Emergency situations in a cosmetologist's office: what is important to know

Sofia Gritsak, dermatologist, anesthesiologist, cosmetologist, founder of the International School of Medical Cosmetology, member of the Association of Preventive and Anti-age Medicine, certified trainer in contour correction and mesotherapy (Ukraine)

The purpose of this article is to improve the knowledge of dermatocosmetologists in the field of treatment and prevention of the most common emergency conditions in aesthetic medicine.

Issues of intensive care of emergency conditions in aesthetic medicine have recently become particularly relevant. This can be explained by an impressive list of aesthetic procedures and their availability to the general public, on the one hand, and on the other, by a decrease in the overall level of health of the nation. In such conditions of growing demand for conservative and invasive procedures of modern aesthetic medicine, it becomes necessary for dermatocosmetologists to be aware of etiopathogenetic links, clinical manifestations and algorithms for providing emergency care for conditions that pose a threat to the patient’s life.

The structure of emergency conditions in aesthetic medicine is dominated by:

• immediate allergic reactions;
• acute cardiovascular and respiratory failure;
• convulsive syndrome;
• metabolic disorders.

It should be noted that the risk of resuscitation syndromes is significantly reduced if the patient’s previous medical history is carefully collected, and the success of intensive care equally depends on the training of the specialist and the availability of medications.

Emergency conditions in aesthetic medicine can be classified as follows:

• allergic reactions;
• certain nosologies of emergency conditions;
• local trophic disturbances;
• threat of infection of medical personnel.

Allergic reactions

The most commonly observed allergic reactions include: simple contact dermatitis, allergic dermatitis, angioedema, anaphylatic shock.

Contact simple irritant dermatitis

Etiological factors : detergents, acids, alkalis, as well as other chemical compounds, sometimes water.

Pathogenesis : lack of sensitization, local degranulation of basophilic granulocytes after exposure to an irritant.

Clinical picture : rashes are localized at the site of action of the irritant. Characteristic is a sequential change of stages - erythematous, bullous, crustous, squamous.

Emergency care : immediately stop contact of the allergen with the skin, if necessary, prescribe topical steroids of high or moderate pharmacological effectiveness.

Allergic contact dermatitis

Etiology : skin exposure to certain metals, such as chromium or nickel; preservatives, SPF, fragrances, as well as various external agents, including hydrocortisone.

Pathogenesis : delayed allergic reaction, characterized by monovalent sensitization.

Clinical picture : develops some time after secondary contact with the allergen, the latent period can range from 12 to 48 hours. Rashes in the form of vesicles are characteristic; when exposed to strong allergens, blisters may appear, as well as hyperemia, swelling, burning sensation and itching to varying degrees. With chronic contact, hyperemia and rashes spread beyond the area of primary contact.

Emergency care : immediately stop the action of the allergen, if necessary, apply topical steroids of high, medium or low pharmacological effectiveness locally (depending on the location of the process), prescribe antihistamines.

Angioedema

Etiology : exposure to allergens or pseudoallergens (substances that cause the formation and release of allergy mediators in a non-immunological, non-specific way).

Pathogenesis: acute hypersensitivity reaction of immediate type (preceded by primary sensitization to the allergen, in response to repeated exposure, a secondary hyperergic reaction develops).

Clinical picture : characterized by damage to the deeper layers of the skin, the main clinical manifestation is swelling, often localized in the head, neck, hands, feet or external genitalia. The skin in the area of swelling appears normal, and patients usually complain of discomfort rather than itching. In 46–49% of cases, a combined development of urticaria and angioedema is observed. It develops acutely and usually has a benign course. An unfavorable outcome is possible with the development of intestinal obstruction, asphyxia and anaphylactic shock.

Urgent Care:

• 0.1% solution of adrenaline hydrochloride 0.2–0.5 ml subcutaneously, every 15–20 minutes until the patient’s condition is stabilized, or intravenously prednisolone 60 mg / dexamethasone 8 mg;
• second and third generation antihistamines - loratadine, cetrin, telfast, erius;
• inhibitors of proteinases and kallikrein – contrical 30–40 units. intravenous drip in 300 ml of 0.9% NaCl solution.

Anaphylactic shock

Etiology : allergen action.

Pathogenesis: immediate systemic allergic reaction resulting from rapid massive IgE-mediated release of mediators from tissue basophils and peripheral blood basophils upon repeated contact of the body with the allergen.

