Shock

SHOCK (from the English shock - impact, concussion). To give a precise definition of shock is difficult, since this term often denotes different states of the body of various etiological origins. For example, one speaks of traumatic shock, operational shock (essentially the same as traumatic), psychic shock, shock from overexertion during exhaustion, infectious shock, shock from large blood losses, anaphylactic shock, hemolytic shock, etc. In all these cases, shock is understood as that severe general disorder of all bodily functions which develops after strong and severe mental shocks and physical injuries and is characterized by a definite clinical picture - paleness of the external coverings, fall in blood pressure, frequent small pulse, shallow breathing, low temperature, etc. Wars, which are traumatic pandemics, injuries in peacetime conditions, as well as the daily work of surgeons have provided and continue to provide abundant material for the study, first of all, of traumatic shock, the clinical picture of which was already classically described by Pirogov in the 1870s under the name traumatic stupor or torpor. "With a torn-off arm or leg, such a stiffened person lies motionless on a dressing station; he does not cry, does not wail, does not complain, takes no part in anything and demands nothing; the body is cold, the face is pale as a corpse; the gaze is motionless and directed into the distance; the pulse, like a thread, is barely perceptible under the finger and with frequent interruptions. To the questions, the stiffened person either does not answer at all or only to himself, in a barely audible whisper, breathing is also barely perceptible. The wound and skin are almost insensitive; but if a large nerve hanging from the wound is irritated by something, the patient with a slight contraction of the facial muscles reveals a sign of feeling. Sometimes this state passes after a few hours from the use of stimulating agents, sometimes it continues unchanged until death." Almost 60 years later, after the world war, the American physiologist Cannon, who worked extensively on the question of traumatic shock, only supplements Pirogov's described clinical picture of shock with modern scientific data: the patient in shock is apathetic, sensitivity is reduced, the skin coverings are pale, the patient is covered with cold sweat with subnormal temperature, the pulse is frequent and thread-like, breathing is shallow, low venous pressure, falling arterial pressure, decreased blood volume with normal or increased number of erythrocytes and percentage of hemoglobin in the peripheral blood, leukocytosis, decreased alkalinity of the blood, decreased metabolism, etc. Traumatic shock can, in terms of time of onset, manifest in two forms: primary, or immediate, shock developing at the moment of injury or immediately after trauma, and secondary shock appearing several hours after injury, even before the multiplication of microorganisms. Further, one also speaks of tertiary shock when there is already toxemia due to infection; secondary shock also occurs in a torpid form and is a transitional stage to collapse, which occurs after shock. If in the description of the picture of shock the opinions of clinicians and physiologists do not generally diverge, then as for the very definition of shock and its division into primary and secondary, as well as in the question of the transition of shock to collapse, by no means all authors agree. Thannhauser, for example, considers shock as overstimulation of the vasomotors, in contrast to the following stage - collapse, when there is already a depressed state, paralysis of the vascular nerves. The author himself emphasizes all the difficulty and complexity of dividing these states. Similarly, Zenen considers that there are two stages - shock and collapse - not only in the clinical picture, but also in the etiological factors. De Quervain strictly separates shock from collapse: while under collapse we generally understand a fall in vital functions, shock represents a fall in these functions caused reflexively, through an effect on the peripheral nervous system. Wieting does not separate shock from collapse, considering them as different stages of one origin. In 1934, Eppinger definitely stated that in essence there is no difference between shock and collapse, and therefore it is generally better to abandon the term "shock," designating this state as collapse. At present, it is still difficult to say to what extent Eppinger's opinion will become generally accepted, but undoubtedly clinical observations and the study of shock as a disorder of the peripheral vascular system give reason to be cautious about dividing shock and the like. The clinical picture of shock was