First aid for long-term compartment syndrome. Long-term compartment syndrome (LCS)

Earthquakes, hurricanes, floods in mountainous areas, and major transport accidents cause the collapse of structures or trees. A person who has fallen under a rubble and is crushed by a weight experiences the so-called crash syndrome.

Crash syndrome is toxic poisoning by waste products of one’s own body in an injured part of the body that is under pressure from a heavy object. If a person has fallen under a rubble and is crushed, it is necessary to free him as soon as possible in order to preserve his health and life. The sooner first aid is provided for long-term compartment syndrome , the greater the chance a person has of avoiding serious complications or death.

The main causes of crash syndrome are massive loss of plasma due to its release through damaged vessels, as a result of which edema and thrombosis of small vessels develop; disruption of metabolic processes in damaged tissues, intoxication of the body with decay products; severe pain.

In case of crash syndrome, you need to try to free the victim from the rubble as quickly as possible and take him to a medical facility.

The main clinical picture of SDS, long-term compression syndrome caused by a blockage, is usually similar to mechanical injuries of the body: fractures, bleeding, hematomas, edema.

What to pay attention to

When providing assistance, a non-specialist must pay attention to the following signs and conditions of the victim:

• fever and chills (may indicate a urinary tract infection);
• decreased blood pressure, decreased heart rate (with cardiovascular failure);
• loss of consciousness, shock.

With such symptoms, you need to try to free the victim from the rubble as quickly as possible, provide first aid, and take him to a medical facility to begin intensive therapy. With strong, prolonged compression, by the end of the first week there is an increase in symptoms of intoxication:

• lethargy and lethargy develops;
• nausea, vomiting;
• motor restlessness increases;
• depression, psychosis, fear;
• delirium may begin.

Head injuries require special care when extricating from the rubble.

Degrees of crash syndrome

Easy degree	Average degree	Severe degree	Severe degree
Compression of small areas, short in time, no more than 4 hours. No impairment of the kidneys or cardiovascular system.	Compression of the soft tissues of both extremities for no more than 6 hours. Mild kidney damage. Symptoms of damage to the cardiovascular system are not pronounced.	Compression for more than 6-7 hours. Symptoms of kidney failure, Disruption of the circulatory system.	Occurs during major accidents or in places where it is difficult for the ambulance team to reach. Compression for more than 8 hours. Often leads to severe complications: heart attack, sepsis, death

The severity of the lesion also depends on:

• from localization: compression of the head, thoracic region, abdomen, pelvic organs, limbs;
• associated pathologies: injuries to internal organs, fractures, chronic pathologies, damage to nerves and large blood vessels.

First aid: algorithm - instructions

First aid depends on the condition of the victim, the complexity of the injuries, and the duration of crushing of the limbs or the entire body under the rubble. Basic actions of a rescuer in case of crash syndrome:

Action	Description
	Remove the victim from under the rubble.
	Clear your mouth and respiratory tract of foreign objects.
	Move to the safest place, cover with a warm blanket.
	The sequence of assistance depends on the degree of injuries and their location (extremities, head) of the victim. Examine the head for damage to the skull bones and compression of the brain.
	Lay the victim on the ground and place a cushion around the neck to reduce head movement. The roller can be rolled out of clothing.
	If necessary, carry out resuscitation measures.
	When restoring heart function and breathing, treat wounds and abrasions on the head.
	When treating wounds on the head, you cannot remove stuck foreign objects or fragments of skull bones from them, so as not to damage the brain. It is enough to apply a clean bandage and take the victim to the hospital or call an ambulance as quickly as possible
	Inspect wounds and cover abrasions with sterile napkins, bandages (for example, from a driver’s first aid kit), clean napkins, handkerchiefs, or a piece of cloth.
	If the victim begins to experience severe swelling of the tissues, it is necessary to unbutton, cut, and tear the clothes in this place to prevent further compression of the body.
	If possible, apply cold to the affected area of ​​the body to reduce swelling.
	If there is bleeding, apply a hemostatic tourniquet or a homemade twist.
	Be sure to write a note about the time the tourniquet is applied. If you don’t have paper or pencil, you can write on your clothes with blood. Further medical care in the hospital will depend on this information.
	Doctors recommend applying a tourniquet to injured limbs above the point of compression, even if there is no bleeding, even before the person is freed from the rubble, especially if a significant amount of time has passed since the injury.
	Important information: Applying a tourniquet will prevent a sudden flow of potassium from the blood plasma to the myocardium (heart muscle), which can prevent collapse, a fatal arrhythmia. If the victim develops gangrene or the limb is almost completely lost, the tourniquet is left in place for a long time, or is removed only in a medical facility.
	Immobilize (immobilize the damaged limb) with any available material or tie it to a healthy limb.
	Provide the victim with plenty of fluids to quickly remove toxins from the body.
	Give a painkiller (Analgin, Baralgin, Ketanov).
	If the heart and breathing stop, emergency resuscitation measures must be carried out: artificial respiration and chest compressions - do 15 chest compressions for every two breaths

The video for this article is an illustration of doctors who briefly tell and show how to behave with the victim, how to properly provide emergency first aid.

What happens next

Further assistance is provided by professional rescuers, ambulance or air ambulance paramedics, and hospital doctors. The main assistance provided by a hospital doctor:

• infusion therapy, hemodialysis;
• plasmaphoresis, hemosorption;
• psychological correction.

In some cases, surgical treatment is performed involving the removal of necrotic tissue areas or amputation of the affected limbs.

