prolongs the antipruritic effect of bencaine and methylene blue: a 10 per cent solution of medicamentous
gelatin, poly vinyl or preferably polyvinylpyrro-lidone (povidone) with a relative molecular mass no lower than
40 000.
Irrigation with ethyl chloride or superficial quenching with carbon-dioxide snow is applied in localized
itching of the scrotum. In some cases of persistent pruritus vulvae, when other methods fail, bilateral resection or
alcoholization of the genital nerves is undertaken.
Localized pruritus is successfully treated with Bucky's and with diadynamic currents (ion-modulator).
Temporary relief is produced by external application of corticosteroid ointments: Synalar, Lo-cacorten, 1-2 per
cent hydrocortisone, 0.5-1.0 per cent prednisolone, 3-5 per cent boric acid-tar ointments, creams containing sex
(mainly androgenic) hormones, namely, methyl testosterone or testosterone propionate in a 0.15-0.25 per cent
concentration on a lanolin base.
Neurodermitis
Neurodermitis is a chronic recurrent inflammatory skin disease manifested by intensive itching, papular
eruptions and marked lichenification.
Circumscribed (neurodermitis circumscripta) and diffuse (neuro-dennitis diffuse) are distinguished. There are
also several atypical forms: hypertrophic neurodermitis (giant lichenification), hyper-keratotic (verrucose),
follicular neurodermitis, diffuse lichenification of the face, etc.
Aetiology and pathogenesis. Neurodermitis results mainly from the effect of endogenic factors, such as
disturbed activity of the nervous system, endocrine glands and internal organs, metabolic disorders, and under the
effect of unfavourable environmental factors. Neurotic disorders of various degrees are observed: increased ex-
citation or restraint, rapid exhaustion, asthenia, emotional lability, insomnia, etc. All this sustains the tormenting
and persistent itching, which is the dominant symptom of neurodermitis. Examination by means of
electroencephalography, plethysmography, chro-naximetry and other methods confirm the existence of functional
disorders of the central nervous system first of all, and then of the vegetative nervous system (stable white
dermatographia, pronounced pilomotor reflex, disturbed thermoregulation, sweat production and sebum
production, etc.).
Disturbed functioning of the higher parts of the central nervous system may be of primary character and
play an aetiological role in the origin of neurodermitis. In some patients they are of secondary character,
appearing as a consequence of a persistent skin disease, protracted and severe itching and insomnia. Secondary
neurotic disorders are of pathogenic significance, they aggravate the course of neurodermitis. A vicious circle is
thus formed: the severe course of neurodermitis and the tormenting itching sustain and intensify the neurotic
disorders, whereas the neurotic disorders aggravate the course of neurodermitis.
Our research disclosed functional disorders in the activity of the adrenal cortex, thyroid and gonads in
patients with neurodermitis. The severe neurotic disturbances (increased excitability, emotional lability, long-term
negative emotions associated with itching, insomnia) are stress factors requiring intensified function of the adrenal
cortex which, under conditions of a protracted and severe inflammatory process, results in drastic diminution of
this function and even to its exhaustion in some cases. When the adrenals are exhausts ed they react to these
increased requirements not by excessive secretion of anti-inflammatory corticosteroid hormones (cortisone, hy-
drocortisone) but by an ever greater decrease in their production. On the other hand, the need for anti-
inflammatory hormones in patients with neurodermitis is increased. The developing paradoxical decrease of
corticosteroid secretion, low as it is, intensifies the inflammatory reaction, i.e. causes an exacerbation of the
pathological skin process, the development or intensification of allergic reactions, etc. This, to some extent,
evidently explains the exacerbation of the skin process in patients with neurodermitis (possibly in some other
dermatoses too) after neuropsychic traumas or long-term negative emotions.
The abovestated testifies to the importance of prescribing a protective regimen for patients with diffuse and
disseminated neurodermitis, the conduct of generally soothing sessions of hypnosis with the suggestion of
pleasant and positive emotions, the use of a complex of electric sleep and hypnosis plus medication with small
gradually decreasing doses of corticosteroid hormones.
The thyroid function in patients with neurodermitis is often increased, less frequently reduced; quite often
they suffer from dysfunction of the gonads. Neuroendocrine disorders and allergic reactions are therefore the
principal factors in the aetiology and pathogenesis of neurodermitis.
Long-term overstrain of the nervous system due to various causes and endocrine disorders create the
background against which allergic reactions as well as 'skin neurosis', i.e. neurodermitis, develop.
The following factors confirm the importance of the allergic state in neurodermitis.
