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Syndrome prolonged compression

What is Long-Term Compartment Syndrome -

Pathological condition defined by the term " long-term compartment syndrome"- SDS (syn.: crash syndrome, traumatic toxicosis, long-term crush syndrome), is characterized by the originality of the clinical picture, the severity of the course, and the high frequency of deaths.

Prolonged limb compression syndrome- this is a peculiar pathological condition of the body, arising, as a rule, in response to prolonged compression of a large mass of soft tissue. Rare cases have been described when SDS develops due to short-term compression of a large mass of soft tissue. The force of compression while the victim remains conscious is usually great, and he is not able to remove the injured limb from under the pressure.

This is observed, for example, during earthquakes, blockages in mines, accidents, etc. The compression force can be small. In this case, SDS develops due to prolonged compression, which is possible in cases where victims various reasons(coma, poisoning, epileptic seizure, etc.) are in an unconscious state. In clinical medicine, the terms “positional compression” and “positional compression” are used to refer to such compression. Experience shows that SDS develops mainly under prolonged (for 2 hours or more) pressure from a large mass of soft tissue.

Pathogenesis (what happens?) during Long-Term Compartment Syndrome:

It is known that at least three theories of the pathogenesis of SDS were previously discussed: the theory of toxemia, the theory of plasma and blood loss, and the theory of the neuro-reflex mechanism. Extensive clinical experience and the results of experimental studies show that all these factors play a role in the development of DFS. According to modern concepts, the leading pathogenetic factor is traumatic toxemia, which develops as a result of the release of decay products of damaged cells into the bloodstream. Hemodynamic disturbances caused by endotoxins include changes in the integrity of the vascular endothelium and activation of the kallikrein cascade.

Capillary "leakage" leads to extravasation of intracellular fluid. Bradykinins, as well as other vasoactive kinins, cause hypotension. As a result of direct exposure to endotoxins and coagulation factor XII, the intravascular coagulation mechanism is activated, which causes fibrinolysis and disseminated intravascular coagulation (DIC). Important role changes in the development of capillary stasis, microcirculation disorders and oxygen starvation of organs play a role rheological properties blood and a decrease in the ability of red blood cells to deform due to endotoxification. The DIC complement system is also activated, leading to further endothelial damage and changes in vasoactivity.

IN pathogenesis different several options SDS(traumatic origin, positional origin, short-term compression with the clinical picture of SDS) there is a common component that determines the fate of the victim in the future - tissue compression, accompanied by ischemia, followed by the resumption of blood circulation and lymph circulation in the damaged tissues.

Each type of compression has features that distinguish them from each other, but acute ischemic disorders (AID) in damaged tissues have a single pathogenesis and, in fact, determine the condition of the majority of victims in the future, unless other damage is added to the ADS (wound, radiation, secondary infection , burns, poisoning, etc.). It is advisable to combine all types of soft tissue compression with the term “compression injury.” If we consider that post-ischemic disorders in compression injury are the main ones and the vital activity of the body or the functioning of the injured limb depends on them, then compression injury can be considered as special case acute ischemic disorders (AID) of any origin, occurring in ischemic tissues after the resumption of blood flow in them. In case of injuries, such conditions are observed in cases of prolonged (pressure of the limb with a tourniquet (tourniquet injury), replantation of the limb (replantation toxicosis), restoration of blood flow in the injured great vessels and their thromboembolism ("switch-on syndrome"), cold injury, etc.

In cases where ischemic disorders threaten the lives of the victims, they can be distinguished as a severe form of acute respiratory syndrome; if they threaten only the function of the damaged organ (limb), then they can be considered as a mild form of OID. This division of IIR will make it possible to establish in which medical institution it is necessary to provide qualified and specialized care to victims, in particular with compression injuries. This is especially important in case of mass lesions, when it is necessary medical triage. Taking into account the above, SDS can be considered as a severe form of compression injury of the limb, threatening the life of the victim, who may die from post-ischemic endotoxicosis associated with the resumption of blood flow and lymph circulation in ischemic tissues. In some cases, it occurs against the background of painful shock (trauma from earthquakes, etc.), in others - without a painful component (positional compression of various origins). Post-ischemic endotoxicosis is not always the most life-threatening for victims of severe compression injury, since its occurrence can be predicted. The development of post-ischemic endotoxicosis must be prevented to the extent that the circumstances of the injury and modern data on its pathogenesis allow.

Limb compression creates anoxia of the injured segment, as a result of which, against the background of painful shock or a coma caused by another reason, redox processes in the anoxia zone are disrupted to the point of being irreversible. This is due to the suppression of the activity of redox enzyme systems of mitochondria in anoxic tissue cells. After decompression, acute ischemic disorders develop in the damaged area, caused by the entry into the body through the blood and lymphatic pathways of under-oxidized products of disturbed metabolism, consisting of elements of the cytoplasm of ischemic cells in toxic concentrations, products of anaerobic glycolysis and peroxide free radical oxidation. The most toxic are the “medium molecular” breakdown products of protein, potassium, myoglobin, etc.

Ischemic tissues, in which blood and lymph circulation are resumed, after decompression lose their normal architecture due to increased permeability of cell membranes, membranogenic edema develops, plasma loss and blood thickening occur. In muscles, normal microcirculation is not restored due to vasoconstriction of toxic origin. The nerve trunks and sympathetic ganglia of not only the injured, but also the symmetrical limb are in a state of morphological deafferentation. Ischemic tissue of the injured limb is toxic. In the presence of a large mass of ischemic tissue, life-threatening post-ischemic toxicosis develops. Under-oxidized toxic products from damaged tissues mainly affect all vital organs and systems: the myocardium (due to the negative inotropic effect of ischemic toxins on it) - the brain, lungs, liver, kidneys; profound disturbances of the erythron system occur, accompanied by hemolysis and a sharp inhibition of regenerative function bone marrow, causing the development of anemia; changes in the blood coagulation system similar to DIC syndrome are observed; All types of metabolism are disrupted due to the consequences of anoxia, the immunological reactivity of the body is sharply inhibited, and the risk of developing a secondary infection increases. Thus, a diverse vicious circle of disorders of all organs and systems of the body arises, described in sufficient detail in the literature, which ultimately often leads to the death of the victim (from 5 to 100%). The foregoing allows us to create a model for the prevention and treatment of SDS. To prevent DFS, it is necessary to exclude post-ischemic toxicosis. The most reliable and simple way to prevent SDS is amputation of the injured limb under a tourniquet applied until the victim is freed from compression. Indications for amputation should be expanded in the event of mass admissions of victims in unfavorable conditions.

In order to prevent SDS without amputation, it is necessary to carry out complex local therapy, which can be called regional resuscitation. This complex consists of measures aimed at stopping anoxia in ischemic tissues: detoxifying them and restoring impaired redox processes in ischemic tissues. Currently, hemosorbents such as SKN are successfully used as detoxifiers; to restore metabolic processes in ischemic tissues, isolated artificial circulation of the injured limb with the connection of the xenopenic liver and hemoperfusion through cryopreserved liver tissue are used. A promising area of ​​regional resuscitation for SDS is directed transport medicinal substances using liposomes.

The most effective in the treatment of already developed VDS are toxicological techniques aimed at freeing the victim’s body from “ischemic toxins” (sorption methods, dialysis, plasmapheresis), and techniques used to break the diverse vicious circle of disorders leading to life-threatening complications (for example, prevention of DIC syndrome, immunostimulation, temporary replacement of the function of affected kidneys). It should be considered erroneous to use any treatment methods that, in the case of severe compression injury, in one way or another contribute to an additional “toxic shock” from injured tissues to vital organs and systems. These include fasciotomy, intensive infusion anti-shock therapy in the absence of tight bandaging and cooling of the limb without detoxification of the body, hyperbaric oxygen therapy(HBO) without taking into account the dangers of the consequences of tissue hypoxia under conditions of increased oxygen concentration.

Symptoms of Long-Term Compartment Syndrome:

Clinical picture of DFS begins to form from the moment of compression of soft tissues; and complications that are life-threatening for victims usually arise after decompression and are associated with the resumption of blood flow and microcirculation in ischemic tissues. The results of numerous experiments and clinical observations show that amputation of the injured limb before the press or tourniquet applied proximal to the compression site is removed from it, as a rule, saves the lives of the victims. In practice, it has been proven that the source of intoxication in severe compression injury is the injured limb and “ischemic toxins” enter the general blood and lymph circulation system after the victims are released from compression. The victim, as a rule, does not die under pressure. Case novocaine blockades as a method of treating SDS turned out to be ineffective. Conduction anesthesia, although more preferable in case of SDS than case blockade, however, in itself does not save victims from death in case of severe compression injury. It has been proven that the nerve trunks of the injured limb undergo morphological deafferentation already during the period of compression. Taking these data into account, the idea of ​​the leading role of the neuroreflex pain component in the pathogenesis of SDS appears differently. The pain syndrome, undoubtedly present in compression injury, creates only an unfavorable background against which post-ischemic endotoxicosis develops and, as a rule, is not the cause of death.

The experimental results showed that after decompression, blood circulation in the compressed limb is restored in a unique way, very reminiscent of that during revascularization of long-term ischemic tissue. With the anatomical preservation of the microvasculature of a limb subjected to long-term compression, after short-term “reactive” hyperemia, blood flow is resumed mainly in connective tissue formations (subcutaneous fatty tissue, fascia, periosteum). In this case, the muscles are almost not supplied with blood, which causes their post-ischemic aseptic necrosis. Post-ischemic changes in muscles are very peculiar: the phenomena of necrosis in them develop unevenly, and it is impossible to see the entire zone of ischemic necrosis with the naked eye, since individual myofibrils are preserved, and some are damaged. It is impossible to excise muscles with post-ischemic avascular necrosis while preserving intact fibers. In addition, it is known that the function of the limb, the muscles of which were ischemic due to compression injury, and at the same time signs were noted flaccid paresis and paralysis, is restored. It has been established that detoxification of an ischemic limb with an adsorbent helps to normalize the distribution of blood in ischemic tissues. It is also known that “ischemic toxins” have a direct vasoactive effect on the smooth muscles of the vascular wall.

The data presented allow us to conclude that “ischemic toxins”, entering the general bloodstream from the injured limb, have a pathogenic effect on vital organs and systems, thereby closing a series of “vicious circles” of endotoxicosis. Not completely clear chemical composition"ischemic toxins", but it is known that these are mainly substances that are part of long-term ischemic tissues, the blood flow in which has been resumed. These substances are “washed out” into the blood and lymph in huge quantities. In addition, in ischemic tissues, oxidation processes are disrupted due to the blockade of redox mitochondrial enzyme systems. In this regard, the oxygen that enters the tissues after the blood flow in them is resumed is not absorbed, but participates in the formation of toxic peroxidation products.

