Compression Syndrome. Prolonged compression syndrome (SDS)

A modern view on the pathogenesis, diagnosis and staged treatment of the syndrome of prolonged compression.

The pathogenesis of the syndrome of prolonged compression

Pathological changes in SDS.

Clinical picture of SDS.

Treatment during the stages of medical evacuation

Among all closed injuries, a special place is occupied by the syndrome of prolonged compression, 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 the syndrome of prolonged compression or crushing.

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

IN pathogenesis compression syndrome, three factors are most important:

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

traumatic toxemia due to the absorption of decay products from damaged tissues (muscles);

plasma loss that occurs secondary as a result of massive edema of damaged limbs.

The pathological process develops as follows:

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

At the same time, large nerve trunks are traumatized and compressed, which causes the corresponding neuro-reflex reactions.

There is a mechanical destruction of mainly muscle tissue with the release of a large amount of toxic metabolic products. Severe ischemia is caused by both arterial insufficiency and venous congestion.

With the syndrome of prolonged compression, a traumatic shock occurs, which acquires a peculiar course due to the development of severe intoxication with renal failure.

The neuro-reflex component, in particular, prolonged pain irritation, plays a leading role in the pathogenesis of the compression syndrome. Painful irritations disrupt the activity of the respiratory and circulatory organs; reflex vasospasm occurs, urination is suppressed, blood thickens, the body's resistance to blood loss decreases.

After the release of the victim from compression or removal of the tourniquet, toxic products, primarily myoglobin, begin to enter the bloodstream. 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 disrupts the filtration capacity 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.

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

Significant plasma loss leads to a violation of the rheological properties of blood.

The development of acute renal failure, which manifests itself differently at different stages of the syndrome. After the compression is eliminated, symptoms resembling traumatic shock develop.

Pathological anatomy.

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

There is swelling of the brain and plethora. The lungs are stagnant and full-blooded, sometimes there are phenomena 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 mucous membrane of the stomach and small intestine. The most pronounced changes in the kidneys: the kidneys are enlarged, the cut shows a sharp pallor of the cortical layer. In the epithelium of the convoluted tubules dystrophic changes. The lumen of the tubules contains granular and small-drop protein masses. Part of the tubules is completely clogged with cylinders of myoglobin.

clinical picture.

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

I period: from 24 to 48 hours after release from compression. In this period, manifestations that can be considered as traumatic shock are quite characteristic: pain reactions, emotional stress, immediate consequences of plasma and blood loss. Perhaps the development of hemoconcentration, pathological changes in the urine, an increase in residual nitrogen in the blood. The syndrome of compression is characterized by a light gap, which is observed after the provision of medical care, both at the scene and in a medical institution. However, the condition of the victim soon begins to worsen again and the second period, or intermediate, develops.

II period - intermediate, - from 3-4th to 8-12th day, - the development of primarily renal failure. The edema of the freed limb continues to grow, blisters and hemorrhages form. The limbs take on the same appearance as in 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. Lethality reaches 35%.

III period - recovery - usually begins with 3-4 weeks of illness. Against the background of normalization of kidney function, positive changes in the protein and electrolyte balance, changes in the affected tissues remain severe. These are extensive ulcers, necrosis, osteomyelitis, purulent complications from the joint, phlebitis, thrombosis, etc. Quite often these serious complications which sometimes come to an end with generalization of a purulent infection lead to a lethal outcome.

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

There are 4 clinical forms of the syndrome of prolonged compression:

Light - occurs when the duration of compression of the limb segments does not exceed 4 hours.

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

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

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

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

One of the early symptoms of the early period of the syndrome is oliguria: the amount of urine during the first 2 days is reduced to 50-200 ml. in severe forms, anuria sometimes occurs. Restoration of 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' state of health improves significantly (light interval), hemodynamic parameters stabilize; swelling of the extremities is reduced. 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, signs of uremia reappear. There are pains in the lower back due to stretching of the fibrous capsule of the kidney. In this regard, a picture of an acute abdomen sometimes develops. Growing symptoms of severe renal failure. There is continuous vomiting. The level of urea in the blood rises to 300-540 mg%, the alkaline reserve of the blood falls. In view of the increase in uremia, the condition of patients gradually worsens, high hyperkalemia is observed. Death occurs 8-12 days after injury against the background of uremia.

