The time of development of the syndrome of prolonged compression. Long crush syndrome

SYNDROME OF LONG-TERM COMPRESSION.

Synonyms used to refer to this term are crush syndrome, traumatic endotoxicosis, tissue compression syndrome.

This syndrome is understood as the development of intravital tissue necrosis, causing endotoxicosis due to prolonged compression of a body segment.

This phenomenon was first described by Dr. Corvisart, Napoleon's personal physician, in 1810.

He noticed that when under the cuirassier - this is a rider, clad in metal armor, they killed a horse, but he could not get out from under it on his own, after the battle and the release of the crushed lower limbs, he died quite quickly, although he did not have any wounds.

At that time, Corvisar did not find an explanation for this, but he described the fact itself.

PATHOGENESIS.

The leading pathogenetic factors of the syndrome of prolonged compression (SDS) are: traumatic toxemia, which develops as a result of the ingress of decay products of damaged cells into the bloodstream, triggering intravascular blood coagulation; plasma loss as a result of severe edema of damaged limbs; pain irritation, leading to discoordination of the process of excitation and inhibition in the central nervous system.

The result of prolonged compression of the limbs is the occurrence of ischemia of the entire limb or its segment in combination with venous congestion. Nerve trunks are also injured. Mechanical tissue destruction occurs with the formation of a large amount of toxic products of cell metabolism, primarily myoglobin. The combination of arterial insufficiency and venous congestion exacerbates the severity of limb ischemia. Developing metabolic acidosis in combination with myoglobin entering the circulation leads to blockade of the kidney tubules, disrupting their reabsorption capacity. Intravascular coagulation blocks filtration. Therefore, myoglobinemia and myoglobinuria are the main factors determining the severity of toxicosis in victims. Significantly affects the patient's condition hyperkalemia, often reaching 7-12 mmol / l. Toxemia is also aggravated by histamine coming from damaged muscles, protein breakdown products, adenylic acid, creatinine, phosphorus, etc.

Already in the early period of SDS, there is a thickening of the blood as a result of plasma loss, a massive edema of damaged tissues develops. AT severe cases plasma loss reaches 1/3 of the volume of circulating blood.

The most severe complication observed in SDS is acute renal failure, which manifests itself differently at the stages of the development of the disease.

CLASSIFICATION.

Type of compression:

crushing,

compression (direct, positional).

By localization:

isolated (one anatomical region),

multiple,

combined (with fractures, damage to blood vessels, nerves, traumatic brain injury).

By severity:

I st. – light (compression up to 4 hours),

II Art. – medium (compression up to 6 hours),

III Art. - severe (compression up to 8 hours),

IV Art. - extremely severe (compression of both limbs for 8 hours or more).

I degree - a slight indurative edema of soft tissues. The skin is pale, at the border of the lesion it bulges slightly above the healthy one. There are no signs of circulatory disorders.

II degree - moderately pronounced indurative edema of soft tissues and their tension. The skin is pale, with areas of slight cyanosis. After 24-36 hours, blisters with a transparent yellowish content may form, which, when removed, expose a moist, pale pink surface. Increased edema in the following days indicates a violation of venous circulation and lymphatic drainage, which can lead to the progression of microcirculation disorders, microthrombosis, increased edema and compression muscle tissue.

III degree - pronounced indurative edema and soft tissue tension. The skin is cyanotic or "marble" appearance. The skin temperature is markedly reduced. After 12-24 hours, blisters with hemorrhagic contents appear. Under the epidermis, a moist surface of a dark red color is exposed. Indurative edema, cyanosis are rapidly growing, which indicates gross violations of microcirculation, vein thrombosis, leading to a necrotic process.

IV degree - indurated edema is moderately pronounced, the tissues are sharply strained. The skin is bluish-purple in color, cold. Separate epidermal blisters with hemorrhagic contents. After removal of the epidermis, a cyanotic-black dry surface is exposed. In the following days, the edema practically does not increase, which indicates deep microcirculation disorders, insufficiency of arterial blood flow, widespread thrombosis of venous vessels.

I period - early (shock period) - up to 48 hours after release from compression. This period can be characterized as a period of local changes and endogenous intoxication. At this time, manifestations of traumatic shock prevail in the clinic of the disease: severe pain syndrome, psycho-emotional stress, hemodynamic instability, hemoconcentration, creatininemia; in the urine - proteinuria and cylindruria. After stabilization of the patient's condition as a result of therapeutic and surgical treatment, a short light period occurs, after which the patient's condition worsens and the II period of SDS develops - the period of acute renal failure. Lasts from 3-4 to 8-12 days. The edema of the extremities, freed from compression, increases on damaged skin bubbles, hemorrhages are found. Hemoconcentration is replaced by hemodilution, anemia increases, diuresis sharply decreases up to anuria. Hyperkalemia and hypercreatininemia reach the highest numbers. Mortality in this period can reach 35%, despite intensive therapy.

From the 3-4th week of the disease, the III period begins - recovery. Kidney function, protein content and blood electrolytes are normalized. Infectious complications come to the fore. The risk of developing sepsis is high.

At the same time, the experience of disaster medicine has shown that the degree of compression and the area of ​​the lesion, the presence of concomitant damage to the internal organs of the bones and blood vessels are of the greatest importance in determining the severity of the clinical manifestations of DFS. The combination of even a short duration of compression of the extremities with any other injury (bone fractures, traumatic brain injury, ruptures of internal organs) sharply aggravates the course of the disease and worsens the prognosis.

The volume of therapeutic measures for SDS is determined by the severity of the condition of the victim.

One of the first necessary prehospital measures should be the imposition of a rubber tourniquet on a compressed limb, its immobilization, the introduction of narcotic analgesics (promedol, omnapon, morphine, morphilong) to relieve shock and emotional stress.

I period. After release from compression, it is necessary to carry out infusion (anti-shock and detoxification) therapy, including intravenous administration of fresh frozen plasma (up to 1 liter per day), polyglucin, rheopolyglucin, the introduction of saline solutions (acesoll, disol), detoxifying blood substitutes - hemodez, neogemodez, neocompensan. Orally applied sorbent - enterodez.