already described by old physicians, mostly military surgeons, among whom John Hunter (1762) was one of the first to point out the severe symptoms observed in persons subjected to sudden violence, gunshot wounds, etc. The term "shock," characterizing the entire picture of the disease, was first introduced by James Latta in 1795. In 1815, Guthrie widely uses this term and warns against any operations in such a condition of patients. More often observed during war, shock naturally attracted the attention of military surgeons, among whom Copland (1858) gave a detailed description of this severe and dangerous complication accompanying severe injuries. A classically correct and complete description of shock was given by N. I. Pirogov in his "Fundamentals of Field Surgery." An equally exhaustive description of the picture of shock was given in Germany by Fischer (H. Fischer, 1870). The development of industry, the construction of railways in the second half of the 19th century, railway accidents created conditions that made it possible to observe the picture of shock also in peacetime conditions (Erichsen, Syme, etc.). With the flourishing of surgery in this same period, the doctrine of shock began to attract the attention of leading physicians (Billroth, Nussbaum, Leyden, Gussenbauer, Engel, Crile, and many others). After the Anglo-Boer, Russo-Japanese, and Balkan wars, no major works on shock appeared, if one does not count individual observations. According to Wieting, in the German literature during the period of the world war, in general, little attention was paid to traumatic shock. In our country after the imperialist war, there are only two printed works on the question of shock - Kruglevsky's and Citron's. The question was much more widely posed by the English, French, Belgians, and Americans, where special committees on shock were created, to the work of which, in addition to major clinicians, such outstanding physiologists as Cannon and others were attracted. The question at present cannot be considered finally studied; work in this direction does not cease, which is confirmed by the works of congresses of American (1934), Soviet (1935) surgeons, etc. Etiology. The main factor in the occurrence of traumatic shock is severe damage to the body. Extensive wounds, crushes, crushings of muscles in the limbs even without fracture of bones, multiple, even if each individually not serious, wounds, subcutaneous ruptures of muscles or organs, wounds of the pleura, abdominal cavity, prolonged laparotomies on weakened patients with evisceration of the intestine, injuries of the pelvis, spine, disarticulation in the hip joint, injuries of the neck, larynx, etc. - all these injuries can each individually become a cause of shock. Along with this, it deserves attention that in very weakened patients even the slightest trauma, the simplest operation can be accompanied by shock. Thus, along with the main factors playing an important role in the occurrence of shock, no less important significance is also attached to predisposing factors in the form of reduced resistance of the body, developing in weakened patients. In such cases, there is the so-called readiness for shock (Schockbereitschaft), which is in a certain dependence on endogenous and exogenous factors. The former should include constitutionally-hereditary factors, which have important significance in the life of neurasthenic individuals. No less, if not greater, importance in the occurrence of shock is attached to external factors. Everything that weakens and enfeebles a soldier at the front, a patient before operative intervention - hunger, thirst, cold, fear, anesthesia, manipulations on damaged tissues, etc. - all this contributes to the occurrence of shock. Prolonged insomnia, fear and physical overexertion in extreme degrees lead, according to Crile, often to complete exhaustion and shock. Similarly, pains and jolts of the wounded during transportation, especially with a poorly immobilized limb, can be the cause of the occurrence of shock, to which Pirogov already drew attention. Cooling of the body in cold and dampness leads to a disturbance of blood circulation, which has important significance in the development of shock. Exhaustion of the body can also be associated with infectious diseases recently undergone, which have important significance in the occurrence of shock. Finally, narcotic substances (chloroform, ether, avertin, etc.), which can themselves cause shock (Franken, Schurmeyer), undoubtedly together with operative intervention contribute to the occurrence of shock in a wounded patient. Pathogenesis. The question of the mechanism of development of shock is not yet finally studied, despite the large number of works devoted to this problem.