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

Treatment at the stages of medical evacuation.

First aid: after releasing the squeezed limb, it is necessary to apply a tourniquet proximal to the compression and tightly bandage the limb to prevent swelling. It is desirable to carry out hypothermia of the limb using ice, snow, cold water. This measure is very important, because to a certain extent it prevents the development of massive hyperkalemia, reduces the sensitivity of tissues to hypoxia. Mandatory immobilization, the introduction of painkillers and sedatives. At the slightest doubt about the possibility of a quick delivery of the victim to medical institutions, after bandaging the limb and cooling it, it is necessary to remove the tourniquet, transport the victim without a tourniquet, otherwise necrosis of the limb is real.

First aid.

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. A bilateral pararenal blockade according to A.V. is also performed. Vishnevsky, 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. Inject drugs and antihistamine preparations (2% solution of pantopon 1 ml, 2% solution of Diphenhydramine 2 ml), cardiovascular agents (2 ml of 10% caffeine solution). Immobilization is carried out with standard transport tires. Give alkaline drink (baking soda), hot tea.

Qualified surgical assistance.

Primary surgical treatment of the wound. 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 shown to drink large amounts of alkaline solutions, the use of high enemas with sodium bicarbonate. To reduce spasm of the vessels of the cortical layer of the kidneys, intravenous drip infusions of a 0.1% solution of novocaine (300 ml) are advisable. during the day, up to 4 liters of fluid are injected into a vein.

Specialized surgical care.

Further receiving infusion therapy, novocaine blockades, correction of metabolic disorders. A full-fledged surgical treatment of the wound, amputation of the limb according to indications is also performed. Extracorporeal detoxification is performed - hemodialysis, plasmapheresis, peritoneal dialysis. After the elimination of acute renal failure, therapeutic measures should be aimed at the fastest restoration of the function of damaged limbs, the fight against infectious complications, and the prevention of contractures. Surgical interventions are performed: opening of phlegmon, streak, removal of necrotic muscle areas. In the future, physiotherapeutic procedures and physiotherapy exercises are applied.

Prolonged compression syndrome (SDS, synonyms: crush syndrome, prolonged crush syndrome, traumatic toxicosis, "release" syndrome, myorenal syndrome) is a pathological symptom complex caused by prolonged (more than 2-8 hours) compression of soft tissues.

The reason is the compression of the limbs, less often the torso by heavy objects, fragments of buildings, rock. It occurs during earthquakes, landslides, as well as in traffic accidents, railway accidents.

The peculiarity of this syndrome is that it develops after the victim is removed from the rubble, when decay products from damaged tissues, especially muscles (myoglobin), enter the general bloodstream.

In the development of the crash syndrome, three factors are important:

severe pain irritation leading to shock;
traumatic toxemia due to the absorption of decay products;
plasma and blood loss due to massive edema of the extremities.

There are three periods in the clinical course of SDS:

early - increase in edema and vascular insufficiency (1-3 days);
intermediate - acute renal failure (from 3-4 days to 1.5 months);
late - recovery (reconvalescence).

Early period characterized by general, local and specific symptoms associated directly with the injury.

General symptoms. After release, the victim develops weakness, chills, fever, tachycardia, a drop in blood pressure up to shock and death.

local symptoms. They develop gradually and cause bursting pains. 30-40 minutes after extraction from the wreckage, the injured limb begins to progressively swell ("thread symptom"), pale skin becomes purple-cyanotic, blisters with serous and hemorrhagic contents appear on it, and zones of necrosis. The pulse and all kinds of sensitivity in the area of damage and below disappear. On palpation, soft tissues have a woody density: when pressed with a finger, no impressions remain on the skin. Movements in the joints are impossible, attempts to make them cause pain in the victim.

specific symptoms. There are signs of thickening of the blood: the content of hemoglobin, the number of erythrocytes, hematocrit increases, azotemia progresses. Urine becomes red, then brown, the protein content in it increases to 600-1200 mg / l. Microscopic examination in the urine sediment is determined by a large number of erythrocytes, casts of tubules from myoglobin.