Immediate provision of first aid for long-term compression syndrome is a guarantee of restoration of health, the ability to avoid amputation, and save life. Particularly quickly, first of all, it is necessary to provide assistance to children who have suffered from prolonged compression, because they endure pain more difficultly, become hypothermic faster, and are more injured.

Quick jump:

Long-term compression syndrome (LCS), 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 the simultaneous entry into the systemic circulation of a large number of products of destruction of striated muscle cells (rhabdomyolysis), primarily myoglobin, proteolytic enzymes, and potassium. Elimination of these substances is carried out by the kidneys, so damage to the latter during development seems to be one of the most common manifestations of DFS.

Epidemiology

Crash syndrome was first described in 1941 by E. Bywaters and D. Beall in the BMJ in an article dedicated to helping victims of the Luftwaffe bombing of London.

Significant progress in studying the pathogenesis of 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 VDS. A serious condition develops within several hours; in the absence of emergency treatment 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 whom 765 (23.8%) developed SDS, while in 78% it was severe or moderate.

Causes of development of long-term compartment syndrome

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

Etiological factors contributing to the development of rhabdomyolysis

Rhabdomyolysis variant	Etiological factors
Traumatic	CDS (crush syndrome), electrical trauma, burns and frostbite, severe combined injury
Ischemic	Positional compression syndrome, tourniquet syndrome, thrombosis, arterial embolism, cardiorenal syndrome
Hypoxic (overexertion and severe hypoxia of muscle tissue)	Excessive physical exertion, marching myoglobinuria, tetanus, convulsions, chills, status epilepticus, delirium tremens
Infectious	Pyomyositis, sepsis, bacterial and viral myositis
Dysmetabolic	Hypokalemia, hypophosphatemia, hypocalcemia, hyperosmolarity, hypothyroidism, diabetes mellitus
Toxic	Snake and insect bites, drug toxicity (amphetamine, barbiturates, codeine, colchicine, lovastatin-itraconazole combination, cyclosporine-simvastatin combination), heroin, N,N-lysergic acid diethylamide, methadone
Genetically determined	McArdle disease (lack of phosphorylase in muscle tissue), Tarui disease (lack of phosphofructomasase)

Pathogenesis of crash syndrome

The most common type is traumatic rhabdomyolysis. It should be remembered that significant damage to soft tissues in severe combined trauma, for example, mine-explosive wounds, can lead to massive resorption of myoglobin from crush sites and 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 to be SDS, which develops under the weight of one’s own body. These facts were not confirmed in the experiment, although it was shown that a prolonged immobile state (the result of alcohol or drug intoxication, acute cerebrovascular accident, surgery) can lead to persistent occlusion of the great vessels or individual muscle branches. As a result, ischemia and necrosis of muscle fibers develops with the release of myoglobin. This is why positional compression should be considered 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 (severity of collateral blood supply and vascular anastomoses); therefore, foci of necrosis are often located outside the compression zone and are located chaotically.

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

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

An infrequent, but difficult to diagnose variant of rhabdomyolysis, caused by 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 caused by combined use with other drugs - cyclosporine, ketoconazole, etc. Toxic metabolites can be formed even when ketoconazole enters the body transconjunctivally. The toxic rhabdomyolysis that develops as a result of 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 exposure, since the cause may be intoxication, impaired blood supply to the myocardium, or another disease requiring specialized treatment.

Acute renal failure in long-term compression syndrome develops with the onset of the compression factor. The main factors determining the development of acute renal failure are hypovolemia and impaired renal perfusion, direct cytotoxicity of myoglobin and intratubular obstruction by insoluble myoglobin globules. Pain leads to the release of adrenaline and normadrenaline into the blood, causing spasm of arterioles and precapillary sphincters. In the glomeruli of the kidneys, microcirculation and the process of filtration of primary urine are sharply disrupted. In addition, under the influence of other hormones (parathyroid hormone, antidiuretic hormone), urine production decreases.

Shock in crash syndrome is characterized by a prolonged period of agitation, no signs of acute blood loss, and preservation of adequate blood supply to the brain and heart.

The redistribution and centralization of blood supply in long-term compartment syndrome 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) and is aimed at supplying blood to vital organs. During the period of compression and the first hours of the post-compression period, spasm of arterioles and precapillary sphincters in the kidney porenchyma occurs. If the duration of the spasm lasts more than 2 hours, it occurs. The permeability of vascular walls increases, blood flow is impaired. 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 pronounced loss of plasma develops, which leads to hemoconcentration, hypoalbuminemia, and hyperproteinemia. The ongoing vasoconstrictor effect of catecholamines on the afferent arterioles of the renal glomeruli, combined with the vasodilatory 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 endothelial cells and the basement membrane of the renal tubular epithelium.

The combination of these factors operates throughout the early period of long-term compartment syndrome.

Under these conditions, the renin-angiotensin system is activated, maintaining spasm of the afferent glomerular arterioles and, as a consequence, reducing glomerular filtration.

Serious changes occur in tissues that have been subjected to compression: often there is a complete absence of blood circulation and lymphatic drainage, reserves of anaerobic respiration 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 cellular elements of the blood. Agglutinates are formed in which the cellular elements of the blood stick together so tightly that after restoration of blood circulation they do not disintegrate, and, in fact, become microemboli. They enter the systemic circulation with the bloodstream, which leads to clogging of the blood vessels of the kidneys and other organs. Their blood circulation is disrupted.