The results of experiments and clinical observations indicate that venous blood in an injured limb is more toxic than blood flowing from. Particularly toxic venous blood injured limb in the first minutes after decompression. In the future, apparently, due to the increase in edema and blocking of the outflow of blood and lymph from ischemic tissues, the toxicity of blood and lymph in the vessels of the injured limb decreases somewhat. Currently, in clinical settings it is possible to monitor the dynamics of the toxicity of biological fluids using methods such as the “paramecium test” and determination of the concentration of “medium molecules”. There are other tests and methods for determining blood and lymph toxicity. These data suggest that in order to detoxify the body, it is more expedient to collect venous blood from the area of ​​injury, for example, from the femoral vein of the injured limb.

The resumption of blood flow in the limb after decompression is accompanied by a violation of the architectonics of ischemic tissues due to an increase in the permeability of their cell membranes - membranogenic edema develops, characteristic of the post-ischemic state of tissues. These disturbances in the architectonics of damaged tissues can be prevented to some extent by gradually restoring blood flow in a gentle manner and local cooling, which reduces blood flow to ischemic tissues.

The question of the pathogenesis and biological significance of edema of ischemic tissues has not been completely resolved. With a compression injury, one can distinguish between predominantly local edema, localized to the area of ​​injured tissue, and general plasma loss with minor local edema, and in both cases, blood thickening can be observed. Experiments have established that the more severe the compression injury, the less pronounced the local post-ischemic edema and the more significant the total plasma loss. These data allowed us to conclude that the severity of local edema reflects the degree of preservation of the body's protective reactions, and edema of ischemic tissues is protective in nature. This conclusion is confirmed by data indicating that the more severe the compression injury, the more significantly the immunological reactivity of the body decreases.

Swelling of ischemic tissues increases as the absorption of toxic substances from the affected tissues decreases. This means that the swelling of injured tissues protects the body from the entry of toxic substances into liquid environments. In this regard, “fighting” the consequences of edema through fasciotomy in case of severe compression injury of a limb inevitably leads to an additional toxic “blow” to the body due to improved blood flow in the injured limb. Thus, trying to preserve the limb and its function, we risk the life of the victim. All therapeutic measures (fasciotomy, necrectomy, fixation of fractures, etc.) to save a limb that has been subjected to compression must be carried out in parallel with intensive therapy, use modern methods active detoxification - hemolymphosorption and hemodialysis.

Significant total plasma loss in severe compression injury secondary to shock is an undoubted indication for intensive infusion therapy, which is a component of anti-shock treatment. However, it should be borne in mind that stimulation of hemodynamic parameters can become dangerous for victims if free communication between the blood and lymphatic beds of the body and the injured limb is maintained. In these cases, as the experiment has shown, stimulation of hemodynamics with the help of anti-shock measures, also increasing blood flow in the ischemic limb, contributes to a more destructive toxic effect, in particular on the liver, as well as other vital organs and systems of injured animals. As a result, infusion antishock therapy in case of severe compression injury, it is effective against the background of separation of the blood and lymphatic beds of the body and the injured limb, which is achieved by tightly bandaging it, cooling it or applying a tourniquet (if the decision is made to amputate).

The main factors of toxemia in SDS are hyperkalemia, heart attack, kidneys and smooth muscles; biogenic amines, vasoactive polypeptides and proteolytic lysosomal enzymes that cause respiratory distress syndrome; myoglobinemia, leading to tubular blockade and impaired renal reabsorption function; development of an autoimmune condition with the formation of autoantibodies to self-antigens. These pathological factors determine the following mechanisms for the development of DFS.

After tissue reperfusion, one of the first barriers to the movement of endotoxins and aggregates from ischemic and damaged tissues is the lungs. The wide microvasculature of the lungs is the main “battlefield” of the body with endotoxins. In victims with DFS, the number of band leukocytes significantly increases and perivascular interstitial edema occurs. Granulocytes penetrate into the interstitium from the lumen of the capillaries, where they degranulate. In addition to granules with enzymes, band leukocytes produce free oxygen radicals that block plasma enzyme inhibitors and increase the permeability of the capillary membrane. The entry of endotoxins into the capillary bed of the lungs and the pulmonary interstitium is regulated by increasing or decreasing physiological or mixed (with pathological) arteriovenous shunting in the pulmonary microcirculation system and a compensatory increase in the rate of lymphatic drainage.

With a massive intake of endotoxins into the lungs, a gradual disruption of the enzyme systems of granulocytes occurs, insufficiency or blockade of lymphatic drainage systems occurs, depletion of the antitoxic function of the lungs and the development of distress syndrome are observed.

Elements of decay muscle tissue, mainly myoglobin, potassium, phosphorus and lactic acid, accumulate in the blood and cause metabolic acidosis. At the same time, fluid exudates from the affected capillaries into the muscle tissue, resulting in severe swelling of the limb and hypovolemia. Due to the development of hypovolemia, myoglobinemia and acidosis against the background of respiratory distress syndrome, acute renal failure occurs. In this case, destruction of the glomerular and tubular epithelium occurs, the development of stasis and thrombosis in both the cortex and medulla. Significant dystrophic changes occur in the renal tubules, the integrity of individual tubules is disrupted, and their lumen is filled with cell decay products. These early-onset and rapidly progressing changes lead to the development renal failure. Myoglobin, hemoglobin formed during hemolysis of red blood cells, as well as impaired ability of red blood cells to deform, increase ischemia of the renal cortex, which contributes to the progression of morphological changes in their glomerular and tubular apparatus and leads to the development of oliguria and anuria.

Long-term compression of the segment, the development of oxygen starvation and hypothermia in its tissues leads to severe tissue acidosis. After the compression is eliminated, under-oxidized metabolic products (lactic, acetoacetic and other acids) flow from the damaged segment into the general bloodstream. Lactic acid is the metabolite that causes a sharp decrease in blood pH and vascular tone, leads to a decrease in cardiac output and the development of irreversible shock.

Developing hypoxia has a negative impact on vital functions important systems. Oxygen deficiency leads to increased permeability of the intestinal wall and disruption of its barrier function, so vasotoxic substances of a bacterial nature freely penetrate the portal system and block the reticuloendothelial system of the liver. Violation of the antitoxic function of the liver and its anoxia contribute to the release of vasopressive factors. Hemodynamic disturbances in this condition are associated not only with the formation of vasopressors. Data have been obtained that with various types of shock, a specific humoral depressive myocardial factor appears. These components may be the causes of inhibition of myocardial contractility and catecholamine response, as well as important factors in the development of shock. With shock, multiple organ failure inevitably occurs if, before severe metabolic acidosis and vascular insufficiency, adequate intensive therapy was not provided.

Depending on the clinical picture The following forms of SDS are distinguished: extremely heavy, heavy, moderate and light. As experience has shown, all these forms of SDS were observed in patients admitted from the earthquake zone.

The clinical course of SDS is divided into four periods.

• I period- compression of soft tissues with the development of traumatic and exotoxic shock.
• II period- local changes and endogenous intoxication. It begins from the moment of decompression and lasts 2-3 days.

Skin on a compressed limb pale in color, cyanosis of the fingers and nails is noted. Swelling increases. The skin becomes dense. Pulsation of peripheral vessels due to dense edema is not detected. As local manifestations deepen, the general condition of the victims worsens. The symptoms of traumatic shock predominate in them: pain syndrome, psycho-emotional stress, unstable hemodynamics, hemoconcentration, creatininemia, fibrinogen concentration increases, plasma tolerance to heparin increases, fibrinolytic activity decreases, and the activity of the blood coagulation system increases. Urine has a high relative density, protein, red blood cells, and casts appear in it.

SDS is characterized by relatively good condition of the victims immediately after the compression is removed. Only after a few hours (if the limb was not “destroyed” as a result of the disaster) local changes appear in the damaged segment - pallor, cyanosis, variegated skin color, lack of pulsation in the peripheral vessels. Over the next 2-3 days, swelling of one or more limbs that have been subjected to compression increases. Edema is accompanied by the appearance of blisters, dense infiltrates, local and sometimes total necrosis of the entire limb. The victim's condition rapidly deteriorates, and acute cardiovascular failure develops.

In the peripheral blood, its thickening, neutrophilic shift, and lymphopenia are noted. Plasma loss leads to a significant decrease in BCC and CV; there is a tendency to thrombus formation.

It is during this period that intensive infusion therapy is required using forced diuresis and detoxification, without which patients develop respiratory distress syndrome.

III period- development of complications manifested by damage to various organs and systems, a period of acute renal failure. The duration of the period is from the 2nd to the 15th day. Analysis of clinical observations showed that there is not always a correspondence between the prevalence and duration of compression of the limbs or limbs and the severity of renal failure. In this regard, in addition to the classification, mild, moderate and severe acute renal failure should be distinguished. During this period, swelling of the compressed limb or its segment increases, and blisters with transparent or hemorrhagic contents appear on the damaged skin. Hemoconcentration is replaced by hemodilution, anemia increases, diuresis sharply decreases, up to anuria. The content of residual nitrogen, urea, creatinine, and potassium in the blood increases. A classic picture of uremia develops with hypoproteinemia, an increase in the amount of phosphorus and potassium, and a decrease in sodium content.

Body temperature rises. The victim's condition sharply worsens, lethargy and lethargy increase, vomiting and thirst appear, icterus of the sclera and skin, indicating involvement of the liver in the pathological process. Despite intensive therapy, up to 35% of victims die. During this period, it is necessary to use methods of extracorporeal detoxification or (in the absence of an artificial kidney apparatus) peritoneal dialysis; as our experience has shown, hemosorption gives good results (preferably with blood sampling from a vein of the affected limb under the control of intoxication tests).

IV period- convalescence. It begins after renal function has been restored. During this period, local changes prevail over general ones. Infectious complications of open injuries resulting from trauma, as well as complications of wounds after fasciotomies, come to the fore. Generalization of infection and sepsis is possible. In uncomplicated cases, swelling of the limb and pain in them disappear by the end of the month. Restoring the function of the joints of the injured limb, eliminating paresis and paralysis of peripheral nerves depend on the degree of damage to the muscles and nerve trunks. As a result of the death of muscle elements, they are replaced connective tissue and the development of limb atrophy, but function can gradually be restored, especially with positional compression.

