Traumatic illness

In recent decades, the problem of injuries and their consequences has been considered in the aspect of a concept called traumatic disease. The importance of this teaching lies in the interdisciplinary approach to examining the functioning of all body systems from the moment of injury to recovery or death of the victim, when all processes (fracture, wound, shock, etc.) are considered in the unity of cause-and-effect relationships.

The importance for practical medicine is connected with the fact that this problem concerns doctors of many specialties: resuscitators, traumatologists, surgeons, therapists, family medicine doctors, psychologists, immunologists, physiotherapists, since a patient who has suffered an injury consistently receives treatment from these specialists both in a hospital and in a clinic.

The term "traumatic disease" appeared in the 50s of the 20th century.

Traumatic disease is a syndrome complex of compensatory-adaptive and pathological reactions of all body systems in response to trauma of various etiologies, characterized by stages and duration of the course, determining its outcome and prognosis for life and ability to work.

Epidemiology of traumatic disease

In all countries of the world, there is a tendency for the annual increase in injuries. Today, this is a priority medical and social problem. Over 12.5 million people are injured per year, of whom over 340 thousand die, and another 75 thousand become disabled. In Russia, the indicator of years of potential life lost from injuries is 4,200 years, which is 39% more than from diseases of the circulatory system, since most patients are young, most able-bodied. These data set specific tasks for traumatologists in the implementation of the priority Russian national project in the field of health care.

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Symptoms of traumatic disease

Trauma is a powerful emotional and painful stress that leads to the development of changes in all systems, organs and tissues of the victims (psychoemotional state, functioning of the central and autonomic nervous system, heart, lungs, digestion, metabolic processes, immunoreactivity, hemostasis, endocrine reactions), i.e. a violation of homeostasis occurs.

Speaking about the role of the nervous system in the formation of clinical variants of post-traumatic disorders, one cannot help but dwell on the specifics of the situation itself, when trauma occurs. In this case, many of the actual needs of the individual are blocked, which affects the quality of life and leads to changes in the system of psychological adaptation. The primary psychological reaction to traumatization can be of two types - anosognosic and anxious.

• In the anosognosic type, up to 2 weeks after the injury, a positive emotional background, a minimum of vegetative manifestations and a tendency to deny or downplay the symptoms of their illness are noted; such features of the psychological reaction to injury are characteristic mainly of young men who lead an active lifestyle.
• Patients with an anxious type in the same period are characterized by a depressed state, suspiciousness, depression, negatively colored emotional background, abundance of vegetative symptoms, pronounced pain syndrome, a feeling of fear, anxiety, uncertainty in a good outcome, poor health, sleep disturbance, decreased activity, which can lead to an exacerbation of concomitant pathology and complicate the course of the underlying disease. Such a reaction is more often characteristic of patients over 50 years old, mainly female.

In further dynamics, by the end of the first month of traumatic disease, the psychoemotional state of most patients with an anxious reaction type begins to stabilize, vegetative manifestations decrease, which indicates a more adequate perception and realistic assessment of their condition and the situation as a whole. Whereas in patients with an anosognostic type, signs of anxiety, frustration, emotional discomfort begin to increase within 1-3 months from the moment of injury, they become aggressive, quick-tempered, concern about the present and the future appears ("anxious assessment of prospects"), which can be partly explained by the inability of patients to cope with the situation on their own. Attempts to attract the attention of relatives and loved ones appear.

By the 3rd month of the disease, only a third of patients experience harmonization of the psychological state, while they note good social adaptation, active participation in the treatment process and acceptance of responsibility for their condition. In most patients, during this period, primary psychological reactions undergo maladaptive development in the form of predominance of pathological types of attitude to the disease, increased anxiety with the predominance of the mental component of anxiety over the vegetative, increased aggressiveness and rigidity. Such development is acquired by the psychoemotional state in half of patients with a primary anosognostic and in 86% of patients with an initially anxious type of reaction to trauma.

Six months after the injury, 70% of patients with traumatic disease retain a maladaptive psychological state associated with frequent hospitalizations and forced long-term isolation from the usual environment. Moreover, half of them develop a dysphoric type, characterized by increased conflict, aggressiveness, selfishness with irritability, weakness, outbursts of anger and hostility towards others, and reduced control over emotions and behavior. In the other part, everything proceeds according to the apathetic type, when self-doubt and a feeling of helplessness prevail, while a pronounced vegetative component is noted, patients lose faith in recovery, a feeling of doom, refusal to communicate, indifference and apathy to everything, including their own health, appear. All this has a significant impact on the patient's rehabilitation process, and therefore requires the mandatory participation of a medical psychologist in the diagnosis and treatment of patients with traumatic disease.