The complex influence of vasoactive components (histamine, kinins, serotonin) and high osmotic pressure leads to the release of albumin and plasma from the vascular bed into the tissue. This leads to a decrease in the oncotic pressure of the blood, fluid is not retained, and blood thickening and coagulation activity increases. As a result of hypoalbuminemia, the consumption of lipoprotein complexes increases. This leads to the release of small globules of deemulsified fat, which clog small vessels and, like microagglutinates, enter the kidneys. Myoglobin is released from destroyed myocytes, which is then filtered in the kidneys, causing 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 urine is up to 5 ng/ml.

In an acidic environment, myoglobin precipitates in the form of acidic hematin. hyperconcentration of myoglobin in urine under acidic conditions 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, preventing the precipitation of pigments, including reducing their concentration due to hemodilution, as well as “alkalinization” of urine are effective means of preventing the development of acute renal failure.

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

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

Symptoms of compartment syndrome

Assessment of the patient's condition and prognosis for long-term compartment syndrome are determined by the functional state of the kidneys during various periods of the disease. Symptoms of victims are usually general and associated with the resulting mechanical injury to a limb or torso. There are usually no symptoms that would indicate kidney damage.

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

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

With a mild degree of long-term compartment syndrome during treatment, it recovers in approximately 3-5 days; in severe cases, 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 usually clearly manifests itself by the 3rd–5th day.

In the intermediate period, diuresis still ranges from 200 to 400 ml, and in some patients it develops. 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 4th–5th day, lower 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, and is bothered by nausea and vomiting.

The progression of intoxication leads to the development of psychosis, motor restlessness, the appearance of feelings 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; cardiac arrest is possible.

Hyperphosphatemia (serum phosphorus concentration up to 2.07–2.49 mmol/l) and hyponatremia are often detected.

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

Renal failure in DFS is characterized by a decrease in the buffer capacity of the blood.

Diagnosis of crash syndrome

In the early and intermediate periods of long-term compression syndrome, and are of greatest importance, as well as blood electrolytes and acid-base balance.

Plasma myoglobin levels may be significantly elevated, 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, acute renal failure does not develop; at a concentration of more than 1000 ng/ml, anuric acute renal failure develops in 80% of cases. Considering the connection 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, it is not the biochemical criteria that come to the fore, but the symptoms, and, first of all, diuresis.

Evidence of serious disturbances in the blood supply to the kidneys is the appearance and, especially, the formation of clots. , increases significantly, grows significantly, comes to light.

In the first hours and days after injury, in patients with long-term compartment syndrome, the specific gravity of urine increases, which, in some cases, reaches 1040–1050. After some time, provided there is no anuria, the relative flatness of the urine decreases, and the degree of decrease is determined by the depth of damage to the renal tubules. In approximately 28% of patients, DFS is 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 is detected in almost all patients with crash syndrome. Determining the concentration of myoglobin, especially in case of mass admission of victims, does not have a decisive diagnostic value. Evidence of the presence of a significant amount of myoglobin in the urine is the color of the urine (dark brown or almost black). Microhematuria occurs in almost all patients with crush syndrome and makes one suspect blunt renal trauma.

Urinary sediment is characterized by:

• availability ;
• increase (subject to the addition of an infectious process);

In the first 2–3 weeks, the vast majority of patients exhibit urate diathesis, and in later periods, oxalate and phosphate diathesis. If in the initial period it predominates, this is most likely evidence of pronounced breakdown of muscle tissue.

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

Possible changes in the kidneys with long-term compression syndrome:

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

Instrumental diagnostics

Ultrasound diagnostics is widely used, which makes it possible to dynamically compare symptoms, laboratory examination data with the structure of the kidneys during different periods of acute renal failure. This allows you to control the flow of the surge arrester. 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 compartment syndrome

Preventing the development of nephropathy in DFS and its treatment is a complex task that combines various methods of conservative, detoxification and surgical treatment and requires the participation of specialists in various fields.

Combating renal ischemia and increasing toxemia.

Non-drug treatment

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

Drug treatment

Prevention of acute renal failure begins in the early period, and treatment begins 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 when providing assistance to victims of the earthquake in Marmaris (Turkey) in 1999. Victims were given an infusion of a mixture of isotonic sodium chloride and 5% bicarbonate as early as possible (often at the first opportunity of venipuncture, even before removal from the rubble). sodium 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.

In severe cases of SDS, patients are given up to 3–4 liters of blood and blood substitutes as anti-shock therapy on the first day.

For the treatment and prevention of complications of DFS in the early phase of disease development, great importance is attached to forcing diuresis with the administration of diuretics - furosemide, mannitol. This prevents hyperconcentration and precipitation of myoglobin in the tubular lumen. In addition, furosemide, by blocking Na-K-ATPase, reduces oxygen consumption by the nephrothelium and increases its tolerance to hypoxia. Prescribing this drug for prophylactic purposes helps maintain a higher creatinine clearance. The administration 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.

Pain relief 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 justified to carry out measures aimed at stopping the flow of impulses from the site of compression. Therefore, complete treatment of the injury site and immobilization of the damaged limb are necessary, which reduces pain, tissue swelling and limits the absorption of toxic substances.

Reducing 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 and increases alkaline reserves.

Renal dysfunction in victims with DFS is reversible with timely and adequate treatment. In most patients, by the 13th–33rd day of treatment, a gradual restoration of renal 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 restored with a continuing decrease in the value of tubular reabsorption.

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

The most common method traditionally remains hemodialysis, based on the diffusion removal of molecules of low molecular weight. While satisfactorily solving the problem of eliminating uremic toxins, hemodialysis is ineffective against “middle molecules.” All methods of extracorporeal detoxification have additional stress and catabolic effects on the body. This is due both to the contact of immunocompetent blood cells with foreign material of the dialyzer membrane and blood lines, and to direct losses of nutrients from the effluent.