Numerous theories: loss of chromaffin substance by the adrenal glands (Vainbridge and Parkinson, Schur and Wiesel), formation of non-reducible hemoglobin^aHbOi), fat embolism (Porter), paralysis of the abdominal sympathetic plexus (Pimenta Bueno), connection with anaphylactic and colloidoclastic shock (Widal and others), etc., have not provided an exhaustive explanation of the pathogenesis of shock and in many cases have been abandoned by the authors themselves. The theory of Henderson deserves attention, which amounts to the fact that deep and rapid breathing after trauma leads to improper gas exchange in the lungs, as a result of which the amount of carbon dioxide in the blood and tissues decreases (acapnia). In connection with this, the venous tone weakens, stagnation develops in the veins, the right ventricle empties, the heart works in vain, blood pressure drops, and the picture of shock is present. Numerous experiments have not confirmed Henderson's position on acapnia as the main factor in the pathogenesis of shock, but they are still of interest because the author began to pay much attention to the state of venous tone even before the start of the world war. The kinetic theory of Krahl and the toxemic theory of Quenu are the most popular. The basic provisions of Krahl's theory amount to the fact that shock is a consequence of primary changes in the ganglion cells of the brain, which leads to their loss of the ability to convert latent energy into kinetic energy. Under normal conditions, the life of a cell is in direct dependence on the dynamic equilibrium between the processes of assimilation and dissimilation, the difference in potentials between the cell plasma and the nucleus, which has a greater acid tension than the plasma. With a strong discharge of nerve energy inside the cell, an excess of acid accumulates, depriving it of the ability to function due to its exhaustion. Nerve tissue also does not have the capabilities of other tissues, which can concentrate acids with reserve alkalinity. In addition, Krahl managed to prove that exhaustion, physical and mental fatigue, cold and hunger, causing deep changes in the body, primarily in the cells of the brain, liver and adrenal gland, are also a cause of exhaustion of nerve cells. A lively exchange of opinions arose around Krahl's theory, and a number of major scientists, including Henderson, Cannon and others, presented evidence against these provisions. The fact that patients in shock retain consciousness, are in a state of agitation with preservation of muscle strength, rather indicates the continuous activity of the central nervous system and to a certain extent refutes the position on the exhaustion of ganglion cells of the brain. Similarly, it has not been proven that ganglion cells change from irritation by centripetal nerves. Rather, blood loss, a drop in blood pressure act on brain cells in this way. Quenu's theory or the theory of traumatic toxemia, developed on the basis of the enormous material of the imperialist war, amounts to the following: in crushed tissues, aseptic decay products are formed, absorbed from the site of injury. These absorbing toxic substances are, in their chemical composition, most likely derivatives of muscle tissue proteins. In support of his theory, Quenu expresses the following considerations. The appearance of shock in most cases is not immediate, but after 2 or more hours, which confirms that a certain period of time is necessary for the formation of tissue decay and the production of toxins. The absorption of decay products of crushed tissue is observed with large muscle wounds and after multiple small wounds, which together constitute a larger wound surface. With subcutaneous crushed tissues with significant wounds, from which decay products are easily absorbed, shock is observed more often than in cases where such damage is open and the conditions for absorption with good outflow or with the application of a tourniquet are much worse. All these clinical observations have found their confirmation in the experimental works of Cannon and Bayliss, who also observed shock in animals after crushing the muscles of the limbs, which occurred even after cutting the nerves or spinal cord. The application of a tourniquet to the limb, ligation of the veins eliminated the appearance of shock, and conversely, improvement of absorption conditions in the form of removal of the tourniquet or ligature from the vein accelerated the onset of shock. Similarly, massage of the damaged veins accelerated the onset of shock. A number of other interesting and well-designed experiments with cross-circulation (MacIver and Haggart) with the introduction under the skin, intraperitoneally or intravenously of muscle autolysates (DeibetH and others) also confirmed Quenu's theory, who called the entire symptom complex traumatic toxemia with depression phenomena. Quenu's theory also met with a number of objections, primarily from Krahl and a number of other physiologists and clinicians. Particularly weighty are the arguments that primary shock, in its clinical course, cannot be explained according to Quenu's theory. Thus, at the present moment, neither of the two theories mentioned, taken separately, gives an exhaustive interpretation of the mechanism of shock development. Most likely, the truth lies in the middle, i.e., one theory complements the other. Primary shock, arising immediately