Traumatic shock. Types, pathogenesis, clinic, treatment. The role of Soviet and domestic scientists in the development of shock issues. Scientific electronic library Traumatic shock pathogenesis and treatment

Traumatic shock – the body’s response to severe mechanical injury, accompanied by disruption of all functions in the body.

Epidemiology.

The frequency of traumatic shock in the wounded in modern combat conditions increases, reaching 25%. Shock with multiple and combined injuries occurs in 11-86% of victims, which on average accounts for 25-30% of all accidents. Etiology. The most common causes of traumatic shock: - damage to the pelvis, chest, lower extremities; — damage to internal organs; - open injuries with extensive crushing of soft tissues when limbs are torn off. Shock can occur with a varied combination of injuries and even with multiple severe bruises of the body.

Pathogenesis.

As a result of a severe wound or trauma, the wounded person develops one or several (in case of multiple or combined injuries) foci of tissue or organ damage. In this case, vessels of various sizes are damaged - bleeding occurs , irritation of a large receptor field occurs - a massive afferent effect on the central nervous system occurs, a more or less extensive volume of tissue is damaged, their decay products are absorbed into the blood - endotoxicosis occurs.

When vital organs are damaged, the corresponding vital functions are disrupted: damage to the heart is accompanied by a decrease in the contractile function of the myocardium; lung damage - decreased volume of pulmonary ventilation; damage to the pharynx, larynx, trachea - asphyxia.

As a result of the action of these pathogenetic factors on the extensive afferent receptor apparatus and directly on organs and tissues, a nonspecific adaptation program for protecting the body is launched. The consequence of this is the release of adaptation hormones into the blood: actg, cortisol, adrenaline, norepinephrine.

A generalized spasm of capacitive vessels (veins) occurs, ensuring the release of blood reserves from the depot - up to 20% of the total blood volume; generalized spasm of arterioles leads to centralization of blood circulation and promotes spontaneous cessation of bleeding; tachycardia ensures the maintenance of proper blood circulation volume. If the severity of the injury and the volume of blood loss exceed the body’s protective capabilities, and medical care is delayed, hypotension and tissue hypoperfusion develop , which are clinical and pathogenetic characteristics of grade III traumatic shock.

Thus, the mechanism of development of traumatic shock is monoetiological (trauma), but polypathogenetic (bleeding, endotoxemia, damage to vital organs, afferent effects on the central nervous system), in contrast to hemorrhagic shock (for example, with stab wounds with damage to large vessels) , where there is only one pathogenetic factor - acute blood loss.

Diagnosis and classification of traumatic shock.

During traumatic shock there are two phases: erectile and torpid.

• Erectile phase relatively short. Its duration ranges from several minutes to several hours. The patient is conscious and restless. Motor and speech excitation are noted. The criticism of the assessment of one's own condition is violated. Pale. The pupils are of normal size, the reaction to light is lively. The pulse is of good quality and rapid. Blood pressure is within normal limits. Increased pain sensitivity and skeletal muscle tone.
• Torpid phase Shock is characterized by inhibition of the vital functions of the body and, depending on the severity of the course, is divided into three degrees:

— shock of the 1st degree. Consciousness is preserved, mild inhibition and slowness of reaction are noted. The pain reaction is weakened. The skin is pale, acrocyanosis. Good quality pulse, 90-100 per minute, systolic blood pressure 100-90 mmHg. Mild tachypnea. Skeletal muscle tone is reduced. Diuresis is not impaired.

— shock 2nd degree. The clinical picture is similar to grade I shock, but is characterized by more pronounced depression of consciousness, decreased pain sensitivity and muscle tone, and significant hemodynamic disturbances. Pulse of weak filling and tension - 110-120 per minute, maximum blood pressure 90-70 mm Hg.

— third degree shock. Consciousness is darkened, the patient is sharply inhibited, the reaction to external stimuli is noticeably weakened. The skin is pale gray, with a bluish tint. Pulse is weak and tense, 130 per minute or more. Systolic blood pressure 70 mm Hg. And below. Breathing is shallow and frequent. Muscle hypotonia, hyporeflexia, decreased diuresis up to anuria are noted. The algover index plays a great diagnostic role in determining the degree of shock: the ratio of heart rate to the level of systolic blood pressure. Using it, you can roughly determine the degree of shock and the amount of blood loss (Table 3).

Shock index

Untimely elimination of the causes that support and deepen traumatic shock prevents the restoration of vital functions of the body, and grade III shock can develop into a terminal state, which is an extreme degree of depression of vital functions, leading to clinical death.

Principles of medical care:

- urgent nature of medical care in case of traumatic shock, due to the threat of irreversible consequences of critical disorders of vital functions and, above all, circulatory disorders, deep hypoxia.

— the feasibility of a differentiated approach when treating the wounded in a state of traumatic shock. Shock should not be treated as
such, not a “typical process” or a “specific pathophysiological reaction”. Anti-shock care is provided to a specific wounded person with dangerous life disorders, which are based on severe trauma (the “morphological substrate” of shock) and, as a rule, acute blood loss. Severe disorders of blood circulation, breathing and other vital functions are caused by severe morphological damage to vital organs and systems of the body. In case of severe injuries, this position takes on the meaning of an axiom and directs the doctor to an urgent search for a specific cause of traumatic shock. Surgical care for shock is effective only with a quick and accurate diagnosis of the location, nature and severity of damage.

— the leading importance and urgent nature of surgical treatment with traumatic shock. Anti-shock care is provided simultaneously by an anesthesiologist-resuscitator and a surgeon. The effective actions of the first determine the rapid restoration and maintenance of airway patency, gas exchange in general, the initiation of infusion therapy, pain relief, drug support of cardiac activity and other functions. However, the pathogenetic meaning is urgent surgical treatment that eliminates the cause of traumatic shock - stopping bleeding, eliminating tension or open pneumothorax, eliminating cardiac tamponade, etc.

Thus, modern tactics of active surgical treatment of a seriously wounded person occupies a central place in the program of anti-shock measures and leaves no room for the outdated thesis - “first bring them out of shock, then operate.” This approach was based on misconceptions about traumatic shock as a purely functional process with a predominant localization in the central nervous system.

Anti-shock measures at the stages of medical evacuation.

First and pre-medical aid includes:

• To stop external bleeding using temporary methods, apply aseptic dressings to the wounds.
• Injection of analgesics using syringe tubes.
• Immobilization of fractures and extensive injuries with transport tires.
• Elimination of mechanical asphyxia (release of the upper respiratory tract, application of an occlusive dressing for open pneumothorax).
• Early initiation of blood replacement infusions using field disposable plastic infusion systems.
• Priority careful transportation of the wounded to the next stage.

First medical aid.

The wounded in a state of traumatic shock should first be sent to the dressing room.

Anti-shock care should be limited to the necessary minimum emergency measures so as not to delay evacuation to a medical facility where surgical and resuscitation care can be provided. It should be understood that the purpose of these measures is not to recover from shock (which is impossible in medical conditions), but to stabilize the condition of the wounded for further priority evacuation.

In the dressing room, the causes of the serious condition of the wounded are identified and measures are taken to eliminate them. For acute breathing problems — Asphyxia is eliminated, external respiration is restored, the pleural cavity is sealed in case of open pneumothorax, the pleural cavity is drained in case of tension pneumothorax, and oxygen is inhaled. In case of external bleeding, it is temporarily stopped, and in the presence of a hemostatic tourniquet, the tourniquet is controlled.

An intravenous infusion of 800-1200 ml of a crystalloid solution (mafusol, lactasol, 0.9% sodium chloride solution, etc.) is carried out, and in case of massive blood loss (2 liters or more), an additional infusion of a colloid solution (polyglucin, etc.) is advisable in a volume of 400 -800 ml. The infusion continues in parallel with the implementation of medical measures and even during the subsequent evacuation.

A mandatory first aid anti-shock measure is pain relief. All wounded with traumatic shock are administered narcotic analgesics. However, the best method of pain relief is novocaine blockade. Transport immobilization is monitored. In case of internal bleeding, the main task of first medical aid is to organize the immediate evacuation of the wounded person to the stage of providing qualified or specialized medical care, where he will undergo emergency surgery to eliminate the source of bleeding.

Qualified and specialized assistance.

The wounded with signs of shock should first be sent to the operating room to perform operations for emergency indications (asphyxia, cardiac tamponade, tension or open pneumothorax, ongoing internal bleeding, etc.) or to the intensive care ward for the wounded - in the absence of indications for emergency surgery ( to eliminate disorders of vital functions, prepare for emergency surgery or evacuation).

For wounded people requiring emergency operations, anti-shock therapy should begin in the emergency department and continue under the guidance of an anesthesiologist-resuscitator simultaneously with surgical intervention. Subsequently after surgery, anti-shock therapy is completed in the intensive care unit. The average time to recover a wounded person from a state of shock in war is 8-12 hours. At the stage of specialized care, after recovery from shock, the wounded with a treatment period not exceeding 60 days are given a full course of treatment. The remaining wounded are evacuated to rear hospitals.

Traumatic shock is defined as the most common clinical form of the serious condition of the wounded, developing as a result of severe mechanical trauma or injury and manifested by a syndrome of low cardiac output and tissue hypoperfusion.

You need to know that, in addition to traumatic shock, there are other clinical forms of the serious condition of the wounded, caused by injury or trauma - traumatic coma, acute respiratory failure and acute heart failure 19 . They have specific triggering mechanisms and require a special approach to diagnosis and treatment, and therefore will be discussed in the relevant chapters.

The frequency of traumatic shock in the wounded in modern combat conditions increases, reaching 25%. This is due to an increase in the destructive power of weapons, unfavorable climatic conditions (hot climate, mountainous desert terrain) and the associated adaptation difficulties, large-scale use of aeromedical evacuation - wounded with extremely severe combat trauma are delivered to medical institutions, many of whom would not be able to endure long-term evacuation by ground transport.

8.1. THE EVOLUTION OF VIEWS ON SHOCK

AND MODERN REPRESENTATIONS

ABOUT ITS PATHOGENESIS

The first observations of unusual retardation in severe wounds belong to Ambroise Paré(XVI century). The medical term “shock” appeared when translated into English by a surgeon James Latta a book by a French military man published in 1737

19 The severity of the wounded person’s condition is an integrative indicator calculated by summing up the most informative symptoms using the “VPH-SP” or “VPH-SG” scales (see Chapter 5). Clinical forms of the serious condition of the wounded are: traumatic shock and terminal condition (63%), traumatic coma (18%), ARF (13%), acute heart failure (6%)

surgeon Henri Ledran, in which a similar word (“secouse”, French - blow, shock) described the serious condition of the wounded from gunshot wounds.

In the history of the study of traumatic shock, three periods can be distinguished - descriptive, theoretical development of the concept and modern - scientific and practical, when the study of pathophysiological processes in response to severe injuries was transferred from experimental laboratories to specialized “anti-shock” centers.

Among the many surgeons from different countries who described traumatic shock, the figure rises N.I. Pirogov, who vividly and deeply presented the picture of traumatic shock in the wounded: “With a torn off leg or arm, such a numb person lies motionless at the dressing station; he doesn't scream, yell or complain; does not take part in anything and does not demand anything; his body is cold, his face is pale, like a corpse; the gaze is motionless and turned into the distance, the pulse, like a thread, is barely noticeable under the finger and with frequent alternations. The numb person either does not answer questions at all, or only in a barely audible whisper to himself; breathing is also barely noticeable. The wound and skin are almost completely insensitive; but if the large nerve hanging from the wound is irritated by something, then the wounded person with one slight contraction of the personal muscles reveals a sign of feeling. Sometimes this condition goes away within a few hours from the use of stimulants, sometimes it continues until death.” 20. The theories of traumatic shock played a special role in the formation of the doctrine of shock: neurogenic, blood plasma loss and toxic.

Neurogenic theory traumatic shock was put forward in the 1890s. American surgeon G. Krail. In the 20th century it was comprehensively developed by a domestic pathophysiologist I.R. Petrov. Proponents of the neurogenic (neuro-reflex) theory associated the “primary breakdown” that occurs in the body after severe wounds and injuries with powerful neuropain impulses from areas of severe mechanical damage to the central nervous system and target organs (adrenal glands and other endocrine organs). Really, modern methods confirm the occurrence of pathological

20 Pirogov N.I. The beginnings of general military field surgery, taken from observations of military hospital practice and memories of the Crimean War and the Caucasian expedition of 1864, 1865-1866. - Collected Works, T. 5. - M., 1961. - P. 71

changes in the central nervous system occurring at the subcellular level. It is possible that they lay the foundation for the development of later complications. However the main provisions of the neurogenic theory of traumatic shock have not been confirmed : she claims an excessive role of neuropainful influences, but to prove the leading role of neuropainful factors, inadequate experimental models were used (many hours of electrical stimulation of large nerve trunks or numerous blows to the limb with heavy metal objects). Besides, studies of all parts of the nervous system did not find signs of its depression during traumatic shock. Inhibition of the cerebral hemispheres actually occurs at the final stage of the terminal state - agony and clinical death, but as a direct consequence of a critical decrease in blood circulation in the brain. At the same time, indication of the limited role of pain impulses in the mechanisms of development of traumatic shock should not give rise to underestimation of pain relief .

At the very beginning of the twentieth century. English explorer A. Malcolm assigned a leading role in the mechanism of development of traumatic shock acute blood plasma loss. The subsequent development and widespread use of objective methods for determining the volume of blood loss (direct measurements of blood volume, etc.) confirmed absolutely priority role of acute blood loss in the pathogenesis of traumatic shock. Severe mechanical damage accompanied by a decrease in blood pressure is usually accompanied by acute blood loss, proportional to the level of hypotension. It is massive blood loss that forms the symptom complex of traumatic shock. The theory of blood plasma loss turned out to be the most fruitful for improving treatment tactics, since it directed doctors to search for the source of acute bleeding, causing a hemodynamic catastrophe (traumatic shock).