Extracorporeal detoxification during this period is represented by plasmapheresis with the extraction of up to 1.5 liters of plasma.

II period. Infusion-transfusion therapy (volume not less than 2000 ml per day, the composition of transfusion media includes fresh frozen plasma 500-700 ml, 5% glucose with vitamins C and group B up to 1000 ml, albumin 5% -10% - 200 ml, 4% sodium bicarbonate solution - 400 ml, glucose-novocaine mixture 400 ml). The composition of transfusion media, the volume of infusions is corrected depending on the daily diuresis, data on acid-base balance, the degree of intoxication, and the surgical intervention performed. Strict accounting of the amount of urine excreted; if necessary - catheterization Bladder.

Plasmapheresis is indicated for all patients who have obvious signs of intoxication, the duration of compression is more than 4 hours, pronounced local changes in the injured limb (regardless of the area of ​​compression).

Sessions of hyperbaric oxygenation - 1-2 times a day in order to reduce the degree of tissue hypoxia.

Drug therapy: stimulation of diuresis by prescribing lasix up to 80 mg per day and eufillin 2.4% - 10 ml; heparin 2.5 thousand under the skin of the abdomen 4 times a day; chimes or trental for the purpose of disaggregation; retabolil 1.0 once every 4 days to enhance protein metabolism; cardiovascular agents according to indications; antibiotics.

The choice of surgical tactics depends on the condition and degree of ischemia of the injured limb. Osteosynthesis is possible only after restoration of normal microcirculation, i.e. should be delayed.

It can be anything, from an accident in transport to an earthquake and a collapse of a mine. In any of these cases, SDS may develop. The syndrome has various causes, pathogenesis, requires mandatory treatment. Let's consider these questions further.

The concept of VTS

As a result of compression of soft tissues, SDS may develop. The syndrome in women occurs with the same frequency as in the male population. It has other names, such as crush syndrome or compression injury. The cause of the syndrome may be:

• Compression of body parts with heavy objects.
• emergency situations.

Such situations often occur after earthquakes, as a result of traffic accidents, explosions, collapses in mines. The force of compression may not always be large, but the duration of such a state plays a role here. As a rule, STS (prolonged compression syndrome) occurs if there is a prolonged impact on soft tissues, usually more than 2 hours. First aid is an important stage on which a person's life depends. That is why it is important to be able to distinguish the manifestations of such a state.

Varieties of SDS

AT medical practice There are several approaches to the classification of the syndrome of compression. Given the type of compression, the following syndromes are distinguished:

• Developing as a result of a collapse of the soil. Occurs as a result of a long stay under a concrete slab or various heavy objects.
• Positional SDS develops due to compression by parts of one's own body.

Localization can also be different, hence the SDS is distinguished:

• limbs.
• heads.
• Belly.
• Breasts.
• pelvis.

After emergencies, SDS often develops. The syndrome is often accompanied by other injuries, so there are:

• Compression syndrome, accompanied by injuries of internal organs.
• With damage to the bone structures of the body.
• SDS with damage nerve endings and blood vessels.

The severity of the syndrome may vary. Based on this fact, there are:

• A mild form of the syndrome, which develops when squeezing the limbs for a short time. Cardiovascular disorders are usually not diagnosed.

• If the pressure on the tissues is more than 5-6 hours, then the average form of SDS develops, in which there may be mild renal failure.
• A severe form is diagnosed when squeezing for more than 7 hours. Signs of renal insufficiency are expressed.
• If pressure is applied to soft tissues for more than 8 hours, then we can talk about the development of an extremely severe form of SDS. Acute heart failure can be diagnosed, which is often fatal.

It often happens when SDS (prolonged compression syndrome) is accompanied by various complications:

• Myocardial infarction.
• Diseases various systems organs is fraught with SDS. The syndrome in women, affecting the lower part of the body, that is, the pelvic organs, is dangerous with severe complications and disruption of the normal functioning of the organs in this area.
• Purulent-septic pathologies.
• Ischemia of the injured limb.

Result of injury: SDS

The cause syndrome has the following:

• Pain shock.

• Loss of plasma that escapes through the vessels into damaged tissues. As a result, the blood becomes thicker and thrombosis develops.
• As a result of tissue breakdown, intoxication of the body occurs. Myoglobin, creatine, potassium and phosphorus from injured tissues enter the bloodstream and cause hemodynamic disorders. Free myoglobin provokes the development
• All these reasons must be eliminated as soon as possible in order to make it possible to save human life.

Periods of the clinical course of SDS

The course of the crash syndrome has several periods:

• The first is the direct compression of soft tissues with the development of traumatic shock.
• In the second period, local changes in the injured area and the onset of intoxication are observed. It can last up to three days.
• The third period is characterized by the development of complications, which are manifested by the defeat of various organ systems.
• The fourth period is convalescence. Its beginning from the moment of restoration of functioning of kidneys.
• Further, in the victims, factors are found that indicate immunological reactivity, bactericidal activity of the blood.

Symptoms of tissue compression syndrome

If the strong pressure on the soft tissues is not immediately eliminated, then SDS gradually progresses. The syndrome has the following symptoms:

• The skin on the squeezed limb becomes pale.
• There is swelling, which only increases with time.
• The pulsation of vessels is not probed.
• The general condition of the victim is deteriorating.
• Observed pain syndrome.
• A person has psycho-emotional stress.

A blood test shows a decrease in fibrinolytic activity, the blood coagulation system also accelerates.

Protein is found in the urine, erythrocytes and casts appear.

These are the manifestations of SDS. The syndrome is characterized by a relatively normal condition of the victims, if the compression of the tissues is eliminated. But after a while there are:

• Cyanosis and pallor of the integument.
• Motley coloration of the skin.
• Over the next few days, the swelling increases.

• Blisters, infiltrates may appear, and in severe cases, necrosis of the limbs occurs.
• Develops cardio vascular insufficiency.
• A blood test shows its thickening and neutrophilic shift.
• Tendency to thrombosis.