after injury, is directly connected with strong irritation of centripetal nerves and their endings in individuals already exhausted and weakened by physical and mental experiences (Krahl). Subsequent development of the torpid stage, secondary shock, collapse is undoubtedly dependent on the absorption of decay products of crushed tissues from the site of injury. At the same time, as a reaction to over-irritation and suppression, primarily of the vegetative centers, the function of the vascular system is impaired. Venous and arterial pressure drops, the amount of circulating blood decreases due to an increase in the amount of deposited (accumulating in depots), the right heart, receiving less blood, decreases in volume. The vasomotor center, in which there is probably also a venomotor center, is obviously suppressed soon after injury. In the capillaries and veins, a large amount of red blood cells and leukocytes accumulates, which leads to an increase in blood viscosity. Due to the drop in venous pressure and stasis of blood in the capillaries, tissue oxygen starvation occurs, the amount of hormones that tone the vascular system decreases. As a result, all the vital functions of the body decrease. All these clinical observations were tested in the laboratory on animals and in many ways found their confirmation. Further research gave Cannon and Bayliss reason to assert that histamine is obviously absorbed from the crushed tissue, the introduction of which in a living being develops a similar picture of shock and collapse. Thus, for example, with intravenous administration of histamine to an animal, arterial and venous pressure drops, a drop in pressure in the right atrium is noted, which indicates a decrease in the amount of circulating blood and poor filling of the heart. In addition, fainting, vomiting, involuntary discharge of feces and urine occur. The decrease in the amount of circulating blood is explained by the fact that histamine causes spasm of the hepatic veins, so that portal blood is completely excluded from the general circulation. At the same time as this spasm, the permeability of the capillary walls increases, through which blood plasma seeps. As a result, the concentration of blood increases and accordingly the number of red blood cells in the capillaries increases, increasing by 2 million in a short time. The clinical picture of postoperative shock is very similar to the experimental histamine shock, all the more so since histamine is present in almost all tissues, especially in the skin. Eppinger, confirming the similarity of traumatic shock with histamine shock in the experiment, could not nevertheless find in such patients a larger amount of histamine than normal. Obviously, with severe injuries, some other harmful substances with a histamine-like action appear in the body (Eppinger). Pathological anatomy. Path-anatomical changes depend on the nature, strength and size of the injury, on the localization and on the time elapsed between the injury and the death of the patient. Of the organs most often subject to path-anatomical changes in shock, the liver, adrenal glands and brain should be mentioned, and often macroscopic changes are very insignificant. The microscopic picture of anatomical changes in these organs initially mainly amounts to hyperchromatism, then to hypochromatism, breakdown of the nucleus, vacuolization, swelling and breakdown of the cell itself (Krahl). Clinical picture. According to the time of appearance and clinical course, primary, or immediate shock, arising at the moment of injury, and secondary shock, developing in the nearest time after injury, in the first 6-8 hours, before the appearance of infection, are distinguished. After this time, the body may become flooded with bacterial toxins, which leads to the development of tertiary shock (Quenu). N. N. Burdenko also 'inclined to introduce this form of shock - tertiary, often observed in many forms of wound infections, most often in anaerobic.'

Primary shock—a psycho-vasomotor symptom complex (Erlenmeyer)—arises as a result of strong psychic excitement associated with received or expected trauma. Likewise, severe damage to those areas of the body that are richly supplied with sensory nerves and fibers of the autonomic nervous system can be the cause of primary shock. It has already been mentioned above that damage to the neck, spinal cord, and pelvis most often causes primary shock. Additionally, in primary shock, an erotic stage and a torpid stage are noted. In the erotic stage observed in primary shock, there is increased reflex excitability, and the pulse is generally of satisfactory filling (Thannhauser). Goldschach was often able to observe in shock an increase in blood pressure. Burdenko also reports this, having observed this form of shock during operations on the central nervous system and in its injuries. Subsequently, with excessive irritation of the central nervous system, the torpid stage develops, which is already associated with inhibition and paralysis of the vasomotor center, clinically expressed by a barely perceptible pulse, a fall in blood pressure, shallow breathing, pallor of all skin covers covered with cold sweat, a generally depressed state with preservation of consciousness and reduced sensitivity of the injured tissues. Primary shock in the erotic stage, observed experimentally, is nevertheless rarely noted in the clinic. Despite the