Mental disorders in patients with traumatic illness are often accompanied by vegetative symptoms.

There are four forms of autonomic nervous system (ANS) response to trauma:

• with a predominance of parasympathetic reactions at all times of the examination;
• with the presence of vagotonia in the early stages of traumatic disease, and sympathicotonia in the later stages;
• with short-term activation of the sympathetic division and persistent eutonia later;
• with stable dominance of sympathicotonia at all times.

Thus, in the case of a pronounced predominance of parasympathetic symptoms in the early stages, the 7th-14th days become critical, when the patients' clinical picture is dominated by apathy, arterial hypotension, orthostatic syncope, bradycardia, respiratory arrhythmia and other symptoms of vagotonia, which were absent before the injury. In the late stages of traumatic disease, the 180th-360th days are considered the most dangerous in terms of the development of vegetative pathology with this form of response. The vicious circle of vegetative imbalance developing in the early stages without appropriate correction in such patients can lead to the formation of pathology in the late stages, up to diencephalic syndrome. The latter manifests itself in several variants: vegetative-visceral, or neurotrophic, syndrome, sleep-wakefulness disorder syndrome, vago-insular crises. This type of response of the autonomic nervous system to trauma is called “decompensated form of the parasympathetic type.”

There is another form of the autonomic nervous system response to trauma, when two diametrically opposed periods are revealed: from the first to the 30th day, the parasympathetic tone prevails, and from the 90th to the 360th day, the sympathetic tone. In the period from the 7th to the 14th day after the trauma, these patients show symptoms of parasympathetic tone prevalence, such as bradycardia (heart rate 49 beats per minute or less), arterial hypotension, extra systole, persistent red dermographism, respiratory arrhythmia; 30-90th days - the period of compensation of autonomic adaptation processes; from the 90th to the 360th day, due to the insufficiency of the compensatory capabilities of the system, a large number of symptoms of the predominance of the sympathetic section of the autonomic nervous system are revealed: tachycardia (in the form of constant sinus or paroxysmal supraventricular and ventricular tachycardia), weight loss, arterial hypertension, a tendency to subfebrile condition. This form of response of the autonomic nervous system to the conditions of traumatic disease should be classified as subcompensated.

The most physiological and common form of response of the autonomic nervous system to trauma conditions in uncomplicated traumatic disease is as follows: short-term (up to 7, maximum 14 days) sympathicotonia, with full restoration of autonomic balance by 3 months, the so-called "compensated form". With this nature of autonomic processes, the body is able to restore the regulatory relationships of the sympathetic and parasympathetic divisions disrupted as a result of trauma without additional correction.

There is another variant of the vegetative response to trauma. It is observed in patients with a history of episodes of increased blood pressure (BP) associated with psychoemotional overstrain or physical exertion. In such patients, sympathetic tone prevails for up to 1 year after the injury. In the early stages, the critical peak of sympathicotonia growth is recorded by the 7th day in the form of tachycardia (up to 120 per minute), arterial hypertension, palpitations, dry skin and mucous membranes, poor tolerance of stuffy rooms, a feeling of numbness in the limbs in the morning, white dermographism. In the absence of appropriate treatment, such dynamics of the autonomic regulation of the heart and blood vessels progressively leads to the development of pathological conditions such as hypertension with frequent crisis course or paroxysmal tachycardia in half of them in the late stages of the disease (90-360th day). Clinically, by the 90th day, these patients experience more frequent attacks of sudden increase in blood pressure (from 160/90 mm Hg to 190/100 mm Hg), requiring an ambulance call. Consequently, the trauma suffered by patients who initially had a predisposition to increased blood pressure becomes a factor provoking the progression of arterial hypertension. It should be noted that the clinical course of hypertensive crises themselves fits into the concept of "sympathoadrenal" or "type I crisis", since blood pressure increases quickly (from 30 minutes to an hour), while tremors of the limbs, facial flushing, palpitations, a feeling of fear, emotional coloring appear, and after a decrease in pressure, polyuria often occurs. This form of response of the autonomic nervous system to trauma should also be classified as decompensated, but of the sympathetic type.

