Complications of SDS. Syndrome of prolonged compression: clinic, diagnosis, treatment at the stages of evacuation

Trauma in peaceful conditions occupies a significant and important place among surgical diseases. In addition to fractures, wounds, open and closed injuries of internal organs, patients from earthquakes, man-made accidents, military operations often have extensive closed muscle injuries due to massive bruises or prolonged crushing of the soft tissues of the body.

The severity of these injuries should not be underestimated, since a significant proportion of victims with extensive muscle damage die from hemodynamic shock-like disorders or uremia. Knowledge of this pathology allows you to make the correct diagnosis in time, prescribe the necessary treatment, as well as prevent complications.

Syndrome of prolonged compression - a specific type of injury associated with massive long-term crushing of soft tissues or compression of the main vascular trunks of the limbs, occurring in 20-30% of cases in case of emergency destruction of buildings, collapses, earthquakes, etc. It is one of the severe injuries, the treatment of which is significant complexity.

At one time, many researchers of this pathology (Bywaters and Bill, A.Ya. Pytel, N.N. Elansky, N.I. Pirogov, Bossar, Silberstern, Kolmers, Frankenthal, Kuttner, Hakkard, Levin, Minami, Kenyu, etc. ) offered their definition based on clinical manifestations or building the pathogenesis of the disease:

Bywaters and Bill (BywatersE., aBeall, 1940 - 1941) - "crash syndrome";

A.Ya.Pytel (1945) - "syndrome of crushing and traumatic compression of the limbs";

N.N.Elansky (1950) - "traumatic toxicosis";

N.I. Pirogov - "local stiffness (local torpor)";

Bossar, Silderstern (Bossar 1882, Silderstern 1909) - "nephritis with albuminuria and hematuria";

Laborit (Laborit) - "Bywaters syndrome";

M.I. Kuzin (1953) - "syndrome of prolonged crushing";

- "VerschuttungsnekrosederMuskelen" - German researchers.

Classification :

1. By type of compression:

Various objects, soil, slabs, etc.

Positional (part of your body)

2. According to the localization of compression:

Limbs (segments)

3. According to the combination of SDS with damage:

internal organs

Bones and joints

Main vessels and nerves

4. By severity:

Medium

heavy

5. According to the clinical course:

Compression period

Post-compression

Early (1-3 days)

Intermediate (4-18 days)

Late (after 18 days)

6. Combination of lesions:

SDS and thermal injury

SDS and radiation injury

SDS and poisoning

SDS and other combinations

7. Complications:

Complicated SDS - diseases of organs and systems

Acute ischemia of the injured limb

Purulent-septic complications

Pathogenesis:

The leading pathogenetic factors of the syndrome of prolonged compression are:

1) traumatic toxemia, which develops as a result of the breakdown products of damaged cells entering the bloodstream;

2) intravascular coagulation, triggered by the decay products of damaged cells;

3) plasma loss as a result of severe edema of the injured limb;

4) pain irritation, leading to a violation of the coordination of the processes 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 destruction of tissues occurs with the formation of a large amount of toxic metabolic products, primarily methemoglobin. The combination of arterial insufficiency and venous congestion exacerbates the severity of limb ischemia. Metabolic acidosis develops, which, in combination with myoglobin entering the bloodstream, 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 the intake of histamine from damaged muscles, protein breakdown products, adenylic acid, creatinine, phosphorus, etc.

Already in the early period of the syndrome of prolonged compression, blood clotting is observed as a result of plasma loss, as a massive edema of damaged tissues develops. In severe cases, plasma loss reaches up to 1/3 of the BCC.

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

Clinic

Compression period: Most victims retain consciousness, but depression often develops, which is expressed in lethargy, apathy or drowsiness. Others experience confusion or even loss of consciousness. Less often there is an excited state. Such victims scream, gesticulate, demand help or sing.

Complaints are caused by pain and a feeling of fullness in the squeezed areas of the body, thirst, shortness of breath. With a significant injury, especially with damage to the internal organs of the abdominal and chest cavity, fractures of long bones, damage to the main vessels and nerves, the phenomena of traumatic shock develop, as well as concomitant damage (intra-abdominal bleeding, pneumohemothorax, craniocerebral injury).

post-compression period. There are 3 periods in the development of this pathological process.

The first period - up to 48 (72) hours after release from compression. This period can be characterized as a period of local changes and endogenous intoxications. At this time, the manifestations of traumatic shock predominate in the clinic of the disease: severe pain syndrome, psycho-emotional stress, hemodynamic instability. Almost all victims remain conscious. Some of them are in an agitated state, but most of them look lethargic, frightened, drowsy, retarded. Some victims die directly at the scene or in the emergency department of a hospital, as a rule, from injuries incompatible with life.

After release from compression, the victims complain of pain in the damaged parts of the body, general weakness, dizziness, nausea, and thirst. The skin is covered with cold sweat. The movements in the limbs are limited due to pain. Tachycardia, hypotension is determined, there is no appetite.

When examining damaged limbs or other parts of the body that have undergone compression, a variety of trophic changes in soft tissues are revealed. Integuments acquire a cyanotic coloration or a marble appearance, swell somewhat over unchanged areas of the skin. In places of compression there are limited hyperemic areas of the skin, sometimes with a purple-cyanotic tint. Often there are hemorrhages, abrasions, macerations, hematomas and imprints of objects pressing on the body on the skin. Moreover, the more pronounced the prints on the skin, the greater the compression force. The absence of such imprints is observed when the body is compressed by soft rock (earth, sand, etc.). In places of greatest compression of the soft tissues, detachment of the epidermis sometimes occurs with the formation of conflicts filled with serous or hemorrhagic fluid. At the same time, depending on the degree of tissue damage, a wet surface of a pale pink or dark red hue can be exposed under the epidermis, and with a significant violation of local blood circulation, a cyanotic, black, dry surface of the underlying tissues.

On damaged limbs, dense, sharply painful infiltrates are often determined on palpation. On the upper extremities, they are usually located along the neurovascular bundle.

With an increase in edema, the skin becomes pale, cold, shiny. The areas of dents are smoothed out. Compressed limbs quickly and significantly increase in volume, sometimes by 10 cm or more in circumference. The tissues become tense, densely elastic,

in some places it has a "woody" consistency, sometimes it takes on a glassy appearance. Palpation of damaged tissues causes severe pain due to the sharp tension of the fascial sheaths, due to an increase in the volume of the muscles contained in them. Edema circularly covers the entire limb or only part of it, directly subjected to compression, and quickly spreads to the buttock and abdomen in case of damage to the lower limbs. In the future (5-10 days of the post-compression period), against the background of complex therapy, as edema, tension, infiltration in soft tissues decrease, sensitivity and movement in the joints can gradually recover, and the pain subsides.

For the differential diagnosis of SDS and other pathological conditions, the “lemon peel” test / Komarov B.D., Shimanko I.I. / is very indicative - the skin of the area subjected to compression is folded with the index and thumb, which is not observed with edema of another origin.