An analysis of the results of observations of victims during the earthquake in Armenia in the IV period of SDS showed that they had long-term severe anemia, hypoproteinemia, dysproteinemia (decrease in albumin, increase in globulin fractions, especially the y-fraction), hypercoagulation of the blood, as well as changes in the urine - the presence of protein and cylinders. All victims have a decreased appetite for a long period. Changes in homeostasis are persistent, and with the help of intensive infusion-transfusion therapy they can be eliminated on average by the end of a month of intensive treatment.

V period - victims, a significant decrease in natural resistance factors, immunological reactivity, bactericidal activity of blood, and serum lysozyme activity is revealed. Of the cellular factors, changes occur mainly in the T-lymphocyte system. The leukocyte intoxication index (LII) remains altered for a long time.

Most victims long time deviations in emotional and mental status persist in the form of depressive or reactive psychoses and hysteria.

Isolated from wounds ( in the presence of open damage), the microflora has peculiarities. In the early period (first 7 days) after the earthquake, the wounds are abundantly contaminated with clostridia, mainly. This indicates a high risk of developing clostridial myonecrosis or “gas gangrene” in these patients. Clostridia in all patients were isolated in association with enterobacteria, pseudomonads, and anaerobic cocci. Influenced surgical treatment and antibacterial therapy, wounds in all patients are cleared of clostridia within 7-10 days.

In most patients admitted at a later stage, microbial associations are isolated, an obligatory component of which is Pseudomonas aeruginosa, and their “companions” are enterobacteria, staphylococci and some other bacteria.

In some victims in the fourth period of DFS, necrosis of the deep muscles of the injured limb or its segment is detected, occurring with scant symptoms or asymptomatically. Healing of a wound of a compressed limb is longer than that of ordinary wounds.

The severity of the clinical manifestations of compartment syndrome and their prognosis depend on the degree of compression of the limb, the mass of the affected tissues and combined damage to other organs and structures (traumatic brain injury, trauma internal organs and systems, bone fractures, damage to joints, blood vessels, nerves, etc.).

Treatment of Long-Term Compartment Syndrome:

Modern treatment victims of earthquakes and other mass disasters with VDS varying degrees severity should be comprehensive, taking into account all aspects of the pathogenesis of a given injury, phasing and continuity in the provision of medical benefits. Complexity involves influencing the macroorganism in order to correct all deviations in hemostasis, the local pathological focus and the microflora of wounds. Stage-by-stage means the provision of a specific and necessary volume and nature of medical care for each stage. Continuity in treatment ensures continuity and purposefulness of treatment measures from the beginning of medical care to the recovery of the victim.

In case of massive lesions, it is advisable to organize three stages of medical care:

• Stage I- assistance in the outbreak of mass destruction,
• Stage II- qualified medical care, which is provided in a medical institution located at a short distance from the mass destruction zone and equipped with everything necessary for sorting and providing qualified assistance for injuries to the musculoskeletal system and internal organs, as well as shock and DFS with initial symptoms of renal failure. Due to the massive influx of victims, stay in this institution is limited to 1-2 days.

On at this stage Medical landing units can be used in the form of “flying hospitals” or “hospitals on wheels”, deploying their activities near the source of destruction. Depending on the situation, these institutions may increase or decrease the amount of care they provide.

• Stage III- specialized medical care. For this purpose, a large surgical and traumatology center is used, equipped with everything necessary to provide specialized assistance for open and closed injuries of the musculoskeletal system and their consequences, as well as resuscitation services for the treatment of shock, post-ischemic toxicosis, sepsis and acute renal failure in full. Thanks to the organization of such centers, temporary transfers of patients to other highly specialized institutions for treatment, for example, acute renal failure, etc., are eliminated, where there are no specialists in the treatment of injuries, infected wounds, etc.

Treatment at the scene. At the scene of the incident, the victim must be given painkillers; if possible, a novocaine blockade (preferably a conduction block) is performed at the base of the limb. A tourniquet is applied only when there is obvious crushing of the limb for the purpose of acute amputation. In other cases, the sequence of assistance at the scene of the incident should be as follows: application of a tourniquet, freeing the limb from the obstruction, tight bandaging of the compressed limb, cold, immobilization, removal of the tourniquet, if there are wounds - their mechanical cleaning, application of dressings that have antiseptic, enzymatic and dehydrating properties. properties, bandaging. If possible, cover the damaged limb segment with ice packs and carry out transport immobilization.

At the stage of qualified and specialized care, intensive infusion and transfusion therapy is continued, and central vein catheterization is carried out (if it was not performed at the previous stage). Treatment is aimed at further increasing urine volume through forced diuresis. The volume of infusion-transfusion therapy is at least 500 ml/hour. The infusion products include fresh frozen plasma (500-700 ml per day), glucose-novocaine mixture (400 ml), 5% glucose solution with vitamins C and group B (up to 1000 ml), 5-10% albumin (200 ml), 4% sodium bicarbonate solution (400 ml), mannitol solution at the rate of 1 g per 1 kg of body weight, detoxification agents ( hemodesis, neohemodes). The composition of fluids and their volume are adjusted depending on diuresis, degree of intoxication, and CBS indicators. Monitor blood pressure, central venous pressure, and urination. To record the amount of urine, catheterization is performed hourly Bladder. Drug therapy: to stimulate diuresis, lasix and aminophylline, heparin, antiplatelet agents (chirantil, trental), retabolil or nerobolil are prescribed, cardiovascular drugs, immunocorrectors. Such treatment should ensure urination in an amount of at least 300 ml/hour.

If conservative treatment is ineffective within 8-12 hours and diuresis decreases to 600 ml/day or lower, the issue of hemodialysis is decided. Anuria, hyperkalemia more than 6 mmol/l, pulmonary and cerebral edema are emergency indications for hemodialysis. The volume of infusion therapy during the interdialytic period is 1500-2000 ml.

In case of bleeding due to uremia and disseminated intravascular coagulation, plasmapheresis is urgently performed, followed by transfusion of up to 1000 ml of fresh frozen plasma and protease inhibitors are prescribed (trasylol, gordox, contrical).

Surgical tactics depends on the condition of the victim, the degree of ischemia of the injured limb, the presence of crushed tissue, bone fractures and must be active.

In the absence of wounds on the compressed limb surgical tactics can be determined by the classification of the degree of ischemia.

• I degree- slight indurative swelling of soft tissues.

The skin is pale, and at the border of the lesion hangs somewhat over the healthy skin. There are no signs of circulatory problems. Conservative treatment gives a pronounced effect.

• II degree- moderately expressed indurative swelling of soft tissues and their tension. The skin is pale, with areas of slight cyanosis. After 24-36 hours, blisters may form containing a clear yellowish liquid, which, when opened, reveal a moist, pale pink surface. Increased swelling in subsequent days indicates a violation of venous circulation and lymphatic drainage. Insufficiently adequate conservative treatment can lead to progression of microcirculation disorders, microthrombosis, increased edema and compression of muscle tissue.
• III degree- pronounced indurative swelling and tension of soft tissues. The skin is cyanotic or “marbled” in appearance. Skin temperature is noticeably reduced. After 12-24 hours, blisters with hemorrhagic contents appear. Under the epidermis, a moist, dark red surface is exposed. Indurative edema and cyanosis quickly increase, which indicates severe microcirculation disorders and venous thrombosis. Conservative treatment is ineffective and leads to the development of a necrotic process. Wide incisions with dissection of the fascial sheaths eliminate tissue compression. Blood flow is restored.
• IV degree- indurative edema is moderately expressed, the tissues are sharply tense. The skin is bluish-purple in color, cold, there are separate epidermal blisters with hemorrhagic contents. After removal of the epidermis, a cyanotic-black, dry surface is exposed. In the following days, the swelling practically does not increase, which indicates deep microcirculation disorders, insufficiency of arterial blood flow, widespread thrombosis venous vessels. Conservative treatment is ineffective. Wide fasciotomy ensures the maximum possible restoration of blood circulation, allows limiting the necrotic process in more distal sections, and reducing the intensity of absorption of toxic products. In most cases, indications are given for limb amputation.

This classification, without claiming to be a complete reflection of the process, helps to choose treatment tactics and significantly reduce the number of amputations.

In the presence of crush wounds on injured limbs, at the second stage of evacuation, a thorough primary surgical treatment is performed with wide opening of the wound, excision of clearly non-viable tissue, removal of foreign bodies and loose bone fragments, copious washing of the wound with antiseptics, sanitation with ultrasound and vacuuming. The application of blind seams is unacceptable. Bandages with antiseptic and dehydrating properties are applied to the wound.

By doing primary surgical treatment at the second stage of evacuation, skin grafting, both free and non-free, should not be performed, since the process of tissue necrosis can continue in the following days. In addition, donor sites after cutting out skin autografts can serve as additional gates for infection, and plastic surgery, by moving local tissues, worsens microcirculation and blood supply to the affected area, which is already impaired as a result of tissue compression, which can lead to deepening and expansion of tissue necrosis. Exposed areas of bone should be covered, if possible, with surrounding soft tissue, applying guiding non-constricting sutures. When deep pockets form, they need to be drained and counter-apertures applied.

Analysis of the results of treatment of victims showed that performing extraosseous and intraosseous osteosynthesis of segments subjected to compression at this stage of medical care should be considered a mistake. Such osteosynthesis worsens the blood circulation of the segment, aggravates the necrotic process, and “opens the gates” of infection. At this stage, stable fixation should be performed using transosseous compression-distraction pin or rod devices, even without final and complete adaptation of the fragments. In the absence of opportunities or conditions for the application of transosseous devices for fixation of the limbs, deep plaster splints are used. Circular plaster casts should not be applied.

After providing qualified assistance at this stage, victims with limb injuries are evacuated to specialized hospital centers (the third stage of medical care), where they are admitted on the 3-7th day after the injury. At this stage, stable fixation of fractures is carried out with transosseous fixation devices, if it was not performed at the previous stage, or correction and adaptation of fragments in the device is continued if they were applied earlier. At the same time, intensive local treatment of wound surfaces is carried out in order to quickly cleanse the wounds of necrotic tissue and prepare for autoplasty or the application of secondary sutures on the 15-20th day after injury. For local treatment of wound surfaces, drugs with antiseptic, enzymatic and dehydrating properties are effective.

After cleansing the wound surface of necrotic tissue and the appearance of fresh granulation tissue, free skin autoplasty is performed with split grafts, perforated in a ratio of 1:2-1:5. Among other types of skin grafting, non-free skin autoplasty (Italian) may be recommended, especially in the presence of wounds in the area of ​​the hand and forearm. Indications for combined skin autoplasty are limited to displaced local tissues, since moving flaps of skin and soft tissue in the area of ​​​​compressed segments can aggravate disturbances of microcirculation and blood supply and lead to necrosis of the flaps.

