General and local reaction of the body to injury. Stages of response to injury According to the nature of bone damage, fractures are divided into

20.06.2020 -

Traumatic disease differs from many diseases in its suddenness, occurrence against the background of complete health and the inevitable significant psychological stress. Often, upon regaining consciousness, the patient suffers morally not so much from the presence of trauma, loss of a limb, but from the sudden collapse of all life plans: work, improvement, habitual hobbies, rest, etc. the patient's condition often ends in suicidal attempts.

Acute trauma, especially polytrauma, creates a number of conditions manifested by a complex of clinical symptoms, general reactions of the body, which makes it possible to distinguish them into separate nosological forms. We give a brief description of them.

Fainting is a sudden short-term loss of consciousness due to a rapidly passing anemia of the brain, which is caused by a reflex vasospasm. The reason is fear, fear, pain. Clinic - sudden discomfort, weakness, nausea, dizziness, tinnitus, darkening of the eyes, pallor, loss of balance with a possible fall. Breathing shallow, slow. Pulse is weak, blood pressure is low. This state lasts for several seconds, rarely minutes.

Collapse - weakened. Pathological state of the body, characterized by depression of the central nervous system, a sharp decrease in arterial and venous pressure, a decrease in the mass of circulating blood and metabolic disorders. Hypoxia and hypoxemia develop. Clinically and pathogenetically, collapse is identical to shock and accompanies it, as well as other serious conditions: blood loss, toxicosis, allergies, myocardial infarction.

Shock - blow - an indifferent state of the body in extreme pain inhibition, according to the definition of N.I. Pirogov and I.P. Pavlova. Currently, traumatic shock is considered as the initial period of a traumatic disease with life-threatening violations of the most important functions of the body, which are expressed in the development of acute cardiovascular and respiratory failure, severe metabolic disorders (hypoxia, acidosis, azotemia, histaminemia, electrolyteemia). In the pathogenesis of shock, the leading role is assigned to the pain factor and blood loss.

There are 3 degrees of shock. At the first, there is slight lethargy, pulse 90-100 beats per minute, satisfactory filling. Systolic blood pressure within 100 mm Hg. Art. In the second degree of shock, the patient is indifferent to the situation, the state of moderate severity, pale. Pulse 110-120 per minute, systolic blood pressure up to 80 mm Hg. Art. The third degree is characterized by extreme severity and indifference to everything. The skin is pale gray, cold, with a marble tint. Tachycardia up to 140 beats per minute. Systolic pressure 80 mm Hg. Art.

Acute blood loss is an indispensable and dangerous complication of all types of injuries with an inevitable breakdown of the cardiovascular, respiratory, endocrine and other vital systems. There are arterial, venous, arteriovenous, capillary and, as its varieties, parenchymal and bone bleeding.

Blood loss can be external, cavitary and interstitial. The latter is a constant companion of all fractures and, unfortunately, is not sufficiently taken into account in practice. But the amount of blood loss is considerable. So, with closed fractures of the bones of the foot or ankles, it is 150-200 ml, the bones of the lower leg - 500-750 ml, the thigh - 800-1200 ml, the pelvis - 1500-2500 ml. With open injuries, blood loss increases by 1.5-2 times. Clinical signs - weakness and shortness of breath, the skin is pale and cold, the pulse is weak, tachycardia, blood pressure is reduced.

Syndrome of prolonged compression - or traumatic toxicosis, crush or crush syndrome, positional and crash syndromes. The pathogenesis consists of shock-like hemoneurodynamic reactions and toxic damage, primarily to the liver, kidneys and other organs and tissues, by the products of muscle breakdown, mainly myoglobin. The clinic is manifested by a syndrome of increasing intoxication and renal and hepatic insufficiency.

Fat embolism - blockage of blood vessels by drops of fat from the bone marrow. The most dangerous, most often fatal complication. There are pulmonary, renal and cerebral forms with the corresponding clinical picture of insufficiency of the primary affected organs and subsequent involvement of others. An embolism can appear immediately after an injury, as well as after a small (hours, days) or long (three days or more) “light period”. Of the external manifestations, a petechial rash and small hemorrhages on the face, upper body and limbs are characteristic. The current is very fast, sometimes instantaneous.

Pathophysiological aspects of trauma. Local and general tissue reaction. From a morphological point of view, the local reaction is simple and manifests itself as a violation of the integrity of damaged organs and tissues - skin and fiber, fascia and muscles, ligaments and bones. Depending on the shape of the wounding projectile and the impact force, the edges of the wounds can be even, with minimal tissue damage, or crushed, with the death of individual sections. All this is accompanied by bleeding, edema, and further necrosis of parabiosis zones and tissue autolysis. Mechanical trauma involves the whole organism in the process. A traumatic disease develops with the activation of adaptive and protective mechanisms. Vital regulators are switched on: the nervous system - the pituitary gland - the adrenal cortex. The release of cortisone and ACTH is stimulated, catabolic reactions are intensified, the metabolic processes of proteins, fats and carbohydrates are disturbed.

In severe injuries, the daily loss of protein reaches 25 g. The activity of transaminases increases 1.5-2 times. The level of blood proteins decreases. There is a dysproteinemia, the ratio between albumins and globulins is disturbed in the direction of the predominance of the latter. Blood sugar rises in response to inhibition of the insular apparatus of the pancreas. The content of iron in the blood decreases. Energy metabolism suffers, the amount of ATP decreases by 1.5-2 times. Vitamin resources are depleted, especially vitamin C. Already in the early stages after injury, the content of calcium and phosphorus sharply increases as a result of activation of bone formation, and alkaline phosphatase is also activated.

Microelements play an important role in the regulation of metabolism. There are about 30 of them in bone tissue. These are copper, strontium, barium, zinc, aluminum, silicon, fluorine, vanadium, gallium and others.

In addition to the above changes, in response to severe mechanical injury, such important adaptation systems as immune and hemostasiological are involved.

So, I. G. Chesnokova studied the state of these body systems in 75 victims for 1.5 years from the moment of injury. It was revealed that traumatic disease is a long-term disease, accompanied by pronounced pathogenetic changes in immune responses and hemostasis at all times. It was noted that during the first month such patients develop immunological insufficiency of a mixed type, later, in the lines up to 6 months - "mosaic shifts of the cellular and humoral links, which are adaptive in nature, and from 6 months to 1.5 years - immunological insufficiency predominantly T-deficient type. Changes in the hemostasis system in traumatic disease in the first 7 days are manifested mainly by stages I and II of DBC syndrome, then up to 6 months - latent coagulopathy, and then from 6 months to 1.5 years - thrombophilia syndrome, thrombocytopenia or depression of fibrinolysis. Such changes determine the nature of the course, the severity of the traumatic disease and its outcome. And the formation in its remote terms (from 6 months to 1.5 years) of clinical and laboratory immunopathological and thrombohemorrhagic symptoms and syndromes proves the need for long-term dispensary, moreover, therapeutic observation with regular consultations of an immunologist and a hematologist.

The obtained results allowed us to propose the following definition: traumatic disease is a syndrome complex of pathological and compensatory-adaptive reactions of all body systems to a severe injury, characterized by duration and staging of the course, which determines the outcome and prognosis for life and working capacity (Kotelnikov G.P., Chesnokova I.G. .).

A team of employees of the Samara State Medical University is conducting research on endocrine, metabolic and neuropsychic changes in severe mechanical injuries, and studying the characteristics of the course of traumatic disease in the elderly.

All this will allow concretizing and clarifying the doctrine of traumatic disease.

Control work on the topic:

General reactions of the body to damage

Introduction

In a person's life, situations often arise when very strong pathogenic factors act on him, causing widespread changes in most or even all physiological systems and organs. In the event of such situations in the body, various general reactions develop, which most often manifest themselves in the form of stress, shock and coma.

1. Stress

Stress- the general reaction of the body in response to the action of emergency or pathogenic stimuli, manifested by an adaptation syndrome. This syndrome is based on adaptive reactions.

Adaptive reaction- the reaction of a biological system under the influence of environmental factors or shifts within the system itself, aimed at its survival, preservation of the state and properties in the new conditions of existence.