1. Diffuse neurodermitis often begins with infantile eczema occurring, as a rule, against the background of
diathesis. Besides infantile eczema, the seborrhoeic and, less frequently, the true forms of eczema may also
transform gradually into neurodermitis when following a protracted course. Such transformation is usually
char acteristic of infantile and in adults of seborrhoeic eczema. In farless frequent cases vesiculation,
weeping in the form of serous or eczematous 'wells', and erythema of an acute inflammatory character
(exudativb neurodermitis) prevail in the clinical picture rather than papular eruptions and infiltration with
lichenification.
2. Allergic eruptions and itching may be encountered on skinareas remotely located from the
principal focus in localized neuro-dermitis.
3. Many patients with neurodermitis are hypersensitive to anti biotics, some other drugs, and to
some food.
4. Neurodermitis is often combined with other allergic diseases, particularly with bronchial asthma,
vasomotor rhinitis, urticaria.
5. According to the results of an examination conducted at our department, immunoallergic
reactions such as Boyden's passive haemagglutination test (PHT), Coombs' and Kuns' antiglobulin
tests, etc. prove to be sharply positive in many patients suffering from neurodermitis. This testifies to
the presence of monovalent antibodies (auto-antibodies) in these patients.
The causes of the origin of neurodermitis discussed from the standpoint of functional disorders in the
central nervous system in the first place, and then in the vegetative and endocrine systems, the role of
allergic states of the body and metabolic disorders in various internal organs do not contradict but even
supplement one another. The frequently encountered combination of functional disorders of the
nervous system with endocrine disturbances (disorders of the hypophyseal-adrenal system and less
frequently of the thyroid and gonads) provide grounds for stating that neuroendocrine disorders play the
leading role in the pathogenesis of neurodermitis.
 Chronic catarrhal inflammation of the mucous membrane of the distal part of the rectum and anal
canal plays an important role in the pathogenesis of localized neurodermitis and itching in the region
of the anus. Chronic gastritis, colitis, enterocolitis and gas-troenterocolitis, which are often attendant to
proctoanusitis, and proctitis and anusitis (cryptitis) themselves, are often attended with retention of
the stool. This leads to absorption of toxic products from the intestine (autotoxicosis of the body). In
diarrhoea or constipation with mucus in the stool, the mucosa and skin in the region of the anus are
irritated, which also creates favourable conditions for the development of exacerbation of neurodermitis
in this region. Fungal and yeast lesions may develop against this back ground. Anal fissures,
haemorrhoids, mostly external and less frequently internal, and helminths (mainly threadworms) may be
conducive to the development of localized skin itching and neurodermitis in the region of the anus.
The principal role in the pathogenesis of localized neurodermitis of the external genitals may be
attributed to neurosexual disorders, various inflammatory processes in the region of the genitals, hor -
monal gonadal dysfunction, and chronic diseases of the sexual sphere (adnexitis and endometritis in
females, prostatitis in males, etc.)
Infiltration with licheni Scation of the skin against the back ground of erythema (of non-acute
inflammatory character) predominate in the clinical picture of diffuse neurodermitis. The foci of
affection are mostly localized on the face, neck, flexor surfaces of the limbs (cubital and popliteal
fossae), in the region of the genitals, medial surfaces of the thighs and on other body areas.
Epidermodermal papules are the commonly encountered primary morphological lesions. They are often
distinguished with difficulty from the healthy skin in colour and in places they coalesce to form areas of
papular infiltration. The skin in the foci of affection is often hy perpigmented and dry and numerous
excoriations and microfur-furaceous scales are seen. Linear fissures are often found in the natural folds
against the background of infiltration. Affection of the skin manifested by severe itching and a
monomorphous eruption, in many cases neurotic disorders of this or that degree, white der-matographia
and marked pilomotor reflex constitute the typical clinical picture of neurodermitis. Hypocorticism in
patients with neurodermitis is manifested by hyperpigmentation, often by hypo- tonia, adynamia, allergic
reactions, reduced secretion of gastric juice, hypoglycaemia, a certain reduction in urine excretion,
loss of body weight, and increased fatiguability.
Diffuse neurodermitis is usually seasonal: the patient's condi tion usually improves in summer and
deteriorates in winter. In some cases the process is combined with bronchial asthma, hay fever, vasomotor
rhinitis, and other allergic diseases. Impetiginization and eczematization of the process are possible
(development of vesiculation, short-term weeping, erythema of an acute inflammatory character).
From the pathohistological aspect, diffuse neurodermitis is characterized by para- and hyperkeratosis,
mild acanthosis, intra- and intercellular oedema, oedema of the papilli, and a round-cell
(lymphohistiocytic) infiltrate found prevalently around mildly dilated vessels in the dermis.