Consequently, the predominance of the parasympathetic division of the autonomic nervous system in the early stages of traumatic disease (from the first to the 14th day) is considered more severe and prognostically unfavorable in relation to the long-term prognosis. Patients with a history of a tendency to increased blood pressure or other risk factors for arterial hypertension require measures to prevent increased sympathetic influence of the autonomic nervous system from the early stages after the injury, systematic blood pressure control and electrocardiographic monitoring, a course of individually selected doses of antihypertensive drugs (for example, enalapril, perindopril, etc.), the use of an integrated approach to rehabilitation: electrosleep, rational psychotherapy, autogenic training, etc.

Among visceral pathology, one of the first places in traumatic disease is occupied by changes in the work of the heart and blood vessels: a decrease in the functional activity of the entire circulatory system as a whole is noted for periods of up to a year or more from the moment of injury. The 1st to 21st day is considered critical in relation to the development of heart failure and post-traumatic myocardial dystrophy, which is manifested in a decrease in the indicators of the stroke index (SI) and ejection fraction (EF). One-time cardiac output depends on several factors: the volume of incoming blood, the state of myocardial contractility and diastole time. In severe mechanical injury, all these factors significantly affect the value of SI, although it is quite difficult to determine the specific weight of each of them. Most often, low values of the SI in victims in the early stages of traumatic disease (from the first to the 21st day) are caused by hypovolemia, a decrease in diastole due to tachycardia, a prolonged hypoxic episode, the effect on the heart of cardiodepressor substances (kinins) released into the blood when large areas of muscle tissue are damaged, hypodynamic syndrome, endotoxicosis, which, undoubtedly, must be taken into account when treating patients with mechanical injuries.

In this case, both extravascular (bleeding, exudation) and intravascular (pathological deposition of blood, rapid destruction of donor erythrocytes) factors should be considered as factors in the development of post-traumatic BCC deficiency.

In addition, severe mechanical trauma is accompanied by a significant increase in the enzymatic activity (2-4 times compared to the norm) of such cardiac-specific enzymes as creatine phosphokinase (CPK), MB-form of creatine kinase (MB-CPK), lactate dehydrogenase (LDH), a-hydroxybutyrate dehydrogenase (a-HBD), myoglobin (MGB), with the highest peak from the first to the 14th day, which indicates a pronounced hypoxic state of cardiomyocytes and a tendency to myocardial dysfunction. This should be especially taken into account in patients with a history of coronary heart disease, since trauma can provoke an attack of angina pectoris, acute coronary syndrome and even myocardial infarction.

In traumatic disease, the respiratory system is extremely vulnerable and suffers among the first. The ratio between lung ventilation and blood perfusion changes. Hypoxia is often detected. Acute pulmonary failure is characterized by the gradual development of arterial hypoxemia. In shock hypoxia, there is a hemic component due to a decrease in the oxygen capacity of the blood due to its dilution and aggregation of erythrocytes. Subsequently, a disorder of external respiration occurs, developing according to the type of parenchymatous respiratory failure. The most formidable complications of traumatic disease from the respiratory system are respiratory distress syndrome, acute pneumonia, pulmonary edema, fat embolism.

After severe injuries, the transport function of the blood (transport of oxygen and carbon dioxide) changes. This occurs due to a decrease in the amount of red blood cells, hemoglobin, nonheme iron by 35-80% in traumatic disease with a decrease in the volume of tissue blood flow, and a limitation in the use of oxygen by tissues; such changes persist on average from 6 months to 1 year from the moment of injury.

The imbalance of oxygen and blood circulation, especially in a state of shock, affects the processes of metabolism and catabolism. Disturbances in carbohydrate metabolism are of particular importance. After an injury, the body develops a state of hyperglycemia, called "trauma diabetes". It is associated with the consumption of glucose by damaged tissues, its release from the depot organs, blood loss, the addition of purulent complications, as a result of which the glycogen reserve of the myocardium decreases, and the carbohydrate metabolism of the liver changes. Energy metabolism suffers, the amount of ATP decreases by 1.5-2 times. Simultaneously with these processes, traumatic disease causes a disorder of lipid metabolism, which in the torpid phase of shock is accompanied by acetonemia and acetonuria, a decrease in the concentration of beta-lipoproteins, phospholipids, and cholesterol. These reactions are restored 1-3 months after the injury.