Stages of stress. The state of stress occurs when the body is exposed to any strong stimuli: hypothermia and overheating, excessive physical activity and immobilization, trauma and drugs, poisons, hypoxia, psycho-emotional stress, etc.

The first stage of stress is characterized by the release of adrenocorticotropic hormone (ACTH) from the adrenohypophysis, which increases the flow of glucocorticoids into the blood. Stress influences activate the sympathetic-adrenal system. These changes in the nervous and endocrine systems cause an urgent mobilization of the body's adaptive forces. The first stage of stress is called the alarm response, and all the changes in metabolism and function are aimed at combating the stressor and repairing the damage that occurs.

In most cases, the body copes with the action of the stress factor, the anxiety reaction disappears, and the resulting damage is eliminated. Synthetic processes are intensified and the supply of glycogen, fats and proteins is replenished, the activity of the nervous and endocrine systems and physiological functions are normalized. The second stage of stress develops, which is called the stage of resistance (resistance of the body).

If stress continues for a long time, the compensatory-adaptive capabilities of the body are exhausted and the third stage of stress occurs - the stage of exhaustion. It is characterized by a weakening of synthetic processes in tissues, inhibition of the functions of physiological systems, a decrease in the formation of hormones of the adrenal cortex.

2. Shock

Shock- an acutely developing, life-threatening pathological process, caused by the action of a superstrong pathogenic stimulus on the body and characterized by severe disturbances in the activity of the central nervous system, blood circulation, respiration and metabolism. Shock develops with gunshot wounds, severe mechanical injuries, widespread burns, transfusion of incompatible blood, sometimes with the introduction of vaccines and sera, etc.

Stages of shock. Shock is characterized by a two-phase change in the activity of the central nervous system: the initial widespread excitation of brain structures (erectile stage) is also replaced by widespread inhibition of their activity (torpid stage). Phase changes in CNS activity are associated with excessive afferent influences of various origins: strong irritation of extero-, intero-, or proprioreceptors, damage to nerve conductors, plexuses, or even brain tissue. In shock, consciousness may be obscured, especially in the torpid stage, but it is not completely lost.

In the erectile stage, the activity of the sympathetic-adrenal and pituitary-adrenal systems increases, the work of the cardiovascular system increases - the heart rate increases, blood pressure rises, the volume of circulating blood in the kidneys, digestive tract, skin and muscles decreases, but increases in the brain and heart . The respiratory rate increases. The erectile stage is usually not long.

In the torpid stage of shock, the activity of the sympathetic-adrenal system decreases, and the level of corticosteroids in the blood falls. Blood pressure drops sharply, heart rate may decrease, deposition and a decrease in the volume of circulating blood occur. There are microcirculation disorders. An increase in the permeability of histohematic barriers leads to the appearance of toxic products in the blood, in connection with which toxemia develops.

Due to respiratory and circulatory disorders, in particular microcirculation disorders, hypoxia always occurs in shock, and the patient's condition largely depends on its severity. Hypoxia contributes to additional damage to organs, primarily the brain, heart and kidneys.

Shock is characterized by the emergence of so-called vicious circles, which play an important role in the increase in the severity of the state of shock. Disorders of the central nervous system during shock leads to respiratory and circulatory disorders. The inhibition of these vital functions causes the development of hypoxia, and the latter aggravates disorders of the central nervous system. Thus, the circle of pathological reactions closes.

During shock, some organs are damaged especially often. Such organs are called "shock organs". These include the lungs and kidneys.

Types of shock. Depending on the cause that caused the shock, there are several types of it.

Traumatic shock occurs with common injuries of bones, muscles and internal organs. In this case, damage to the nerve endings, trunks and plexuses always occurs. The course of traumatic shock is aggravated by bleeding and infection of wounds.

Burn shock develops with extensive thermal damage to the skin. The severity of shock depends primarily on the area of the affected body and the degree of burn. With burn shock, toxemia occurs very early, so the erectile stage quickly turns into a torpid one. In the later stages of the burn process, due to the appearance of altered proteins, it is possible to develop autoallergy with damage to microvessels and cells of parenchymal organs. This condition is called "burn disease".

Anaphylactic shock is the most formidable and dangerous manifestation of an immediate allergy in humans. It occurs with the introduction of therapeutic sera or vaccines, certain drugs, ingestion of a number of insects into the blood.

Anaphylactic shock develops rapidly. The erectile stage is very short, it is manifested by a feeling of fear, anxiety, motor excitement. Often there is itching of the skin and pronounced sweating. CNS function depression quickly occurs, seizures may develop. Often there is a feeling of suffocation, asphyxia develops. Allergy mediators cause a drop in blood pressure and sharply disrupt microcirculation. Disseminated intravascular coagulation occurs.

Transfusion shock is the result of a transfusion of donor blood that is incompatible with the recipient's blood in terms of group factors, the Rh factor, or individual antigens. Shock can develop if poor quality blood is used.

Transfusion shock develops rapidly. After a short erectile stage, manifested by motor excitation, increased and difficult breathing, pain in different parts of the body, especially in the kidneys, the torpid stage begins. Against the background of general weakness, immobility, blood pressure drops. Blood clotting decreases and multiple hemorrhages occur in different areas of the body and in internal organs. A characteristic of transfusion shock and often a factor that determines its course is impaired renal function.

3. Collapse

Collapse- acutely developing vascular insufficiency, characterized by a drop in vascular tone and a decrease in the mass of circulating blood. It is manifested by a sharp decrease in arterial and venous pressure, signs of cerebral hypoxia and inhibition of vital body functions. Collapse is a consequence of a primary circulatory disorder that develops when the volume of circulating blood is less than the volume of the vascular bed. Such a discrepancy occurs either as a result of a rapid drop in the volume of circulating blood (for example, with massive blood loss), or as a result of an acute drop in vascular tone and their sharp expansion (for example, when the endocrine system is disrupted).

4. Coma

stress coma shock

Coma- a state of deep depression of the functions of the central nervous system, characterized by a complete loss of consciousness, loss of reactions to external stimuli and profound disorders in the regulation of vital body functions. Coma is one of the most severe and life-threatening conditions. Coma is characterized by progressively increasing inhibition of brain activity and loss of consciousness.

Causes of coma. Coma that occurs under the influence of various pathogenic environmental factors is called exogenous coma. It can be traumatic, toxic, thermal, alimentary, radiation, infectious-toxic, hypoxic, etc. If various diseases become the cause of coma, then they talk about endogenous coma.

Coma mechanisms. In the occurrence of coma, there are several general mechanisms. The most important of them - intoxication - is associated with the action of exogenous poisons or metabolic products to be removed from the body. Another common mechanism for the development of coma, largely associated with intoxication of the body, is oxygen and energy starvation of the brain. The third, which plays an important role in the occurrence of coma, are violations of the acid-base, electrolyte and water balance of the body.

Characteristic of various coma are circulatory disorders, especially microcirculation in the brain, depression of the respiratory center and the development of pathological forms of respiration (Kussmaul, Cheyne-Stokes), which often ends in the death of the patient.

Trubitsyna L.V. The trauma process. - M., 2005. - S.67-83, 115-126, 130-144

Stages of reaction to trauma

Psychological trauma should be considered as a process, and this process should be studied in dynamics, starting from the most traumatic event (or even from the expectation of it, which in itself can be traumatic) and to the most remote consequences.

Different authors distinguish various stages and stages of the development of trauma, which sometimes seem not very compatible. So, in the USA, there are 4 phases of the dynamics of psychogenic disorders due to extreme situations: 1 - the “heroic” phase, lasting several hours, it is characterized by altruism, heroic behavior caused by the desire to help people, save themselves and survive; 2 - the "honeymoon" phase, lasting from a week to 6 months, it is characterized by a strong sense of pride among the survivors for having overcome all the dangers and survived, as well as the belief that soon all problems and difficulties will be resolved ; 3 - phase of disappointment, lasting from 2 months to 2 years, with experiences of anger, disappointment, indignation; 4 - the recovery phase, in which people begin to take responsibility for solving their problems.

It is customary for us to distinguish 5 stages of PTSD: mobilization, immobilization, aggression, depressive reactions, and the recovery process.

Horowitz, a well-known researcher on the problems of psychological trauma, distinguishes a short phase of despair, or "cries", then a phase of denial, or numbness, followed by a phase of obsession.

