Long-term compression syndrome. Features of the course of the syndrome of short-term collapse and positional compression of soft tissues Positional compression

Long-term compartment syndrome (traumatic anuria, Bywaters syndrome, traumatic rhabdomyolysis) is a pathological condition associated with the restoration of blood circulation in tissues that have been deprived of it for a long time. SDS occurs when victims are removed from the rubble, where they end up during earthquakes, man-made disasters, and terrorist attacks. A variation of this pathology is positional compression syndrome, which occurs in the limbs of people who remain immobile for a long time (coma, alcohol intoxication). In this case, compression of the limbs occurs under the weight of the patient’s own body.

Most often, people suffer from crash syndrome in regions where military operations are ongoing, during earthquakes, and in car accidents. In recent years, terrorism has become increasingly important as a cause of SDS, in which explosions of buildings can lead to victims falling under the rubble.

In all these cases, with the exception of car accidents, situations arise with the mass arrival of victims in medical institutions. Therefore, it is especially important to quickly identify the development of DFS and begin its treatment at the prehospital stage.

Types of compartment syndrome

This pathological condition is classified according to several criteria:

• According to the type of compression, it is divided into crushing (traumatic muscle damage), direct and positional compression;
• by localization - chest, abdominal, pelvic areas, hand, forearm, thigh, lower leg, foot in various combinations;
• in combination with damage to other parts of the body:
  • internal organs;
  • bones, joints;
  • main vessels, nerve trunks;
• the presence of complications;
• degree of severity;
• combinations with other types of injury:
  • burns or frostbite;
  • radiation sickness;
  • poisoning, etc.

What happens in the body during crash syndrome

The basis of this pathology is the massive death of muscle cells. There are several reasons for this process:

• their direct destruction by a traumatic factor;
• cessation of blood supply to the compressed muscle;
• cellular hypoxia associated with hemorrhagic shock, often accompanying massive trauma.

As long as the muscle is compressed, there is no crash syndrome. It begins after the pinched part of the body is released from external pressure. At the same time, the compressed blood vessels open, and blood, saturated with the breakdown products of muscle cells, rushes into the main channel. Once it reaches the kidneys, myoglobin (the main muscle protein) clogs the microscopic kidney tubules, blocking urine production. Within a few hours, tubular necrosis and kidney death develop. The result of these processes is acute renal failure.

The course of the disease directly depends on both the duration of compression and the volume of affected tissue. So, when the forearm is compressed for 2-3 hours, there will be no acute renal failure, although a decrease in urine production is still noted. There are no intoxication phenomena that are inevitable with longer compression. Such patients almost always recover without consequences.

Extensive compression lasting up to 6 hours leads to moderate crash syndrome. In this case, there are striking signs of endotoxicosis (intoxication) and impaired renal function for a week or more. The prognosis depends on the timing of first aid and the timeliness and volume of subsequent intensive care.

When compression lasts for more than 6 hours, SDS develops in severe form. Endotoxicosis rapidly increases, the kidneys shut down completely. Without hemodialysis and powerful intensive care, a person inevitably dies.

The symptoms of crash syndrome depend on the period of development of the pathology.

In the early period (1-3 days), there are mainly symptoms of shock: pallor, weakness, tachycardia, low blood pressure. The most dangerous moment in this period is the direct extraction of the victim from the rubble. As soon as blood circulation is restored in the affected limb, a large amount of potassium is released into the blood, which can lead to instant cardiac arrest. But even without this, in severe forms of DFS, the phenomena of renal-liver failure and pulmonary edema, as well as cardiac arrhythmias, develop already in the first day.

The early period is characterized by local manifestations on the affected limbs:

• skin condition - tense (due to interstitial edema), pale, bluish, cold to the touch;
• there are blisters on the skin;
• there is no pulse in the peripheral arteries;
• all forms of sensitivity are either suppressed or absent;
• the ability for active movements of the affected limb is reduced or absent.

More than half of the victims are also diagnosed with corresponding bones.

In the intermediate period (4-20 days), intoxication and acute renal failure come first. Initially, the patient’s condition stabilizes for a short period of time, but then begins to rapidly deteriorate, disturbances of consciousness appear, up to deep stupor. The urine becomes brown, its amount drops to zero, and this condition can last up to 3 weeks. With a favorable course of the disease, this phase passes into the phase of polyuria, in which the amount of urine excreted increases sharply. It is in the intermediate period that infectious complications tend to generalize (spread throughout the body) most often develop, and pulmonary edema is also possible.

If during the intermediate period the patient does not die, then the third period begins - late. It lasts from 3-4 weeks to several months. At this time, the functions of all affected organs - lungs, liver and, most importantly, kidneys - are gradually normalized.

The development of long-term compartment syndrome can be suspected already at the scene of the incident. Information about a natural disaster, about a person’s long stay under the rubble, suggests the possible development of VDS. Objective data allow us to make a diagnosis of crash syndrome with a fairly high degree of confidence.

In laboratory conditions, you can obtain information about hemoconcentration (blood thickening), electrolyte disturbances, increased levels of glucose, creatinine, urea, and bilirubin. A biochemical blood test reveals an increase in liver transaminases and a decrease in protein concentration. An analysis of the acid-base state of the blood shows the presence of acidosis.

In the urine analysis, at first there are no changes, but then the urine becomes brown in color, its density increases, protein appears in it, and the pH shifts to the acidic side. Microscopic examination reveals a large number of cylinders, erythrocytes, and leukocytes.

First aid measures for compartment syndrome depend on who is providing it, as well as the availability of forces involved and the availability of qualified personnel. An untrained person can do little to prevent the development of severe complications, while professional rescuers, through their actions, seriously improve the prognosis for the patient.

First of all, the one removed from under must be moved to a safe place. Wounds and abrasions identified during a superficial examination should be covered with aseptic dressings. If there is bleeding, measures should be taken to stop it as soon as possible; fractures are immobilized with special splints or improvised means. If starting an intravenous infusion at this stage is not possible, the patient must be provided with plenty of fluids. These measures can be carried out by any person participating in rescue operations.

The issue of applying a tourniquet to the injured limb is currently being debated. Practice, however, shows the effect of this method when applied correctly. It is advisable to apply a tourniquet before the victim is released; the place of application is above the place of compression. The tourniquet helps prevent the influence of large doses of potassium, which simultaneously reach the heart muscle and lead to the development of collapse and fatal cardiac arrhythmias. It is recommended to leave it for a long time only in two cases:

• with complete destruction of a limb;
• with gangrene.

At the next stage, assistance is provided by trained people - rescuers, paramedics, nurses. At this stage, the victim must be given an intravenous catheter (although it is ideal to do this even before liberation from the wreckage), with the help of which the infusion of saline blood-substituting solutions without potassium content is started. Infusion therapy should continue for as long as possible; it is advisable not to interrupt it even when evacuating the victim to a medical facility. Adequate pain relief is mandatory. If help is provided by a specialist, he can use narcotic analgesics (Promedol); if not, using any painkiller like baralgin or ketorolac will be better than refusing analgesia. At this stage, you can cut off the clothing if there is significant swelling of the affected limb.

In parallel, patients are injected intravenously with a solution of sodium bicarbonate to correct acidosis, calcium chloride to neutralize excess potassium, and glucocorticoids to stabilize cell membranes.

In a hospital setting, measures are taken to stimulate kidney function - the administration of diuretics in parallel with infusions of saline solutions and sodium bicarbonate. It is possible to use blood purification methods, with preference given to the most gentle of them - hemosorption, plasmapheresis. They should be used with caution and only in case of obvious onset of pulmonary edema or uremia.

Antibiotic therapy is used only when there are clear signs of wound infection. Heparin prophylaxis helps prevent the development of disseminated intravascular coagulation syndrome, a particularly severe complication of DIC.

Surgical treatment of long-term compartment syndrome involves amputation of a nonviable limb. In case of severe swelling leading to compression of the great vessels, fasciotomy surgery in combination with plaster immobilization is indicated.

Complications

The main complication of crash syndrome is acute renal failure. It is the main cause of death in this pathology.

Pulmonary edema is a life-threatening condition in which the lung tissue becomes saturated with fluid escaping from the blood vessels. At the same time, gas exchange in the alveoli worsens and hypoxia increases.