Clinical picture: characterized by rapidly developing generalized reactions, including itching, urticaria, angioedema (especially laryngeal edema), arterial hypotension, wheezing and bronchospasm, nausea, vomiting, abdominal pain, cardiac arrhythmia, followed by asphyxia. Such clinical manifestations can be monosymptomatic or in various combinations and usually develop immediately after exposure to the irritant (sometimes after 30–60 minutes, and in some cases more than an hour later). Sometimes the course of anaphylactic shock is biphasic: symptoms can regress independently or as a result of treatment and reappear after a few hours.

Emergency care : place the patient in a horizontal position, ensure airway patency, and, if possible, administer oxygen therapy:

• 0.1% solution of adrenaline hydrochloride 0.2–0.5 ml intravenously or sublingual injection every 15–20 minutes until the patient’s condition is stabilized;
• if anaphylactic shock develops after injection of the drug - 0.15–0.3 ml of adrenaline hydrochloride 0.1% at the site of allergen injection;
• dexamethasone 8 mg intravenously to reduce the risk of relapse or continuation of anaphylaxis;
• second and third generation antihistamines - loratadine, cetrin, telfast, erius;
• post-syndromic therapy - maintaining a normal level of blood pressure (if necessary, vasoconstrictors, replenishing blood volume), eliminating bronchospasm - aminophylline 2.4% intravenously slowly 10 ml, drotaverine hydrochloride (NO-SPA) 40 mg intravenously;
• hospitalization in a specialized department of a medical hospital.

Selected nosologies of emergency conditions

Reflex bronchospasm

Etiology: acute allergic reaction as a complication as a result of the use of certain medications, in cases of damage to the respiratory system by toxic substances, psychosomatic disorders (the most common cause in the group of emotionally labile patients).

Pathogenesis : the leading role is played by swelling and/or spasm of the smooth muscles of the tracheobronchial tree.

Clinical picture: difficulty breathing with prolonged exhalation, tension in the muscles of the neck, chest, anterior abdominal wall, cyanotic skin, noisy, wheezing breathing that can be heard from a distance. With total bronchospasm, there are no breath sounds.

Urgent Care:

• give the patient a sitting position, provide free access to fresh air, and, if possible, administer oxygen therapy;
• desensitization therapy: dexamethasone 8 mg intravenously or intramuscularly;
• post-syndromic therapy: elimination of bronchospasm - aminophylline 2.4% intravenously slowly 10 ml, drotaverine hydrochloride (NO-SPA) 40 mg intravenously;
• if necessary, sedatives and anxiolytics;
• second and third generation antihistamines - loratadine, cetrin, telfast, erius (not prescribed in case of severe bronchospasm).

Acute vascular insufficiency - syncope

Etiology: neurogenic, orthostatic, symptomatic and cardiac factors are distinguished.

Pathogenesis: short-term loss of consciousness, occurring suddenly, with a violation of postural tone and rapid, complete and independent restoration of normal tone. It is a mild form of acute cerebral vascular insufficiency caused by brain hypoxia.

Clinical picture: there is loss of consciousness, muscle atony, bradycardia, hypotension, pale skin, shallow breathing.

Urgent Care:

• give the patient a horizontal position in order to improve cerebral blood supply and provide free access to fresh air;
• measures aimed at irritation: intensive rubbing of the earlobes, mechanical stimulation of reflexogenic zones, etc.;
• if necessary, 0.1% solution of atropine sulfate 0.75–1.0 ml intravenously or 0.1% solution of adrenaline hydrochloride 0.2–0.5 ml intravenously;
• symptomatic therapy.

If the above measures are ineffective, you should immediately begin chest compressions and continue administering adrenaline.

Heart rhythm disturbance

Etiology: the most common causes are myocardial pathology, neuroendocrine disorders, and electrolyte imbalance.

Pathogenesis : depends on the trigger mechanism for the development of heart rhythm disturbances; disorders of automaticity, excitability and conductivity of the myocardium are distinguished.

Clinical picture: depending on the type of heart rhythm disturbance, sinus tachycardia or bradycardia, extrasystole, paroxysmal tachycardia, atrial fibrillation and atrial or ventricular flutter (with asystole) may be observed. In most cases, patients will complain of interruptions in heart function, a feeling of fear and lack of air.

