Prolonged crush syndrome: causes, symptoms, diagnosis, treatment

Crush syndrome (synonyms: traumatic toxicosis, crush syndrome, crush syndrome, myorenal syndrome, "release" syndrome, Bywaters syndrome) is a specific type of injury associated with massive prolonged crushing of soft tissues or compression of the main vascular trunks of the extremities, characterized by a severe clinical course and high mortality.

ICD-10 code

• T79.5. Traumatic anuria.
• T79.6. Traumatic muscle ischemia.

Epidemiology of crush syndrome

They occur in 20-30% of cases of emergency destruction of buildings, during earthquakes, rock falls and in mines.

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What causes crush syndrome?

The main factors in the pathogenesis of crush syndrome are traumatic toxemia, plasma loss, and pain irritation. The first factor occurs as a result of the breakdown products of damaged cells entering the bloodstream, causing intravascular blood coagulation. Plasma loss is the result of significant swelling of the extremities. The pain factor disrupts the coordination of excitation and inhibition processes in the central nervous system.

Long-term compression leads to ischemia and venous congestion of the entire limb or its segment. Nerve trunks are injured. Mechanical tissue destruction occurs with the formation of a large number of toxic products of cellular metabolism, primarily myoglobin. Metabolic acidosis in combination with myoglobin leads to intravascular blood coagulation, while the filtration capacity of the kidneys is blocked. The final stage of this process is acute renal failure, which is expressed differently at different periods of the disease. 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, massive edemas of damaged tissues appear. Plasma loss can reach 30% of the circulating blood volume.

Symptoms of Crush Syndrome

The course of crush syndrome can be divided into three periods.

Period I (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 picture is dominated by manifestations of traumatic shock: severe pain syndrome, psychoemotional stress, hemodynamic instability, hemoconcentration, creatinemia; in urine - proteinuria and cylinruria. 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 - the next period develops.

Period II is the period of acute renal failure. It lasts from the 3rd to the 8-12th day. Edema of the damaged limb increases, blisters and hemorrhages appear on the skin. Hemoconcentration is replaced by hemodilution, anemia increases, diuresis drops sharply to anuria. The highest hyperkalemia and hypercreatinemia. Despite intensive therapy, mortality reaches 35%.

Period III - recovery, begins from the 3rd-4th week. Kidney function, protein content and blood electrolytes are normalized. Infectious complications come to the fore, sepsis may develop.

Summarizing the experience of observing victims of the earthquake in Armenia, clinicians came to the conclusion that the severity of clinical manifestations of prolonged crush syndrome primarily depends on the degree of compression, the area of damage and the presence of concomitant injuries. The combination of short-term compression of the limb with bone fractures, craniocerebral trauma, and damage to internal organs sharply aggravates the course of traumatic disease and worsens the prognosis.

Classification of crush syndrome

According to the types of compression, a distinction is made between compression (positional or direct) and crushing.

By localization of the lesion: head (chest, abdomen, pelvis, limbs).

By combination of soft tissue damage:

• with damage to internal organs;
• with damage to bones and joints;
• with damage to the main vessels and nerve trunks.

By severity of the condition:

• mild degree - compression up to 4 hours;
• moderate degree - develops with compression for up to 6 hours;
• severe form - occurs when the entire limb is compressed for 7-8 hours; signs of acute renal failure and hemodynamic disorders are characteristic;
• extremely severe form - compression of one or both limbs with exposure over 8 hours.

By periods of clinical course:

• compression period;
• post-compression period: early (1-3 days), intermediate (4-18 days) and late.

By combination:

• with burns, frostbite;
• with acute radiation sickness;
• with damage from chemical warfare agents.

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Complications of crush syndrome

The most common complications that develop are:

• from the organs and systems of the body - myocardial infarction, pneumonia, pulmonary edema, peritonitis, neuritis, psychopathological reactions, etc.;
• irreversible limb ischemia;
• purulent-septic complications;
• thromboembolic complications.