The skin over the affected area during this period has a lemon-yellow color (due to absorbable muscle pigment) with a clear boundary at the transition to intact tissue. With the restoration of blood circulation, the increase in edema and tension in the compressed tissues against the background of a violation of metabolic processes and the addition of a secondary infection, secondary necrosis of damaged tissues develops.

With severe edema, the pulsation of the arteries in the distal parts of the limb weakens or is not even detected. The limb becomes cold to the touch. With a further increase in edema and tension of the soft tissues, hemo-, lymphodynamic and neurological disorders increase. Movements in the joints of the injured limbs are limited or completely absent, most often due to severe pain caused by compression of the nerve trunks and the development of ischemic neuritis. The pains are so severe that the victims groan, cannot find a comfortable position in which their intensity would decrease. At the same time, they note a feeling of fullness in the damaged limb, constant tension in it. Sometimes victims are disturbed by pain even in the absence or deep violation of sensitivity, which is believed to be due to the humoral nature of their occurrence. Pain in injured limbs and other parts of the body is most pronounced during the first 3-5 days of the post-compression period.

Local changes in damaged areas of the body are accompanied by a sharp decrease or loss of all types of sensitivity (pain, tactile, temperature), the severity of which depends on the strength and duration of compression and its localization. So, with damage to the upper limbs, there is a violation of superficial and deep sensitivity, a decrease or absence of tendon and periosteal reflexes, muscle atony, the development of paresis or paralysis with damage to the median, radial or ulnar nerves. If the lower extremities are damaged, hypoesthesia, weakening or absence of the knee, akhilova and plantar reflexes, a sharp violation of deep sensitivity, often in combination with limb paralysis, are observed.

A frequent manifestation of the syndrome of prolonged compression are traumatic neuritis and plexitis that occur at the time of injury and in the early post-compression period in the form of sensitivity disorders, active movements, moderate pain at first, and then 4-5 days after the injury - constant debilitating pain that disrupts night sleep and not amenable to elimination with analgesics. Upon admission, up to 80% of patients are encountered.

Swelling of the soft tissues of damaged limbs is accompanied by a sharp blood loss with the development of hemoconcentration (increase in hemoglobin, hematocrit, decrease in BCC and BCP), pronounced protein and electrolyte disorders. Plasma loss is largely due to increased capillary permeability as a result of exposure to endogenous toxins and, therefore, is not the main, but a secondary factor. Thickening of the blood due to the development of traumatic edema, violation of its physicochemical properties, slowing of blood flow due to acute vascular insufficiency lead to hypercoagulability in the early period of the syndrome of prolonged compression. All this, undoubtedly, enhances the manifestation of shock and contributes to the further accumulation of toxic products of the metabolism disturbed by trauma.

Changes in soft tissues, especially in victims with a large affected area, are accompanied by endogenous intoxication, the severity of which is aggravated as pathological changes in the compressed tissues increase. In this case, intoxication is manifested by malaise, lethargy, lethargy, nausea, repeated vomiting, dry mouth, fever up to 38 ° C and above. These phenomena are mainly associated with the entry into the blood of the products of impaired metabolism, the decay of ischemic tissues. Tachycardia appears, accompanied by shortness of breath, weakening of heart sounds, in some victims there is an increase in blood pressure.

In the early post-compression period of the syndrome of prolonged compression, respiratory failure often develops. These phenomena may be due to the occurrence of a massive fat embolism. It is known that fat embolism is manifested by various and non-specific symptoms, primarily due to circulatory disorders in various organs. Intravital diagnosis of a fatty embolism is quite difficult. There are pulmonary (most common), brain and generalized form of fat embolism. In the sequential manifestation of the clinic of fat embolism of all forms, neurological symptoms are usually recorded first, then acute respiratory failure with constant arterial hypoxemia joins. The pulmonary form at the height of manifestation is characterized by tachycardia, cyanosis, cough, and a progressive decrease in ventilation function. The appearance of moist rales, frothy sputum with an admixture of blood indicates an adjoining pulmonary edema. X-ray reveals disseminated foci of blackout (“snowstorm”), enhanced vascular-bronchial pattern, dilatation of the right heart. The evidence that fat embolism can be the cause of acute respiratory failure is the increase in the early post-compression period of the syndrome of prolonged compression of hypoproteinemia and hypoalbuminemia - indirect signs of fat embolism. So, on the 2nd day of this period of the syndrome of prolonged compression, the albumin-globulin index in the victims is 0.98±0.85. The intense catabolism of proteins occurring at the same time is confirmed, in addition, by the high content of residual nitrogen and urea in the blood. Throughout the early period of the syndrome of prolonged compression, the content of glucose in the blood remains elevated. This is explained, firstly, by the high concentration of catecholamines in the blood, which cause active glycogenolysis in the liver and muscles, i.e. the level of hyperglycemia is proportional to the severity of aggressive influences on the body, and, secondly, by the fact that hyperglycemia is promoted by intense protein catabolism, as a result of which a large number of amino acids are released, the main part of which, with energy deficiency that develops under conditions of prolonged compression syndrome, turns into glucose.

Significant disorders of electrolyte metabolism were found in the victims in the early period of the syndrome of prolonged compression. Thus, the content of calcium (2.23 ± 0.05 mmol/l) is below the norm, probably due to the transition to the interstitial spaces along with plasma and albumin, as well as as a result of its increased consumption in the process of progressive blood coagulation, and, conversely, a high the content of phosphorus (1.32 ± mmol/l), apparently due to the enhancement of its reabsorption in the tubular apparatus of the kidneys under the influence of calcitonin. In turn, severe hyperphosphatemia indicates severe violations of the ratio in the body of the content of calcium, sodium, potassium salts, the presence of dystrophic processes in the liver, impaired tubular reabsorption in the kidneys, especially in conditions of a change in the acid-base state (CBS) to the acid side, which is characteristic of the early period of the syndrome of prolonged compression. An increase in potassium and sodium is more common in patients with a severe degree of the syndrome of prolonged compression. The content of chlorides, especially in the first day of the early period, usually exceeds normal values ​​(140 ± 16 mmol / l), which can be associated with a violation of the excretory function of the kidneys.

The amount of urine excreted decreases sharply from the very beginning of the early post-compression period. It acquires a lacquer-red color due to the release of hemoglobin and myoglobin entering the bloodstream from damaged muscles, and has a high relative density, a pronounced shift to the acid side. Later, the urine becomes dark brown in color. It contains a large amount of protein, leukocytes, erythrocytes, and in the sediment - cylinders and cylinder-like brownish ribbon-like formations, similar to casts of convoluted tubules of the kidneys, which consist of desquamated epithelium, clumps of amorphous myoglobin, hematin crystals.

