Long crush syndrome

Long crush syndrome

Syndrome of prolonged crushing – a shock-like condition after prolonged compression of body parts by heavy objects, manifested by oligo- or anuria due to impaired renal function by decay products of crushed tissues (for example, muscle myoglobin).


    • In peacetime, cases of prolonged crush syndrome are mainly observed during collapses in mines, strong earthquakes, especially occurring near large cities (up to 24% of the total number of victims)
    • The most common damage occurs to the limbs (up to 80%), mainly the lower (60% of cases). Classification.
    • By type of compression
    • Compression (positional or various objects, soil, etc.)
    • Crushing.
    • By localization: head, chest, abdomen, pelvis, limbs.
    • Combination of soft tissue injuries
    • With damage to internal organs
    • With damage to bones, joints
    • With damage to the main vessels and nerve trunks.
    • According to the severity of the condition
    • Mild degree occurs when the limb segments are compressed for up to 4 hours
    • The average degree develops with compression of the entire limb for 6 hours
    • A severe form occurs when the entire limb is compressed for 7–8 hours. Symptoms of acute renal failure and hemodynamic disorders are clearly manifested
    • An extremely severe form develops when both limbs are compressed for more than 6 hours.
    • By periods of clinical course
    • Compression period
    • Post-compression period
    • Early (1–3 days)
    • Intermediate (4–18 days)
    • Late.
    • By combination
    • With burns, frostbite
    • With acute radiation sickness
    • With the defeat of chemical warfare agents.
    • Complications
    • From the organs and systems of the body (MI, pneumonia, pulmonary edema, peritonitis, neuritis, psychopathological reactions, etc.)
    • Irreversible limb ischemia
    • Purulent-septic
    • Thromboembolic.

Pathogenesis. The syndrome of prolonged crushing develops as a general reaction of the body in response to pain, prolonged compression of tissues with impaired microcirculation, causing their ischemia (with subsequent necrosis) and edema. Tissue decay products, myoglobin, potassium ions and bacterial toxins coming from the area of ​​damage and other places (intestines, respiratory organs), cause endogenous intoxication, the main pathogenetic factor of the long-term crush syndrome.


    • The compressed limb is sharply edematous, the skin is pale with a large number of abrasions and bruises.
    • Subcutaneous tissue and muscles are saturated with yellowish edematous fluid
    • The muscles are imbibed with blood, have a dull appearance, the integrity of the vessels is not broken. Microscopic examination of the muscles reveals a characteristic pattern of wax degeneration.
    • Often

observe cerebral edema and plethora

    • The lungs are stagnant and plethoric, sometimes edema and pneumonia are noted.
    • The most pronounced changes in the kidneys: the kidneys are enlarged, the cut shows a sharp pallor of the cortical layer. In the epithelium of the convoluted tubules dystrophic changes. In the lumen of the tubules are cylinders of myoglobin.

Clinical picture and course of the disease. In the development of the syndrome of prolonged crushing, the following periods (stages) are distinguished.