Many distinguish smaller stages at first after the experienced event, lasting from several hours to several days.

One of the attempts to explain the development of trauma connects it with the development of dissociation, and different stages of trauma - with different types of dissociation. “There are three distinct but interrelated patterns of dissociation: primary dissociation that occurs at the first moment a person enters a traumatic situation. Primary dissociation is characterized by disintegrative and fragmentary perception of a threat situation, which is accompanied by intense emotions of fear, horror and helplessness. Secondary or peritraumatic dissociation - further disintegration of personal experience in the face of ongoing serious threat; tertiary dissociation - the development of characteristic ego states containing traumatic experiences. A high intensity of peritraumatic dissociation is one of the most significant predictors of post-traumatic stress disorder.”

Quite different stages are distinguished when considering the development of psychological trauma after a long stay in captivity. Allocate the shock of admission, changes during a long stay, release. Or in another way: the phase of the primary reaction, the phase of adaptation, the phase of asthenia. Or on release: apathy, followed by anxiety, and then aggression and hostility. In this case, which phases and periods are singled out largely depends on the moment at which the development of the process of psychological trauma begins to be considered and at what moment it ends, as well as how detailed the different stages of the process are considered.

When considering the trauma of loss of loved ones, we practically consider the stages of grief. Although, when considering grief, there is more agreement between the authors in the allocation of stages, however, there are also more discrepancies in terms. But we will return to the question of the reaction to the death of loved ones later. It should also be taken into account that in all cases it is necessary to distinguish between the process of normal experience of psychological trauma (that is, the process of experiencing trauma and recovering from it) and the pathological process, “protracted”, “stuck”, leading to the development of various pathological conditions, chronic disorders and changes.

Depending on how long a person has been in traumatic conditions, and also on whether the trauma was associated with the loss of the closest people or not, the process of a normal reaction to trauma may take different times and include different stages. It does not take a psychologist to understand that normal grief from the loss of a loved one will last longer than a normal reaction to an accident, and after a long time in captivity, readaptation periods will be required. Therefore, we will consider the stages of trauma development in three cases: after a short-term traumatic event, after a long stay in a traumatic situation, and somewhat lower - in the case of grief after the death of loved ones.

Trauma is always accompanied by a violation of the general condition of the victim. Pain, blood loss, dysfunction of damaged organs, negative emotions, etc. contribute to the development of various pathological reactions of the body.

Fainting- sudden short-term loss of consciousness due to acute anemia of the brain. Under the influence of fright, acute pain, sometimes with a sharp change in position from horizontal to vertical, a person suddenly loses consciousness, becomes covered with cold sweat, turns pale sharply. At the same time, the pulse is slowed down, blood pressure is reduced, the pupils are constricted. Rapidly onset anemia of the brain sharply reduces the function of the motor and autonomic centers. Sometimes, before fainting, patients report dizziness, nausea, ringing in the ears, and blurred vision.

Fainting usually lasts 1-5 minutes. A longer loss of consciousness indicates more severe pathological disorders in the body.

Treatment. The patient should be laid in a horizontal position, raise his legs, unfasten the collar, belt and all parts of clothing that restrict breathing. Let the ammonia vapor inhale (to expand the vessels of the brain).

Collapse(from lat. collaborator- fall) - one of the forms of acute cardiovascular insufficiency, characterized by a sharp drop in vascular tone or a rapid decrease in the mass of circulating blood, which leads to a decrease in venous flow to the heart, a decrease in arterial and venous

pressure, hypoxia of the brain and inhibition of vital body functions. With injuries, the development of collapse is facilitated by damage to the heart, blood loss, severe intoxication, severe pain irritation.

clinical symptoms. Consciousness is preserved or darkened, the patient is indifferent to the environment, the reaction of the pupils to light is sluggish. Complaints of general weakness, dizziness, chilliness, thirst; body temperature decreases. The facial features are pointed, the extremities are cold, the skin and mucous membranes are pale with a cyanotic tinge. The body is covered with cold sweat. The pulse is small and frequent, blood pressure is lowered. Breathing is shallow and rapid. Diuresis is reduced.

Treatment. Elimination of the cause that caused the collapse, and the fight against vascular and heart failure. With blood loss, intravenous infusion of crystalloid and colloid solutions should be immediately established. With massive blood loss, transfusion of erythrocyte mass and fresh frozen plasma may be required in a ratio of 1: 3. The use of vasopressor drugs (mezaton, dopamine, adrenaline) is possible only after restoration of circulating blood volume). Prednisolone (60-90 mg), 1-2 ml of cordiamine, 1-2 ml of 10% caffeine solution, 2 ml of 10% sulfocamphocaine solution are administered intravenously. Along with infusions produce anesthesia.

TRAUMATIC SHOCK

Traumatic shock is a severe pathological process that occurs in the body as a general reaction to severe mechanical damage to tissues and organs. This process is characterized by increasing inhibition of the basic vital functions of the body due to violations of nervous regulation, hemodynamics, respiration and metabolic processes.

The serious condition of the victims is associated primarily with massive blood loss, ARF, acute disorders of the functions of damaged vital organs (brain, heart), fat embolism, etc. Shock should be expected in patients with multiple fractures of the bones of the lower extremities, pelvis , ribs, with damage to internal organs, with open fractures with extensive crushing of soft tissues, etc.

The totality of all processes (protective and pathological) that develop in the body in response to severe trauma (including shock), and all diseases that develop in the post-shock period (pneumonia, sepsis, meningoencephalitis, shock lung, pleurisy, fat embolism, thromboembolism, peritonitis, DIC -syndrome and many others), began to unite under the name "traumatic disease". However, the clinical diagnosis of "traumatic shock" for practitioners most acutely signals the critical condition of the victim, the need for emergency anti-shock assistance.

In the clinical picture of traumatic shock, hemodynamic disturbances are most clearly manifested. The main hemodynamic parameters are blood pressure, pulse rate, cardiac output (CO), circulating blood volume (CBV) and CVP. Critical Level

blood pressure - 70 mm Hg. Art., below this level, the process of irreversible changes in vital organs (in the brain, heart, kidneys, liver, lungs) begins. You can roughly determine the dangerous level of blood pressure by the pulsation of the main arteries. If it is not possible to palpate the pulsation of the radial arteries, but the pulsation of the femoral arteries is preserved, then we can assume that the arterial pressure is near a critical level. If the pulsation is determined only on the carotid arteries, then the level of blood pressure is below critical. "Threaded", periodically disappearing pulse indicates a decrease in blood pressure below 50 mm Hg. Art., which is typical for the terminal state and the development of dying processes.

A change in heart rate is an earlier sign of a circulatory disorder than blood pressure. It is generally accepted that the value obtained after subtracting the patient's age in years from 220 is considered a safe limit for increased heart rate; with more frequent contractions, there is a threat of myocardial exhaustion as a result of developing hypoxia. A pronounced increase in the frequency of heart contractions (120 beats / min or more) with a satisfactory arterial pressure indicates occult bleeding.

More precisely, the amount of blood loss can be judged by the shock index (Table 6), proposed by Algover and determined by the formula:

where SHI - shock index;

Π - pulse rate, bpm;

BP - blood pressure, mm Hg. Art.

Table 6 Relationship between blood loss, shock index and shock severity

Note. * DOCK = Μ ? K, where DOCC - proper BCC, ml; Μ - body weight, kg; K - constitutional factor, ml/kg (for obese patients K = 65 ml/kg, for asthenics K = 70 ml/kg, for athletes K = 80 ml/kg).

The amount of blood loss is also determined by the hematocrit number, the hemoglobin content in the blood and the relative density of the blood (Table 7).

Usually, with closed fractures, there is blood loss: with fractures of the bones of the lower leg - up to 0.5 l, femur - up to 1.5 l, pelvic bones - up to 3.5 l.

Clinical signs of violation of regional hemodynamics. Pale and cold to the touch skin indicates circulatory disorders in the skin and muscles. A parametric indication of these disorders is possible, determined by the time of refilling the capillaries of the skin of the patient's forearms or lips with blood after pressing on it with a finger for 5 s. This time is normally 2 s. Exceeding the specified period says

about circulatory disorders in this area. This sign is important for predicting the outcome of the injury.

