Positional compression syndrome microbial 10. Prolonged compression syndrome: causes, symptoms, diagnosis, help and treatment

Syndrome of prolonged compression (crash syndrome) is a serious condition, which, fortunately, rarely occurs in everyday life. In peacetime, victims with such an injury are found under rubble in mines, after collapses of buildings and other structures as a result of earthquakes and other cataclysms.

The form of this syndrome, which can occur in everyday life, will stand out separately - positional compression. Pathology develops with prolonged squeezing of a part of the body while in an unconscious state or deep sleep under the influence of drugs or alcohol.

Briefly about what happens with a crash syndrome

When a part of the body is compressed (most often the limbs suffer), there is a violation of the blood supply to the tissues below the place of squeezing. The tissues begin to experience oxygen starvation (hypoxia), the death (necrosis) of muscle tissue gradually begins with the release of a large amount of toxic substances.

Often, already at the time of injury, massive muscle destruction occurs, bone fractures, damage to blood vessels and, as a result, bleeding are possible. There is also a pronounced pain syndrome, as a result of which the victims may develop.

Signs of the syndrome of prolonged compression

The condition of the victim and the prognosis directly depend on the time spent under the rubble, the area of ​​the lesion, the force of pressure and some other factors.

The clinical picture largely depends on which limb was compressed, whether the affected area is large, the force of external pressure and, of course, the time spent under the rubble. Victims who have suffered prolonged compression of both legs at the level of the thigh will have a more serious condition and a worse prognosis than victims after compression of the hand at the level of the forearm.

The condition of a person at the time of discovery can be quite satisfactory, or it can be extremely difficult:

• If a little time has passed since the start of compression, then the limb will be edematous, the skin will be pale and cold to the touch, the peripheral pulsation will be reduced or completely absent.
• If the victim was under the rubble for a long time (4-6 hours or more), then the affected areas of the body may be red-bluish in color, strongly edematous, there is no pulsation of the vessels, movement of the limbs is impossible, attempts to move them cause severe pain.

First aid

Upon detection of victims who were under any squeezing objects, it is categorically impossible to release the transferred limbs immediately. First of all, it is necessary to apply a tourniquet above the injury site, and only after that you can carefully remove the objects under which the person was. If you remove them immediately, without applying a tourniquet, the toxic products formed during the massive destruction of muscle tissue will enter the general bloodstream. This will cause rapid kidney damage, development, which can quickly lead to the death of the victim before they can be delivered to a medical facility.

The injured limb must be tightly bandaged, cooled and immobilized as much as possible, after removing clothes and shoes from it, if we are talking about the lower limbs. Open wounds (abrasions, cuts) should be treated if possible. If possible, it is necessary to give the patient any analgesics. If the wounded is conscious and there is no suspicion of an abdominal injury, then he can be given a drink.

The victim must be taken to a medical facility as soon as possible for qualified assistance. It should be noted that a note must be attached to the tourniquet, which will indicate the time of application. In summer, it must be removed half an hour after application, in the cold season - after an hour.

The clinical picture of the crash syndrome

After providing first aid to the wounded, he should be taken to a medical facility as soon as possible.

The clinic of the syndrome of prolonged compression is complex and can be very different for different wounded. The longer the victim was under compression, and the stronger the pressure was, the faster local and general pathological changes in the body occur, the more severe the syndrome and the worse the prognosis.

1. In the early period (1-3 days after release from compression), as a result of prolonged massive compression, traumatic shock may develop in victims, acute renal failure rapidly increases, and other conditions that threaten the patient's life. In cases where the wounded were quickly removed from the rubble, and the force of compression was not very high, their condition during this period may remain quite satisfactory (light interval). But they are worried about severe pain in the injured limbs, they remain swollen, blisters may appear on the skin, sensitivity is impaired or absent altogether.
2. After three days, an intermediate period of the syndrome of prolonged compression occurs, which can last up to 20 days, depending on the severity of the injury. The condition of patients worsens, symptoms of insufficiency of the functions of various organs appear, kidney damage comes first and acute renal failure develops. Swelling of damaged limbs may increase, foci of tissue necrosis may appear, infection may be attached. This is especially dangerous, since against the background of multiple organ failure, the rapid development of sepsis is possible.
3. In the late period, which can last several months, there is a restoration of the functions of the affected organs, as well as the damaged limb. The course of this period can be complicated by infectious complications. Due to the violation of trophism on damaged limbs, they can form, so the risk of developing infectious complications remains high.

Unfortunately, the restoration of limb functions is not always possible. Doctors continuously evaluate the viability of damaged tissues throughout the entire period of treatment. Patients at any stage may require surgical treatment: removal of necrotic muscle areas, suturing of damaged nerve trunks, in the worst case, amputation of the damaged limb.

It is difficult to single out the most important stages in helping the wounded with the syndrome of prolonged compression. However, it is very important to remove the victims from the rubble as soon as possible and deliver them to medical facilities for qualified assistance. This can not only prevent the disability of the wounded, but also save their lives.

Which doctor to contact

If you suspect a syndrome of prolonged compression (for example, after severe alcohol intoxication), you should contact a traumatologist. Additionally, it may be necessary to consult an anesthesiologist, nephrologist, dermatologist, cardiologist and other specialists, since this pathology leads to multiple organ failure.