Recognition of the leading role of acute blood loss in the pathogenesis of traumatic shock still does not provide grounds for identifying traumatic and hemorrhagic shock. In case of severe mechanical damage, the pathological effect of acute blood loss is inevitably accompanied by the negative effect of pain - nociceptive impulse, consequences of visceral injuries, and for wounds accompanied by the formation of extensive foci of primary necrosis (gunshot wounds), crushing or crushing of tissue - severe endotoxicosis. Toxic substances enter the systemic circulation in large quantities - products of destroyed tissues,

impaired metabolism, resolving large hematomas. All these substances negatively affect the autonomic centers in the brain, heart, and lungs, which ensure adequate blood circulation and breathing. When the integrity of the hollow organs of the abdomen is damaged, toxic products enter the bloodstream and are absorbed through the extensive surface of the peritoneum. The listed toxic substances have a depressing effect on hemodynamics, gas exchange and contribute to the formation of irreversible changes in cells. For the first time, French doctors drew attention to the large role of the toxic factor in severe mechanical damage during the First World War. E. K enyu And P. Delbe- authors toxic theory traumatic shock.

Thus, the clinical and pathogenetic basis of traumatic shock is the syndrome of acute circulatory disorders (hypocirculation), which occurs as a result of the combined effect on the wounded body of the life-threatening consequences of injury - acute blood loss, damage to vital organs, endotoxicosis, as well as neuropainful influences. Domestic scientists from the “Group” came to this conclusion. 1", who studied traumatic shock on the battlefields of the Great Patriotic War ( N.N. Elansky, M.N. Akhutin, 1945).

Views on traumatic shock as a hypocirculation syndrome were confirmed in the third historical period of development of the doctrine of shock, which chronologically coincided with the formation in the 1960s. a new medical specialty - resuscitation. During these years, specialized departments and centers began to be organized, where seriously injured people with symptoms of traumatic shock were concentrated, and not only surgeons and resuscitators, but also clinical physiologists took part in their treatment. In our country, the first such center - a research laboratory for the study of shock and terminal conditions at the Department and Clinic of Military Field Surgery of the Military Medical Academy - was created by a famous surgeon A.N. Berkutov in 1961. Since this period, the clinical manifestations and pathogenetic mechanisms of the development of traumatic shock began to be studied directly in a wounded person, depending on the methods of his treatment. In the 1970s the debate over the fundamental theory of the development of traumatic shock ends. Traumatic shock is defined as a syndrome of hypocirculation and tissue hypoperfusion that develops as a result of severe mechanical injury. Researched in

direct connection with treatment, traumatic shock began to be viewed not as a scientific theory, but as treatment-tactical concept, i.e. methodology of pathogenetically based treatment.

To date pathogenesis of traumatic shock simplified as follows. As a result of severe injury or trauma, the wounded person develops one or more (for multiple or combined injuries) foci of damage tissues or organs. In this case, vessels of various sizes are damaged - there is bleeding ; irritation of a large receptor field occurs - formation massive afferent effect on the central nervous system ; a more or less extensive volume of tissue is damaged, the products of their breakdown are absorbed into the blood - a endotoxemia . In case of damage to vital organs there is a violation of the corresponding vital functions: damage to the heart is accompanied by a decrease in the contractile function of the myocardium; lung damage - decreased volume of pulmonary ventilation; damage to the pharynx, larynx, trachea - asphyxia. Thus, mechanism of development of traumatic shock monoetiological (trauma), but at the same time polypathogenetic (the listed pathogenetic factors) in contrast to hemorrhagic shock (for example, with stab wounds with damage to large vessels), where there is only one pathogenetic factor - acute blood loss.

Massive afferent influence to the central nervous system (nociceptive afferent impulses) from the lesion(s) of damage and information impact through the baroreceptors of the walls of arterial vessels to the centers of the autonomic nervous system (hypothalamus) about the volume of blood loss is a trigger for launching a nonspecific adaptation program to protect the body . Its main task is the survival of the body in an extreme situation. The direct “organizer” and “executor” of this program is the hypothalamic-pituitary-adrenal system, which implements evolutionarily formed mechanisms of neuro-endocrine regulation aimed at saving the life of the wounded.

Having received information from the center and periphery, the hypothalamus launches an adaptation program by isolating stress-releasing factors affecting the corresponding areas of the pituitary gland. The pituitary gland, in turn, sharply increases the secretion of stress hormones and above all adrenocorticotropic hormone (ACTH). Thus, in response to injury, a stress cascade of neurohumoral interactions is launched, the result of which is a sharp

activation of the adrenal and cortical adrenal systems . They release large amounts of adrenaline, norepinephrine and glucocorticoid hormones into the blood.

Following this are implemented effector mechanisms of the adaptation program. As a result of increased nervous sympathetic efferentation and a sharp release of a large amount of catecholamines (adrenaline and norepinephrine) into the bloodstream, generalized spasm of small vessels in the periphery(limbs, pelvis, abdominal cavity). The first reaction in time to compensate for blood loss is spasm of the capacitance vessels of the veins. Venoconstriction, which reduces the capacity of the venous reservoir, mobilizes up to 1 liter of blood for circulation. Venous capacitance system contains 75-80% of all blood, rich in adrenergic receptors, therefore is the first-line effector of emergency compensation for blood loss. The second most time-consuming compensatory reaction to injury and blood loss is spasm of arterioles and precapillary sphincters. The resulting increase in total peripheral resistance is aimed at maintaining minimally sufficient blood pressure. The biological meaning of these processes consists primarily of mobilizing blood from blood depots, mobilizing fluid into the vascular bed, redistributing blood to maintain perfusion of the brain and heart due to the death of the periphery, stopping or reducing the intensity of bleeding . These processes are called "centralization of blood circulation" . They are the most important and early defense mechanism, aimed at compensating blood volume and stabilizing blood pressure. Thanks to the “centralization of blood circulation”, the body can independently compensate for blood loss of up to 20% of the bcc.

With the progression of bleeding and the action of other factors of traumatic shock, blood volume and blood pressure decrease, and circulatory and tissue hypoxia develops. The second level of protection is activated. To compensate for the deficit of blood volume, circulatory hypoxia, and ensure the proper volume of blood circulation, heart contractions become more frequent - tachycardia develops, the severity of which is directly proportional to the severity of the shock. Compensation for hypoxia is also carried out by slowing blood flow in the lungs as a result of spasm of post-capillary sphincters; slowing down the passage of blood through the pulmonary capillaries increases the time of saturation of red blood cells with oxygen (Fig. 8.1).

The protective-adaptive reactions listed above are realized within the first hour after injury; pathogenetically they represent a stage of compensation, and clinically they represent traumatic shock of degrees I and II.

At severe traumatic brain injury or trauma An obligatory component of the injury is primary or secondary (due to swelling and dislocation of the brain) damage to the structures of the interstitial brain and brainstem, where numerous centers of neurohumoral regulation of all vital functions of the human body are concentrated. The main result of such damage is failure of the body's adaptation program to protect itself . In the damaged hypothalamus, the processes of formation of releasing factors are disrupted, and feedback between the pituitary gland and the effector endocrine glands, primarily the adrenal glands, is disrupted. As a result, centralization of blood circulation and tachycardia do not develop, and the metabolism acquires a hypercatabolic character that is unfavorable for the body. A pathogenetic and clinical picture of traumatic coma develops, which is characterized by: loss of consciousness and reflex activity, muscle hypertonicity up to convulsions, arterial hypertension

Rice. 8.1. Scheme of the pathogenesis of traumatic shock I-II degrees

and bradycardia, i.e. a symptom complex opposite to the manifestations of traumatic shock.

If the pathogenetic factors of shock continue to act, and medical care is delayed or ineffective, defensive reactions acquire the opposite quality and become pathological, exacerbating the pathogenesis of traumatic shock. Begins stage of decompensation . As a result of prolonged generalized spasm of small vessels microcirculatory hypoxia develops, which causes generalized hypoxic damage to cells, is the main factor in the pathogenesis of grade III traumatic shock that is prolonged in dynamics.

Progressive disorders of oxygen transport in cells are accompanied by a pronounced decrease in the content of adenosine triphosphoric acid (ATP), the main energy carrier, the occurrence of energy deficiency in cells. Energy production in cells switches to the path anaerobic glycolysis, and underoxidized metabolites accumulate in the body(lactic, pyruvic acids, etc.). Metabolic acidosis develops. Tissue hypoxia leads to increased lipid peroxidation, which causes damage to cell membranes. As a result of destruction of cell membranes and energy deficiency The high-energy potassium-sodium pump stops working. Sodium penetrates into the cell from the interstitial space, and water moves into the cell with sodium. The cell edema, following the destruction of membranes, completes the cycle of cell death.

As a result of the destruction of lysosomal membranes, they are released and lysosomal enzymes enter the bloodstream, which activate the formation of vasoactive peptides (histamine, bradykinin). These biologically active substances, together with acidic anaerobic metabolites, cause persistent paralysis of the precapillary sphincters. Total peripheral resistance drops critically, and arterial hypotension becomes irreversible. It should be remembered that when SBP drops below 70 mm Hg. kidneys stop producing urine - acute renal failure develops . Microcirculation disorders are aggravated by internal combustion engine. Initially being a protective reaction to stop bleeding, at subsequent stages of the pathological process DIC syndrome causes microthrombosis in the lungs, liver, kidneys, heart, accompanied by dysfunction (dysfunction) of these organs(DIC I, II degrees), or the cause of the development of severe fibrinolytic bleeding (DIC III-IV degrees). Developing multiple organ dysfunction vital

important organs , that is, simultaneous dysfunction of the lungs, heart, kidneys, liver and other organs of the gastrointestinal tract, which has not yet reached critical levels.

Pathological processes occurring in the stage of decompensation are characteristic of prolonged (hours) cases of traumatic shock. Quickly initiated and correctly carried out resuscitation measures are often effective in case of third degree traumatic shock, less often - in a terminal condition (in cases of isolated injuries). Therefore, the widespread practice of emergency medicine has included the “golden hour” rule, the meaning of which is that medical care for severe injuries is effective only during the first hour ; During this time, the wounded person should be provided with pre-hospital resuscitation care, and he should be taken to a hospital.

The last stage of development of pathological processes in prolonged traumatic shock of the third degree is the progression of dysfunction of vital organs and systems. Wherein disruption of their function reaches critical levels, beyond the threshold of which the function of the organs is no longer sufficient to ensure the vital functions of the body, polyogranic insufficiency (POF) develops (Fig. 8.2).

In the vast majority of cases, its outcome is terminal condition and death. In certain situations, with excellently organized resuscitation care in specialized centers for the treatment of severe injuries correction of multiple organ dysfunction of vital organs and even MODS is possible using complex expensive and high-tech methods: mechanical ventilation devices of III-IV generations with numerous modes of artificial respiration, multiple sanitary fibrobronchoscopy, large-volume extracorporeal blood oxygenation, various methods of extracorporeal detoxification, hemofiltration, hemodialysis, proactive surgical treatment, targeted antibacterial therapy, correction of disorders in the immune system, etc.

Upon successful resuscitation MODS in most cases transforms into a number of complications that have their own etiology and pathogenesis, those. are already new etiopathogenetic processes. The most typical of them are: fat embolism, thromboembolism, pneumonia, gastrointestinal bleeding, various types of aerobic and anaerobic infections of various locations. In 40% of cases, the immediate outcome of MOF is sepsis.

In 30% of cases with sepsis, in 60% with severe sepsis and in 90% with septic shock, the outcome is death. Thus, the heroic efforts of specialists (resuscitators, surgeons, anesthesiologists, etc.) when using expensive and modern treatment methods can bring back to life only 30-40% of the wounded who have suffered MODS, which developed as a result of prolonged traumatic shock of the third degree.

Rice. 8.2. Scheme of the pathogenesis of traumatic shock of the third degree

The possibility of treating wounded people with severe wounds and injuries accompanied by third-degree shock appeared in the 1960s. due to the rapid development of anesthesiology and resuscitation and the emergence of specialized multidisciplinary centers for the treatment of severe injuries. Our country has been a leader in this direction. During these same years, an obvious paradox emerged: the faster and more effectively the wounded with severe injuries receive medical care at the prehospital stage and in the anti-shock departments of specialized centers, the higher the likelihood of their immediate survival, i.e. according to formal indicators (sBP), they are removed from the state of shock. But this fact does not mean recovery. After recovering the wounded from a state of III degree shock, 70% of them develop severe complications in subsequent periods, the treatment of which is often more difficult than recovery from shock.

Thus, in case of severe and extremely severe injuries or wounds, removing the wounded from a state of traumatic shock, especially stage III, is only the first stage of treatment. Subsequently, these wounded people develop new etiopathogenetic processes, defined as organ failure or complications, the treatment of which has serious specifics. Nevertheless, all protective and pathological processes that develop in the wounded after severe injuries or wounds are determined by trauma and are interconnected by cause-and-effect relationships. All of them constitute the pathogenetic essence traumatic disease (TB) .

8.2. MODERN CONCEPTS ABOUT TRAUMATIC DISEASE.

In the 1970s In our country, theoretical and clinical prerequisites for new tactics for treating wounded and seriously injured people began to form. They were based on the concept of traumatic disease, the founders of which were Russian scientists, primarily pathophysiologist S.A. Seleznev and military field surgeon I.I. Deryabin.

TB is defined as a therapeutic-tactical concept, i.e. methodology for treating severe wounds and injuries. As a concept, it explains the mechanisms and sequence of development of protective and pathological processes, and on this basis provides the ability to predict the dynamics of their development, timely prevention and treatment.

Consequently, traumatic shock as a treatment and tactical concept is a methodology for saving the lives of the wounded in the first hours after severe wounds and injuries, and TB is a methodology for treating them until the final outcome.

There are 4 periods during TB.

1st period (acute) - period of acute disturbance of vital functions. In 63% of cases, impairment of vital functions manifests itself in the form of traumatic shock or terminal condition, in 18% - traumatic coma with severe brain damage, in 13% - ARF with severe chest injuries, in 6% - acute heart failure with heart damage. It begins immediately after the injury and lasts 6-12 hours depending on the severity of the injury and the effectiveness of treatment measures. During this period, the wounded receive pre-hospital care and resuscitation care in the anti-shock departments of specialized centers or in the resuscitation and intensive care units (ICU) of district (regional) hospitals, medical hospitals, MOSN, VG. The main therapeutic task during this period is to identify the causes of violations of vital functions and the systems in which they occurred; active, in t.including instrumental, damage diagnostics; performing emergency and urgent surgical interventions and conservative resuscitation measures: puncture and catheterization of large veins and even arteries, ITT, mechanical ventilation, monitoring of vital functions, etc. It is during this period that the wounded are removed from the state of traumatic shock. The optimal place for treating the wounded in the first period of TB is anti-shock operating rooms, where it is possible to create conditions for simultaneous instrumental invasive diagnostics (pleural, lumbar and other types of punctures, laparocentesis, laparoscopic and thoracoscopy, etc.); performing emergency and urgent surgical interventions; invasive intensive care measures (puncture and catheterization of veins and arteries, tracheostomy) . During this period, up to 10% of those seriously wounded or suffering from life-threatening consequences of injuries die. The period ends with the final diagnosis of damage, elimination of the causes of violations of vital functions, compensation of blood loss and relative stabilization of the main indicators of the respiratory and circulatory systems.