At this stage, it is important to conduct a timely intensive infusion therapy with the use of forced diuresis and detoxification.

Symptoms of the third period

The third stage of the development of the syndrome (SDS) is characterized by the development of complications, it lasts from 2 to 15 days.

Symptoms at this time may include the following:

• Damage to various organ systems.
• development of renal failure.
• The swelling gets bigger.
• The appearance of blisters with transparent or hemorrhagic contents can be observed on the skin.
• Anemia is starting to show up.
• Decreased diuresis.
• If you do a blood test, then the concentration of urea, potassium and creatinine increases.
• The classic picture of uremia with hypoproteinemia appears.
• There is an increase in body temperature of the victim.
• The general condition worsens.
• There is lethargy and lethargy.
• There may be vomiting.
• Scleral staining indicates involvement of the liver in pathological process.

It can not even always save a person if SDS is diagnosed. The syndrome, if it reaches this period, then in 35% of cases leads to the death of the victims.

In such cases, only extracorporeal detoxification can help.

Further development of the VTS

The fourth period is convalescence. It begins after the kidneys restore their work. At this stage, local changes prevail over general ones.

Symptoms may be as follows:

• If there are open injuries, then infectious complications are observed.
• Sepsis may develop.
• If there are no complications, then the swelling begins to subside.
• How quickly the mobility of the joints is restored will depend on the severity of the damage.
• Since muscle tissues die, they begin to be replaced by connective tissue, which does not have the ability to contract, therefore, atrophy of the limbs develops.
• Anemia still persists.
• The victims have no appetite.
• There are persistent changes in homeostasis, and if intensive infusion-transfusion therapy is used, they can be eliminated after a month of intensive treatment.

During the last period, the victims show a decrease in natural resistance factors, bactericidal activity of the blood. The leukocyte index remains unchanged for a long time.

For a long time, the victims experience emotional and mental instability. frequent depressive states, psychosis and hysteria.

How to recognize SDS?

The syndrome, the diagnosis of which should be carried out only by a competent specialist, requires special attention and treatment. You can determine the presence of pathology on the basis of the following indicators:

• The clinical picture and the circumstances of the injury are taken into account.
• Do not go unnoticed the results of the analysis of urine, blood.
• Held instrumental diagnostics, which allows you to compare the dynamics of laboratory symptoms and the structure of the kidneys.

People undergoing heart diagnostics sometimes hear this diagnosis, but not everyone understands what the syndrome is. SDS in the cardiogram of the heart may indicate the presence of a pathology that affects the chest. Being under the rubble can significantly affect the work of the heart muscle.

Laboratory diagnostics is carried out in order to:

• Detection of the level of myoglobin in the blood plasma: usually in this condition it rises significantly.
• Determination of the concentration of myoglobin in the urine. If the indicators reach 1000 ng / ml, then we can talk about developing acute renal failure with DFS.
• The syndrome can also be manifested by an increase in blood transaminases.
• Increased creatinine and urea.

Doctors determine the degree of kidney damage by analyzing urine. The study reveals:

• Increased white blood cells, if there is complicated SDS.
• Salt concentration increases.
• The content of urea increases.
• cylinders are present.

A correct diagnosis allows doctors to prescribe effective therapy in order to help the victim restore all body functions as quickly as possible.

How to provide first aid?

From rendering emergency assistance the condition of the victim depends, and maybe his life, if SDS develops. Syndrome, first aid should be provided as soon as possible, will not lead to serious complications if you help the victim according to the following algorithm:

1. Give pain medication.
2. Then begin to release the affected area of ​​the body.

As such funds suitable: "Analgin", "Promedol", "Morphine". All drugs are administered only intramuscularly.

Many people ask why a tourniquet should be applied with SDS syndrome? This is done in the presence of a strong arterial bleeding or extensive damage to the limbs so that the victim does not die from blood loss.

• Inspect the damaged area.
• Remove the tourniquet.
• All existing wounds must be treated with an antiseptic and covered with a sterile napkin.
• Try to cool the limb.
• Give the victim plenty of fluids, tea, water, coffee or soda-salt solution will do.
• Warm the victim.
• If there are blockages, then the person must be provided with oxygen as soon as possible.
• To prevent heart failure, administer Prednisolone to the victim.

• Send the victim to the nearest hospital.

Compression syndrome therapy

There may be varying degrees of severity of SDS. The syndrome, the treatment of which should be carried out in a complex manner, will not cause serious complications considering the pathogenesis of damage. Comprehensively influence means:

• Take measures to eliminate deviations of homeostasis.
• Provide a therapeutic effect on the pathological focus of damage.
• Normalize the microflora of wounds.

Therapeutic measures should be carried out almost continuously, starting from the moment of first aid and until the complete recovery of the victim.

If the injuries are significant, then medical care consists of several stages:

• The first begins directly at the scene.
• The second is assistance in a medical facility, which can be quite far from the site of the tragedy, so “flying hospitals”, “hospitals on wheels” are often used. It is very important that there is appropriate equipment to provide assistance in case of damage to the musculoskeletal system and internal organs.

• At the third stage, specialized assistance is provided. This usually happens in a surgical or trauma center. It has all the necessary equipment to provide assistance in case of serious damage to the musculoskeletal system or internal organs. There are resuscitation services to remove a person from a state of shock, treat sepsis or kidney failure.

Medical therapy

The earlier this stage of therapy is started, the more likely the patient is to survive. Medical assistance at this stage is as follows:

• Victims are given an infusion of a mixture of sodium chloride and 5% sodium bicarbonate in a 4:1 ratio.
• If a severe form of the syndrome is observed, then 3-4 liters of blood or a blood substitute are administered to the victims as an anti-shock measure.
• To prevent the development of complications, diuresis is performed with the introduction of Furosemide or Mannitol.
• Reducing the intoxication of the body is achieved by replacing the blood and the use of gamma-hydroxybutyric acid at an early stage. It has an inhibitory effect on the central nervous system and has a hypertensive effect.