By this time, the prevalence of necrosis of bone areas subjected to compression is fully revealed; the boundaries of bone tissue necrosis can be determined using radionuclide research. In order to remove clearly necrotic areas of the bone, radical sequesterectomy, longitudinal and segmental resections are performed. The resulting postoperative bone cavities are replaced with demineralized bone grafts and muscles. For defects, compression-distraction osteosynthesis has proven itself well.

At stages qualified and specialized assistance The use of modern methods of active detoxification is of paramount importance. An increase in blood and lymph toxicity in patients can be detected earlier than they appear clinical symptoms toxicosis, therefore, without waiting for the patients’ condition to worsen, a blood test for toxicity should be performed using the paramecium test and the concentration of “medium molecules”. In case of increased toxicity, hemolymphosorption and enterosorption are indicated; in case of disturbances in homeostasis and hyperhydration, hemodialysis is indicated. When toxicosis, overhydration and disturbances of homeostasis are combined, hemo-, lympho-, enterosorption and hemodialysis are simultaneously carried out in the ultrafiltration mode, if necessary - repeatedly. At the same time, they carry out targeted antibacterial therapy: immunocorrection, as well as rehabilitation measures that are carried out throughout the entire process of treating the victim.

Thus, in the treatment of compartment syndrome with open and closed injuries of the musculoskeletal system, constant work of trauma surgeons, resuscitators, toxicologists, therapists, and nephrologists is required. Victims who have suffered SDS require follow-up medical supervision.

Prevention of Long-Term Compartment Syndrome:

In order to prevent wound infection, a combination of antibiotics is administered with the mandatory inclusion of an antibiotic of the penicillin group (given the frequent isolation of clostridial anaerobes from the wound). Prophylactic use Antibiotics, without completely preventing subsequent wound suppuration, prevent the development of clostridial myonecrosis (gas heating), for the development of which in this situation there are favorable conditions. It is important as early as possible, if possible, even before the victim is completely freed from the rubble, to begin infusion therapy in order to normalize the blood volume, increase the volume and alkalinize the urine. Crystalloids, rheopolyglucin, 4% sodium bicarbonate solution, and mannitol should be used as the first infusion media. The rate of fluid administration during infusion is at least 500 ml/h.

The above measures, carried out at the scene and during the evacuation stages, are measures to prevent shock, renal failure and gas gangrene.

Which doctors should you contact if you have Long-Term Compartment Syndrome:

• Traumatologist
• Surgeon

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Other diseases from the group Trauma, poisoning and some other consequences of external causes:

Arrhythmias and heart block in cardiotropic poisonings

Depressed skull fractures

Intra- and periarticular fractures of the femur and tibia

Congenital muscular torticollis

Congenital malformations of the skeleton. Dysplasia

Lunate dislocation

Dislocation of the lunate and proximal half of the scaphoid (de Quervain's fracture dislocation)

Tooth luxation

Dislocation of the scaphoid

Dislocations of the upper limb

Dislocations of the upper limb

Dislocations and subluxations of the radial head

Dislocations of the hand

Dislocations of the foot bones

Shoulder dislocations

Vertebral dislocations

Forearm dislocations

Metacarpal dislocations

Foot dislocations at the Chopart joint

Dislocations of the phalanges of the toes

Diaphyseal fractures of the leg bones

Diaphyseal fractures of the leg bones

Old dislocations and subluxations of the forearm

Isolated fracture of the ulnar shaft

Deviated nasal septum

Tick ​​paralysis

Combined damage

Bone forms of torticollis

Posture disorders

Knee instability

Gunshot fractures in combination with soft tissue defects of the limb

Gunshot injuries to bones and joints

Gunshot injuries to the pelvis

Gunshot injuries to the pelvis

Gunshot wounds of the upper limb

Gunshot wounds of the lower limb

Gunshot wounds to joints

Gunshot wounds

Burns from contact with Portuguese man-of-war and jellyfish

Complicated fractures of the thoracic and lumbar spine

Open injuries to the diaphysis of the leg

Open injuries to the diaphysis of the leg

Open injuries to the bones of the hand and fingers

Open injuries to the bones of the hand and fingers

Open injuries of the elbow joint

Open foot injuries

Open foot injuries

Frostbite

Wolfsbane poisoning

Aniline poisoning

Antihistamine poisoning

Antimuscarinic drug poisoning

Acetaminophen poisoning

Acetone poisoning

Poisoning with benzene, toluene

Toadstool poisoning

Poisoning with poisonous wech (hemlock)

Halogenated hydrocarbon poisoning

Glycol poisoning

Mushroom poisoning

Dichloroethane poisoning

Smoke poisoning

Iron poisoning

Isopropyl alcohol poisoning

Insecticide poisoning

Iodine poisoning

Cadmium poisoning

Acid poisoning

Cocaine poisoning

Poisoning with belladonna, henbane, datura, cross, mandrake

Magnesium poisoning

Methanol poisoning

Methyl alcohol poisoning

Arsenic poisoning

Indian hemp drug poisoning

Poisoning with hellebore tincture

Nicotine poisoning

Carbon monoxide poisoning

Paraquat poisoning

Poisoning by smoke vapors from concentrated acids and alkalis

Poisoning by oil distillation products

Poisoning with anti-depressant drugs

Salicylate poisoning

Lead poisoning

Hydrogen sulfide poisoning

Carbon disulfide poisoning

Poisoning with sleeping pills (barbiturates)

Poisoning with fluoride salts

Poisoning by central nervous system stimulants

Strychnine poisoning

Tobacco smoke poisoning

Thallium poisoning

Tranquilizer poisoning

Acetic acid poisoning

Phenol poisoning

Phenothiazine poisoning

Phosphorus poisoning

Poisoning with chlorine-containing insecticides

Poisoning with chlorine-containing insecticides

Cyanide poisoning

Ethylene glycol poisoning

Ethylene glycol ether poisoning

Poisoning with calcium ion antagonists

Barbiturate poisoning

Beta blocker poisoning

Poisoning with methemoglobin formers

Poisoning with opiates and narcotic analgesics

Poisoning with quinidine drugs

Pathological fractures

Maxillary fracture

Fracture of the distal radius

Long-term compartment syndrome (traumatic anuria, Bywaters syndrome, traumatic rhabdomyolysis) is a pathological condition associated with the restoration of blood circulation in tissues, for a long time deprived of it. SDS occurs when victims are removed from the rubble, where they end up during earthquakes, man-made disasters, and terrorist attacks. A type of this pathology is positional compression syndrome, which occurs in the limbs of people who remain immobile for a long time (coma, alcohol intoxication). In this case, compression of the limbs occurs under the mass own body sick.

Most often, people suffer from crash syndrome in regions where military operations are ongoing, during earthquakes, and in car accidents. In recent years, terrorism has become increasingly important as a cause of SDS, in which explosions of buildings can lead to victims falling under the rubble.

In all these cases, with the exception of car accidents, situations arise with the mass arrival of victims in medical institutions. Therefore, it is especially important to quickly identify the development of DFS and begin its treatment at the prehospital stage.

Types of compartment syndrome

This pathological condition is classified according to several criteria:

• Based on the type of compression, it is divided into crushing ( traumatic injury muscles), direct and positional compression;
• by localization - chest, abdominal, pelvic areas, hand, forearm, thigh, lower leg, foot in various combinations;
• in combination with damage to other parts of the body:
  • internal organs;
  • bones, joints;
  • main vessels, nerve trunks;
• the presence of complications;
• degree of severity;
• combinations with other types of injury:
  • burns or frostbite;
  • radiation sickness;
  • poisoning, etc.

What happens in the body during crash syndrome

The basis of this pathology is the massive death of muscle cells. There are several reasons for this process:

• their direct destruction by a traumatic factor;
• cessation of blood supply to the compressed muscle;
• cellular hypoxia associated with hemorrhagic shock, often accompanying massive trauma.

As long as the muscle is compressed, there is no crash syndrome. It begins after the pinched part of the body is released from external pressure. At the same time, the compressed blood vessels open, and the blood rich in products the breakdown of muscle cells rushes into the mainstream. Once it reaches the kidneys, myoglobin (the main muscle protein) clogs the microscopic kidney tubules, blocking urine production. Within a few hours, tubular necrosis and kidney death develop. The result of these processes is acute renal failure.

The course of the disease directly depends on both the duration of compression and the volume of affected tissue. So, when the forearm is compressed for 2-3 hours, there will be no acute renal failure, although a decrease in urine production is still noted. There are no intoxication phenomena that are inevitable with longer compression. Such patients almost always recover without consequences.

Extensive compression lasting up to 6 hours leads to moderate crash syndrome. In this case, there are striking signs of endotoxicosis (intoxication) and impaired renal function for a week or more. The prognosis depends on the timing of first aid and the timeliness and volume of subsequent intensive care.

When compression lasts for more than 6 hours, SDS develops in severe form. Endotoxicosis rapidly increases, the kidneys shut down completely. Without hemodialysis and powerful intensive care, a person inevitably dies.

The symptoms of crash syndrome depend on the period of development of the pathology.

In the early period (1-3 days), there are mainly symptoms of shock: pallor, weakness, tachycardia, low blood pressure. The most dangerous moment in this period is the direct extraction of the victim from the rubble. As soon as blood circulation is restored in the affected limb, a large amount of potassium is released into the blood, which can lead to instant cardiac arrest. But even without this, in severe forms of DFS, the phenomena of renal-liver failure and pulmonary edema, as well as cardiac arrhythmias, develop already in the first day.

For early period Local manifestations of the affected limbs are typical:

• skin condition - tense (due to interstitial edema), pale, bluish, cold to the touch;
• there are blisters on the skin;
• there is no pulse in the peripheral arteries;
• all forms of sensitivity are either suppressed or absent;
• the ability for active movements of the affected limb is reduced or absent.

More than half of the victims are also diagnosed with corresponding bones.

In the intermediate period (4-20 days), intoxication and acute renal failure come first. Initially, the patient's condition is short term stabilizes, but then begins to rapidly deteriorate, disturbances of consciousness appear, up to deep stupor. The urine becomes brown, its amount drops to zero, and this condition can last up to 3 weeks. With a favorable course of the disease, this phase passes into the phase of polyuria, in which the amount of urine excreted increases sharply. It is in the intermediate period that infectious complications tend to generalize (spread throughout the body) most often develop, and pulmonary edema is also possible.