As you know, the state of the excretory function of the kidneys is used to judge the severity of SDS, the effectiveness of ongoing therapeutic and preventive measures, predict the course of SDS and often its outcome. The more severe the compression injury and the more pronounced the endogenous intoxication, the lower the diuresis. With a severe degree of SDS, already in the early post-compression period, complete anuria may occur, continuing until the death of the victim. In the first 12 hours after the release of the body from compression in patients with prolonged compression syndrome, even against the background of intensive treatment, including infusion therapy and forced diuresis, the average amount of urine excreted is 604 ± 69 ml / day, gradually increasing by the end of the first day to 1424 ± 159 ml/day, 2 days - up to 1580±503 ml/day. The value of daily diuresis objectively indicates the restoration of the excretory function of the kidneys. However, these figures alone do not give a real idea of ​​the true state of kidney function, since diuresis fluctuations in patients with prolonged compression syndrome throughout the entire observation period can be in the range from 0 to 500 ml. A more accurate idea of ​​kidney function is given by the study of the amount of creatinine. Its content in the blood on the first day of the early post-compression period exceeds the normal values ​​by 2 times, and on the 2nd day - by 5 times.

The appearance of fresh erythrocytes in the urine should be considered as a result of severe endotoxin damage to the vascular apparatus of the renal glomeruli in the early period of the syndrome of prolonged compression. Another indicator of the degree of kidney damage is the presence of leukocytes in the urine, the number of which gradually increases.

Protein in the urine is determined in almost all victims. By the end of the first day, its concentration reaches 0.28±0.077%, on the third day it reaches 0.2±0.06%. This also confirms the presence of severe nephropathy in the victims, which is based on damage to the vascular apparatus of the glomeruli and tubular basement membrane, which in turn leads to impaired glomerular filtration and tubular reabsorption. At this time, according to the ultrasound examination, in patients with acute renal failure, a thickening of the renal parenchyma and an expansion of its cavitary system are detected.

A sign of severe endogenous intoxication in the syndrome of prolonged compression is the presence of granular cylinders in the urine on the 1st day of the post-compression period. Their presence indicates deep degenerative changes occurring in the renal tubules. It is especially important to note that their granularity is due to protein particles or fat droplets. In this regard, the appearance of granular casts in the urine can be considered an objective sign of fatty globulinemia.

In the pathogenesis of SDS in the early post-compression period, the main role belongs to changes in the microcirculation system, which are of a generalized nature, and are not limited only to the place of direct impact of the compressing agent on the body of the victim. This circumstance is a pathogenetic justification for carrying out appropriate therapeutic and preventive measures in the early period.

Depending on the duration of compression, scale, localization, depth of damage to the compressed soft tissues and the individual reaction of the body to this aggression, three degrees of severity of the course of the syndrome of prolonged compression are distinguished.

1) light severity- small depth and area of ​​the lesion, 4-6 hours. At the same time, local changes prevail, the general clinical manifestations of endogenous intoxication are slightly expressed. Moderate, transient disorders of general and renal hemodynamics. In the urine there are no signs of gross violations of kidney function. Urine may be red-brown or brown in color, quickly freed from myoglobin and acquires a normal color. With more pronounced muscle damage, myoglobinuria lasts for several days, which is observed with mild nephropathy. Oliguria persists for 2-4 days. By the 4th-6th day, against the background of targeted intensive therapy, pain and swelling usually disappear, sensitivity in damaged tissues is restored, body temperature and diuresis normalize. Laboratory parameters return to normal by 5-7 days after the injury. After that, the victims can be discharged for outpatient treatment. In the study of kidney function 15-20 days after the injury, deviations from the norm are not determined. Conducting intensive complex therapy in patients with mild severity of the syndrome of prolonged compression, as a rule, prevents the possible development of severe complications.

2) medium severity- with more extensive damage, at least 6 hours, accompanied by moderately pronounced signs of endogenous intoxication. Kidney dysfunction is characteristic of moderate nephropathy and manifests itself in the form of myoglobinuric nephrosis with more pronounced pathological changes in the blood and urine composition than in mild SDS. Myoglobinuria and oliguria usually persist for 3-5 days. In the blood there is a moderate increase in the content of residual nitrogen, urea and creatinine. These indicators of nitrogen metabolism with an average degree of SDS usually return to normal on the 12-20th day after the injury. In the study of the functional state of the kidneys, a decrease in the concentration index of creatinine, glomerular filtration and tubular reabsorption of water is revealed. In the peripheral blood, all the victims have a pronounced leukocytosis with a shift of the leukocyte formula to the left. Untimely or insufficiently qualified medical care at the scene and subsequent intensive infusion therapy can lead to rapid progression of acute renal failure and the development of severe infectious complications.

3) severe severity- even more extensive damage, more than 6 hours. Endogenous intoxication is rapidly growing and leads to the development of severe complications up to death. With this degree of SDS, the most formidable and determining the fate of the affected pathological process is acute renal failure. With untimely provision of medical care, as well as with insufficiently effective intensive therapy for hemodynamic disorders that have arisen, the condition of the victims progressively worsens, and a significant part of them die within 1-2 days after the compression injury.

There is no doubt that the combination of even an insignificant compression of soft tissues with damage to internal organs, bones, blood vessels, nerve trunks significantly complicates the clinical course of the syndrome of prolonged compression, and the syndrome of prolonged compression, in turn, aggravates the course of the pathological process from the side of the internal organs - the syndrome mutual burden.

Thus, already from the moment of impact on the victim of compression, a clinical picture of systemic and organ failure arises, which can be characterized as a syndrome of multiple organ failure. A feature of this syndrome in SDS is its early development (starting from the period of compression) and the preservation of signs throughout all periods of the clinical course of the syndrome of prolonged compression.

If, as a result of surgical and therapeutic treatment, the patient's condition stabilizes, then a short light period occurs, after which the patient's condition worsens.

Interim period.

There comes the 2nd period of the syndrome of prolonged compression - the period of acute renal failure, it lasts from 3-4 to 8-12 days. During this period, in addition to acute renal failure, rapidly progressive hyperhydration and hypoproteinemia (anemia) pose a great danger to life. At the same time, degenerative-necrotic changes continue to grow at the site of application of the squeezing agent, which are complicated by the development of a local infection. Due to impaired urination and metabolic disorders, accompanied by an increase in the production of endogenous water in the body, edema continues to increase in the extremities released from compression, and edema appears in other parts of the body. Bubbles filled with a cloudy liquid form on the damaged skin, hemorrhages appear. The progression of local changes in soft tissues, mainly purulent-necrotic, determine the severity of endogenous intoxication and the severity of acute renal failure. Later, general purulent-septic complications may occur, such as pneumonia, purulent pleurisy, pericarditis, peritonitis, osteomyelitis, parotitis, etc. Anaerobic infection often joins. One of the reasons for the development of infectious complications in the interim period is the metabolic immunosuppression that occurs at this time.

The clinical picture of acute renal failure in patients with prolonged compression syndrome correlates with the severity of its clinical course and, as a rule, manifests itself after the victim recovers from shock, corrects hemodynamic and homeostasis disorders. However, acute renal failure can also occur in the period of compression, especially against the background of hypothermia, hypovolemia, starvation, and then only continue its development in the early and intermediate periods of the syndrome of prolonged compression.