If all conservative methods of therapy do not give the desired result, then surgical treatment is required, which is based on the use of the following detoxification methods:

• sorption methods.
• Dialysis-filtration (hemodialysis, ultrafiltration).
• Feretic (plasmapheresis).

May be required and which cannot be returned to normal life.

Can SDS be prevented?

If you avoid getting serious injury did not work out, then in most cases SDS develops. The syndrome, the prevention of which is mandatory, will not lead to disastrous consequences if you immediately start action. This requires antibiotics. penicillin series. Usage antibacterial agents may not save from suppuration, but it is quite possible to prevent gas gangrene in this way.

Even before removing the victim from the rubble, it is important to start to normalize the bcc. Often, Mannitol, a 4% solution of magnesium bicarbonate, is used for these purposes.

If all these actions are carried out directly at the scene, then it is quite possible to prevent the development of serious complications of SDS, such as gas gangrene and kidney failure.

We examined in detail the SDS (prolonged compression syndrome) of the internal organs with the weight of one's own body or heavy objects. This condition often occurs during emergencies. It should be noted that timely assistance can save a person's life. But in the literature and on the pages of modern magazines you can find a completely different interpretation. It is also called - SDS syndrome - female disease century. This concept from a completely different area and should not be confused with such a serious pathology. This is a topic for a completely different article, but it should be briefly noted what such a syndrome means. Often it strikes women burdened with power. Selfishness, lack of self-criticism, prejudice against men, confidence in one's own infallibility and similar "symptoms" are characteristic of syndrome among women.

Fast passage:

Syndrome of prolonged compression (SDS), or crash syndrome (crush-syndrome)- a symptom complex that develops as a result of reperfusion of soft tissues subjected to compression and acute ischemia. The basis of the pathogenesis of SDS is a simultaneous entry into the systemic circulation a large number products of destruction of striated muscle cells (rhabdomyolysis), primarily myoglobin, proteolytic enzymes, potassium. Elimination of these substances is carried out by the kidneys, so damage to the latter with development seems to be one of the most common manifestations of SDS.

Epidemiology

For the first time, the crash syndrome was described in 1941 by E. Bywaters and D. Beall in BMJ in an article devoted to helping victims of the bombing of London by Luftwaffe aircraft.

Significant progress in the study of the pathogenesis of the crash syndrome is associated with natural and man-made disasters. The most significant of them are earthquakes in Armenia (1988), Turkey (1998), Iran (2003). During catastrophes and natural disasters, during earthquakes, destruction of industrial and residential buildings by bombing, rocket attacks, 3.5-23.8% of victims develop SDS. A severe condition develops within a few hours; in the absence of emergency therapeutic measures, death occurs in 85–90% of cases.

G.G. Savitsky, V.K. Agapov (1990) after the catastrophic earthquake in Armenia (1988) observed 3203 victims, of which 765 (23.8%) developed SDS, while in 78% it was severe or moderate.

Causes of the development of the syndrome of prolonged compression

Destruction of striated muscles (rhabdomyolysis) with myoglobin resorption is possible in various pathological conditions presented in the table.

Etiological factors contributing to the development of rhabdomyolysis

Crash syndrome pathogenesis

Traumatic rhabdomyolysis is the most common. At the same time, it should be remembered that significant damage to soft tissues in severe concomitant trauma, for example, mine-explosive wounds, can lead to massive resorption of myoglobin from crush foci, the development of acute renal failure, although there is no mechanism of limb compression as such.

For many years, one of the variants of traumatic rhabdomyolysis was considered SDS, which develops under the weight of one's own body. In the experiment, these facts were not confirmed, although it was shown that a long immobile state (the result of alcohol or drug intoxication, acute violation cerebral circulation, surgical intervention) can lead to persistent occlusion of the great vessels or individual muscle branches. As a result, ischemia and necrosis of muscle fibers develop with the release of myoglobin. That is why positional compression should be considered as ischemic rather than traumatic rhabdomyolysis. Most often, positional compression develops in the upper or lower extremities, the blood supply of which is carried out through the main neurovascular bundles (brachial and femoral arteries). The severity of necrosis depends on the individual characteristics of the victim (the severity of collateral blood supply and vascular anastomoses); therefore, often the foci of necrosis are outside the zone of compression and are located randomly.

With thrombosis or embolism of the arterial highways or complete external occlusion of the vessels of the limb (“turnstile syndrome”), as a rule, necrosis of all muscles of the limb distal to the occlusion zone develops, and, as a rule, with a clear demarcation line. A special variant of ischemic rhabdomyolysis is cardiorenal syndrome, which complicates myocardial infarction. The striated muscles of the heart are destroyed as a result of ischemia; this process can also be accompanied by a significant release of myoglobin, myoglobinuria and acute renal failure. Most often, cardiorenal syndrome complicates circular transmural myocardial infarctions.

An increased load on muscle tissue leads to a discrepancy between the oxygen supply of myocytes to their needs. Developing hypoxia is accompanied by the destruction of muscle cells and myoglobinuric nephrosis. Excessive physical activity can be both conscious and caused by chills, convulsions, etc.

An infrequent, but difficult to diagnose variant of rhabdomyolysis, due to toxic and especially drug interactions. The widespread use of various statins to prevent the progression of atherosclerosis has led to the identification of their toxic effects on striated muscles, which is due to the combined use with other drugs - cyclosporine, ketoconazole, etc. Toxic metabolites can be formed even with transconjunctival ingestion of ketoconazole into the body. The toxic rhabdomyolysis resulting from this interaction is also often complicated by acute renal failure. The variety of mechanisms of rhabdomyolysis requires a thorough examination of patients and victims with myoglobinemia and acute renal failure, especially in the absence of a clear fact of traumatic effects, since the cause may be intoxication, impaired blood supply to the myocardium, or another disease requiring specialized treatment.