An alternative to hemodialysis for 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 convective mass transfer, allows one to achieve sufficient elimination of medium-molecular substances. The combination of severe uremic and medium molecular intoxication determines the use of hemodiafiltration, which combines the physical principles of diffusion and convection on one membrane, as the method of choice.

Indications for emergency hemodialysis:

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

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

Unremoved foci of muscle necrosis and endotoxicosis deplete the body's adaptive mechanisms, cause gross dysfunction of other organs and systems, and contribute to a delay in the restoration 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 endotoxemia and persistent necrotic lesions in the muscles.

Surgical treatment

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

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

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

When treating SDS, the rules for removing all necrotic tissue, which is the morphological substrate of intoxication, the development of acute renal failure, and septic infection, which often lead to death, are strictly adhered to.

Crash syndrome 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 of acute lung injury and acute respiratory distress syndrome.

In victims with DFS, the development of hemodynamic disorders due to the hypokinetic type of blood circulation (with low cardiac output) is noted, which is associated with the development of severe endotoxicosis as a result of acute renal failure. Clinical manifestations of acute renal failure with adequate treatment are on the decline. In some cases, acute renal failure has a rapid course, leading to death in the first days of the intermediate period.

On the 9th–12th day, the polyuric stage of acute renal failure begins, which proceeds quite typically. The dynamics of diuresis restoration has prognostic significance. If diuresis is restored quickly and immediately becomes abundant, the prognosis is favorable. Otherwise, irreversible kidney damage should be assumed.

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

Stages and symptoms of the disease

There are four stages of the disease:

Toxic shock - immediately after compression, a painful shock occurs, which is usually not accompanied by a significant decrease in blood pressure (it is rarely below 90 mm Hg). Severe pain after compression lasts from several minutes to 2 hours. When the compression is eliminated, they can immediately collapse will occur and death. If this does not happen, you should determine the affected area, which is easily identified by the reduced temperature and density of the affected tissues. Characteristic purple-violet skin color. Approximately 1 hour after decompression, woody swelling appears and increases rapidly. If the urine discharged from the bladder is dirty-brown in color, this indicates a severe form of DFS. An even more unfavorable sign of anuria is when, after 200-300 ml of urine has been released, it ceases to be excreted altogether. In this situation, hyperkalemia is extremely dangerous. Ischemia a compressed limb leads to numbness and disappearance of pain. After decompression, toxemia occurs due to the entry of ischemic toxins into the bloodstream; myoglobinuria plays an important role, which leads to necrosis of the renal tubules and the development of acute renal failure. The level of potassium in the blood increases sharply, which can be a direct cause of death. Damage to internal organs may occur - erosive gastritis, enteritis, gangrene of the cecum or sigmoid colon. The victims are concerned about weakness, thirst, nausea, and may experience vomiting. There is little urine, it becomes yellow-brown or reddish in color. Swelling of areas of the body that have been subjected to compression appears and progresses; the skin over these areas is pale bluish, cold, shiny, easily wounded, the tissues are dense to the touch. Possible blisters, abrasions, hematomas, and often contaminated wounds. All this together creates a picture post-compression toxic shock with a very high mortality rate in severe forms of long-term compartment syndrome. This stage lasts up to 48 hours after the compression is released.

Light Gap- inconsistent. After the patient’s condition has stabilized as a result of treatment, a short period of light (“imaginary well-being”) occurs, after which the condition worsens again.

Acute renal failure. Lasts from 3-4 days to 8-12 days. There is an increase in the extremities freed from compression. The composition of the blood changes, anemia increases, urine output sharply decreases, up to anuria. A sharp worsening of the condition, the patient is lethargic, apathetic. Vomit. Areas of limb tissue necrosis. The pulse is frequent and weak. Blood pressure is reduced.

Recovery stage. Begins from the 3-4th week of the disease. Kidney function, protein content and blood composition are normalized. Infectious complications come to the fore. High risk of sepsis.

Possible complications:

1) Toxic damage to the liver, kidneys and other organs due to increasing intoxication.

2) Fat embolism - blockage of blood vessels (pulmonary, renal, cerebral, etc.) with drops of fat from the bone marrow. Thromboembolism of the same vessels is possible. Consequently, necrosis (destruction) of the relevant organs may occur. That is, a heart attack.

3) Immediately after the injury, or after a light interval (hours to a day or more), a rash and small hemorrhages develop on the face, upper torso and limbs. The skin becomes purple-bluish in color, with blisters.

Ksenia Skrypnik about long-term compression syndrome, which occurs in victims during combat operations, landslides, earthquakes, terrorist attacks, and road accidents

The syndrome was first identified as a separate disease in 1941 by English physician Eric Bywaters, who treated people affected by the London bombings during World War II. In patients who spent a long time under rubble with compressed limbs, a special form of shock was observed. The peculiarity was that if the injuries were not too severe (the internal organs of such patients, as a rule, were not injured), after a set of therapeutic measures the patients’ condition improved significantly, but then a sharp deterioration occurred. Most patients developed acute renal failure and soon died. There are several options for the names of this syndrome: compartment syndrome, compression injury, crash syndrome (from the English crush - “crushing, crushing”), traumatic toxicosis.

Bywaters was able to identify three successive stages leading to the development of crash syndrome:

1. compression of the limb and subsequent tissue necrosis;
2. development of edema at the site of compression;
3. development of acute renal failure and ischemic toxicosis.

Pathogenesis

Bywaters syndrome occurs as a result of compression of the limb, damage to the main vessels and main nerves. This type of injury occurs in approximately 30% of people injured in natural or man-made disasters.