Protein metabolism disorders persist for up to 1 year and manifest themselves early (up to 1 month) as hypoproteinemia due to increased catabolic processes (the concentration of functional proteins decreases: transferrins, enzymes, muscle proteins, immunoglobulins). In severe injuries, daily protein loss reaches 25 g. Later (up to 1 year), prolonged dysproteinemia is recorded, associated with a violation of the ratio between albumins and globulins towards the predominance of the latter, an increase in the amount of acute phase proteins and fibrinogen.

In trauma, electrolyte and mineral metabolism is disrupted. Hyperkalemia and hyponatremia are detected, most pronounced in a state of shock and recovering fairly quickly (by 1 month of illness). Whereas a decrease in calcium and phosphorus concentration is noted even 1 year after the injury. This indicates that bone tissue mineral metabolism suffers significantly and for a long time.

Traumatic disease leads to changes in water-osmotic homeostasis, acid-base balance, pigment metabolism, and depletion of vitamin resources.

Particular attention should be paid to the functioning of such important systems as the immune, endocrine and homeostasis systems, since the clinical course of the disease and the restoration of the damaged organism largely depend on their condition and response.

The immune system influences the course of traumatic disease, while mechanical trauma disrupts its normal functioning. Changes in the body's immunological activity in response to trauma are considered as manifestations of the general adaptation syndrome,

In the early post-traumatic periods (up to 1 month from the moment of injury) a pronounced immunodeficiency of mixed genesis develops (on average, most indicators of the immune status are reduced by 50-60%). Clinically, at this time the greatest number of infectious and inflammatory (in half of the patients) and allergic (in a third of the patients) complications occur. From 1 to 6 months, multidirectional shifts of an adaptive nature are recorded. Despite the fact that after 6 months an adequate bone callus is formed and the supporting function of the limb is restored (which is confirmed by radiography), immunological shifts in such patients are prolonged and do not disappear even by 1.5 years from the moment of injury. In the long term (from 6 months to 1.5 years), patients develop an immunological deficiency syndrome, predominantly of the T-deficiency type (reduced number of T-lymphocytes, T-helpers/inducers, complement activity, number of phagocytes), which is clinically manifested in half, and laboratory-appearing in all, who have suffered severe trauma.

Critical periods for the occurrence of possible immunopathological complications:

• the first day, the period from the 7th to the 30th day and from 1 year to 1.5 years are prognostically unfavorable in relation to infectious and inflammatory complications;
• periods from the first to the 14th day and from the 90th to the 360th day - in relation to allergic reactions.

Such long-term immune shifts require appropriate correction.

Severe mechanical trauma leads to serious changes in the hemostasis system.

In the hemostasis status of patients in the first 7 days, thrombocytopenia with intravascular platelet aggregation and multidirectional shifts in coagulation tests are detected:

• fluctuations in thrombin time;
• prolongation of activated partial thromboplastin time (APTT);
• decrease in prothrombin index (PTI);
• decreased activity of antithrombin III;
• a significant increase in the amount of soluble fibrin monomer complexes (SFMC) in the blood;
• positive ethanol test.

All this indicates the presence of disseminated intravascular coagulation syndrome (DIC syndrome).

DIC syndrome in the examined patients is a reversible process, but produces a long-term after-effect. Most often, it is associated with a deep lesion of the compensatory mechanisms of the hemostasis system under the influence of severe mechanical trauma. Such patients develop long-term coagulopathy (up to 6 months from the moment of injury). Thrombocytopenia, thrombophilia and disturbances of fibrinolysis reactions are recorded from 6 months to 1.5 years. Laboratory data during these periods may show a decrease in the number of platelets, antithrombin III activity, fibrinolysis activity; an increase in the amount of RFMC in plasma. Clinically, some patients experience spontaneous gingival and nasal bleeding, skin hemorrhages of the petechial-spotty type, and some - thrombosis. Consequently, in the pathogenesis of the formation and development of the nature of the course of traumatic disease, one of the leading factors is disturbances in the hemostasis system, they must be diagnosed and corrected in a timely manner.

The endocrine system in a functional state is one of the dynamic systems, it regulates the activity of all morphofunctional systems of the body, is responsible for homeostasis and resistance of the body.

In mechanical injuries, the stages of functional activity of the pituitary gland, thyroid and pancreas, and adrenal glands are determined. There are three periods of endocrine reactions in patients with traumatic disease: the first period - from the first to the 7th day; the second period - from the 30th to the 90th day; the third period - from 1 to 1.5 years.