enormous material from the imperialist war, the number of observations of primary shock is negligible, which even gave some authors reason to deny its existence altogether. The existence of primary shock is undeniable (Cowell, Picqe, Burdenko, etc.), but a huge number of such patients with severe injuries and blood loss quickly die without coming under the care of a physician. However, secondary shock, arising from toxemia associated with the absorption of breakdown products from crushed tissue, is often observed in conditions of battle, in surgical work in peacetime, etc. This form of shock—secondary—is essentially what the extensive literature on shock is devoted to. The clinical picture, basically given in the classic description by Pirogov, also refers for the most part to secondary shock, which, as already mentioned above, many clinicians and physiologists consider to be collapse. Thus, the torpid form of primary shock is clinically a transitional stage to secondary shock—collapse. As for the tertiary form, it is hardly possible to distinguish it clinically, since the resulting infection and the associated toxemia only complicate the course of the process, affecting individual symptoms—temperature, consciousness, the cardiovascular apparatus, etc. The cause and mechanism of the fall in blood pressure have already been mentioned above. Likewise, the pallor of the mucous membranes and external covers is associated with the outflow of blood from the skin capillaries, a change in the concentration of blood, and generally with an improper distribution of blood in the body. The decrease in the general metabolism, the reduction in gas exchange, the significant heat loss through the skin, sweating—all this is the cause of a noticeable decrease in temperature. Only in later stages, when the blood pressure in the peripheral vessels noticeably falls and simultaneously the pressure in the coronary vessels falls, the blood supply to the heart muscle noticeably deteriorates, which must affect both the nutrition and the function of the heart. Simultaneously with the fall in venous and arterial pressure, the amount of circulating blood may be reduced by 40-60%, even in the absence of external bleeding. Breathing in shock may at the moment of trauma stop altogether for a short time, only to subsequently, especially in the secondary stage, become shallow, interrupted only by deep sighs and groans. The shallowness of breathing finds its explanation in the fall of metabolism, the decrease in internal respiration, which sharply reduces the need for oxygen. Intermittent, Cheyne-Stokes breathing, etc., is observed in the last minutes of life in shock. Generally, dyspnea in shock is as a rule not observed. The morphological picture of blood turns out to be definitely changed—the amount of hemoglobin is increased, and the number of red and white blood cells in the capillaries is also increased. Particularly characteristic is the circumstance that with simultaneous counting of erythrocytes in venous and capillary blood, the latter contains a larger number of erythrocytes, sometimes 2-2.5 million more per 1 mm³ (Kennon). The latter, as already mentioned, is explained by the increased concentration of capillary blood in shock. Metabolism in shock is found to be sharply disturbed. True, the conditions for observing and studying patients with shock have not so far allowed a complete picture of the disturbance of metabolism in them to be presented, but still the available experimental and clinical observations allow one to assert that the basic metabolism in shock is lowered by almost 70% against the initial level (Aub). The amount of oxygen in the venous blood is also found to be lowered, and finally there is always acidosis, with the decrease in the alkaline reserve going parallel with the fall in vascular pressure (Kennon). From the side of the nervous system, special depression, inhibition, and indifference to the surroundings have already been noted, with full consciousness and memory. The patient, correctly answering the questions posed, does so somehow reluctantly and sluggishly. Pathognomonic is the fact that even in the most severe cases of shock consciousness nevertheless remains preserved (Viting). Disturbance of consciousness may give reason to deny shock or to look for deep special damage to the central nervous system. Skin and tendon reflexes are diminished and may be completely absent. Sensitivity is noticeably diminished, sometimes to complete anesthesia. A number of other general symptoms are observed in shock. A quiet, hoarse voice, ptosis, nausea accompanied by vomiting, hiccups, dilation of the pupils, retention of urine, up to anuria, sometimes also incontinence of urine and feces, etc., may be noted in shock, without being pathognomonic for this condition. Old surgeons also described a purely local shock, limited only to a certain area of damaged tissue. The corresponding limb is cold to the touch, the skin on it is pale or cyanotic, there is no sensitivity or ability to move, so that patients do not complain of any suffering. In other cases, patients complain of a feeling of running ants and other abnormal sensations in the injured limb. This picture, described by Mosettig, has been known for a long time, since Pirogov, who called local shock local asphyxia. Along with this, it is beyond doubt that in a certain number of such patients one was dealing with