Table7. Approximate determination of the amount of blood loss (according to G. A. Barashkov)

With circulatory disorders, diuresis decreases to 40 ml / h or less. Lack of blood supply to the brain affects the state of consciousness (stunning, stupor). However, this sign is rare in patients with traumatic shock due to the phenomenon of centralization of blood circulation, which ensures an adequate supply of blood to the brain until the development of a terminal state. More complete information about the state of regional blood circulation can be obtained by using the method of impedance rheography.

In the clinical picture of traumatic shock, erectile and torpid phases are distinguished.

erectile phase characterized by general arousal of the patient. The victim is restless, verbose, fussy, randomly moving. The pulse is quickened (up to 100 beats / min), blood pressure increases abruptly with a difference in maximum and minimum values up to 80-100 mm Hg. Art., breathing uneven, frequent, up to 30-40 in 1 min. The appearance of an excited patient, as a rule, does not correspond to the significant severity of his injuries.

Torpid phase traumatic shock is characterized by the inhibition of all vital functions of the body. The victim is inhibited, indifferent to the environment, to his condition, his pain sensitivity is reduced, blood pressure decreases, the pulse is frequent, of weak filling, breathing is shallow, rapid. Depending on the severity of the condition of the victim, the torpid phase of shock is conditionally divided into four degrees.

I degree: consciousness is preserved, moderate pallor of the skin and mucous membranes, blood pressure 90-100 mm Hg. Art., rhythmic pulse, satisfactory filling, 90-100 bpm, SI less than or equal to 0.8, blood loss up to 1000 ml.

II degree: consciousness is preserved, depression, lethargy are expressed, the skin and mucous membranes are pale, blood pressure is in the range of 70-90 mm Hg. Art., pulse 100-120 beats / min, weak filling, SI equal to 0.9-1.2, blood loss 1500 ml.

II degree: consciousness is preserved (if the brain is not damaged), the skin and mucous membranes are sharply pale, weakness, blood pressure is below 70 mm Hg. Art., thready pulse, 130-140 bpm, SI greater than or equal to 1.3, blood loss more than 1500 ml.

IV degree - a terminal state in which three stages are distinguished (according to V. A. Negovsky): a preagonal state, an agonal state and clinical death.

Preagonal state - consciousness is confused or absent. The skin and mucous membranes are grayish-pale ("earthy"), the body temperature is reduced, blood pressure and pulse on the peripheral arteries are not determined, the pulse on the carotid and femoral arteries is determined with difficulty, threadlike, disappearing, up to 140-150 beats per minute, but maybe less. Breathing is shallow, quite rhythmic, blood loss is more than 2000 ml.

Agonal state - consciousness is absent, weakness, breathing becomes periodic, convulsive, accompanied by general motor excitation, the intervals between breaths increase. Flashes of sharp hypoxic excitation are possible. There are general tonic convulsions, involuntary urination, defecation.

Clinical death - this is the state of the body after the disappearance of all clinical manifestations of life (cessation of blood circulation, cardiac activity, pulsation of all arteries, respiration, complete disappearance of all reflexes). This state lasts an average of 5 minutes (from the moment the pulsation of the carotid arteries ceases), however, with a long preceding preagonal state (more than 1-2 hours), the duration of clinical death may be less than 1 minute; on the contrary, with sudden cardiac arrest against the background of sufficiently high hemodynamic parameters, the duration of clinical death can increase up to 7-8 minutes, and with a decrease in brain temperature (hypothermia) - up to 10 minutes or more. During this period, it is still possible to restore the vital activity of the cells of the cerebral cortex with the resumption of blood flow. If irreversible changes occur in the cells of the cerebral cortex and they die, then we should talk about the onset of brain death. In this state, with the help of active resuscitation, it is possible to restore the activity of the heart and breathing, but it is impossible to restore the function of the cerebral cortex. Clinical signs of decortication of the brain are the maximum expansion of the pupils and their complete absence of reaction to light after the restoration of blood circulation and respiration. After the death of all structures (departments) of the CNS, biological death occurs, although the vital activity of individual organs and tissues can be temporarily restored when blood flow resumes in them, but it is no longer possible to restore the life of the organism as a whole.

Of particular severity is the course of shock in patients with fractures of the bones of the extremities in combination with fractures of the ribs, spine, and pelvis. The causes of such severe injuries are road accidents, falls from a height, landslides in mines, etc.

minor damage to several areas of the body, such as skeletal fractures, ruptures of internal organs, TBI.

Treatment. The provision of early care for injuries complicated by shock continues to be one of the main problems in medicine. In cities, this assistance is provided by specialized resuscitation teams that quickly leave for the scene.

Resuscitation should be understood not only as the restoration of the vital activity of an organism in a state of clinical death, but also all measures aimed at preventing cardiac and respiratory arrest. The main tasks of resuscitation are:

1) restoration of cardiac activity, blood circulation and creation of the most favorable conditions for the blood supply to the brain;

2) restoration of gas exchange in the lungs;

3) restoration of the BCC.

Practically at the scene, only the first tasks are feasible, and before the arrival of medical workers, only the people around the victim will be able to provide real assistance. Therefore, not only doctors and paramedical workers, but also all people should master simple methods of restoring cardiac activity and respiration.

The main methods of resuscitation are indirect (external) heart massage and mechanical ventilation by blowing air through the mouth or nose of the victim (Fig. 49).

Technique of indirect heart massage. The principle of indirect massage is the periodic compression of the heart between the sternum and the spine, while at the time of compression, blood is pushed out of the heart cavities into the aorta and pulmonary arteries, and after the compression stops, it enters the heart cavities from the venous vessels. An absolute indication for the beginning of indirect massage is the cessation of the pulsation of the carotid arteries. The victim is quickly placed on a rigid base (or a shield is placed under the back) and the sternum is jerkily shifted to the spine at a frequency of 80-120 times per minute. Pressure is exercised with both hands, while the base of the right palm is placed on the lower third of the sternum, and the left palm rests on the right hand from above. If the heart massage is carried out effectively, then a distinct pulsation appears on the carotid arteries, the pupils narrow, the lips turn pink, blood pressure rises to 60-80 mm Hg. Art. In children, massage should be done with only one hand, and in newborns - only with your fingers. In this case, complications are possible: fractures of the ribs, sternum, damage to the heart, liver, spleen and other organs.

Artificial lung ventilation technique. It should be noted that squeezing the chest during heart massage restores to some extent the ventilation of the lungs, and thus the gas exchange in them. However, for proper ventilation, it is necessary to blow air into the lungs of the victim through the mouth or nose. It is first necessary to check the patency of the upper respiratory tract: insert a finger into the victim's mouth to determine the presence or absence of foreign bodies (teeth, prostheses, etc.), extend the tongue, extend the lower

Rice. 49. Resuscitation in case of clinical death: a - closed heart massage; b - artificial lung ventilation

put a cushion under the victim’s lower jaw so that the head is thrown back and the neck is arched (if there are no symptoms of a fracture of the cervical vertebrae!). If it is possible to apply the "mouth-to-mouth" method, then after closing the patient's nasal passages, the resuscitator takes a deep breath and blows air into the victim's mouth with force until the chest rises, then quickly moves away and takes a deep breath, the victim at this time makes a passive exhalation. The first 5-10 breaths must be done quickly (to eliminate life-threatening hypoxia), then at a rate of 12-20 breaths per minute until spontaneous breathing occurs. If the victim develops bloating, then it is necessary to gently press the area of \u200b\u200bthe stomach with your hand, without stopping the blows. If the victim has damage to the jaws or a severe spasm of the chewing muscles occurs, then blowing is carried out through the nose.

For mechanical ventilation, it is advisable to use an S-shaped air duct and a portable manual respirator.

The fight against blood loss must begin at the scene by temporarily stopping the bleeding.

If resuscitation is carried out in a medical institution, then additional medication and cardiac defibrillation can be used. When erratic contractions of myocardial fibers occur,

yes, as seen on the ECG, defibrillation is shown. The electrodes are pre-wrapped with gauze napkins moistened with isotonic sodium chloride solution, one is placed under the back at the level of the left shoulder blade, the other is pressed tightly against the anterior surface of the chest to the left of the sternum, current is applied to the electrodes (discharge energy 360 J), 1 mg 0 is injected intravenously, 1% solution of adrenaline, with asystole - atropine.

