PMP with prolonged compression syndrome briefly. Syndrome of long crush. Prevention of Prolonged Compression Syndrome

Prolonged compression syndrome is one of the most severe types of injuries that usually occur as a result of catastrophes, natural disasters, landslides, and so on.

What happens to the limbs during prolonged compression?

In another way, the syndrome of prolonged squeezing is called traumatic toxicosis. This process begins as a result of squeezing one or more large segments of any limb with a pronounced array. Basically, this is the area of ​​​​the buttocks, lower legs, thighs.

Any part of the human body, after prolonged squeezing, provokes a violation of tissue circulation and stops the flow of oxygen and nutrients to them. All this leads to tissue necrosis, and, as we know, atrophied tissues begin to emit toxic products that enter the human body. These poisons are called autotoxins.

As soon as the limb is released from compression, autotoxins immediately begin to flow into the blood, and in large quantities. At this time, the patient's condition worsens significantly. There are cases when everything can end in cardiac arrest. Such poisons can instantly stop all activity of the heart, as well as adversely affect the functioning of the central nervous system, liver and kidneys.

If autotoxins have significantly affected the kidneys, then the process of urination may completely stop in a person. In severe cases of violations of the liver, kidneys and heart, death can occur in 3-5 days.

As soon as a person is released from prolonged squeezing, the process of swelling of the damaged segments of the limbs begins. You can see how the tissue structure is instantly compacted.

The skin is initially pale, but then abruptly becomes purplish with a pronounced blue tint. Sometimes you can see foci of small hemorrhages. Often, light or bloody vesicles are observed on the skin of a squeezed limb. By themselves, the skin is quite cold, and there is practically no sensitivity. As for the pulse, it is very difficult to feel it.

The syndrome of prolonged compression is divided into three stages. It all depends on how much the limb was squeezed. The stage is also determined by the duration of compression.

So, this syndrome is divided into such degrees of severity:

• light - the squeezing time does not exceed four hours;
• medium - does not exceed six hours;
• heavy - more than eight hours.

Providing first aid for the syndrome of prolonged compression

First aid should be provided immediately at the place where the victim is located. Before you begin to release a person from a pressing object, it is necessary to eliminate pain syndromes and restore the patient's psycho-emotional state. As an anesthetic, you can use analgin, promedol solution or any other sedative drugs. If you notice that the patient's abdominal region is not compressed, then you can give him any strong liquor to drink.

Proper liberation of a person begins from the head to the torso. But there are exceptions, so you need to be guided by the situation. It is very important not to let the patient suffocate, which happens quite often. To do this, if possible, it is necessary to place the person in a comfortable position and clear all upper respiratory tracts. This way you can avoid asphyxia. If you notice external bleeding in a person, you should immediately stop it.

Getting Started with First Aid

First, remember that never and under no circumstances should you sharply lift an object that crushed a person. We lift only one part, and at this time we begin to slowly bandage the squeezed limb with an elastic bandage. It is very important to bandage with an elastic bandage, of course, if it is not available, then you can use gauze. You are faced with the task of gradually lifting the object and bandaging the limb. All this is done until she is completely freed. Why not just pick up the object and bandage the entire limb? The fact is that when squeezed, the tissues atrophy and begin to release toxins, and if we do it the wrong way, then all the toxic substances will abruptly enter the body, and everything will end in the death of the victim. Therefore, slow and confident movements can save a person's life.

After you release the person from under the squeezing object, it is necessary to cover the injury site with something cold. Put something soft under the limb itself (jacket, bag, any rags, and so on).

After that, the victim can be transported. During this period, it is important to monitor his condition as much as possible.

Touch the stomach, if there is no damage to the internal organs, then it will be soft. In this case, a person needs to be given a lot to drink. You can add a vessel to warm water, this can improve the condition of his kidneys. If you feel any seals in the abdomen, then the internal organs are damaged.

Do not apply a tourniquet to the limb, it can harm a person. It is allowed to use it only if bleeding is present, or the limb has lost its vitality.

It is impossible to immediately say how this situation will end. It all depends on most factors. There are cases when a person was crushed for a whole day and fully recovered after treatment, and it happens that people are under the rubble for several hours and die.

If you cannot release the victim within twenty minutes, then stop your actions and wait for the arrival of the rescue team and ambulance.