2nd period - a period of relative stabilization of vital functions. During this period, formal indicators of vital functions (blood pressure, pulse, oxygen tension in the blood, blood counts) approach normal values ​​or deviate slightly, but compensation of functions is unstable, breakdowns are possible. This period

lasts from 12 to 48 hours. Its importance is very great in the treatment of the wounded, because . it is at this time that conditions are created for the prevention of severe, life-threatening complications, mainly through surgery: operations on the great vessels of the limbs, long bones, bones and pelvic organs, spine and spinal cord. This is especially important in case of combined injuries (polytraumas), when several areas of the body are simultaneously damaged, and multiple foci of damage and multiple fractures are sources of enzymatic aggression, blood loss, excessive afferent impulses and physical inactivity. Surgical interventions are performed in specially equipped operating rooms, often simultaneously on several areas of the body by multidisciplinary surgical teams; anesthesia and intensive care are carried out by specially trained anesthesiologists with monitoring of vital functions. This active treatment tactic was defined as surgical resuscitation., and surgical interventions refer to deferred categories. The place of treatment for the wounded in the second period of TB is the intensive care unit and intensive care unit. During this period, up to 5% of seriously wounded and victims die, mainly from early MODS 1 .

3rd period - the period of maximum likelihood of complications developing.

During this period, optimal conditions are created for the development of complications. Due to large blood loss, endotoxicosis, DIC syndrome, systemic inflammatory response in the internal organs (lungs, heart, spleen, liver, intestines, kidneys) formed multiple foci of microthrombosis . These lesions are a target for microorganisms entering the bloodstream from wounds, the upper respiratory tract and the intestines; blood macrophages, fixing together with bacteria on the endothelium of the vascular wall and thereby disrupting the already compromised microcirculation in the organs.

Particularly favorable conditions for the development of severe complications are created in the lungs.

1. Microthrombi and fat emboli affect the lungs at the level of arterioles, precapillaries, capillaries - when a critical level is reached, such life-threatening complications develop as thromboembolism of small branches of the pulmonary artery or fat embolism with a mortality rate of up to 50%.

1 Early MODS - insufficiency of functions of vital organs, which has reached critical levels and is caused by traumatic shock of the third degree. Late MODS - failure of vital organs due to generalization of infectious complications (sepsis)

2. Biologically active substances, fat, enzymes of destroyed cells, toxins of various origins, circulating in the blood, passing through the pulmonary capillaries, affect the basement membrane of the alveoli and cause “chemical” inflammation in it - the permeability of the capillary wall increases, protein penetrates the basement membrane, and she becomes impermeable to oxygen- diffusion of gases in the alveoli is disrupted, oxygen tension in the blood decreases - develops acute respiratory distress syndrome with a mortality rate of up to 90%.

3. With prolonged traumatic shock of the third degree, the protective vascular reaction in the lungs (spasm of pulmonary postcapillaries), aimed at slowing down the rate of passage of red blood cells through the pulmonary capillaries to increase the time they are enriched with oxygen, turns into its opposite and becomes pathological. As a result of prolonged spasm of pulmonary postcapillaries pressure in the pulmonary artery system increases. Hypovolemia, movement of Na + ions into cells, cellular hyperhydration, intravascular dehydration lead to a decrease in osmotic pressure in the vascular sector - the osmotic gradient is directed towards the alveoli. As a result of these two processes Liquid from the capillaries sweats into the alveoli, and the activity of surfactant decreases(a surfactant that prevents the walls of the alveoli from sticking together), the airiness of the alveoli decreases, then they stick together or fill with liquid - microatelectases are formed. As the process progresses, microatelectasis merges into larger foci of atelectasis - a focal pneumonia . The average period of development of pneumonia in wounded with severe trauma is 3-6 days. With extremely severe injuries, with acute massive blood loss, pathological processes in the lungs occur more rapidly and dramatically: the alveoli quickly fill with fluid - the formation of “wet” (“wet”, “shock”) lung syndrome , which, as the process progresses, turns into pulmonary edema usually ending in death.

Systemic processes of microthrombosis occur in damaged internal organs, segments and tissues of the musculoskeletal system - they are a good environment for development local, visceral and generalized infectious complications .

1st etiological a factor in the occurrence of such complications is endogenous microflora. There is also a philosophical

the law of “unity and struggle of opposites”, when the defensive reaction of centralization of blood circulation leads to profound disturbances of blood circulation and metabolism in the intestinal wall. As a result the natural barrier of the intestinal tube is disrupted, i.e. the wall of the intestinal capillaries becomes permeable to microorganisms growing in the lumen of the intestine of a healthy person. Thus, enterobacteria, Proteus, Klebsiella, Escherichia coli and other conditionally pathogenic microorganisms enter the blood, circulate in it and settle in foci of microthrombosis, in damaged tissues, where they interact with tissue and blood macrophages and other immune defense factors. This microbiological phenomenon is called hematogenous translocation, i.e. the migration of microorganisms through the blood into a new habitat with the subsequent formation of a new (metastatic) pathological microbiocenosis.

2nd important factor condition of the source of damage: wounds, fracture areas, skin detachment areas, etc. The state of the lesion is determined by the volume of necrotic tissue, their functional significance, the degree of disruption of the blood supply to the damaged organ or segment, and ultimately, the likelihood of progression or regression of necrosis in the lesion. The effectiveness of therapeutic measures is also significant: complete removal of necrotic tissue during surgical treatment, restoration of adequate blood circulation in the damaged organ (segment), creation of conditions for restoration of microcirculation in the area of ​​damage and tissue regeneration.

3rd factor influencing the likelihood of developing infectious complications is microbial invasion. In case of open injuries, invasion occurs through a wound - this route of microbial contamination is the least dangerous, since after surgical removal of the necrosis focus, 1 g of healthy tissue independently destroys 1 million microbial bodies. Invasion of hospital microflora is more dangerous, resistant even to modern antibacterial agents. It is carried out through the upper respiratory tract during mechanical ventilation and sanitation measures, through the urinary tract during catheterization, as well as through the skin during numerous invasive therapeutic and diagnostic procedures. The infectious process caused by hospital microflora has been defined as a hospital or nosocomial infection.

The 3rd period of TB begins on the 3rd day and ends on the 10th. At the same time, on the 3-4th day the maximum number of visceral infectious complications develops, mainly pneumonia; on the 6th-10th - the maximum number of local and generalized infectious complications: purulent tracheobronchitis, peritonitis, various forms of local purulent infection of various locations (abscesses, cellulitis, anaerobic cellulitis, myositis, etc.), as well as sepsis.

It should be understood that complications do not always develop in the 3rd period of TB, but the likelihood of their development during these periods is pathogenetically justified and scientifically proven. That's why The therapeutic and tactical feasibility of identifying the 3rd period of TB consists in purposefully focusing the attention of surgeons and resuscitators on the active detection of visceral infectious pulmonary complications on the 3-4th, infectious complications of other localizations and sepsis - on the 6-10th day, on building intensive care on the principle of preventing the development of complications, building rational antibacterial and immune therapy, rationally determining indications for reconstructive operations and carrying them out with an appropriate preventive component. In the 3rd period, up to 15% of seriously wounded people and victims of complications of injuries die from TB.

During TB they are released 4 types: 1st - favorable course with recovery (40%), 2nd - complicated course with recovery (30%), 3rd - complicated course with death (20%), 4th - unfavorable course with death ( 10%).

In type 1, the 2nd period of TB is spent entirely in the intensive care unit, and the 3rd period of stay of the wounded in the ICU can be reduced to 2-4 days if the likelihood of complications is minimized. These wounded people enter the 4th period of TB early and are transferred to specialized surgical departments for recovery treatment and rehabilitation. With types 2 and 3 of TB, the wounded develop complications, and as a result they must be transferred from a “clean” ICU to a specialized ICU for the treatment of wounded with IO injuries. This department performs surgical interventions at the site of injury and intensive care of wound infections. After the elimination of infectious complications, the wounded are transferred to specialized departments. In type 4 TB, death occurs on the 1st day before complications develop.

4th TB period - period of complete stabilization of vital functions. During this period, all vital signs are restored to normal values ​​or close to them. There are no time parameters for this period- they vary significantly depending on the severity of the injury, the location of the injury (for example, severe brain damage is especially distinguished by the duration of previous periods), the severity and nature of the complications. The objective criterion for the transition of a wounded person to the 4th period of TB is stabilization of the condition to the level of compensation according to the scales “VPH-SG and VPH-SS”(see Appendix 1).

During this period, the wounded are treated in specialized (neurosurgery, trauma, etc.) departments in accordance with the location of the leading injury. They perform planned surgical interventions in order to restore the structure and function of damaged tissues, organs and systems, and carry out medical rehabilitation measures.

The average mortality rate of wounded with severe and extremely severe gunshot wounds is up to 10%, with severe and extremely severe combined injuries - up to 30%, the average duration of their treatment is long and exceeds 50 days.

8.3. CLINICAL, DIAGNOSIS AND CLASSIFICATION OF TRAUMATIC SHOCK

The main criteria for traumatic shock are clinical signs of circulatory disorders such as hypocirculation in combination with the presence of a severe wound or mechanical injury.

To the clinical manifestations of traumatic shock This includes severe pallor or gray coloration of the skin, sticky cold sweat, cyanosis of the lips and subungual beds, increased relief of the superficial veins. The facial features are sharpened, and when pressure is applied to the skin of the forehead, a white spot that does not disappear for a long time is formed. A decrease in blood pressure, the most striking and reliable symptom of traumatic shock, does not appear immediately due to the action of compensation mechanisms. However, in the practical diagnosis of traumatic shock, it is the reduction of SBP that is given decisive importance.

In the absence of arterial hypotension, the diagnosis of traumatic shock is not made.

Symptoms of hypocirculation due to acute blood loss are subject to specific features of certain types of severe injuries. For example, with penetrating wounds breasts and severe hypoxia, psychomotor agitation occurs, increased muscle tone, a short-term increase in blood pressure, followed by a sharp decrease. In cases of penetrating injuries belly with ongoing internal bleeding and damage to hollow organs, the symptoms of peritonitis with its characteristic picture are superimposed on the phenomena of hypocirculation. For traumatic brain injury (TBI) The symptom-tomocomplex of shock is observed only in cases of mild brain damage and blood loss either from the integumentary tissues of the head or from other foci of damage in case of combined injuries. In cases of severe brain damage, a picture of traumatic coma develops, which is both pathogenetically and clinically opposite to the manifestations of traumatic shock. The “classical” clinic of traumatic shock, described by N.I. Pirogov, classified as seriously injured limbs at a late stage of circulatory disorders, close to traumatic shock of the third degree.

ABOUT amount of blood loss, confirming the diagnosis of traumatic shock, can be judged by the level of systolic blood pressure, pulse rate, specific gravity of blood, number of red blood cells in mm 3, hemoglobin and hematocrit. For bone fractures, the approximate amount of blood loss is determined by the location and nature of the fracture: fractures of the humerus - up to 500 ml, shin bones - 500-700 ml, hips - up to 1000 ml, with multiple fractures of the pelvic bones - more than 1000 ml. Upon completion of emergency surgery and radical hemostasis, the most accurate information is provided by direct measurements of the blood spilled into the cavity. The dependence of the severity of traumatic shock on the amount of blood loss is presented in Table. 8.1.

About the progression of traumatic shock evidence of increased pallor of the skin and lips, increased heart rate and deterioration, and decreased blood pressure. Against, criteria for recovery from traumatic shock should be considered the appearance of a pink color of the skin, warming of the skin, and the disappearance of cold sweat. The pulse becomes less frequent, and its quality characteristics improve. There is an increase in blood pressure and an increase in its amplitude.

To divide traumatic shock by severity in emergency care practice, of the many parameters available for registration, the most informative is SBP level . The thing is

Table 8.1. Dependence of the severity of traumatic shock on the amount of blood loss, blood pressure level, and pulse rate

that it is SBP that has the closest inverse correlation with the amount of blood loss, which primarily determines the clinical picture of traumatic shock. Other parameters lack such correlation. For example, in addition to hypovolemia, heart rate is significantly affected by psycho-emotional stress, administered medications, concomitant head injury and other factors. For this reason, the so-called “shock index” (HR/BP) is not of great value in the diagnosis of traumatic shock, especially with associated injuries.

Classification of traumatic shock.

According to the level of sBP and the severity of clinical symptoms, traumatic shock is divided into 3 degrees of severity, after which a new qualitative category arises - the next form of serious condition of the wounded is the terminal condition.

Traumatic shock I degree most often occurs as a result of isolated wounds or trauma. It is manifested by pallor of the skin and minor hemodynamic disturbances. SBP is maintained at 90-100 mmHg. and is not accompanied by high tachycardia (pulse up to 100 per minute).

Traumatic shock II degree characterized by lethargy of the wounded person, severe pallor of the skin, and significant hemodynamic impairment. Blood pressure drops to 85-75 mm Hg, pulse quickens to 110-120 beats per minute. In case of insolvency

compensatory mechanisms, as well as in case of unrecognized severe injuries, late stages of assistance, the severity of traumatic shock increases.

Traumatic shock III degree usually occurs with severe combined or multiple wounds (traumas), often accompanied by significant blood loss (the average blood loss in grade III shock reaches 3000 ml, while in grade I shock it does not exceed 1000 ml). The skin becomes pale gray in color with a cyanotic tint. The pulse is greatly increased (up to 140 per minute), sometimes even thread-like. SBP falls below 70 mm Hg. Breathing is shallow and rapid. Restoring vital functions in stage III shock presents significant difficulties and requires the use of a complex set of anti-shock measures, often combined with emergency surgical interventions.