Acute renal failure in the syndrome of prolonged compression is formed with the onset of the action of the compressive factor. The main factors determining the development of acute renal failure are hypovolemia and impaired perfusion of the kidneys, direct cytotoxicity of myoglobin, and intratubular obstruction by insoluble myoglobin globules. Pain leads to the fact that adrenaline and normadrenaline are released into the blood, a spasm of arterioles and precapillary sphincters occurs. In the glomeruli of the kidneys, microcirculation and the process of primary urine filtration are sharply disturbed. In addition, under the influence of other hormones (hormone parathyroid glands, antidiuretic hormone) decreases urine production.

Shock in crush syndrome is characterized by a prolonged period of excitement, the absence of signs of acute blood loss, and the preservation of adequate blood supply to the brain and heart.

The redistribution and centralization of blood supply in the syndrome of prolonged compression does not differ from that in traumatic shock. Blood circulation in the kidneys and other organs does not stop. Blood circulation is carried out through a system of arteriovenular anastomoses (shunts), aimed at providing blood to vital organs. During the period of compression and the first hours of the post-compression period, there is a spasm of arterioles and precapillary sphincters in the kidney porenchyma. If the duration of the spasm lasts more than 2 hours, it occurs. The permeability of the vascular walls increases, blood flow is disturbed. The lumen of the renal tubules, especially the straight ones, is closed by swollen cells as a result of edema and swelling, active filtration of the liquid part of the blood through the capillary wall into the interstitium.

A marked loss of plasma develops, leading to hemoconcentration, hypoalbuminemia, and hyperproteinemia. The ongoing vasoconstrictive effect of catecholamines on the afferent arterioles of the renal glomeruli, in combination with the vasodilating effect of vasoactive substances on the venular structure of the glomeruli, leads to a pronounced disturbance of blood flow in the renal cortex.

Severe toxemia is the cause of damage to vascular endotheliocytes and the basement membrane of the epithelium of the tubules of the kidneys.

The combination of these factors act throughout the early period of the syndrome of prolonged compression.

Under these conditions, the "renin-angiotensin" system is activated, which maintains spasm of the adductor glomerular arterioles and, as a result, reduces glomerular filtration.

Serious changes occur in tissues that have been subjected to compression: often, blood circulation and lymphatic drainage are completely absent, anaerobic respiration reserves are depleted, which leads to the accumulation of under-oxidized products (lactic acid, pyruvic acid, and others) - metabolic acidosis develops. After 4-6 hours, destruction processes develop, in the vessels - stasis with adhesion and aggregation of blood cell elements. Agglutinates are formed, in which the cellular elements of the blood stick together so tightly that after the restoration of blood circulation they do not disintegrate, and, in fact, become microemboli. They enter the systemic circulation with the blood flow, which leads to blockage of the vessels of the kidneys and other organs. Their circulation is disrupted.

The complex effect of vasoactive components (histamine, kinins, serotonin) and high osmotic pressure leads to the release of albumin and plasma from the vascular bed into the tissues. This leads to a decrease in oncotic blood pressure, fluid is not retained, blood clotting and clotting activity increase. As a result of hypoalbuminemia, the consumption of lipoprotein complexes increases. This leads to the release of small globules of demulsified fat, they clog small vessels and, like microagglutinates, enter the kidneys. Myoglobin is released from the destroyed myocytes, which is then filtered in the kidneys, having a direct toxic effect and forming insoluble globules with the development of intratubular obstruction.

Myoglobin is an iron-containing protein, an intracellular oxygen carrier in striated muscles (molecular weight 18,800 Da, content in muscles - 4 mg per 1 g of tissue). The normal concentration of myoglobin in blood plasma is 0.5-7 ng / ml. Normally, it is filtered in the glomeruli and undergoes tubular catabolism, the maximum concentration in the urine is up to 5 ng / ml.

In an acidic environment, myoglobin precipitates as acidic hematin. hyperconcentration of myoglobin in the urine in an acidic environment leads to the formation of insoluble conglomerates that block the outflow of urine in the tubules. Intratubular hypertension causes leakage of filtrate into the interstitium, interstitial edema, and ischemia of the tubular epithelium. In this regard, the prevention of precipitation of pigments, including a decrease in their concentration due to hemodilution, as well as "alkalinization" of urine, serve effective means prevention of the development of acute renal failure.

Myoglobinuria, according to the degree of kidney damage, is subdivided into:

• simple myoglobinuria - does not cause damage to the nephrons;
• myoglobinuric nephropathy - there is a lesion of nephrons with the appearance of cylinders in the urine;
• malignant nephropathy - severe damage to the kidney parenchyma with the appearance of signs of acute renal failure.

Symptoms of the syndrome of prolonged compression

The assessment of the patient's condition and the prognosis for the syndrome of prolonged compression are determined by the functional state of the kidneys at different periods of the disease. The symptoms of the victims are usually of a general nature and are associated with a mechanical injury to the limb or trunk. There are usually no symptoms that would indicate kidney damage.

An increase in body temperature and the addition of chills give reason to suspect a urinary tract infection. Blood pressure levels help assess the severity of shock. Arterial hypertension is usually reactive and rarely observed.

In the early and intermediate periods, the main symptoms of crush syndrome can be identified: shock, toxemia, generalized microcirculation disorders, anemia, acute renal failure, cardiovascular failure, infectious and septic complications, traumatic neuritis.

With a mild degree of the syndrome of prolonged compression against the background of treatment, it is restored after about 3-5 days; with a severe degree - the general condition does not improve. Acute renal failure, as a rule, continues to develop. It should be said that acute renal failure can develop without previous signs of shock and is usually clearly manifested by the 3-5th day.

In the interim, diuresis still ranges from 200 to 400 ml, and some patients develop. Due to the cessation of myoglobin secretion, the urine becomes lighter, its relative density decreases, and the reaction becomes acidic. Microscopic examination reveals hyaline, granular, epithelial casts.

On the 4-5th day, back pain appears due to stretching of the fibrous capsule of the kidneys due to edema.

By the end of the 1st week, the patient's condition worsens due to an increase in uremic intoxication. The patient becomes lethargic, lethargic, he is disturbed by nausea and vomiting.

