Traumatic shock

With traumatic shock changes that happen to the blood circulationcaused by the changes of the functional state of the Central nervous system and peripheral nervous system under the influence of persistent destructive (pain) or irritation at the site of the injury.
Decided to allocate and erectile torpid phase of shock.
At the earliest date after the injury pain and mental factors cause drastic action in the bark of the big hemispheres and in different subcortical departments, in particular in the hypothalamic region, resulting in increased functional activity of endocrine glands (pituitary, adrenal gland, thyroid gland), increases the tone of sympathetic nervous system. Functional changes the body initially manifested complex adaptive reactions aimed at creating the most favorable conditions for the blood supply to vital organs. Occurs common spasm of small peripheral vessels of the skin and most of the internal organs, while the arteries of the brain, the heart and the working muscles can even expand, i.e. the flow of blood in the body is redistributed by the centralization of a circulation.
When pronounced these reactions occur very short-term (10-20 minutes) erectile phase of shock (phase excitation). If the adaptive response of the organism are sufficient and the impact of trauma eliminated timely remedial measures can be normalization of all body functions.
If the flow of pain impulses continues, energy resources nerve cells are depleted and the result is the inhibition of functional activity of the Central and peripheral nervous systems, including centres of breathing and blood circulation, - erectile phase of shock goes into a torpid (phase braking).
Long-term narrowing of the small arteries and the opening of additional arterio-venous anastomoses, supports the centralization of a circulation, lead to permanent shutdown of certain sections of the vascular system of blood circulation (the so-called sequestration of blood flow), and the emergence of the lack of oxygen in the tissues of the distal arterial narrowing of the branches. In the tissues, deprived of adequate oxygen supply to accumulate toxic products of metabolism. They lead to the paralysis of smooth muscles of the arterioles and capillaries, expanding, and the stasis of blood in the result of the circulating blood remains peripheral vessels and does not return to the heart, is not involved in the circulation. Decrease volume of circulating blood (hypovolemia) also contributes to the rapidly emerging in the conditions of oxygen starvation of tissues violation of the permeability of the vascular wall (see Permeability) and liquid output from the vascular bed in the surrounding tissue.
With traumatic shock gipovolemia constantly grows, as all the large amount of blood stagnate in paralyzed vessels. Because of decreasing venous return blood heart all the time "empty", its impact and the minute volume falls, progressive decreases blood pressure.
Violations of regional blood circulation in shock reinforce the violation of blood coagulation due to hypoxia, which leads to the formation of blood clots in small vessels. Oxygen starvation of tissues supports further reduced vascular tone, which ultimately lose inherent in normal conditions, the ability to shrink under the influence of adrenaline and nor-adrenaline. Vicious circle from which the body without treatment cannot go.
The severity of the shock and the onset of irreversible changes in the internal organs depend not only on the extent hypotension, and its duration, i.e. the duration of oxygen starvation of tissues. External or internal bleeding in most cases accompanied by severe and multiple damages and aggravates a traumatic shock, as in this case, relative to hypovolemia associated with the centralization of circulatory shock, joins true hypovolemia due to loss of blood (see Blood loss).
With other types of pain shock along with the above changes are identified specific pathophysiological features that define the clinical course, for example, shock if frostbite, burns shock and other

Traumatic (exogenous) shock. The direct cause of traumatic shock in most cases is heavy mechanical injury, but not all, severe injuries complicated by the shock. The degree of personal reaction to the damage is determined, on the one hand, its localization and severity, on the other hand,a particular state of the organism at the time of injury and the circumstances in which the injury received.
Contribute to the emergence of shock oppression of the psyche, hemorrhage, cooling, heat, starvation, exposure to ionizing radiation. At adverse influences of an environment shock can develop at pains relatively low intensity.
According to the materials of the Scientific-research Institute of emergency medical aid to them. Sklifosovsky, in time of peace injuries of various localization about 2% of the cases are complicated by shock. On the first place on the frequency of shocks are multiple injuries, combined with craniocerebral trauma; then there are fractures of pelvic bones, multiple fractures of the ribs. A long and traumatic surgery for lack of anesthesia may also be complicated by the shock.
The pathogenesis of the traumatic shock is complex and not fully understood. The most exhaustively the occurrence and during shock reveals serverelement theory, according to which the injury, the effects on nerve endings in the tissues, causing the flow of super-strong impulses in the Central nervous system. Inadequate irritation causes changes of the functional state of subcortical structures and bark of the big hemispheres. Shock may occur off the bark (for example, in a comatose state), when the pain signals react only subcortical centers. Emerging spilled stimulation of the nervous system helps increase blood pressure, spasm of peripheral vessels, capillaries of the brain and myocardium, strengthening the functions of the endocrine glands (pituitary, adrenal) and increase metabolism. In cases where the adaptive response of the organism are sufficient can be normalization irritable and inhibitory processes in the Central nervous system with the subsequent disappearance of the symptoms of shock. If the flow of pain impulses ongoing, region centers of bark and cortex is concentrated excitement, challenge, as a rule, braking, which is clinically manifested in the development of torpid phase traumatic shock.
As a result of violations reflex regulation changes peripheral circulation, preventing normal tone of vessels, there is hypoxia of organs and tissues and pathological deposition of a blood, what is the reduced mass of circulating blood. Along with reduction of volume of circulating blood and is an absolute reduction of its volume due to the condensation caused by increased prepodavanie plasma through the vascular wall permeability which is increased.
Disorders of tissue respiration and metabolism caused by circulation and ventilation of the lungs, leading to the development of acidosis in organs and tissues. Thus, the mechanism of shock at the height of its development is a difficult complex of numerous violations mutually reciprocally and forming a vicious circle. This mechanism, reaching its full development, continue regardless of the reasons which prompted him, even after the pain will be eliminated. Extreme irritation shock character is the starting torque, resulting in a complex mechanism of shock, which further develops according to the principle of the self.