Prolonged hypotension with a decrease in systolic blood pressure to 70-60 mm Hg. is accompanied by a decrease in diuresis, profound metabolic disorders and can lead to irreversible changes in vital organs and systems of the body. In this regard, the indicated level of SBP is usually called “critical”.

Untimely elimination of the causes that support and deepen traumatic shock prevents the restoration of vital functions of the body, and third degree shock can develop into terminal state, which is an extreme degree of depression of vital functions, turning into clinical death.

The terminal condition develops in 3 stages.

1. Preagonal state characterized absence of pulse in the radial arteries if it is present on the carotid and femoral arteries and not determined by the usual blood pressure method.

2. Agonal state has the same features as preagonal, but combined with respiratory disorders(arrhythmic breathing of the Cheyne-Stokes type, severe cyanosis, etc.) and loss of consciousness.

3. Clinically I am death begins from the moment of the last breath and cardiac arrest. There are no clinical signs of life in the wounded patient. However, metabolic processes in brain tissue continue for an average of 5-7 minutes. Isolating clinical death as a separate form of the serious condition of the wounded is advisable, since in cases where the wounded does not have injuries incompatible with life, this condition can be reversible with the rapid application of resuscitation measures.

It should be emphasized that resuscitation measures taken in the first 3-5 minutes, it is possible to achieve complete restoration of the vital functions of the body , while resuscitation carried out at a later date can lead to the restoration of only somatic functions (blood circulation, breathing, etc.) in the absence of restoration of central nervous system functions. These changes can be irreversible, resulting in permanent disability (defects of intelligence, speech, spastic contractures, etc.) - “a disease of a revitalized organism.” The term “resuscitation” should not be understood narrowly as the “revival” of the body, but as a set of measures aimed at restoring and maintaining the vital functions of the body.

The irreversible condition is characterized by a complex of signs: complete loss of consciousness and all types of reflexes, absence of spontaneous breathing, heart contractions, absence of brain biocurrents on the electroencephalogram (“bioelectric silence”). Biological death is declared only when these signs cannot be resuscitated for 30-50 minutes.

8.4. PRINCIPLES OF TREATMENT OF TRAUMATIC SHOCK

1. Urgency of medical care with traumatic shock. This principle is dictated by the threat of irreversible consequences of critical disorders of vital functions and, above all, circulatory disorders and deep hypoxia. The diagnosis of shock is important as an alarm signal indicating the need for priority treatment to save the life of the wounded.

2. The feasibility of a differentiated approach when treating the wounded in a state of traumatic shock. It is not the shock itself that should be treated, nor the “typical process” or the “specific pathophysiological reaction” (both terms are outdated). Anti-shock care is provided to a specific wounded person with dangerous life disorders, which are based on severe trauma (the “morphological substrate” of shock) and, as a rule, acute blood loss. Severe disorders of blood circulation, breathing and other vital functions are caused by severe morphological damage to vital organs and systems of the body. This position is

severe injuries acquires the meaning of an axiom and targets the doctor for an urgent search for a specific cause of traumatic shock. Surgical care for shock is effective only with a quick and accurate diagnosis of the location, nature and severity of damage.

3. The leading importance and urgent nature of surgical treatment with traumatic shock. Anti-shock care is provided simultaneously by an anesthesiologist-resuscitator and a surgeon. The effective actions of the first determine the rapid restoration and maintenance of airway patency, gas exchange in general, the start of infusion therapy, pain relief, drug support of cardiac activity and other functions. However, urgent surgical treatment has a pathogenetic meaning, eliminating the cause of traumatic shock- stopping bleeding, eliminating tension or open pneumothorax, eliminating cardiac tamponade, etc. Thus, modern tactics of active surgical treatment of a seriously wounded person occupies a central place in the program of anti-shock measures and leaves no room for the outdated thesis - “first get out of shock, then operate.”

8.5. HELP WITH TRAUMATIC SHOCK AT THE STAGES OF MEDICAL EVACUATION

At provision of first and pre-medical aid(battlefield, MPb) the salvation of the wounded in a state of shock depends on their rapid search, stopping external bleeding, eliminating acute respiratory disorders and priority evacuation. Therefore, mandatory measures at the stages of first aid and pre-medical aid are: stopping external bleeding (pressure bandage, tight wound tamponade, application of a standard hemostatic tourniquet), restoration of breathing (elimination of asphyxia, insertion of an air duct, oxygen inhalation and even mechanical ventilation) in the absence of hopelessly severe brain damage, infusion of crystalloid plasma substitute by connecting a special polyethylene container with a capacity of 800-1000 ml to the wounded person through a peripheral vein; it is placed under the back of the wounded person, and the infusion continues during the evacuation process under the influence of the weight of the wounded person and a special drop dispenser in the system. For pain relief on the battlefield, 1 ml of 2% promedol is injected from a syringe tube. The medical assistant has the ability to

ability to enhance analgesia by administering morphine and bupranal. Inhalation autoanalgesia with inhalin and trichlorethylene through special evaporators is possible. Effective immobilization of fractures and laying on a stretcher in a functionally advantageous position should also be considered as an essential element of pain relief in its broad semantic meaning.

At the stage of providing first aid wounded in a state of traumatic shock should first go to the dressing room .

Anti-shock care in the hospital (med) should be limited to the necessary minimum of urgent measures so as not to delay evacuation to a medical facility where surgical and resuscitation care can be provided. It should be understood that the purpose of these measures is not to recover from shock (which is impossible in the conditions of emergency medicine), but to stabilize the condition of the wounded for further priority evacuation.

In the dressing room, the causes of the serious condition of the wounded are identified and measures are taken to eliminate it. For acute breathing problems Asphyxia is eliminated, external respiration is restored, the pleural cavity is sealed in case of open pneumothorax, the pleural cavity is drained in case of tension pneumothorax, and oxygen is inhaled. For external bleeding it is temporarily stopped, and if there is a hemostatic tourniquet, it is monitored.

An important anti-shock measure is intravenous infusion

800-1200 ml of crystalloid solution (lactasol, 0.9% sodium chloride solution, etc.), and in case of massive blood loss (2 liters or more), an additional infusion of colloid solution (polyglucin, rheopolyglucin, etc.) in a volume of 400 ml is advisable . The infusion system is installed by a paramedic or nurse immediately when the wounded person is placed on the dressing table. Accelerating the rate of infusion is possible by connecting a special device in the form of a rubber bulb (Richardson balloon) to the system through an air needle (“air”). It is possible to install two systems for infusion into two veins. The infusion continues in parallel with the implementation of medical measures and even during the subsequent evacuation.

In case of internal bleeding, the main task of first aid is immediate helicopter evacuation of the wounded person to the stage of providing qualified or specialized (at close range) medical care, where he will undergo emergency surgery to eliminate the source of bleeding. The main first aid measure before evacuation is the installation

infusion system into a peripheral vein through a flexible catheter or a special flexulu and start of infusion crystalloid, and in case of shock of the third degree - colloid solution at a moderate pace so as not to increase bleeding. Reducing the intensity of intrapelvic and intraperitoneal bleeding is possible with the availability of special anti-shock inflatable suits (NATO countries have MASS (military anti-shock suit) anti-shock suits available due to inflating the pelvic or abdominal section.

A mandatory first aid anti-shock measure is anesthesia . All wounded with traumatic shock are administered narcotic analgesics. However, the best method of pain relief is novocaine blockades. In case of damage to the chest organs with open pneumothorax, a vagosympathetic blockade is effective; in case of multiple rib fractures, a paravertebral or intercostal blockade is effective. For fractures of the long bones of the extremities, conductor or case novocaine blockades are mandatory. Novocaine blockades are effective for multiple fractures of the pelvic bones, especially the posterior half-ring. After performing novocaine blockades, a mandatory first aid measure is transport immobilization damaged segments of the limbs, pelvis and spine.

The priority task for saving the lives of the wounded in a state of shock is fast delivery to the stage of providing qualified or specialized assistance. Here, already during the reception and selective triage, the wounded in a state of shock are quickly identified. In the emergency diagnosis of shock, the simultaneous participation of surgeons and anesthesiologists-resuscitators is necessary.

Injured patients showing signs of shock should be taken to the operating room first to perform operations for emergency indications (asphyxia, cardiac tamponade, tension or open pneumothorax, ongoing internal bleeding, etc.) or to the intensive care ward in the absence of indications for emergency surgery (to eliminate disorders of vital functions, prepare for emergency interventions or evacuation).

In wounded patients requiring emergency surgery, anti-shock therapy should begin in the emergency department and continue under the guidance of an anesthesiologist-renimatologist simultaneously with surgical intervention. Subsequently after surgery, anti-shock therapy is completed in the intensive care unit.

In the intensive care ward, work continues to replenish blood loss and restore blood volume, which began in the operating room, and measures are also being taken to restore the function of the circulatory system and correct the consequences of acute blood loss. These events are conditionally grouped in several areas.

Recovery BCC for blood loss of up to 1 liter is carried out using crystalloid (Ringer's solution, 5% glucose, lactosol) and colloid (polyglucin, rheopolyglucin) blood replacement solutions with a total volume of up to 2-2.5 liters per day; for blood loss up to 2 liters - from blood and blood substitutes in a 1:2 ratio with a total volume of up to 3.5-4 liters per day; with massive blood loss exceeding 2 liters, mainly due to blood with a ratio of blood and blood substitutes of 2:1, and the total volume of injected fluid exceeds 4 liters; with blood loss exceeding 3 liters, mainly due to large doses of blood (3 liters or more); in this case, blood transfusion is carried out at a rapid pace into two large veins or into the aorta through the femoral artery. It should be remembered that in case of intracavitary bleeding, blood from the cavities must be reinfused (in the absence of damage to hollow organs). Must be as a rule, replacement of lost blood in the first 2 days after injury . The criteria for effectively compensated blood loss are: stabilization of systolic blood pressure at a level of more than 100 mm Hg, a stable decrease in heart rate less than 100 per minute, restoration of red blood parameters (red blood cells - up to 3.0x10 12 / l, hemoglobin - up to 100 g / l , hematocrit - up to 0.32-0.34 l/l, central venous pressure - 6-12 cm water column).

Stimulation of peripheral vascular tone to increase and stabilize SBP - as a necessary condition for the functioning of the heart, lungs, liver, and kidneys. It is effective for adequately compensated blood loss and is carried out by drip administration of dopamine at a dose of 10-15 mcg/kg per minute or norepinephrine at a dose of 1.0-2.0 ml of a 0.2% solution in 400 ml of 5% glucose at a rate of 40-50 drops in a minute.

Hemodynamic stabilization with glucocorticoids(prednisolone 10-30 mg/kg per day during the first two days), which improve myocardial contractile function, relieve peripheral vascular spasm, stabilize cell membranes, and reduce the permeability of the vascular wall.

Improving the rheological properties of blood the use of rheologically active blood substitutes (reopolyglucin, reogluman), crystalloid solutions (5% glucose solution, Ringer's solution, lactosol), disaggregants (trental, aspisol).

Correction of the blood coagulation system, determined by the severity of DIC syndrome: for DIC syndrome of the first degree (hypercoagulation, isocoagulation), heparin 50 IU/kg 4-6 times a day, prednisolone 1.0 mg/kg 2 times a day, trental, rheopolyglucin are used; for DIC syndrome of the second degree (hypocoagulation without activation of fibrinolysis), heparin is used up to 30 IU/kg per day (no more than 5000 IU), prednisolone 1.5 mg/kg 2 times a day, albumin, plasma, rheopolyglucin, whole blood for no more than 3 days of preservation; for DIC syndrome of the third degree (hypocoagulation with the beginning activation of fibrinolysis), prednisolone 1.5 mg/kg 2 times a day, contrical 60,000 units per day, albumin, plasma, short-term preserved blood, fibrinogen, gelatin, dicinone are used; for stage IV DIC syndrome (generalized fibrinolysis), prednisolone up to 1.0 g per day, contrical 100,000 units per day, plasma, fibrinogen, albumin, gelatin, dicinone, alkaline solutions are used. In addition, a mixture of: 100 ml of a 5% solution of ε-aminocaproic acid, 5 ml of adroxon, 400-600 units of dry thrombin is injected locally through drainages into the serous cavities for 30 minutes.

Correction of metabolism during blood loss replenishment. It comes down to the correction of acidosis, caused, on the one hand, by multifactorial tissue hypoxia, and on the other, by the transfusion of a large volume of canned blood. To correct acidosis, buffer solutions of sodium bicarbonate (70-100 mmol per day) or trisamine are used. In order to prevent the adverse effects of the blood preservative (sodium citrate) during large volumes of transfusion, 15 ml of a 10% calcium chloride solution must be administered for every 500 ml of blood.

Neutralization of enzymatic aggression, which is an inevitable consequence of injury, blood loss, hypoxia and blood transfusions. It is carried out by introducing enzyme inhibitors into the infusion therapy (contrical 100,000-160,000 units, trasylol 300,000-500,000 units).

Restoring and maintaining kidney function. With timely and adequate replenishment of blood loss and normalization of hemodynamics, renal blood flow and glomerular filtration are restored, which is manifested by diuresis exceeding 50-60 ml of urine per hour. Prolonged hypotension and large volumes of transfused blood inhibit renal function and lead to the development of prerenal renal failure, the initial manifestation of which is an hourly urine output level below 50 ml . Therefore, in the process of replenishing blood loss, constant catheterization of the bladder and recording of hourly urine output are necessary.

The indication for stimulation of renal function is the development of prerenal renal failure, despite the restoration of systemic hemodynamics. Stimulation begins with intravenous administration of saluretics (Lasix 60 mg once, 200-300 mg per day), since they increase diuresis only due to blockade of sodium reabsorption in the renal tubules; It should be remembered that saluretics reduce blood volume and can only be used when replenishing blood volume. When an adequate response to the use of saluretics is obtained, adequate diuresis is maintained by stimulating hemodynamics and renal blood flow by including rheologically active blood substitutes, disaggregants, osmotic (1 g/kg mannitol per day) and oncotic (1 g/kg albumin per day) in the infusion-transfusion therapy. day) diuretics. Osmodiuretics increase blood volume by increasing plasma osmolarity, and due to weak reabsorption in the renal tubules, they provide an increase in diuresis.