The progression of intoxication leads to the development of psychosis, motor restlessness, the appearance of a feeling of fear, delirium; changes in red blood parameters are expressed; dangerous changes in potassium metabolism, the level of which can reach 7.5-11.3 mmol / l. With the development of hyperkalemia, characteristic electrocardiographic changes are noted; possible cardiac arrest.

Often, hyperphosphatemia (serum phosphorus concentration up to 2.07-2.49 mmol / l), hyponatremia are detected.

With an increase in the level of magnesium in the blood serum, depressive states characteristic of victims with acute renal failure, periodically accompanied by aggressiveness, are associated.

For renal failure in SDS, a decrease in the buffer capacity of the blood is characteristic.

Diagnostics of the crash syndrome

In the early and intermediate periods of the syndrome of prolonged compression, the most important are, and, as well as blood electrolytes and acid-base balance.

Plasma myoglobin levels may be elevated significantly, but their concentration does not correlate with the severity of kidney damage. On the contrary, it serves as an informative prognostic criterion for renal damage. At a myoglobin concentration of up to 300 ng / ml, AKI does not develop; at a concentration of more than 1000 ng / ml - in 80% of cases, anuric acute renal failure develops. Given the relationship of renal damage with the resorption of rhabdomyolysis products, an additional (confirming) diagnostic sign of the latter will be an increase in the concentration of transaminases, primarily creatine phosphokinase, the concentration of which can exceed the normal one by several thousand times.

When determining the severity of kidney damage, not biochemical criteria come to the fore, but symptoms, and, first of all, diuresis.

Evidence of serious violations of the blood supply to the kidneys is the appearance, and even more so the formation of clots. , increases significantly, grows significantly, is revealed.

In the first hours and days after injury, in patients with the syndrome of prolonged compression, the specific gravity of urine increases, which, in some cases, reaches 1040-1050. After some time, in the absence of anuria, the relative flatness of urine decreases, and the degree of decrease is determined by the depth of damage to the tubules of the kidneys. Approximately 28% of patients with SDS are detected in the first 2 weeks (up to 0.5–1%), which indicates damage to the proximal nephron.

Protein in the urine up to 2 g/l, detected in almost all patients with crush syndrome. Determining the concentration of myoglobin, especially in the case of mass admission of victims, is not of decisive diagnostic value. Evidence of presence significant amount myoglobin in urine is the color of urine (dark brown or almost black). Microhematuria occurs in virtually all patients with crush syndrome and raises the suspicion of blunt trauma to the kidney.

Urinary sediment is characterized by:

• Availability ;
• increase (subject to the attachment of an infectious process);

In the first 2–3 weeks, the vast majority of patients develop urate diathesis, and later, oxalate and phosphate diathesis. If it prevails in the initial period, this, with a sick probability, is evidence of a pronounced breakdown of muscle tissue.

The transition of acute renal failure from (or anuric) stage to is accompanied by an increase in urinary sediment with an increase in cylindruria, leukocyturia,. This is not associated with an inflammatory process, but, in fact, is a “washing out” of the lumen of the tubules and collecting ducts against the background of the restoration of glomerular filtration.

Possible changes in the kidneys in the syndrome of prolonged compression:

• "shock kidney";
• toxic and infectious (tubulointerstitial nephropathy);
• compression of the kidney by a perirenal hematoma;
• other conditions leading to disruption of the normal passage of urine;

Instrumental diagnostics

Widely used ultrasound diagnostics, which allows you to dynamically compare symptoms, data laboratory examination with the structure of the kidneys in various periods of acute renal failure. This makes it possible to control the course of acute renal failure. Normalization of the condition (according to ultrasound of the kidneys) occurs within a period of several weeks to 1-2 months and depends on the severity.

Treatment of the syndrome of prolonged compression

Prevention of the development of nephropathy in SDS and its treatment is a complex task that combines various methods of conservative, detoxification and surgical benefits and requires the participation of specialists of various profiles.

Fight against renal ischemia and increasing toxemia.

Non-drug treatment

• hypothermia to the area of ​​injury reduces shock, plasma loss, reduces the rate of formation of toxins;
• hyperbaric oxygenation reduces the degree of tissue hypoxia, and also participates in the normalization of the activity of the cardiovascular system;
• plasmapheresis reduces the toxic effect of myoglobin on the kidneys, improves blood rheology, normalizes the coagulation system, reduces the concentration of cytokines and autoantibodies.

Medical treatment

Prevention of acute renal failure begins in the early period, and treatment - in the intermediate period of SDS. Of fundamental importance is the elimination of hypovolemia and the prevention of myoglobin precipitation.

The importance of this was convincingly demonstrated during the care of victims during the earthquake in Marmaris (Turkey) in 1999. The victims were infused as early as possible (often at the first opportunity of vein puncture, even before being removed from the rubble) isotonic solution sodium chloride and 5% sodium bicarbonate in a ratio of 4:1. As a result, out of 43,953 victims, only 639 developed acute renal failure, of which only 340 victims had its most severe (oliguric) form.

With a severe degree of SDS, patients on the first day are administered up to 3–4 liters of blood and blood substitutes as antishock therapy.

Of great importance for the treatment and prevention of complications of SDS in early phase the development of the disease is given to forcing diuresis with the introduction of diuretics - furosemide, mannitol. This prevents hyperconcentration and precipitation of myoglobin in the lumen of the tubules. In addition, furosemide, by blocking Na-K-ATPase, reduces oxygen consumption by the nephrothelium and increases its tolerance to hypoxia. Purpose this drug With preventive purpose contributes to maintaining a higher creatinine clearance. The appointment of mannitol is advisable only in the initial period of acute renal failure, when there are still no gross morphological changes in the epithelium of the renal tubules.

Anesthesia is of great importance. Since the main thing in the pathogenesis of acute renal failure is a violation of blood circulation in the kidneys of a neuro-reflex nature, it is reasonable to carry out measures aimed at stopping the flow of impulses from the place of compression. Therefore, a complete treatment of the focus of injury and immobilization of the injured limb are necessary, which reduces pain, tissue swelling and limits the absorption of toxic substances.