Pediatrician E. O. Komarovsky talks about the syndrome of prolonged squeezing:

A specialist at the Moscow Doctor clinic talks about the syndrome of prolonged squeezing:

Positional Compression Syndrome (SPS) is a type of PDS. Its main difference is the absence of initial damage to soft tissues by heavy crushing violence. Positional compression occurs when the victim is unconscious and is associated with an uncomfortable posture in which the limbs are either pressed down by the body, or bend over a solid object, or hang down under the influence of their own gravity.

Deep alcohol intoxication or unconsciousness caused by other reasons, sometimes forced to be in an uncomfortable position for 10-12 hours. As a result, severe neuro-ischemic disorders occur in the extremities, leading to tissue necrosis and toxic effects due to the absorption of autolysis products.

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

clinical picture. Waking up and recovering, patients note significant pain and a sharp violation of the functions of the affected limb. Weakness, headache aggravate the general condition. Local disorders are expressed in pallor and coldness of the diseased limb, decreased skin sensitivity, severe limitation of function, lethargy, weakening or complete absence of pulsation of the arteries. Body temperature is normal or slightly elevated, blood pressure is unchanged.

If the patient was admitted a few hours after the onset of the disease, then increasing edema appears on the limbs, the skin becomes purple in color. In the correct recognition of suffering, anamnesis plays a huge role. Meanwhile, patients are reluctant to report severe intoxication, talk about trauma or an unknown cause. Most often, doctors diagnose thrombophlebitis, and in some advanced cases - an anaerobic infection, and therefore make wide incisions.

Growing woody edema, pronounced neurovascular disorders are aggravated by severe changes in kidney function. The daily amount of urine decreases sharply until the development of anuria.

TREATMENT

In the first period of development of SDS, nonspecific antishock therapy, adequate to the state of the patient's hemodynamics, significantly improves his life prognosis.

Complex therapy should include the following activities:

Correction of hemodynamic disorders;

Relief of respiratory failure;

detoxification;

Elimination of acute renal failure;

Prevention and treatment of DIC;

Increasing the general and specific immune resistance of the body;

Stimulation of regenerative processes.

Algorithm of first aid measures for prolonged compression syndrome:

1. Applying a tourniquet proximal to the site of compression.

2. Tight bandaging of the limb.

3. Cooling of the damage zone.

4. Immobilization of the limb.

5. Pain relief.

6. Anti-shock measures (in / in infusion, hormones, adrenaline).

Measures to eliminate hemodynamic disorders are in many ways reminiscent of the treatment of traumatic shock. The elimination of the pain factor and stress as the main link in the neuroreflex pathogenetic chain should begin already in the compression period of the crush syndrome. For this, injections of neuroleptics (droperidol 0.1-0.2 mg / kg) or tableted tranquilizers (seduxen, chlozepid, diazepam, etc.) are used. After decompression, narcotic and non-narcotic analgesics are used: if necessary, general anesthesia.

The following activities are carried out locally.

The tourniquet is applied proximal to the injury site until the limb is released from compression, then the bandage is tightly bandaged and the injury area is cooled. After that, the tourniquet is removed and appropriate transport immobilization is performed. This order of procedures is aimed both at stopping pain and at reducing the general intoxication of the body. If the prognosis for saving the limb is unfavorable, and the general condition of the patient does not allow immediate amputation, then the tourniquet-cold isolation of the injured area is provided by flashing its main vessels and applying ice. If the indications for amputation are obvious and the doctor has the appropriate equipment, then the operation should be carried out as soon as possible.

Emergency medical care should include pararenal novocaine blockade according to A.V. Vishnevsky, case novocaine blockade of the injured limb. 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 the tourniquet has not been applied, the blockade is performed proximal to the level of compression. It is more useful to introduce broad-spectrum antibiotics into the novocaine solution, tetanus toxoid is injected.

In parallel with these events, infusion-transfusion therapy begins. Plasma substitutes are transfused intravenously (rheopoliglyukin, polyglukin, gelatinol, hemodez, albumin, etc.)

If possible, start transfusion of fresh frozen plasma (1000-1500 ml / day) with heparin 2500 IU 4 times under the skin of the abdomen as early as possible to combat DIC and plasmorrhagia. .

The fight against acidosis - the introduction of a 3-5% solution of sodium bicarbonate in an amount of 300-500 ml. prescribe large doses (15-25 g per day) of sodium citrate, which has the ability to alkalize urine, which prevents the formation of myoglobin deposits. It is also indicated to drink large amounts of alkaline solutions, the use of high sodium bicarbonate enemas.

Heart remedies and antihistamines, drugs to restore acid-base balance and water-electrolyte balance are also used. The average daily transfusion volume for SDS is 5 liters.

If there is no improvement in hemodynamic parameters against the background of the transfusion of these drugs, steroid hormones are prescribed. The victim is administered prednisolone at the rate of 1-3 mg per 1 kg of body weight at once, followed by the addition of a half dose every 4-6 hours.