Interim period characterized by a progressive increase in acute renal failure (ARF) and restoration of blood circulation.

Patients have better blood circulation. Swelling of the limb slowly subsides, the pain subsides; blood pressure normalizes, moderate tachycardia remains - the pulse corresponds to a temperature of 37.3-37.5 ° C. However, ARF is progressing. Oliguria turns into anuria, the concentration of createnin and urea in the blood plasma increases; hemoconcentration is replaced by anemia; increasing intoxication, azotemia; changes in acid-base balance (acidosis).

With extensive tissue damage, treatment may be ineffective, in these cases, uremia develops on the 4-7th day and the patients die.

With a favorable course of traumatic toxicosis, the function of the kidneys begins to recover, the third period begins.

Late period characterized by a predominance of local symptoms. The general condition of the victims improves, azotemia decreases, the amount of urine increases, erythrocytes and cylinders disappear in it. However, against the background of an improvement in the general condition, a burning pain in the limb appears; extensive areas of necrosis of the skin and deep tissues (gray muscles, osteomyelitis), ulcers are determined; muscle atrophy increases; stiffness in the joints. Perhaps the accession of a purulent infection.

With a favorable course of SDS after rejection or removal of necrotic tissues, the viability of the remaining tissues is restored, the function of the kidneys and other internal organs is normalized, and recovery occurs.

Algorithm for providing first aid in case of SDS at the scene:

Pain relief before or in parallel with the release of the injured limb (promedol, morphine or analgin with diphenhydramine intramuscularly). Releasing the victim, starting with the head.
The imposition of a rubber tourniquet on the limbs until the victim is completely released.
Examination of the limb.
Release of the limb from the tourniquet. Remember: the tourniquet is left only with arterial bleeding and extensive crushing of the limb.
The imposition of an aseptic dressing on abrasions, wounds, if any.
Tight bandaging of the limb with an elastic or regular bandage from the periphery to the center.
Transport immobilization of the limb.
Cooling of the limb.
Drink plenty of water in the absence of damage to the abdominal organs: - hot tea, coffee with the addition of alcohol (50 ml 40-70%); - soda-salt solution (1/2 teaspoon of baking soda and 1 teaspoon of table salt per 1 liter of water).
Warming (warmly cover).
Oxygen therapy (access to fresh air, oxygen).
Prevention of cardiovascular insufficiency (prednisolone).
Transportation to hospitals on a stretcher in the supine position.

V.Dmitrieva, A.Koshelev, A.Teplova

"Prolonged compression syndrome, cause, symptoms, first aid" and other articles from the section

Long-term compression syndrome (SDS) is a severe pathological condition that occurs as a result of closed damage to large areas of soft tissues under the influence of large and / or long-acting mechanical force, accompanied by a complex of specific pathological disorders (shock, cardiac arrhythmias, acute kidney injury, compartment- syndrome), most often in the limbs for more than 2 hours.

For the first time, SDS was described by N. I. Pirogov in 1865 in the “Principles of General Military Field Surgery” as “local asphyxia” and “toxic tissue tension”. The SDF attracted particular attention during the Second World War. In 1941, English scientists Bywaters E. and Beall D., taking part in the treatment of victims of the bombing of London by German aircraft, identified this syndrome as a separate nosological unit. Among the inhabitants of London, who suffered from fascist bombings, SDS was registered in 3.5-5% of cases and was accompanied by high mortality. In 1944, Bywaters E. and Beall D. determined that myoglobin plays a leading role in the development of renal failure.

In the domestic literature, SDS was described for the first time under the name “syndrome of crushing and traumatic compression of the limbs” in 1945 by Pytel A. Ya. and an opinion was expressed about the leading role of toxicosis in the development of the clinical picture.

In peacetime, SDS most often occurs in victims of earthquakes and man-made disasters (Table 1).

Table 1

Frequency of development of SDS during earthquakes

Most often (79.9% of cases) SDS occurs with a closed injury of the soft tissues of the lower extremities, in 14% - with damage to the upper and in 6.1% - with simultaneous damage to the upper and lower extremities.