    • Initial period (up to 3 days)
    • Complaints of pain in the area of ​​injury, weakness, nausea. In severe cases, vomiting, severe headache, depression, euphoria, perceptual disturbances, etc. are possible. The skin is pale, in severe cases – gray
    • CCC
    • BP and CVP are traditionally reduced, sometimes significantly (BP – 60/30 mm Hg, CVP indicators are negative)
    • Tachycardia, arrhythmias
    • When the injured limb is released without prior application of a tourniquet, tissue decay products begin to enter the bloodstream, which is accompanied by a sharp deterioration in the condition of the victim, a drop in blood pressure, loss of consciousness, involuntary defecation and urination (turnstile shock)
    • Asystole often occurs. Causes – hyperkalemia and metabolic acidosis
    • Other organs and systems. Possible pulmonary edema, encephalopathy
    • locally. On the skin – wounds, blisters with serous and hemorrhagic contents. The extremity is cold, the skin is cyanotic. Sensitivity and ability to active movements are sharply reduced or absent. In severe cases, muscle contracture of the limb develops. After elimination of the compressive factor, a dense (subfascial) edema of the limb quickly develops.
    • The toxic period begins with a deterioration in the condition (usually for 4–5 days) due to intoxication and the development of acute renal failure.
    • Intoxication at this stage is caused not only by the decay products of tissues, but also by the massive influx of bacterial toxins into the blood from the affected area and intestines (up to the development of toxic hepatitis and endotoxin shock).
    • OPN develops as a result of myoglobin entering the kidneys from the affected area and its transition in the acidic environment of the renal tubules into insoluble hydrochloric hematin. In addition, myoglobin itself can cause necrosis of the tubular epithelium.
    • Clinical picture
    • Complaints remain the same, pain in the lumbar region is detected. The patient is inhibited, in severe cases – loss of consciousness (coma). Severe edema, anasarca. Body temperature rises to 40 °C, with the development of endotoxin shock it can decrease to 35 °C.
    • s – CCC. Hemodynamics is unstable, blood pressure is often lowered, CVP is significantly increased (up to 20 cm of water column), tachycardia (up to 140 per minute). Various forms of arrhythmias due to severe hyperkalemia. Toxic myocarditis and pulmonary edema often develop.
    • Other organs and systems
    • GIT. Diarrhea or paralytic ileus
    • Kidneys. Necrosis of the renal tubules, severe oliguria, up to anuria.
    • Test Data
    • Lacquer red or brown urine (high content of myoglobin and Hb), severe albumin and creatinuria
    • Blood: anemia, leukocytosis with a significant shift to the left, hypoproteinemia, hyperkalemia (up to 20 mmol/l), increased levels of creatinine up to 800 µmol/l, urea up to 40 mmol/l, bilirubin up to 65 µmol/l, transferase levels increased by more than 3 times, violation of the blood coagulation system (up to the development of DIC).
    • locally. Foci of necrosis in places of compression, suppuration of wounds and eroded surfaces.
    • The period of late complications begins from 20-30 days of illness. With adequate and timely treatment, the phenomena of intoxication, acute renal failure, and cardiovascular insufficiency are significantly reduced. The main problems of this stage are all kinds of complications (for example, immunodeficiency, sepsis, etc.) and local changes (for example, atrophy of viable limb muscles, contractures, suppuration of wounds).


    • Urgent care. Tourniquets are applied to the limb above the place of compression, and only after that it is released. Then the limb in the affected area is tightly bandaged and immobilized. Treatment of associated wounds and injuries.
    • Infusion therapy is aimed at combating shock and acute renal failure, improving microcirculation and is carried out under strict control of diuresis and CVP
    • Completion of plasma loss and detoxification – solutions of albumin, sodium chloride (0.9%), glucose (5%), fresh frozen plasma, gemodez
    • Improving microcirculation – rheopolyglucin and heparin (5,000 units)
    • Compensation of metabolic acidosis – 400-1 200 ml 4% solution of sodium bicarbonate, lactosalt
    • Fighting hyperkalemia.
    • Broad spectrum antibiotics.
    • Symptomatic therapy (for example, antihistamine products, narcotic and non-narcotic analgesics, diuretics, antiarrhythmic products).
    • Case, conductor novocaine blockade.
    • Surgery
    • Fasciotomy
    • Indications: pronounced subfascial edema with impaired blood supply to the limb while maintaining viable muscle tissue
    • Make an incision 5-7 cm long
    • Revision of muscle bundles is carried out, necrotic ones are excised
    • After stopping the edema, stabilizing the general condition and in the absence of local infectious complications (traditionally on the 3rd-4th day), the wound is sutured.
    • Amputation of the affected limb
    • Carried out under general anesthesia
    • In case of irreversible ischemia, the limb is amputated proximal to the site of the tourniquet application.
    • In other cases, excision of necrotic tissues is performed (probably leaving viable muscle bundles)
    • The viability of muscle tissue is determined during the operation by normal coloration, its probability of contraction when touched by power tools (electric scalpel) and bleeding
    • The wound is abundantly washed with antiseptic solutions. Primary sutures are strictly contraindicated. Healing is by secondary intention.
    • Extracorporeal detoxification (plasmapheresis, hemodialysis, hemo- and plasma sorption) must begin at the probably early stages of the disease.


    • Traumatic toxicosis
    • Bywaters syndrome
    • Myorenial syndrome
    • crush syndrome

See also Renal failure, acute KSD

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

Note. Positional compression syndrome occurs when the victim is immobile for a long time (more than 8 hours) on a hard plane. More often it develops in persons who are in a state of alcoholic or drug intoxication, in case of poisoning with sleeping pills. Usually there is a lesion of the upper limbs, tucked under the body. According to the pathogenesis, clinical picture and methods of treatment, it is similar to the syndrome of prolonged compression, but stiffness of the muscles, pronounced phenomena of intoxication and acute renal failure appear much less frequently. Literature. Syndrome of long compression. Nechaev EA, Revskiy AK, Savitskiy GG. M.: Medicine, 1993

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