Thus, the main task of qualified medical care - saving the lives of the wounded - is realized by removing them from a state of traumatic shock by performing emergency surgical interventions and carrying out anti-shock intensive care measures.

To remove the wounded from a state of traumatic shock (including after performing emergency operations in the operating room), two intensive care wards are deployed at the stages of providing qualified medical care: 1st - for the wounded, 2nd - for burnt patients with 14-16 beds each. The average time to recover a wounded person from a state of shock in war is 8-12 hours. Consequently, with a massive flow of wounded in one “intensive bed,” 2 wounded receive anti-shock care, i.e. the capabilities of the stage of providing qualified medical care for the wounded in a state of traumatic shock are 28-32 wounded per day when using one intensive care unit and 56-64 when using two.

This chapter presents the standard of resuscitation care for traumatic shock. It is likely that it will not always be feasible in a large-scale war due to massive flows of wounded, a shortage of anesthesiologists and resuscitators, a shortage of drugs and other reasons. At the same time, in local wars (Afghanistan, 1979-1989) and counter-terrorism operations (North Caucasus, 1994-1996, 1999-2002)

all of the listed activities were actually carried out in all medical hospitals (Afghanistan), in the MoSN and in the 1st echelon VG (North Caucasus).

Control questions:

1. Are there other clinical forms of the serious condition of the wounded, besides traumatic shock?

2. List the main pathophysiological mechanisms of traumatic shock of the I-II degree (compensation stage).

3. Is tachycardia characteristic of traumatic coma? What other clinical signs characterize the development of traumatic coma?

4. Is the centralization of blood circulation preserved during traumatic shock of the third degree (stage of decompensation)? What clinical signs characterize this stage of shock?

5. List the possible variants of violations of vital functions that develop immediately after injury.

6. How, in your opinion, is it possible to reduce the frequency and severity of complications of injuries after the wounded person is brought out of shock?

7. List the reasons for the development of pulmonary complications in trauma.

8. How does endogenous microflora become one of the causes of the development of infectious complications?

9. List the degrees and severity criteria of traumatic shock.

10. Describe the contribution of domestic scientists to the development of the doctrine of traumatic shock.

11.What happens after a wounded person is brought out of third degree shock? What are the names of the clinical and pathogenetic processes that develop in a wounded person after recovery from shock?

Traumatic shock develops as a result of traumatic damage to various organs and parts of the body, accompanied by pain, blood loss that occurs with severe mechanical damage, and poisoning due to the absorption of decay products from ischemic tissues. Factors predisposing to the development of shock and aggravating its course are hypothermia or overheating, intoxication, starvation, and overwork.

Severe injuries are the third leading cause of death in adults after cardiovascular diseases and malignant neoplasms. Causes of injury include motor vehicle accidents, fall injuries, and rail injuries. Medical statistics show that recently polytraumas - injuries involving damage to several areas - have become more common. They are distinguished by severe violations of the vital functions of the body, and primarily by circulatory and respiratory disorders.

In the pathogenesis of traumatic shock, an important place belongs to blood and plasma loss, which accompanies almost all traumatic injuries. As a result of injury, vascular damage occurs and the permeability of vascular membranes increases, which leads to the accumulation of large volumes of blood and plasma in the area of ​​injury. And the severity of the victim’s condition largely depends not only on the volume of blood lost, but also on the rate of bleeding. Thus, blood pressure remains at the values ​​​​that were before the injury if bleeding occurs at a slow rate and the blood volume decreases by 20%. With a high bleeding rate, a loss of circulating blood of 30% can lead to the death of the victim. A decrease in the volume of circulating blood - hypovolemia - leads to an increase in the production of adrenaline and norepinephrine, which have a direct effect on capillary circulation. As a result of their influence, the precapillary sphincters close and the postcapillary sphincters expand. Impaired microcirculation causes disruptions in the metabolic process, resulting in the release of large amounts of lactic acid and its accumulation in the blood. A significantly increased amount of under-oxidized products leads to the development of acidosis, which in turn contributes to the development of new circulatory disorders and a further decrease in circulating blood volume. A low volume of circulating blood cannot provide sufficient blood supply to vital organs, which include primarily the brain, liver, kidneys, and brain. Their functions are limited, resulting in irreversible morphological changes.

During traumatic shock, two phases can be traced:

Erectile, which occurs immediately after injury. During this period, the consciousness of the victim or patient is preserved, motor and speech agitation, and lack of a critical attitude towards oneself and the environment are noted; the skin and mucous membranes are pale, sweating is increased, the pupils are dilated and react well to light; blood pressure remains normal or may increase, and the pulse quickens. The duration of the erectile shock phase is 10-20 minutes, during this time the patient’s condition worsens and enters the second phase;

The course of the torpid phase of traumatic shock is characterized by a decrease in blood pressure and the development of severe lethargy. The change in the condition of the victim or patient occurs gradually. To assess the patient’s condition during the torpid phase of shock, it is customary to focus on indicators of the level of systolic blood pressure.

I degree- 90-100 mHg. Art.; in this case, the condition of the victim or patient remains relatively satisfactory and is characterized by pallor of the skin and visible mucous membranes, muscle tremors; the victim’s consciousness is preserved or slightly inhibited; pulse up to 100 beats per minute, number of respirations up to 25 per minute.

II degree- 85-75 mm Hg. Art.; the victim’s condition is characterized by clearly expressed retardation of consciousness; pale skin, cold sticky sweat, decreased body temperature are noted; the pulse is increased - up to 110-120 beats per minute, breathing is shallow - up to 30 times per minute.

III degree- pressure below 70 mm Hg. Art., often develops with multiple severe traumatic injuries. The victim’s consciousness is greatly inhibited, he remains indifferent to his surroundings and his condition; does not respond to pain; the skin and mucous membranes are pale, with a grayish tint; cold sweat; pulse - up to 150 beats per minute, breathing is shallow, frequent or, conversely, rare; consciousness is darkened, pulse and blood pressure are not determined, breathing is rare, shallow, diaphragmatic.

Without the provision of timely and qualified medical care, the torpid phase ends in a terminal condition, which completes the process of development of severe traumatic shock and, as a rule, leads to the death of the victim.

Main clinical signs. Traumatic shock is characterized by inhibited consciousness; pale skin color with a bluish tint; impaired blood supply, in which the nail bed becomes cyanotic; when pressed with a finger, the blood flow is not restored for a long time; the veins of the neck and limbs are not filled and sometimes become invisible; breathing rate increases and becomes more than 20 times per minute; pulse rate increases to 100 beats per minute or higher; systolic pressure drops to 100 mmHg. Art. and below; there is a sharp cooling of the extremities. All these symptoms are evidence that a redistribution of blood flow occurs in the body, which leads to disruption of homeostasis and metabolic changes, becoming a threat to the life of the patient or injured person. The likelihood of restoration of impaired functions depends on the duration and severity of shock.

Shock is a dynamic process, and without treatment or with delayed medical care, its milder forms become severe and even extremely severe with the development of irreversible changes. Therefore, the main principle of successful treatment of traumatic shock in victims is to provide comprehensive assistance, including identifying violations of the vital functions of the victim’s body and carrying out measures aimed at eliminating life-threatening conditions.

Emergency care at the prehospital stage includes the following stages.

Restoration of airway patency. When providing first aid to a victim, it should be remembered that the most common cause leading to deterioration of the victim’s condition is acute respiratory failure resulting from aspiration of vomit, foreign bodies, blood and cerebrospinal fluid. Traumatic brain injuries almost always involve aspiration. Acute respiratory failure develops with multiple rib fractures as a result of hemopneumothorax and severe pain. In this case, the victim develops hypercapnia and hypoxia, which aggravate the phenomenon of shock, sometimes causing death due to suffocation. Therefore, the first task of the person providing assistance is to restore the airway.

Respiratory failure, which appears as a result of suffocation due to retraction of the tongue or severe aspiration, is caused by the general anxiety of the victim, severe cyanosis, sweating, retraction of the chest and neck muscles during inspiration, hoarse and arrhythmic breathing. In this case, the person providing assistance must ensure the patency of the upper respiratory tract for the victim. In this case, he should tilt the victim’s head back, move the lower jaw forward and aspirate the contents of the upper respiratory tract.

Intravenous infusions of plasma-substituting solutions, if possible, are carried out simultaneously with measures to restore normal ventilation of the lungs, and depending on the size of the injury and the amount of blood loss, a puncture of one or two veins is performed and an intravenous infusion of solutions is started. The goal of infusion therapy is to compensate for the deficit in circulating blood volume. The indication for starting the infusion of plasma replacement solutions is a decrease in systolic blood pressure below 90 mmHg. Art. In this case, to replenish the volume of circulating blood, the following volume-replacing solutions are usually used: synthetic colloids - polyglucin, polydes, gelatinol, rheopolyglucin; crystalloids - Ringer's solution, lactasol, isotonic sodium chloride solution; salt-free solutions - 5% glucose solution.

If it is impossible to use infusion therapy at the prehospital stage in case of blood loss, the victim is placed in a lying position with the head end down; in the absence of injuries to the upper and lower extremities, they are given a vertical position, which will help increase the central volume of circulating blood. In critical situations, in the absence of the possibility of infusion therapy, the administration of vasoconstrictors is indicated to increase blood pressure.

Stopping external bleeding, which is carried out by applying a tight bandage, hemostatic clamp or tourniquet, packing the wound, etc. Stopping bleeding contributes to more effective infusion therapy. Prompt hospitalization is necessary if the victim has internal bleeding, signs of which are pale skin covered with cold sweat: rapid pulse and low blood pressure.

Anesthesia should be performed before removing the victim from under heavy objects, placing him on a stretcher, before applying transport immobilization, and carried out only after all measures have been taken to restore vital functions, which include sanitation of the respiratory tract, administration of solutions in case of large blood loss, and stopping bleeding.

Under the condition of rapid (up to 1 hour) transportation, mask anesthesia is used using AP-1, Trintal devices and the use of methoxyflurane and local anesthesia with novocaine and trimecaine.

During long-term transportation (more than 1 hour), narcotic and non-narcotic analgesics are used, and they are also used in cases of precise diagnosis (for example, amputation of a limb). Since absorption from tissues is impaired in the acute period of severe trauma, analgesic drugs are administered intravenously, slowly, under the control of breathing and hemodynamics.

Immobilization: transportation and removal (removal) of the victim from the scene and, if possible, rapid hospitalization.

Fixation of injured limbs prevents the appearance of pain that intensifies shock, and is indicated in all necessary cases, regardless of the condition of the victim. Standard transport tires are being installed.

Placing the victim on a stretcher for transportation plays an equally important role in his rescue. In this case, the victim is placed in such a way as to avoid aspiration of the respiratory tract with vomit, blood, etc. The conscious victim should be placed on his back. An unconscious patient should not place a pillow under his head, since in such a position the tongue may close the airways with reduced muscle tone. If the patient or victim is conscious, he is placed on his back. Otherwise, you must remember that with reduced muscle tone, the tongue closes the airways, so you should not place a pillow or other objects under the victim’s head. In addition, in this position, a bent neck can cause kinking of the airways, and if vomiting occurs, vomit will easily enter the airways. If there is bleeding from the nose or mouth of a victim lying on his back, the flowing blood and stomach contents will freely enter the airways and close their lumen. This is a very important point in transporting a victim, since according to statistics, approximately a quarter of all victims of accidents die in the first minutes due to aspiration of the respiratory tract and incorrect position during transportation. And if in this case the victim survives in the first hours, then in most cases later he develops post-aspiration pneumonia, which is difficult to treat. Therefore, in order to avoid such complications, in such cases it is recommended to lay the victim on his stomach and ensure that his head is turned to the side. This position will facilitate the outflow of blood from the nose and mouth, in addition, the tongue will not interfere with the free breathing of the victim.

Positioning the victim on his side with his head turned to his side will also help avoid aspiration of the airway and tongue retraction. But to prevent the victim from turning onto his back or face down, the leg on which he lies should be bent at the knee joint: in this position it will serve as a support for the victim. When transporting a victim, it should be borne in mind that if the chest is wounded, in order to facilitate breathing, it is better to lay the victim down, raising the upper part of the body; if the ribs are fractured, the victim should be laid on the damaged side, and then the body weight will act like a splint, preventing painful movements of the ribs when breathing.

When transporting a victim from the scene of an accident, the person providing assistance must remember that his task is to prevent the shock from deepening, to reduce the severity of hemodynamic and respiratory disorders, which pose the greatest danger to the life of the victim.

First aid for shock

Shock is the body's general reaction to an emergency (trauma, allergy). Clinical manifestations: acute cardiovascular failure and, necessarily, multiple organ failure.

The main link in the pathogenesis of traumatic shock is disorders caused by injury to tissue blood flow. Trauma leads to disruption of the integrity of blood vessels and blood loss, which is a trigger for shock. There is a deficit of circulating blood volume (CBV), bleeding (ischemia) of organs. At the same time, in order to maintain blood circulation in vital organs (brain, heart, lungs, kidneys, liver) at the expense of others (skin, intestines, etc.), compensatory mechanisms are activated, i.e. blood flow is redistributed. This is called centralization of blood circulation, due to which the functioning of vital organs is maintained for some time.

The next compensation mechanism is tachycardia, which increases the passage of blood through the organs.

But after some time, compensatory reactions take on a pathological character. At the level of microcirculation (arterioles, venules, capillaries), the tone of the capillaries and venules decreases; blood collects (pathologically deposits) in the venules, which is equivalent to repeated blood loss, since the area of ​​the venules is huge. Then the capillaries also lose their tone, they do not stretch, they fill with blood, it stagnates, which causes massive microthrombi to form - the basis for hemocoagulation disorders. There is a violation of the patency of the capillary wall, plasma leakage, and blood again flows in place of this plasma. This is an irreversible, terminal phase of shock, capillary tone is not restored, and cardiovascular failure progresses.

In other organs during shock, changes due to decreased blood supply (hypoperfusion) are secondary. The functional activity of the central nervous system is preserved, but complex functions are impaired as the brain is ischemic.