In the pathogenesis of this disease, three factors are of leading importance: regulatory, associated with the painful effect on the body, significant plasma loss and, finally, tissue toxemia. Note that such factors are observed to one degree or another in almost any injury, but in crash syndrome they manifest themselves especially clearly. Each of these factors contributes to the clinical picture of long-term compartment syndrome.

Painful effect affects the person trapped under the rubble most strongly. There is a reflex spasm of the vessels of peripheral organs and tissues, which leads to disruption of gas exchange and subsequent tissue hypoxia. Vascular spasm and developing hypoxia cause dystrophic changes in the epithelium of the renal convoluted tubules, and glomerular filtration decreases significantly.

Plasma loss develops soon after injury and even after eliminating the cause of compression.

Plasma loss is associated with an increase in capillary permeability due to injury, which leads to the release of blood plasma from the bloodstream.

The volume of circulating blood decreases, viscosity increases, and oxygen transport becomes more difficult. Swelling and numerous hemorrhages develop at the site of injury, the outflow of blood from the compressed limb is disrupted, since the edematous fluid leads to a narrowing of the lumen of the blood vessels until they are completely blocked. As a result, limb ischemia develops, cellular metabolic products accumulate in tissues, and the amount of myoglobin, creatinine, potassium and calcium ions increases. An increase in the concentration of myoglobin in the circulating blood and developing metabolic acidosis have a detrimental effect on the functioning of the renal tubules. Exacerbate toxemia and other protein factors that accumulate as a result of compression of the limb and damage to muscle tissue. After blood circulation is restored, they “in one gulp” begin to enter the vascular bed. At this moment, a number of symptoms characteristic of ischemic toxicosis appear.

Intoxication of the body is more pronounced, the greater the mass of compressed tissues and the duration of the compression effect.

Severity of crash syndrome

Depending on the amount of damage and the duration of compression, there are 4 degrees of severity of the syndrome.

Light degree- compression of a small segment of a limb for no more than two hours. In this case, toxemia is mild, although acute renal failure and hemodynamic disturbances are noted. In most cases, with timely therapy, improvement occurs within a week.

Average degree occurs when the entire limb is compressed for four hours. This condition is characterized by intoxication, myoglobinuria and oliguria.

Prolonged compression of the limbs (4-7 hours) leads to the manifestation of symptoms characteristic of severe Bywaters syndrome. Significant hemodynamic disturbances are noted, symptoms of intoxication are pronounced, and acute renal failure quickly develops.

Untimely and incorrect provision of medical care in most cases leads to death.

It is also important to act correctly and quickly if a patient is diagnosed extremely severe crash syndrome. This diagnosis is made when there is compression of the lower extremities for 8 hours or more. Developing ischemic toxicosis will be disastrous for the patient soon after decompression. The mortality rate of such patients is extremely high even with timely treatment.

Treatment

The choice of treatment approach begins with assessing the degree of compression and duration of compression of the limbs. For specialists taking part in rescue operations, it is important to try to free the maximum number of victims in the first two hours after the emergency occurs. It is in this case that the prognosis will be favorable for most patients.

During the earthquake in Marmara (Türkiye) in 1999, many children were injured. At that time, enormous experience was accumulated in eliminating the consequences of compression injury in young patients. The specificity of treatment for Bywaters syndrome in children is due to the fact that their injuries are often much more severe than in adults.

It is more difficult to communicate with children during a rescue operation, so they often spend more time under the rubble than adults. Children's bodies are more susceptible to hypothermia and fluid loss, so special attention should be paid to rehydration immediately after rescuing the child.

Regardless of the severity and age of the patient, anti-shock measures are carried out: analgesics and cardiovascular drugs are administered to normalize blood pressure. In most cases, this is done before the victim is removed from the rubble.

Treatment started before the abdomen is removed makes it possible to avoid the development of ischemic toxicosis. This primarily applies to extensive compression injuries.

After releasing the injured limb, a tourniquet is applied to the site of compression, which helps prevent a “volley” release of accumulated toxic substances into the bloodstream. This is an important feature of providing medical care for Bywaters syndrome. After moving the victim and removing the compression, the limb is bandaged with an elastic bandage, and only then the tourniquet is removed. Cooling of the injured limb is also recommended.

Following the sequence of treatment steps for patients with compression injuries is very important. Timely use of infusion therapy and understanding the pathogenesis of Byouters syndrome significantly increases the number of lives saved.

For mild cases of the syndrome, surgical treatment is not performed; such patients are often treated on an outpatient basis. With moderate severity, hemodynamic disturbances are quite pronounced: swelling increases, microcirculation is disrupted, and the number of microthromboses increases, but surgical treatment in this case is not always indicated. Infusion therapy is recommended to prevent the development or progression of acute renal failure.

In cases of severe and extremely severe crash syndrome, conservative treatment is ineffective and surgical treatment is necessary. A fasciotomy of the injured limb is performed, which helps restore blood circulation and makes it possible to avoid complete necrotization of the limb. It is often necessary to amputate distal limbs to save the patient.

In parallel, acute renal failure is treated - a strict drinking regimen, hemodialysis, plasmapheresis and infusion therapy (administration of glucose solutions, albumin, etc.) are prescribed.

During the rehabilitation period, attention should be paid to physiotherapy (for example, massage) and physical therapy, which contribute to more effective restoration of the limb, minimizing atrophy of muscles and nerves.