After removing the victim from the state of clinical death, it is necessary to carry out intensive therapy within 2-3 days: to carry out mechanical ventilation (with automatic respirators) according to indications, correction of metabolic acidosis (administration of large doses of corticosteroids, ascorbic acid, concentrated protein solutions), correction of water and electrolyte balance, protein-carbohydrate metabolism and prevention of infectious complications.

If active resuscitation for 30-40 minutes is ineffective (cardiac activity and spontaneous breathing are not restored, the pupils remain as dilated as possible without any reaction to light), then resuscitation should be stopped and the onset of biological death should be ascertained. 10-15 minutes after the onset of biological death, the "cat's eye" phenomenon is observed, which consists in the fact that when the eyeball is squeezed, the pupil acquires an oval shape (in a living person, the shape of the pupil does not change).

Carrying out resuscitation is impractical: in case of severe head injury with severe deformation of the skull; crushed chest with signs of damage to the internal organs of the abdomen and massive blood loss; severe combined injuries of three or more areas of the body (for example, avulsion of both hips in combination with intra-abdominal bleeding and severe TBI).

All measures to remove victims from shock can be divided into four groups: the fight against hypovolemia; fight against ODN; the fight against pain and the fight against metabolic disorders.

Hypovolemia is the basis of traumatological shock. It occurs due to blood loss, plasma loss (with burns), violation of the rheological properties of blood (catecholaminemia). Effective replenishment of blood loss is possible only after bleeding has stopped, therefore, victims with intracavitary bleeding need an emergency operation for health reasons, regardless of the severity of the general condition.

The basis for the treatment of acute massive blood loss is infusion-transfusion therapy. A prerequisite for its implementation is adequate and reliable access to the vessel. According to modern standards, it is provided by catheterization of vessels with various plastic catheters.

The qualitative and quantitative composition of transfused media is determined by the amount of blood loss. To quickly restore intravascular volume and improve the rheological properties of blood, heterogeneous colloidal solutions are most effective: dextran (polyglucin, rheopolyglucin) and hydroxyethyl starch (voluven, venofundin, hemohes, HAES-steril). Crystalloid solutions (Ringer's solution, Ringer's lactate, lactasol, quatrasol, etc.) are necessary to correct the interstitial volume. Fast Boost

low-volume infusion of a hypertonic-hyperoncotic solution (7.5% sodium chloride solution in combination with a dextran solution) is capable of improving systemic arterial pressure and improving microcirculation. The rate of infusion of plasma-substituting and electrolyte solutions is determined by the patient's condition. The more severe the shock, the higher the volumetric infusion rate should be, up to the injection of infusion solutions into 1-2 veins under pressure. Red blood cell transfusion is indicated only in the case of an established deficiency of oxygen carriers, provided that it is adequately delivered. An indication for erythrocyte transfusion in acute anemia due to massive blood loss is the loss of 25-30% of the BCC, accompanied by a decrease in hemoglobin below 70-80 g / l, a hematocrit below 0.25 and the occurrence of hemodynamic disorders. The ratio of volumes of transfused fresh frozen plasma and erythrocytes is 3:1.

For liquidation ODN use oxygen inhalation, carry out mechanical ventilation with the help of automatic respirators, introduce respiratory analeptics.

Ensuring good airway patency is a necessary condition for normalization of lung ventilation and prevention of post-traumatic pulmonary complications. The trachea and bronchi, the cavity of the nasopharynx and mouth are cleaned by regular suction of pathological contents through sterile catheters or probes. The effectiveness of the procedure is ensured by a sufficient vacuum in the system (at least 30 mm Hg) and a wide catheter lumen (at least 3 mm). The duration of suction should not exceed 10-15 s, since during this period the ventilation of the lungs deteriorates sharply. The indication for the transfer of the victim to a ventilator is the extreme degree of ARF. The half-sitting position, insufflation of humidified oxygen through nasal catheters, prevention of retraction of the tongue, etc. improve respiratory function.

The indications for the imposition of a tracheostomy are severe injuries of the facial skeleton, larynx, trachea, cervical spine, prolonged unconsciousness of the victim with severe head injury, the need for many days to carry out mechanical ventilation (Fig. 50).

Fighting pain is one of the important anti-shock measures. At the scene, analgesics (promedol, morphine) are administered, blockades (Fig. 51) of fracture sites with 0.5% novocaine solution (40-80 ml), case (100 ml of 0.5% novocaine solution), conduction (20-30 ml of 1% solution of novocaine), a cross-section above the applied tourniquet (200-300 ml of 0.25% solution of novocaine), vagosympathetic (40-60 ml of 0.5% solution of novocaine), intrapelvic (200 ml of 0.25% solution of novocaine) , give a mask surface anesthesia with nitrous oxide mixed with oxygen (1: 1).

Mandatory measures to combat the pain factor are careful immobilization of injured limbs and gentle transportation of the victim. The use of narcotic analgesics is contraindicated in case of head injury, signs of damage to the internal organs of the abdomen, with damage to the cervical spine, in a terminal state, with severe injuries of the chest. In a specialized antishock

Rice. 50. Types of tracheotomy: a - thyrotomy; b - conicotomy; c - cricotomy; d - upper tracheotomy; e - lower tracheotomy

In the department, antipsychotics, ganglion blockers, neuroleptanalgesia, and endotracheal anesthesia can be used to combat shock.

When conducting anti-shock treatment, constant monitoring of the dynamics of biochemical changes in the blood and urine, the excretory function of the kidneys, the body's temperature reactions, and the function of the gastrointestinal tract is necessary.

Rice. 51. Novocaine blockades: a - fracture sites; b - case blockade; c - blockade of the cross section; d - cervical vagosympathetic blockade according to A.V. Vishnevsky; e - blockade of the pelvis according to Shkolnikov-Selivanov (1-3 - change in the position of the needle when advancing it

inside the pelvis)

LONG-TERM CRUSHING SYNDROME

Long-term crushing syndrome (SDR) is observed in people who find themselves for a long time littered with the rubble of buildings, rock in mines, earth during blasting. The general condition of the liberated does not inspire much alarm, but after a short time they suddenly die with phenomena close to shock.

Limb compression syndrome can develop as a result of improper application of a plaster cast.

Clinical picture SDR manifests itself in the form of local and general disorders. The skin of the parts of the limbs subjected to compression may initially be unchanged, but after 3-4 hours their soft tissues noticeably swell, after 12 hours the swelling reaches a maximum. By this time, the limb becomes cold, its skin is purple-cyanotic, blisters appear, filled with serous or hemorrhagic fluid. Trophic disorders increase in muscles, vessels and nerves, the pulsation of peripheral vessels weakens and

disappears, the conduction of the nerves is sharply disturbed, and at the same time the function of the limbs is impaired. The patient complains of severe pain. Blood pressure decreases, the pulse becomes weak and frequent. Acute renal failure (ΟΠΗ) develops, in the pathogenesis of which many factors are involved: damage to the epithelium of the distal tubules of the kidneys by protein breakdown products and inorganic substances; blockade of tubules by myoglobin, which precipitates; spasm of blood vessels; reflex effect of pain.

The absence of pulsation of the peripheral arteries indicates the blockade of the main vessels. Already the first portions of urine have a dark brown color (myo- and hemoglobinuria), the content of protein (60-120 g/l), cylinders, desquamated epithelium and hematin crystals is increased. In the blood, the hematocrit number, the content of hemoglobin, erythrocytes, residual nitrogen, urea, creatinine, potassium, and phosphorus are increased. The development of acute liver failure is evidenced by an increase in the blood content of bilirubin, enzyme activity (alkaline phosphatase, creatine phosphokinase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase).

According to the clinical picture, several forms of SDR are distinguished:

1) very severe - observed with extensive crushing for more than 6-8 hours of both lower limbs (the victim dies in the first two days);

2) severe - with crushing of one lower limb (characterized by a severe course and high mortality);

3) moderate severity - observed after a short-term (less than 6 hours) crushing of a relatively small part of the limb (with this form, the phenomena of renal failure are clearly expressed);

4) mild - with a predominance of local changes and mild disorders of hemodynamics and kidney function.