Urgent Care:

• in case of tachyarrhythmia - vagal tests (pressing on the eyeballs with eyes closed, holding the breath); β-blockers (atenolol 50–150 mg/day), Ca2 channel blockers (verapamil 2.5–10 mg IV), antiarrhythmic drugs (Rhythmilen 150 mg IV, propanorm 150 mg per os); lidocaine (1–1.5 mg/kg) - do not prescribe to patients with hypersensitivity, SSS (sick sinus syndrome - especially in elderly patients), AV block III degree, SA block, WPW syndrome, cardiogenic shock, disorders intraventricular conduction;
• in case of bradyarrhythmia - symptomatic therapy, atropine sulfate 1 mg every 3-5 minutes intravenously or sublingually by injection until a total dose of 0.04 mg/kg is reached, (O2)

Pulmonary embolism (PE)

Etiology: occlusion of the arterial bed of the lungs by a thrombus, which primarily formed in the veins of the systemic circulation or in the cavity of the right heart and migrated into the vessels of the lungs with the blood flow.

Pathogenesis: embolic obstruction of the vascular bed stops blood flow in the area supplied by this vessel and redistributes it to free zones, causing an increase in intrapulmonary shunting. Non-perfused but ventilated areas of lung tissue appear, respiratory sections collapse and bronchial obstruction occurs in the affected area. A decrease in vascular capacity due to thromboembolism leads to an increase in vascular resistance, the development of pulmonary hypertension and acute right ventricular failure. Left ventricular failure is associated not only with obstruction of the pulmonary vessels, but also with another physiological mechanism: high pressure in the right parts of the heart displaces the heart septum to the left - and the volume of the left ventricle, sandwiched between the “inflated” right ventricle and the pericardial membrane, is significantly reduced. A decrease in pressure in the aorta in combination with its increase in the right atrium causes a decrease in perfusion pressure in the coronary arteries, leads to the development of myocardial ischemia and, as a result, to an even greater decrease in IOC.

Clinical picture: sudden shortness of breath at rest, pain syndrome: angina-like, pulmonary-pleural, abdominal, mixed. Arterial hypotension, pronounced cyanosis of the upper half of the body, and pallor of the skin are also observed.

Emergency treatment:

• VHF support, O2 therapy;
• anesthesia;
• thrombolytic therapy – tissue plasminogen activator (tPA), in a total dose of 100 mg/kg intravenously;
• anticoagulants – heparin 10,000–20,000 units. (if thrombolysis was not carried out), then they switch to administration in a hospital according to approved regimens.

Hypertensive crisis

Etiology: acute increase in blood pressure in response to psycho-emotional or other factors.

Pathogenesis: a rapid increase in blood pressure leads to disruption of regional circulation and is accompanied by an increase in existing symptoms or the appearance of new signs.

The clinical picture and subsequent emergency care depend on the form of the hypertensive crisis:

neurovegetative: characteristic sudden onset, a feeling of pulsation in the head, facial flushing, sweating, chills, tachycardia, anxiety, pain in the heart, which intensifies with a periodic rise in blood pressure with a predominant increase in systolic and a significant pulse difference;
water-salt: swelling of the eyelids and puffiness of the face are noted, which intensify in the morning, oliguria, numbness of the fingers, paresthesia. Both systolic and diastolic pressure increase, often with a decrease in pulse pressure;
convulsive.
Emergency care: gradually lower blood pressure by prescribing conventional antihypertensive drugs orally or sublingually:

• in the case of a mild neurovegetative crisis, nifedipine 10 mg sublingually every 30 minutes, can be combined with clonidine 0.15 mg orally, furosemide 40 mg intravenously or orally under the control of blood pressure dynamics;
• for water-salt crisis - furosemide 40-80 mg orally once and nifedipine 10 mg sublingually (every 30 minutes) or furosemide 20 mg orally once and captopril 6.25 mg sublingually and 25 mg every 30-60 minutes until the effect is achieved;
• relief of convulsive syndrome - diazepam 10–20 mg intravenously slowly, magnesium sulfate 2.5 mg intravenously very slowly, furosemide 40–80 mg intravenously slowly.

Hyperglycemic (ketoacidotic) coma

Etiology: diabetic ketoacidosis is a complication of diabetes mellitus and develops as a result of severe insulin deficiency, due to inadequate insulin therapy or increased need for insulin (trauma, pain, surgery, pregnancy, infectious intercurrent processes).