Localized neurodermitis develops on a circumscribed skin area but is agonizing for the patient
because of very severe itching, which usually appears in the evening or at night. The favoured localiza -
tion is the posterior and lateral surfaces of the neck, the anal-geni tal region (in these patients the skin of
the medial surface of the thighs is often involved in the process), the intergluteal folds, and the flexor
surfaces of the large joints. At first the skin on the lo calized area remains unchanged. With time,
however, papular lesions of a dense consistency and covered with furfuraceous scales in places appear
in combination with itching and scratching. After that individual, predominantly the lichenoid,
papules coalesce and form flat plaques of various size (continuous papular infiltra tion) palepink to
brownish-red in colour with oval or rounded contours. The skin pattern gradually becomes markedly
exaggerated, i.e. lichenification develops. The skin turns shagreen-like of the process in localized
neurodennitis: a central zone with li-chenification, a middle zone with isolated shiny, often with a smooth surface,
pale-pink papules, and a peripheral zone with hyperpig-mentation. Excoriations (fresh or covered with haemorrhagic
crusts) are often seen against the background of erythema, which is of a non-inflammatory character. In exacerbation
of the process disseminated pruriginous lesions are sometimes seen besides the grouped coalesced lichenoid
papules, scaling intensifies and erythema becomes brighter. The disease follows a protracted course measured in
years.
Histopathology. The histological picture is marked by parakerato-sis (less frequently by hyperkeratosis),
acanthosis, infiltration of the papillary and frequently of the reticular dermal layers.
Treatment. Sedative therapy and psychotherapy in combination with low, gradually decreasing doses of anti-
inflammatory and hyposensitizing corticosteroid hormones (Urbasone syn. methyl-prednisolone, dexamethasone)
are recommended for patients with a diffuse process. These hormones are prescribed in a persistent course of the
disease, severe itching, and a tendency to dissemination of the foci of affection when the process responds poorly to
other methods of treatment. The activity of the central nervous system is normalized and neurotic reactions reduced
by means of electric sleep combined with hypnosis, preparations of bromide and valeriana, neuro-plegics
(meprobamate, trioxazine, chlordiazepoxide, Librium, Se-duksen) ganglion-blocking agents (nanophyn,
chlorpromazine hyd-rochloride, hexamethonium, etc.), and antihistaminic antipruritic agents (Tavegil, Dimedrol,
Suprastin, Diprazin, etc.). Vitamins of the В complex, and vitamins PP and A are prescribed (in a dis persed
form for children and as drops of a concentrated oil vitamin A solution for adults; vitamins A and E are given as
intramuscular injections separately or as aevit). Elderly patients are prescribed methyltestosterone. Sulphurated
hydrogen and radon baths, ultraviolet irradiation and heliotherapy (photochemotherapy) are the recommended
physiotherapeutic measures. Baths with bur-marigold, oak bark or chamomile decoction are advisable. After the
bath the dry skin areas are smeared with nutrient cream (Lanolini, 01. Olivarum, Aq. destill. aa 30.0) or olive oil.
Keratoplastic ointments with naphthalan, tar, sulphur, ichthammol, ASD solution are applied.
Ointments containing corticosteroids (Synalar, Locacorten, Flucinar, Ftorokort, etc.) are applied to the
affected areas. Aniline dyes, Gastellani's paint and Oxycort, Geocorton, Locacorten N, Locacorten-Vioform
ointments are used for external therapy of secondary infection. Patients with localized neurodermitis, like those
with diffuse and disseminated processes, are given sedatives and antihistaminic agents, a diet with restriction of
spicy and smoked foods and exclusion of salt foodstuffs. Alcoholic beverages and food which intensifies itching and
the inflammatory process of the skin are not allowed. Intracutaneous injections of a 0.15 per cent methy-lene blue
solution with a 2 per cent bencaine or procaine hydrochlo-ride solution with the prolongator gelatin or
polyvinylpyrrolidone around the foci of affection are recommended in localized neurodermitis. Injections of
hydrocortisone emulsion around the foci are advisable in pronounced lichenification and infiltration of the foci.
Treatment with Bucky's rays has a favourable effect. A long stay in the south in summer is recommended for the
prevention of recurrences and prolongation of the achieved remission, as well as a rational hygienic regimen,
treatment of foci of chronic infection, and removal of food, drug and household allergens (animals* fur, everyday
household chemicals, household dust, etc.).