To eliminate respiratory failure, the patency of the airways is restored, humidified oxygen is used, and the tracheobronchial tree is sanitized. Respiratory analeptics are used only when breathing is preserved.

The set of measures to remove intoxication, in addition to the indicated local and infusion-transfusion procedures, includes methods of active detoxification.

The choice of the method of active detoxification in the early decompression period in SDS should be decided in principle as follows:

In patients with moderate manifestations of endogenous intoxication against the background of early post-compression syndrome without signs of renal and hepatic failure, hemodilution, rapid buffering of the internal environment and stimulation of diuresis can be limited.

· In patients with moderate SDS and obvious clinical and laboratory signs of endogenous intoxication, but with the preservation of the urinary function of the kidneys, therapeutic plasmapheresis is considered the first choice of efferent therapy. Taking into account the high molecular weight of myoglobin and its practical nondialyzability through semipermeable membranes, it is plasmapheresis that can be considered one of the main variants of the task of removing myoglobin from the circulating blood, although the role of hemosorption is also recognized.

· In patients with a clinical picture of renal failure, as one of the components of multiple organ failure, hemofiltration is currently considered the first choice method.

· In the absence of the possibility of haemofiltration and haemodiafiltration (indicated with significant dyselectricemia and metabolic disorders of the CBS) in the early decompression period, alternative solutions have to be used. These include the method of ultrafiltration followed by hemosorption or plasmapheresis or detoxification plasmapheresis with plasmasorption and subsequent hemodialysis, sometimes in combination with hemosorption.

Daily plasmapheresis and hyperbaric oxygenation make it possible to avoid amputation even in cases where patients were under debris for 5-7 days. Starting from the second period of the intoxication stage, acute renal failure becomes the leading symptom in the clinical picture of traumatic toxicosis. All of the above measures are aimed at eliminating OPN and its consequences. It remains to add only a number of specific procedures for the treatment of acute renal failure. Against the background of the described infusion-transfusion therapy, a 10% solution of mannitol is administered intravenously at the rate of 1 g per 1 kg of the patient's body weight. 2 hours later, the hourly urine output should be about 50 ml. If this does not happen, then re-introduce mannitol at the same dose and again wait 2 hours. Lack of response to these measures from the kidneys is an indication for hemodialysis. If successful with the use of mannitol, it should be administered repeatedly under the control of diuresis. Furosemide can also be used for forced diuresis.

Recently, prostaglandin E2 (prostenon) has been used in the treatment of acute renal failure. After diagnosing SDS, it is recommended to inject 1.0 ml intravenously. 0.1-0.5% solution of prostenon in 300 ml of isotonic sodium chloride solution. Continue for 3-5 days.

With the onset of the polyuric stage of acute renal failure (the stage of convalescence of SDS), specific therapy is stopped.

In order to increase the body's immune resistance, patients are prescribed hyperimmune plasma, targeted gamma globulin, lysozyme and other drugs. To prevent infection, broad-spectrum antibiotics are prescribed, enterosorption is performed.

During the period of convalescence, non-narcotic analgesics, prozerin, galantamine, reflexology, injections of B vitamins, therapeutic massage, exercise therapy, UHF therapy are used to eliminate traumatic neuritis.

The question of the choice of adequate surgical tactics in the treatment of local manifestations of DFS remains difficult. The authors believe that an extremely severe form of DFS and compression for more than 24 hours are absolute indications for amputation. In conditions of a shortage of extracorporeal blood purification agents, severe and extremely severe forms of SDS can be considered an indication for amputation.

The method of surgical decompression of soft tissues in the post-compressive period of traumatic toxicosis is fasciotomy. The usefulness of this method is currently disputed. Fasciotomy opens additional gates of wound infection, which, under conditions of a weakened body, can cause severe complications during SDS. Therefore, some authors recommend not to perform fasciotomy if it is possible to carry out a full-fledged active blood purification and local cooling of the extremities with ice. If such conditions are not feasible at the stage of qualified medical care and it is impossible to quickly transport the patient to a specialized hospital, then fasciotomy should be performed.

Indications for fasciotomy:

Severe subfascial edema

Progressive disturbance of lymph and blood circulation,

Ischemic muscle contracture (limited),

Purulent anaerobic infection.

Primary surgical treatment of wounds of the victim is carried out at the stage of qualified medical care in the focus of the disaster. Surgical interventions are performed: opening of phlegmon, streaks, removal of necrotic muscle areas. It should be remembered that the imposition of deaf primary sutures on the wound is strictly contraindicated. In the future, physiotherapeutic procedures and physiotherapy exercises are applied.

The course of SDS can be complicated by the presence of bone fractures and extensive wounds of the damaged segment in the patient. In the treatment of fractures at present, the method of choice is the use of compression-distraction devices (Ilizarov, Volkov-Oganesyan, etc.). In some cases, with SDS, the reposition of fragments by the method of skeletal traction is allowed. The imposition of plaster casts in SDS is contraindicated due to their pronounced compressive effect.

CONCLUSION

The syndrome of prolonged compression occupies a special place among the numerous forms of closed injuries due to the complexity and diversity of the mechanisms underlying its pathogenesis and determining the unusual clinical course, which manifests itself in the presence of a “light” gap that hides early signs of the development of severe functional and metabolic disorders in the vital important organs and systems.