the initial stages of gas gangrene. The fact that during the imperialist war surgeons paid little attention to this form of shock is explained by Viting as follows: that main attention was paid in such cases to gas gangrene, which most likely developed in tissues with local shock. This local shock, little known to modern surgeons, nevertheless deserves definite attention, since, in the opinion of the same author, the possibility of the development of general shock from local cannot be excluded. Diagnosis. Recognition of shock often presents great difficulties, especially in conditions of the front, due to complications with other ailments that confuse and obscure the diagnosis. To no lesser extent hinders the correct establishment of diagnosis the uncertainty, confusion of the very concept of 'shock,' the desire to separate it from collapse, considering the latter almost as an independent picture of the disease in trauma, etc. Only the division of shock into primary, manifesting in the erotic and torpid form, with the transition of the latter into secondary, which is essentially already collapse, allows one to more easily and better orient oneself in the diagnosis of this severe and formidable complication in trauma. The presence of predisposing factors—hunger, overwork, psychic trauma, etc., sudden and strong action of physical trauma, often with multiple fractures of tubular bones, etc., the characteristic general habitus (indifferent, indifferent gaze, pallor, cold clammy sweat, etc.), fall in blood pressure, barely perceptible pulse, corresponding changes in blood, metabolism, etc.—are the objective data that facilitate the establishment of the correct diagnosis. In differential diagnosis, a number of complications in trauma can confuse the picture of the disease. Such complications should include fainting, nervous shock, acute bleeding with significant blood loss, fat and air embolism, concussion of the brain, and acute infections. In fainting, arising in connection with fright, pain, and generally with rapid and improper distribution of blood in the body, there is always complete loss of consciousness and sensitivity, pallor, cold sweat, and general weakness; the pulse is weak and accelerated; no changes in blood are observed. Likewise, so-called nervous shock, developing in connection with severe psychic experiences after attacks, explosions of heavy shells, great emotional shocks, undoubtedly exists and can be diagnosed as such.

The clinical picture of the disease is more complex when there is also traumatic damage to the tissues at the same time. Analysis of the entire clinical picture, the condition of the cardiovascular system, blood, etc., allows for differentiation between traumatic shock and purely nervous shock. In the differential diagnosis of severe hemorrhages and Shock, attention should be paid to the nature of the pallor of the skin coverings - pale, marble-like shiny whiteness in hemorrhages and pale yellow, matte pallor in Shock. Next are characteristic hyperhemoglobinemia and an increase in the number of red blood cells in Shock and hypohemoglobinemia and a decrease in the number of red blood cells in hemorrhages. Nevertheless, it must be remembered that with severe injuries, which are the cause of Shock, there are often also significant hemorrhages present. Fat embolies differ in their course from Shock with characteristic symptoms: in the pulmonary form - shortness of breath, cough, bloody sputum, unconscious state, elevated temperature, etc., and in the cerebral - unconscious state, tonic and clonic convulsions, epileptiform seizures, pareses and paralyses. In concussions of the brain, loss of consciousness and a number of symptoms of increased intracranial pressure are noted. Special difficulties for diagnosis are cases when severe skull injuries are accompanied by Shock. Gas phlegmon, developing at the site of injury, most often gives rise to diagnostic errors. Finally, it should be borne in mind that anaphylactic Shock, developing after the administration of anti-tetanus and other serums. The prognosis in each individual case depends on a number of conditions: the condition of the patient himself, the severity of the injury, blood loss, the duration of suffering, the impending surgical intervention, etc. Great importance is attached to the time that has passed from the moment of injury to the examination of the patient, since during this period of time the strength of the patient further decreases, blood pressure decreases even more, etc., and after 6-8 hours after traumatic injury, infection joins, further complicating the already serious condition of the patient. Surgical interventions in the pre-shock state or with already developed manifestations of Shock sometimes have a negative effect on the course of the disease and require special precautions. - Preventive measures are of great importance in the fight against Shock. Fighting the cooling of the body, maintaining psychological calm as much as possible, eliminating pain, fighting hemorrhages - these are in essence the main tasks in the fight against possible Shock. On the front, these measures are basically reduced to the following: frequent replacement of troops in the front line with fresher forces from the reserve; satisfactory, nourishing food and careful supply of warm clothing in the autumn and winter seasons. Special attention deserves the transport of wounded