Your main task is to try to correctly release the pinched limb. If you succeeded, then bandage it and cover it with cold objects. Let the patient drink a lot. These actions are the essence of first aid, and then it remains to wait for the medical team.

Prolonged compression syndrome (SDS) occurs after prolonged compression of the limbs during the collapse of buildings as a result of strong earthquakes or during military operations. The circulation of blood flow in the tissues is disturbed and oxygen and nutrients are not supplied to them in normal quantities.

As a result of oxygen starvation, tissues die, and many toxic substances are released. After a person has received this injury, the muscles begin to collapse, even fractures, damage to blood vessels and heavy bleeding are possible. In this case, a pain syndrome occurs and then the patient has every chance of getting a traumatic shock. The condition and future prognosis depend on how much time he spent under the rubble and on the force of compression, as well as the total area of ​​​​the affected area.

Types of VTS

There are many criteria for classifying this condition.

By type:

• crushing;
• straight ;
• positional compression;

By localization:

• Rib cage;
• Abdomen;
• Pelvic area;
• Hands;
• forearm;
• Thigh, foot and lower leg in different variations;

In combination with injuries of body parts:

• Internal organs;
• Bones and joints;
• Main vessels and nerve trunks;

By the presence of complications:

• Pulmonary edema;
• DIC;

In terms of severity:

• Satisfactory;
• Extremely serious condition;

By association with injuries and illnesses:

• After burns and frostbite;
• After radiation sickness;
• Nausea, vomiting;

In addition to these criteria, there are others, but they are less significant.

Signs of a crash syndrome.

The clinical picture and further prognosis depend on many factors. Of great importance is how long the compression lasted, and what area of ​​​​the lesion, during military operations 90% of the body is affected, in other cases from 70 to 80%.
Victims who have compression of both limbs at the level of the thigh have a much worse prognosis than those who have passed hands.

Stages of SDS, at the time of detection of the victim:

• Light
  If 30-40 minutes have passed since the beginning of the compression, his hands or feet will begin to swell, and the skin will be cold and pale, the pulsation is either absent or weak. Timely therapy will allow you to return to normal in a week;
• Medium
  If the compression was no more than 4 hours, intoxication, myoglobinuria and oliguria begin;
• heavy
  Squeezing from 4 to 7 hours leads to a serious condition, kidney failure progresses, body temperature rises to 39 degrees;
• Extremely heavy
  If a person has been under the rubble for 8 hours or more, then the areas subject to compression will be red-cyanotic in color with severe swelling. No pulsation, Inability to move limbs. At any attempt to do this, the victim feels severe pain. The chance of death is too high.

After detecting signs of SDS, it is urgent, before the arrival of doctors, to provide first aid.

First aid

Anesthesia is carried out at the very beginning until release. When conducting first aid, much depends on the qualifications of the one who provides it. Who, without special training, can do little to prevent serious consequences.

But when professionals get down to business, the forecast improves significantly:

• Specialists often resort to narcotic analgesics, usually Promedol. If it is absent, then drugs such as Baralgin and Ketorolac are suitable. With severe swelling, cut off clothes;
• At the same time, the victim is injected with a solution of sodium bicarbonate, calcium chloride intravenously and glucocorticoids. They stabilize cell membranes;
• After extraction from the wreckage, an elastic bandage is applied to the damaged limb from the base of the fingers. To do this, give the victim a comfortable position for access from all sides. A tourniquet is used if the compression has lasted 15 hours or more, or if there is severe crushing and bleeding. The damaged area must be cooled with ice, snow or a cold water bottle;
• The victim must be moved away from the scene, to a safe distance;
• The wounds revealed during his examination are covered with aseptic dressings. With open bleeding, a pressure bandage must be stopped, and this must be done as quickly as possible. To do this, it is necessary to apply several sterile gauze napkins to the wound, and a cotton ball on top of them. After fixing everything with circular tours of the bandage;
• In the presence of fractures, tires or improvised materials are applied.

If it is impossible to start an intravenous infusion, it is necessary to provide the patient with a large amount of alkaline water (baking soda solution). Anyone involved in rescue work can take such measures.

tourniquet

Many argue about the advisability of applying a tourniquet. Practice shows that this method is quite effective if everything is done correctly. In order for the tourniquet to work positively, it must be applied even before the person is released, it is used above the place where the compression occurred. This prevents the influence of large doses of potassium, which at one moment reach the heart muscle, which leads to the development of fatal cardiac arrhythmias.