• In the first period, a significant decrease in the activity of the hypothalamic-pituitary-thyroid system is noted, combined with a sharp increase in the activity of the pituitary-adrenal system, a decrease in the endogenous function of the pancreas and an increase in the activity of somatotropic hormone.
• In the second period, increased activity of the thyroid gland is observed, the activity of the pituitary gland is reduced with normal functioning of the adrenal glands, and the synthesis of somatotropic hormone (STH) and insulin is reduced.
• In the third period, increased activity of the thyroid gland and pituitary gland is recorded with low functional capacity of the adrenal glands, the content of C-peptide increases, and the amount of somatotropic hormone returns to normal.

Cortisol, thyroxine (T4), insulin, and somatotropic hormone have the greatest prognostic value in traumatic disease. Differences in the functioning of individual links of the endocrine system in the early and late stages of traumatic disease have been noted. Moreover, from 6 months to 1.5 years after the injury, patients were found to have hyperfunction of the thyroid gland due to T4, hypofunction of the pancreas due to insulin, decreased activity of the pituitary gland due to adrenocorticotropic (ACTH) and thyroid-stimulating hormones (TTT), and increased activity of the adrenal cortex due to cortisol.

It is important for a practicing physician that endocrine shifts in response to trauma are ambiguous: some are adaptive, transient in nature and do not require correction. Other changes, designated as pathological, require specific therapy, and such patients require long-term observation by an endocrinologist.

In patients with traumatic disease, metabolic and destructive changes occur in the digestive organs depending on the location and severity of the injury. The development of gastrointestinal bleeding, erosive gastroenteritis, stress ulcers of the stomach and duodenum, cholecystopancreatitis is possible, sometimes the acidity of the gastrointestinal tract and absorption of food in the intestine are disrupted for a long time. In severe cases of traumatic disease, the development of hypoxia of the intestinal mucosa is noted, which may result in hemorrhagic necrosis.

Classification of traumatic disease

The classification of traumatic disease was proposed by I.I. Deryabin and O.S. Nasonkin in 1987. Forms of the course of the disease.

By severity:

• light;
• average;
• heavy.

By character:

• uncomplicated;
• complicated.

By outcome:

• favorable (recovery is complete or incomplete, with anatomical and physiological defects);
• unfavorable (with a fatal outcome or transition to a chronic form).

Periods of illness:

• spicy;
• clinical recovery;
• rehabilitation.

Clinical forms:

• head injuries;
• spinal injuries;
• isolated chest injuries;
• multiple abdominal injuries;
• combined pelvic injuries;
• combined limb injuries.

The classification of forms of traumatic disease according to the degree of compensation of the functions of organs and systems is as follows:

• compensated;
• subcompensated;
• decompensated.

A practicing physician dealing with the problem of trauma and post-traumatic pathology must take into account the following principles:

• syndromic approach to diagnosis;
• reaching the level of diagnostics of pre-diseases and their timely correction;
• individual approach to rehabilitation;
• treating not the disease, but the patient.

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Treatment of traumatic disease

Treatment of traumatic disease depends on the severity and period of the disease, but despite the general principles, the most important thing is an individual approach taking into account the complex of syndromes in a particular patient.

The first stage (prehospital) begins at the scene of the incident and continues with the participation of a specialized ambulance service. It includes emergency bleeding control, restoration of airway patency, artificial ventilation of the lungs (ALV), closed heart massage, adequate pain relief, infusion therapy, application of aseptic dressings to wounds and transport immobilization, delivery to a medical facility.

The second stage (inpatient) continues in a specialized medical institution. It consists of eliminating traumatic shock. All patients with trauma have a pronounced pain reaction, so they need adequate pain relief, including modern non-narcotic drugs (lornoxicam, ketorolac, tramadol + paracetamol), narcotic analgesics, psychotherapy aimed at pain relief. Blood loss in a hip fracture is up to 2.5 liters, therefore, the volume of circulating blood must be replenished. For this, there are modern drugs: hydroxyethyl starch, gelatin, antioxidants and detoxifiers (reamberin, cytoflavin). During the period of shock and early post-shock reaction, catabolic processes are launched. In severe injuries, daily protein loss reaches 25 g, with the so-called "eating" of one's own skeletal muscles, and if the patient is not helped during this period, muscle mass is restored on its own only by the age of 1 year (and not in all patients). One should not forget about parenteral and enteral nutrition in patients with traumatological profiles; balanced mixtures such as Nutricomb for enteral nutrition and "three in one" preparations for parenteral nutrition (Kabiven, Oliklinomel) are best suited for this. If the listed problems are successfully solved, the BCC is normalized, hemodynamic disorders are restored, which ensures the delivery of oxygen, plastic substances and energy to tissues, and therefore stabilizes homeostasis as a whole. In addition to the loss of muscle mass, protein metabolism disorders support the existing post-traumatic immunodeficiency, which leads to the development of inflammatory complications and even sepsis. Therefore, along with adequate nutrition, it is necessary to correct immune disorders (for example, polyoxidonium).