Case from practice

A 21-year-old man spent 10 hours trapped in a damaged vehicle after a car accident. He was taken to a hospital in Nizwa (Oman) while fully conscious. The examination showed that the chest, abdomen, back and pelvis were not damaged. At the same time, swelling of the right shoulder was observed, and the right upper limb was immobilized. X-ray examination revealed a fracture of the right clavicle.

Swelling of the right lower limb was also noted, but the skin was not damaged. There was diffuse swelling in the left leg involving the calf and thigh, as well as deep abrasions. Both legs were practically immobile at the ankle joints, and there were sensory disturbances in the shin area. A Doppler ultrasound study showed impaired venous blood flow in the foot and leg. Further observation revealed rapid accumulation of creatinine, myoglobin, potassium in the blood serum, as well as myoglobinuria.

Infusion therapy was carried out: saline solution, glucose, sodium bicarbonate. Despite this, the patient developed anuria and blood potassium levels continued to rise. The victim was prescribed hemodialysis and underwent fasciotomy of the left thigh and lower leg, as a result of which it was discovered that part of the thigh muscles was necrotic. On the 7th day of treatment, gram-negative bacteria were found in a smear from the wound - E. coli and bacteria of the genus Proteus. The patient was prescribed adequate antibiotic therapy, and the wound was regularly treated with antiseptics. The patient's condition progressively worsened. Despite taking antibiotics, bacterial septicemia developed and amputation of the left leg was recommended, but the patient and his family refused. They decided to continue treatment abroad, where the victim died of severe sepsis three days after arrival.

Resume

Bywaters syndrome was identified as a nosological entity not so long ago - only in the middle of the 20th century. When rescuing and subsequently treating victims with severe compression injuries, coordinated actions of rescuers and doctors are important. Quickly removing people from the rubble and providing first aid even before removing the press will minimize the severe consequences of long-term limb compression syndrome and help save the patient’s life.

2.Rudaev V.I. Krichevsky A.L., Galeev I.K. Crash syndrome in disaster conditions. - Methodological recommendations for resuscitation and anti-shock groups of the VGSCh, specialized teams of constant readiness of the Disaster Medicine Service and resuscitation ambulance teams. 1999.

3.Dario Gonzalez. Crush syndrome. Crit Care Med. 2005. Vol. 33, No. 1 (Suppl.). S.34-41.

4.Dinesh Dhar, T.P. Varghese. Crush Syndrome Case Report and Literature Review. Macedonian Journal of Medical Sciences. 2010 Sep 15; 3(3):319-323.

Long-term compartment syndrome- symptoms and treatment

What is compartment syndrome? We will discuss the causes, diagnosis and treatment methods in the article by Dr. Nikolenko V.A., a traumatologist with 10 years of experience.

Definition of disease. Causes of the disease

Long-term compression syndrome(crash syndrome, CDS) is a life-threatening condition that occurs due to prolonged compression of any part of the body and its subsequent release, causing traumatic shock and often leading to death.

Two conditions contribute to the occurrence of this syndrome:

These factors lead to the fact that after the release of a compressed body part, the injury goes beyond the damage and local traumatic reaction.

In the compression zone, toxic products are formed (free myoglobin, creatinine, potassium, phosphorus), which are not “washed out” by the liquid that has accumulated due to a mechanical obstacle to the circulation of its current. In this regard, after eliminating the cause of the compression, a systemic reaction of the body occurs - the products of destroyed tissues enter the bloodstream. This is how the body is poisoned - toxemia.

A special form of crash syndrome is positional compression syndrome (PCS). In this situation, there is no external traumatic factor, but tissue compression occurs from an unnatural and prolonged body position. Most often, SPS is characteristic of a person in a state of severe intoxication: depression of consciousness and pain sensitivity, combined with a prolonged immobile position, lead to critical ischemia (decreased blood supply in a separate area of ​​the body). This does not mean at all that in order to achieve positional compression, a person must “rest” on an arm or leg for hours. Tissue necrosis can be caused by maximum flexion of the joint for a sufficiently long time, which leads to compression of the vascular bundle and disruption of the blood supply to the tissue. Concomitant shifts in homeostasis (self-regulation of the body), characteristic of the biochemistry of intoxication, accompany the described positional syndrome.

Positional compression differs from true SDS in the rate of increase in toxemia and the rare incidence of irreversible organ damage.

Particular and least destructive is neurological symptom. It occurs quite rarely and is a separate component of crash syndrome. This symptom manifests itself in the form of damage or disruption to a particular nerve (neuropathy). In this case, there is no underlying chronic neurological disease or injury. This condition is reversible.

If you notice similar symptoms, consult your doctor. Do not self-medicate - it is dangerous for your health!

Symptoms of compartment syndrome

The symptoms of crash syndrome are extensive and varied. It consists of local (local) and general manifestations, any of which in itself is a serious injury.

During the initial examination of the patient, local symptoms may be interpreted incorrectly due to the non-obviousness of the damage: the affected tissues in the early stages look healthier than they actually are. Necrotic (dying) zones clearly appear only after a few days, and their delimitation can continue in the future.

The scale of local disturbances becomes apparent already at the stage of complications. This fact requires a special tactic from the surgeon - a secondary revision (examination) of the victim.

Local symptoms are primarily represented by injuries encountered in everyday life, but their massiveness is more significant. SDS is characterized by combined and combined injuries and polytraumas. These include open and closed fractures, extensive wounds, detachments of skin with tissue, crush injuries, traumatic amputations of limbs, torsion injuries (rotation of the bone around its axis).