Hemorrhagic shock due to massive blood loss is observed when large vessels are damaged. The situation is worsened by the fact that in the affected area the ability of tissues to withstand the damaging effects of external factors is sharply reduced.

DIC syndrome develops as a consequence of bleeding, as well as due to direct damage to blood vessels by decay products of the affected tissues. This is the most severe complication of DFS with a high mortality rate.

Infectious and septic complications often accompany crash syndrome. Due to reduced tissue viability, the damaged area is easily affected by microorganisms, especially anaerobic ones. The result is severe illnesses that worsen the course of the underlying pathology.

In case of crash syndrome, the timing of the start of assistance is important. The sooner the victim is removed from the rubble, the more complete the scope of measures taken, the greater his chances of survival.

Bozbey Gennady Andreevich, emergency doctor

Positional crush syndrome is a type of long-term crush syndrome. Its main difference is the absence of initial damage to soft tissues by severe and crushing violence. Positional compression occurs when the victim is unconscious and is associated with an uncomfortable posture in which the limbs are either pressed down by the body, or bent over a solid object, or hang down under the influence of their own gravity. Deep alcoholic intoxication or unconsciousness caused by other reasons sometimes forces one to remain in an uncomfortable position for 10-12 hours. As a result, severe ischemic disorders occur in the limbs, leading to tissue necrosis and toxic phenomena due to the absorption of the products of their autolysis.

The outcome of the pathological process depends on the duration of compression, early correct diagnosis and rational treatment. In patients in whom the diagnosis was not made at all during life or was recognized very late, the prognosis is disappointing. Often, patients are left with irreversible neurological and trophic disorders after positional compression.

Clinical picture

Having woken up and come to their senses, patients note significant pain and a sharp dysfunction of the affected limb. Weakness and headache aggravate the general condition. Local disorders are expressed in pallor and coldness of the affected limb, decreased sensitivity of the skin, severe limitation of functions, lethargy, weakening or complete absence of pulsation of the arteries. Body temperature is normal or slightly increased, blood pressure is not changed. If the patient was admitted several hours after the onset of the disease, then increasing swelling appears on the limb, and the skin becomes purple. Anamnesis plays a huge role in correctly recognizing suffering. Meanwhile, patients are reluctant to report severe intoxication, talk about injury or an unknown reason. Most often, doctors diagnose “thrombophlebitis”, and in some advanced cases, “anaerobic infection”, and therefore make wide incisions. Increasing edema of a woody nature, pronounced neurovascular disorders are aggravated by severe impairment of renal function. The daily amount of urine decreases sharply, until anuria develops.

Principles of treatment

The main therapeutic measures for positional compression should be aimed at normalizing the functioning of the cardiovascular system and kidneys; the administration of analgesics, antihistamines, osmodiuretics is indicated, and endotheliotropic therapy is mandatory. To prevent swelling, the limb is tightly bandaged with an elastic bandage and cooled. For severe swelling, a fasciotomy with a small skin incision is indicated. The infusion of fluids is controlled by the excretory function of the kidneys. In severe cases of the process, hemosorption and hemodialysis are used using an “artificial kidney” apparatus in specialized departments.

In Fig. Figures 1-5 show photographs of a patient who, while intoxicated, lay motionless on his right forearm for more than 12 hours (Figure 1-3). By the end of the first day of the patient’s stay in the hospital, he was found to have a pinpoint hemorrhagic rash (Fig. 4-5), which was not associated with the main suffering. Upon repeated questioning, it was found that the patient had drank a large amount of alcohol substitutes the day before and that previously the use of substitutes had caused similar changes on the skin (toxic hepatitis).

Pathogenesis, clinical manifestations and treatment can be schematically presented as follows.

Compartment syndrome

Local hypertensive ischemic syndrome (compartment syndrome - compression syndrome) develops in skeletal muscles limited by rigid osteofascial sheaths.

Pathogenesis:

- increased pressure in the closed fascial space;

- minimal circulation syndrome;

- capillary leak syndrome;

- tissue swelling.

Diagnostics:

1. Severe pain that does not correspond to the severity of the lesion.

2. Dense tense swelling.

3. Paresthesia or anesthesia in the area of ​​innervation of ischemic nerves.

4. Pain during passive stretching of the affected muscles.

5. Invasive injection determination of subfascial pressure (more than 10 mm Hg, normal - 8 mm Hg).

2. Normalization of central hemodynamics: crystalloids, colloids.

3. Normalization of microcirculation and rheology: rheopolyglucin, trental, L-lysine escinate.

4. Stabilization of vascular membranes: L-lysine aescinate (endotheliotropic therapy), in the absence of L-lysine aescinate, glucocorticoids can be prescribed, especially in case of hypotension.

5. Improving venous and lymphatic drainage, relieving vasospasm: L-lysine escinate or other bioflavonoids.

6. Anti-inflammatory therapy: steroids, NSAIDs.

7. If necessary, dehydration. It must be remembered that the administration of diuretics can lead to aggravation of the rheological properties of blood and microcirculatory block.

8. Vitamin therapy: B1, B6, B12, ascorbic acid.

9. Surgical decompression: fasciotomy.

10. Antibacterial therapy.

L-lysine aescinate

1. In the first 2-4 hours - 15-25 ml.

2. In the following days - 10 ml 2 times a day (6-8 days).

Remember: the bioavailability of the tissues of the fascial-bone sheath for medications is limited.

In our experience, it is advisable to administer L-lysine aescinate at an early prehospital stage.

According to a number of authors and our observations, such tactics for managing such victims allows us to achieve the following results: in 71.4-80.5% of cases, there is regression of clinical symptoms and a decrease in subfascial pressure by 12-21 mm Hg, this allows us to limit ourselves to conservative therapy in 64% of cases.

Table of contents of the topic "Long-term compression syndrome. Crash syndrome (CDS). First aid (emergency care) for crash syndrome (CDS).":
1. Long-term compression syndrome. Definition of crash syndrome. Causes (etiology), pathogenesis of crash syndrome (CDS).

3. Classification of long-term compartment syndrome (CPS). Forms of the course of crash syndrome (cds)..
4. Periods of long-term compartment syndrome (LCS). Compression period of crash syndrome (CCS). Early post-compression period. Intermediate period.
5. Clinic (manifestations) of long-term compartment syndrome (LCS). Diagnosis of crash syndrome (cds)..
6. Principles of treatment of long-term compartment syndrome (CPS). Pre-hospital medical care. First aid (emergency care) for crash syndrome (CDS).
7. Qualified medical care for long-term compartment syndrome (CPS).
8. Surgery(s) for long-term compartment syndrome (LCS). Fasciotomy. Amputation.
9. Lamp incisions for long-term compartment syndrome (LCS). Specialized medical care for crash syndrome (CDS).

Positional compression syndrome (ATP) is a common type of SDS and occurs with prolonged compression of the limbs by the weight of one’s own body in patients in a coma (I. I. Shimanko, S. G. Musselius, 1993).

If at SDS Diagnosis issues in connection with clear causative factors do not present any difficulties, but SPS is rarely diagnosed in a timely manner. This is due to the obligatory presence of a period of coma (for example, alcoholic coma, carbon monoxide poisoning, barbiturates, etc.). After emerging from a comatose state or while still in it, victims usually end up in therapeutic departments. Sometimes patients, after regaining consciousness in the initial stages of the disease, do not seek medical help at all, and only the appearance of signs of acute renal failure forces them to do so.

Etiology. Trigger factor ATP is a prolonged comatose state, most often due to poisoning (alcohol and its surrogates, carbon monoxide, sleeping pills, sedatives, etc.), and the resulting positional compression of soft tissues when the victim is in an uncomfortable position for a long time. Usually he lies on a hard surface in a forced position with his compressed or bent limbs tucked under him.

Pathogenesis of SPS is quite complex and is associated with the main etiological factors, poisoning with exotoxic substances of narcotic action and positional trauma, which occurs during a prolonged coma. In the pathogenesis of SPS, toxemia is of great importance, associated with the proteolysis of tissue enzymes killed as a result of ischemia, plasma loss and pain. The impact of myoglobin and other toxic metabolites released from the focus of compressed and ischemic tissues is manifested by severe endotoxemia, leading to disruption of the functions of many organs and systems (I. I. Shimanko, S. G. Musselius, 1993).