Table 2 lists the main causes leading to SDS.

table 2

The main etiological factors of SDS

Options	Etiological factors
Traumatic	Electrical injury, burns, frostbite, severe concomitant injury
Ischemic	Positional compression syndrome, tourniquet syndrome, thrombosis, arterial embolism
Hypoxic (overstrain and severe hypoxia of muscle tissue)	Excessive physical activity, "marching myoglobinuria", tetanus, convulsions, chills, status epilepticus, delirium tremens
Infectious	Pyomyositis, sepsis, bacterial and viral myositis
Dysmetabolic	Hypokalemia, hypophosphatemia, hypocalcemia, hyperosmolarity, hypothyroidism, diabetes mellitus
Toxic	Snake and insect bites, drug toxicity (amphetamine, barbiturates, codeine, colchicine, lovastatin-itraconazole combination, cyclosporine-simvastatin combination), heroin, lysergic acid N,N-diethylamide, methadone
genetically determined	McArdle disease (lack of phosphorylase in muscle tissue), Tarui disease (lack of phosphofructomase)

As a result of tissue compression, there is a violation of blood flow in the vessels and the accumulation of tissue waste products. After restoration of blood flow, cellular decay products (myoglobin, histomin, serotonin, oligo- and polypeptides, potassium) begin to enter the systemic circulation. Pathological products activate the blood coagulation system, which leads to the development of DIC. It should be noted that another damaging factor is the deposition of water in damaged tissues and the development of hypovolemic shock. A high concentration of myoglobin in the renal tubules under acidic conditions leads to the formation of insoluble globules, causing intratubular obstruction and acute tubular necrosis.

As a result of hypovolemia, DIC, cytolysis products entering the bloodstream, in particular myoglobin, multiple organ failure develops, the leading place in which is occupied by acute kidney injury (AKI).

Depending on the extent and duration of tissue compression, three degrees of severity of the course of DFS are distinguished (Table 3).

Table 3

SDS classification by severity

The severity of the current	Area of limb compression	indicative compression time	The severity of endotoxicosis
mild SDS	Small (forearm or lower leg)	No more than 2-3 hours	Endogenous intoxication is insignificant, oliguria is eliminated after a few days	Favorable
moderate SDS	Larger areas of pressure (thigh, shoulder)	From 2-3 to 6 hours	Moderate endotoxicosis and AKI within a week or more after injury	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	More than 6 hours	Severe endogenous intoxication rapidly increases, multiple organ failure develops, including AKI	In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable.

The clinical picture of SDS has a clear periodicity.

The first period (from 24 to 48 hours after release from compression) is characterized by the development of tissue edema, hypovolemic shock and pain.

The second period of SDS (from 3-4 to 8-12 days) is manifested by an increase in edema of compressed tissues, impaired microcirculation and the formation of AKI. In laboratory blood tests, progressive anemia is detected, hemoconcentration is replaced by hemodilution, diuresis decreases, and the level of residual nitrogen increases. If treatment is ineffective, anuria and uremic coma develop. Mortality during this period reaches 35%.

In the third period (from 3-4 weeks of the disease), clinical manifestations of multiple organ failure are observed, including AKI, acute lung injury, heart failure, DIC, and gastrointestinal bleeding. During this period, it is possible to attach a purulent infection, which can lead to the development of sepsis and death.

SDS ends with a period of convalescence and restoration of lost functions. This period begins with a brief polyuria, indicating resolution of the AKI. Homeostasis is gradually restored.

Diagnosis of SDS is based on anamnestic and clinical and laboratory data.

Laboratory signs of SDS consist of elevated levels of creatine phosphokinase, metabolic acidosis, hyperphosphatemia, uric acid, and myoglobin. Evidence of severe kidney damage is the acid reaction of urine, the appearance of blood in the urine (gross hematuria). Urine becomes red, its relative density increases significantly, protein in the urine is determined. Signs of AKI are a decrease in diuresis to oliguria (daily diuresis less than 400 ml), an increase in the level of urea, creatinine, and serum potassium.

Therapeutic measures should begin at the prehospital stage and include pain relief, intravenous fluid infusion, heparin administration. The victim must be taken to the hospital as soon as possible. When observing and treating patients, it is necessary to take into account the risk of developing hyperkalemia soon after the release of the affected limb, carefully monitor for the development of shock and metabolic disorders.