If during the intermediate period the patient does not die, then the third period begins - late. It lasts from 3-4 weeks to several months. At this time, the functions of all affected organs - lungs, liver and, most importantly, kidneys - are gradually normalized.

The development of long-term compartment syndrome can be suspected already at the scene of the incident. Information about a natural disaster, about a person’s long stay under the rubble, suggests the possible development of VDS. Objective data allow us to make a diagnosis of crash syndrome with a fairly high degree of confidence.

In laboratory conditions, you can obtain information about hemoconcentration (blood thickening), electrolyte disturbances, increased levels of glucose, creatinine, urea, and bilirubin. A biochemical blood test reveals an increase in liver transaminases and a decrease in protein concentration. An analysis of the acid-base state of the blood shows the presence of acidosis.

In the urine analysis, at first there are no changes, but then the urine becomes brown in color, its density increases, protein appears in it, and the pH shifts to the acidic side. Microscopic examination reveals a large number of cylinders, erythrocytes, and leukocytes.

First aid measures for compartment syndrome depend on who is providing it, as well as the availability of forces involved and the availability of qualified personnel. An untrained person can do little to prevent the development of severe complications, while professional rescuers, through their actions, seriously improve the prognosis for the patient.

First of all, the one removed from under must be moved to a safe place. Wounds and abrasions identified during a superficial examination should be covered with aseptic dressings. If there is bleeding, measures should be taken to stop it as soon as possible; fractures are immobilized with special splints or improvised means. If starting an intravenous infusion at this stage is not possible, the patient must be provided with plenty of fluids. These measures can be carried out by any person participating in rescue operations.

The issue of applying a tourniquet to the injured limb is currently being debated. Practice, however, shows the effect of this method when used correct use. It is advisable to apply a tourniquet before the victim is released; the place of application is above the place of compression. The tourniquet helps prevent the influence of large doses of potassium, which simultaneously reach the heart muscle and lead to the development of collapse and fatal cardiac arrhythmias. It is recommended to leave it for a long time only in two cases:

• with complete destruction of a limb;
• with gangrene.

At the next stage, assistance is provided by trained people - rescuers, paramedics, nurses. At this stage, the victim must have an intravenous catheter installed (although it is ideal to do this even before liberation from the wreckage), with the help of which the infusion of saline blood-substituting solutions without potassium content is started. Infusion therapy should continue for as long as possible; it is advisable not to interrupt it even when evacuating the victim to a medical facility. Adequate pain relief is mandatory. If help is provided by a specialist, he can use narcotic analgesics (Promedol); if not, using any painkiller like baralgin or ketorolac will be better than refusing analgesia. At this stage, you can cut off the clothing if there is significant swelling of the affected limb.

In parallel, patients are injected intravenously with a solution of sodium bicarbonate to correct acidosis, calcium chloride to neutralize excess potassium, and glucocorticoids to stabilize cell membranes.

In a hospital setting, measures are taken aimed at stimulating kidney function - administering diuretics in parallel with infusions saline solutions and sodium bicarbonate. It is possible to use blood purification methods, with preference given to the most gentle of them - hemosorption, plasmapheresis. They should be used with caution and only in case of obvious onset of pulmonary edema or uremia.

Antibiotic therapy is used only when there are clear signs of wound infection. Heparin prophylaxis helps prevent the development of disseminated intravascular coagulation syndrome, a particularly severe complication of DIC.

Surgical treatment of long-term compartment syndrome consists of amputation of a nonviable limb. In case of severe swelling leading to compression of the great vessels, fasciotomy surgery in combination with plaster immobilization is indicated.

Complications

The main complication of crash syndrome is acute renal failure. It is the main cause of death in this pathology.

Pulmonary edema is a life-threatening condition in which the lung tissue becomes saturated with fluid escaping from the blood vessels. At the same time, gas exchange in the alveoli worsens and hypoxia increases.

Hemorrhagic shock due to massive blood loss is observed when large vessels are damaged. The situation is worsened by the fact that in the affected area the ability of tissues to withstand the damaging effects of external factors is sharply reduced.

DIC syndrome develops as a consequence of bleeding, as well as due to direct damage to blood vessels by decay products of the affected tissues. This is the most severe complication of DFS with a high mortality rate.

Infectious and septic complications often accompany crash syndrome. Due to reduced tissue viability, the damaged area is easily affected by microorganisms, especially anaerobic ones. The result is severe illnesses that worsen the course of the underlying pathology.

In case of crash syndrome, the timing of the start of assistance is important. The sooner the victim is removed from the rubble, the more complete the scope of measures taken, the greater his chances of survival.

Bozbey Gennady Andreevich, emergency physician

is a shock-like state that occurs after prolonged compression of the torso, limbs or their segments by heavy objects. Manifested by pain, deterioration, swelling of the affected parts of the body, acute renal failure. Without medical care, patients die from acute renal failure, increasing intoxication, pulmonary or cardiovascular failure. Treatment includes detoxification and plasma replacement infusion therapy, extracorporeal hemocorrection, antibiotic therapy, excision of areas of necrosis or amputation of a crushed limb.

ICD-10

T79.5 Traumatic anuria

General information

Long-term crush syndrome (CDS), other names - traumatic toxicosis, crash syndrome, Bywaters syndrome, myorenal syndrome - a pathological shock-like condition that occurs after prolonged compression of the torso, limbs or their segments by heavy objects. Crash syndrome develops immediately after the release of the patient and restoration of blood and lymph flow in the affected parts of the body. Accompanied by a deterioration in general condition, the development of toxemia and acute renal failure, and with a large area of ​​damage, it often ends in the death of the patient. In traumatology and orthopedics, a common type of crash syndrome is distinguished - the so-called positional compression syndrome (PCS), which develops as a result of prolonged (more than 8 hours) compression of body parts while a person is stationary on a hard surface.

Reasons for SDR

Typically, long-term crush syndrome occurs in victims of landslides, earthquakes, mine collapses, construction work, road accidents, logging, explosions and the destruction of buildings as a result of bombing.

Positional compression syndrome is usually detected in patients who, at the time of injury, were in a state of poisoning with sleeping pills, drugs or alcohol. The upper limbs tucked under the body are more often affected. For the reasons of development, symptoms and treatment methods, positional crush syndrome is practically no different from long-term crush syndrome, however, it usually proceeds more favorably due to the smaller area of ​​​​the lesion.

Pathogenesis

The occurrence of long-term crush syndrome is due to a combination of three factors:

• pain syndrome;
• massive loss of plasma caused by the release of the liquid part of the blood through the walls of blood vessels into damaged tissues;
• traumatic toxemia (intoxication of the body with tissue decay products).

Prolonged painful stimulation during crash syndrome leads to the development of traumatic shock. Loss of plasma causes blood to thicken and cause thrombosis small vessels. Traumatic toxemia in crash syndrome develops due to the absorption of tissue decay products of injured muscles into the blood. Immediately after the limb is released from the damaged tissue, a significant amount of potassium ions enters the vascular bed, which can cause arrhythmia, and in severe cases, cessation of the functioning of the lungs and heart.

Subsequently, the crushed muscle tissue of a patient with crush syndrome loses up to 66% of potassium, 75% of myoglobin, 75% of phosphorus and 70% of creatinine. Decomposition products enter the blood, causing acidosis and hemodynamic disturbances (including a sharp narrowing of the vessels of the renal glomeruli). Myoglobin damages and clogs the kidney tubules. All this leads to the development of acute renal failure, which threatens the life of a patient with crash syndrome.

Classification

By severity:

• Mild form of crash syndrome. Occurs when segments of a limb are crushed for 4 hours or less.
• Moderate form of crash syndrome. Develops as a result of crushing one limb within 4-6 hours. With timely initiation of treatment, the prognosis is favorable.
• Severe form of crash syndrome. Occurs when one limb is crushed for 6-8 hours. Accompanied by hemodynamic disorders and acute renal failure. With timely initiation of treatment, the prognosis is relatively favorable.
• An extremely severe form of crash syndrome. Develops as a result of crushing of two or more limbs for 6 or more hours. Accompanied by severe shock. The prognosis is unfavorable.

According to clinical symptoms:

• early period (from the moment of release to 3 days);
• toxic period (begins on days 4-5);
• period of late complications (develops 20-30 days after the injury).

Symptoms of SDR

Immediately after the compression is removed, the general condition of the victim improves. A patient with long-term crush syndrome experiences pain and limited movement in the crushed limb. During the first hours after release, swelling of the affected area gradually increases, becoming dense and woody. Blisters with serous-hemorrhagic contents form on the skin of the limb. When examining the damaged part of the body, a weakening of the pulsation of the arteries, a decrease in sensitivity and local temperature are revealed.

Growing general symptoms. The condition of the victim with crash syndrome is deteriorating. After a short period of excitement, the patient becomes lethargic and inhibited. There is a decrease in blood pressure and body temperature, arrhythmia, tachycardia, and severe pallor of the skin. The skin of a patient with crash syndrome is covered with sticky cold sweat. Possible loss of consciousness, involuntary defecation and urination. Sometimes pulmonary edema develops. The amount of urine excreted decreases. Without adequate medical care, there is a risk of death within 1 or 2 days.

Foci of necrosis form on the crushed limb. When dead tissue is sloughed away, the muscles that have characteristic appearance boiled meat. Suppuration of wounds and eroded surfaces develops. Acute renal failure appears and gradually increases. On days 5-6, patients with long-term crush syndrome develop uremic syndrome. An increase in potassium levels in the blood causes arrhythmia and bradycardia.

On days 5-7, signs of pulmonary insufficiency appear. Increasing intoxication, caused by the entry into the bloodstream of tissue decay products and bacterial toxins from a crushed limb, causes toxic hepatitis. Endotoxic shock is possible. The symptoms of multiple organ failure in patients with crash syndrome gradually decrease within 2-3 weeks.

Acute renal failure in crash syndrome resolves approximately a month after the injury. The patient's condition improves, his body temperature returns to normal. Pain and swelling of the limb are reduced. Necrotic muscles are replaced by connective tissue, which leads to muscle atrophy and the development of contractures. In case of unfavorable development of events, local (suppuration) and general (sepsis) complications are possible.

Diagnostics

In order to compensate for metabolic acidosis, a patient with crash syndrome is given a 4% sodium bicarbonate solution by drip. Broad-spectrum antibiotics are prescribed intramuscularly. Symptomatic therapy is carried out (diuretics, analgesics, antihistamines and antiarrhythmic drugs). In case of long-term crush syndrome, extracorporeal hemocorrection (hemodialysis, plasma and hemosorption) is carried out as early as possible.