Bibliography:

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2. Kavalersky G.M., Silin L.L., Garkavi A.V., Musalatov Kh.A. Traumatology and Orthopedics: Textbook for students of higher educational institutions / Ed. G.M. Kavalersky. - M .: Publishing Center "Academy", 2005.

3. Kornilov N. V., Gryaznukhin E. G. Traumatological and orthopedic care in the clinic: A guide for doctors. - St. Petersburg: Hippocrates, 2004.

4. Krichevsky A. L., Vodyanov A. M. et al. Compression injury of the limb. – M.: Rus. Panorama, 1995.

5. Musalatov Kh. A., Silin L. L., Brovkin S. V. et al. Medical care in disasters: Textbook. – M.: Medicine, 1994.

6. "Emergency Medical Care", ed. J. E. Tintinalli, Rl. Crouma, E. Ruiz, Translated from English by Dr. med. Sciences V.I. Candrora, MD M.V. Neverova, Dr. med. Sciences A.V. Suchkova, Ph.D. A.V. Nizovy, Yu.L. Amchenkova; ed. MD V.T. Ivashkina, D.M.N. P.G. Bryusov; Moscow "Medicine", 2001.

7. Nechaev E. A., Savitsky G. G. Diagnosis and pathogenetic treatment of the syndrome of prolonged compression. - M .: Military publishing house, 1992.

8. Sokolov V.A. Multiple and combined injuries. M. : GEOTAR Media, 2006.

9. Shaposhnikova Yu. G. Traumatology and orthopedics / Guide for doctors. In 3 volumes. T.1 - M.: Medicine, 1997.

- this is a shock-like condition that occurs after prolonged compression of the trunk, limbs or their segments with heavy objects. It is 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 insufficiency. 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

Prolonged Crush Syndrome (SDR), other names - traumatic toxicosis, crash syndrome, Bywaters syndrome, myorenal syndrome - a pathological shock-like condition that occurs after prolonged compression of the trunk, limbs or their segments with heavy objects. Crash syndrome develops immediately after the release of the patient and the restoration of blood and lymph flow in the affected parts of the body. Accompanied by a deterioration in the general condition, the development of toxemia and acute renal failure, with a large area of ​​​​damage often ends in the death of the patient. In traumatology and orthopedics, a domestic variety of crash syndrome is distinguished - the so-called positional compression syndrome (SPS), which develops as a result of prolonged (more than 8 hours) squeezing of body parts during a person's immobile position on a hard surface.

Causes of SDR

Usually, the syndrome of prolonged crushing occurs in victims during landslides, earthquakes, collapses in mines, construction works, road accidents, logging, explosions and destruction of buildings as a result of bombardment.

The 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 most often affected. In terms of developmental causes, symptoms, and methods of treatment, positional crush syndrome is practically the same as long-term crush syndrome, however, it usually proceeds more favorably due to the smaller area of ​​\u200b\u200bthe lesion.

Pathogenesis

Prolonged crush syndrome occurs due to a combination of three factors:

• pain syndrome;
• massive loss of plasma due to 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 pain irritation with a crash syndrome leads to the development of traumatic shock. Loss of plasma causes blood to thicken and cause thrombosis of small vessels. Traumatic toxemia in crush syndrome develops due to the absorption of tissue breakdown products of injured muscles into the blood. Immediately after the release of the limb from the damaged tissues, a significant amount of potassium ions enter the vascular bed, which can cause arrhythmia, and in severe cases, the cessation of the lungs and heart.

In the future, the crushed muscle tissue of a patient with a crush syndrome loses up to 66% potassium, 75% myoglobin, 75% phosphorus and 70% creatinine. The decay 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 a crush syndrome.

Classification

By severity:

• Mild form of crush syndrome. Occurs when crushing limb segments for 4 hours or less.
• Moderate form of crash syndrome. It develops as a result of crushing one limb within 4-6 hours. With timely initiation of treatment, the prognosis is favorable.
• Severe crash syndrome. It 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. It develops as a result of crushing 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 4-5 days);
• the period of late complications (develops after 20-30 days from the moment of injury).

Symptoms of SDR

Immediately after the removal of compression, the general condition of the victim improves. A patient with prolonged crush syndrome is concerned about pain and limited movement in the crushed limb. During the first hours after release, the swelling of the affected area gradually increases, which becomes dense, 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 the crash syndrome worsens. After a short period of excitement, the patient becomes sluggish, inhibited. There is a decrease in blood pressure and body temperature, arrhythmia, tachycardia, severe pallor of the skin. The skin of a patient with crush syndrome is covered with sticky cold sweat. Possible loss of consciousness, involuntary defecation and urination. Sometimes pulmonary edema develops. Decreases the amount of urine produced. Without adequate medical care, there is a chance of death within 1 or 2 days.

Foci of necrosis form on the crushed limb. When dead tissues are rejected, muscles are exposed that have the characteristic appearance of boiled meat. Suppuration of wounds and eroded surfaces develops. Appears and gradually increases acute renal failure. On the 5th-6th day, patients with prolonged crushing syndrome develop uremic syndrome. An increase in the level of potassium in the blood causes arrhythmia and bradycardia.