In the hospital, according to indications, surgical treatment of the affected areas is carried out, including “lamp” incisions with a mandatory dissection of the skin, subcutaneous tissue and fascia within the edematous tissues. This is necessary to relieve the secondary compression of the affected tissues. In case of detection of necrosis of only part of the muscles of the limb, their excision is performed - myectomy. Non-viable limbs with signs of dry or wet gangrene, as well as ischemic necrosis (muscle contracture, complete lack of sensitivity, with a diagnostic dissection of the skin - the muscles are dark or, on the contrary, discolored, yellowish, do not contract and do not bleed when cut) are subject to amputation above the level of the compression boundary, in within healthy tissues.

Massive infusion therapy is mandatory. Fluid therapy is aimed at correcting fluid and electrolyte disturbances, shock, metabolic acidosis, preventing DIC, and reducing or preventing AKI.

Antibacterial therapy should begin as early as possible and is used not only for treatment, but, above all, for the prevention of infectious complications. In this case, it is necessary to exclude the use of nephro- and hepatotoxic drugs.

More than 10% of victims require extracorporeal detoxification. Anuria during the day with the ineffectiveness of conservative therapy, hyperazotemia (urea more than 25 mmol / l, creatinine more than 500 μmol / l), hyperkalemia (more than 6.5 mmol / l), persistent hyperhydration and metabolic acidosis require the immediate initiation of renal replacement therapy - hemodialysis , hemofiltration, hemodiafiltration. Methods of renal replacement therapy make it possible to remove medium- and low-molecular toxic substances from the bloodstream, eliminate acid-base disorders and water-electrolyte disorders.

On the first day, plasmapheresis (PF) is indicated. According to the data presented by P. A. Vorobyov (2004), PF showed high efficiency in the treatment of patients affected by the earthquake in Armenia in 1988. PF performed on the first day after decompression reduced the incidence of AKI to 14.2%. The effectiveness of PF is associated with the rapid removal of myoglobin, tissue thromboplastin, and other cellular decay products.

SDS is currently on an upward trend worldwide. This is due, among other things, to the increase in the number of victims of road traffic accidents. It is rather difficult to predict the course of the disease, since most of the data come from the sources of earthquakes and other man-made disasters. According to the available data, mortality depends on the timing of the start of treatment and ranges from 3 to 50%. In the case of AKI, the mortality rate can reach 90%. The use of methods of renal replacement therapy has reduced mortality to 60%.

Literature

Vorobyov P. A. Actual hemostasis. - M.: Publishing house "Newdiamed", 2004. - 140 p.
Gumanenko E. K. Military field surgery of local wars and military conflicts. A guide for doctors / ed. Gumanenko E.K., Samokhvalova I.M. - M., GEOTAR-Media, 2011. - 672 p.
Genthon A. , Wilcox S. R. Crush syndrome: a case report and review of the literature. // J. Emerg. Med. - 2014. - Vol. 46. - No. 2. - P. 313 - 319.
Malinoski D. J. , Slater M. S. , Mullins R. J. Crush injury and rhabdomyolysis. // Crit. care. - 2004. - Vol. 20 - P. 171 - 192.
Sever MS. Rhabdomyolysis. // Acta. Clin. Belg. Suppl. - 2007. - Vol. 2. - P. 375 - 379.

Topic: a modern view on the pathogenesis, diagnosis and staged treatment of the syndrome of prolonged compression.

Abstract plan.

1. Pathogenesis of the syndrome of prolonged compression

2. Pathological changes in SDS.

3. Clinical picture of SDS.

4. Treatment during the stages of medical evacuation

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

IN pathogenesis compression syndrome, three factors are most important:

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

Traumatic toxemia due to the absorption of decay products from damaged tissues (muscles);

Plasma loss secondary to massive edema of damaged limbs.

The pathological process develops as follows:

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

2. At the same time, large nerve trunks are traumatized and compressed, which causes the corresponding neuro-reflex reactions.

3. There is a mechanical destruction of mainly muscle tissue with the release of a large amount of toxic metabolic products. Severe ischemia is caused by both arterial insufficiency and venous congestion.