The severity of acute renal failure largely depends on the quality of medical care at the scene, the timeliness of its diagnosis and the start of complex therapy. In addition, the severity of acute renal failure is significantly affected by complications that often accompany kidney disorders - hepatitis, pneumonia, etc.

The clinical picture of acute renal failure in the interim period develops as follows. After some improvement in well-being, which is usually observed 2-3 days after the injury, the victim's condition worsens again. A headache appears, adynamia increases, lethargy, in severe cases a coma occurs, convulsions, tachycardia or, conversely, bradycardia appear. The victims are worried about nausea, frequent vomiting, thirst. Sometimes intoxication paresis of the intestine develops with peritoneal phenomena, which can cause an unreasonable operation. Often there are pains in the lumbar region, due to stretching of the fibrous capsule of the kidneys, and therefore, some victims may experience a clinical picture of an acute abdomen.

Kidney function continues to decline with the development of oliguria. The content of residual nitrogen, urea, creatinine increases in the blood, which serves as a harbinger of the development of uremia. Gradually increasing, oliguria in some cases passes into anuria. Uremic intoxication is accompanied by metabolic acidosis and hypochromic anemia. Due to the increase in uremia, the condition of the patients worsens. Often there are periodic bouts of motor anxiety, accompanied by a feeling of fear, delirium. Severe disorders of protein and water-electrolyte metabolism, especially those occurring against the background of acute renal failure, can lead to serious neuropsychiatric disorders.

The course of mild acute renal failure is characterized by a short period of oliguria, a moderate content of urea and creatinine in the blood, and a rare occurrence of hyperkalemia. The concentration index of creatinine, minute diuresis and tubular reabsorption remain within normal values. In this case, glomerular filtration is significantly reduced. Timely targeted therapy allows you to quickly (within 7-10 days) normalize diuresis, urea and creatinine in the blood.

The oligoanuric phase of acute renal failure usually lasts 2-3 weeks and, with adequate treatment, is gradually replaced by a polyuric phase, which is accompanied by appropriate clinical symptoms. However, with mild and moderate acute renal failure, the polyuric phase begins even on the 3rd-5th day of the oligoanuric period, often with a rather rapid increase in diuresis. Initially, the victim excretes 150 ml/day of urine with an increase in its amount to 500-600 ml/day. At the same time, homeostasis indicators remain unchanged. This condition remains stable for 2-3 days. Then the actual phase of polyuria begins, during which the daily diuresis exceeds 1800 ml / day of urine, gradually reaching 4-7 l / day. Moreover, light, myoglobin-free urine with a low relative density begins to stand out. It contains a large number of leukocytes, epithelial cells, bacteria, and sometimes erythrocytes.

Azotemia during this period, although not immediately, gradually decreases. But even with severe polyuria, the concentration of creatinine, urea and residual nitrogen in the blood can not only decrease, but also increase. This is due to the slow recovery of the nitrogen excretion function of the kidneys. Usually only glomerular filtration is restored during this period, and tubular reabsorption remains insufficient. This is confirmed by the low content of urea in the urine on the first day of the diuresis recovery period.

A characteristic feature of the initial period of recovery of diuresis is hypercalcemia, which occurs due to the release of deposited calcium from the muscle tissue of damaged limbs. At the same time, there is a thickening of the plasma, as a result of which the concentration of proteins increases. This hyperproteinemia is associated with hemoconcentration as a result of the rapid loss of salts and water in the urine.

Polyuria, as a rule, is accompanied by a decrease in body weight, the disappearance of peripheral edema and free fluid in the cavities, the normalization of blood pressure, a decrease in intoxication, and an improvement in the general condition and well-being of the victims.

The duration of the phase of polyuria and restoration of diuresis largely depends on the degree of hydration and the amount of fluid administered during infusion therapy.

However, the transition to the polyuric phase of acute renal failure is fraught with many dangers, often difficult to tolerate by the victims, so during this period it is necessary to strictly monitor changes in homeostasis and correct them in time. The harbinger of the polyuric phase is increasing hypertension against the background of uremic intoxication, accompanied by severe tachycardia. Hypertension is caused by the movement of fluid from the intercellular space into the blood, which often leads to re-hyperhydration of the lungs and an increase in azotemia. All this may be the basis for active detoxification and hypohydration. A certain danger in the period of polyuria is represented by hydrolytic disorders arising from dehydration and a large loss of electrolytes. Thus, intensive excretion of potassium from the body, especially with insufficient correction of fluctuations in its content, leads to severe hypokalemia, in which myocardial dysfunction can be observed up to cardiac arrest.

The characteristic changes on the ECG are a reflection of the hypokalemia developing with polyuria: a progressive decrease in the tooth T, prong T inverted with increased amplitude (segment QT elongated), increased intervals R-R ectopic atrial rhythm. In addition, hypochloremia and hyponatremia are often detected, less often - hypomagnesemia and hypocalcemia. Water-electrolyte disorders can be manifested by asthenia, lethargy, severe lethargy, repeated vomiting, a significant decrease in body weight, and even the onset of a coma. Normalization of the water-electrolyte balance leads to an improvement in the condition of the victims.

Usually, the onset of recovery from acute renal failure in patients with SDS is noted from the moment of normalization of the nitrogen content in the blood, which, as a rule, refers to the late period of SDS, since renal dysfunction persists for a long time (polyuria, nocturia, decreased glomerular filtration, etc.). This period of acute renal failure in SDS is the longest and can last several months.

For the intermediate period of SDS, the development of hypochromic anemia is characteristic. The most pronounced decrease in the number of erythrocytes was noted on the 4th-5th day of the post-compression period of SDS, when an increased adhesive-aggregative activity of blood cells and, above all, erythrocytes, joins the deficiency of erythrocytes due to blood sequestration in the microcirculation system. This is also facilitated by a progressive increase in vascular permeability, thickening of the blood. Despite ongoing infusion therapy aimed at maintaining hemodilution and improving the rheological properties of blood, hypohydration and hemoconcentration continue to increase, reaching the most pronounced values ​​by the 5th day of the post-compression period. At the same time, deformation and a decrease in the volume of erythrocytes occur, which is associated with changes in the degree of hydration of tissue structures due to a violation of the water-electrolyte metabolism, the transition of plasma into interstitial spaces, and an increase in blood clotting activity. In turn, the deformation of erythrocytes leads to a violation of microcirculation, since rigid, rigid erythrocytes occlude the capillary bed.

In the intermediate period of SDS, as a result of proteolysis, the predominance of catabolic processes and impaired renal function, not only the products of nitrogen metabolism, but also potassium, magnesium, phosphates and sulfates increase in the blood, the acid-base state is disturbed towards the development of metabolic acidosis. Moreover, hyperphosphatemia is accompanied by the occurrence of hypocalcemia. On the 4th-9th day of the post-compression period, the plasma protein content again reaches normal values ​​due to a decrease in protein catabolism under the influence of the treatment, mainly due to replenishment of the loss of proteins by transfusions of blood products (erythrocyte mass, plasma, albumin, proteins and amino acids). However, at 2-3 weeks of the interim period, a decrease in the content of proteins in the plasma again occurs, which indicates the depletion of the anabolic capabilities of the body, as well as the development by this time of severe complications, primarily infectious ones.