With crash syndrome, large areas of destruction (destruction), organ-destructive and irreversible injuries occur. In addition to skeletal trauma and soft tissue injuries, SDS is often accompanied by neurotrauma (damage to the nervous system), thoracic (chest injuries) and abdominal (intra-abdominal) injuries. The victim’s condition can be aggravated by continued bleeding at the scene of the incident and infectious complications that arose earlier.

Local damage triggers a general process such as shock. Its appearance in DFS is due to multiple injuries, prolonged pain impulses and lack of blood supply to the compressed body segment.

Shock in crash syndrome is multicomponent: the mechanism of prolonged compression leads to the development of such types of stress in the body as hypovolemic (decrease in circulating blood volume), infectious-toxic and traumatic. Particularly dangerous in case of SDS are the toxic components of shock, which are characterized by suddenness: in large quantities, after the release of a compressed part of the body, they immediately enter the bloodstream. The combination of severe local damage and the toxic effect of one’s own tissues determines the course of the disease and can lead to a fatal outcome.

Pathogenesis of long-term compartment syndrome

The human body has compensatory capabilities- the body’s reaction to damage, in which the functions of the affected part of the body are performed by another organ. Against the background of a person’s long stay in conditions hypovolemia(decrease in circulating blood volume), intense pain, forced position and accompanying injuries to internal organs, such body abilities are at the limit or completely dry up.

Violation of the volume of red blood cells in the blood and the flow of plasma into the interstitial space causes ischemia, slowing blood flow and increasing capillary permeability. Sweating of plasma into the tissue and interstitial space also leads to the accumulation of myoglobin (a protein that creates oxygen reserves in the muscles). A drop in blood pressure maintains hypoperfusion (insufficient blood supply), plasma loss, and increased tissue edema.

During the entire time of compression, tissue breakdown products entering the bloodstream affect the kidneys. After the victim is released, there is a sharp increase in the release of toxic substances and a massive “washing out” of tissue detritus (destroyed cells) into the bloodstream. Freed from the compression block, the blood flow resumes, inevitably filling the circulating blood volume with the resulting autotoxins. This leads to the appearance acute renal failure, resulting in immediate autoimmune reactions: temperature crises, generalized disorders of humoral regulation (metabolic processes).

Kidney failure develops due to the blocking of the kidney tubules by the myoglobin of destroyed muscles and the cessation of the vital process of reabsorption (reabsorption of water). This is greatly aggravated by ionic disturbances. Tissue breakdown products additionally entering the blood have an uncontrollable effect on the diameter of the lumen of blood vessels. As a result, the vessels narrow, including in the filtration glomeruli of the kidneys, which leads to thrombosis and complete cessation of filtration.

In connection with acute renal failure, the resulting decompensation is aggravated by increasing ion imbalance (hyperkalemia). This leads to gross violations of the body’s self-regulation and “acidification” of internal environments - acidosis.

The phenomenon of mutual aggravation (hypovolemia + pain impulses + toxemia) is now unfolding in full. Symptoms become maximally pronounced, cascading and increasing, and the likelihood of their elimination by the body’s forces becomes impossible.

The described disorders are accompanied by a collapse of hemodynamics (blood movement through the vessels) due to blood loss and reflex hypotension (lowering blood pressure). This leads to a stepwise increase in severity and the formation of a vicious circle. It is possible to interrupt pathological processes in case of long-term compression syndrome only with medical intervention - timely, coordinated and competent.

Classification and stages of development of long-term compartment syndrome

The classification of crash syndrome is based on the severity of the clinical manifestation, which depends on the area and duration of compression.

VTS forms:

Due to the knowledge of the pathogenesis of crash syndrome and the knowledge of the prognosis of each form of SDS, this classification is generally accepted and remains unchanged for a long time. And although it is quite simplified and does not take into account the details of local damage, this systematization proves its importance in the distribution of patient flows in disaster conditions, thereby increasing the efficiency of medical care.

• according to the predominant clinical component of shock;
• according to the picture of toxinemia;
• according to the ratio of local damage, injuries to internal organs and the severity of the toxic-shockogenic component.

However, these scales are of little use for quickly assessing the condition of patients, as they slow down the provision of assistance through laboratory and instrumental studies.

Before diagnosing and analyzing the clinical picture, it is important to assess which stage a particular DDS belongs to:

• Early period- lasts less than three days from the moment the patient is removed from under the compressive objects. This stage is characterized by the development of complications characteristic of shock, with the addition of acute renal failure.
• Interim period- lasts 3-12 days. The clinical picture of acute renal failure develops completely, reaching the terminal stage. The general clinical picture is expressed by obvious demarcation zones and the volume of damage.
• Late period- lasts from 12 days to 1-2 months. It is a period of reparation (recovery): no violations of vital functions have occurred, the body mobilizes compensatory capabilities. The duration of the period up to two months is arbitrary - the duration depends on which structures are damaged and how seriously they are damaged, as well as how adequate the treatment is provided.

Complications of compartment syndrome

The severity of crash syndrome and the likelihood of its outcome depend on the complications that arise. The main complications of DFS include:

The chronology of complications plays a leading role in long-term compartment syndrome, explaining many clinical patterns.

Due to the severity of the damage, favorable conditions arise for the development of “intensive separation” problems:

• distress syndrome (respiratory failure);
• fatty, air and thromboembolism (blockage);
• disseminated intravascular coagulation syndrome;
• nosocomial pneumonia.

These complications do not always occur with SDS, but their manifestation often causes the death of a large percentage of victims.

Also, with DDS, local complications of wounds occur:

• wound infection with the addition of anaerobic flora;
• destruction (destruction) of the anatomical structure: severe and poorly drained extensively scalped wounds, multiple “pockets”, detachments, ischemic foci.