On the 5-7th day, signs of pulmonary insufficiency are revealed. Increasing intoxication due to the entry into the bloodstream of tissue decay products and bacterial toxins from a crushed limb causes toxic hepatitis. Possible endotoxic shock. The phenomena of multiple organ failure in patients with crush syndrome gradually decrease over 2-3 weeks.

Acute renal failure with crush syndrome stops about a month after the injury. The patient's condition improves, his body temperature returns to normal. Reduced pain and swelling of the limb. Necrotized muscles are replaced by connective tissue, which leads to muscle atrophy and the development of contractures. With an unfavorable development of events, local (suppuration) and general (sepsis) complications are possible.

Diagnostics

In order to compensate for metabolic acidosis, a patient with crush syndrome is given a 4% solution of sodium bicarbonate by drip. Prescribe broad-spectrum antibiotics intramuscularly. Carry out symptomatic therapy (diuretics, analgesics, antihistamines and antiarrhythmic drugs). With prolonged crushing syndrome, extracorporeal hemocorrection (hemodialysis, plasma and hemosorption) is carried out as early as possible.

While maintaining the viability of muscle tissues and severe subfascial edema with impaired local circulation, the traumatologist performs fasciotomy with revision and excision of necrotic muscle bundles. If there is no suppuration, the wound is sutured for 3-4 days, after the swelling decreases and the general condition of the patient with crush syndrome improves.

In cases of irreversible ischemia, the limb is amputated above the site of the tourniquet. In other cases, excision of necrotic areas is indicated with preservation of viable muscle bundles. Muscle viability is determined during surgery. The criteria for viability are the preservation of normal coloration, the ability to bleed and contract. After excision of tissues, the wound is abundantly washed with antiseptics. Seams are not applied. The wound heals by secondary intention.

In the long term, patients with prolonged crush syndrome are shown courses of rehabilitation treatment (massage, exercise therapy) aimed at restoring muscle strength and eliminating contractures.

The pathological condition defined by the term " long-term compression syndrome"- SDS (syn.: crash syndrome, traumatic toxicosis, prolonged crushing syndrome), is characterized by the peculiarity of the clinical picture, the severity of the course, and the high frequency of deaths.

Syndrome of prolonged limb compression- this is a kind of pathological condition of the body, which occurs, as a rule, in response to prolonged compression of a large mass of soft tissues. Rare cases are described when SDS develops with short-term compression of a large mass of soft tissues. The force of compression with the victim's consciousness preserved, as a rule, is great, and he is not able to extract the injured limb from under the press.

This is observed, for example, during earthquakes, blockages in mines, accidents, etc. The pressure force may be small. At the same time, SDS develops due to prolonged compression, which is possible in cases where the victims are unconscious for various reasons (coma, poisoning, epileptic seizures, etc.). In clinical medicine, the terms "positional compression", "positional compression" are used to refer to such compression. Experience shows that SDS develops mainly with prolonged (for 2 hours or more) pressure of a large mass of soft tissues.

Pathogenesis (what happens?) during Prolonged Compression Syndrome:

It is known that at least three theories of the pathogenesis of DFS were previously discussed: the theory of toxemia, the theory of plasma and blood loss, and the theory of the neuroreflex 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 ingress 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 leak leads to extravasation of intracellular fluid. Bradykinins, like other vasoactive kinins, cause hypotension. As a result of direct exposure to endotoxins and clotting factor XII, the intravascular coagulation mechanism is activated, which causes fibrinolysis and disseminated intravascular coagulation (DIC). An important role in the development of capillary stasis, disorders of microhemocirculation and oxygen starvation of organs is played by a change in the rheological properties of blood and a decrease in the ability of erythrocytes to deform due to endotoxication. The DIC complement system is also activated, leading to further damage to the endothelium and changes in vasoactivity.

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

Each variant of compression is characterized by features that distinguish them from each other, but acute ischemic disorders (AIR) in damaged tissues have a single pathogenesis and, in fact, determine the condition of most victims in the future, if other injuries (wound, radiation, secondary infection) do not join SDS. , burns, poisoning, etc.). It is advisable to combine all variants 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 organism or the functioning of the injured limb depends on them, then compression injury can be considered as a special case of acute ischemic disorders (AID) of any genesis that occur in ischemic tissues after the resumption of blood flow in them. . With 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 OIR; if they threaten only the function of the damaged organ (limb), then they can be considered as a mild form of OIR. Such a division of the IIR will make it possible to determine in which medical institution it is necessary to provide qualified and specialized assistance to the victims, in particular those with compression injuries. This is especially important in mass lesions, when medical triage is necessary. Taking into account the above, SDS can be considered as a severe form of compression injury of the limb, life-threatening to the victim, who may die from postischemic endotoxicosis associated with the resumption of blood flow and lymph circulation in ischemic tissues. In some cases, it occurs against the background of pain shock (injuries during earthquakes, etc.), in others - without a pain 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 postischemic endotoxicosis must be prevented to the extent that the circumstances of the injury and current data on its pathogenesis allow.

Limb compression creates anoxia of the injured segment, as a result of which, against the background of a painful shock or a coma caused by another cause, redox processes are disrupted in the anoxia zone, up to irreversible ones. This is due to the suppression of the activity of the redox enzyme systems of the mitochondria of anoxic tissue cells. After decompression, acute ischemic disorders develop in the damage zone, caused by the ingestion of incompletely oxidized products of impaired metabolism into the body through the blood and lymphatic pathways, 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" products of protein breakdown, potassium, myoglobin, etc.

Ischemic tissues, in which blood and lymph circulation resumes, after decompression lose their normal architectonics due to increased permeability of cell membranes, membranogenic edema develops, plasma is lost and blood thickens. 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 tissues of the injured limb are toxic. In the presence of a large mass of ischemic tissues, a life-threatening postischemic toxicosis develops. Underoxidized toxic products from damaged tissues mainly affect all vital organs and systems: myocardium (due to the negative inotropic effect of ischemic toxins on it) - the brain, lungs, liver, kidneys; deep violations of the erythron system occur, accompanied by hemolysis and a sharp inhibition of the regenerative function of the bone marrow, causing the development of anemia; there are changes in the blood coagulation system according to the type of DIC; all types of metabolism are disturbed due to the consequences of anoxia, the immunological reactivity of the body is sharply suppressed, 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 makes it possible to create a model for the prevention and treatment of DFS. For the prevention of SDS, it is necessary to exclude postischemic toxicosis. The most reliable and simplest way to prevent SDS is to amputate the injured limb under a tourniquet applied before the victim is released from compression. Indications for amputation should be expanded in case of mass admissions of victims in an unfavorable environment.

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 disturbed redox processes in ischemic tissues. Hemosorbents of the SKN type are currently successfully used as detoxifiers; isolated artificial circulation of the injured limb with the connection of xenoliver and hemoperfusion through cryopreserved liver tissue are used to restore metabolic processes in ischemic tissues. A promising area of ​​regional resuscitation in DFS is targeted transport of drugs using liposomes.

The most effective in the treatment of already developed SDS are toxicological methods aimed at freeing the body of the victim from "ischemic toxins" (sorption methods, dialysis, plasmapheresis), and methods used to break the diverse vicious circle of disorders leading to life-threatening complications. (eg, prevention of DIC, immunostimulation, temporary replacement of affected kidney function). It should be considered erroneous to use any treatment methods that, in severe compression injury, to some extent contribute to an additional "toxic blow" 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 oxygenation (HBO) without taking into account the danger of the consequences of tissue hypoxia in conditions of high oxygen concentration.

Symptoms of Prolonged Compression Syndrome:

Clinical picture of SDS begins to form from the moment of soft tissue compression; and life-threatening complications usually occur 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 is removed from it, applied proximal to the place of compression, as a rule, saves the life 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. Under pressure, the victim, as a rule, does not die. Case novocaine blockades as a method of treating SDS were ineffective. Conduction anesthesia, although more preferable for SDS than case blockade, however, does not in itself save victims from death with 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 into account these data, the idea of ​​the leading role of the neuroreflex pain component in the pathogenesis of DFS appears differently. Pain syndrome, undoubtedly present in compression injury, creates only an unfavorable background against which postischemic endotoxicosis develops, as a rule, is not the cause of death.

The results of the experiments showed that after decompression, the blood circulation in the compressed limb is restored in a peculiar way, very similar to that during revascularization of long-term ischemic tissues. With the anatomical preservation of the microvasculature of the limb subjected to prolonged compression, after a short-term "reactive" hyperemia, the blood flow resumes mainly in the connective tissue formations (subcutaneous fatty tissue, fascia, periosteum). At the same time, the muscles are almost not supplied with blood, which causes their postischemic aseptic necrosis. Postischemic muscle changes 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 aseptic necrosis while preserving intact fibers. In addition, it is known that the function of the limb, the muscles of which were ischemic during compression injury, and signs of flaccid paresis and paralysis were noted, is restored. It has been established that detoxification of an ischemic limb with an adsorbent contributes to the normalization of blood distribution in ischemic tissues. It is also known that "ischemic toxins" have a direct vasoactive effect on the smooth muscles of the vascular wall.

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

The results of experiments and clinical observations indicate that venous blood in an injured limb is more toxic than blood flowing from. The toxicity of the venous blood of the injured limb is especially high in the first minutes after decompression. In the future, apparently due to the increase in edema and blockage 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 the clinic, it is possible to control the dynamics of the toxicity of biological fluids using methods such as the "paramecium test" and the determination of the concentration of "medium molecules". There are other tests and methods for determining blood and lymph toxicity. These data suggest that for detoxification of the body, it is more expedient to take venous blood from the injury zone, 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, which is characteristic of the postischemic state of tissues. These violations of the architectonics of damaged tissues can be prevented to some extent by gradually restoring blood flow in a gentle mode and local cooling, which reduces blood flow to ischemic tissues.

The question of the pathogenesis and biological significance of edema in ischemic tissues has not been finally resolved. With a compression injury, one can distinguish between predominantly local edema, localized in the area of ​​injured tissues, and general plasma loss with slight local edema, and in both cases, blood clotting can be observed. It has been established in experiments that the more severe the compression injury, the less local postischemic edema and the greater the total plasma loss. These data led to the conclusion that the severity of local edema reflects the degree of preservation of the protective reactions of the body, and the edema of ischemic tissues is protective. This conclusion is confirmed by the data indicating that the more severe the compression injury, the more significantly the immunological reactivity of the body decreases.

The edema of ischemic tissues increases as the absorption of toxic substances from the affected tissues decreases. This means that the edema of injured tissues protects the body from the entry of toxic substances from them into liquid media. In this regard, the "struggle" with the consequences of edema by fasciotomy in severe compression injury of the limb inevitably leads to an additional toxic "blow" on the body due to improved blood flow in the injured limb. Thus, trying to save the limb, its function, we risk the life of the victim. All therapeutic measures (fasciotomy, necrectomy, fixation of fractures, etc.) to save a compressed limb should be carried out in parallel with intensive therapy, the use of modern methods of active detoxification - hemolymphosorption and hemodialysis.

A significant total plasma loss in severe compression injury against the background of shock is an undoubted indication for intensive infusion therapy, which is a component of anti-shock treatment. At the same time, however, it should be borne in mind that stimulation of hemodynamic parameters can become dangerous for victims if free communication is maintained between the blood and lymphatic channels of the body and the injured limb. In these cases, as the experiment showed, stimulation of hemodynamics with the help of anti-shock measures, while 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 anti-shock therapy in severe compression injury is effective against the background of separation of the blood and lymphatic channels of the body and the injured limb, which is achieved by tight bandaging, cooling or applying a tourniquet (if a decision is made to amputate).

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

After tissue reperfusion, the lungs are one of the first barriers to the movement of endotoxins and aggregates from ischemic and damaged tissues. A wide microvasculature of the lungs is the main "battlefield" of the body with endotoxins. In patients with SDS, the number of stab 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, stab leukocytes release free oxygen radicals that block plasma inhibitors of enzymes and increase the permeability of the capillary membrane. The entry of endotoxins into the capillary bed of the lungs and 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 outflow.

With a massive intake of endotoxins into the lungs, a gradual violation 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 muscle breakdown, mainly myoglobin, potassium, phosphorus and lactic acid, accumulate in the blood and cause metabolic acidosis. At the same time, fluid is exuded from the affected capillaries into the muscle tissue, resulting in severe limb edema 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, the development of stasis and thrombosis both in the cortical and in the medulla occur. In the renal tubules, significant dystrophic changes occur, the integrity of individual tubules is disturbed, their lumen is filled with cell decay products. These early and rapidly progressive changes lead to the development of renal failure. Myoglobin, hemoglobin formed during hemolysis of erythrocytes, as well as a violation of the ability of erythrocytes to deform, increase ischemia of the cortical layer of the kidneys, which contributes to the progression of morphological changes in their glomerular and tubular apparatus and leads to the development of oliguria and anuria.

Prolonged compression of the segment, the development of oxygen starvation and hypothermia in its tissues lead to pronounced tissue acidosis. After the compression is removed, the incompletely oxidized metabolic products (lactic, acetoacetic and other acids) come 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 the functions of vital systems. Oxygen deficiency leads to an increase in the permeability of the intestinal wall and a violation of its barrier function, therefore, vasotoxic substances of a bacterial nature freely penetrate into 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 a specific humoral depressive myocardial factor appears in various types of shock. These components may be the causes of inhibition of myocardial contractility and catecholamine response, as well as important factors in the development of shock. In shock, multiple organ failure inevitably occurs if adequate intensive care has not been carried out before severe metabolic acidosis and vascular insufficiency have developed.

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

There are four periods in the clinical course of SDS.

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

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

SDS is characterized by a relatively good condition of the victims immediately after the removal of compression. Only after a few hours (if the limb was not "destroyed" as a result of a catastrophe) local changes appear in the damaged segment - pallor, cyanosis, variegated skin color, absence of pulsation in peripheral vessels. Over the next 2-3 days, swelling of one or more limbs that have undergone compression increases. Edema is accompanied by the appearance of blisters, dense infiltrates, local and sometimes total necrosis of the entire limb. The condition of the victim is rapidly deteriorating, 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 BCC; there is a tendency to thrombosis.

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- the development of complications, manifested by the defeat of various organs and systems, the period of acute renal failure. The duration of the period is from 2 to 15 days. An 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. In this period, swelling of the compressed limb or its segment increases, 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, potassium increases in the blood. A classic picture of uremia develops with hypoproteinemia, an increase in the amount of phosphorus and potassium, and a decrease in sodium content.

The body temperature rises. The condition of the victim deteriorates sharply, lethargy and lethargy increase, vomiting and thirst appear, icterus of the sclera and skin, indicating involvement in the pathological process of the liver. Despite intensive care, up to 35% of those affected die. In 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 the vein of the affected limb under the control of intoxication tests).

• IV period- convalescence. It begins after the restoration of kidney function. In 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. Restoration of the function of the joints of the damaged limb, elimination of 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 by connective tissue and the development of limb atrophy, but the function can gradually recover, especially with positional compression.

An analysis of the results of observations of the victims during the earthquake in Armenia in the IV period of the SDS showed that they have a long history of severe anemia, hypoproteinemia, dysproteinemia (decrease in albumin, increase in globulin fractions, especially the y-fraction), hypercoagulability 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, 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 reveal a significant decrease in natural resistance factors, immunological reactivity, bactericidal activity of blood, activity of serum lysozyme. Of the cellular factors, changes occur mainly in the T-lymphocyte system. For a long time, the leukocyte index of intoxication (LII) remains changed.

In the majority of victims, a deviation in the emotional and mental status persists for a long time in the form of depressive or reactive psychoses and hysteria.

Isolated from the wounds ( in the presence of open lesions) microflora has features. In the early period (the first 7 days) after the earthquake, the wounds were abundantly seeded with clostridium, mainly. This indicates a high risk of developing clostridial myonecrosis or "gas gangrene" in these patients. Clostridia in all patients isolated in association with enterobacteria, Pseudomonas, anaerobic cocci. Under the influence of surgical treatment and antibacterial therapy, wounds in all patients are cleared of clostridium in 7-10 days.

In most patients arriving at a later date, microbial associations are isolated, the mandatory component of which is Pseudomonas aeruginosa, and their "companions" are enterobacteria, staphylococci and some other bacteria.

In some victims in the IV period of SDS, necrosis of the deep muscles of the injured limb or its segment is detected, occurring with scanty symptoms or asymptomatically. The healing of a wound of a compressed limb is longer than conventional wounds.

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

Treatment for Prolonged Compression Syndrome:

Modern treatment victims of earthquakes and other mass disasters with SDS of varying severity should be comprehensive, taking into account all aspects of the pathogenesis of this damage, stages and continuity in the provision of medical benefits. The complexity provides for the impact on the macroorganism in order to correct all deviations of hemostasis, the local pathological focus and the microflora of wounds. Staged means the provision of a specific and necessary for each stage of the volume and nature of medical care. Continuity in treatment ensures the continuity and purposefulness of therapeutic measures from the beginning of medical care to the recovery of the victim.

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

• I stage- assistance in the focus of mass destruction,
• II stage- qualified medical care, which is provided in a medical facility located at a short distance from the zone of mass destruction and equipped with everything necessary for sorting and providing qualified assistance in case of damage to the musculoskeletal system and internal organs, as well as shock and SDS with initial symptoms of renal failure. In connection with the mass flow of victims, stay in this institution is limited to 1-2 days.

At this stage, medical landing units in the form of "flying hospitals" or "hospitals on wheels" deploying their activities near the lesion center can be used. Depending on the situation, these institutions may increase or decrease the amount of medical care provided.

• Stage III- specialized medical care. For this purpose, a large surgical and trauma center is used, equipped with everything necessary to provide specialized care for open and closed injuries of the musculoskeletal system and their consequences, as well as a resuscitation service for the treatment of shock, postischemic 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 the treatment of, for example, acute renal failure, etc., where there are no specialists in the treatment of injuries, infected wounds, etc., are excluded.

Treatment at the scene. At the scene of the incident, the victim must be injected with painkillers, if possible, a novocaine blockade (preferably conductive) is performed at the base of the limb. A tourniquet is applied only with a clear crush of the limb in order to sharpen the amputation. In other cases, the sequence of assistance at the scene of the incident should be as follows: applying a tourniquet, freeing the limb from obstruction, tight bandaging of the squeezed limb, cold, immobilization, removing the tourniquet, if there are wounds, their mechanical cleaning, applying dressings that have antiseptic, enzymatic and dehydrating properties, bandaging. If possible, the damaged limb segment is covered with ice packs and transport immobilization is carried out.

At the stage of qualified and specialized care, intensive infusion-transfusion therapy is continued, central vein catheterization is performed (if it was not performed at the previous stage). Treatment is aimed at further increasing the volume of urine by forced diuresis. The volume of infusion-transfusion therapy is not less than 500 ml/h. The composition of infusion agents includes 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 ( hemodez, neohemodez). The composition of fluids and their volume is corrected depending on diuresis, the degree of intoxication, and KOS indicators. Carry out monitoring of blood pressure, CVP, urination. To account for the amount of urine, bladder catheterization is performed hourly. Drug therapy: to stimulate diuresis, lasix and eufillin, heparin, antiplatelet agents (curantil, trental), retabolil or nerobolil, cardiovascular agents, immunocorrectors are prescribed. Such treatment should provide urination in an amount of at least 300 ml / h.

With the ineffectiveness of conservative treatment for 8-12 hours and a decrease in diuresis to 600 ml / day and below, the issue of hemodialysis is decided. Anuria, hyperkalemia over 6 mmol/l, pulmonary and cerebral edema are urgent indications for hemodialysis. The volume of infusion therapy during the interdialysis period is 1500-2000 ml.

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

Surgical tactics depends on the condition of the victim, the degree of ischemia of the injured limb, the presence of crushed tissues, bone fractures, and should 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 soft tissue edema.

The skin is pale, on the border of the lesion hangs over the healthy one. There are no signs of circulatory disorders. Conservative treatment gives a pronounced effect.

• II degree- moderately expressed indurative edema of soft tissues and their tension. The skin is pale, with areas of slight