The creation of neurogenic or reflex, the theory of the origin of the traumatic shock is a merit of Soviet scientists - followers of the I. P. Pavlova.
Some authors (D. Shushkov) leading the importance attached to the processes namely parabiosis in the afferent part of a reflex arc. Many scientists studying the pathogenesis of shock mainly in the experiment, tied his appearance with damage to centres of vegetative nervous system and cerebral cortex, a violation of vascular tone, acapnia, intoxication decay products of damaged tissues and toxins developing in them microflora, embolism, and so on, While etiological factors often mixed with pathogenetic, the main neurogenic mechanism of shock was substituted separate pathogenetic aspects that are only a consequence of the impact of trauma on the nervous system. However, for the disclosure of the pathogenesis of shock study of these mechanisms is of paramount importance.
Clinically in shock observed rapid breathing. Henderson (J. Henderson) in experiment on animals using a special pump reached breathing rate 60-120 in 1 min After 10-30 minutes this hyperventilation decreased the content of carbonic acid in the alveolar air and the blood and the animal appeared unstable hemodynamics, characteristic of shock. The disadvantage of carbonic acid in the blood, the author explained the falling tone respiratory and vasomotor centers, and its shortage in venous blood - lowering the tone veins, in which blood flow to the heart sharply decreases, and the cavity of the heart insufficiently filled with decreases in systolic and minute volume, which leads to lowering blood pressure. Lowering blood pressure leads to oxygen starvation of tissues and the development of acidosis, which increases the permeability of the vascular wall, reduces the amount of circulating blood, which causes a further fall in blood pressure and the development of shock. Supporters akanishi theory does not take into account that changes breath in shock are only a secondary and not the only consequence of the violation of the nervous regulation, so that acapnia and its results should be considered only as one of the aspects of pathogenesis of shock.
Theory toxemia well explains the origin of the shock of having toxic nature, although anamnesticeskih and associated with the trauma. In some cases humoral factor may have additional etiological significance and in shock to pain of origin. Keno (E. A. Quenu) believed that toxic products generated in compressed tissues after removal of the cause of embarrassment enter the bloodstream and cause intoxication leading to death of the victim. Cannon, Bayliss (W. C. Cannon, VV. M. Bayliss) in experiment on animals with cross-circulation, causing injury to one animal, caused the development of shock from the other.
Together with the products of tissue decay in the development toksemicheskim shock can have a value products disturbed metabolism of proteins, fats and carbohydrates and bacterial toxins circulating in the blood.
Attempts to detect toxic substances in the blood of humans and animals in the initial period torpid phase traumatic shock still did not succeed. However, there is no doubt that in the damaged tissues in shock toxic substances are formed. However, they linger on the site of its formation in the damaged tissues, as the latter have a high ability to adsorb as colloid and crystalloid substances (I. R. Petrov). In later periods toxic substances can enter the blood from damaged tissues.
Thus, toxaemia in the late stage of shock can develop again.
Blalock (A. Blalock), Parsons and Demister (E. Parsons, D. C. Pheinister), Freeman (N. E. Freeman) and TCS. say that in the basis of the pathogenesis of shock lies primary reduction in the mass of circulating blood, caused by blood loss and plasmopara due to increased permeability of blood vessels. However, Gregersen (M. J. Gregersen) with shock, caused by mechanical injury, and N. I. Kochetygov if you burn shock showed that the decrease in blood volume has a secondary character and caused by the reflex regulation disturbances of blood circulation and pathological deposition of a blood (I. R. Petrov).
Thus, the most complete picture of the development of the traumatic shock gives neurogenic theory. Other theories cover only certain aspects of its pathogenesis.