Prolonged compression syndrome (compression) is a massive traumatic injury to soft tissues, often leading to persistent hemodynamic disorders, shock and uremia. This is a traumatic toxicosis that develops in the tissues of the extremities when they are released after prolonged compression. The breakdown products of muscle cells, which are normally excreted by the kidneys, are released into the blood. When the kidneys are damaged, they accumulate and clog the renal tubules, which leads to the death of nephrons and the development of acute renal failure.

The variety of clinical signs of the syndrome is due to prolonged soft tissue ischemia, endotoxemia, hyperkalemia and renal dysfunction. This disease is a consequence of accidents: road accidents, earthquakes, destruction of buildings, blockages in mines, man-made disasters, terrorist attacks, landslides, construction work, logging, bombing. The compression force is so great that the victim cannot independently remove the affected limb.

It is possible to develop a special form of the syndrome that affects the limbs of immobilized patients. This is a positional syndrome that develops under the pressure of one’s own body weight on soft tissues. It occurs with severe alcohol intoxication or alcoholic coma. Such patients spend a long time in an unnatural position, often lying on an uneven surface. The development of the syndrome is caused by hypoxia and dyscirculatory changes, leading to a decrease in the volume of intravascular fluid and endotoxemia.

The pathology was first described during the First World War by the French surgeon Quenu. He watched an officer whose legs were crushed by a log after the explosion. The limbs below the compression site were dark red, and the wounded man himself felt well during the rescue. When the log was removed from his feet, toxic shock developed, from which the officer died. Several decades later, a scientist from England, Bywaters, studied in detail the pathogenetic factors and mechanism of development of the syndrome and identified it as a separate nosology.

The syndrome has various causes, complex pathogenesis, requires mandatory treatment and characterized by a high incidence of deaths. It occurs equally often in women and men. A shock-like state develops immediately after the victim is released and blood circulation and lymph flow are restored in the affected parts of the body. The causes of death of patients are: traumatic shock, endogenous toxemia, myoglobinuric nephrosis, heart and pulmonary failure. Treatment of the pathology is complex, including detoxification, replacement and antimicrobial therapy, necrectomy or amputation of the affected limb.

Most often, people living in regions where there is active hostilities or frequent earthquakes suffer from long-term compartment syndrome. Terrorism is a current problem and the cause of the syndrome.

Crush syndrome is a serious injury, the treatment of which causes many difficulties and difficulties.

Classification

Based on the location of the lesion, compartment syndrome is distinguished:

• thoracic region,
• abdominal area,
• heads,
• limbs,
• pelvic area.

The syndrome is often accompanied by damage:

1. vital organs,
2. bone structures,
3. articular joints,
4. arteries and veins,
5. nerve fibers.

Long-term compartment syndrome is often combined with other ailments:

• burns,
• frostbite,
• exposure to radioactive radiation,
• acute poisoning.

Etiopathogenetic links and factors

The main cause of prolonged compartment syndrome is mechanical trauma resulting from an accident at work, at home or in war. Compression of body parts occurs during accidents, earthquakes, explosions and other emergency situations.

Long-term compression of soft tissues leads to damage to blood vessels and nerves, the development of ischemia of the affected area and the appearance of areas of necrosis. The syndrome develops a few minutes after the removal of compressive objects and the resumption of lymph and blood supply to the damaged area. That is why first aid is provided directly at the scene of the incident.

Pathogenetic links of the syndrome:

1. pain shock,
2. increasing capillary permeability,
3. release of proteins and plasma from the vascular bed,
4. disruption of the normal tissue structure,
5. swelling of tissues,
6. loss of the liquid part of the blood - plasma,
7. changes in hemodynamics,
8. dysfunction of the blood coagulation system,
9. thrombus formation,
10. toxemia as a result of tissue breakdown,
11. penetration of microelements from injured tissues into the blood,
12. a shift in the acid-base balance towards increasing acidity,
13. the appearance of myoglobin in the blood and urine,
14. formation of hematin hydrochloride from methemoglobin,
15. development of tubular necrosis,
16. death of kidney cells,
17. acute uremia,
18. entry into the systemic circulation of inflammatory mediators,
19. multiple organ failure.

Vasoconstriction and changes in normal microcirculation in the muscles lead to disruption of sensory stimulation in both the affected and healthy limbs.

Multiple organ failure is characterized by damage to internal organs and systems:

• cardiovascular, excretory, respiratory, digestive,
• hematopoietic system with the development of anemia, hemolysis of red blood cells, disseminated intravascular coagulation syndrome,
• metabolism,
• immune system with the development of secondary infection.

The outcome of multiple organ failure in most cases is the death of the patient.

Factors involved in the development of pathology:

1. toxemia,
2. plasma loss,
3. neuro-reflex mechanism.

Pathomorphological changes in long-term compartment syndrome:

• The first degree is characterized by swelling and pallor of the skin, no signs of ischemia.
• The second degree is tension of edematous tissues, bluishness of the skin, the formation of blisters with purulent exudate, signs of impaired blood and lymph circulation, microthrombosis.
• Third degree - “marbling” of the skin, local hypothermia, blisters with blood, gross dyscirculatory changes, venous thrombosis.
• Fourth degree – purple skin color, cold and sticky sweat, foci of necrosis.

Symptoms

The symptoms of the pathology depend on the duration of compression of the soft tissues and the area of ​​the lesion.

The compression or first period is characterized by a clinical picture of shock:

1. bursting pain in the affected area,
2. shortness of breath,
3. signs of general asthenia of the body,
4. nausea,
5. paleness of the skin,
6. drop in blood pressure,
7. rapid heartbeat,
8. indifference to current events, lethargy or anxiety, sleep disturbance.

After removing the victim from the rubble, the second period of clinical manifestations begins - toxic. At this time, the swelling in the affected area increases, the skin becomes tense, purple-bluish with many abrasions, bruising, and blisters with blood.

• Any movement brings excruciating pain to the victim.
• The pulse is weak, thread-like.
• Hyperhidrosis.
• Loss of sensitivity.
• Oliganuria develops.
• Proteinuria, leukocyturia, hematuria, myoglobinuria, cylindruria, urine acidification.
• In the blood - erythrocytosis, azotemia, blood thickening.
• Involuntary release of feces and urine.
• Euphoria and loss of consciousness.

The third period is characterized by the development of severe complications, which significantly worsen the condition of patients and can lead to death. These include:

1. kidney dysfunction,
2. anemia,
3. uremia with hypoproteinemia,
4. fever,
5. vomit,
6. foci of necrosis,
7. muscle exposure,
8. suppuration of wounds and erosions,
9. lethargy, hysteria, psychosis,
10. toxic liver damage,
11. endotoxicosis.

By the end of the first week, uremic intoxication increases and the condition of patients worsens. They experience motor restlessness and psychosis, depression gives way to aggressiveness, hemogram parameters change, potassium metabolism is disrupted, and cardiac arrest is possible.

The fourth period is convalescence. In patients, the functioning of internal organs is restored, hemogram and water-electrolyte balance are normalized.

The severity of the clinical manifestations of the syndrome depends on the area of ​​the lesion and the duration of compression:

• If the patient's forearm tissues were compressed for 2-3 hours, his condition remains satisfactory, uremia and severe intoxication do not develop. There was a rapid recovery of the victims without consequences or complications.
• When a large surface of the human body is compressed for more than six hours, severe endotoxicosis and complete shutdown of the kidneys develop. Without extrarenal blood purification and powerful intensive therapy, the patient may die.

Complications of the syndrome: kidney dysfunction, acute pulmonary failure, hemorrhagic shock, disseminated intravascular coagulation syndrome, secondary infection, acute coronary insufficiency, pneumonia, psychopathy, thromboembolism. Early removal of victims from the rubble and the fullest possible scope of treatment measures increase the patients’ chances of survival.

Diagnostics

The diagnosis of long-term compression syndrome can be schematically represented as follows:

1. study of clinical signs of pathology,
2. obtaining information about the victim’s presence under the rubble,
3. visual examination of the patient,
4. physical examination,
5. sending clinical material to biochemical and microbiological laboratories.