In the intermediate period of SDS, pronounced shifts in the blood coagulation system are observed, which are of a phase nature. At first, the phenomena of hyper- and then hypocoagulation develop, which is a sign of thrombohemorrhagic syndrome. The trigger mechanism for the development of this syndrome is the massive intake of thromboplastin from damaged tissues. Thrombohemorrhagic syndrome worsens the condition of the victims and is often the cause of severe complications. In the study of indicators of the blood coagulation system in the early period of acute renal failure, it is possible to identify the initial signs of hypercoagulability: a slight decrease in the time of blood clotting and plasma recalcification, a decrease in the prothrombin index, and an increase in plasma tolerance to heparin. At the same time, thrombin time and fibrinogen concentration do not change significantly, although fibrinolytic activity increases slightly. Hypercoagulation is caused by the activation of blood coagulation not only due to external, but also internal mechanisms, i.e. not only due to the entry into the blood of thromboplastic substances from damaged tissues, but also due to the activation of the contact phase of coagulation.

One of the frequent complications that develop in the intermediate period of SDS is liver damage - from a mild degree to the development of acute liver failure. The degree of liver dysfunction depends on the extent of soft tissue damage and the duration of compression. Acute hepatitis is manifested by icterus of the sclera and skin, an increase in the liver and its pain on palpation. The content of intracellular liver enzymes in the blood plasma increases. The concentration of bilirubin increases to 100 mmol / l or more. With a favorable course of SDS, the normal content of enzymes and bilirubin is restored, and clinical signs of liver damage gradually disappear.

The most constant manifestation of the clinical picture of DFS in the interim period is hyperkalemia, especially in moderate and severe DFS. It is mainly due to the entry into the bloodstream of a large amount of potassium from damaged muscle tissue. The danger of hyperkalemia for victims with SDS is determined mainly by the toxic effect of high concentrations of potassium on the heart muscle. Moreover, the toxicity of potassium increases in the conditions of development of acidosis and hypocalcemia. In this regard, ECG changes are more informative indicators of hyperkalemia than can be expected from the results of a direct determination of blood potassium.

Clinical signs of hyperkalemia in victims in the intermediate period of SDS are:

Sharp muscle weakness, periodic convulsions, sometimes motor agitation, hallucinations;

· Bradycardia;

Decrease in the height of the P wave, elongation of the QRS complex, the appearance of a giant T wave with a sharpening of its apex, sinoauricular block, A-B block, premature contraction of the ventricles, their flicker;

Increase in plasma potassium above 6 mmol / l.

It cannot be ruled out that hyperkalemia in severe SDS can become

cause of death.

In addition to hyperkalemia, hyperhydration is a particular danger to the life of the victim in the intermediate period of SDS, due, as a rule, to inadequate and intensive infusion therapy, unlimited fluid intake against the background of developing oliguria. This serious complication is difficult to diagnose in a timely manner due to the initial paucity of specific clinical signs, especially against the background of severe manifestations of DFS, and therefore it can quickly lead to the development of severe respiratory failure, often predetermining an unfavorable prognosis for DFS.

Symptoms of developing overhydration are:

The appearance of pastosity, cyanosis and general edema;

· Dry cough with the appearance of oral crepitus;

Overflow of the neck veins;

Intense pulse and tachycardia;

Increase in blood pressure up to 160-200 mmHg., which becomes refractory to most antihypertensive drugs;

· An increase in CVP over 130-150 mm of water column;

Dullness of percussion pulmonary sound with the appearance of moist dry rales;

Enlargement of the boundaries of the liver and the appearance of bursting pains in the right hypochondrium;

The appearance of exudate in the cavities;

Appearance of a “wet lung” pattern on radiographs of the lungs.

Hyperhydration may present predominantly with cerebral edema, anasarca, ascites, acute subcapsular renal edema, or a combination thereof. However, most often hyperhydration is manifested by changes in the lungs. In these cases, moderate shortness of breath, hard breathing, mild cyanosis, rare wet rales appear first. The number of wet rales increases rapidly until it matches the clinical picture of pulmonary edema. The reason for the increase in blood pressure during hyperhydration can be explained by an increase in intravascular resistance and, above all, a deterioration in the function of microcirculation, as well as the development of acute renal failure. The increase in heart rate observed at the same time indicates a deterioration in the work of the heart, pronounced microcirculatory disorders. At this time, the ECG shows signs of diffuse changes in the myocardium, repolarization disorders and hypoxia, and ventricular extrasystoles can often be seen.

An x-ray examination can determine the fluid in the pericardial cavity, pleural and abdominal cavities. The study allows you to control the effectiveness of dehydration methods and identify associated complications: pneumonia, pleurisy, pericarditis, overload of the heart. Radiologically, an increase in the bronchovascular pattern from the roots to the periphery is determined. Severe hyperhydration is characterized by an intense inhomogeneous decrease in the transparency of the lung fields and multiple confluent or cloudy shadows. The roots are mostly butterfly-shaped. The lower parts of the lungs are intensely darkened due to effusion. Attention is drawn to the change in the configuration of the heart with a predominant increase in the right sections.

With long-term hyperhydration, especially with the presence of effusion in the pleural cavity and alveolar edema, pneumonia often develops. However, the diagnosis of pneumonia against the background of hydration is difficult and in some cases is possible only after dehydration.

The interim period of SDS is characterized by the manifestation of multiple organ failure. In this case, the pathology of the internal organs most often develops, due primarily to the severity of the injury itself and endogenous intoxication. During this period, SDS occurs mainly in such forms of secondary pathology of internal organs as purulent-resorptive fever, anemia, myocardial dystrophy, pneumonia, hypertensive reactions, and pulmonary edema. Moreover, changes prevail, both due to general syndromes and due to secondary pathology.

Mortality in this period can reach 35%, despite intensive therapy.

Edema of the extremities freed from compression increases, blisters, hemorrhages are found on the damaged skin, blood thickening is replaced by hemodilution, anemia increases, diuresis sharply decreases up to anuria. The content of potassium and creatinine in the blood increases significantly.

Late (recovery) period.

The third period - recovery begins with 3-4 weeks of illness. During this period of SDS, there is a gradual restoration of the function of the affected organs. Its rate depends on the severity and severity of SDS. The condition of the victims gradually improves, but remains satisfactory for a long time. Body temperature normalizes. The victims are mainly concerned about pain in the area of ​​injury, limitation of movements in the injured limbs.