Pathogenesis: progressive insulin deficiency causes a decrease in glucose utilization and energy starvation of tissues, triggers alternative pathways for energy production, which are under the control of counter-insular hormones (catecholamines, glucagon, growth hormone, ACTH, GCS and thyroid hormones). This causes an increase in non-glycogenic substrates, and in parallel, lipolysis increases. Insulin deficiency leads to the fact that the oxidation of fatty acids ends in intermediate products - ketone bodies, which depress the central nervous system and negatively affect the cardiovascular system, which is manifested by a decrease in vascular tone, a decrease in stroke and minute volume of blood flow with a further decrease in hemodynamics, cerebral blood flow and depression of the central nervous system. .

Clinical picture: ketone bodies contribute to the occurrence of acidosis, which excites the respiratory center with the subsequent development of hyperventilation (the exhaled air has the smell of acetone, which makes it possible to distinguish it from hyperosmolar).

Emergency care : rehydration with physiological NaCl solution (at least 1 liter for 1–2 hours), intravenous administration of insulin per injection Dyn = Sgl - 6, where Dyn is the dose of insulin, units; Gg – blood glucose concentration, mmol/l. Posyndromic therapy.

Hyperosmolar hyperglycemic coma

Etiology: most often this type of coma develops in patients with a long history of insulin-dependent diabetes mellitus; its development is facilitated by various provoking factors.

Pathogenesis: high glucose levels stimulate urination; as a result of dehydration and increased electrolyte concentrations, hyperosmolarity develops, tachycardia and arterial hypotension progress.

Clinic : gradual loss of consciousness, focal, mildly expressed symptoms may occur, convulsions are possible.

Emergency care : the same as for ketoacidotic coma.

Hypoglycemic coma

Etiology : a condition that develops as a complication of diabetes mellitus with an overdose of insulin or excessive consumption of glucose.

Pathogenesis: a lack of glucose entering the brain leads to the fact that nerve cells quickly deplete their reserves, their activity decreases sharply, and then irreversible changes occur. Therefore, hypoglycemic coma is always more dangerous than hyperglycemic coma.

Clinical picture: feeling of hunger, anxiety, then excitement, external manifestations are very characteristic: pale skin covered with cold sweat, small frequent muscle contractions (fibrillations), sometimes blood pressure may increase, then loss of consciousness occurs, often accompanied by convulsions, constriction of the pupils.

Emergency care : administration of glucose 40% intravenously, in extreme cases orally sublingually. In case of complicated differential diagnosis of hyper- and hypo-osmolar coma, administer a 40% glucose solution preventively. Syndromic therapy, stabilization of hemodynamics and breathing.

Acute adrenal insufficiency

Etiology : acute adrenal insufficiency can occur as a result of rapid decompensation of chronic adrenal insufficiency, with acute damage, intoxication, or sudden withdrawal of steroid hormones. Various factors that cause tension in homeostasis can be provoking: infectious diseases, stress, operations, other painful interventions.

Pathogenesis: due to the lack of synthesis of gluco- and mineralocorticoids in acute adrenal insufficiency, there is a loss of sodium and chloride ions, a decrease in their absorption in the intestine, which leads to dehydration and the secondary transfer of water from the extracellular space into the cell. Due to severe dehydration, the volume of circulating blood decreases and shock develops. The concentration of potassium in the blood serum, in the intercellular fluid and in the cells increases and leads to impaired myocardial contractility.

Clinical picture : initial symptoms of acute adrenal insufficiency, such as adynamia, muscle hypotension, depressed reflexes, pallor, anorexia, decreased blood pressure, tachycardia, oliguria, non-localized abdominal pain of varying intensity, including acute abdominal syndrome. Without treatment, hypotension quickly progresses, signs of microcirculation disorders appear in the form of acrocyanosis, “marbling” of the skin. Heart sounds are dull, pulse is thready. Vomiting and frequent loose stools occur, which leads to exicosis and anuria.

The clinical picture, up to coma, develops quite suddenly, sometimes without any prodromal phenomena (bilateral hemorrhage of various origins in the adrenal glands, glucocorticosteroid withdrawal syndrome).