In the clinical course of SDR, three periods are distinguished: early (lasting 2-3 days), intermediate (from the 3rd to the 12th day) and late.

AT early period the focus should be on the treatment of acute cardiovascular insufficiency and the prevention of disorders of kidney function; it is also characterized by mental disorders, pain reaction, intense plasma loss, respiratory failure.

AT interim period the main attention is paid to the treatment of ΟΠΗ.

AT late period after normalization of hemodynamics and kidney function, the main task of treatment is the healing of extensive wounds after tissue necrosis, the elimination of contractures and neurological disorders.

In the early period, the clinical condition of the victim has much in common with traumatic shock. Therefore, therapeutic measures should be aimed at normalizing hemodynamics, respiratory function, excretory system, etc.

First aid is provided at the scene. Before release from compression or immediately after it, a tourniquet is applied to the limb proximal to the injured tissues. The entire limb is tightly bandaged, immobilized and, if possible, cooled. The victim is parenterally administered analgesic

tics, sedatives, cardiac drugs. Prompt hospitalization is indicated.

Treatment. As early as possible, the victim must be blocked with novocaine of the cross section of the limb proximal to the compression boundary (if a tourniquet is applied, then above it, after which the tourniquet is removed). Make a bilateral perirenal novocaine blockade. To combat swelling, the limb is tightly bandaged with an elastic bandage and cooled. If the edema increases, then it is necessary to perform a subcutaneous or open fasciotomy along the entire limb. With the manifestation of signs of non-viability of the crushed part, emergency amputation of the limb is indicated. At the same time, massive antibiotic therapy is carried out, tetanus prophylaxis, analgesics (promedol, omnopon), antihistamines (diphenhydramine, diprazine, suprastin), osmodiuretics (mannitol, urea, lasix) are administered. To improve the excretory function of the kidneys and compensate for plasma loss, low molecular weight colloidal and saline solutions, plasma and protein preparations are injected intravenously. For the prevention and control of acidosis, a solution of sodium bicarbonate is administered intravenously, an abundant drink of alkaline solutions and high enemas with a solution of baking soda are prescribed. If oliguria progressively increases, anuria develops, then it is necessary to carry out hemodialysis using the "artificial kidney" apparatus. Less effective peritoneal dialysis. In the recovery period, infectious complications are prevented, physiotherapy procedures, general strengthening treatment are carried out.

Lethality does not exceed 30%. In the acute period, victims die from shock (5%), later - from acute renal failure (85%), pulmonary complications (13%) and other causes. With a favorable course, kidney function is restored 5-38 days after injury. In 70% of those who have recovered, disability occurs, mainly after limb amputations or due to extensive muscle atrophy, paralysis.

POSITIONAL PRESSURE SYNDROME

Positional compression syndrome is a type of SDR. Its main difference is the absence of initial damage to soft tissues by heavy and crushing violence. Positional compression occurs when the victim is unconscious and is associated with an uncomfortable posture in which the limbs are either pressed down by the body, or bent over a solid object, or hang down under the influence of their own gravity. Deep alcohol intoxication or unconsciousness caused by other reasons sometimes forces one to be in an uncomfortable position for 10-12 hours. As a result, severe ischemic disorders occur in the extremities, leading to tissue necrosis and toxic effects due to the absorption of their autolysis products.

In a state of alcoholic intoxication, the truck driver slept in the cab in an uncomfortable position for 10 hours, as a result of which severe violations developed in the right

shins. The leg was amputated. For the same reason, another patient slept on his haunches for 8 hours. As a result, severe ischemic disorders developed in the lower extremities. A 55-year-old woman who suffered from alcoholism slept for 12 hours on a short chest with both legs hanging down. The result is severe distress. Died on the 4th day.

The outcome of the pathological process depends on the duration of compression, early correct diagnosis and rational treatment. Patients died in whom the diagnosis during their lifetime was not made at all or was recognized with a great delay. Often in patients after positional compression, irreversible neurological disorders remain.

clinical picture. Waking up and recovering, patients note significant pain and a sharp violation of the functions of the affected limb. Weakness, headache aggravate the general condition. Local disorders are expressed in pallor and coldness of the diseased limb, decreased skin sensitivity, severe limitation of functions, lethargy, weakening or complete absence of pulsation of the arteries. Body temperature is normal or slightly elevated, blood pressure is not changed.

If the patient was admitted several hours after the onset of the disease, then an increasing edema appears on the limb, the skin becomes purple. In the correct recognition of suffering, anamnesis plays a huge role. Meanwhile, patients are reluctant to report severe intoxication, talk about trauma or an unknown cause. Most often, doctors diagnose "thrombophlebitis", and in some advanced cases - "anaerobic infection", in connection with which they make wide incisions. Increasing woody edema, pronounced neurovascular disorders are aggravated by severe impairment of kidney function. The daily amount of urine decreases sharply until the development of anuria.

Principles of treatment. The main therapeutic measures for positional compression should be aimed at normalizing the functioning of the cardiovascular system and kidneys. The introduction of analgesics, antihistamines, osmodiuretics is shown. To prevent edema, the limb is tightly bandaged with an elastic bandage and cooled. In severe edema, a fasciotomy with a small skin incision is indicated. The infusion of fluids is controlled by the excretory function of the kidneys. In severe cases of the process, hemosorption and hemodialysis are used using the "artificial kidney" apparatus in specialized departments.

TRAUMATIC ASPHYXIA

Causes: general compression of the chest in catastrophes with a large number of victims.

Signs. The upper half of the body becomes purple, blue-violet, purple-blue and even black in color, small hemorrhages appear on the skin and mucous membranes of the mouth, tongue, especially noticeable on the conjunctiva. Exophthalmos and significantly pronounced swelling of the soft tissues of the face are noted. There may be bleeding from the ears, nose, mouth.

Death occurs from prolonged compression of the chest with impaired external respiration and severe congestion in the system of the superior vena cava.

First aid. Rapid transportation of the victim to the intensive care unit in a half-sitting position on a stretcher with a soft mattress and pillows; restoration of patency of the upper respiratory tract by suction or insertion into the mouth of a finger wrapped in gauze; elimination of retraction of the tongue (with a concomitant fracture of the lower jaw); the introduction of painkillers and cardiotonic drugs. With a considerable distance to the hospital, the most sparing and fastest transport is air ambulance.

Treatment. In the hospital, therapeutic measures are primarily aimed at improving breathing and blood circulation. Tension pneumothorax is eliminated, blood that has poured into the pleural cavity is removed, blood loss is replenished (blood transfusion and plasma-substituting solutions). To improve breathing, it is necessary to restore the shape and frame of the chest and achieve good anesthesia.

ELECTRIC INJURY

The widespread use of electricity in everyday life, in industry and in transport leads to an increase in the number of accidents caused by this physical factor. Electrical injuries account for 2-2.5% of the total number of industrial injuries. Sometimes the cause of electrical injury is the defeat of atmospheric electricity - lightning.

Electrical injury is a severe injury, often fatal, so the treatment of this injury is of great practical importance. The most common cause is the contact of the body with bare wires, contacts. The main factors that determine the severity of electrical injury are the strength, voltage and duration of the electric current, the type of tissues through which the electric current passes, the general resistance of the body, and individual characteristics. Of particular importance is the condition of the skin in places of direct contact with conductors of electric current. Dry and dense skin has a high resistance, thin and damp skin has a small resistance. Of the tissues of the body, the skin has the greatest resistance, the fascia, tendons, bones, nerves, muscles have the least resistance, and the blood has the smallest. Electric current in tissues with high electrical resistance causes a burn, in tissues with low electrical resistance, mechanical and chemical changes. Characteristic local changes in the form of current signs are located at the points of its entry and exit. With significant destruction in the tissues, through tunnels and multiple foci of necrosis are formed. Early tissue changes occur immediately or within 2-3 hours, late - after a few days or even months.