If the viability of the muscle tissue is preserved and there is pronounced subfascial edema with impaired local circulation, the traumatologist performs a fasciotomy with revision and excision of necrotic muscle bundles. If there is no suppuration, the wound is sutured on the 3-4th day, after swelling has decreased and the general condition of the patient with crash syndrome has improved.

In cases of irreversible ischemia, amputation of the limb is performed above the site of application of the tourniquet. In other cases, excision of necrotic areas while preserving viable muscle bundles is indicated. Muscle viability is determined during surgery. The criteria for viability are the preservation of normal color, the ability to bleed and contract. After tissue excision, the wound is washed generously with antiseptics. No stitches are required. The wound heals by secondary intention.

In the long term, patients with long-term crush syndrome are advised to take courses rehabilitation treatment(massage, exercise therapy) aimed at restoring muscle strength and eliminating contractures.

CHAPTER 7 BLEEDING AND BLOOD LOSS. INFUSION-TRANSFUSION THERAPY. PREPARATION AND BLOOD TRANSFUSION IN WAR

CHAPTER 10 TACTICS OF PROGRAMMED MULTISTAGE SURGICAL TREATMENT OF WOUNDS AND INJURIES (DAMAGE CONTROL SURGERY)

CHAPTER 11 INFECTIOUS COMPLICATIONS OF COMBAT SURGICAL INJURIES

CHAPTER 20 COMBAT CHEST INJURY. THORACOABDOMINAL WOUNDS

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

The first descriptions of the SDS clinic for earthquake victims date back to the beginning of the 20th century. During the Second World War E. Byuo-ters presented a detailed description of a specific pathology in the wounded recovered from the ruins after the bombing of London, calling it “crash syndrome” (from the English word “crush” - crush, crush). In our country, the most famous researchers of SDS were AND I. Pytel(observations of the wounded during the bombing of Stalingrad), M.I. Kuzin(earthquake in Ashgabat 1948), E. A. N echaev, G. G. Savitsky(earthquake in Armenia 1988).

9.1. TERMINOLOGY, PATHOGENESIS

AND CLASSIFICATION OF THE SYNDROME

PROLONGED COMPRESSION

A complex of specific pathological disorders that develops after the release of the wounded from the rubble, where they were crushed by heavy debris for a long time (for 1 hour or more), is called long-term compartment syndrome. The emergence of SDS, which is described under different names (long-term crush syndrome, crush syndrome, traumatic toxicosis, traumatic rhabdomyolysis etc.), is associated with the resumption of blood circulation in damaged and long-term ischemic tissues. In a large-scale war, the frequency of development of SDS can reach 5-20%.

In wounded people with SDS, damage to the extremities is mainly observed (more than 90% of cases), because Compression of the head and torso due to damage to internal organs is often fatal.

In injury surgery, in addition to SDS, there is also positional compression syndrome as a result of ischemia of parts of the body (limb, shoulder blade area, buttocks, etc.) from prolonged compression by the victim’s own weight lying in one position (coma, alcohol intoxication). Recirculation syndrome develops after restoration of a damaged artery in a long-term ischemic limb or removal of a long-term tourniquet.

basis pathogenesis the above similar pathological conditions is endogenous intoxication by products of tissue ischemia and reperfusion . In compressed tissues, along with areas of direct traumatic necrosis, ischemic zones are formed where sour foods anaerobic metabolism. After the wounded are released from compression, blood and lymph circulation is resumed in ischemic tissues, characterized by increased capillary permeability. This is called tissue reperfusion. In this case, toxic substances (myoglobin, products of impaired lipid peroxidation, potassium, phosphorus, polypeptides, tissue enzymes - histamine, bradykinin, etc.) enter the general bloodstream.

Happening toxic damage to internal organs, primarily the lungs, with the formation of ARF.

Hyperkalemia may lead to acute disorder heart activity.

Under-oxidized products of anaerobic metabolism (lactic acid, etc.) are also washed out from ischemic tissues, which cause pronounced metabolic acidosis.

The most dangerous is release into the blood from ischemic striated muscles large quantities squirrel myoglobin. Myoglobin is freely filtered in the renal glomeruli, but clogs the renal tubules, forming insoluble hematin hydrochloride under conditions of metabolic acidosis (if the urine pH is greater than 6, the likelihood of developing renal failure in DFS is reduced). In addition, myoglobin has a direct toxic effect on the epithelium of the renal tubules, which together leads to myoglobinuric nephrosis and acute renal failure(OP N).

Rapidly developing post-ischemic edema of damaged and long-term compressed tissues causes acute hypovolemia with hemo concentration (BCV decreases by 20-40% or more). This is accompanied by a clinical picture of shock and, ultimately, also contributes to the deterioration of kidney function.

Severity of the current	Area of ​​limb compression	Approximate timing of compression	Severity of endotoxicosis	Forecast
mild degree	Small (forearm or lower leg)	No more than 2-3 hours	Endogenous intoxication insignificant, oliguria is eliminated through several days	With proper treatment, favorable
Moderate SDS	More extensive compression	From 2-3 to 6 o'clock	Moderate endo- toxicosis and acute renal failure in a week and more after	Determined by the timing and quality of first aid and treatment with early use of extracorporeal detoxification
Severe SDS	Compression of one or two limbs		Endogenous intoxication rapidly increases, acute renal failure, MODS and other life-threatening complications develop	In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable

oliguria stops after a few days. The prognosis for mild DFS with proper treatment is favorable.

Moderate SDS develops with larger areas of compression of the limb for up to 6 hours. It is accompanied by endotoxicosis and impaired renal function for a week or more after the injury. The prognosis of moderate SDS is determined by the timing and quality of first aid, as well as subsequent treatment with the early use of extracorporeal detoxification.

Severe SDS develops when one or two limbs are compressed for more than 6 hours. With severe DFS, endogenous intoxication quickly increases, acute renal failure, MODS and other life-threatening complications develop. In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable.

It should be noted that There is no complete correspondence between the severity of disorders of the functions of vital organs and the scale and duration of tissue compression. Mild DFS with untimely or inadequate medical care can lead to anuria or other fatal complications. On the other hand, with very long periods of compression of the extremities (more than 2-3 days), DFS may not develop due to the lack of restoration of blood circulation in necrotic tissues.

9.2. PERIODIZATION, CLINICAL SYMPTOMATICS OF LONG-TERM COMPRESSION SYNDROME

Early, intermediate and late periods of the course of SDS are distinguished (Table 9.2).

Table 9.2. Periodization of long-term compartment syndrome

VTS periods	Development timeframe	Main content
		With mild DFS, there is a hidden course. With moderate and severe SDS, the picture of traumatic shock
Intermediate		acute renal failure and endotoxicosis (pulmonary and cerebral edema, toxic myocarditis, disseminated intravascular coagulation syndrome, intestinal paresis, anemia, immunosuppression)
Late (restorative)	From 4 weeks to 2-3 months after compression	Restoration of kidney function, liver, lungs and other internal organs. High danger development

9.2.1. Early period of compartment syndrome

Early period clinic (1-3 days) varies significantly among different wounded people. With moderate and severe SDS, after release from compression, a picture of traumatic shock may develop: general weakness, pallor, arterial hypotension and tachycardia.

Due to hyperkalemia, cardiac arrhythmias are recorded (sometimes up to cardiac arrest). In the next 1-2 days, the clinical picture manifests itself as instability in the respiratory and circulatory systems. With severe DFS, symptoms develop already in the first days acute renal failure and swelling of the lungs x(the earlier signs of anuria appear, the more dangerous they are prognostically).

In other cases, the general condition is initially satisfactory. In the absence of severe craniocerebral injuries, consciousness in all wounded patients with SDS is, as a rule, preserved.

The wounded, freed from the rubble, complain of severe pain in an injured limb that swells quickly. The skin of the limb becomes tense, pale or bluish, cold to the touch, and blisters appear. Pulsation of peripheral arteries due to edema may not be detected, sensitivity and active movements reduced or absent. More than half of the wounded with SDS also have fractures of the bones of the compressed limbs, Clinical signs which may complicate the early diagnosis of DFS.

Due to severe edema, tissue pressure in the muscles of the limbs, enclosed in dense osteofascial sheaths, can exceed the perfusion pressure in the capillaries (40 mm Hg) with further deepening of ischemia. This pathological condition, which can occur not only with SDS, is designated by the term compartment syndrome (from the English “compartment” - sheath, vagina) or the syndrome of “increased intracase pressure”.

In the majority of wounded people with moderate and mild SDS, with prompt medical care, the general condition is temporarily stabilized (“bright period” of SDS).

Laboratory research blood reveals signs of hemoconcentration (increased hemoglobin numbers, hematocrit, decreased BCC and CV), pronounced electrolyte disturbances (increased potassium and phosphorus content), increased levels of creatinine, urea, bilirubin, glucose. Hyperfermentemia, hypoproteinemia, hypocalcemia, and metabolic acidosis are noted. There may be no changes in the first portions of urine, but then due to the release of myoglobin urine turns brown, is characterized by a high relative density with a pronounced shift in pH to the acidic side. A large amount of protein, red blood cells, white blood cells, and casts are also detected in the urine.

9.2.2. Intermediate period of long-term compartment syndrome

In the intermediate period of SDS (4-20 days) symptoms of endotoxemia and acute renal failure come to the fore. After short-term stabilization, the condition of the wounded worsens, and signs of toxic encephalopathy (profound stupor, stupor) appear.

For severe DFS dysfunction of vital organs increases rapidly. The development of acute renal failure is signaled by oligonuria (a decrease in the rate of hourly diuresis of less than 50 ml/h). Anuria can last up to 2-3 weeks with a transition in favorable cases to the polyuric phase of acute renal failure. Due to overhydration, overload of the pulmonary circulation is possible, up to pulmonary edema. Cerebral edema, toxic myocarditis, disseminated intravascular coagulation syndrome, intestinal paresis, persistent toxic anemia, and immunosuppression develop.

SDS of moderate and mild severity characterized mainly by signs of oligoanuria, endotoxemia and local manifestations.

Swelling of the injured limbs persists or increases even more. In the muscles of the compressed limbs, as well as in areas of positional compression, foci of progressive secondary necrosis are formed, supporting endogenous intoxication. In ischemic tissues, infectious (especially anaerobic) complications often develop, which tend to generalize.

Laboratory research with the development of oligoanuria, a significant increase in creatinine and urea is detected. Hyperkalemia, uncompensated metabolic acidosis, and severe anemia are noted. Under microscopy, urine sediment reveals cylindrical formations consisting of desquamated tubular epithelium, myoglobin and hematin crystals.