The local status of wounds in long-term compartment syndrome always causes concern and has an unfavorable prognosis, even with the condition of complete and timely surgical treatment. Healing of wounds, open fractures, and damage to internal organs occurs with significant difficulties due to the accompanying shock. The phenomenon of mutual burden is clearly expressed.

Diagnosis of long-term compartment syndrome

The diagnosis of SDS is complex, that is, it can be established by adding and combining the components of the injury, taking into account its mechanism. Diagnosis of crash syndrome is preventive - it is of a cautionary nature. The doctor, taking into account the circumstances and conditions of the injury, determines SDS as the expected diagnosis.

Despite the severity and variety of clinical manifestations, DFS can present a challenge for many experienced specialists. This is due to the rare occurrence of the syndrome in peacetime.

Diagnosis becomes very difficult if the injury history is unknown. In this case, the only correct tactical decision for the surgeon is a cautious approach. It manifests itself in the assumption of SDS in the absence of contact with the patient, with polytrauma of unknown duration, severe segmental injuries with a compressive nature of the injury. Infected wounds, signs of compression of the extremities, and a discrepancy between the local manifestations of injury and the general condition of the patient may also indicate the likelihood of crash syndrome.

To detail the diagnosis, generally accepted research schemes are used: clarification of complaints, anamnesis, mechanism of injury, focusing on the duration of compression and activities preceding release from compression.

When collecting a life history, attention is paid to previous kidney diseases: glomerulonephritis, pyelonephritis, chronic renal failure, as well as nephrectomy (removal of a kidney or part thereof).

When assessing the objective status, a close examination of the patient is indicated in order to assess the massiveness of the damage. Clear consciousness, insignificance of complaints, the active position of the patient should not mislead the doctor, since it is possible that the examination is carried out during the “light” period, when the body is subcompensated and symptoms do not appear.

Objective parameters are assessed: arterial and central venous pressure, heart rate, respiratory rate, saturation, diuresis (urine volume). Laboratory screening is carried out.

The parameters of biochemical tests and “renal” markers are indicative: concentration of creatinine, blood urea, creatinine clearance. Early informative indicators will be blood ionic shifts.

Inspection of wounds and damage resulting from tissue compression is performed primarily. It is a therapeutic and diagnostic procedure that allows us to clarify the depth and extent of tissue destruction.

In order to exclude specialized injuries, narrow specialists are involved: urologists, neurosurgeons, abdominal surgeons, gynecologists.

For diagnosis, radiography, computed tomography and magnetic resonance imaging (optional) are also used. Patients are subject to continuous monitoring even if their condition was stable at the time of admission.

Treatment of compartment syndrome

The fundamental points in the treatment of crash syndrome are related to the release and evacuation of the victim. The correctness of the doctor’s actions at the scene largely determines the success of inpatient treatment.

Preliminary and most effective assistance depends on the stage of SDS. And although the general treatment of crash syndrome is complex, the priority method of treatment also depends on the stage of this condition.

Immediately after detection, the victim is given analgesics, including narcotic, antihistamines, sedatives and vascular drugs proximally, that is, closer to the area of ​​compression of the limb, and a tourniquet is also applied. Without removing the tourniquet, the damaged segment is bandaged with an elastic bandage, immobilized and cooled. After this initial amount of medical care has been completed, the tourniquet can be removed.

Then the wounds are cleaned and aseptic dressings are applied. Permanent venous access (peripheral) is established, and solutions are infused. Against the background of ongoing analgesia (relief of pain symptoms), the patient is transported to the hospital under the control of hemodynamic parameters (blood movement through the vessels). Treatment is effective in an intensive care unit. Puncture and catheterization of the central vein, continuation of infusion-transfusion therapy (introduction of necessary biochemical fluids) with transfusion of fresh frozen plasma, crystalloid and high molecular weight solutions are indicated. Plasmapheresis, hemodialysis (purification of blood outside the body), oxygen therapy, hyperbaric oxygenation (treatment with high pressure oxygen) are performed.

Based on the indications, symptomatic treatment is also carried out. Continuous monitoring of diuresis, heart rate, pulse, and central venous pressure is carried out. Control the ionic composition of the blood.

The effectiveness of general measures directly depends on local surgical treatment. There are no universal schemes for treating wounds and managing the victim. Active prevention of compartment syndrome (swelling and compression of muscles in fascial sheaths) is carried out, including early implementation of subcutaneous fasciotomy.

Assessing tissue viability during primary surgical treatment can be difficult: the lack of delineation between healthy and damaged areas, borderline and mosaic perfusion disorders (blood release through body tissues) keep surgeons from taking radical actions.

In case of doubt, amputation of the limb with dissection of most of the fascial sheaths, additional access for adequate examination, drainage, application of delayed sutures or packing of the wound is indicated.

The clinical picture of local damage is poor in the initial period of DFS. Therefore, there is a need for a secondary examination of the wound or revision of the limb after 24-28 hours. Such tactics make it possible to sanitize (clean) the emerging foci of necrosis against the background of secondary capillary thrombosis, assess the viability of the tissues and the segment as a whole, and adjust the surgical plan.

Forecast. Prevention

The prognosis of DFS depends on the duration of compression and the area of ​​compressed tissue. The number of deaths and the percentage of disability predictably decreases depending on the quality of medical care, the experience of the surgical team, the equipment of the hospital and the capabilities of the intensive care unit.

Knowledge of the pathogenesis and stages of crash syndrome allows the doctor to select a priority treatment method according to the situation. In a significant number of cases, with the exception of severe forms of the syndrome, this leads to functionally favorable outcomes.