Emergency care : immediate intravenous administration of 125 mg of hydrocortisone or 60 mg of prednisolone in an isotonic NaCl solution, DOXA 5–10 mg intramuscularly. In case of a sharp decrease in blood pressure - 0.2% norepinephrine 1 ml or 1% mesaton 0.3–0.5 ml, cordiamine 1–2 ml intravenously.

Convulsive syndrome

Etiology : multifactorial syndrome. There are primary factors (genetic and idiopathic) and secondary (degenerative, infectious, metabolic, neoplastic, toxic, traumatic, vascular, etc.). It is important to remember that any, even the slightest stimulating effect on a patient with a history of seizures can lead to a relapse of seizures.

Pathogenesis: in the development of convulsive syndrome lies the process of the emergence of a focus of pathological excitability in the brain.

Clinical picture: seizures can be single or serial. Depending on the cause that caused the development of convulsions, both preservation of consciousness and loss of consciousness are possible. There are tonic (characterized by increasing muscle tone, to “wooden” density), clonic (tonic phase is replaced by a relaxation phase), hormeotonic (similar to clonic, but differ in greater expressiveness of both phases, especially relaxation) convulsions.

Emergency care at the prehospital stage is to prevent trauma to the patient and retraction of the tongue:

• ensuring airway patency, oxygen therapy;
• anticonvulsant therapy: 0.5% sibazone 2.0 ml or diazepam 10–20 mg intravenously slowly;
• magnesium sulfate 2.5 mg intravenously very slowly, furosemide 40–80 mg intravenously slowly.

Local tissue trophic disorders

Tissue ischemia followed by necrosis

Etiology : embolization of vessels or their compression due to excessive injection of filler in areas with poorly developed arterial collaterals (glabella, columns of the philtrum) or with an increased risk of occlusion by pressure (glabella, forehead, nose, nasolabial fold).

Pathogenesis : the main role in pathogenesis is played by impaired blood circulation in tissues, mainly the skin.

Clinical picture: symptoms of ischemia can develop quite quickly or gradually increase over the course of hours. In the case of fulminant development of ischemia, the patient complains of severe pain, which is not similar to his sensations during the procedure. The focus of ischemia turns white, with a gradual predominance of a cyanotic-violet hue. In case of progression, ischemic processes become irreversible and transform into necrosis.

Emergency care : since the skin is quite resistant to trophic disorders and necrotic processes start after two hours of ischemia, during this time the doctor has the opportunity to carry out measures to restore adequate blood circulation in the tissues, including:

• maximum possible aspiration of the injected material;
• massage of the ischemic area followed by application of a warm compress;
• application of drugs with vasodilating, anticoagulant and disaggregant properties (for example, lyoton, thrombocide, and nitroglycerin solution 10%). Since the external use of nitroglycerin solution has a limited effect, and there is no cream with nitroglycerin in Ukraine, it is possible to use this drug sublingually in tablet form, which will give a more pronounced vasodilator effect;
• in case of progression or lack of effect from the above-mentioned measures, it is necessary to proceed to the administration of hyaluronidase (in case of ischemia development after the injection of hyaluronic acid-based filler) or longidase. In the place where hyaluronic acid is located, it is necessary to inject hyaluronidase in an approximate dose of 30 IU;
• if necessary, resort to hyperbaric oxygenation.

Recently, reports have increasingly appeared in the scientific medical literature about transient or irreversible visual impairment in patients after contouring procedures using absorbable and permanent fillers in the forehead and glabella as a result of compression of the vessels supplying the eye.

Retrobulbar hematoma

Etiology: damage to the vessels of the fatty tissue of the eye when performing injection correction of aesthetic defects in the periorbital area beyond the bony edge of the orbit.

Pathogenesis: the leading role is played by increased intraocular pressure and compression of the optic nerve.

Clinical picture : characteristic symptoms of retrobulbar hematoma are: exophthalmos, increased intraocular pressure, limited mobility of the eyeball. There may be a decrease in visual function, which is associated with compression of the optic nerve in its orbital part. A sharp increase in pressure in the orbit can lead to reflex nausea, vomiting, and slowing of the pulse. Such hemorrhages are localized under the skin of the eyelids or under the conjunctiva, which reduces the tactile sensitivity of the facial skin under the orbital edge.

Emergency care : immediate hospitalization in the ophthalmic surgery department.