9.2.3. Late period of long-term compartment syndrome In the late (recovery) period of SDS - after 4 weeks and up to

up to 2-3 months after compression - in favorable cases, there is a gradual improvement in the general condition of the wounded. There is a slow restoration of the functions of the affected internal organs (kidneys, liver, lungs, heart, etc.). However, toxic and dystrophic disorders in them, as well as severe immunosuppression, can persist for a long time. The main threat to the life of the wounded with SDS during this period is generalized IO.

Local changes are expressed in long-term non-healing purulent and purulent-necrotic wounds of the extremities. The functional outcomes of treatment of limb injuries with DFS are often unsatisfactory: atrophy and connective tissue degeneration of muscles, joint contractures, and ischemic neuritis develop.

Examples of diagnosis of SDS:

1. Severe DFS of both lower extremities. Terminal state.

2. SDS of moderate degree in the left upper limb.

3. Severe right DDS lower limb. Gangrene of the right leg and foot. Traumatic shock of the third degree.

9.3. ASSISTANCE AT THE STAGES OF MEDICAL EVACUATION

First and first aid. The content of first aid to the wounded during SDS can vary significantly depending on the conditions of its provision, as well as on the forces and means of the medical service involved.

On the battlefield the wounded, pulled out of the rubble, are taken to a safe place. Orderlies or the military personnel themselves, in the form of mutual assistance, apply aseptic dressings to wounds (casualties) formed by compression of the limbs. In case of external bleeding, it is stopped (pressure bandage, tourniquet). Anesthetic is administered from a syringe tube (1 ml of 2% pro-medol solution), transport immobilization with improvised means. If consciousness is preserved and there are no abdominal injuries, the wounded are provided with plenty of fluids.

Pre-medical care for the wounded with suspected VDS necessarily involves intravenous administration of crystalloid solutions (0.9% sodium chloride solution, 5% glucose solution, etc.), which, if possible, continues during further evacuation. The paramedic corrects mistakes made during first aid, bandages wet bandages, and improves transport immobilization. In case of severe swelling, shoes are removed from the injured limb and uniforms are cut off. Give plenty of fluids.

In case of organizing assistance to the wounded outside the zone of direct enemy influence(removal of rubble after bombings, earthquakes or terrorist attacks), medical assistance is provided directly at the site of injury by medical and nursing teams. Depending on the training and equipment, such teams carry out urgent measures first medical and even qualified resuscitation care.

For the wounded released from the rubble, intravenous administration of crystalloid solutions is immediately established in order to eliminate blood plasma loss (it is even better to start infusion therapy before liberation from the rubble). If the development of VDS is suspected, 4% sodium bicarbonate 200 ml is administered intravenously (“blind correction of acidosis”) to eliminate acidosis and alkalinization of urine, which prevents the formation of hematin hydrochloride and blockage renal tubules. Also, 10 ml of a 10% calcium chloride solution is injected intravenously to neutralize the toxic effect of potassium ions on the heart muscle. In order to stabilize cell membranes, they are introduced large doses glucocorticoids. Painkillers and sedatives are administered, along with symptomatic therapy.

Before freeing the wounded from the rubble (or immediately after extraction), rescuers apply a tourniquet above the area of ​​compression of the limb to prevent the development of collapse or cardiac arrest from hyperkalemia. Immediately after this, the wounded person is removed to assess the viability of the compressed area of ​​the limb by a doctor.

The tourniquet is left on the limb (or applied if it has not been applied previously) in following cases:

limb destruction(extensive soft tissue damage to more than half the circumference of the limb, bone fracture, damage to great vessels); limb gangrene(distal to the demarcation line, the limb is pale or blue-spotted, cold, with wrinkled skin or desquamated epidermis; sensation and passive movement in the distal joints are completely absent). For the rest of the wounded, aseptic stickers are attached to the wounds of the extremities with adhesive tape (circular bandages can compress the limb and impair blood circulation), and transport immobilization is performed.

If possible, priority evacuation (preferably by helicopter) is provided for all wounded with SDS directly to the stage of providing specialized medical care.

First medical aid. Upon admission to the medical center (med), the wounded with signs of SDS are sent to the dressing room first.

1000-1500 ml of crystalloid solutions, 200 ml of 4% sodium bicarbonate solution, 10 ml of 10% calcium chloride solution are administered intravenously. The bladder is catheterized, the color and amount of urine are assessed, and diuresis is monitored.

A long-term compressed limb is examined. If available destruction or gangrene- a tourniquet is applied. If in these cases the tourniquet was applied earlier, it is not removed.

In the remaining patients with DFS, against the background of infusion therapy, administration of cardiovascular and antihistamines, tourniquet removal, novocaine blockade (conductor or cross-section type above the compression area), and transport immobilization are performed.

Cooling of the injured limb is provided (ice packs, cryopacks). If the condition of the wounded allows, an alkaline-salt drink is given (made at the rate of a teaspoon of baking soda and table salt per 1 liter of water). Urgent evacuation, preferably by helicopter, preferably immediately to the stage of specialized medical care, where there are conditions for the use of modern methods of extracorporeal detoxification.

Qualified medical care. In armed conflict

with established aeromedical evacuation of the wounded from medical companies directly to the 1st echelon MVG, when delivering the wounded from the SDS to the Omedb (Omedo Special Forces) - they only carry out pre-evacuation preparation in the scope of first medical aid. CCP is provided only for health reasons.

In conditions of large-scale war or when the evacuation of the wounded is disrupted The medical hospital (omedo) provides clinical and clinical care. Already during selective triage, the wounded with SDS are first of all sent to the intensive care ward for the wounded in order to assess their condition and identify life-threatening consequences.

In the event of massive sanitary losses, a number of wounded with severe SDS, unstable hemodynamics and severe endotoxemia (coma, pulmonary edema, oligoanuria) can be classified as agonizing.

In the intensive care ward To compensate for plasma loss, crystalloids (do not inject potassium!) and low-molecular colloid solutions are administered intravenously, while stimulating urination with Lasix and maintaining diuresis of at least 300 ml/h. For every 500 ml of blood substitutes, in order to eliminate acidosis, 100 ml of 4% sodium bicarbonate solution is administered to achieve a urine pH of at least 6.5. With the development of oliguria, the volume of infusion therapy is limited according to the amount of urine excreted. A 10% calcium chloride solution, glucocorticoids, painkillers and sedatives are administered.

In case of DFS, the administration of nephrotoxic antibiotics is contraindicated: aminoglycosides (streptomycin, kanamycin) and tetracyclines. Non-toxic antibiotics (penicillins, cephalosporins, chloramphenicol) are administered in half doses and only for the treatment of developed wound infections (but not for prophylactic purposes).

After stabilization of hemodynamic parameters, the wounded with SDS are examined in the dressing room for the seriously wounded(Table 9.3).

For signs of compartment syndrome(intense swelling of the limb with the absence of pulsation of the peripheral arteries, coldness of the skin, decreased or absent sensitivity and active movements) is indicated wide open fasciotomy . Indications for fasciotomy for SDS should not be expanded, because incisions are the gateway to wound infection. In the absence of signs of compartment syndrome, dynamic monitoring of the condition of the limb is carried out.

Fasciotomy is performed from 2-3 longitudinal skin incisions (above each osteofascial sheath) at least 10-15 cm long with dissection of dense fascial plates with long scissors throughout the entire segment of the limb. Wounds after fasciotomy are not sutured, because with significant tissue edema, this can impair blood circulation, and they are covered with napkins with water-soluble ointment. Immobilization is carried out with plaster splints.

“Lampas” incisions to the bone along the lateral surface of the limb or “subcutaneous” fasciotomy from small incisions are not used for DFS.

If necrosis of individual muscles or muscle groups limbs are excised - necrectomy .

Non-viable limbs with signs of dryness or wet gangrene, as well as ischemic necrosis (muscle contracture, complete lack of sensitivity), after a diagnostic dissection

Table 9.3. Surgical tactics for DFS

Clinical signs
Swelling of the limb is moderate, arterial pulsation and sensitivity are reduced	There is no threat to the viability of the limb	Treatment is conservative; monitoring of the condition of the limb is necessary.
Intense swelling of the limb; absence of pulsation of peripheral arteries; cold skin, decreased or absent all types of sensitivity and active movements	Compartment- syndrome (increased intracase pressure syndrome)	Shown open fascio
Lack of sensitivity, contracture of a muscle group (within the sheath) or the entire segment of the limb. During diagnostic dissection of the skin, the muscles are dark or discolored, yellowish, and do not contract or bleed when incised.	Ischemic necrosis of a muscle group or the entire compressed area of ​​a limb	Excision of necrotic muscles is indicated. With extensive necrosis - limb amputation
Distal to the line of demarcation, the limb is pale or blue-spotted, cold, with wrinkled skin or desquamated epidermis; Sensation and passive movements in the distal joints are completely absent	Gangrene of the limbs	Limb amputation indicated

skin lesions (muscles are dark or, conversely, discolored, yellowish, do not contract or bleed when cut) - are subject to amputation.

Amputation with SDS is performed above the level of the compression boundary, within healthy tissues. With a tourniquet applied, amputation is performed over the tourniquet. Lateral incisions on the limb stump being formed are used to monitor the viability of the overlying tissues. Wide subcutaneous fasciotomy of the limb stump is required. Primary sutures are not applied to the skin of the stump due to the threat of anaerobic infection and the high probability of the formation of new foci of necrosis.

If there is doubt about the non-viability of a limb, a relative indication for urgent amputation may be an increase in endotoxicosis and oligoanuria.

Urgent evacuation is indicated for the wounded with SDS of any severity, due to the real threat of acute renal failure and the need for specific detoxification methods. It is preferable to evacuate such wounded people to the stage of providing SCP by air, with the obligatory continuation of intensive care during the flight.

Specialized medical care wounded with SDS in the absence of surge arrester turns out in a general surgical hospital.

Modern view on the pathogenesis, diagnosis and staged treatment of long-term compartment syndrome.

Pathogenesis of long-term compartment syndrome

Pathological changes with SDS.

Clinical picture of DFS.

Treatment during the stages of medical evacuation

Among all closed injuries, a special place is occupied by long-term compression syndrome, which occurs as a result of prolonged compression of the limbs during landslides, earthquakes, destruction of buildings, etc. It is known that after the atomic explosion over Nagasaki, about 20% of the victims had more or less pronounced clinical signs of prolonged compression or crush syndrome.