Prurigo
Two principal varieties of prurigo are distinguished: infantile (prurigo infantum, seu strophulus) and adult
(adultorum). A less frequent variety is nodular prurigo (prurigo nodularis).
Prurigo nodularis is a disease well denned clinically and his-topathologically. The morphological lesions are
semispherical hard pustules, 5-12 mm in diameter, often with a verrucose surface. They are usually localized on
the extensor surfaces of the lower limbs and less frequently on the upper limbs and trunk. The disease greatly
resembles the hypertrophic form of lichen rubrum planus. It is mainly encountered among middle-aged females and
is characterized by a protracted chronic course. Emotional stress and mosquito bites are among the causative
factors noted. A very severe and persistent itching leads to changes in the nerve receptors.
The histological picture is marked by thickening of the horny and, in places, of the granular epidermal
layers. The interpapillary strands penetrate the derma to great depths (sharply pronounced acanthosis). Massive
cellular infiltrate of lymphocytes, fibroblasts and histiocytes is found in the dermis (mainly in the upper part
of the reticular layer). No collagenous or elastic fibres are seen in the central parts of the infiltrates. A very
pronounced hyperplasia of the nerve endings and nerve bundles and thickened Schwann's membranes of the nerve
trunk are noted. Degeneration of nerve fibres are seen here and there as non-structural ruptured bundles.
Treat^nt. Injections of a 0.25 per cent methylene blue solution on a 1-2 per cent bencaine or procaine
hydrochloride solution with a prolongator (medicinal gelatin or polyvinylpyrrolidone) are made around some of
the pustules. Some pruriginous nodular lesions are destroyed by means of liquid nitrogen, carbon dioxide or diather-
mocoagulation. Antihistaminic agents and sedatives are prescribed at this time.
Infantile prurigo (syn. strophulus, papular urticaria in chil dren, infantile urticaria) prevails among
children of 5 months to 3 years of age suffering from exudative diathesis. It usually sets in during the first year
of life. An important role in its pathogenesis is played by sensitization to food: to the protein of the mother's
or cow's milk (caseinogen) in infants. Exacerbation of the disease in older children is usually attributed to
chocolate, canned foods» citrous fruit, eggs, less frequently to mushrooms, strawberries, some kinds of fish
and other products, and sometimes to drugs.
Besides sensitization to food and drugs, autotoxicosis and auto-sensitization from the intestine play a definite
role in the development of prurigo.
Clinical picture. In addition to itching, which usually occurs in paroxysms the child develops diffuse
papulovesical or, less frequently, urticarial-macular eruptions on the face, scalp, trunk, buttocks and extensor
surfaces of the limbs. The mucous membranes are not involved. Papular lesions with vesicles on their tops are
the most typical, punctate erosions and serous crusts come next.
The histo logical picture is displayed by oedema of the dermal papillary layer. In the epidermal prickle-cell
layer there are peri-vascular infiltration, acanthosis, and intra- and intercellular oedema, as a result of which
small cavities with a serous exudate form.
In many children prurigo disappears after they are weaned. Less frequently it develops into chronic prurigo
of adults, pruriginous eczema or diffuse neurodermitis (atopic dermatitis) or Besnier's prurigo (disseminated
neurodermitis). Such children with persistent prurigo have white dermatographia, a marked neurotic state, dry
skin, disturbed sweat secretion, and enlarged lymph nodes (inguinal and femoral in particular). The plantar reflex
is absent and the abdominal reflex diminished.
The neurotic disorders (increased irritability, fretfulness, partial or complete insomnia) may be of primary
character inherited from parents together with an exudative-catarrhal constitution and abnormal lability of the
nervous system. They may also be caused by the disease itself; this is characterized by very intensive itching,
which is in turn a manifestation of the toxico-allergic reaction in these patients.
Diagnosis. Prurigo is distinguished from neurodermitis only by certain morphological features of the
eruption and its localization: in neurodermitis the eruption prevails on the flexor surfaces of the limbs, whereas in
prurigo it is found on the extensor surfaces. Differential diagnosis is also made with scabies and drug disease.
Treatment. Dietetic treatment is very important. The diet for children calls for particular scrupulousness (see
the corresponding section). Before all else, the child should not be overfed, and carrot juice, yoghurt and cottage
cheese should be given as early as possible, gradually increasing their amount. For the purpose of hypo-
sensitization it is advisable to give the infant 10-15 drops of strained mother's milk 15-20 minutes before it is
given the breast.