with multiple fractures and significant damage to soft tissues. Those transported in poor, bumpy carts with poorly applied splints, or even without splints at all, often develop a picture of severe Shock. Cannon definitely points out that thanks to the use of splints when dressing the wounded on the front lines, the number of cases of Shock in the British army significantly decreased in the last war. Decisive importance is timely and rapid surgical help, which can not only prevent Shock, but also improve the outcome in cases where Shock has already developed. In surgical interventions, preventive measures against operative Shock are reduced to more correct preoperative care in the form of appropriate diet, eliminating all disturbing and upsetting moments for the patient; minimizing all thermal, painful, visual and auditory irritations during the operation itself and the choice of appropriate anesthesia, etc., create the most favorable conditions for fighting the possibility of developing Shock. Treatment. Therapeutic measures for the erectic form of primary Shock, observed, as already mentioned, extremely rarely, should be aimed at clarifying the local cause of Shock and eliminating it, if not surgically, then by conduction anesthesia (Kraille) or circular anesthesia - circular block. Maximum attention is required for the condition of blood pressure, which can suddenly drop. But with a significant drop in blood pressure, there will be a torpid form with transition to secondary Shock. Since in this stage the drop in blood pressure is directly related to the decrease in the amount of circulating blood, all therapeutic measures should be directed in this direction and are basically reduced according to Eppinger to the following: 1) means acting on the vasomotor center; 2) means acting on the peripheral vascular system and directed directly at mobilizing depot blood, in order to thereby increase the amount of circulating blood; 3) increasing the absolute amount of blood and finally 4) improving the function of the abdominal press, which has important significance in better emptying blood from the abdominal depots. First of all, inhalation of carbon dioxide is recommended, which is the best irritant of the vasomotor center and reflexively acts on the cutaneous and portal venous system. In practice, it is best to give the patient to inhale a gas mixture of 10% carbon dioxide and 50% oxygen. A good effect on the vasomotor system is exerted by strychnine in doses of 0.005-0.01 per day. A good effect is obtained from strychnine also in Shock in infectious patients. Weaker than strychnine act camphor and cardizole, which also affect the peripheral vessels. Caffeine and digalen are also recommended. Adrenaline has a powerful but quickly passing effect; the best effect is obtained with constant intravenous drip infusion of glucose with an admixture of adrenaline. Good effect is exerted by intravenous infusion of 500 cm³ of Baylis solution: Nat. chlorat. 20.0; Kal. chlorat., Calc. chlor. aa 0.5; Gummi arabici pulv. 50.0; Aq. dest. 1,000.0. Blood transfusion has a brilliant effect in cases where there is simultaneously significant blood loss, but in all other cases the effect is less significant, and after apparent improvement, deterioration often occurs, associated with the fact that peripheral tone is not restored and the transfused blood again accumulates in the depots. Warm wraps, but not to overheating, bandaging of the abdomen, etc., contribute to improving the tone of peripheral vessels and better function of the abdominal press, which has significance in the sense of better mobilization of blood from depots. As for surgical interventions, this issue is decided according to the urgency of the indication. It is necessary to keep in mind the negative effect of anesthesia (chloroform, ether, avertin) on patients in a state of Shock. Regional or infiltrative anesthesia according to the creeping infiltrate method (Vishnevsky) and the smallest doses of ether will make it possible to complete the operation successfully. The administration of serum for preventive purposes is not recommended, at least in the first hours after injury, when the danger of Shock has not yet passed. Only the presence or even suspicion of the development of anaerobic infection serves as an indication for the administration of anti-anaerobic serum. In a number of cases, success is achieved by all these measures, but in a considerable number of cases, despite the use of all precautions and energetic treatment, patients still die. In such cases, there is reason to assert that shock developed in the body, already sharply weakened and reduced in all its functions. Lit.: Alipov G., Traumatic Shock, J. Contemp. Surg., vol. V, No. 5-6, 1930 (lit.); Andreev L., General effect of injuries on the body (General Surgery, ed. by E. Hesse, S. Girgolav and V. Shaak, vol. I, M.-L., 1923); Burdenko N., Shock, Centr. Med. Zhurn., vol. XII, pp. 393-406; ibid., On Shock, Works of the XXIII All-Union Congress of Surgeons, M., 1936; Cannon W., On Traumatic Shock, Sov. Surg., 1936, No. 1; Levit V., On Postoperative Shock, Works of the XXIII All-Union Congress of Surgeons, M., 1936; Eppinger H., Uber den postoperativen Symptomenkomplex, Wien. klin. Wochenschr., 1922, p. 618; ibid., Uber Kollapszustände, ibid., 1934, No. 1-2; Herbst B., Uber Klinik und Aetiologie des reintraumatischen Schocktodes, ibid., 1924, No. 28.