In the pathology clinic, signs of pain, dyspepsia, asthenia, and depression predominate. During the examination, specialists identify pallor or cyanosis of the skin, abrasions and blisters with serous-hemorrhagic contents in the affected area, foci of necrosis, and suppuration of wounds. A physical examination reveals a decrease in blood pressure, tachycardia, edema, fever, and chills. In the late stage - atrophy of viable muscles of the limb and contracture.

Laboratory diagnostics include:

Therapeutic measures

Treatment of the pathology is multicomponent and multistage:

1. At the first stage, patients are provided with emergency medical care at the scene of the incident.
2. At the second stage, patients are hospitalized in a hospital in special intensive care vehicles equipped with all the necessary equipment to provide pre-medical care.
3. The third stage is the treatment of patients in surgery or traumatology by highly qualified specialists.

First aid algorithm:

All victims with prolonged compartment syndrome are hospitalized in a hospital. Drug treatment in the hospital consists of prescribing the following groups of drugs:

Extrarenal blood purification is carried out in severe cases when other treatment methods do not produce positive results. If it is not possible to control electrolyte disturbances with medication, pulmonary edema and metabolic acidosis persist, and symptoms of uremia appear, patients are prescribed hemodialysis, ultrafiltration, plasmapheresis, hemosorption, hemodiafiltration, plasmasorption, lymphoplasmasorption. Hyperbaric oxygenation sessions are carried out 1-2 times a day in order to saturate the tissues with oxygen.

Surgical treatment - dissection of the fascia, removal of necrotic tissue, amputation of the limb. In a hospital, it is necessary to strictly observe the rules of asepsis and antiseptics when carrying out diagnostic and treatment procedures, disinfect environmental objects, and keep all premises, equipment and inventory perfectly clean.

Rehabilitation of patients consists of massage, physical therapy, physiotherapeutic techniques and sanatorium-resort treatment. Reconstructive interventions are performed according to indications.

The prognosis of the pathology is determined by the timeliness of medical care, the extent of the lesion, the characteristics of the course of the syndrome, and the individual characteristics of the victim.

Video: about help with long-term compartment syndrome

LONG-TERM POSITIONAL COMPRESSION SYNDROME

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

The severity of these injuries cannot 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 a correct diagnosis in time, prescribe the necessary treatment, and also prevent complications.

Long-term compression syndrome is 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 during emergency destruction of buildings, collapses, earthquakes, etc. It is among the severe injuries the treatment of which is very difficult.

At one time, many researchers of this pathology (Bywaters and Bill, A.Ya. Pytel, N.N. Elansky, N.I. Pirogov, Bossard, Silberstern, Colmers, Frankenthal, Küttner, Gaccard, Levin, Minami, Quenu, etc. ) offered their definition based on clinical manifestations or the pathogenesis of the disease:

Bywaters and Bill (Bywaters E., a Beall, 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 numbness (local torpor)”;

Bossar, Silberstern (Bossar 1882, Silderstern 1909) - “nephritis with albuminuria and hematuria”;

Laborit - "Bywaters syndrome";

M.I.Kuzin (1953) - “long-term crush syndrome”;

- "Verschuttungsnekrose der Muskelen" - German researchers.

Classification:

1. By type of compression:

Various objects, soil, slabs, etc.

Positional (with part of your body)

2. By localization of compression:

Limbs (segments)

3. According to the combination of SDS with damage:

Internal organs

Bones and joints

Great vessels and nerves

4. By severity:

Average

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 injuries

SDS and radiation injuries

SDS and poisoning

SDS and other combinations

7. Complications:

DFS complicated - diseases of organs and systems

Acute ischemia of the injured limb

Purulent-septic complications

Pathogenesis:

The leading pathogenetic factors of long-term compartment syndrome are:

1) traumatic toxemia, which develops due to the entry into the bloodstream of decay products of damaged cells;

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

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

4) painful stimulation, leading to disruption of the coordination of excitation and inhibition processes 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 stagnation. Nerve trunks are also injured. Mechanical destruction of tissue occurs with the formation of a large amount of toxic metabolic products, primarily methemoglobin. The combination of arterial insufficiency and venous congestion aggravates 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 ability. Intravascular coagulation blocks filtration. Consequently, myoglobinemia and myoglobinuria are the main factors determining the severity of toxicosis in victims. Hyperkalemia, often reaching 7-12 mmol/l, significantly affects the patient’s condition. Toxemia is also aggravated by the intake of histamine, protein breakdown products, adenylic acid, creatinine, phosphorus, etc. from damaged muscles.

Already in the early period of long-term compartment syndrome, blood thickening is observed as a result of plasma loss, as massive swelling of damaged tissues develops. In severe cases, plasma loss reaches up to 1/3 of the bcc.

The most severe complication observed in long-term compartment syndrome is acute renal failure, which manifests itself differently at the stages of disease development.

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. An excited state occurs less often. Such victims shout, gesticulate, demand help, or sing.

Complaints are caused by pain and a feeling of fullness in compressed areas of the body, thirst, and difficulty breathing. With significant trauma, especially with damage to the internal organs of the abdominal and thoracic cavity, fractures of long tubular bones, damage to the great vessels and nerves, the phenomena of traumatic shock develop, as well as collateral damage (intra-abdominal bleeding, pneumohemothorax, traumatic brain injury).

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

The first period is 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 clinical picture of the disease is dominated by manifestations of traumatic shock: severe pain, psycho-emotional stress, and hemodynamic instability. Almost all victims remain conscious. Some of them are in an excited state, but most look lethargic, frightened, drowsy, and lethargic. Some victims die directly at the scene of the incident or in the hospital emergency department, usually from injuries incompatible with life.

After being released from the compression, victims complain of pain in the damaged parts of the body, general weakness, dizziness, nausea, and thirst. The skin becomes covered with cold sweat. Movement in the limbs is limited due to pain. Tachycardia, hypotension, and lack of appetite are detected.

When examining damaged limbs or other parts of the body that have been subjected to compression, a variety of trophic changes in the soft tissues are revealed. The skin acquires a cyanotic color or a marbled appearance, and bulges somewhat over the unchanged areas of the skin. In places of compression there are limited hyperemic areas of the skin, sometimes with a purplish-bluish tint. Often the skin has hemorrhages, abrasions, macerations, hematomas and imprints of objects pressing on the body. Moreover, the more pronounced the imprints 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 soft tissues, detachment of the epidermis sometimes occurs with the formation of conflicts filled with serous or hemorrhagic fluid. In this case, depending on the degree of tissue damage under the epidermis, a wet surface of a pale pink or dark red hue may be exposed, and if local blood circulation is significantly impaired, a cyanotic, black, dry surface of the underlying tissues may be exposed.

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

As swelling increases, the skin becomes pale, cold, and shiny. Dent areas 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 places it has a “woody” consistency, sometimes it takes on a glassy appearance. Palpation of damaged tissue causes severe pain due to the sharp tension of the fascial sheaths, caused by an increase in the volume of the muscles contained in them. Swelling circumferentially covers the entire limb or only the part directly subjected to compression, and quickly spreads to the buttock and abdomen in case of damage to the lower extremities. In the future (5-10 days of the post-compression period), against the background of complex therapy, as swelling, tension, and infiltration in the soft tissues decrease, sensitivity and movement in the joints can gradually be restored, and the pain subsides.

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

The skin over the affected area during this period has a lemon-yellow color (due to absorbable muscle pigment) with a clear boundary when transitioning into undamaged tissue. As blood circulation is restored, swelling and tension increase in the compressed tissues against the background of metabolic processes disturbances 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 further increase in edema and tension of soft tissues, hemo-, lymphodynamic and neurological disorders intensify. Movement in the joints of the injured limbs is limited or completely absent, most often due to severe pain caused by compression of the nerve trunks and the development of ischemic neuritis. The pain is so severe that the victims groan and cannot find a comfortable position in which their intensity would decrease. At the same time, they note a feeling of fullness in the injured limb, constant tension in it. Sometimes victims are bothered by pain even in the absence or profound impairment of sensitivity, which is believed to be associated with 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 location. Thus, when the upper extremities are damaged, 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 when the median, radial or ulnar nerves are damaged. When the lower extremities are damaged, hypoesthesia, weakening or absence of the knee, Achilles and plantar reflexes, a sharp violation of deep sensitivity, often in combination with limb paralysis, are observed.

A frequent manifestation of long-term compression syndrome is traumatic neuritis and plexitis, which occurs at the time of injury and in the early post-compression period in the form of sensory disturbances, active movements, initially moderate pain, and then 4-5 days after injury - constant debilitating pain that disturbs night sleep and cannot be eliminated with analgesics. Upon admission of patients, this occurs in up to 80%.

Swelling of the soft tissues of injured extremities is accompanied by sudden blood loss with the development of hemoconcentration (hemoglobin and hematocrit levels increase, volume of blood volume and blood volume decreases), and pronounced protein and electrolyte disturbances. Plasma loss is largely due to increased capillary permeability as a result of exposure to endogenous toxins and, therefore, is not a primary, but a secondary factor. Blood thickening caused by the development of traumatic edema, a violation of its physicochemical properties, and a slowdown in blood flow due to acute vascular insufficiency lead to hypercoagulation in the early period of long-term compression syndrome. All this undoubtedly enhances the manifestation of shock and contributes to the further accumulation of toxic products of 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 worsens as pathological changes in the compressed tissues increase. In this case, intoxication is manifested by malaise, lethargy, lethargy, nausea, repeated vomiting, dry mouth, increased body temperature to 38°C and above. These phenomena are associated mainly with the entry into the blood of products of disturbed metabolism and the breakdown of ischemic tissues. Tachycardia appears, accompanied by shortness of breath, weakening of heart sounds, and some victims experience a rise in blood pressure.

In the early post-compression period of long-term compression syndrome, respiratory failure often develops. These phenomena may be due to the occurrence of massive fat embolism. It is known that fat embolism manifests itself in various and non-specific symptoms, caused primarily by circulatory disorders in various organs. Intravital diagnosis of fat embolism is quite difficult. There are pulmonary (the most common), cerebral and generalized forms of fat embolism. In the sequential clinical manifestation of fat embolism of all forms, neurological symptoms are usually recorded first, followed by acute respiratory failure with constant arterial hypoxemia. 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, foamy sputum mixed with blood indicates additional pulmonary edema. The radiograph reveals disseminated foci of darkening (“blizzard”), an enhanced vascular-bronchial pattern, and dilatation of the right parts of the heart. Evidence that the cause of acute respiratory failure can be fat embolism is the increase in the early post-compression period of prolonged compression syndrome, hypoproteinemia and hypoalbuminemia - indirect signs of fat embolism. Thus, on the 2nd day of this period of long-term compression syndrome, the albumin-globulin index in victims is 0.98±0.85. The intense catabolism of proteins that occurs is also confirmed by the high content of residual nitrogen and urea in the blood. Throughout the early period of long-term compartment syndrome, blood glucose levels remain elevated. This is explained, firstly, by the high concentration of catecholamines in the blood, which determine 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, to the fact that hyperglycemia is promoted by intense protein catabolism, as a result of which a large number of amino acids are released, the main part of which, during energy deficiency, developing in conditions of long-term compression syndrome, is converted into glucose.

Significant disorders of electrolyte metabolism were found in victims of the early period of long-term compartment syndrome. Thus, the calcium content is below normal (2.23±0.05 mmol/l), probably due to the transition into the interstitial spaces along with plasma and albumin, as well as as a result of its increased consumption in the process of progressive blood coagulation activity, and, conversely, high phosphorus content (1.32±mmol/l), apparently due to increased reabsorption in the renal tubular apparatus under the influence of calcitonin. In turn, severe hyperphosphatemia indicates severe disturbances in the ratio of calcium, sodium, and potassium salts in the body, the presence of degenerative processes in the liver, and impaired tubular reabsorption in the kidneys, especially in conditions of changes in the acid-base state (ABS) in the acidic direction, which is characteristic of the early period of long-term compartment syndrome. Increases in potassium and sodium are more common in victims with severe compartment syndrome. The chloride content, especially in the first day of the early period, usually exceeds normal values ​​(140±16 mmol/l), which can be associated with impaired 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 varnish-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 acidic 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, and hematin crystals.

As is known, the state of the excretory function of the kidneys is used to judge the severity of DFS, the effectiveness of ongoing treatment and preventive measures, and predict the course of DFS and often its outcome. The more severe the compression injury and the more pronounced the endogenous intoxication, the lower the diuresis. In severe cases of SDS, complete anuria may occur already in the early post-compression period, continuing until the death of the victim. In the first 12 hours after releasing the body from compression in victims with long-term 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 amount 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 fluctuations in diuresis in victims with long-term compartment syndrome throughout the entire observation period can range from 0 to 500 ml. A more accurate picture of kidney function is given by studying the amount of creatinine. Its content in the blood on the first day of the early post-compression period exceeds normal values ​​by 2 times, and on the 2nd day – by 5 times.

The appearance of fresh red blood cells in the urine should be considered as a result of severe damage to the vascular apparatus of the renal glomeruli by endotoxins in the early period of long-term compartment syndrome. 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 detected in almost all victims. By the end of the first day, its concentration reaches 0.28±0.077%, on the third day – 0.2±0.06%. This also confirms the presence of severe nephropathy in 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 disruption of glomerular filtration and tubular reabsorption. At this time, according to ultrasound, in victims with acute renal failure, thickening of the renal parenchyma and expansion of its cavity system are detected.

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

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

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

1) mild severity – small depth and area of ​​damage, 4-6 hours. In this case, local changes predominate, the general clinical manifestations of endogenous intoxication are insignificantly expressed. Moderate, transient disorders of general and renal hemodynamics. There are no signs of gross renal dysfunction in the urine. Urine may be red-brown or brown in color; it is quickly freed from myoglobin and acquires its normal color. With more severe muscle damage, myoglobinuria lasts for several days, which is observed with mild nephropathy. Oligouria persists for 2-4 days. By the 4-6th day, against the background of targeted intensive therapy, pain and swelling usually disappear, sensitivity in damaged tissues is restored, body temperature and diuresis are normalized. Laboratory parameters return to normal by 5-7 days after injury. After this, victims can be discharged for outpatient treatment. When examining kidney function 15-20 days after injury, no deviation from the norm is detected. Carrying out intensive complex therapy for victims with mild severity of long-term compartment syndrome, as a rule, prevents the possible development of severe complications.

2) moderate severity - with more extensive damage, at least 6 hours, accompanied by moderately pronounced signs of endogenous intoxication. Impaired renal function is characteristic of moderate nephropathy, and manifests itself in the form of myoglobinuric nephrosis with more pronounced pathological changes in the composition of blood and urine than with mild DDS. Myoglobinuria and oliguria usually persist for 3-5 days. There is a moderate increase in the content of residual nitrogen, urea and creatinine in the blood. These indicators of nitrogen metabolism with an average degree of SDS usually return to normal 12-20 days after injury. When examining the functional state of the kidneys, a decrease in the creatinine concentration index, glomerular filtration and tubular reabsorption of water is revealed. In the peripheral blood of all victims there is pronounced leukocytosis with a shift in the leukocyte formula to the left. Untimely or insufficiently qualified provision of medical care at the scene of an 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 quickly increases and leads to the development of severe complications, including death. At this degree of SDS, the most threatening pathological process that determines the fate of the victim is acute renal failure. If medical care is not provided in a timely manner, as well as with insufficiently effective intensive therapy for the resulting hemodynamic disorders, 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 minor compression of soft tissues with damage to internal organs, bones, blood vessels, and nerve trunks significantly complicates the clinical course of long-term compression syndrome, and long-term compression syndrome, in turn, aggravates the course of the pathological process on the part of internal organs - syndrome mutual burden.

Thus, from the moment the victim is exposed to compression, a clinical picture of systemic and organ failure arises, which can be characterized as multiple organ failure syndrome. A feature of this syndrome in DFS is its early development (starting from the period of compression) and the persistence of symptoms throughout all periods of the clinical course of long-term compression syndrome.

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

Intermediate period.

The 2nd period of long-term compression syndrome begins - 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 progressing overhydration and hypoproteinemia (anemia) pose a great danger to life. At the same time, degenerative-necrotic changes continue to increase at the site of application of the compressive agent, complicated by the development of local infection. Due to impaired urination and metabolic disorders, accompanied by an increase in the production of endogenous water in the body, swelling of the extremities freed from compression continues to increase, and swelling also appears in other parts of the body. On damaged skin, blisters filled with cloudy liquid form and hemorrhages appear. The progression of local changes in soft tissues, mainly purulent-necrotic, determines 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, mumps, etc. An anaerobic infection is often associated. One of the reasons for the development of infectious complications in the intermediate period is the metabolic immunosuppression that occurs at this time.

The clinical picture of acute renal failure in victims with long-term compartment syndrome correlates with the severity of its clinical course and appears, as a rule, after the victim recovers from shock and corrects hemodynamic and homeostasis disorders. However, acute renal failure can also occur during the period of compression, especially against the background of hypothermia, hypovolemia, and fasting, and then only continue to develop in the early and intermediate periods of long-term compression syndrome.

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

The clinical picture of acute renal failure in the intermediate 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, lethargy intensifies, in severe cases a coma occurs, convulsions, tachycardia or, conversely, bradycardia appear. The victims are worried about nausea, frequent vomiting, and thirst. Sometimes intoxication paresis of the intestine with peritoneal phenomena develops, which can cause an unnecessary operation. Pain often appears in the lumbar region, caused by 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, and creatinine in the blood increases, which serves as a harbinger of the development of uremia. Gradually increasing, oliguria in some cases turns into anuria. Uremic intoxication is accompanied by metabolic acidosis and hypochromic anemia. Due to the increase in uremia, the condition of patients worsens. Periodic attacks of motor restlessness often appear, accompanied by a feeling of fear and delirium. Severe disturbances in protein and input-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, moderate levels of urea and creatinine in the blood, and the rare occurrence of hyperkalemia. The creatinine concentration index, minute diuresis and tubular reabsorption remain within normal values. In this case, glomerular filtration is significantly reduced. Timely implementation of targeted therapy allows you to quickly (within 7-10 days) normalize diuresis, urea and creatinine levels in the blood.

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

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 restoration of nitrogen excretion function of the kidneys. Usually during this period only glomerular filtration is restored, and tubular reabsorption remains insufficient. This is confirmed by the low urea content in the urine on the first day of the recovery period of diuresis.

A characteristic feature of the initial period of diuresis recovery is hypercalcemia, which occurs due to the release of deposited calcium from the muscle tissue of the damaged limbs. At the same time, plasma thickening is observed, as a result of which the concentration of proteins increases. This hyperproteinemia is associated with hemoconcentration resulting from 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, normalization of blood pressure, a decrease in intoxication, and an improvement in the general condition and well-being of 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 and is often difficult for victims to tolerate, so during this period it is necessary to strictly monitor changes in homeostasis indicators and correct them in a timely manner. The harbinger of the polyuric phase is growing 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 repeated hyperhydration of the lungs and an increase in azotemia. All this can be the basis for active detoxification and hypohydration. Hydrolytic disorders arising from dehydration and large loss of electrolytes pose a certain danger during the period of polyuria. Thus, intensive excretion of potassium from the body, especially with insufficient correction of fluctuations in its content, leads to severe hypokalemia, in which disturbances in myocardial function can occur, including cardiac arrest.

The hypokalemia developing with polyuria is reflected by characteristic changes on the ECG: a progressive decrease in the T wave, the T wave is inverted with increased amplitude (the QT segment is lengthened), increased PR intervals, ectopic atrial rhythm. In addition, hypochloremia and hyponatremia are often detected, and less commonly, hypomagnesemia and hypocalcemia. Input-electrolyte disturbances can manifest as asthenia, lethargy, severe lethargy, repeated vomiting, a significant decrease in body weight, and even the occurrence of a coma. Normalization of the input-electrolyte balance leads to an improvement in the condition of the victims.

Typically, the beginning of recovery in acute renal failure in victims with DFS is noted from the moment of normalization of the nitrogen content in the blood, which usually refers to the late period of DFS, 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.

The intermediate period of SDS is characterized by the development of hypochromic anemia. The most pronounced decrease in the number of erythrocytes was noted on days 4-5 of the post-compression period of SDS, when the deficiency of erythrocytes caused by sequestration of blood in the microcirculation system is accompanied by increased adhesive-aggregation activity of blood cells and, above all, erythrocytes. This is also facilitated by a progressive increase in vascular permeability and blood thickening. 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 red blood cells occur, which is associated with changes in the degree of hydration of tissue structures caused by a violation of input-electrolyte metabolism, the transition of plasma into the interstitial spaces, and an increase in blood coagulation activity. In turn, deformation of erythrocytes leads to disruption of microcirculation, since hard, 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, there is an increase in the blood of not only the products of nitrogen metabolism, but also potassium, magnesium, phosphates and sulfates, the acid-base state is disrupted towards the development of metabolic acidosis. Moreover, hyperphosphatemia is accompanied by the occurrence of hypocalcemia. On days 4-9 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 the replenishment of protein loss by transfusions of blood products (erythrocyte mass, plasma, albumin, proteins and amino acids). However, at 2-3 weeks of the intermediate period, a decrease in the protein content in the plasma occurs again, which indicates the depletion of the body’s anabolic capabilities, as well as the development by this time of severe complications, primarily infectious.

In the intermediate period of SDS, pronounced changes in the blood coagulation system are observed, which are of a phase nature. First, hyper- and then hypocoagulation phenomena develop, which is a sign of thrombohemorrhagic syndrome. The trigger for the development of this syndrome is the massive intake of thromboplastin from damaged tissues. Thrombohemorrhagic syndrome worsens the condition of victims and often causes severe complications. When studying the parameters of the blood coagulation system in the early period of acute renal failure, initial signs of hypercoagulation can be identified: a slight decrease in blood clotting time and plasma recalcification, a decrease in the prothrombin index, and an increase in plasma tolerance to heparin. In this case, 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 of thromboplastic substances into the blood from damaged tissues, but also due to the activation of the contact phase of coagulation.

One of the frequent complications that develops in the intermediate period of DFS is liver damage - from mild 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 jaundice of the sclera and skin, enlargement of 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 DFS, the normal content of enzymes and bilirubin is restored, and clinical signs of liver damage gradually disappear.

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

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

· Severe muscle weakness, periodic convulsions, sometimes motor agitation, hallucinations;

· Bradycardia;

· Decrease in the height of the P wave, prolongation of the QRS complex, the appearance of a giant T wave with a sharpening of its apex, sinoauricular block, A-V block, premature contraction of the ventricles, their fibrillation;

· Increased plasma potassium above 6 mmol/l.

It cannot be ruled out that hyperkalemia in severe DFS may become

cause of death.

In addition to hyperkalemia, a particular danger to the life of a victim in the intermediate period of SDS is overhydration, which is usually caused by 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 pronounced manifestations of DFS, and therefore it can quickly lead to the development of severe respiratory failure, often predetermining an unfavorable prognosis during DFS.

Symptoms of developing overhydration are:

· Appearance of pastiness, cyanosis and general edema;

· Dry cough with the appearance of oral crepitus;

· Congestion of the neck veins;

· Intense pulse and tachycardia;

· Increased blood pressure to 160-200 mmHg., which becomes refractory to most antihypertensive drugs;

· Increase in central pressure over 130-150 mm water column;

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

· Enlargement of the borders of the liver and the appearance of bursting pain in the right hypochondrium;

· The appearance of exudate in cavities;

· The appearance of a “wet lung” pattern on radiographs of the lungs.

Overhydration may manifest primarily as cerebral edema, anasarca, ascites, acute subcapsular edema of the kidneys, or a combination of these. However, most often overhydration is manifested by changes in the lungs. In these cases, moderate shortness of breath, harsh breathing, mild cyanosis, and rare moist rales initially appear. The number of moist rales quickly increases until it corresponds to the clinical picture of pulmonary edema. The reason for the increase in blood pressure during overhydration can be explained by an increase in intravascular resistance and, above all, a deterioration in microcirculatory function, as well as the development of acute renal failure. The observed increase in heart rate indicates a deterioration in heart function and 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.

X-ray examination can detect fluid in the pericardial cavity, pleural and abdominal cavities. The study allows you to monitor the effectiveness of dehydration methods and identify additional complications: pneumonia, pleurisy, pericarditis, overload of the heart. X-ray examination reveals an increase in the bronchovascular pattern from the roots to the periphery. Severe overhydration is characterized by an intense, inhomogeneous decrease in the transparency of the pulmonary fields and multiple confluent or cloud-like shadows. The roots are mostly butterfly shaped. The lower parts of the lungs are intensely darkened due to effusion. Noteworthy is the change in the configuration of the heart with a predominant increase in the right sections.

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

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

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

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

Late (recovery) period.

The third period - recovery begins from 3-4 weeks of illness. During this period of DFS, the function of the affected organs is gradually restored. Its pace depends on the severity and severity of SDS. The condition of the victims is gradually improving, but remains satisfactory for a long time. Body temperature normalizes. Victims are mainly concerned about pain in the area of ​​injury and limited movement in the injured limbs.

The clinical picture of the late period of DFS is dominated by 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 a gradual restoration of limb function occurs. When studying the motor chronaxy of damaged limbs, restoration of electrical excitability of the damaged nerve trunks is noted. After the edema decreases, residual effects of polyneuritis remain, leading to atrophy of individual muscles and expressed by numbness in the area of ​​​​the compressed nerve trunk, decreased tendon reflexes, limited function and trophic changes in the damaged limb. Some victims, due to the development of traumatic neuritis, experience severe pain resembling causalgic pain. They become especially intense at night and persist for a long time. The time to restore movement and sensitivity in damaged limbs depends on the degree of damage to the nerve trunks and muscles. A faster recovery of nerve function is characteristic of ischemic damage. However, 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 limitation of movements in the joints.

Under the influence of treatment, kidney function normalizes. The nitrogen excretion function of the kidneys is restored, which ensures the cleansing of the affected body from metabolic products. An improvement in the excretory function of the kidneys is indicated by an increase in the level of excretion of molecules of average mass in the urine. Partial renal dysfunction persists for a longer period of time. Some victims continue to have oliguria, which requires continued intensive treatment measures. The persistence of manifestations of acute renal failure contributes to the development of infectious complications during this period and aggravates the clinical course of DFS. At least, septic complications with progressive dystrophic and necrotic changes in damaged tissues that arise against the background of acute renal failure are the main cause of death for victims in the late period of DFS.

Among the organopathological changes, anemia, varying degrees of acute renal failure, and myocardial dystrophy are especially common during this period. As the phenomena of purulent-resorptive fever and azotemia decrease, blood counts improve, the number of red blood cells and hemoglobin increases. The ECG retains pathological changes 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 victims with DFS. As complex therapy is carried out, liver function is restored, which is confirmed by the disappearance of clinical symptoms of toxic hepatitis and the normalization of the content of enzymes, bilirubin, protein and blood coagulation parameters in the blood.

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

A decrease in the immunobiological strength of the victim’s body is clinically manifested by 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, mumps, abscess pneumonia, pleural empyema, etc., which often determines the outcome of the course of DFS. At this time, some victims develop limited skin necrosis and even gangrene of the distal segment of the limb. After rejection of necrotic areas, they become 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 DFS and purulent complications of wounds have a slow, sluggish course of the wound process, despite the use of broad-spectrum antibiotics. The low level of immunological protection in victims with DFS often leads to generalization of the purulent-septic process. Moreover, the clinical manifestations of sepsis are often overlooked because of their similarity to 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 are usually accompanied by purulent-resorptive fever, which is manifested by neutrophilic leukocytosis with an increase in band forms and ESR, an increase in the activity of creatine kinase, LDH, AST, ALT and the number of average weight molecules in the blood.

Reflections of endogenous intoxication are severe hypoproteinemia, hypocholesterolemia, hyperbilirubinemia and high ALT activity, indicating the development of toxic hepatitis. In this case, hypercoagulation is noted, although it does not reach critical values. Some victims may experience signs of toxic and degenerative damage to the liver, kidneys and myocardium, symptoms of acute coronary insufficiency, and circulatory failure. Clinical manifestations of purulent intoxication correlate with the nature of changes in laboratory parameters, reflecting the state of the liver, homeostasis system, water and electrolyte balance, and CBS.

Prolonged compression and the associated disruption of blood supply leads to the development of gangrene of the crushed limb. The question of the viability of an injured limb often presents great difficulties. The presence of edema, sharp tissue tension and subsequent compression of blood vessels, combined 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 cold weather and the absence of pulsation of the peripheral arteries on the injured limb due to spasm and compression of the vessels by edematous tissue.

Limited skin necrosis is detected 4-5 days after injury at the site of slight tissue crushing. Dead skin is rejected after 8-9 days, and 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 the fascia and muscles undergo necrosis. After the dead skin is rejected, swollen, partially dead muscles begin to protrude through the resulting defect. In these cases, a secondary infection easily occurs and extensive phlegmon occurs.

Cellulitis during prolonged compartment syndrome, with timely modern use of antibacterial therapy and the use of sulfonamide drugs, does not occur often. Often occur with the penetration of infection into damaged and crushed muscles, either from superficial infected skin abrasions and wounds, or from wounds arising in connection with skin necrosis or, finally, from wounds specifically inflicted to relieve tension in the tissues of the affected limb. The possibility of hematogenous and lymphogenous infection also cannot be excluded.

The peculiarity of these phlegmons is their extensiveness and the difficulty of diagnosis. The injured limb, even in the absence of phlegmon, appears sharply swollen and painful on palpation. Body temperature in the first days is usually elevated, regardless of complications. It is impossible to monitor changes 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 observation of the patient, when the disorders caused by long-term compression syndrome begin to subside, or rather, should have decreased, but they are still present (pain, swelling, increased body temperature).

Of greatest importance in determining the severity of clinical manifestations of long-term compartment syndrome are the degree of compression and area of ​​damage, the presence of concomitant lesions of internal organs, bones, and blood vessels. The combination of even short-term compression of the limbs with any other injury (bone fractures, traumatic brain injury, ruptures of internal organs) sharply aggravates the course of the disease and worsens the prognosis.

Intensive therapy for long-term compartment syndrome includes a number of stages.

First aid should include immobilization of the injured limb and bandaging it.

First medical aid consists of establishing infusion therapy, regardless of blood pressure levels, checking and correcting immobilization, and administering painkillers and sedatives. It is advisable to use rheopolyglucin, 5% glucose solution, and 4% sodium bicarbonate solution as the first infusion media.

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

These include:

· infusion therapy, which necessarily includes the use of fresh frozen plasma,

· low-molecular dextrans / reopolyglucin /, detoxification agents / hemodez, etc./;

· extracorporeal detoxification /plasmopheresis, hemosorption/;

· hyperbaric oxygenation to improve microcirculation and reduce the degree

· severity of hypoxia of peripheral tissues;

· hemodialysis using artificial kidney devices during acute renal failure;

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

Strict adherence to asepsis and antiseptics, quartzing of all premises is necessary,

dietary regimen /restriction of water and exclusion of fruits/ during acute kidney disease

insufficiency.

The characteristics of the therapy depend on the period of development of the disease.

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

perform a puncture of the central vein;

1. Infusion therapy in a volume of at least 2 liters per day. 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,

· detoxification drugs,

· low-molecular drugs (dextrans).

The composition of transfusion media and the volume of infusions are adjusted depending on daily diuresis, acid-base status, degree of intoxication, and surgical intervention performed. Strict monitoring of the amount of urine excreted is necessary, and, if necessary, catheterization of the bladder.

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

3. Hyperbaric oxygenation (HBO) sessions 1-2 times a day to reduce tissue hypoxia.

4. Drug therapy:

Stimulation of diuresis by prescribing diuretics (up to 80 mg of Lasix per day, aminophylline),

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

To prevent thrombosis and disseminated intravascular coagulation, heparin is prescribed at a dose of 2500 units subcutaneously 4 times a day,

Antibacterial therapy for the prevention of purulent complications,

Cardiovascular drugs according to indications.

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

1st degree - slight indurative swelling of soft tissues and their tension. The skin is pale, at the border of the lesion it bulges somewhat above the healthy skin. There are no signs of circulatory disorders. Conservative treatment is indicated, which gives a beneficial effect.

2nd degree - moderately expressed indurative swelling of soft tissues and their tension. The skin is pale, with areas of slight cyanosis. 24-36 hours after the compression is released, bubbles with transparent yellowish contents may form - conflicts, upon removal of which a moist, pale pink surface is revealed. Increased swelling in the following days indicates a violation of venous circulation and lymph flow. Insufficiently adequate conservative treatment can lead to progression of microcirculation disorders, microthrombosis, increased edema and compression of muscle tissue.

3rd degree - pronounced indurative swelling and tension of soft tissues. The skin is cyanotic or “marbled” in appearance. Skin temperature decreases noticeably. 12-24 hours after the compression is released, blisters with hemorrhagic contents appear. Under the epidermis, a moist, dark red surface is exposed. Indurative edema and cyanosis rapidly increase, which indicates severe microcirculation disorders and venous thrombosis. Conservative treatment in this case is not effective and leads to a necrotic process. It is necessary to make wide strip incisions with dissection of the fascial sheaths to eliminate tissue compression and restore blood flow. The resulting abundant wound plasma loss reduces the degree of intoxication.

4th degree - indurative edema is moderately expressed, but the tissues are sharply tense. The skin is bluish-purple in color and cold. On the surface of the skin there are epidermal blisters with hemorrhagic contents. After removal of the epidermis, a cyanotic-black, dry surface is exposed. In the following days, the swelling practically does not increase, which indicates a deep disturbance of microcirculation, insufficiency of arterial blood flow, and widespread thrombosis of the venous vessels.

Wide fasciotomy in these cases ensures the maximum possible restoration of blood circulation, allows limiting the necrotic process in more distal sections, and reduces the intensity of absorption of toxic products. If necessary, amputation is performed in 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. When diuresis decreases to 600 ml per day, hemodialysis is performed, regardless of the level of nitrogenous waste in the blood. Emergency indications for hemodialysis are anuria, hyperkalemia more than 6 mmol/l, pulmonary edema, cerebral edema.

Infusion therapy during 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 long-term compression syndrome, the task of treating local manifestations and purulent complications comes to the fore. Particular 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 classic purulent infection.

Thus, intensive therapy of long-term compartment syndrome requires the active work of a team of doctors - surgeons, anesthesiologists, therapists, nephrologists, traumatologists, each of whom at a certain stage becomes a leader.

Positional compression syndrome.

Positional compression syndrome is one of the “everyday” varieties of long-term compression syndrome, but unlike the latter, it has a number of specific features relating to etiology and pathogenesis, clinical course and treatment tactics. For the development of this disease, a combination of several factors is necessary. On the one hand, it is necessary for the patient to remain in a comatose state for a long time or in a state of deep pathological sleep, which is most often caused by poisoning with alcohol or its surrogates, drugs, carbon dioxide or exhaust fumes. On the other hand, a necessary condition for the development of positional compression syndrome is injury to soft tissues, most often the limbs, caused by positional compression by body weight during a long stay of the victim in an uncomfortable position with compressed or bent limbs tucked under him, or when a limb hangs for a long time over the edge of some any hard 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 monoxide, etc.) leads to severe disturbances of homeostasis, with disruption of water-electrolyte balance, acid-base balance, disruption of macro- and microcirculation, often with the development of collapse. Quite often this comatose state is accompanied by general hypothermia of the body. A prolonged comatose state and positional compression of tissues leads to both local changes in the compressed tissues and general intoxication.

Local changes are characterized by:

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

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

neuritis), disruption of vital functions 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 developing:

1. Disorder of the central nervous system function of neurohumoral origin.

2. Circulatory disorders, hypotension, microcirculation disorders.

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

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

5. Development of myoglobinemia, myoglobinuria.

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

Clinical picture.

The clinical course of positional compression syndrome is divided into 4 periods:

1. Acute period. Comatose state developing 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 recovery from a coma).

3. Intermediate 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 specific to the substances that caused the poisoning are observed.

In the second period of the disease, upon the return of consciousness and an attempt to change position, patients feel a “numbness of the stiff” 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 that have been subjected to compression. Upon examination, in places of compression there are delimited hyperemic areas of skin, sometimes with a purplish-blue tint. Herpetic rashes, abrasions, macerations, and hematomas are often found on the skin.

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

Subsequently, as blood circulation in the compressed tissues is restored, rapid development of edema is noted. As swelling increases, the skin becomes pale, cold, and shiny. The tissues are sharply tense, densely elastic, and in places woody in consistency, sharply painful on palpation, which is caused by the tension of the facial sheaths due to a sharp swelling of the muscles, subcutaneous fatty tissue and an increase in the volume of the affected muscles. With severe swelling, the pulsation of the arteries in the distal limbs is either absent or sharply weakened, movements in the joints of the 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.

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

Myoglobinemia is determined. Following myoglobinemia, myoglobinuria appears. Urine contains protein, leukocytes, red blood cells, and casts. Oligouria gradually develops and the disease moves into the third period.

Distinctive features of SPS from long-term compartment syndrome are:

Exotoxic poisoning and coma in the acute period;

No 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 of long-term compartment syndrome.

Treatment of positional compartment syndrome follows the same principles as long-term compartment syndrome. In the acute period, coma caused by exogenous intoxication and its complications is treated.

Appendix 1.

Summary of the main signs of compartment syndrome.

Signs	Early period	Interim period	Late period
General condition	Heavy, lethargy, indifference, lethargy	What is satisfactory then gradually becomes difficult; drowsiness, sometimes on the contrary - excitement, delirium (at the end of the period)	Satisfactory
Consciousness	Saved	Preserved, in severe cases lost, delirium.	Saved
Pulse	100-120 beats per minute or more, sometimes arrhythmic, barely noticeable	Normal frequency. At the height of uremia, 100-120 per minute, satisfactory filling.	Normal frequency (increased with complications).
Blood pressure	Low to 80-60 mmHg.	Normal, often elevated (up to 140-160 mmHg)	Normal or slightly increased.
Temperature	Normal, or reduced to 35º.	Increased to 38-39º.	Normal.
Nausea, vomiting	Common (early appearance).	As a rule, (late vomiting) is observed with increasing uremia	No.
Changes in urine	Oliguria, rarely anuria; low pH, high sp. Weight, Albuminuria, myoglobinuria, microhematoma riya. Cylindruria (grainy and hyaline).	Oliguria to complete anuria. Urine is acidic. Low specific gravity Albuminuria, less pronounced. Myoglobinuria. The cylinders are hyaline, granular, pigmented.	Norm. Sometimes there are traces of protein, some red blood cells and food casts in the preparation.
Blood counts	Significantly higher than normal	Below normal, less often normal.	Norm
Hemoglobin	Above normal (up to 120-150%)	Normal, often below normal.	Normal or below normal
Red blood cells	An increase in their number by 1-2 million above the norm	Normal, often below normal	Norm. On the 20–30th day, secondary anemia
Leukocytes	Moderate non-centrophilic leukocytosis. Lymphatic singing.	Same	The formula has not been changed
Biochemical blood test	Increased content: residual nitrogen, urea, phosphorus, protein, creatinine, bilirubin. Reducing the amount of: chlorides, reserve alkalinity.	A sharp increase in the content of residual nitrogen, urea, phosphorus, creatinine. Further decline in reserve alkalinity	No

Changes in the injured limb

Signs	Early period	Interim period	Late period
Skin coloring	Crimson-bluish coloration in the compression zone	Crimson-bluish, unevenly spotted color.	The purple-bluish color disappears.
Swelling crushed limbs	Sharply expressed.	Sharply expressed at the beginning, decreases at the end of the period.	No.
Presence of bubbles	Bubbles appear filled with hemorrhagic or serous fluid.	Bubbles in the zone of greatest compression.	Usually not.
Temperature of the affected limb	Cold to the touch.	Warm, sometimes remains cold.	Warm.
Pulsation of peripheral vessels	Absent or barely noticeable.	Not always determined.	Normal or slightly weakened.
Movements	Severely limited or impossible.	Paralysis, limitation of movements.	Same. Gradual recovery.

G., allowed not only to develop new approaches to the provision of surgical and resuscitation care for this pathology, but also to develop a new classification of the syndrome (Table 2). Table 1. Frequency of development of long-term compression syndrome during earthquakes Place of earthquake, year, author Number of victims Frequency of SDS, % Ashgabat, 1948 (M.I. Kuzin) 114 3.8 Morocco, 1960 ...

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