With a large current strength, death can occur in the next 2-3 minutes. Its causes are paralysis of the central nervous system centers, spasm of the coronary arteries

heart, ventricular fibrillation, spasm of the glottis, convulsive contractions of the muscles of the chest. An alternating current with a frequency of 50 Hz is the most dangerous, as it causes fibrillation of the ventricles of the heart; a current with a frequency of 200 Hz is most dangerous for breathing. In the long term, the causes of death are shock, coma, electrical burns, acute heart failure (pulmonary edema), severe vascular damage.

Death from respiratory arrest. Tetanic contraction of the respiratory muscles occurs when current passes along the body. At the moment of closing the current, a strong exhalation occurs. Death occurs when a current is applied for more than 1 minute. With a high current, death occurs immediately from paralysis of the respiratory center.

Death from cardiac arrest occurs when current passes through the heart. Tachyor bradycardia, blockade of atrioventricular conduction, blockade of the legs of the His bundle, extrasystoles, paroxysmal tachycardia, ventricular fibrillation are observed. Cardiac arrest is possible when exposed to current in the "vulnerable" phase of the cardiocycle, on the ECG - in the region of the top of the tooth T. Cardiac arrest can also occur from irritation of the vagus nerve. Ischemic myocardial disorders always occur.

Histological examination of tissues and internal organs reveals changes in the structure of nerve cells (tigrolysis, swelling of processes), rupture of muscle fibers, muscle necrosis, changes in the walls of blood vessels, edema, hemorrhages in the myocardium and tissues of internal organs.

Clinical signs. Darkening of consciousness with pronounced motor excitation. retrograde amnesia. Headache, weakness, irritability, photophobia, fear. The disappearance of normal and the appearance of pathological reflexes. The pulse is slow, tense, heart sounds are muffled, arrhythmia. Severe ECG and EEG changes

Features of the clinical picture: a pronounced discrepancy between relatively good health and significant deviations from the norm of objective data. Severe lesions are characterized by pulmonary edema, acute liver failure, enteritis. With mild damage, increased fatigue, weakness, depressed mood, decreased memory, hearing, vision, and sense of smell are noted.

First aid. Immediate assistance at the scene is crucial.

1. It is necessary to release the victim from the action of electric current. At the same time, it is necessary to observe strict personal safety measures: have good insulation from the ground (rubber boots, rubber mat, wooden shield, board), do not touch the victim with bare hands, remove the current conductor from him with a dry wooden stick, pull the victim out of the affected area by clothes, remember that within a radius of 10 m around the fallen wire, the earth is energized, so it is necessary to approach the victim in small steps to avoid the effects of the so-called step voltage.

2. In the absence of breathing, ventilation is immediately started.

3. In the absence of cardiac activity, a closed heart massage is started (for the full restoration of cardiac activity, as a rule, defibrillation is necessary).

4. When the patient is excited, Seduxen (Relanium) is administered - 10-20 mg. Injections of agents that excite the respiratory center are shown: lobeline (1 ml of a 1% solution), bemegride (10 ml of a 0.5% solution), etimizole (5 ml of a 1.5% solution). The introduction of strophanthin (1 ml of a 0.05% solution) is shown.

5. In case of electric burns, aseptic dressings are applied.

6. Transportation in the supine position to the intensive care unit (at burn or therapeutic clinics).

Principles of hospital treatment. The nature of the treatment is determined by the severity of the condition. Resuscitation continues: mechanical ventilation, heart massage, defibrillation, etc. After the restoration of cardiac activity and respiration, the patient is constantly monitored, since acute cardiovascular failure can develop again after a few hours or even days. You need to repeat the ECG. Complications: lability of the cardiovascular system, nervous disorders, mental disorders, general weakness, apathy, headache, etc.

Local treatment electrical burns is different from the treatment of thermal burns. This is due to deep tissue damage and the need for early surgical interventions, which include necrectomy, ligation of blood vessels, amputation and exarticulation of limbs, restoration of the skin in various ways, and opening of purulent streaks.

Prevention electrical burns and electrical injuries consists in observing the safety rules for the operation of electrical installations in everyday life and at work, maintaining sanitary and hygienic order and constant vigilance of adults in relation to children, who are more often victims of electric shock in everyday life.

DROWNING

Resuscitation of the drowned occupies a significant place in the practice of resuscitation service. Every year, thousands of people die from drowning, mostly young people. The results of resuscitation largely depend on the timeliness of pathogenetic treatment.

There are four main types of death in water:

1) primary, true, or "wet", drowning;

2) asphyxic or "dry" drowning;

3) secondary drowning;

4) death in water.

For true drowning characterized by the penetration of fluid into the lungs. True drowning accounts for 75-95% of all water accidents.

Asphyxial drowning occurs without aspiration of water, as a result of laryngospasm due to fluid irritation of the upper respiratory tract.

Most often it occurs in children and women, observed in 5-20% of all drowned. This type of resuscitation gives the best results.

In primary cardiac and respiratory arrest ("syncope drowning") the skin is pale ("marble"), there is a picture of acute myocardial ischemia - a reflex reaction to the aspiration of water.

Loss of consciousness associated with trauma, an epileptic attack, etc., leads to secondary drowning, if the victim is in the water. In some cases, even in good swimmers, prolonged exposure to water causes a sharp decrease in oxygen tension in the blood and an increase in carbon dioxide tension, which leads to loss of consciousness and drowning. Water shock ("ice shock", sinking syndrome) associated with a sharp temperature drop, leading to overstimulation of thermoreceptors, vasospasm, cerebral ischemia, reflex cardiac arrest.

Contribute to drowning overfatigue, full stomach, alcohol intoxication, hypothermia, especially in water temperatures below 20 ° C. At a water temperature of 4 ... 6 ° C, a person cannot make active movements after 15 minutes due to rigor mortis. Cooling the body down to 20...25 °C leads to darkening of consciousness, death occurs within an hour even in physically strong people.

Changes in the lungs. With true drowning, the volume of the lungs increases due to the retention of water in them, spasm of the bronchioles, and the formation of foam. In fresh water, the swelling of the lungs is more pronounced, but there is less fluid in the alveoli than when drowning in salt water. Often at the same time there is obturation of the bronchi with solid particles. Pulmonary edema is more pronounced and occurs immediately when drowning in salt water due to the release of the liquid part of the blood into the alveoli. Fresh water causes the destruction of the surface layer of the alveoli, which provides their surface tension, which leads to edema in the later stages. This is also facilitated by stagnation of blood in the pulmonary circulation, the development of heart failure.

Violation of the function of the cardiovascular system. During the first minute of immersion in water, blood pressure rises by 1.5-2 times, then it decreases. CVP rises, arrhythmia, extrasystole, ventricular fibrillation occur. With true drowning, the right ventricle expands, with asphyxia - the left one. Asphyxia and acidosis lead to excitation of the sympathoadrenal system, resulting in an increase in the content of catecholamines in the blood.

Death from drowning can occur during the aspiration of water, immediately after removing the victim from the water, in the early and late post-resuscitation period (from complications).

The main role is played by hypoxia, a violation of the acid-base state, a smaller one - changes in the electrolyte composition of the blood, respiratory and cardiovascular disorders associated with these changes.

When drowning in fresh water, after 2 minutes, 50% of the aspirated fluid passes into the blood. This leads to hemodilution and hemolysis, a decrease in the concentration of electrolytes, plasma proteins. In the initial period after the transfer

hay drowning, gas exchange in the lungs is sharply disturbed due to the presence of different sizes of zones (areas of the lung) with impaired microcirculation. The saturation of arterial blood with oxygen decreases, the collapse of the alveoli, the edema of the lung tissue, and the decrease in lung perfusion (up to 2 days) persist. There is a constant risk of developing pulmonary edema. Hyperkalemia causes disruption of the heart.

When drowning in sea water, the opposite occurs - the liquid part of the blood passes into the alveoli, and the electrolytes into the blood. BCC decreases, hematocrit increases. After equalizing the concentration of salts, osmotic pressure, the liquid begins to be absorbed back into the vascular bed. The tension of oxygen in the arterial blood decreases, acidosis increases, edema of the lung tissue and atelectasis of the lungs develop, microcirculation is disturbed. Aspiration of sea water is more dangerous than fresh water.