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Diagnosis of crush syndrome

Anamnesis

In the initial period - complaints of pain in the area of injury, weakness, nausea. In severe cases - vomiting, severe headache, possible depression, euphoria, disturbances of perception, etc.

Toxic period. Complaints remain the same, pain in the lumbar region is added.

The period of late complications. Complaints depend on the complications that have developed.

Inspection and physical examination

In the initial period, the skin is pale, in severe cases - gray. Blood pressure and central venous pressure are usually reduced, sometimes significantly (blood pressure - 60/30 mm Hg, central venous pressure indicators are negative). Tachycardia, arrhythmia are detected, asystole may develop. If the injured limb is released without first applying a tourniquet, the patient's condition sharply worsens, blood pressure drops, consciousness is lost, and involuntary urination and defecation occur. Abrasions and blisters with serous and hemorrhagic contents are locally visible on the skin. The limb is cold and bluish.

Toxic period. The patient is inhibited, in severe cases loss of consciousness occurs. Pronounced edema and anasarca develop. Body temperature rises to 40 °C, with the development of endotoxin shock it can decrease to 35 °C. Hemodynamics are unstable, blood pressure is often decreased, central venous pressure is significantly increased (up to 20 cm H2O), tachycardia is characteristic (up to 140 per minute). Arrhythmias (due to severe hyperkalemia), toxic myocarditis and pulmonary edema develop. Diarrhea or paralytic ileus. Due to necrosis of the renal tubules - pronounced oliguria, up to anuria. Locally - foci of necrosis in places of compression, suppuration of wounds and eroded surfaces.

The period of late complications. With adequate and timely treatment, intoxication, symptoms of acute renal failure, cardiovascular failure are significantly reduced. The main problems are various complications (e.g., immunodeficiency, sepsis, etc.) and local changes (e.g., wound suppuration, atrophy of viable limb muscles, contractures).

Laboratory and instrumental diagnostics of crush syndrome

Laboratory test results depend on the duration of crush syndrome.

• Initial period - hyperkalemia, metabolic acidosis.
• Toxic period. Blood shows anemia, leukocytosis with a significant shift in the leukocyte formula to the left, hypoproteinemia, hyperkalemia (up to 20 mmol/l), creatinine up to 800 μmol/l, urea up to 40 mmol/l, bilirubin up to 65 μmol/l, transferase activity increased by 3 times or more, myoglobin, bacterial toxins (from the affected area and intestines), blood coagulation disorder (up to the development of DIC). Urine is varnish-red or brown (high content of myoglobin and Hb), pronounced albumin and creatinuria.
• The period of late complications. The data of laboratory and instrumental studies depend on the type of complications that have developed.

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Treatment of crush syndrome

Indications for hospitalization

All victims are subject to hospitalization.

First aid

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

First aid

First aid consists of correction or manipulations not performed at the first stage, and establishment of infusion therapy (regardless of hemodynamic parameters). Dextran [mol. mass 30,000-40,000], 5% dextrose solution and 4% sodium bicarbonate solution are desirable for infusion.

Conservative treatment of crush syndrome

Treatment of prolonged crush syndrome is complex. Its features depend on the period of the disease. However, it is possible to highlight the general principles of conservative treatment.

• Infusion therapy with the infusion of fresh frozen plasma up to 1 l/day, dextran [mol. mass 30,000-40,000], detoxifying agents (sodium bicarbonate, sodium acetate + sodium chloride). Plasmapheresis with the extraction of up to 1.5 l of plasma in one procedure.
• Hyperbaric oxygen therapy to reduce hypoxia of peripheral tissues.
• Early application of arteriovenous shunt, hemodialysis, hemofiltration - daily during acute renal failure.
• Sorption therapy - povidone orally, locally after surgery - charcoal fabric AUG-M.
• Strict observance of asepsis and antisepsis.
• Dietary regimen - water restriction and exclusion of fruits during acute renal failure.