Vegetables (carrots, cabbage, spinach, peas, sorrel) and fruits are given in abundance. Sour dairy foods
(yoghourt, keffir, sour milk) and cooked meat (lamb and beef) are recommended. Vegetable oil is given. The food
should be sparce in salt, with no excess of carbohydrates or fats, it should be rich in vitamins С, В and A, with a
sufficient amount of vegetables.
In planning the diet of a child suffering from exudative diathesis it is therefore essential to adhere to the
following rule: the amount of proteins in the diet should accord to the physiological age norm (2.0-2.5 g/kg daily in
the first three months of life, 3 g/kg at three to six months of age, 3.5-4.0 g/kg from the age of 6 to 12 months
and older). Fats and carbohydrates are given in amounts that are slightly less than the physiological norm, i.e. less
than 6-7 g/kg fats and less than 12-14 g/kg carbohydrates after the age of 12 months.
All food listed above and other foodstuffs, which induce exacerbation of a pruritic allergic dermatosis, are
removed from the diet of infants of nursery, рге-school and school age.
Expectant mothers and mothers in the period of lactation are not allowed eggs, fish, citrous fruit, strong meat
broth and pork; salty foods and fats should be restricted. Vegetables and fruits should be given in abundance.
Sour dairy foods and boiled beef are recommended.
Test for helminths must be conducted and if these are detected not only children, but also expectant and
nursing mothers must be treated, because helminths, nematode worms in particular, cause a strong allergenic
effect. Special care should be accorded to the detection of various foci of infection (chronic tonsillitis and chole-
cystitis, sinusitis, otitis, carious teeth, etc.) in patients with exudative diathesis. Obligatory and timely
treatment of these foci reduces the possibility of the development of infectious allergy and auto-allergy.
Children with prurigo are given antihistaminic and neuroplegic agents, sedatives, vitamins of the В complex
and vitamin A, rutin, ascorbic acid. Calcium preparations are advisable in vagotonia (red diffuse
dermatographia, which is often of a stable character). Corticosteroid hormones are used in low and gradually reduced
doses in particularly persistent cases.
Ultraviolet irradiation with suberythema doses (every other day to a total of 20 exposures) are among the
indicated physiotherapeutic methods. Older children are treated by lumbar inductothermia. In the absence of
pyococcal infection, a favourable effect is caused by baths with decoctions of bur-marigold or oak bark,
chamomile and sometimes with bran. Sea bathing is beneficial.
External treatment is of an auxiliary character and is applied only in combination with a rational diet and
general therapeutic measures. Ointments and creams with corticosteroid hormones and aqueous-zinc shake
lotions with glycerin are prescribed.
In lesions complicated by pyococcal infections the skin is rubbed with Alibur's solution.
Rp: Sol. Zinci sulf. 0.25%
Sol. Cupri sulf. 0.5% aa 50.0
Sp. Vini 96% 20.0
MDS. For external application
The skin may also be rubbed with a 1 per cent vinegar in 60 per cent ethyl alcohol. The pustules are
opened and painted with a 1-2 per cent solution of aniline dyes, 1-2 per cent potassium permanganate solution
or a 5-10 per cent silver nitrate solution. If crusts (purulent or seropurulent) have formed, ointments like Oxy-
cort, Geocorton, Locacorten or ointments with vioform, neomycin or mycerin-prednisolone are prescribed.
 Prurigo of adults (prurigo adultorum, seu temporanea) is manifested by itching and papular eruptions mainly
on the extensor surface of the limbs as well as on the back, abdomen, loins, and buttocks. The flexor surf ace of the
limbs and face is usually not involved in the process. The papules are scattered, hard in consistency, conic or
semispherical in shape (ranging in size from a pin-head to a millet or hemp grain). They are pinkish-red and
may have haemorrhagic crusts on their surface as the result of excoriations. Because of oedema some papules
acquire an urticarial appearance.
Pustules form if secondary pyococcal infection develops. The disease lasts from several weeks to many
months. Neurotic disorders and troubled sleep develop in chronic prurigo. Such patients have enlarged lymph
nodes and eosinophilia.
Differential diagnosis is made with Dtihring's disease, which is characterized by pleomorphic eruptions
(vesicles, bullae, urticarial, erythematous and papular lesions) a tendency of the vesicular lesions to gather in
groups, hypersensitivity of the patients to potassium iodine and increased number of eosinophils in the bullae
fluid. Scabies is characteristically localized on the flexor surface of the limbs and other typical sites and the
scabies mite is found in the papulovesicular lesions.
Treatment of patients with prurigo is the same as for diffuse neu-rodermitis.
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 che-
mically 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 re-
nal 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 urti caria 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 ap pearance 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. Angioneurotic 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 short lived 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, vita mins 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.