The clinical picture of the late period of SDS is dominated by the positive dynamics of changes in the injured limbs. With a favorable course of the process, under the influence of treatment, swelling and pain decrease and there is a gradual restoration of the function of the limbs. In the study of motor chronaxy of damaged limbs, restoration of the electrical excitability of damaged nerve trunks is noted. After the reduction of edema, residual effects of polyneuritis persist, leading to atrophy of individual muscles and expressed by numbness in the area of ​​the compressed nerve trunk, decreased tendon reflexes, limited function, and trophic changes in the damaged limb. Some victims in connection with the development of traumatic neuritis experience severe pain, reminiscent of causalgia. They become especially intense at night and persist for a long time. The recovery time of movements and sensitivity in the injured limbs depends on the degree of damage to the nerve trunks and muscles. A faster recovery of nerve function is characteristic of ischemic injury. However, a complete restoration of the functions of nerves and muscles in the initial stages of the late period has not yet been observed, and restriction of movement in the joints and impaired sensitivity continue to persist. Over time, part of the muscle fibers of the injured limb dies, being replaced by connective tissue, which leads to the development of atrophy, contractures, and limited movement in the joints.

Under the influence of treatment, kidney function is normalized. The nitrogen excretion function of the kidneys is restored, which ensures the cleansing of the body of the victim from metabolic products. An increase in the level of urinary excretion of molecules of average mass indicates an improvement in the excretory function of the kidneys. For a longer time, a violation of the partial functions of the kidneys persists. In some victims, oliguria persists, which requires the continuation of intensive therapeutic measures. Preservation of manifestations of acute renal failure contributes to the development of infectious complications in this period and aggravates the clinical course of SDS. At the very least, septic complications with progressive dystrophic and necrotic changes in damaged tissues that have arisen against the background of acute renal failure are the main cause of death in patients in the late period of SDS.

Among the organopathological changes, anemia, varying degrees of acute renal failure, and myocardial dystrophy are especially common in this period. As the phenomena of purulent-resorptive fever and azotemia decrease, blood counts improve, the number of erythrocytes and hemoglobin increases. Pathological changes remain on the ECG, indicating the presence of electrolyte and metabolic changes, diffuse changes in the myocardium, ischemia, overload of the right heart, bundle branch block, extrasystole, which in turn indicates the development of myocardial dystrophy, myocarditis and coronary insufficiency in patients with SDS. As the complex therapy is carried out, the liver function is restored, which is confirmed by the disappearance of the clinical symptoms of toxic hepatitis and the normalization of the blood levels of enzymes, bilirubin, protein and indicators of the blood coagulation system.

Of the clinical manifestations of the late period of SDS, infectious complications come to the fore in terms of their importance. These complications are primarily due to the development of metabolic immunosuppression.

The decrease in the immunobiological forces of the victim's body is clinically manifested by the inhibition of reparative processes in the wound and the occurrence of purulent-septic complications in the form of suppuration of wounds, the development of phlegmon, osteomyelitis, parotitis, abscess pneumonia, pleural empyema, etc., which often determines the outcome of the course of SDS. In some victims, limited skin necrosis and even gangrene of the distal segment of the limb are formed at this time. After rejection of necrotic areas, they are re-infected with the subsequent development of severe phlegmon. Surgical interventions undertaken for purulent complications are often complicated by the development of a secondary infection with rapid progression of muscle necrosis, which is difficult to treat. All victims with SDS and purulent complications of wounds have a slow, sluggish course of the wound process, despite the use of broad-spectrum antibiotics. A low level of immunological protection in patients with SDS often leads to a generalization of the purulent-septic process. Moreover, the clinical manifestations of sepsis are often viewed because of their similarity with uremic symptoms. Often, against this background, candidiasis develops, the occurrence of which is facilitated by significant amounts of antibiotics that the victims receive.

Complications of a wound infection, as a rule, are accompanied by purulent-resorptive fever, which is manifested by neutrophilic leukocytosis with an increase in stab forms and ESR, an increase in the activity of creatine kinase, LDH, AST, ALT, and the number of medium-weight molecules in the blood.

A reflection of endogenous intoxication is severe hypoproteinemia, hypocholesterolemia, hyperbilirubinemia and high ALT activity, indicating the development of toxic hepatitis. At the same time, hypercoagulability is noted, although not reaching critical values. Some victims may experience signs of toxic and degenerative lesions of the liver, kidneys and myocardium, the phenomena of acute coronary insufficiency, circulatory failure. Clinical manifestations of purulent intoxication correlate with the nature of changes in laboratory parameters that reflect the state of the liver, homeostasis system, water and electrolyte balance, CBS.

Prolonged squeezing and the associated circulatory disturbance leads to the development gangrene of a crushed limb. The question of the viability of the injured limb often presents great difficulties. The presence of edema, a sharp tension in the tissues and subsequent compression of the vessels, in combination with extensive subcutaneous hemorrhages, gives the limb a gangrenous appearance from the very beginning. The similarity with developing gangrene increases even more in the presence of a cold snap and the absence of pulsation of the peripheral arteries on the injured limb due to spasm and compression of the vessels by edematous tissues.

Limited skin necrosis is detected 4-5 days after the injury at the site of a slight crushing of the tissues. Dead skin is torn off after 8-9 days, a wound with smooth edges appears in this area (7.8%). Sometimes the process of skin necrosis is limited only to the formation of a relatively superficial wound, and in some cases, fascia and muscles undergo necrosis. After the dead skin is rejected through the formed defect, edematous, partially already dead muscles begin to bulge. In these cases, a secondary infection easily joins, extensive phlegmons occur.

Phlegmon during the syndrome of prolonged compression, with the timely modern use of antibiotic therapy and the use of sulfa drugs, it is not common. Often occurs with the penetration of infection into damaged and crushed muscles, either from superficial infected skin abrasions and wounds, or from wounds arising in connection with skin necrosis, or, finally, from wounds specially inflicted to relieve the tension of the tissues of the affected limb. The possibility of hematogenous and lymphogenous infection also cannot be ruled out.

A feature of these phlegmon is their vastness and the difficulty of diagnosis. The injured limb, even in the absence of phlegmon, appears sharply edematous and painful on palpation. Body temperature in the first days is usually increased, regardless of complications. It is impossible to monitor the change in skin color due to the presence of extensive subcutaneous and intradermal hemorrhages. The function of the affected limb is impaired. Suspicion of the presence of deep phlegmon arises during dynamic monitoring of the patient, when the disorders caused by the syndrome of prolonged compression begin to subside, or rather, should decrease, but they are still retained (pain, swelling, fever).

The degree of compression and the area of ​​the lesion, the presence of concomitant lesions of the internal organs, bones, and blood vessels are of the greatest importance in determining the severity of the clinical manifestations of the syndrome of prolonged compression. 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.

Treatment.

Intensive care of the syndrome of prolonged compression includes a number of stages.

First aid should include immobilization of the injured limb, its bandaging.

First aid consists in establishing infusion therapy, regardless of the level of blood pressure, checking and correcting immobilization, administering painkillers and sedatives. As the first infusion media, it is desirable to use reopoliglyukin, 5% glucose solution, 4% sodium bicarbonate solution.

Treatment in a hospital is based on a complex combination of several therapeutic methods, each of which becomes the leading one in a certain period of the disease.