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

I period.

Catheterization of a large vein, determination of blood type and Rh factor. Infusion-transfusion therapy of at least 2000 ml/day: fresh frozen plasma 500-700 ml, 5% dextrose solution up to 1000 ml with ascorbic acid, B vitamins, 5-10% albumin - 200 ml, 4% sodium bicarbonate solution - 400 ml, dextroseprocaine mixture - 400 ml. The amount and type of transfusion agents are determined by the patient's condition, laboratory parameters and diuresis. Strict accounting of excreted urine is mandatory.

HBO therapy sessions - 1-2 times a day.

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

Drug treatment for crush syndrome:

• furosemide up to 80 mg/day, aminophylline 2.4% 10 ml (stimulation of diuresis);
• heparin sodium 2.5 thousand under the skin of the abdomen 4 times a day;
• dipyridamole or pentoxifylline, nandrolone once every 4 days;
• cardiovascular drugs, antibiotics (after microflora culture for antibiotic sensitivity).

After surgical treatment of crush syndrome (if performed), the volume of infusion therapy per day increases to 3000-4000 ml, includes up to 1000 ml of fresh frozen plasma, 500 ml of 10% albumin. HBO therapy - 2-3 times a day. Detoxification - infusion of sodium bicarbonate up to 400 ml, intake of povidone and activated carbon. AUG-M carbon fabric is used locally.

II period. Fluid intake is restricted. Hemodialysis is indicated when diuresis decreases to 600 ml/day. Emergency indications for it include anuria, hyperkalemia over 6 mmol/l, pulmonary or cerebral edema. In case of severe hyperhydration, hemofiltration is indicated for 4-5 hours with a fluid deficit of 1-2 l.

During the interdialysis period, infusion therapy is carried out with the same drugs as in the first period, with a total volume of 1.2-1.5 l/day, and in the presence of surgical interventions - up to 2 l/day.

With timely and adequate treatment, renal failure is relieved by the 10th-12th day.

III period. Treatment consists of therapy of local manifestations of prolonged crush syndrome, purulent complications and prevention of sepsis. Treatment of infectious complications is carried out according to the general laws of purulent surgery.

Surgical treatment of crush syndrome

General principles of surgical treatment are strict adherence to asepsis and antisepsis, fasciotomy (“lampas incisions”), necrectomy, amputation (according to strict indications).

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

• Grade I - minor indurative edema. The skin is pale, raised above the healthy skin at the compression border. Conservative treatment is effective, so there is no need for surgical intervention.
• II degree - moderate tissue swelling and tension. The skin is pale, with areas of cyanosis. There may be blisters with transparent-yellowish contents, with a wet pink surface underneath.
• Grade III - pronounced indurative edema and tissue tension. The skin is cyanotic or "marbled", its temperature is reduced. After 12-24 hours, blisters with hemorrhagic contents appear, under them - a moist dark red surface. Signs of microcirculation disorder progressively increase. Conservative therapy is ineffective, leads to necrosis. Lampas incisions with dissection of fascial sheaths are indicated.
• IV degree - moderate edema, tissues are sharply tense. Skin is bluish-purple, cold. Blisters with hemorrhagic contents, under them - bluish-black dry surface. Subsequently, the edema does not increase, which indicates deep circulatory disorders. Conservative treatment is ineffective. Wide fasciotomy ensures the maximum possible restoration of blood circulation, allows to limit the necrotic process in more distal parts, reduces the intensity of absorption of toxic products. In case of subsequent amputation, its level will be significantly lower.

Estimated period of disability and prognosis

The period of disability and prognosis depend on the timeliness of the assistance provided, the extent of the lesion, the characteristics of the course of the crush syndrome and the individual characteristics (for example, age, presence of severe chronic diseases) of each specific patient.