First aid

1. It is necessary to overcome fear, to correctly navigate the situation, to find the best option for saving the victim.

2. When removing the victim from the surface of the water, his condition is due to mental trauma and hypothermia. His consciousness may be preserved or confused, excitation and depression may prevail, the skin is pale, cyanosis of the mucous membranes, "goose bumps", shortness of breath, tachycardia, blood pressure - within normal limits. Tranquilizers (trioxazin, elenium, seduxen), sedatives (bromides, valerian tincture, valocordin), hot drinks, rubbing, massage, warming, oxygen inhalation are effective.

3. When removing the victim from under the water, he may be in an unconscious state, a state of agony and clinical death. It can be saved only with the help of emergency resuscitation measures:

a) quickly clean the oral cavity and pharynx from water, foreign bodies, mucus;

b) at the same time, they begin to carry out mechanical ventilation by blowing air through the mouth or nose and remove water from the lungs and stomach by quickly turning the victim on his side and stomach and pressing (in between air blows) on the lower half of the chest and epigastric region;

c) in the absence of a pulse on the carotid arteries, a closed heart massage is performed;

d) after the victim is removed from the state of clinical death, he is warmed up, the limbs are massaged.

Shown: oxygen therapy, the introduction of sedatives and antihypoxants (seduxen, sodium oxybutyrate), analeptics (cordiamin, caffeine, camphor), for bradycardia and hypotension - atropine, blood substitutes (rheopolyglucin).

Victims on the water are hospitalized in a therapeutic hospital, where they are observed for at least 2 days and prevent possible complications (pneumonia, pulmonary edema, renal failure).

REPARATIVE BONE REGENERATION

Damage to bone tissue leads to complex general and local changes in the body. The adaptive and compensatory systems of the body are the first to be activated due to neurohumoral mechanisms, which eliminate changes in homeostasis and restore damaged areas of the bone. Local changes in the fracture zone contribute to the evacuation of protein breakdown products and other substances from the injury area, tissue differentiation and bone cell protein biosynthesis.

The general reaction of the body during bone fractures occurs along with local changes and is called the fracture syndrome. It is characterized by two phases: catabolic, when decay processes dominate, and anabolic, when catabolic processes decrease and synthesis processes dominate.

This general reaction of the body depends on the severity of the damage, the age of the patient, the reactivity of the body, concomitant diseases, etc.

Bone tissue regeneration can be physiological and reparative. Physiological regeneration is expressed in bone renewal, during which, throughout the life of the organism, partial or complete resorption and the formation of new structural bone formations occur. It is aimed at restoring the anatomical structure of the bone and adapting it to the appropriate function.

Reparative regeneration occurs due to the proliferation of cells of the cambial layer of the periosteum, endosteum, poorly differentiated cells of the bone marrow stroma, due to metaplasia of poorly differentiated mesenchymal adventitia cells of ingrowing vessels.

In 1988, G. A. Ilizarov registered the discovery of a general biological pattern, according to which, with dosed stretching of bone and soft tissue structures, regeneration processes are initiated in them, while energy metabolism, proliferative and biosynthetic activity of cells increases.

There is an active growth of bones, muscles, fascia, tendons, skin, nerves, blood and lymphatic vessels. On the basis of this discovery, numerous techniques have been developed to replace bone and soft tissue defects, restore the length of limb segments, lengthen limbs, and eliminate any skeletal deformities.

There are three theories about the sources of osteogenesis. The first - neoplastic - is based on the strict specificity and sequence of bone formation from the cambial layer of the bone; according to the second - metaplastic - sources of osteoblasts and osteocytes are undifferentiated mesenchymal progenitor cells, and preosteoclasts and osteoclasts are progenitor cells of the hematopoietic series. The third theory combines the first two. It should be borne in mind that in the process of bone tissue regeneration, an important role is played by the rate of restoration of microcirculation and blood supply to the regenerate by increasing oxygenation and the influx of substances necessary for the vital activity of cells. Since the speed of the

the formation of the regenerate in different parts of the damaged bone is uncertain, conditionally, the entire cycle of bone tissue restoration is usually divided into four stages.

First stage. Catabolism of tissue structures with necrosis and necrobiosis of cells, followed by differentiation and proliferation of specialized cellular structures.

Second stage. Formation and differentiation of tissue structures that form the basis of bone regenerate. At this stage, osteoid tissue is formed. If the regeneration conditions are less favorable, then chondroid tissue is formed, which is gradually replaced by bone tissue.

During the period of calcification of bone tissue, chondroid and fibroblastic structures gradually resolve.

Third stage. The formation of a bone structure, when the blood supply is restored and the protein base of the regenerate is mineralized with the restoration of bone beams and osteon channels.

Fourth stage. Restructuring of the primary bone regenerate and bone restoration. At this time, the periosteum, the cortical layer and the medullary cavity are determined.

This is the way of natural bone regeneration with the gradual restoration of its anatomical form and function.

There are the following types of callus at the fracture site: periosteal callus formed due to the periosteum; endosteal callus, formed from the endosteum of the tubular bone; an intermediate callus that fills the junction of the compact layer of the bone itself at the fracture site, and, finally, the paraossal callus, which forms in the form of a bridge passing from one bone fragment to another over the fracture site (Fig. 52).

The biological process of bone tissue regeneration is the same, but physiologically the calluses are different.

Thus, the process of bone regeneration in periosteal and endosteal callus includes a cartilaginous stage, which then passes into a bone one, and an intermediary callus is characteristic of bone formation without a preliminary cartilaginous stage. In the latter case, the union of the fracture occurs at an earlier time.

Rice. 52. Components of callus: 1 - periosteal; 2 - endosteal; 3 - intermediate; 4 - paraossal

Comparing the process of consolidation with the healing of soft tissue wounds by primary and secondary intention, the union of bone fragments is usually defined as primary (intermediary callus) and secondary (periosteal and endosteal calluses).

The union of a spongy bone fracture proceeds somewhat differently: it is connected not with the cortical layer, but with bone beams in the endosteal zone of the fracture. At the same time, a large mechanical pro-

The integrity of the callus is achieved by bringing the fragments as close as possible, in particular with impacted fractures. In this case, callus formation takes place without a cartilaginous phase; periosteal callus is not expressed in these fractures.

In conclusion, it should be noted that atraumatic and accurate reposition of fragments, stability of their fixation with observance of the terms of immobilization play a significant role in the reparative regeneration of bone tissue.

Failure to comply with these principles can lead to various complications in the form of delayed fracture consolidation or the development of a false joint.

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Fainting usually lasts 1-5 minutes. A longer loss of consciousness indicates more severe pathological disorders in the body.

Treatment. The patient should be laid in a horizontal position, raise his legs, unfasten the collar, belt and all parts of clothing that restrict breathing. Let the ammonia vapor inhale (to expand the vessels of the brain).

Collapse(from lat. collabor - fall) is one of the forms of acute cardiovascular insufficiency, characterized by a sharp drop in vascular tone or a rapid decrease in the mass of circulating blood, which leads to a decrease in venous flow to the heart, a decrease in arterial and venous pressure, cerebral hypoxia and inhibition of vital body functions. With injuries, the development of collapse is facilitated by damage to the heart, blood loss, severe intoxication, severe pain irritation.

clinical symptoms. Consciousness is preserved or darkened, the patient is indifferent to the environment, the reaction of the pupils to light is sluggish. Complaints of general weakness, dizziness, chilliness, thirst; body temperature decreases. The facial features are pointed, the extremities are cold, the skin and mucous membranes are pale with a cyanotic tinge. The body is covered with cold sweat. The pulse is small and frequent, blood pressure is lowered. Breathing is shallow and rapid. Diuresis is reduced.

Treatment. Elimination of the cause that caused the collapse, and the fight against vascular and heart failure. With blood loss, intravenous infusion of crystalloid and colloid solutions should be immediately established. With massive blood loss, transfusion of red blood cells and fresh frozen plasma in a ratio of 1:3 may be required. The use of vasopressor drugs (mezaton, dopamine, adrenaline) is possible only after the restoration of circulating blood volume). Prednisolone (60-90 mg), 1-2 ml of cordiamine, 1-2 ml of 10% caffeine solution, 2 ml of 10% sulfocamphocaine solution are administered intravenously. Along with infusions produce anesthesia.

General and local reaction of the body to injury. Stages of response to injury According to the nature of bone damage, fractures are divided into

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