List of necessary medications for emergency care at the prehospital stage

• adrenaline hydrochloride 0.1%
• cordiamine 25%
• GCS: dexamthasone, prednisolone, etc.
• nitroglycerine
• magnesium sulfate 25%
• lidocaine 2%
• Diphenhydramine 1%
• drotaverine hydrochloride (NO-SPA) 2%
• aminophylline 2%
• glucose 5, 40%
• sodium chloride 0.9%
• sodium bicarbonate 2.4%
• hyaluronidase, longidase

Threat of infection of medical personnel due to contact with blood

If contact with blood or biological fluids was accompanied by a violation of the integrity of the skin (injection, cut), then the victim must:

• remove gloves with the working surface facing inward;
• squeeze blood out of the wound;
• treat the damaged area with a disinfectant (70% ethyl alcohol solution, 5% tincture of iodine, 3% hydrogen peroxide solution);
• wash your hands thoroughly with soap and running water, and then wipe them with a 70% ethyl alcohol solution;
• apply a plaster to the wound, put on a finger guard;
• if necessary, continue working, put on new medical gloves;
• immediately inform the management of the treatment and prevention institution about the incident in order to carry out emergency prevention of HIV infection.

When contaminated with blood, biological fluids, biomaterials without damaging the skin:

• treat the area of contamination with a disinfectant (70% ethyl alcohol solution, 3% hydrogen peroxide solution, 3% chloramine solution);
• Wash your hands thoroughly with soap and running water, and then wipe them with a 70% ethyl alcohol solution.

If blood, biological fluids, or biomaterial gets on the mucous membranes:

• oral cavity - rinse with 70% ethyl alcohol solution;
• nasal cavity - instill 30% albucide solution;
• eyes - rinse with water, drop in 30% albucide solution.

International Standard for Cardiopulmonary Resuscitation

Knowledge of the main stages of cardiopulmonary resuscitation (CPR) is not only an absolute responsibility of medical personnel of various qualifications, but also an opportunity to prevent death in conditions that pose a threat to human life (Fig. 1).

Rice. 1. "Chain of Survival"

A step-by-step cardiopulmonary resuscitation (CPR) framework approved by the American Heart Association and recognized as a standard throughout the world.

Rice. 2. Cardiopulmonary resuscitation

The correct position of the doctor’s hands during chest compressions is: deep compressions in the middle of the chest, in the area slightly above the xiphoid process, with a frequency of at least 60–70 compressions per minute.

Rice. 3. Correct position of the doctor’s hands during chest compressions

How to properly perform artificial pulmonary ventilation (ALV) and ensure airway patency: the patient’s head is thrown back, the lower jaw is pushed forward, the mouth is open.

Rice. 4. Technique for ensuring airway patency

For the most effective ventilation, it is desirable to introduce an air duct. Ventilation is carried out using a mask, an Ambu bag or (in its absence) by the mouth-to-mouth method using a special filter to prevent infection of medical personnel. Make 14–16 respiratory movements per minute. A marker of the correctness of mechanical ventilation is the rise of the chest at the moment of inspiration. Having the ability to ventilate the patient with 100% oxygen significantly improves the results of mechanical ventilation (Fig. 5).

Rice. 5. Joint CPR - mechanical ventilation and chest compressions

CONCLUSION

Issues of intensive care of emergency conditions are relevant for medical workers of various specialties, since they allow them to navigate difficult situations when the patient’s condition becomes terminal and there is a need to take emergency measures to stabilize or even replace certain vital functions of the body. It should be emphasized that success in emergency care is determined by the competence and actions of the doctor, as well as the necessary resuscitation support to provide primary intensive care before the arrival of the resuscitation team.

Literature

• Usenko L.V. et al. Basics of intensive care. – Ternopil: Ukrmedkniga. – 2002.
• Order dated January 17, 2005 No. 24 “On the approval of protocols for the provision of medical assistance for the specialty “Emergency Medicine.”
• Manevich A. Z., Plokhoy A. D. Fundamentals of intensive care, resuscitation and anesthesiology. – Moscow: Triad H. – 2000.
• Dranik G. N. Clinical immunology and allergology. – Kyiv: Polygraph Plus. – 2010.
• Adaskevich V.P., Kozin V.M. Skin and venereal diseases. – Moscow: Medical literature. – 2009.

First published in Les Nouvelles Esthetiques 2015/№2