The development of a syndrome similar to the syndrome of compression is observed after removal of a tourniquet applied for a long time.

IN pathogenesis compartment syndrome, three factors are of greatest importance:

painful irritation causing a violation of the coordination of excitatory and inhibitory processes in the central nervous system;

traumatic toxemia caused by the absorption of decay products from damaged tissues (muscles);

plasma loss occurring secondary to massive edema of injured limbs.

The pathological process develops as follows:

As a result of compression, ischemia of a segment of the limb or the entire limb occurs in combination with venous stagnation.

At the same time, large nerve trunks are exposed to trauma and compression, which causes corresponding neuro-reflex reactions.

Mechanical destruction occurs mainly of muscle tissue with the release of a large number of toxic metabolic products. Severe ischemia is caused by arterial insufficiency and venous congestion.

Long-term compartment syndrome occurs traumatic shock, which acquires a peculiar course due to the development of severe intoxication with renal failure.

The neuro-reflex component, in particular prolonged painful stimulation, is of leading importance in the pathogenesis of compartment syndrome. Painful irritations disrupt the functioning of the respiratory and circulatory organs; A reflex vascular spasm occurs, urination is suppressed, the blood thickens, and the body’s resistance to blood loss decreases.

After the victim is released from the compression or the tourniquet is removed, toxic products and, above all, myoglobin begin to enter the blood. Since myoglobin enters the bloodstream against the background of severe acidosis, the precipitated acidic hematin blocks the ascending limb of the loop of Henle, which ultimately impairs the filtration ability of the renal tubular apparatus. It has been established that myoglobin has a certain toxic effect, causing necrosis of the tubular epithelium. Thus, myoglobinemia and myoglobinuria are significant, but not the only factors that determine the severity of intoxication in the victim.

Entry into the blood of other toxic substances: potassium, histamine, adenositriposphate derivatives, products of autolytic breakdown of proteins, adenyl acid and adenosine, creatine, phosphorus. When muscles are destroyed, a significant amount of aldolase enters the blood (20-30 times higher than normal). The level of aldolase can be used to judge the severity and extent of muscle damage.

Significant plasma loss leads to disruption of the rheological properties of blood.

Development of acute renal failure, which is various stages syndrome manifests itself in different ways. After the compression is eliminated, symptoms reminiscent of traumatic shock develop.

Pathological anatomy.

The compressed limb is sharply swollen. The skin is pale, with a large number of abrasions and bruises. Subcutaneous fatty tissue and muscles are saturated with edematous fluid, yellowish in color. The muscles are imbibed with blood, have a dull appearance, the integrity of the blood vessels is not impaired. Microscopic examination of the muscle reveals a characteristic pattern of waxy degeneration.

Brain swelling and plethora are observed. The lungs are congestive and full of blood, sometimes there are symptoms of edema and pneumonia. In the myocardium - dystrophic changes. In the liver and organs of the gastrointestinal tract there is plethora with multiple hemorrhages in the gastric mucosa and small intestine. The most pronounced changes are in the kidneys: the kidneys are enlarged, and the section shows a sharp pallor of the cortex. There are dystrophic changes in the epithelium of convoluted tubules. The lumen of the tubules contains granular and small-droplet protein masses. Some of the tubules are completely clogged with myoglobin cylinders.

Clinical picture.

There are 3 periods in the clinical course of compartment syndrome (according to M.I. Kuzin).

I period: from 24 to 48 hours after release from compression. During this period, manifestations that can be considered as traumatic shock are quite characteristic: pain reactions, emotional stress, the immediate consequences of plasma and blood loss. It is possible to develop hemoconcentration, pathological changes in the urine, and an increase in residual blood nitrogen. Compartment syndrome is characterized by a clear interval that is observed after medical care is provided, both at the scene of the incident and in a medical facility. However, the victim’s condition soon begins to deteriorate again and the second period, or intermediate, develops.

II period - intermediate, - from the 3-4th to the 8-12th day, - the development, first of all, of renal failure. The swelling of the freed limb continues to increase, blisters and hemorrhages form. The limbs take on the same appearance as during an anaerobic infection. A blood test reveals progressive anemia, hemoconcentration is replaced by hemodilution, diuresis decreases, and the level of residual nitrogen increases. If treatment is ineffective, anuria and uremic coma develop. Mortality reaches 35%.

The third period - recovery - usually begins with 3-4 weeks of illness. Against the background of normalization of kidney function, positive changes in protein and electrolyte balance, changes in the affected tissues remain severe. These are extensive ulcers, necrosis, osteomyelitis, purulent complications of the joint, phlebitis, thrombosis, etc. Often it is these severe complications, which sometimes end in the generalization of a purulent infection, that lead to death.

A special case of long-term compression syndrome is positional syndrome - a prolonged stay in an unconscious state in one position. With this syndrome, compression occurs as a result of tissue compression under its own weight.

There are 4 clinical forms of long-term compartment syndrome:

Mild - occurs in cases where the duration of compression of limb segments does not exceed 4 hours.

Moderate - compression, as a rule, of the entire limb for 6 hours. In most cases, there are no pronounced hemodynamic disorders, and renal function suffers relatively little.

The severe form occurs due to compression of the entire limb, most often the thigh and lower leg, for 7-8 hours. Symptoms of renal failure and hemodynamic disorders are clearly manifested.

An extremely severe form develops if both limbs are subjected to pressure for 6 hours or more. Victims die from acute renal failure within the first 2-3 days.

The severity of the clinical picture of compression syndrome is closely related to the strength and duration of compression, the area of ​​damage, as well as the presence of concomitant damage to internal organs, blood vessels, and bones; nerves and complications developing in crushed tissues. After release from compression, the general condition of most victims is usually satisfactory. Hemodynamic parameters are stable. Victims experience pain in injured limbs, weakness, and nausea. The limbs are pale in color, with traces of compression (dents). There is a weakened pulsation in the peripheral arteries of the damaged limbs. Edema of the extremities quickly develops, they significantly increase in volume, acquire a woody density, and vascular pulsation disappears as a result of compression and spasm. The limb becomes cold to the touch. As the swelling increases, the victim's condition worsens. General weakness, lethargy, drowsiness, pale skin, tachycardia appear, and blood pressure drops to low levels. Victims experience significant pain in the joints when trying to make movements.

One of early symptoms The early period of the syndrome is oliguria: the amount of urine during the first 2 days decreases to 50-200 ml. in severe forms, anuria sometimes occurs. Restoring blood pressure does not always lead to an increase in diuresis. Urine has a high density (1025 and above), an acidic reaction and a red color due to the release of hemoglobin and myoglobin.

By the 3rd day, by the end of the early period, as a result of treatment, the patients’ well-being significantly improves (light period), hemodynamic parameters stabilize; swelling of the limbs decreases. Unfortunately, this improvement is subjective. Diuresis remains low (50-100 ml). on the 4th day, the clinical picture of the second period of the disease begins to form.

By the 4th day, nausea, vomiting, general weakness, lethargy, lethargy, apathy, and signs of uremia reappear. Lower back pain occurs due to stretching of the fibrous capsule of the kidney. In this regard, sometimes a picture of an acute abdomen develops. Symptoms of severe renal failure increase. Continuous vomiting occurs. The urinary level in the blood increases to 300-540 mg%, the alkaline reserve of the blood decreases. Due to the increase in uremia, the patients' condition gradually worsens, and high hyperkalemia is observed. Death occurs 8-12 days after injury due to uremia.

With proper and timely treatment, by 10-12 days all symptoms of renal failure gradually subside and a late period begins. In the late period, local manifestations of compartment syndrome come to the fore, swelling and pain in the injured limb gradually decrease and completely disappear by the end of the month. Complete restoration of limb function usually does not occur, which is due to damage to large nerve trunks and muscle tissue. Over time, most muscle fibers dies, being replaced by connective tissue, which leads to the development of atrophy and contractures. During this period, severe purulent complications of a general and local nature are observed.

Treatment during the stages of medical evacuation.

First aid: After releasing the compressed limb, apply a tourniquet proximal to the compression and bandage the limb tightly to prevent swelling. It is advisable to perform hypothermia of the limb using ice, snow, cold water. This measure is very important, since to a certain extent it prevents the development of massive hyperkalemia and reduces the sensitivity of tissues to hypoxia. Immobilization, administration of painkillers and sedatives are required. If there is the slightest doubt about the possibility of quickly delivering the victim to medical institutions, it is necessary, after bandaging the limb and cooling it, remove the tourniquet and transport the victim without a tourniquet, otherwise necrosis of the limb will result.

First medical aid.

A novocaine blockade is performed - 200-400 ml of a warm 0.25% solution proximal to the applied tourniquet, after which the tourniquet is slowly removed. If a tourniquet has not been applied, the block is performed proximal to the level of compression. It is more useful to introduce broad-spectrum antibiotics into the novocaine solution. Bilateral perinephric blockade according to A.V. is also performed. Vishnevsky is injected with tetanus toxoid. Cooling of the limb with tight bandaging should be continued. Instead of tight bandaging, the use of a pneumatic splint to immobilize fractures is indicated. In this case, uniform compression of the limb and immobilization will be carried out simultaneously. Drugs and antihistamines (2% pantopon solution 1 ml, 2% diphenhydramine solution 2 ml), cardiovascular drugs (2 ml 10% caffeine solution) are administered. Immobilization is carried out using standard transport tires. Give alkaline drink (baking soda), hot tea.

Qualified surgical care.

Primary surgical treatment of the wound. The fight against acidosis is the introduction of a 3-5% sodium bicarbonate solution in an amount of 300-500 ml. large doses (15-25 g per day) of sodium citrate are prescribed, which has the ability to alkalize urine, which prevents the formation of myoglobin sediments. Drinking large quantities of alkaline solutions and using high enemas with sodium bicarbonate are also recommended. To reduce spasm of the vessels of the renal cortex, intravenous drip infusions of a 0.1% novocaine solution (300 ml) are advisable. During the day, up to 4 liters of liquid are injected into a vein.

Specialized surgical care.

Further receipt of infusion therapy, novocaine blockades, correction of metabolic disorders. Full surgical debridement of the wound and amputation of a limb according to indications are also performed. Extracorporeal detoxification is performed - hemodialysis, plasmapheresis, peritoneal dialysis. After the elimination of acute renal failure, treatment measures should be aimed at quickly restoring the function of damaged limbs, combating infectious complications, and preventing contractures. Produced surgical interventions: opening of phlegmon, numbness, removal of necrotic areas of muscles. In the future, physiotherapeutic procedures and physical therapy are used.