The tourniquet is allowed to be left for a long time when gangrene appears, and also when the limb is completely destroyed.

With an intact limb, the tourniquet must be removed after a maximum of 1.5 hours.

Infusion therapy

Further, professional rescuers and medical workers should start working. At this stage, an intravenous catheter is installed and with its help saline blood-substituting solutions are poured in, in which there is no potassium. Infusion therapy is carried out as long as possible. The most correct thing is its implementation even during evacuation to the hospital.

Treatment in a hospital

Upon delivery to the hospital, it is necessary for the victim to introduce diuretics along with infusions of saline solutions and sodium bicarbonate. This procedure stimulates the kidneys. Sometimes sparing methods of blood purification are used: hemosorption and plasmapheresis. This is done very carefully and only when pulmonary edema or uremia has begun.
Wound infections are treated with antibiotics.
To avoid a possible complication after a crash syndrome, DIC - syndrome (a problem with blood clotting), heparin prophylaxis is used.

During surgical treatment, an amputation of a non-viable limb is performed. With pronounced edema leading to compression of the fascia, a fasciotomy is performed along with plaster immobilization.

Possible Complications

The main complication that occurs with SDS is acute renal failure. It often leads to death.

There are other complications:

• Pulmonary edema is a life-threatening condition, the lung tissue is saturated with blood from torn vessels and hypoxia is growing;
• Hemorrhagic shock - observed with a large loss of blood;
• DIC - a syndrome - often leads to death due to the fact that the blood vessels are damaged by toxic substances released by the affected tissues;
• Infectious - septic complications - lead to serious diseases due to tissue damage by microorganisms.

To avoid dangerous consequences, it is of great importance to help the patient as quickly as possible.

The victim, with his quick release from the rubble and providing him with medical support, has a much better chance of saving and keeping his arms and legs intact. The longer the compression lasts, the worse the consequences for the human body will be and the treatment will become much more complicated.

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 extremities, 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 own 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 prevail 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. 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, in case of 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 occur.

Swelling of the soft tissues of damaged limbs is accompanied by a sharp blood loss with the development of hemoconcentration (hemoglobin and hematocrit levels increase, BCC and BCP decrease), 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 consistent 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 protein catabolism that occurs 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, most 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 together 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, lumps 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, the basis of which is damage to the vascular apparatus of the glomeruli and the basement membrane of the tubules, 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 victims 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 of the incident 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 the syndrome of prolonged compression correlates with the severity of its clinical course and manifests itself, as a rule, after the victim recovers from shock, correction of hemodynamic and homeostasis disorders. However, acute renal failure can also occur during 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 limits. 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 disturbances 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 in acute renal failure in patients with SDS is noted from the moment the nitrogen content in the blood is normalized, 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 4-5th day of the post-compression period of SDS, when the 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 4-9th 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.

The 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, a decrease in tendon reflexes, limitation of 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 movements in the joints and impaired sensitivity continue to persist. Over time, part of the muscle fibers of the damaged 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 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 DFS.

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 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 that occur 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 held (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 ensures the maximum possible restoration of blood circulation, allows you to delimit the necrotic process in more distal sections, 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 "everyday" 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, it is necessary for the patient to stay in a coma for a long time or in a state of deep pathological sleep, which is most often caused by alcohol poisoning 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 an injury to soft tissues, 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, squeezed 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 purplish-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 in consistency, sharply painful on palpation, which is due to the tension of the facies cases due to a sharp swelling of the muscles, subcutaneous fatty 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

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

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

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

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

Table 1

Frequency of development of SDS during earthquakes

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

Table 2 lists the main causes leading to SDS.

table 2

The main etiological factors of SDS

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

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

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

Table 3

SDS classification by severity

The clinical picture of SDS has a clear periodicity.

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

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

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

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

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

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

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

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

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

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

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

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

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

Literature

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

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

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

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

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

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

There are three periods in the clinical course of SDS:

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

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

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

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

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

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

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

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

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

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

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

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

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

V.Dmitrieva, A.Koshelev, A.Teplova

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