Shock is accompanied by respiratory failure, as there is hypoperfusion of blood in the lungs. Tachypnea and hyperpnea begin as a result of hypoxia. The so-called non-respiratory functions of the lungs (filtering, detoxification, hematopoietic) suffer; blood circulation in the alveoli is disrupted and the so-called “shock lung” occurs - interstitial edema. In the kidneys, a decrease in diuresis is initially observed, then acute renal failure occurs, “shock kidney”, since the kidney is very sensitive to hypoxia.

Thus, multiple organ failure quickly develops, and without taking urgent anti-shock measures, death occurs.

Shock clinic. In the initial period, excitement is often observed, the patient is euphoric, and does not realize the severity of his condition. This is the erectile phase and is usually short. Then comes the torpid phase: the victim becomes inhibited, lethargic, and apathetic. Consciousness is preserved until the terminal stage. The skin is pale and covered in cold sweat. For an ambulance paramedic, the most convenient way to roughly determine blood loss is by systolic blood pressure (SBP).

1. If SBP is 100 mm Hg, blood loss is no more than 500 ml.

2. If SBP is 90-100 mm Hg. Art. - up to 1 l.

3. If SBP is 70-80 mm Hg. Art. - up to 2 l.

4. If SBP is less than 70 mm Hg. Art. - more than 2 l.

Shock of the first degree - there may be no obvious hemodynamic disturbances, blood pressure is not reduced, the pulse is not increased.

Second degree shock - systolic pressure reduced to 90-100 mm Hg. Art., the pulse is rapid, the skin becomes pale, and the peripheral veins collapse.

III degree shock is a serious condition. SBP 60-70 mm Hg. Art., pulse increased to 120 per minute, weak filling. Severe pallor of the skin, cold sweat.

IV degree shock is an extremely serious condition. Consciousness is confused at first, then fades away. Against the background of pale skin, cyanosis and a spotted pattern occurs. SBP 60 mm Hg. Tachycardia is 140-160 per minute, the pulse is determined only in large vessels.

General principles of shock treatment:

1. Early treatment, as shock lasts 12-24 hours.

2. Etiopathogenetic treatment, i.e. treatment depending on the cause, severity, course of shock.

3. Complex treatment.

4. Differentiated treatment.

Urgent Care

1. Ensuring airway patency:

Slightly tilting the head back;

Removing mucus, pathological secretions or foreign bodies from the oropharynx;

Maintaining patency of the upper respiratory tract using an airway.

2. Breathing control. Carry out an excursion of the chest and abdomen. If there is no breathing, urgent artificial respiration “mouth to mouth”, “mouth to nose” or using portable breathing apparatus.

3. Control of blood circulation. Check the pulse in the large arteries (carotid, femoral, brachial). If there is no pulse, urgently perform indirect cardiac massage.

4. Providing venous access and starting infusion therapy.

For hypovolemic shock, isotonic sodium chloride solution or Ringer's solution is administered. If hemodynamics do not stabilize, then ongoing bleeding can be assumed (hemothorax, ruptures of parenchymal organs, fracture of the pelvic bones).

5. Stopping external bleeding.

6. Pain relief (promedol).

7. Immobilization for injuries of the limbs and spine.

8. Stopping the intake of allergen during anaphylactic shock.

In case of traumatic shock, first of all, it is necessary to stop the bleeding (if possible) by applying tourniquets, tight bandages, tamponade, applying clamps to the bleeding vessel, etc.

In case of shock of I-II degree, intravenous infusion of 400-800 ml of polyglucin is indicated, which is especially appropriate for preventing the deepening of shock when transporting over long distances is necessary.

In case of shock of I-III degree, after transfusion of 400 ml of polyglucin, 500 ml of Ringer's solution or 5% glucose solution should be transfused, and then resume the infusion of polyglucin. Add 60 to 120 ml of prednisolone or 125-250 ml of hydrocortisone to the solutions. In case of severe injury, infusion into two veins is advisable.

Along with infusions, pain relief should be carried out in the form of local anesthesia with a 0.25-0.5% solution of novocaine in the area of ​​fractures; if there is no damage to internal organs, or skull injuries, solutions of promedol 2% - 1.0-2.0, omnopon 2% - 1-2 ml or morphine 1% - 1-2 ml are administered intravenously.

In case of shock of III-IV degree, anesthesia should be performed only after transfusion of 400-800 ml of polyglucin or rheopolyglucin. Hormones are also administered: prednisolone (90-180 ml), dexamethasone (6-8 ml), hydrocortisone (250 ml).

You should not try to quickly raise blood pressure. The administration of pressor amines (mesaton, norepinephrine, etc.) is contraindicated.

For all types of shock, oxygen is inhaled. If the patient’s condition is extremely serious and there is a long distance to be transported, especially in rural areas, there is no need to rush. It is advisable to at least partially compensate for blood loss (BCB), carry out reliable immobilization, and stabilize hemodynamics if possible.

The classic description of shock made by I.I. Pirogov, was included in almost all shock manuals. For a long time, research on shock was carried out by surgeons. The first experimental work in this area was carried out only in 1867. Until now, there is no unambiguous definition of the concept of “shock” for pathophysiologists and clinicians. From the point of view of pathophysiology, the most accurate is the following: traumatic shock is a typical pathological process that occurs as a result of damage to organs, irritation of receptors and nerves of injured tissue, blood loss and the entry of biologically active substances into the blood, that is, factors that together cause excessive and inadequate reactions of adaptive systems, especially the sympathetic-adrenal system, persistent violations of the neuroendocrine regulation of homeostasis, especially hemodynamics, violations of specific functions of damaged organs, disorders of microcirculation, oxygen regime of the body and metabolism. It should be noted that the general etiology of traumatic shock in the form of a stable theory has not yet been developed. Nevertheless, there is no doubt that all the main factors of etiology take part in the development of shock: the traumatic factor, the conditions in which the injury was received, the body’s response. Environmental conditions are of great importance for the development of traumatic shock. Traumatic shock is promoted by: overheating, hypothermia, malnutrition, mental trauma (it has long been noted that in the defeated, shock develops faster and is more severe than in the winners).

The significance of the state of the body for the occurrence of shock (data are still scarce): 1. Heredity - these data are difficult to obtain in humans, but they are available in experimental animals. Thus, dogs’ resistance to injury depends on the breed. At the same time, dogs of pure lines are less resistant to injury than mongrels. 2. Type of nervous activity - animals with increased excitability are less resistant to injury and shock develops after a minor injury. 3. Age – shock is easier to get in young animals (puppies) and more difficult to treat than in adults. In old and senile age, trauma affects a significantly weakened body, characterized by the development of vascular sclerosis, hyporeactivity of the nervous system, endocrine system, so shock develops more easily and mortality is higher. 4. Diseases preceding the injury. The development of shock is promoted by: hypertension; neuropsychic stress; physical inactivity; blood loss preceding the injury. 5. Alcohol intoxication - on the one hand, increases the likelihood of injury (nervous dysfunction), and at the same time is used as an anti-shock liquid. But even here it should be remembered that with chronic alcoholism, changes are observed in the nervous and endocrine systems, leading to a decrease in resistance to injury. Discussing the role of various pathogenetic moments in the origin of traumatic shock, most researchers note the different times of their inclusion in the general mechanism of development of the process and their unequal significance in different periods of shock. Thus, it is quite obvious that consideration of traumatic shock is unthinkable without taking into account its dynamics - its phase development.

There are two phases in the development of traumatic shock: erectile, occurring after the injury and manifested by activation of functions, and torpid, expressed by inhibition of functions (both phases were described by N.I. Pirogov, and substantiated by N.N. Burdenko). The erectile phase of shock (from the Latin erigo, erectum - straighten, raise) is a phase of generalized excitation. In recent years it has been called adaptive, compensatory, non-progressive, early. During this phase, activation of specific and nonspecific adaptive reactions is observed. It is manifested by pallor of the integument and mucous membranes, increased arterial and venous pressure, tachycardia; sometimes urination and defecation. These reactions have an adaptive orientation. They provide, under extreme conditions, the delivery of oxygen and metabolic substrates to tissues and organs, and the maintenance of perfusion pressure. As the degree of damage increases, these reactions become excessive, inadequate and uncoordinated, which significantly reduces their effectiveness. This largely determines the severe or even irreversible self-aggravating course of shock conditions. Consciousness is not lost during shock. Usually there is nervous, mental and motor arousal, manifested by excessive fussiness, agitated speech, increased responses to various stimuli (hyperreflexia), and screaming. In this phase, as a result of generalized excitation and stimulation of the endocrine apparatus, metabolic processes are activated, while their circulatory support is insufficient. In this phase, prerequisites arise for the development of inhibition in the nervous system, circulation disorders, and oxygen deficiency occurs. The erectile phase is short-lived and usually lasts minutes. If the adaptation processes are insufficient, the second stage of shock develops.

The torpid phase of shock (from the Latin torpidus - sluggish) is a phase of general inhibition, manifested by physical inactivity, hyporeflexia, significant circulatory disorders, in particular arterial hypotension, tachycardia, respiratory disorders (tachypnea at the beginning, bradypnea or periodic breathing at the end), oliguria, hypothermia etc. In the torpid phase of shock, metabolic disorders are aggravated due to disorders of neurohumoral regulation and circulatory support. These disorders are not the same in different organs. The torpid phase is the most typical and prolonged phase of shock; its duration can range from several minutes to many hours. Currently, the torpid phase is called the stage of disadaptation (decompensation). At this stage, two substages are distinguished: progressive (consisting in the depletion of compensatory reactions and tissue hypoperfusion) and irreversible (during which changes incompatible with life develop).

In addition to the erectile and torpid phases of traumatic shock in severe shock ending in death, it is advisable to distinguish the terminal phase of shock, thereby emphasizing its specificity and difference from the pre-mortem stages of other pathological processes, usually united by the general term “terminal conditions”. The terminal phase is characterized by certain dynamics: it begins to be revealed by disorders of external respiration (Biot or Kussmaul breathing), instability and a sharp decrease in blood pressure, and slowing of the pulse. The terminal phase of shock is characterized by a relatively slow development, and therefore a greater depletion of adaptation mechanisms, more significant than, for example, with blood loss, intoxication, and more profound dysfunction of organs. The restoration of these functions during therapy occurs more slowly.

Traumatic shock should be classified according to the time of development and severity. Based on the time of development, primary shock and secondary shock are distinguished. Primary shock develops as a complication soon after the injury and may subside or lead to the death of the victim. Secondary shock usually occurs several hours after the patient recovers from primary shock. The cause of its development is most often additional trauma due to poor immobilization, difficult transportation, premature surgery, etc. Secondary shock is much more severe than primary shock, since it develops against the background of very low adaptive mechanisms of the body, which were exhausted in the fight against primary shock, therefore mortality in secondary shock is significantly higher. According to the severity of the clinical course, mild shock, moderate shock and severe shock are distinguished. Along with this, shock is divided into four degrees. This division is based on the level of systolic blood pressure. I degree of shock is observed when the maximum blood pressure is above 90 mm Hg. Art. – mild stupor, tachycardia up to 100 beats/min, urination is not impaired. Blood loss: 15–25% of the total blood volume. II degree – 90–70 mm Hg. Art., stupor, tachycardia up to 120 beats/min, oliguria. Blood loss: 25–30% of the total blood volume. III degree – 70–50 mm Hg. Art., stupor, tachycardia more than 130–140 beats/min, no urination. Blood loss: more than 30% of the total blood volume. IV degree – below 50 mm Hg. Art., coma, pulse in the periphery is not detected, the appearance of pathological breathing, multiple organ failure, areflexia. Blood loss: more than 30% of the total blood volume. Should be regarded as a terminal condition. The clinical picture of shock is influenced by the type of nervous system, gender, age of the victim, concomitant pathology, infectious diseases, and a history of trauma accompanied by shock. An important role is played by blood loss, dehydrating diseases and conditions that affect the blood volume and lay the basis for hemodynamic disorders. A certain idea about the degree of decrease in blood volume and the depth of hypovolemic disorders allows us to obtain a shock index. It can be calculated using the following formula: shock index = pulse rate / systolic blood pressure. Normally, the shock index is 0.5. In the case of an increase in the index to 1 (pulse and blood pressure are equal to 100), the approximately decrease in blood volume is equal to 30% of the expected value; when it increases to 1.5 (pulse is 120, blood pressure is 80) the blood volume is 50% of the expected value, and with shock index values 2.0 (pulse – 140, blood pressure – 70), the volume of circulating blood in active circulation is only 30% of what it should be, which, of course, cannot provide adequate perfusion of the body and leads to a high risk of death for the victim. The main pathogenetic factors of traumatic shock can be identified as follows: inadequate impulses from damaged tissues; local blood and plasma loss; the entry into the blood of biologically active substances resulting from cell destruction and oxygen starvation of tissues; loss or dysfunction of damaged organs. Moreover, the first three factors are nonspecific, that is, inherent in any injury, and the last characterizes the specificity of the injury and the shock that develops.

In its most general form, the pathogenesis of shock is presented as follows. The traumatic factor acts on organs and tissues, causing their damage. As a result, cell destruction occurs and their contents escape into the intercellular environment; other cells are subject to contusion, as a result of which their metabolism and inherent functions are disrupted. Primary (due to the action of a traumatic factor) and secondary (due to changes in the tissue environment) numerous receptors in the wound are irritated, which is subjectively perceived as pain, but objectively characterized by numerous reactions of organs and systems. Inadequate impulses from damaged tissues have a number of consequences. 1. As a result of inadequate impulses from damaged tissues, a pain dominant is formed in the nervous system, which suppresses other functions of the nervous system. Along with this, a typical defensive reaction occurs with stereotypical autonomic accompaniment, since pain is a signal to flee or fight. The most important components of this autonomic reaction are: the release of catecholamines, increased blood pressure and tachycardia, increased breathing, activation of the hypothalamic-pituitary-adrenal system. 2. The effects of painful stimulation depend on its intensity. Weak and moderate irritation causes stimulation of many adaptive mechanisms (leukocytosis, phagocytosis, increased function of the SFM, etc.); strong irritations inhibit adaptive mechanisms. 3. Reflex tissue ischemia plays an important role in the development of shock. In this case, under-oxidized products accumulate, and the pH decreases to values ​​borderline acceptable for life. On this basis, microcirculation disorders, pathological blood deposition, and arterial hypotension occur. 4. Pain and the entire situation at the time of injury certainly cause emotional stress, mental tension, and a feeling of anxiety about danger, which further enhances the neurovegetative reaction.