In the presence of DIC syndrome, fresh frozen plasma containing all the necessary components of the anticoagulant system (antithrombin III, protein C, etc.) in combination with heparin should be added to the indicated therapy; antiplatelet agents (pentoxifylline, dipyridamole); therapeutic plasmapheresis to unblock the mononuclear phagocyte system and detoxify the body; polyvalent protease inhibitors (aprotinin); peripheral alpha-blockers (phentolamine, droperidol).

Treatment of post-traumatic acute respiratory failure (ARF) should be pathogenetic. For emergency restoration of airway patency, the upper airways are examined, eliminating the retraction of the tongue and lower jaw. Then, using an electric suction device, mucus, blood and other liquid components are aspirated from the tracheobronchial tree. If the patient is conscious and adequate breathing has been restored, inhalation oxygen therapy is prescribed and ventilation of the lungs is monitored. In severe cases of failure of external respiration or in case of its excessive strain, tracheal intubation (less often tracheotomy) with subsequent artificial ventilation of the lungs (ALV) is indicated. It is also used to prevent and treat adult respiratory distress syndrome. The next and most difficult section of the fight against ARF is the restoration of the rib cage frame in case of chest trauma and the elimination of pneumothorax. At all stages of the fight against ARF, it is necessary to provide sufficient oxygen saturation of tissues using artificial ventilation of the lungs, and, at the first opportunity, in a pressure chamber.

Victims with psychogenic disorders (aggressive behavior, pronounced agitation, etc.) require the administration of one of the following drugs: chlorpromazine, haloperidol, levomepromazine, bromdihydrochlorophenylbenzodiazepine. An alternative to this is the administration of a mixture consisting of chlorpromazine, diphenhydramine and magnesium sulfate. In the pregnant state, a 10% solution of calcium chloride (10-30 ml) is injected intravenously, sometimes rausch anesthesia is used. In anxiety-depressive states, amitriptyline, propranolol, clonidine are prescribed.

After the victim has been removed from the acute condition and emergency surgery has been performed, it is necessary to conduct a full examination of the patient, delayed surgeries or other manipulations aimed at eliminating defects (imposition of skeletal traction, plaster casts, etc.). After determining the leading clinical syndromes, it is necessary, along with the treatment of the main process (trauma of a particular area), to correct the general reactions of the body to the injury. Timely administration of drugs that help restore homeostasis, such as antihomotoxic drugs and systemic enzyme therapy (phlogenzym, wobenzym) can improve the course of traumatic disease, reduce the risk of infectious and allergic complications, restore neuroendocrine reactions, tissue respiration, regulate microcirculation, and, consequently, optimize reparative and regenerative processes in the presence of bone fractures, avoid the development of acquired immunological deficiency, hemostasis system pathology syndromes in the distant future. The complex of rehabilitation measures should include adequate physiotherapy (massage, UHF, electrophoresis of calcium and phosphorus ions, laser therapy of bioactive points, exercise therapy), hyperbaric oxygenation (no more than 5 sessions), acupuncture, gravitational therapy. Good results are achieved by using preparations containing mineral-vitamin complexes.

Given the psychogenic effects of trauma, it is necessary to involve psychologists and use a range of different psychotherapeutic methods, medications and social rehabilitation programs. The most common combination is situational protection, emotional support and cognitive psychotherapy methods, preferably in group settings. It is necessary to avoid prolonging the course of psychosocial interventions in order to avoid the formation of a secondary benefit effect from the disease.

Thus, traumatic disease is of great interest to a wide range of practical medical doctors, since the rehabilitation process is long and requires the involvement of specialists of various profiles, and also requires the development of fundamentally new therapeutic and preventive measures.