4. With the syndrome of prolonged compression, a traumatic shock occurs, which acquires a peculiar course due to the development of severe intoxication with renal failure.

5. The neuro-reflex component, in particular, prolonged pain irritation, plays a leading role in the pathogenesis of the compression syndrome. Painful irritations disrupt the activity of the respiratory and circulatory organs; reflex vasospasm occurs, urination is suppressed, blood thickens, the body's resistance to blood loss decreases.

6. After the release of the victim from compression or removal of the tourniquet, toxic products and, above all, myoglobin begin to flow into 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 disrupts the filtration capacity 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.

8. Significant plasma loss leads to a violation of the rheological properties of blood.

9. The development of acute renal failure, which manifests itself differently at different stages of the syndrome. After the compression is eliminated, symptoms resembling traumatic shock develop.

Pathological anatomy.

clinical picture.

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

There are 4 clinical forms of the syndrome of prolonged compression:

1. Light - occurs when the duration of compression of the limb segments does not exceed 4 hours.

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

3. A severe form occurs as a result of compression of the entire limb, more often the thigh and lower leg, within 7-8 hours. Symptoms of renal failure and hemodynamic disorders are clearly manifested.

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

Treatment at the stages of medical evacuation.

First aid: after releasing the compressed limb, it is necessary to apply a tourniquet proximal to the compression and tightly bandage the limb to prevent swelling. It is desirable to carry out hypothermia of the limb using ice, snow, cold water. This measure is very important, because to a certain extent it prevents the development of massive hyperkalemia, reduces the sensitivity of tissues to hypoxia. Mandatory immobilization, the introduction of painkillers and sedatives. At the slightest doubt about the possibility of a quick delivery of the victim to medical institutions, after bandaging the limb and cooling it, it is necessary to remove the tourniquet, transport the victim without a tourniquet, otherwise necrosis of the limb is real.

First aid.

Qualified surgical assistance.

Specialized surgical care.

References.

1. Lectures and practical exercises on military field surgery, ed. Prof. Berkutov. Leningrad, 1971

2. Military field surgery. A.A. Vishnevsky, M.I. Schreiber, Moscow, medicine, 1975

3. Military field surgery, ed. K.M. Lisitsyna, Yu.G. Shaposhnikov. Moscow, medicine, 1982

4. Guide to traumatology MS GO. Ed. A.I. Kuzmina, M. Medicine, 1978.

The syndrome of prolonged compression is understood as a number of symptoms after a long tissue hypoxia caused by mechanical compression of the vessels. In severe cases, SDS leads to necrosis of muscle and nerve tissues. First aid to the wounded with SDS helps to prevent complications of tissue hypoxia, including toxemia, liver and kidney failure, which are accompanied by traumatic toxicosis.

There are several classifications of the syndrome of prolonged compression. If we talk about the types of compression, then there are:

positional pressure syndrome- local damage mainly to the limbs under the weight of its own weight in case of prolonged immobility;
crushing- an open type of injury;
direct compression- occurs when an object of large mass is pressed for a long period.

Traumatic toxicosis has a different clinical course, which is due to the scale of the damage and the severity of the injury. A mild compression injury does not cause significant disturbances, and blood circulation is fully restored over time. Another thing is compression injuries of internal organs and the spine. coupled with the syndrome of prolonged compression can lead to death. and are considered the most dangerous. Pain syndrome often causes shock, and tissue hypoxia - necrosis and coma.

The concept of traumatic toxicosis includes violations of the following intensity:

mild crush syndrome- involves squeezing mainly the limbs for up to 4 hours. The prognosis of mild SDS is favorable;
mild syndrome- a symptom complex with developing hypoxia, occurs during compression for a period of 4-6 hours;
severe crush syndrome- occurs after 6 hours of compression, accompanied by renal failure, the appearance of areas of necrosis. Severe by definition, but successfully treated if detected early;
extremely severe crush syndrome– this condition occurs after 8 hours of compression. The term "extremely severe traumatic toxicosis" implies life-threatening conditions.

During traumatic toxicosis, physicians distinguish three periods:

a period of increased swelling and vascular disorders;
involvement in the pathological process of the kidneys, liver, lungs;
recovery stage.