These include:

infusion therapy, including the mandatory use of fresh frozen plasma,

low molecular weight dextrans / rheopolyglucin /, detoxification agents / hemodez, etc. /;

extracorporeal detoxification /plasmapheresis, hemosorption/;

hyperbaric oxygen therapy to improve microcirculation and reduce the degree

the severity of hypoxia of peripheral tissues;

hemodialysis with artificial kidney devices during acute renal failure;

surgical interventions according to indications - fasciotomy, necrectomy, amputation of limbs;

Strict observance of asepsis and antisepsis is necessary, quartzization of all premises,

dietary regimen / water restriction and exclusion of fruits / during acute renal

insufficiency.

Features of the therapy depends on the period of development of the disease .

Therapy during the period of endogenous intoxication without signs of acute renal failure:

produce a puncture of the central vein;

1. Infusion therapy in a volume of at least 2 liters per day. The composition of transfusion media should include:

fresh frozen plasma 500-700 ml / day,

glucose solution with vitamins C, B 5% up to 1000 ml,

albumin 5%-200 ml (5%-10%),

sodium bicarbonate solution 4% - 400 ml,

Detoxifying drugs

low molecular weight drugs (dextrans).

The composition of transfusion media, the volume of infusions is corrected depending on the daily diuresis, data on the acid-base state, the degree of intoxication, and the surgical intervention performed. A strict accounting of the amount of urine excreted is necessary, if necessary - catheterization of the bladder.

2. Extracorporeal detoxification, primarily plasmapheresis, is indicated for all patients with signs of intoxication, duration of compression over 4 hours, pronounced local changes in the injured limb, regardless of the area of ​​compression.

3. Sessions of hyperbaric oxygenation (HBO) 1-2 times a day to reduce tissue hypoxia.

4. Drug therapy:

Stimulation of diuresis by the appointment of diuretics (up to 80 mg of lasix per day, aminophylline),

The use of antiplatelet agents and agents that improve microcirculation (chimes, trental, nicotinic acid),

For the prevention of thrombosis and DIC, heparin is prescribed at 2500 IU s / c 4 r / day,

Antibacterial therapy for the prevention of purulent complications,

Cardiovascular drugs according to indications.

5. Surgical treatment. Tactics depends on the condition and degree of ischemia of the injured limb. There are 4 degrees of limb ischemia:

Grade 1 - slight indurated swelling of soft tissues and their tension. The skin is pale, at the border of the lesion it swells slightly above the healthy one, there are no signs of circulatory disorders. Shown conservative treatment, which gives a favorable effect.

Grade 2 - moderately pronounced indurative edema of soft tissues and their tension. The skin is pale, with areas of slight cyanosis. 24-36 hours after release from compression, blisters with transparent yellowish contents can form - conflicts, which, when removed, reveal a moist, pale pink surface. Increased edema in the following days indicates a violation of venous circulation and lymph flow. Insufficiently adequate conservative treatment can lead to the progression of microcirculation disorders, microthrombosis, increased edema and compression of muscle tissue.

Grade 3 - pronounced indurative edema and soft tissue tension. The skin is cyanotic or marbled. The skin temperature is markedly reduced. 12-24 hours after release from compression, blisters with hemorrhagic contents appear. Under the epidermis, a moist surface of a dark red color is exposed. Indurated edema, cyanosis is growing rapidly, which indicates gross violations of microcirculation, vein thrombosis. Conservative treatment in this case is not effective, leading to a necrotic process. It is necessary to make wide stripe incisions with dissection of fascial cases to eliminate tissue compression and restore blood flow. The abundant wound plasma loss that develops at the same time reduces the degree of intoxication.

Grade 4 - indurated edema is moderately pronounced, but the tissues are sharply strained. The skin is bluish-purple in color, cold. On the surface of the skin 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 a deep violation of microcirculation, insufficiency of arterial blood flow, widespread thrombosis of venous vessels.

Wide fasciotomy in these cases provides the maximum possible restoration of blood circulation, allows you to delimit the necrotic process in more distal parts, and reduces the intensity of absorption of toxic products. If necessary, amputation is performed in the more distal parts of the limb.

It should be especially noted that in patients after surgical intervention (fasciotomy, amputation), the total volume of infusion therapy increases to 3-4 liters per day. In the composition of infusion media, the volume of fresh frozen plasma and albumin increases due to pronounced plasma loss through the wound surface.

During the period of renal failure, fluid intake is limited. With a decrease in diuresis to 600 ml per day, hemodialysis is performed regardless of the level of nitrogenous slags in the blood. Emergency indications for hemodialysis are anuria, hyperkalemia more than 6 mmol/l, pulmonary edema, cerebral edema.

Infusion therapy in the interdialysis period includes mainly fresh frozen plasma, albumin, 10% glucose solution, 4% sodium bicarbonate solution. The total volume of infusion is reduced to 1000 - 1500 ml per day.

In the 3rd period of the syndrome of prolonged compression, the task of treating local manifestations and purulent complications comes to the fore. Special attention is required to prevent the generalization of infection with the development of sepsis. The principles of treatment of infectious complications are the same as for classical purulent infection.

Thus, intensive care of the syndrome of prolonged compression requires the active work of a team of doctors - surgeons, anesthesiologists, therapists, nephrologists, traumatologists, each of whom becomes the leader at a certain stage.

Positional compression syndrome.

The positional compression syndrome is one of the "household" varieties of the syndrome of prolonged compression, however, unlike the latter, it has a number of specific features regarding the etiology and pathogenesis, clinical course and therapeutic tactics. A combination of several factors is necessary for the development of this disease. On the one hand, a long stay of the patient in a coma or in a state of deep pathological sleep is necessary, which is most often caused by poisoning with alcohol or its surrogates, drugs, carbon monoxide or exhaust gases. On the other hand, a necessary condition for the development of the positional compression syndrome is soft tissue injury, more often the limbs, caused by positional compression by the body weight during a long stay of the victim in an uncomfortable position with the limbs tucked under him or bent at the joints, or with prolonged hanging of the limb over the edge of some some solid object.

Pathogenesis.

The mechanism of development of SPS is complex and associated with the main etiological factors: poisoning with narcotic substances and positional trauma. Exogenous intoxication with narcotic substances (alcohol, its surrogates, carbon monoxide and exhaust gases, etc.) leads to severe homeostasis disorders, with a violation of the water-electrolyte balance, acid-base balance, a violation of macro- and microcirculation, often with the development of collapse. Quite often, this coma is accompanied by a general hypothermia of the body. Prolonged coma and positional compression of tissues leads to both local changes in the compressed tissues and general intoxication.

Local changes are characterized by:

1. Violation of blood and lymph circulation, tissue ischemia, circulatory hypoxia, lymphostasis.

2. Violation of tissue metabolism, ischemic damage to nerve cells (ischemic

neuritis), impaired vital activity and death of soft tissues.

3. Damage to lysosomal membranes and release of proteolysis products (myoglobin, creatinine, histamine, etc.) into the blood.