The role of the nervous system. When the body is exposed to a damaging mechanical agent in the damaged area, various nerve elements are irritated, not only receptors, but also other elements - nerve fibers passing through the tissues that are part of the nerve trunks. While the receptors have a certain specificity in relation to the stimulus, characterized by differences in the threshold value for different stimuli, the nerve fibers in relation to mechanical stimulation do not differ so sharply from each other, therefore mechanical stimulation causes excitation in conductors of various types of sensitivity, and not only painful or tactile. This is precisely why injuries accompanied by crushing or rupture of large nerve trunks are characterized by more severe traumatic shock. The erectile phase of shock is characterized by generalization of excitation, which is externally manifested in motor restlessness, speech excitation, screaming, and increased sensitivity to various stimuli. Excitation also covers the autonomic nerve centers, which is manifested by an increase in the functional activity of the endocrine apparatus and the release of catecholamines, adaptive and other hormones into the blood, stimulation of heart activity and an increase in the tone of resistance vessels, activation of metabolic processes. Prolonged and intense impulses from the site of injury, and then from organs with impaired functions, changes in the lability of nerve elements due to disorders of blood circulation and oxygen regime determine the subsequent development of the inhibitory process. The irradiation of excitation—its generalization—is a necessary prerequisite for the occurrence of inhibition. Of particular importance is the fact that inhibition in the zone of the reticular formation protects the cerebral cortex from the flow of impulses from the periphery, which ensures the safety of its functions. At the same time, elements of the reticular formation that facilitate the conduction of impulses (RF+) are more sensitive to circulatory disorders than those that inhibit the conduction of impulses (RF–). It follows from this that circulatory disorders in this area should contribute to a functional blockade of impulse conduction. Gradual inhibition extends to other levels of the nervous system. It tends to deepen due to impulses from the area of ​​injury.

The role of the endocrine system.
Traumatic shock is also accompanied by changes in the endocrine system (in particular, the hypothalamic-pituitary-adrenal system). During the erectile phase of shock, the content of corticosteroids in the blood increases, and during the torpid phase, their amount is reduced. However, the adrenal cortex remains responsive to externally administered ACTH. Consequently, the inhibition of the cortical layer is largely due to the insufficiency of the pituitary gland. Hyperadrenalineemia is very typical for traumatic shock. Hyperadrenalineemia, on the one hand, is a consequence of intense afferent impulses caused by damage, on the other hand, a reaction to the gradual development of arterial hypotension.

Local blood and plasma loss.
With any mechanical injury, there is a loss of blood and plasma, the extent of which is very variable and depends on the degree of tissue trauma, as well as on the nature of vascular damage. Even with a minor injury, exudation into the injured tissue is observed due to the development of an inflammatory reaction, and hence loss of fluid. However, the specificity of traumatic shock is still determined by neuropainful injury. Neuropainful injury and blood loss are synergistic in their effect on the cardiovascular system. With painful stimulation and loss of blood, vasospasm and the release of catecholamines first occur. With blood loss immediately, and with painful stimulation later, the volume of circulating blood decreases: in the first case due to exit from the vascular bed, and in the second - as a result of pathological deposition. It should be noted that even small bloodletting (1% of body weight) sensitizes (increases the body’s sensitivity) to mechanical damage.

Circulatory disorders.
The very concept of “shock” includes obligatory and severe hemodynamic disturbances. Hemodynamic disturbances during shock are characterized by sharp deviations in many parameters of the systemic circulation. Disorders of systemic hemodynamics are characterized by three cardinal signs - hypovolemia, decreased cardiac output and arterial hypotension. Hypovolemia has always been considered important in the pathogenesis of traumatic shock. On the one hand, it is caused by blood loss, and on the other, by the retention of blood in capacitive vessels (venules, small veins), capillaries - by its deposition. The exclusion of some blood from circulation can be clearly detected already at the end of the erectile shock phase. By the beginning of the development of the torpid phase, hypovolemia is even more pronounced than in subsequent periods. One of the most typical symptoms of traumatic shock is phase changes in blood pressure - its increase in the erectile phase of traumatic shock (the tone of resistive and capacitive vessels increases, as evidenced by arterial and venous hypertension), as well as a short-term increase in the volume of circulating blood, combined with a decrease in the capacity of the functioning vascular bed of organs. The increase in blood pressure, typical for the erectile phase of traumatic shock, is the result of an increase in total peripheral vascular resistance due to activation of the sympathoadrenal system. An increase in the tone of resistive vessels is combined with the activation of arteriovenous anastomoses and the rejection of blood from the system of high pressure vessels (arterial bed) into the system of low pressure vessels (venous bed), which leads to an increase in venous pressure and prevents the outflow of blood from the capillaries. If we take into account the fact that most capillaries do not have sphincters at their venous end, then it is not difficult to imagine that under such conditions not only direct, but also retrograde filling of the capillaries is possible. Numerous researchers have shown that hypovolemia limits afferent impulses from baroreceptors (stretch receptors) of the aortic arch and sinocarotid zone, as a result of which the pressor formations of the vasomotor center are excited (disinhibited) and spasm of arterioles occurs in many organs and tissues. Sympathetic efferent impulses to the blood vessels and heart are enhanced. As blood pressure decreases, tissue blood flow decreases, hypoxia increases, which causes impulses from tissue chemoreceptors and further activates the sympathetic effect on the vessels. The heart empties more completely (residual volume decreases), and tachycardia also occurs. A reflex also arises from the vascular baroreceptors, leading to an increased release of adrenaline and norepinephrine by the adrenal medulla, the concentration of which in the blood increases 10-15 times. In a later period, when renal hypoxia develops, vascular spasm is maintained not only by increased secretion of catecholamines and vasopressin, but also by the release of renin by the kidneys, which is the initiator of the renin-angiotensin system. It is believed that this generalized vasoconstriction does not involve the vessels of the brain, heart and liver. Therefore, this reaction is called centralization of blood circulation. Peripheral organs are increasingly suffering from hypoxia, as a result of which metabolism is disrupted and under-oxidized products and biologically active metabolites appear in the tissues. Their entry into the blood leads to acidosis of the blood, as well as the appearance in it of factors that specifically inhibit the contractility of the heart muscle. Another mechanism is also possible here. The development of tachycardia leads to a reduction in diastole time - the period during which coronary blood flow occurs. All this leads to disruption of myocardial metabolism. With the development of the irreversible stage of shock, the heart can also be affected by endotoxins, lysosomal enzymes and other biologically active substances specific to this period. Thus, blood and plasma loss, pathological blood deposition, and fluid extravasation lead to a decrease in the volume of circulating blood and a decrease in venous blood return. This, in turn, along with metabolic disorders in the myocardium and a decrease in the performance of the heart muscle leads to hypotension, characteristic of the torpid phase of traumatic shock. Vasoactive metabolites that accumulate during tissue hypoxia disrupt the function of vascular smooth muscles, which leads to a decrease in vascular tone, and therefore to a drop in the overall resistance of the vascular bed and, again, to hypotension.
Disorders of capillary blood flow deepen as a result of a violation of the rheological properties of blood, aggregation of red blood cells, which occurs as a result of increased activity of the coagulation system and thickening of the blood due to the release of fluid into the tissue. Breathing disorders. In the erectile stage of traumatic shock, frequent and deep breathing is observed. The main stimulating factor is irritation of the receptors of injured tissues, which causes stimulation of the cerebral cortex and subcortical centers, and the respiratory center of the medulla oblongata is also excited.
In the torpid phase of shock, breathing becomes more rare and superficial, which is associated with depression of the respiratory center. In some cases, as a result of progressive brain hypoxia, periodic respiration of the Cheyne-Stokes or Biot type appears. In addition to hypoxia, various humoral factors have an inhibitory effect on the respiratory center - hypocapnia (caused by hyperventilation - but later CO2 accumulates), low pH. The development of hypoxia, one of the very important aspects of the pathogenesis of traumatic shock, is closely related to circulatory and respiratory disorders. In the genesis of shock hypoxia, the hemic component also occupies a certain place, caused by a decrease in the oxygen capacity of the blood due to its dilution and aggregation of red blood cells, as well as external respiration disorders, but the main importance still belongs to tissue perfusion and the redistribution of blood flow between terminal vessels.

Abnormalities in the lungs and the effects they cause are combined into a symptom complex called respiratory distress syndrome. This is an acute disorder of pulmonary gas exchange with life-threatening severe hypoxemia as a result of a decrease to a critical level and below the number of normal respirons (respiron is a terminal or final respiratory unit), which is caused by negative neurohumoral influences (neurogenic spasm of pulmonary microvessels with pathological pain), damage to the pulmonary capillary endothelium with cytolysis and destruction of intercellular connections, migration of blood cells (primarily leukocytes), plasma proteins into the pulmonary membrane, and then into the lumen of the alveoli, the development of hypercoagulation and thrombosis of the pulmonary vessels.

Metabolic disorders. Energy exchange.
Shock of various etiologies through microcirculation disorders and destruction of the histohematic barrier (exchange capillary - interstitium - cell cytosol) critically reduces oxygen delivery to mitochondria. As a result, rapidly progressing disorders of aerobic metabolism occur. The links in the pathogenesis of dysfunctions at the level of mitochondria in shock are: - swelling of mitochondria; - disorders of mitochondrial enzyme systems due to a deficiency of necessary cofactors; - decrease in magnesium content in mitochondria; - increase in calcium content in mitochondria; - pathological changes in the content of sodium and potassium in mitochondria; - disorders of mitochondrial functions due to the action of endogenous toxins (free fatty acids, etc.); - free radical oxidation of mitochondrial membrane phospholipids. Thus, during shock, the accumulation of energy in the form of high-energy phosphorus compounds is limited. A large amount of inorganic phosphorus accumulates, which enters the plasma. Lack of energy disrupts the function of the sodium-potassium pump, causing excess sodium and water to enter the cell and potassium to leave the cell. Sodium and water cause mitochondria to swell, further uncoupling respiration and phosphorylation. As a result of decreased energy production in the Krebs cycle, the activation of amino acids is limited, and as a result, protein synthesis is inhibited. A decrease in ATP concentration slows down the combination of amino acids with ribonucleic acids (RNA), the function of ribosomes is disrupted, resulting in the production of abnormal, incomplete peptides, some of which may be biologically active. Severe acidosis in the cell causes rupture of lysosome membranes, as a result of which hydrolytic enzymes enter the protoplasm, causing the digestion of proteins, carbohydrates, and fats. The cell dies. As a result of insufficient cell energy and metabolic disorders, amino acids, fatty acids, phosphates, and lactic acid enter the blood plasma. Apparently, mitochondrial dysfunctions (like any pathological processes) develop in different organs and tissues asynchronously, mosaically. Damage to mitochondria and disorders of their functions are especially pronounced in hepatocytes, while in neurons of the brain they remain minimal even in decompensated shock.
It should be noted that mitochondrial damage and dysfunction are reversible in compensated and decompensated shock and are reversed by rational analgesia, infusions, oxygen therapy and hemorrhage control. Carbohydrate metabolism. During the erectile phase of traumatic shock, the concentration of insulin antagonists, catecholamines, which stimulate the breakdown of glycogen, glucocorticoids, which enhance the processes of gluconeogenesis, thyroxine and glucagon in the blood increases as a result of increased activity of the endocrine glands. In addition, the excitability of the sympathetic nervous system (hypothalamic centers) is increased, which also contributes to the development of hyperglycemia. In many tissues, glucose consumption is inhibited. In general, a false-diabetic picture is revealed. In the later stages of shock, hypoglycemia develops. Its origin is associated with the complete use of liver glycogen reserves available for consumption, as well as a decrease in the intensity of gluconeogenesis due to the use of substrates necessary for this and relative (peripheral) corticosteroid deficiency.
Lipid metabolism. Changes in carbohydrate metabolism are closely associated with lipid metabolism disorders, which manifest themselves in the torpid phase of shock as ketonemia and ketonuria. This is explained by the fact that fats (as one of the main energy sources) are mobilized from the depot during shock (their concentration in the blood increases), and oxidation is not complete.
Protein metabolism. A manifestation of its disturbance is an increase in the content of non-protein nitrogen in the blood, mainly due to polypeptide nitrogen and, to a lesser extent, urea nitrogen, the synthesis of which is disrupted with the development of shock. Changes in the composition of serum proteins during traumatic shock are expressed by a decrease in their total amount, mainly due to albumin. The latter may be associated both with metabolic disturbances and with changes in vascular permeability. It should be noted that with the development of shock, the content of α-globulins in the serum increases, which, as is known, is directly related to the vasoactive properties of the blood. The accumulation of nitrogenous products and changes in the ionic composition of plasma contribute to impaired renal function. Oliguria, and in severe cases of shock, anuria are constant during this process. Renal dysfunction usually corresponds to the severity of shock. It is known that with a decrease in blood pressure to 70-50 mm Hg. Art. the kidneys completely stop filtering in the glomerular apparatus of the kidney due to changes in the relationships between hydrostatic, colloidosmotic and capsular pressure. However, in traumatic shock, renal dysfunction is not solely a consequence of arterial hypotension: shock is characterized by limitation of cortical circulation due to increased vascular resistance and shunting through the juxtaglomerular pathways. This is determined not only by a decrease in cardiac performance, but also by an increase in the tone of the vessels of the cortical layer.
Ion exchange. Significant shifts are detected in the ionic composition of the plasma. With traumatic shock, a gradual convergence occurs, the concentration of ions in the cells and extracellular fluid, while normally the ions K+, Mg2+, Ca2+, HPO42-, PO43- predominate in the cells, and in the extracellular fluid Na+, C1-, HCO3-. Receipt of biologically active substances into the blood. For the subsequent course of the process, the release of active amines from cells, which are chemical mediators of inflammation, is of great importance. Currently, over 25 such mediators have been described. The most important of them, appearing immediately after damage, are histamine and serotonin. With extensive tissue damage, histamine can enter the general bloodstream, and since histamine causes dilation of precapillaries and venous spasm without directly affecting the capillary bed, this leads to a decrease in peripheral vascular resistance and a drop in blood pressure. Under the influence of histamine, channels and gaps are formed in the endothelium, through which blood components, including cellular elements (leukocytes and erythrocytes), penetrate into the tissues. As a result of this, exudation and intercellular edema occur. Under the influence of injury, the permeability of vascular and tissue membranes increases, but still, due to circulatory disorders, the absorption of various substances from injured tissues slows down. Enzymes of lysosomes of tissue cells and neutrophils play a major role in the development of secondary alteration. These enzymes (hydrolases) have pronounced proteolytic activity. Along with these factors, plasma kinins (bradykinin), as well as prostaglandins, play a certain role in circulatory disorders. These factors also affect the microcirculation system, causing expansion of arterioles, capillaries and an increase in their permeability, which occurs first (mainly in venules) due to the formation of intercellular gaps and transendothelial channels. Later, the permeability of the capillary and precapillary sections of the vascular bed changes.