A decrease in intoxication in the early period of SDS is achieved by replacing blood, using gamma-hydroxybutyric acid in the early period of SDS, which has an inhibitory effect on the central nervous system and a hypertensive effect, and increases the concentration of plasma sodium, increases alkaline reserves.

Kidney dysfunctions in patients with DFS are reversible with timely and adequate treatment. In most patients, by the 13–33rd day of treatment, a gradual recovery of kidney function is noted with complete normalization of nitrogen metabolism and the level of medium molecules by the end of the 2nd month of treatment. By this time, as a rule, the value of glomerular filtration is also restored, with a continuing decrease in the value of tubular reabsorption.

The most effective measure in the elimination of toxemia, prevention and treatment of acute renal failure should be considered infusion therapy aimed at fulfilling the volume of circulating plasma, increasing diuresis, and improving the rheological properties of blood. More than 10% of victims require extracorporeal detoxification. The methods of substitution therapy for acute renal failure differ in the physical principle and the range of substances removed, as well as in duration.

The most common method traditionally remains hemodialysis, based on the diffusion removal of molecules of small molecular weight. Satisfactorily solving the problem of eliminating uremic toxins, hemodialysis is ineffective in relation to "medium molecules". All methods of extracorporeal detoxification have additional stress and catabolic effects on the body. This is due to both the contact of immunocompetent blood cells with foreign material of the dialyzer membrane and blood-conducting lines, and direct loss of nutrients with the effluent.

An alternative to hemodialysis in acute renal failure is hemofiltration, which uses highly permeable and biocompatible synthetic membranes that do not activate the complement system. In addition, hemofiltration based on convection mass transfer makes it possible to achieve sufficient elimination of medium molecular substances. The combination of severe uremic and medium molecular intoxication determines the appointment as a method of choice for hemodiafiltration, combining physical principles diffusion and convection on the same membrane.

Indications for emergency hemodialysis:

• (more than 6–7 µmol/l);
• hyperhydration with the threat of pulmonary edema;
• clinic of uremic intoxication.

Anuria during the day with inefficiency conservative therapy, hyperazotemia (urea 20-25 mmol / l, creatinine more than 500 μmol / l), persistent hyperhydration and metabolic acidosis require planned hemodialysis.

Unremoved foci of muscle necrosis and endotoxicosis deplete the adaptive mechanisms of the body, cause gross violations of the function of other organs and systems, contribute to the delay in the recovery of kidney function and the elimination of acute renal failure. That is why prolonged anuria for 4–5 weeks serves as a marker of severe endotoxicosis and persistent necrotic foci in the muscles.

Surgical treatment

The ineffectiveness of conservative treatment dictates the need for surgical methods of detoxification, which include sorption methods (blood, lymph, intestines), dialysis-filtration (hemodialysis, hemodiafiltration, ultrafiltration), feretic (plasmapheresis, plasma sorption, lymphoplasmic sorption).

Among the methods of surgical rehabilitation of the damaged area, fasciotomy without stripe incisions, necrectomy, amputation of non-viable limbs, etc. are recommended.

The severity of acute renal failure is directly dependent on the massiveness of hemorrhage into soft tissues, and therefore, early emptying of hematomas is necessary to prevent toxic effects on the kidneys.

In the treatment of SDS, the rule of removal of all necrotic tissues, which are the morphological substrate of intoxication, the development of acute renal failure, septic infection, often leading to death, is strictly adhered to.

Crash prognosis

One of the severe complications of acute renal failure in the intermediate period of SDS is severe respiratory failure as a result of the development acute injury mild and acute respiratory distress syndrome.

In patients with SDS, the development of hemodynamic disorders according to the hypokinetic type of blood circulation (with low cardiac output) is noted, which is associated with the development of a severe degree of endotoxicosis as a result of acute renal failure. Clinical manifestations of acute renal failure against the background of adequate treatment are on the wane. In some cases, acute renal failure has a rapid course, leading to death in the first days of the interim period.

On the 9-12th day, the polyuric stage of acute renal failure occurs, which proceeds quite typically. The dynamics of diuresis recovery has prognostic value. If diuresis recovers quickly and immediately becomes abundant, the prognosis is favorable. Otherwise, the irreversible nature of kidney damage should be assumed.

In the long term, a decrease in the partial functions of the kidneys is noted: a decrease in the filtration charge of sodium, a decrease in the renal plasma flow, a decrease in the excretion of sodium and chlorine in the absence of changes in potassium secretion.

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Syndrome of prolonged compression

What is Prolonged Compression Syndrome -

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 different reasons(coma, poisoning, epilepsy, etc.) are in an unconscious state. 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. Big clinical experience and the results of experimental studies show that all these factors play a role in the development of SDS. 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.

AT pathogenesis several different options SDS(traumatic genesis, 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 case of mass lesions, when it is necessary triage. 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 affect basically all vital important organs and systems: myocardium (due to the negative inotropic effect of ischemic toxins on it) - the brain, lungs, liver, kidneys; there are profound disorders of the erythron system, 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 allows you to create a model for the prevention and treatment of SDS. 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 situation.

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 increased concentration oxygen.

Symptoms of Prolonged Compression Syndrome:

Clinical picture 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" get into common system circulation of blood and lymph after the release of victims 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 smooth muscle 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 huge 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. Particularly high toxicity venous blood injured limb 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 defensive reactions organism, and the edema of ischemic tissues is protective. This conclusion is supported by data indicating that the more severe the compression injury, the more significantly the immunological reactivity of the body decreases.

Edema of ischemic tissues increases as absorption decreases toxic substances from the affected tissues. 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 "fight" 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, striking 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. AT 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 renders Negative influence 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 has been received that various options shock, a specific humoral depressive myocardial factor appears. These components can be the causes of oppression. contractility myocardial 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 easy. As experience has shown, all these forms of SDS were observed in patients coming from the earthquake zone.

AT clinical course SDS is divided into four periods.