General changes are due to the developing:

1. Disorder of the CNS function of neurohumoral genesis.

2. Circulatory disorders, hypotension, impaired microcirculation.

3. Violation of the respiratory function - hypoventilation with the development of respiratory and circulatory hypoxia.

4. Violation of homeostasis - metabolic and respiratory acidosis, violation of water - electrolyte balance.

5. Development of myoglobinemia, myoglobinuria.

All these changes lead to intoxication of acute renal failure and renal and hepatic failure, which can lead to the death of the patient.

clinical picture.

In the clinical course of the positional compression syndrome, 4 periods are distinguished:

1. Acute period. A coma that develops as a result of exogenous intoxication (duration from several hours to several days).

2. Early period. The period of local changes in soft tissues and early endogenous intoxication (1-3 days after leaving the coma).

3. Interim period or period of acute renal failure and complications from other organs and systems (from 5 to 25 days).

4. Late or recovery period, when infectious complications come to the fore.

During the period of clinical manifestations of acute exogenous intoxication, characteristic symptoms are observed, specific for the substances that caused poisoning.

In the second period of the disease, upon the return of consciousness and an attempt to change position, patients feel "numbness of stiffened" in the compressed areas of the body, a decrease or loss of sensitivity, a feeling of fullness, pain, and a lack of active movements in the limbs subjected to compression. When viewed in places of compression, there are delimited hyperemic areas of the skin, sometimes with a purple-blue tint. Often, herpetic eruptions, abrasions, macerations, hematomas are found on the skin.

In places of greatest compression, epidermal detachment sometimes occurs with the formation of vesicles (conflict) filled with serous or hemorrhagic fluid. All patients have dense, sharply painful infiltrates on palpation.

In the future, as the restoration of blood circulation in the compressed tissues, there is a rapid development of edema. With an increase in edema, the skin becomes pale, cold, shiny. The tissues are sharply tense, densely elastic, and in some places woody consistency, sharply painful on palpation, which is due to the tension of the facies cases due to a sharp swelling of the muscles, subcutaneous adipose tissue and an increase in the volume of the affected muscles. With a sharp edema, the pulsation of the arteries in the distal extremities is either absent or sharply weakened, movements in the joints of the extremities are limited or completely absent, most often due to severe pain due to compression of the nerve trunks and the development of ischemic neuritis.

Changes in soft tissues already in the early period of SPS after recovery from a coma are accompanied by severe endogenous intoxication, which is aggravated as changes in compressed tissues increase. Intoxication is manifested by malaise, lethargy, lethargy, nausea, vomiting, dry mouth, fever up to 38C and above. Tachycardia is detected, accompanied by shortness of breath, weakening of the heart tones and a decrease in blood pressure. Blood tests reveal leukocytosis with a shift to the left, thickening of the blood, manifested by an increase in hematocrit and red blood cell count.

Myoglobinemia is determined. Following myoglobinemia, myoglobinuria appears. Urine contains protein, leukocytes, erythrocytes, cylinders. Oliguria gradually develops and the disease passes into the third period.

Distinctive features of SPS from the syndrome of prolonged compression are:

Exotoxic poisoning and coma in the acute period;

Absence of traumatic shock;

Less pronounced and slower developing local changes;

Slowly increasing plasma loss.

The clinical picture during acute renal failure and the recovery period is similar to that in the syndrome of prolonged compression.

The treatment of positional compression syndrome is carried out according to the same principles as for the syndrome of prolonged compression. In the acute period, coma therapy is carried out due to exogenous intoxication and its complications.

Attachment 1.

Summary of the main features of the syndrome of prolonged compression.

Changes in the injured limb

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, mandatory treatment is required. 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

In medical practice, there are several approaches to the classification of compression syndrome. 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 to 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 of various organ systems are 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.
• There is a 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.
• Cardiovascular insufficiency develops.
• A blood test shows its thickening and neutrophilic shift.
• Tendency to thrombosis.

At this stage, it is important to conduct timely intensive infusion therapy using 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.
• The staining of the sclera indicates the involvement of the liver in the 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. Depressive states, psychoses and hysteria are frequent.

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.
• Instrumental diagnostics is carried out, which allows you to compare laboratory symptoms and the structure of the kidneys in dynamics.

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?

The condition of the victim, and maybe his life, if SDS develops, depends on the provision of emergency assistance. 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 severe 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, given the pathogenesis of the 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 it was not possible to avoid serious injuries, then in most cases SDS develops. The syndrome, the prevention of which is mandatory, will not lead to disastrous consequences if you immediately start taking action. To do this, it is necessary to introduce antibiotics of the penicillin series. The use of antibacterial agents may not save you 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 - a female disease of the century. This concept is 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 the DFS syndrome in women.

Stages and symptoms of the disease

There are four stages of the disease:

Toxic shock - immediately after compression, a pain 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 pressure is eliminated, they can immediately collapse and death. If this does not happen, then determine the affected area, which is easily identified by the reduced temperature and density of the affected tissues. Characteristic purplish-purple coloration of the skin. Approximately 1 hour after decompression, a woody edema develops rapidly. If the urine discharged from the bladder has a dirty brown color, then this indicates a severe form of SDS. An even more unfavorable sign of anuria is when, after 200-300 ml of urine has been released, it ceases to be excreted at all. In this situation, hyperkalemia is extremely dangerous. Ischemia of a compressed limb leads to its numbness and the 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 rises sharply, which can be a direct cause of death. There may be lesions of internal organs - erosive gastritis, enteritis, gangrene of the blind or sigmoid colon. Victims are concerned about weakness, thirst, nausea, and vomiting may occur. There is little urine, it acquires a yellow-brown or reddish color. Edema appears and progresses in areas of the body that have undergone compression, the skin over these areas is pale cyanotic, cold, shiny, easily injured, the tissues are dense to the touch. Blisters, abrasions, hematomas, often contaminated wounds are possible. All this together creates a picture post-compression toxic shock with a very high level of mortality in severe forms of the syndrome of prolonged compression. This stage lasts up to 48 hours after release from compression.

light gap- not always. After stabilization of the patient's condition as a result of treatment, a short light period ("imaginary well-being") occurs, after which the condition worsens again.

Acute renal failure. Lasts from 3-4 days to 8-12 days. Increasing flow of extremities released from compression. The composition of the blood changes, anemia increases, urine output decreases sharply, up to anuria. A sharp aggravation of the condition, the patient is lethargic, apathetic. Vomit. Areas of tissue necrosis of the limb. Pulse is frequent, weak. Arterial pressure is reduced.

Recovery stage. It starts 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 by drops of fat from the bone marrow of blood vessels (pulmonary, renal, cerebral, etc.). Possible thromboembolism of the same vessels. 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 up to a day or more), a rash and small hemorrhages develop on the face, upper body and limbs. The skin becomes purple-bluish in color, with blisters.

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

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

Briefly about what happens with a crash syndrome

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

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

Signs of the syndrome of prolonged compression

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

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

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

First aid

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

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

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

The clinical picture of the crash syndrome

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

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

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

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

Which doctor to contact

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

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

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