A few words about wound toxemia. The issue of wound toxin has not been finally resolved. However, it is firmly established that toxic substances cannot enter the blood from injured tissues, because reabsorption in them is reduced. The source of toxic substances is the extensive zone of tissue contusion around the wound channel. It is in this zone that under the influence of potassium, histamine, serotonin, lysosomal enzymes, ATP, AMP, vascular permeability sharply increases. The toxin is formed within 15 minutes after ischemia, but has a relative molecular weight of 12,000 and is a product of intense protein breakdown. Administration of this toxin to intact animals leads to hemodynamic disorders typical of shock. The vicious circles that form during traumatic shock can be represented in the form of a diagram shown in Figure 1. Fig. 1. The main vicious circles in shock. Dysfunctions of damaged organs. Most researchers consider shock to be a functional pathology, although an organic component always plays a role in etiology and pathogenesis, which includes a decrease in the volume of circulating blood and, consequently, a decrease in the number of red blood cells.
A significant factor complicating the analysis of the pathogenesis of shock in the clinic is the presence of organic damage, which can accelerate the development of shock and modify its course. Thus, damage to the lower extremities, limiting the mobility of the wounded, forces them to take a horizontal position, often on the cold ground, which, causing general cooling, provokes the development of shock. When the maxillofacial area is injured, victims lose a large amount of saliva, and along with it water and protein, which, when it is difficult to take liquids and food, contributes to the development of hypovolemia and blood thickening. With traumatic brain injuries, symptoms of brain dysfunction occur, consciousness is lost, and excessive vascular spasm occurs, which often masks hypovolemia. When the pituitary gland is damaged, neuroendocrine regulation is sharply disrupted, which in itself causes the development of shock and complicates the course of the post-shock period. Fundamentals of pathogenetic therapy of shock The complexity of the pathogenesis of traumatic shock, the variety of disturbances in the functioning of many body systems, and differences in ideas about the pathogenesis of shock determine a significant difference in recommendations for the treatment of this process. We will focus on established things. Experimental studies allow us to determine possible directions in the prevention of traumatic shock. For example, the use of certain drug complexes before severe mechanical injury prevents the development of shock. Such complexes include the combined use of drugs (barbiturates), hormones, and vitamins. Long-term stimulation of the pituitary gland-adrenal cortex system with the introduction of ACTH increases the resistance of animals to shockogenic injury; the introduction of ganglion blockers also has a preventive effect. However, situations in which shock prevention is appropriate may not occur very often. Much more often we have to deal with the treatment of developed traumatic shock and, unfortunately, not always in its early periods, but in most cases in its later stages. The basic principle of treating shock is the complexity of therapy. Taking into account the phases of shock development is important in the treatment of shock. The treatment carried out should be as fast and vigorous as possible. This requirement also determines the methods of administration of certain medications, most of which are administered directly into the vascular bed. When treating shock in the erectile phase, when circulatory disorders have not yet fully developed, deep hypoxia and advanced metabolic disorders have not yet occurred, measures should be limited to preventing their development. During this phase, means that limit afferent impulses are widely used; various types of novocaine blockades, analgesics, neuroplegics, narcotic substances. Analgesics that inhibit impulse transmission, suppress autonomic reactions, and limit the feeling of pain are indicated in early periods of shock. An important point limiting impulses from the site of damage is rest of the damaged area (immobilization, bandages, etc.). In the erectile phase of shock, it is recommended to use saline solutions containing neurotropic and energetic substances (Popov, Petrov, Filatov liquids, etc.). Significant disorders of circulation, tissue respiration and metabolism that occur in the torpid phase of shock require various measures aimed at their correction. To correct circulatory disorders, blood transfusions or blood substitutes are used. In severe shock, intra-arterial transfusions are more effective. Their high effectiveness is associated with stimulation of vascular receptors, increased capillary blood flow and the release of part of the deposited blood. Due to the fact that during shock there is predominantly deposition of formed elements and their aggregation, it seems very promising to use low-molecular colloidal plasma substitutes (dextrans, polyvinol), which have a disaggregating effect and reduce blood viscosity at low shear stresses. Caution should be exercised when using vasopressor agents. Thus, the introduction of one of the most common vasopressor substances, norepinephrine, in the initial period of the torpid phase slightly increases the minute volume of blood circulation due to the release of part of the deposited blood and improves blood supply to the brain and myocardium. The use of norepinephrine in later periods of shock even aggravates the centralization of blood circulation characteristic of it. Under these conditions, the use of norepinephrine is advisable only as an “emergency” remedy. The use of saline plasma-substituting solutions, although it leads to a temporary revival of blood flow, still does not provide a long-term effect. These solutions, with significant disturbances in capillary blood flow and changes in the ratios of colloid-osmotic and hydrostatic pressures characteristic of shock, leave the vascular bed relatively quickly. Hormones - ACTH and cortisone, administered to normalize metabolic processes, have a noticeable effect on blood flow during traumatic shock. During the development of shock, relative and then absolute adrenal insufficiency is detected first. In light of these data, the use of ACTH appears to be more appropriate in the early stages of shock or in its prevention. Glucocorticoids administered in the torpid phase have a diverse effect. They change the response of blood vessels to vasoactive substances, in particular they potentiate the effect of vasopressors. In addition, they reduce vascular permeability. And yet, their main effect is associated with the influence on metabolic processes and, above all, on the metabolism of carbohydrates. Restoration of oxygen balance in conditions of shock is ensured not only by restoration of circulation, but also by the use of oxygen therapy. Recently, oxygen barotherapy has also been recommended. In order to improve metabolic processes, vitamins are used (ascorbic acid, thiamine, riboflavin, pyridoxine, calcium pangamate). Due to the increased resorption of biogenic amines and, above all, histamine from damaged tissues, the use of antihistamines may be important in the treatment of traumatic shock. An essential place in the treatment of shock is occupied by the correction of acid-base balance. Acidosis is typical of traumatic shock. Its development is determined by both metabolic disorders and the accumulation of carbon dioxide. The development of acidosis is also facilitated by disruption of excretory processes. To reduce acidosis, the use of sodium bicarbonate is recommended; some consider the use of sodium lactate or Tris buffer to be better.

Traumatic shock– a syndrome that occurs with severe injuries; characterized by a critical decrease in blood flow in tissues (hyperfusion) and is accompanied by clinically pronounced circulatory and respiratory disorders.

Traumatic shock occurs: a) as a result of mechanical trauma (wounds, bone fractures, tissue compression, etc.); b) due to burn injury (thermal and chemical burns); c) when exposed to low temperature - cold shock; d) as a result of electrical injury - electric shock.

Types of traumatic shock:- wound shock (cerebral, pleuropulmonary, visceral, with multiple wounds of the limb, combined); - operating; - hemorrhagic; - combined.

Pathogenesis: In the development of traumatic shock, the main pathogenetic factors are the pain factor and blood loss (plasma loss), which lead to acute vascular insufficiency with microcirculation disorder and the development of tissue hypoxia. Not only the total volume of blood loss matters, but also the rate of bleeding. At slow

Blood loss\Bcc by 20-30% causes noticeable\BP, and with rapid blood loss, its decrease by 30% can lead to death. A decrease in blood volume (hypovolemia) is the main pathogenetic link of traumatic shock.

Shock phases: 1 – Erectile phase– short, occurs immediately after injury, characterized by tension of the sympathetic-adrenal system. The skin is pale, the pulse is frequent, blood pressure is elevated, the patient is excited. 2 – Torpid phase– lethargy, blood pressure, thready pulse .

4 degrees of torpid phase of shock.

I degree – consciousness is preserved, the patient is communicative, slightly inhibited. SBP decreased to 90 mm Hg. Art, pale skin. When pressing with a finger on the nail bed, the restoration of blood flow is slowed down.

P degree - the patient is lethargic, the skin is pale, cold, sticky sweat, cyanosis of the nail bed; when pressed with a finger, blood flow is restored very slowly. SBP decreased to 90-70 mm Hg. Art. Pulse is weak, 110-120 per minute, central venous pressure is reduced, shallow breathing

Grade III is a serious condition: he is adynamic, inhibited, and does not respond to pain. The skin is pale, cold, with a bluish tint. Breathing is shallow and frequent. The pulse is frequent, up to 130-140 per minute. SBP 70-50 mm Hg. Art. CVP ~ O or negative. Urination stops.

IV degree – preagonal state: the skin and mucous membranes are pale, with a bluish tint, breathing is frequent, shallow, pulse is rapid, weak filling, SBP - 50 mm Hg. Art. and below.

Treatment: first aid: 1 – stopping bleeding (applying a tourniquet, tight bandage, squeezing the damaged vessel), 2 – ensuring airway patency (turn the victim’s head to one side, clean the mouth, tilt his head back or move the lower jaw forward; it is possible to use an air duct) , 3 – transfusion therapy (polyglucin, rheopolyglucin, gelatinol), 4 – adequate pain relief (non-narcotic – analgin, ketorol; and narcotic analgesics – promedol, omnopon; nitrous oxide with O2 1:1), 5 – immobilization for fractures (splint) , gentle transportation. TREATMENT OF TRAUMATIC SHOCK At the scene of the incident: 1. Termination of the traumatic factor. 2. Temporary stop of bleeding. 3. Restoration of patency of the upper respiratory tract; if necessary, mechanical ventilation and closed cardiac massage. 4. Closing the wound with an aseptic dressing.
5. Pain relief; blockade, therapeutic anesthesia, administration of promedol, fentanyl, diprazine, suprastin. Narcotic analgesics are not administered for traumatic brain injury, respiratory depression, or suspected damage to the abdominal organs; if there are clear signs of damage to intra-abdominal organs, drug administration is advisable. The best pain relief is anesthesia at the analgesic stage. 6. Immobilization and rational positioning of the patient. 7. Preventing the victim from cooling down, wrapping him in a blanket, clothes, warming him up (you can give the victim hot tea if an abdominal injury is excluded). 8. Intravenous administration of blood substitutes. After emergency measures, with the continued administration of blood substitutes, oxygen inhalation or anesthesia, transportation of the victim can begin. It is important to prevent the shock from deepening under the influence of inevitable additional injuries and to reduce the severity of disorders that pose an immediate threat to life.

The term “shock,” as noted in all scientific works, was introduced by James Latta (1795). However, there are indications that already before Lyatt, at the beginning of the 18th century, the French scientist and physician Le Dran not only described the main features of traumatic shock, but also systematically used the term “shock” in his writings. To treat shock, Le Dran recommended warming, resting the patient, alcoholic drinks, opium, i.e. those means of combating shock that are still used today (E. A. Asratyan).
In Russia, already in 1834, P. Savenko correctly assessed the state of shock as a severe lesion of the nervous system and pointed out that with severe and widespread burns that “kill” the patient, “the container of painful irritation is the general sensory,” i.e., the brain. For the first time in the world, N. I. Pirogov correctly understood the pathogenesis of shock, classically describing it and outlining methods of prevention and treatment. He distinguished erectile shock from torpid shock, saw the difference between shock and collapse, which some foreign scientists dispute, etc.

The teaching of I. M. Sechenov and his students - I. P. Pavlov and N. E. Vvedensky - about the role of the central nervous system as the main factor determining the development, nature, forms, phases of shock phenomena and, accordingly, the construction of a method for treating shock - the first a necessary condition in understanding shock and in organizing pathogenetic treatment.
The merit of Soviet surgeons and physiologists is a correctly, methodologically constructed doctrine of shock, based not only on analysis, but also on the synthesis of clinical and experimental data. The problem of shock was most intensively dealt with by N. N. Burdenko, A. V. Vishnevsky, E. A. Asratyan, Yu. Yu. Dzhanelidze, S. I. Banaitis, I. R. Petrov, B. N. Postnikov, G. F. Lang et al. They accumulated clinical, laboratory and experimental material. During the Great Patriotic War, shock treatment methods were tested comprehensively by teams of specialists.
Thanks to the participation of physiologists and pathologists in the development of the problem of shock, a solid basis was laid for the synthesis of the data obtained, based on the principles of nervism, the principles of I. P. Pavlov on the therapeutic and protective role of inhibition. Numerous conferences and congresses of surgeons, meetings of scientific councils with the participation of N. N. Burdenko, M. N. Akhutin, S. I. Banaitis, A. A. Vishnevsky and others, conferences of clinicians, physiologists, pathophysiologists and pathologists made it possible to find out the main issues of pathogenesis and therapy of shock.
The clinical picture of shock is vividly described by N. I. Pirogov. “With a torn off leg or arm, a numb person lies motionless at a dressing station; he does not shout, does not yell, does not complain, does not take part in anything and does not demand anything; the body is cold, the face is pale, like a corpse; the gaze is motionless and directed into the distance, the pulse, like a thread, is barely noticeable under the finger and with frequent alternations. The numb person either doesn’t answer questions at all, or only in a barely audible whisper to himself; breathing is also barely noticeable. The wound and skin are almost completely insensitive; but if the diseased nerve hanging from the wound is irritated by something, then the patient with one slight contraction of the personal muscles reveals a sign of feeling. Sometimes this condition disappears within a few hours from the use of stimulants, sometimes it continues until death.”
From this description, the following symptoms of shock are visible: sharp depression of the psyche, apathy, indifference to the environment while maintaining the patient’s consciousness, depression of the centers of the nervous and cardiovascular system, small, rapid pulse, pallor, cold sweat, drop in temperature, drop in blood pressure. These symptoms are accompanied by oxygen starvation of tissues (hypoxia), oliguria and anuria, changes in blood composition, increased quality of red blood cells, decreased amount of blood plasma, metabolic disorders, and acidosis. Consciousness is always preserved.