• I period- compression of soft tissues with the development of traumatic and exotoxic shock.
• II period- local changes and endogenous intoxication. It 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 is high relative density, protein, erythrocytes, cylinders 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) changes appear local character in the damaged segment - pallor, cyanosis, variegated coloration of the skin, absence of pulsation in the 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 the 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, their replacement occurs connective tissue and development of limb atrophy, but 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 y-fraction), hypercoagulability of blood, as well as changes in 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 are identified significant reduction factors of natural resistance, 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 testifies to high risk development in these patients of clostridial myonecrosis or "gas gangrene". 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 the majority of patients arriving at a later date, microbial associations are isolated, mandatory integral part which is Pseudomonas aeruginosa, and their "companions" - 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 traumatological 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 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, perform novocaine blockade(preferably conductive) 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, catheterization is carried out central vein(if it was not made 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. Part infusion means 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 classifying 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 cyanosis. After 24-36 hours, blisters may form, containing a clear yellowish liquid, upon opening of which a moist, pale pink surface is exposed. Increased edema in the following days indicates a violation of venous circulation and lymphatic drainage. Insufficiently adequate conservative treatment can lead to the progression of microcirculation disorders, microthrombosis, increased edema and compression of muscle tissue.
• III degree- Pronounced indurative edema and soft tissue tension. The skin is cyanotic or marbled. Skin temperature is markedly reduced. After 12-24 hours, blisters with hemorrhagic contents appear. Under the epidermis, a moist surface of a dark red color is exposed. Indurated edema and cyanosis are rapidly growing, which indicates gross violations of microcirculation and vein thrombosis. Conservative treatment is ineffective, leading to the development of a necrotic process. Wide incisions with dissection of fascial cases eliminate tissue compression. The blood flow is restored.
• IV degree- indurated edema is moderately pronounced, the tissues are sharply strained. The skin is bluish-purple, cold, there are separate epidermal blisters with hemorrhagic contents. After removal of the epidermis, a cyanotic-black dry surface is exposed. In the following days, the edema practically does not increase, which indicates deep microcirculation disorders, insufficiency of arterial blood flow, widespread thrombosis of venous vessels. Conservative treatment is ineffective. Wide fasciotomy provides the maximum possible restoration of blood circulation, allows you to limit the necrotic process in more distal parts, reduce the intensity of absorption of toxic products. In most cases, indications are given for amputation of the limb.

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

In the presence of crushed wounds on damaged limbs, at the second stage of evacuation, a thorough primary surgical treatment is performed with a wide opening of the wound, excision of obviously non-viable tissues, removal foreign bodies and free-lying bone fragments, abundant washing of the wound with antiseptics, sanitation with ultrasound and vacuum. The imposition of deaf seams is unacceptable. Bandages with antiseptic, dehydrating properties are applied to the wound.

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

An analysis of the results of treatment of the victims showed that the implementation of external and intraosseous osteosynthesis of the segments subjected to compression at this stage of medical care should be considered a mistake. Such osteosynthesis worsens the blood circulation of the segment, exacerbates the necrotic process, "opens the gates" of infection. At this stage, stable fixation should be performed using transosseous compression-distraction wire or rod devices, even without the final and complete adaptation of the fragments. In the absence of opportunities or conditions for the imposition of transosseous devices for fixation of the limbs, gypsum deep splints are used. Circular casts should not be applied.

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

After cleansing wound surface from necrotic tissues and the appearance of fresh granulation tissue perform free skin autoplasty with split grafts, perforated in a ratio of 1:2-1:5. From other types of skin plastics, non-free skin autoplasty (Italian) can be recommended, especially in the presence of wounds in the area of ​​the hand and forearm. The indications for performing combined skin autoplasty with displaced local tissues are limited, since the movement of skin and soft tissue flaps in the area of ​​compressed segments can aggravate microcirculation and blood supply disorders and lead to flap necrosis.

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

At the stages qualified and specialized assistance the use of modern methods of active detoxification is of paramount importance. An increase in the toxicity of the blood and lymph in patients can be detected earlier than the clinical symptoms of toxicosis appear, therefore, without waiting for the deterioration of the patients' condition, a blood test for toxicity should be carried out according to the paramecium test and the concentration of "medium molecules". In case of increased toxicity, hemolymphosorption and enterosorption are indicated, in case of violation of homeostasis and hyperhydration - hemodialysis. With a combination of toxicosis, hyperhydration and homeostasis disturbance, hemo-, lymph-, enterosorption and hemodialysis are simultaneously carried out in the ultrafiltration mode, if necessary, repeatedly. In parallel, purposeful antibacterial therapy is carried out: immunocorrection, as well as rehabilitation measures that are carried out during the entire process of treating the victim.

In this way, in the treatment of the syndrome of prolonged compression with open and closed injuries of the musculoskeletal system, the constant work of trauma surgeons, resuscitators-toxicologists, therapists, and nephrologists is necessary. Victims who have undergone SDS need follow-up follow-up.

Prevention of Prolonged Compression Syndrome:

For the purpose of prevention wound infection a combination of antibiotics is administered with the obligatory inclusion of an antibiotic of the penicillin group (taking into account frequent discharge from wounds of clostridial anaerobes). Prophylactic use of antibiotics, without completely preventing wound suppuration in the future, prevents the development of clostridial myonecrosis (gas heat), for the development of which in this situation there are favorable conditions. It is important as soon as possible, if possible, even before the complete release of the victim from the rubble, to start infusion therapy in order to normalize the BCC, increase the volume and alkalinize the urine. Crystalloids, rheopolyglucin, 4% sodium bicarbonate solution, mannitol should be used as the first infusion media. The rate of fluid administration during infusion is not less than 500 ml / h.

The above activities performed at the scene and during the evacuation stages are measures to prevent shock, kidney failure and gas gangrene.

Which doctors should you contact if you have Prolonged Compression Syndrome:

• Traumatologist
• Surgeon

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

Syndrome of prolonged compression (crash syndrome) - 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 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 arm 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

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 severe pain in damaged limbs, they remain edematous, 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. AT 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 a severe alcohol intoxication) you should consult 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: