Long-term compartment syndrome treatment principles. Long-term compartment syndrome, cause, symptoms, first aid

Synonyms: traumatic toxicosis, crash syndrome, crush syndrome, myorenal syndrome, “release” syndrome.

Long-term crush syndrome - a specific type of injury associated with massive long-term crushing of soft tissues or compression of the main vascular trunks of the extremities, characterized by a severe clinical course and high mortality. It occurs in 20-30% of cases of emergency destruction of buildings, during earthquakes, rock falls and in mines.

The leading factors in the pathogenesis of SDS are: traumatic toxemia, plasma loss and painful irritation. The first factor arises due to the entry of breakdown products of damaged cells into the bloodstream, which causes intravascular coagulation. Plasma loss results from significant swelling of the extremities. The pain factor disrupts the coordination of excitation and inhibition processes in the central nervous system.

Prolonged compression leads to ischemia and venous stagnation of the entire limb or its segment. Nerve trunks are injured. Mechanical destruction of tissue occurs with the formation of a large number of toxic products of cell metabolism, primarily myoglobin. Metabolic acidosis in combination with myoglobin leads to intravascular coagulation, while the filtration ability of the kidneys is blocked. The final stage of this process is acute renal failure, expressed differently in different periods diseases. Toxemia is aggravated by hyperkalemia (up to 7-12 mmol/l), as well as histamine, protein breakdown products, creatinine, phosphorus, adenylic acid, etc., coming from damaged muscles.

As a result of plasma loss, blood thickening develops and massive swelling of damaged tissues appears. Plasma loss can reach 30% of circulating blood volume.

Clinic and diagnostics. The course of long-term compartment syndrome can be divided into three periods.

Iperiod(initial or early), the first 2 days after release from compression. This time is characterized as a period of local changes and endogenous intoxication. The clinical manifestations of traumatic shock predominate: severe pain, psycho-emotional stress, hemodynamic instability, hemoconcentration, creatinemia; in the urine - proteinuria and cylinuria. After conservative and surgical treatment, the patient’s condition stabilizes in the form of a short clear interval, after which the patient’s condition worsens and the next period develops.

II period - acute period renal failure. Lasts from 3rd to 8-12th day. Swelling of the injured limb increases, blisters and hemorrhages appear on the skin. Hemoconcentration gives way to hemodilution, anemia increases, diuresis drops sharply down to anuria. Maximum hyperkalemia and hypercreatinemia. Despite intensive therapy, mortality reaches 35%.

III period - restorative, starts at 3-4 weeks. Kidney function, protein content and blood electrolytes are normalized. Infectious complications come to the fore, and the development of sepsis is possible.

According to the severity of the course of SDS, they are divided into 4 degrees. The gradation is based on the duration of compression of the limb: mild degree - compression up to 4 hours, average - up to 6 o'clock, heavy - until 8 o'clock and extremely severe degree - compression of one or both limbs with exposure over 8 hours.

Summarizing the experience of monitoring victims during the earthquake in Armenia, clinicians came to the conclusion that the severity of the clinical manifestations of SDS primarily depends on the degree of compression, the area of ​​the lesion and the presence of concomitant injuries. A combination of short-term compression of a limb with bone fractures, traumatic brain injury, damage internal organs sharply worsen the course of the traumatic disease and worsen the prognosis.

First aid. After the compression is removed, the limb is bandaged, immobilized, cold is applied, and painkillers and sedatives are prescribed. If a limb is compressed for more than 10 hours and there is doubt about its viability, a tourniquet should be applied according to the level of compression.

First aid consists of correcting or performing manipulations that were not performed at the first stage, and establishing infusion therapy (regardless of hemodynamic parameters). For infusion, rheopolyglucin, 5% glucose solution or 4% sodium bicarbonate solution are desirable.

Treatment. Therapy should be comprehensive and include:

1. Infusion therapy with infusion of fresh frozen plasma up to 1 liter per day, rheopolyglucin, detoxification agents (neohemodez, neocompensan, disol). Plasmapheresis with extraction of up to 1.5 liters of plasma in one procedure.

2. Hyperbaric oxygen therapy to reduce hypoxia of peripheral tissues.

3. Early application of arteriovenous shunt, hemodialysis, hemophilic filtration - daily during the period of acute renal failure.

4. Fasciotomy (“lamp incisions”), necrectomy, amputation - according to strict indications.

5. Sorption therapy - enterodesis orally, locally after operations - carbon tissue AUG-M.

6. Strict adherence to asepsis and antiseptics.

7. Dietary regimen - limiting water and excluding fruits during the period of acute renal failure.

The specific treatment for each patient depends on the stage of care and the clinical period of the compartment syndrome.

Treatment inIperiod (endogenous intoxication and local changes). Catheterization of a large vein, determination of blood group and Rh factor. Infusion and transfusion therapy of at least 2000 ml per day. Of these: fresh frozen plasma 500-700 ml, 5% glucose up to 1000 ml with vitamins C and B, albumin 5-10% 200 ml, 4% sodium bicarbonate solution 400 ml, glucosone-caine mixture 400 ml. The quantity and quality of transfusion agents are determined by the patient’s condition, laboratory parameters and diuresis. Strict recording of urine excretion is required.

HBO therapy sessions 1-2 times a day.

Plasmapheresis is indicated for obvious signs intoxication, exposure to compression for more than 4 hours, pronounced local changes in the injured limb.

Drug therapy: lasix up to 80 mg per day, aminophylline 2.4% 10 ml (stimulation of diuresis); heparin 2.5 thousand under the skin of the abdomen 4 times a day; chimes or trental, retabolil 1.0 times every 4 days; cardiovascular drugs, antibiotics.

Surgical treatment depends on the condition and degree of ischemia of the injured limb.

I degree - minor indurative edema. The skin is pale, rises above the healthy skin at the border of compression. Conservative treatment is effective.

II degree - moderate swelling of tissues and their tension. The skin is pale with areas of cyanosis. There may be bubbles with transparent yellowish contents, underneath them there is a moist pink surface.

III degree - pronounced indurative swelling and tissue tension. The skin is bluish or “marbled”, its temperature is reduced. After 12-24 hours, blisters with hemorrhagic contents appear, underneath them there is a moist dark red surface. Signs of microcirculation disorders are progressively increasing. Conservative therapy is not effective and leads to necrosis. Lamp incisions with dissection of the fascial sheaths are shown.

IV degree - moderate swelling, tissues are sharply tense. The skin is bluish-purple, cold. Bubbles with hemorrhagic contents, underneath them there is a bluish-black dry surface. Subsequently, the swelling does not increase, which indicates deep circulatory disorders. Conservative treatment is not effective. Wide fasciotomy 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. In case of subsequent amputation, its level will be significantly lower.

After surgical treatment, the volume of infusion therapy per day increases to 30,004,000 ml, which includes up to 1000 ml of fresh frozen plasma, 500 ml of 10% albumin. HBO therapy 2-3 times a day. Detoxification - infusion of neohemodesis up to 400 ml, administration of enterodesis and activated carbon. Coal fabric AUG-M is used topically. Culture of microflora for sensitivity to antibiotics.

Treatment duringIIperiod (acute renal failure). Limiting fluid intake. Hemodialysis is indicated when diuresis is reduced to 600 ml per day. Emergency indications for it are anuria, hyperkalemia more than 6 mmol/l, pulmonary and cerebral edema. In case of severe hyperhydration, hemofiltration is indicated for 4-5 hours with a fluid deficit of 1-2 liters.

During the interdialytic period, infusion therapy with the same drugs as in the first period with a total volume of 1.2-1.5 liters per day, and in the presence of surgical interventions - up to 2 liters per day.

With timely and adequate treatment, renal failure is stopped by 10-12 days.

Treatment inIIIperiod consists of treating local manifestations of SDS, purulent complications and preventing sepsis. Treatment of infectious complications is carried out according to the general laws of purulent surgery.

LONG-TERM COMPRESSION SYNDROME.

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

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

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

He noticed that when a horse was killed under a cuirassier, a horseman clad in metal armor, and he could not get out from under it on his own, after the battle and the release of his crushed lower limbs, he died quite quickly, although he had no injuries.

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

PATHOGENESIS.

The leading pathogenetic factors of long-term compartment syndrome (PCS) are: traumatic toxemia, which develops due to the entry into the bloodstream of decay products of damaged cells that trigger intravascular coagulation; plasma loss as a result of severe edema of injured limbs; painful irritation leading to discoordination of the process of excitation and inhibition in the central nervous system.

The result of prolonged compression of the limbs is the occurrence of ischemia of the entire limb or its segment in combination with venous stagnation. Nerve trunks are also injured. Mechanical destruction of tissue occurs with the formation of a large number of toxic products of cell metabolism, primarily myoglobin. The combination of arterial insufficiency and venous congestion aggravates the severity of limb ischemia. Developing metabolic acidosis in combination with myoglobin entering the circulation leads to blockade of the kidney tubules, impairing their reabsorption capacity. 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 histamine, protein breakdown products, adenylic acid, creatinine, phosphorus, etc., coming from damaged muscles.

Already in the early period of DFS, blood thickening is observed as a result of plasma loss, and massive swelling of damaged tissues develops. In severe cases, plasma loss reaches 1/3 of the circulating blood volume.

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

CLASSIFICATION.

By type of compression:

crushing,

compression (direct, positional).

By localization:

isolated (one anatomical area),

multiple,

combined (with fractures, vascular damage, nerves, traumatic brain injury).

By severity:

I Art. – mild (compression up to 4 hours),

II Art. – medium (compression up to 6 o’clock),

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

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

I degree – minor indurative swelling of soft tissues. The skin is pale and at the border of the lesion bulges slightly above the healthy skin. There are no signs of circulatory problems.

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

III degree – pronounced indurative swelling and tension of soft tissues. The skin is cyanotic or “marbled” in appearance. Skin temperature is noticeably reduced. After 12-24 hours, blisters with hemorrhagic contents appear. Under the epidermis, a moist, dark red surface is exposed. Indurative edema and cyanosis quickly increase, which indicates gross disturbances of microcirculation, vein thrombosis, leading to a necrotic process.

IV degree – indurative edema is moderately expressed, the tissues are sharply tense. The skin is bluish-purple in color and cold. Individual 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 deep microcirculation disorders, insufficiency of arterial blood flow, and widespread thrombosis of venous vessels.

I period – early (period of shock) – up to 48 hours after release from compression. This period can be characterized as a period of local changes and endogenous intoxication. At this time, the clinical manifestations of the disease are dominated by manifestations of traumatic shock: severe pain, psycho-emotional stress, hemodynamic instability, hemoconcentration, creatininemia; in the urine - proteinuria and cylindruria. After stabilization of the patient’s condition as a result of therapeutic and surgical treatment, a short clear period begins, after which the patient’s condition worsens and the second period of DDS develops - the period of acute renal failure. Lasts from 3-4 to 8-12 days. Swelling of the extremities, freed from compression, increases; blisters and hemorrhages are found on damaged skin. Hemoconcentration gives way to hemodilution, anemia increases, and diuresis sharply decreases down to anuria. Hyperkalemia and hypercreatininemia reach the highest numbers. Mortality in this period can reach 35%, despite intensive therapy.

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

At the same time, the experience of disaster medicine has shown that highest value In determining the severity of clinical manifestations of DFS, the degree of compression and area of ​​damage, the presence of concomitant damage to the internal organs of 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.

The scope of treatment measures for SDS is determined by the severity of the victim’s condition.

One of the first pre-hospital necessary measures should be the application of a rubber tourniquet to the compressed limb, its immobilization, and the administration of narcotic analgesics (promedol, omnapon, morphine, morphilong) to relieve shock and emotional stress.

I period. After release from compression, it is necessary to carry out infusion (anti-shock and detoxification) therapy, including intravenous administration of fresh frozen plasma (up to 1 liter per day), polyglucin, reopolyglucin, administration saline solutions(acesol, disol), detoxification blood substitutes – hemodez, neohemodez, neocompensan. The sorbent – ​​enterodesis – is applied orally.

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

II period. Infusion-transfusion therapy (volume of at least 2000 ml per day, transfusion media includes fresh frozen plasma 500-700 ml, 5% glucose with vitamins C and group B up to 1000 ml, albumin 5%-10% - 200 ml, 4% sodium bicarbonate solution - 400 ml, glucose-novocaine mixture 400 ml). The composition of transfusion media and the volume of infusions are adjusted depending on daily diuresis, acid-base balance data, degree of intoxication, and surgical procedures performed. Strict recording of the amount of urine excreted; if necessary - catheterization Bladder.

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

Hyperbaric oxygenation sessions – 1-2 times a day to reduce the degree of tissue hypoxia.

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

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

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

CHAPTER 9 LONG-TERM COMPRESSION SYNDROME

The first descriptions of the SDS clinic for earthquake victims date back to the beginning of the 20th century. During the Second World War E. Byuo-ters presented detailed description specific pathology in the wounded recovered from the ruins after the bombing of London, calling it “crash syndrome” (from English word“crush” - crush, crush). In our country, the most famous researchers of SDS were AND I. Pytel(observations of the wounded during the bombing of Stalingrad), M.I. Kuzin(earthquake in Ashgabat 1948), E. A. N echaev, G. G. Savitskiy(earthquake in Armenia 1988).

9.1. TERMINOLOGY, PATHOGENESIS

AND CLASSIFICATION OF THE SYNDROME

PROLONGED COMPRESSION

Complex of specific pathological disorders, developing after the release of the wounded from the rubble, where they long time(for 1 hour or more) were crushed by heavy debris, called long-term compartment syndrome. The emergence of SDS, which is described under different names (long-term crush syndrome, crush syndrome, traumatic toxicosis, traumatic rhabdomyolysis etc.), is associated with the resumption of blood circulation in damaged and long-term ischemic tissues. In a large-scale war, the frequency of development of SDS can reach 5-20%.

In wounded people with SDS, damage to the extremities is mainly observed (more than 90% of cases), because Compression of the head and torso due to damage to internal organs is often fatal.

In injury surgery, in addition to SDS, there is also positional compression syndrome as a result of ischemia of body parts (limb, shoulder blade area, buttocks, etc.) from prolonged compression by the victim’s own weight lying in one position (coma, alcohol intoxication). Recirculation syndrome develops after restoration of a damaged artery in a long-term ischemic limb or removal of a long-term tourniquet.

basis pathogenesis above similar pathological conditions is endogenous intoxication by products of tissue ischemia and reperfusion . In compressed tissues, along with areas of direct traumatic necrosis, ischemic zones are formed, where acidic products of anaerobic metabolism accumulate. After the wounded are released from compression, blood and lymph circulation is resumed in ischemic tissues, characterized by increased capillary permeability. This is called tissue reperfusion. Wherein toxic substances

(myoglobin, products of impaired lipid peroxidation, potassium, phosphorus, polypeptides, tissue enzymes - histamine, bradykinin, etc.) enter the general bloodstream. Happening toxic damage internal organs

, primarily the lungs, with the formation of ARF. Hyperkalemia may lead to acute disorder

heart activity. Under-oxidized products of anaerobic metabolism (lactic acid, etc.) are also washed out from ischemic tissues, which cause pronounced metabolic.

acidosis The most dangerous is release into the blood from ischemic striated muscles large quantities squirrel. Myoglobin is freely filtered in the renal glomeruli, but clogs the renal tubules, forming insoluble hematin hydrochloride under conditions of metabolic acidosis (if the urine pH is greater than 6, the likelihood of developing renal failure in DFS is reduced). In addition, myoglobin has a direct toxic effect on the epithelium of the renal tubules, which together leads to myoglobinuric nephrosis and acute renal failure

(OP N). Rapidly developing post-ischemic edema of damaged and long-term compressed tissues causes acute hypovolemia

In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable

oliguria stops after a few days. The prognosis for mild DFS with proper treatment is favorable. SDS medium degree

develops with larger areas of compression of the limb for up to 6 hours. It is accompanied by endotoxicosis and impaired renal function for a week or more after the injury. The prognosis of moderate SDS is determined by the timing and quality of first aid, as well as subsequent treatment with the early use of extracorporeal detoxification. Severe SDS

develops when one or two limbs are compressed for more than 6 hours. With severe DFS, endogenous intoxication quickly increases, acute renal failure, MODS and other life-threatening complications develop. In the absence of timely intensive treatment using hemodialysis, the prognosis is unfavorable. It should be noted that full compliance with the severity of vital function disorders important organs Mild DFS with untimely or inadequate medical care can lead to anuria or other fatal complications. On the other hand, with very long periods of compression of the extremities (more than 2-3 days), DFS may not develop due to the lack of restoration of blood circulation in necrotic tissues.

9.2. PERIODIZATION, CLINICAL SYMPTOMATICS OF LONG-TERM COMPRESSION SYNDROME

Early, intermediate and late periods of the course of SDS are distinguished (Table 9.2).

Table 9.2. Periodization of long-term compartment syndrome

9.2.1. Early period of compartment syndrome

Clinic early period(1-3 days) varies significantly among different wounded people. With moderate and severe SDS, after release from compression, a picture of traumatic shock may develop: general weakness, pallor, arterial hypotension and tachycardia.

Violations are recorded due to hyperkalemia heart rate(sometimes to the point of cardiac arrest). In the next 1-2 days clinical picture manifests itself as instability in the respiratory and circulatory systems. With severe DFS, symptoms develop already in the first days acute renal failure and swelling of the lungs x(the earlier signs of anuria appear, the more dangerous they are prognostically).

In other cases general state initially satisfactory. In the absence of severe craniocerebral injuries, consciousness in all wounded patients with SDS is, as a rule, preserved.

The wounded, freed from the rubble, complain of severe pain in an injured limb that swells quickly. The skin of the limb becomes tense, pale or bluish, cold to the touch, and blisters appear. The pulsation of peripheral arteries may not be detected due to edema, sensitivity and active movements are reduced or absent. More than half of the wounded with SDS also have fractures of the bones of the compressed limbs, Clinical signs which may complicate the early diagnosis of DFS.

Due to severe edema, tissue pressure in the muscles of the limbs, enclosed in dense osteofascial sheaths, can exceed the perfusion pressure in the capillaries (40 mm Hg) with further deepening of ischemia. This pathological condition, which can occur not only with SDS, is designated by the term compartment syndrome (from the English “compartment” - sheath, vagina) or the syndrome of “increased intrasheath pressure”.

In the majority of wounded people with moderate and mild SDS, with prompt medical care, the general condition is temporarily stabilized (“bright period” of SDS).

Laboratory research blood reveals signs of hemoconcentration (increased hemoglobin numbers, hematocrit, decreased BCC and CV), pronounced electrolyte disturbances (increased potassium and phosphorus content), increased levels of creatinine, urea, bilirubin, glucose. Hyperfermentemia, hypoproteinemia, hypocalcemia, and metabolic acidosis are noted. There may be no changes in the first portions of urine, but then due to the release of myoglobin urine turns brown, is characterized by a high relative density with a pronounced shift in pH to the acidic side. Also detected in urine a large number of protein, erythrocytes, leukocytes, cylinders.

9.2.2. Intermediate period of long-term compartment syndrome

In the intermediate period of SDS (4-20 days) symptoms of endotoxemia and acute renal failure come to the fore. After short-term stabilization, the condition of the wounded worsens, and signs of toxic encephalopathy (profound stupor, stupor) appear.

For severe DFS dysfunction of vital organs increases rapidly. The development of acute renal failure is signaled by oligonuria (a decrease in the rate of hourly diuresis of less than 50 ml/h). Anuria can last up to 2-3 weeks with a transition in favorable cases to the polyuric phase of acute renal failure. Due to overhydration, overload of the pulmonary circulation is possible, up to pulmonary edema. Cerebral edema, toxic myocarditis, disseminated intravascular coagulation syndrome, intestinal paresis, persistent toxic anemia, and immunosuppression develop.

SDS of moderate and mild severity characterized mainly by signs of oligoanuria, endotoxemia and local manifestations.

Swelling of the injured limbs persists or increases even more. In the muscles of the compressed limbs, as well as in areas of positional compression, foci of progressive secondary necrosis are formed, supporting endogenous intoxication. In ischemic tissues, infectious (especially anaerobic) complications often develop, prone to generalization.

Laboratory research with the development of oligoanuria, a significant increase in creatinine and urea is detected. Hyperkalemia, uncompensated metabolic acidosis, and severe anemia are noted. Under microscopy, urine sediment reveals cylindrical formations consisting of desquamated tubular epithelium, myoglobin and hematin crystals.

9.2.3. Late period of long-term compartment syndrome In the late (recovery) period of SDS - after 4 weeks and up to

up to 2-3 months after compression - in favorable cases, there is a gradual improvement in the general condition of the wounded. There is a slow restoration of the functions of the affected internal organs (kidneys, liver, lungs, heart, etc.). However, toxic and dystrophic disorders in them, as well as severe immunosuppression, can persist for a long time. The main threat to the life of the wounded with SDS during this period is generalized IO.

Local changes are expressed in long-term non-healing purulent and purulent-necrotic wounds of the extremities. The functional outcomes of treatment of limb injuries with DFS are often unsatisfactory: atrophy and connective tissue degeneration of muscles, joint contractures, and ischemic neuritis develop.

Examples of diagnosis of SDS:

1. Severe DFS of both lower extremities. Terminal state.

2. SDS of moderate degree in the left upper limb.

3. Severe SDS of the right lower limb. Gangrene of the right leg and foot. Traumatic shock III degree.

9.3. ASSISTANCE AT THE STAGES OF MEDICAL EVACUATION

First and first aid. The content of first aid to the wounded during SDS can vary significantly depending on the conditions of its provision, as well as on the forces and means of the medical service involved.

On the battlefield the wounded, pulled out of the rubble, are taken to a safe place. Orderlies or the military personnel themselves, in the form of mutual assistance, apply aseptic dressings to wounds (accidents) formed by compression of the limbs. In case of external bleeding, it is stopped (pressure bandage, tourniquet). Anesthetic is administered from a syringe tube (1 ml of 2% pro-medol solution), transport immobilization with improvised means. If consciousness is preserved and there are no abdominal injuries, the wounded are provided with plenty of fluids.

First aid for the wounded with suspected SDS in mandatory provides for intravenous administration of crystalloid solutions (0.9% sodium chloride solution, 5% glucose solution, etc.), which, if possible, continues during further evacuation. The paramedic corrects mistakes made during first aid, bandages wet bandages, and improves transport immobilization. In case of severe swelling, shoes are removed from the injured limb and uniforms are cut off. Give plenty of fluids.

In case of organizing assistance to the wounded outside the zone of direct enemy influence(removal of rubble after bombings, earthquakes or terrorist attacks), medical assistance is provided directly at the site of injury by medical and nursing teams. Depending on the training and equipment, such teams carry out urgent measures first medical and even qualified resuscitation care.

For the wounded released from the rubble, intravenous administration of crystalloid solutions is immediately established in order to eliminate blood plasma loss (it is even better to start infusion therapy before liberation from the rubble). If the development of DFS is suspected, 4% sodium bicarbonate 200 ml is administered intravenously (“blind correction of acidosis”) to eliminate acidosis and alkalinization of urine, which prevents the formation of hematin hydrochloride and blockage of the renal tubules. Also, 10 ml of 10% calcium chloride solution is injected intravenously to neutralize toxic effect potassium ions on the heart muscle. In order to stabilize cell membranes, they are introduced large doses glucocorticoids. Painkillers are administered and sedatives, symptomatic therapy.

Before freeing the wounded from the rubble (or immediately after extraction), rescuers apply a tourniquet above the area of ​​compression of the limb to prevent the development of collapse or cardiac arrest from hyperkalemia. Immediately after this, the wounded person is removed to assess the viability of the compressed area of ​​the limb by a doctor.

The tourniquet is left on the limb (or applied if it has not been applied previously) in following cases:

limb destruction(extensive soft tissue damage to more than half the circumference of the limb, bone fracture, damage to great vessels); limb gangrene(distal to the demarcation line the limb is pale or with blue spots, cold, with wrinkled skin or desquamated epidermis; Sensitivity and passive movements in the distal joints are completely absent). For the rest of the wounded, aseptic stickers are attached to the wounds of the extremities with adhesive tape (circular bandages can compress the limb and impair blood circulation), and transport immobilization is performed.

If possible, priority evacuation (preferably by helicopter) is provided for all wounded with SDS directly to the stage of providing specialized medical care.

First medical aid. Upon admission to the medical center (med), the wounded with signs of SDS are sent to the dressing room first.

1000-1500 ml of crystalloid solutions, 200 ml of 4% sodium bicarbonate solution, 10 ml of 10% calcium chloride solution are administered intravenously. The bladder is catheterized, the color and amount of urine are assessed, and diuresis is monitored.

A long-term compressed limb is examined. If available destruction or gangrene- a tourniquet is applied. If in these cases the tourniquet was applied earlier, it is not removed.

In the rest of the wounded with SDS, against the background of infusion therapy, administration of cardiovascular and antihistamines the tourniquet is removed, novocaine blockade(conductive or cross-sectional type above the compression area), transport immobilization.

Cooling of the injured limb is provided (ice packs, cryopacks). If the condition of the wounded allows, an alkaline-salt drink is given (made at the rate of a teaspoon baking soda and table salt per 1 liter of water). Urgent evacuation, preferably by helicopter, preferably immediately to the stage of providing specialized medical care, where there are conditions for use modern methods extracorporeal detoxification.

Qualified medical care. In armed conflict

with established aeromedical evacuation of the wounded from medical companies directly to the 1st echelon MVG, when delivering the wounded from the SDS to the Omedb (Omedo Special Forces) - they only carry out pre-evacuation preparation in the scope of first medical aid. CCP is provided only for health reasons.

In conditions of large-scale war or when the evacuation of the wounded is disrupted The medical hospital (omedo) provides clinical and clinical care. Already during selective triage, the wounded with SDS are first of all sent to the intensive care ward for the wounded in order to assess their condition and identify life-threatening consequences.

In the event of massive sanitary losses, a number of wounded with severe SDS, unstable hemodynamics and severe endotoxemia (coma, pulmonary edema, oligoanuria) can be classified as agonizing.

In the intensive care ward To compensate for plasma loss, crystalloids (do not inject potassium!) and low-molecular colloid solutions are administered intravenously, while stimulating urination with Lasix and maintaining diuresis of at least 300 ml/h. For every 500 ml of blood substitutes, in order to eliminate acidosis, 100 ml of 4% sodium bicarbonate solution is administered to achieve a urine pH of at least 6.5. With the development of oliguria, the volume of infusion therapy is limited according to the amount of urine excreted. A 10% calcium chloride solution, glucocorticoids, painkillers and sedatives are administered.

In case of DFS, the administration of nephrotoxic antibiotics is contraindicated: aminoglycosides (streptomycin, kanamycin) and tetracyclines. Non-toxic antibiotics (penicillins, cephalosporins, chloramphenicol) are administered in half doses and only for the treatment of developed wound infections (but not for prophylactic purposes).

After stabilization of hemodynamic parameters, the wounded with SDS are examined in the dressing room for the seriously wounded(Table 9.3).

For signs of compartment syndrome(intense swelling of the limb with the absence of pulsation of the peripheral arteries, coldness of the skin, decreased or absent sensitivity and active movements) is indicated wide open fasciotomy . Indications for fasciotomy for SDS should not be expanded, because incisions are the gateway to wound infection. In the absence of signs of compartment syndrome, dynamic monitoring of the condition of the limb is carried out.

Fasciotomy is performed from 2-3 longitudinal skin incisions (above each osteofascial sheath) at least 10-15 cm long with dissection of dense fascial plates with long scissors throughout the entire segment of the limb. Wounds after fasciotomy are not sutured, because with significant tissue edema, this can impair blood circulation, and they are covered with napkins with water-soluble ointment. Immobilization is carried out with plaster splints.

“Lampas” incisions to the bone along the lateral surface of the limb or “subcutaneous” fasciotomy from small incisions are not used for DFS.

If necrosis of individual muscles or muscle groups of the limb is detected during wound inspection, their excision is performed - necrectomy .

Non-viable limbs with signs of dryness or wet gangrene, as well as ischemic necrosis (muscle contracture, complete lack of sensitivity), after a diagnostic dissection

Table 9.3. Surgical tactics for DFS

skin lesions (muscles are dark or, conversely, discolored, yellowish, do not contract or bleed when cut) - are subject to amputation.

Amputation with SDS is performed above the level of the compression boundary, within healthy tissues. When a tourniquet is applied, amputation is performed over the tourniquet. Side slits on the limb stump being formed, they are used to control the viability of the overlying tissues. Wide subcutaneous fasciotomy of the limb stump is required.

Primary sutures are not applied to the skin of the stump due to the threat of anaerobic infection and the high probability of the formation of new foci of necrosis.

If there is doubt about the non-viability of a limb, a relative indication for urgent amputation may be an increase in endotoxicosis and oligoanuria. Injured with SDS of any severity, due to the real threat of acute renal failure and the need to carry out specific methods detoxification, urgent evacuation is indicated. It is preferable to evacuate such wounded people to the stage of providing SCP by air

, with mandatory continuation of intensive care during the flight. Specialized medical care wounded with SDS in the absence of surge arrester turns out.

in a general surgical hospital As a result of the impact on After a few hours of heavy objects, a person begins to develop long-term compression syndrome. IN medical practice This condition has several definitions: crash syndrome, traumatic toxicosis, positional syndrome or compression syndrome.

Long-term compression syndrome, for which first aid is of paramount importance, appears in people who have been in the area of ​​earthquakes, rubble, collapses, and car accidents.

Also distinguished positional compression, which develops due to a person’s prolonged exposure to pressure or gravity own body in a state of sleep or unconsciousness. Most often, this condition occurs as a result of taking alcohol or drugs, when a person cannot control the level of danger.

A characteristic feature of SDS is the development pathological changes after removing the heaviness from the patient’s body. At this moment, active restoration of the stopped blood flow begins, in which tissue breakdown products have already accumulated.

Clinic and its manifestations

In case of long-term compression syndrome, the main criterion for the development of pathology is mass destruction muscle tissue, which occurs for the following reasons:

• Damage and subsequent cell death due to the traumatic factor itself;
• Lack of blood flow through the compressed muscle;
• Cell hypoxia resulting from hemorrhagic shock.

Note!

At the moment of compression of the muscle, there is no crash syndrome. Their manifestations begin after the injured person is released from under heavy objects.

Constricted or crushed vessels and muscles, in which their decay products have accumulated, open up. All toxic substances rush through the bloodstream. Having reached the kidneys, a special muscle protein (myoglobin) blocks the tubules of the organ, preventing urine from being produced.

A few hours are enough for tubular necrosis to occur, and irreversible processes in the kidneys begin, the result of which will be.

First honey assistance will depend on the length of time the body remains under the rubble.

There are 3 stages of pathology development:

• Early ( characteristic symptoms manifests itself in the first three days);
• Intermediate (manifestations last one and a half months);
• Late (time period until complete recovery).

Each of these periods has characteristic symptoms and features of their manifestation.

After correctly rendered emergency care with long-term compartment syndrome late period The body begins to independently reject dead tissue and restore the functioning of all vital organs.

In particularly severe cases, surgical removal of necrotic tissue is required.

The specifics of care for long-term compartment syndrome will depend on several other factors:

• Type: crushing or squeezing;
• Location: chest, pelvis, abdominal area, limbs;
• Combination of injury with complications: violations of the integrity of internal organs, large vessels and nerves;
• The severity and area of ​​damage;
• Combination with other injuries: poisoning, etc.

When providing primary care, it is mandatory to determine the severity of injuries.

Doctors distinguish 4 degrees:

1. Easy. The compression lasts no more than 3-4 hours. It has the most favorable prognosis, since renal dysfunction is insignificant.
2. Average. The duration of exposure to gravity is 5-6 hours. Fatalities are about 30%;
3. Heavy. Development of necrosis due to 7-8 hours of being under rubble. There are always serious complications. Mortality accounts for up to half of all cases.
4. Very severe degree is characterized by compression of large areas of the body for more than 9 hours. Death inevitable a day after liberation from the rubble.

Specifics of urgent measures

First aid for long-term compartment syndrome has a number of characteristic features.

Note!

Its main feature is a categorical prohibition on releasing a person from under a heavy object without first applying a tourniquet or a pressure bandage.

Apply above the damaged area and only after that remove the weights. If this rule is violated, the released toxins will immediately begin to spread throughout systemic blood flow, calling irreversible damage kidneys and liver. Then there will be no need to provide medical care: the victim will die.

If the limbs are compressed, first aid consists of completely immobilizing them.

General algorithm for rendering first aid comes down to the following steps:

• Secure the injured part with a tourniquet or bandage above the injury site;
• Give for prevention painful shock(if possible, administer it intramuscularly);
• Release the victim from the effects of heavy loads;
• Cool the affected part of the body;
• several days open wounds they will need to be disinfected;
• Remove the tourniquet;
• Apply a pressure bandage using the same principle;
• Immobilize the limb;
• If there are no signs of abdominal injury, the patient is given warm drinking plenty of fluids;
• For the purpose of prevention cardiovascular disorders You can give the victim prednisolone.

Note!

Long-term use of a tourniquet is allowed only in case of arterial bleeding or obvious signs of incipient gangrene.

Immediately after the actions taken, you need to write a note indicating the exact time of application of the device.

Further first aid for prolonged compression is provided in a health care facility, where the victim is taken on a stretcher.

Anything can happen, from a transport accident to an earthquake and a mine collapse. In any of these cases, DFS may develop. The syndrome has various reasons, pathogenesis, required compulsory treatment. Let's consider these questions further.

The concept of VTS

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

• Compression of body parts by heavy objects.
• Emergency situations.

Such situations often occur after earthquakes, as a result of road accidents, explosions, and mine collapses. The force of compression may not always be great, but the duration of this state plays a role here. Typically, SCS (long-term compartment syndrome) occurs when there is prolonged impact on soft tissue, usually more than 2 hours. First aid is an important stage, on which human life depends. That is why it is important to be able to distinguish between the manifestations of such a condition.

Types of SDS

In medical practice, there are several approaches to the classification of compartment syndrome. Considering the type of compression, the following syndromes are distinguished:

• Developing as a result of a soil collapse. Occurs as a result of prolonged exposure to a concrete slab or various heavy objects.
• Positional SDS develops due to compression by parts of one’s own body.

Localization can also be different, hence the SDS:

• Limbs.
• Heads.
• Belly.
• Breasts.
• Taza.

After emergency situations VDS often develops. The syndrome is often accompanied by other injuries, so it is distinguished:

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

The severity of the syndrome may vary. Based on this fact, we distinguish:

• A mild form of the syndrome, which develops when the limbs are compressed for a short time. Disorders of the cardiovascular system are usually not diagnosed.

• If pressure is applied to the tissue for more than 5-6 hours, then a moderate form of DFS develops, which may result in mild renal failure.
• A severe form is diagnosed when compression lasts more than 7 hours. Signs of renal failure are evident.
• If pressure is applied to soft tissues for more than 8 hours, then we can talk about the development of an extremely severe form of SDS. Acute heart failure can be diagnosed, which is often fatal.

It often happens when SDS (long-term compression syndrome) is accompanied by various complications:

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

Result of injury: SDS

The syndrome has the following causes:

• Pain shock.

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

Periods of the clinical course of SDS

The course of crash syndrome has several periods:

• The first is the direct compression of soft tissues with the development of traumatic shock.
• In the second period there are local changes in the injured area and the onset of intoxication. It can last up to three days.
• The third period is characterized by the development of complications, which are manifested by damage to various organ systems.
• The fourth period is convalescence. It begins with the restoration of kidney function.
• Further, the victims exhibit factors that indicate immunological reactivity and bactericidal activity of the blood.

Symptoms of tissue compression syndrome

If it is not eliminated immediately strong pressure on soft tissues, then SDS gradually progresses. The symptoms of the syndrome are as follows:

• The skin on the compressed limb becomes pale.
• Swelling appears, which only increases over time.
• The pulsation of blood vessels is not palpable.
• The general condition of the victim is deteriorating.
• Pain syndrome is observed.
• A person has psycho-emotional stress.

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

Protein is detected in the urine, red blood cells and casts appear.

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

• Blueness and pallor of the skin.
• Variegated skin color.
• Over the next 24 hours, the swelling increases.

• Blisters, infiltrates may appear, and in severe cases, necrosis of the extremities occurs.
• Cardiovascular failure develops.
• A blood test shows thickening and neutrophil shift.
• Tendency to thrombosis.

At this stage, it is important to carry out timely intensive infusion therapy using forced diuresis and detoxification.

Symptoms of the third period

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

The following symptoms may appear at this time:

• Damage to various organ systems.
• Development of renal failure.
• The swelling gets bigger.
• The appearance of blisters with transparent or hemorrhagic contents can be observed on the skin.
• Anemia begins to manifest itself clearly.
• Diuresis decreases.
• If you do a blood test, the concentration of urea, potassium and creatinine increases.
• A classic picture of uremia with hypoproteinemia appears.
• There is an increase in the victim's body temperature.
• The general condition worsens.
• Lethargy and lethargy appear.
• There may be vomiting.
• Staining of the sclera signals the involvement of the liver in the pathological process.

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

In such cases, only extracorporeal detoxification can help.

Further development of SDS

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

Symptoms may include:

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

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

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

How to recognize SDS?

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

• The clinical picture and circumstances of the injury are taken into account.
• The results of urine and blood tests are not ignored.
• Held instrumental diagnostics, which allows you to compare in dynamics laboratory symptoms and kidney structure.

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

Laboratory diagnostics are carried out for the purpose of:

• Detecting the level of myoglobin in the blood plasma: usually in this condition it increases significantly.
• Determination of myoglobin concentration in urine. If the indicators reach 1000 ng/ml, then we can talk about developing acute renal failure in DFS.
• The syndrome can also manifest itself as an increase in transaminases in the blood.
• Creatinine and urea increase.

Doctors use a urine test to determine the extent of kidney damage. The study reveals:

• An increase in leukocytes if there is complicated DFS.
• The concentration of salts increases.
• The urea content increases.
• There are cylinders.

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

How to provide first aid?

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

1. Give a painkiller.
2. Then begin to release the affected area of ​​the body.

Suitable products include: “Analgin”, “Promedol”, “Morphine”. All medicines are administered only intramuscularly.

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

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

• Send the victim to the nearest hospital.

Therapy for compartment syndrome

May be varying degrees severity of SDS. The syndrome, which must be treated comprehensively, will not cause serious complications, if we take into account the pathogenesis of damage. To have a comprehensive impact means:

• Carry out measures to eliminate deviations in homeostasis.
• Provide therapeutic effect to the pathological focus of damage.
• Normalize the microflora of wounds.

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

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

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

• At the third stage it turns out specialized assistance. This usually occurs in a surgical or trauma center. Everything is here necessary equipment to provide assistance for serious injuries to the musculoskeletal system or internal organs. There are resuscitation services to remove a person from state of shock, treatment of sepsis or renal failure.

Drug therapy

The earlier this stage of therapy is started, the greater the patient's chances of survival. Health care at this stage is as follows:

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

If all conservative methods therapy does not give the desired result, then it is required surgery, which is based on the use following methods detoxification:

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

May be required and cannot be returned to normal activities.

Is it possible to prevent SDS?

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

Even before removing the victim from the rubble, it is important to begin to normalize the blood volume. Mannitol, a 4% solution of magnesium bicarbonate, is often used for these purposes.

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

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