ICD 10 injury code

Since DFS has many synonymous diagnoses, it is difficult to identify the disease. In case of detection of such violations, an ICD code is assigned - T79.5. Traumatic anuria is hidden under this coding, it is also Bywaters syndrome or crush, SDS, SPS, myorenal syndrome, traumatic toxicosis.

Causes

The syndrome of prolonged compression of soft, predominantly muscle tissues develops as a result of a combination of three essential elements:

loss of the liquid part of the blood due to trauma to blood vessels and other tissues;
development of pain syndrome, possibly shock conditions;
poisoning of the body with necrotic tissues and other toxic products formed during tissue decay.

The pathogenesis of the syndrome of prolonged compression is due to a long stay in conditions of tissue hypoxia. The causes of such conditions are earthquakes, collapses and blockages due to natural disasters. In children, signs of compression appear faster than in adults. While the victim is removed from the heavy rubble, he can lose a lot of blood and develop kidney failure.

Common causes of mild SDS are prolonged squeezing of limbs by one's own body when falling while under the influence of alcohol or drugs. By the time a person wakes up, his soft tissues have time to survive hypoxia.

Symptoms

You can name the exact clinic of the syndrome of prolonged compression based on the stage of the process. Severe pain syndrome is observed immediately after the injury. Then, when squeezed, the sensitivity decreases, the limb becomes cold, the vessels cannot cope with the transport function. The patient's condition worsens every hour. The edema of the injured limbs increases, the site of injury turns blue. With trauma to the vertebrae or skull, symptoms of functional insufficiency quickly increase.

If the victim does not receive help for a long time, death occurs. If one limb has undergone compression, necrosis develops. Signs of limb death are:

suppuration, erosion;
muscle exposure;
damaged tissues acquire the color of boiled meat.

At the same time, acute renal failure increases, signs of cardiac arrhythmia and bradycardia appear.

Clinical manifestations of moderate and severe SDS are associated with the functions of internal organs. The general condition sharply worsens, toxic hepatitis with the possible development of multiple organ failure is not excluded.

In the intermediate period of the syndrome of prolonged compression, physicians identify the main pathological manifestations: a decrease in acute symptoms within 2 weeks from the moment of injury, an increase in long-term complications - atrophy, contractures, local inflammatory reactions. The clinic of the syndrome of prolonged compression is reduced in case of timely medical care.

First aid

Immediately after release from the rubble or other unfavorable conditions in case of prolonged compression syndrome, first aid is provided. The algorithm of actions includes:

above the compression part, tighten the tourniquet on the injured limb;
apply a pressure bandage;
wounds are sanitized;
give painkillers, narcotic analgesics are not excluded.

Pre-hospital tourniquet application for DFS is essential to stop the spread of toxins. For the same purpose, tight bandaging is shown. Methods and means of pain relief at different stages of medical care vary. Emergency care at the scene of an accident with a syndrome of prolonged compression does not exclude resuscitation. The timing and quality of first aid determines how successful the recovery of the victim with prolonged crush syndrome will be.

If less than 2 hours have passed since the accident, then the sequence of actions when providing medical assistance to the victim will be different. A patient with a syndrome of prolonged squeezing in the absence of signs of necrotization - cyanosis, swelling, loss of sensitivity, is allowed to warm.

The syndrome of prolonged compression in the first stage does not have time to have a destructive effect on the body, which means that first aid for the syndrome of prolonged compression allows the use of methods and means that stimulate blood flow. If the time of the tragedy is unknown, standard first aid is provided, a feature of which is the refusal to quickly release the pressure load.

Diagnostics

It is possible to identify traumatic toxicosis during the examination of the victim. In the case of prolonged disturbances of blood microcirculation, stagnation occurs, possibly with necrosis. To assess the risk of compression allow laboratory diagnostic methods that determine the viscosity of the blood and the inflammatory process. Electrolyte disturbances are observed, the concentration of glucose and bilirubin increases.

In traumatology and orthopedics, radiodiagnostics is used: X-ray, CT, MRI. In case of damage to the kidneys and liver, urine tests are of great importance. A high level of myoglobin indicates kidney failure. With the development of acidosis, acidity increases.

Metabolic acidosis develops already at the initial stage of SDS. In the toxic period, blood clotting is disturbed, the content of creatine in the urine increases, and serum albumin is detected.

Treatment

Intoxication develops rapidly, so it is important to reduce the toxic effect of decay products inside the body. For this purpose, a glucose solution and saline solutions are prescribed. By decision of the doctor, albumin preparations are used. In the early period 1, detoxification of the body alone is sufficient to eliminate the main symptoms of long-term crush syndrome, however, specific treatment is required to restore limb function.

If a patient has endotoxicosis, glucocorticoids will help out, which preserve the integrity of cell membranes. Other necessary preparations are 10% calcium chloride, 4% sodium bicarbonate. They are used in disaster medicine to support kidney function and reduce toxic effects on the heart muscle.

The main treatment for crush syndrome is carried out in a hospital. As part of intensive care, infusion drugs are prescribed to support vital signs. The acute period, which can last several days, requires constant medical monitoring. With the development of acute renal failure, stimulation of diuresis is necessary.

Treatment of acute renal failure should be concomitant with other consequences of SDS. With prolonged compression, extracorporeal hemocorrection is required. According to the doctor's prescription, hemodialysis, hemosorption, membrane or discrete plasmapheresis can be used. With acute renal failure adhere to a strict diet. Limit water intake.

Symptomatic therapy includes taking analgesics, diuretics, agents to maintain cardiac activity. In traumatology, treatment tactics are determined taking into account damage to the musculoskeletal system. The specific treatment of individual organs depends on their localization, the degree of crushing, and the duration of tissue hypoxia. As part of general therapy, heparin sodium, nandrolone decanoate are prescribed.

Surgical treatment

If a surgical pathology is detected during compression, it must be corrected immediately. With the development of contracture and large-scale edema, fasciotomy is indicated. Compression injury with tissue necrosis requires surgical removal of dead areas, blood clots, abscesses. After excision of the anesthetized fibers, the wound is sutured. Drainage is installed as needed.

Necrosis of muscle fibers, which is irreversible, forces amputation of the limb. At the slightest opportunity to preserve the viability of the muscles, other surgical and medical measures are carried out. The ability of muscles to recover is determined by the degree of contraction and the type of bleeding. If all signs point to irreversible ischemia, the operation should not be delayed.

After surgical treatment, increased attention is paid to infusion therapy. Enter up to 1 liter of plasma per day. Activated charcoal is used as a detoxifying agent, sodium bicarbonate is used to equalize the acid-base balance. Strictly adhere to the rules of asepsis in order to avoid purulent complications.

Rehabilitation

Recovery from traumatic toxicosis takes a short period if the compression was mild. Otherwise, rehabilitation is delayed, and it is not possible to fully restore the viability of muscle tissue.

The task of rehabilitation therapy is to restore the functionality of the affected parts of the body, get rid of contractures and residual pain. To do this, use hardware physiotherapy, exercise therapy, massage.

The presence of comorbidities and advanced age reduce the likelihood of a full recovery. The prognosis depends on the clinical picture and the individual characteristics of the victim's body.

Complications and consequences

The main and most dangerous complication of SDS is liver failure, which develops rapidly in the absence of adequate treatment. It is she who becomes the culprit in the death of the victim in most cases. Let's single out other negative consequences, which are indicated in order of prevalence:

DIC- a companion of severe toxic toxicosis, characterized by increased mortality;
pulmonary edema- leads to total hypoxia and death;
hemorrhagic shock- accompanies mainly crushing, is associated with large-scale blood loss;
infectious and septic complications- arise due to infection of the injured area, require urgent medical intervention, sometimes amputation of the limb.

Dear readers of the 1MedHelp website, if you have any questions on this topic, we will be happy to answer them. Leave your feedback, comments, share stories of how you survived a similar trauma and successfully coped with the consequences! Your life experience may be useful to other readers.

Article author:| orthopedic doctor Education: diploma in the specialty "Medicine" received in 2001 at the Medical Academy. I. M. Sechenov. In 2003, she completed postgraduate studies in the specialty "Traumatology and Orthopedics" at the City Clinical Hospital No. N.E. Bauman.