Crush syndrome is a shock–like condition that occurs after prolonged compression of the trunk, limbs or their segments with heavy objects. It is manifested by pain, deterioration, swelling of the affected parts of the body, acute renal failure. Without medical care, patients die from acute respiratory failure, increasing intoxication, pulmonary or cardiovascular insufficiency. Treatment includes detoxification and plasma replacement infusion therapy, extracorporeal hemocorrection, antibiotic therapy, excision of necrosis sites or amputation of a crushed limb.
ICD 10
T79.5 Traumatic anuria
Meaning
Crush syndrome, other names – traumatic toxicosis, prolonged crushing syndrome, Bywaters syndrome, myorenal syndrome is a pathological shock–like condition that occurs after prolonged compression of the trunk, limbs or their segments with heavy objects. Crush syndrome develops immediately after the release of the patient and the restoration of blood and lymph flow in the affected parts of the body. It is accompanied by a deterioration of the general condition, the development of toxemia and acute renal failure, with a large lesion area, it often ends with the death of the patient. In traumatology and orthopedics, there is a household type of crush syndrome – the so–called positional compression syndrome, which develops as a result of a long (more than 8 hours) compression of body parts during the stationary position of a person on a hard surface.
Crush syndrome causes
Usually, the crush syndrome occurs in victims during landslides, earthquakes, collapses in mines, construction work, road accidents, logging, explosions and destruction of buildings as a result of bombing.
Positional compression syndrome is usually detected in patients who, at the time of injury, were in a state of poisoning with sleeping pills, narcotic or alcoholic intoxication. The upper limbs tucked under the trunk are more often affected. For reasons of development, symptoms and methods of treatment, the syndrome of positional compression practically does not differ from the syndrome of prolonged crushing, however, it usually proceeds more favorably due to a smaller lesion area.
Pathogenesis
The occurrence of prolonged crushing syndrome is caused by a combination of three factors:
- pain syndrome;
- massive plasma loss caused by the release of the liquid part of the blood through the vessel walls into damaged tissues;
- traumatic toxemia (intoxication of the body by products of tissue decay).
Prolonged pain irritation with crush syndrome leads to the development of traumatic shock. The loss of plasma causes blood to thicken and causes thrombosis of small vessels. Traumatic toxemia in crush syndrome develops due to the absorption into the blood of the products of tissue decay of injured muscles. Immediately after the limb is released from the damaged tissues, a significant amount of potassium ions enters the vascular bed, which can cause arrhythmia, and in severe cases, the cessation of the work of the lungs and heart.
In the future, the crushed muscle tissues of a patient with crush syndrome lose up to 66% of potassium, 75% of myoglobin, 75% of phosphorus and 70% of creatinine. Decay products enter the bloodstream, causing acidosis and hemodynamic disorders (including a sharp narrowing of the vessels of the renal glomeruli). Myoglobin damages and clogs the renal tubules. All this leads to the development of acute renal failure, which threatens the life of a patient with crush syndrome.
Classification
By severity:
- A mild form. Occurs when the limb segments are crushed for 4 or less hours.
- A moderate form. Develops as a result of crushing one limb within 4-6 hours. With the timely start of treatment, the prognosis is favorable.
- Severe form. Occurs when one limb is crushed for 6-8 hours. It is accompanied by hemodynamic disorders and acute renal failure. With the timely start of treatment, the prognosis is relatively favorable.
- An extremely severe form. Develops as a result of crushing two or more limbs for 6 or more hours. Accompanied by severe shock. The prognosis is unfavorable.
According to clinical symptoms:
- early period (from the moment of release to 3 days);
- toxic period (starts on 4-5 days);
- the period of late complications (develops 20-30 days after the injury).
Crush syndrome symptoms
Immediately after the compression is eliminated, the general condition of the victim improves. A patient with prolonged crushing syndrome is concerned about pain and restriction of movement in the crushed limb. During the first hours after release, swelling of the affected area gradually increases, which becomes dense, woody. Bubbles with serous-hemorrhagic contents form on the skin of the limb. When examining the damaged part of the body, a weakening of the pulsation of the arteries, a decrease in sensitivity and local temperature are revealed.
The general symptoms are increasing. The condition of the victim with crush syndrome is deteriorating. After a short period of excitement, the patient becomes sluggish, inhibited. There is a decrease in blood pressure and body temperature, arrhythmia, tachycardia, pronounced pallor of the skin. The skin of a crush syndrome patient is covered with a sticky cold sweat. Possible loss of consciousness, involuntary defecation and urination. Sometimes pulmonary edema develops. The amount of urine excreted decreases. Without adequate medical care, there is a possibility of death within 1 or 2 days.
Necrosis foci form on the crushed limb. When dead tissues are rejected, muscles that have the characteristic appearance of boiled meat are exposed. Suppuration of wounds and eroded surfaces develops. Acute renal failure appears and gradually increases. On 5-6 days, patients with prolonged crushing syndrome develop uremic syndrome. An increase in the level of potassium in the blood causes arrhythmia and bradycardia.
On 5-7 days, signs of pulmonary insufficiency are detected. The increasing intoxication caused by the entry into the bloodstream of tissue decay products and bacterial toxins from the crushed limb causes toxic hepatitis. Endotoxic shock is possible. The phenomena of multiple organ failure in patients with crush syndrome gradually decrease within 2-3 weeks.
Acute renal failure with crush syndrome is stopped about a month after the injury. The patient’s condition improves, his body temperature normalizes. Pain and swelling of the limb are reduced. Necrotized muscles are replaced by connective tissue, which leads to muscle atrophy and the development of contractures. With an unfavorable development of events, local (suppuration) and general (sepsis) complications are possible.
Diagnostics
Pathology is diagnosed by a traumatologist on the basis of a characteristic anamnesis (prolonged compression of a body part), complaints and external examination data. To assess the general condition, a complex of laboratory tests is prescribed. Laboratory monitoring of kidney function is carried out for the timely detection and treatment of acute kidney injury.
Crush syndrome treatment
Before releasing the limb, it is necessary to apply a tourniquet above the injury site. After the compression is eliminated, the limb is tightly bandaged and fixed on the tire. Wounds and superficial skin injuries are treated according to general rules. A patient with prolonged crushing syndrome is injected with narcotic analgesics. The limb is covered with hot-water bottles with ice. If possible, perform a case novocaine blockade of the crushed limb or a paranephral blockade according to Vishnevsky. The victim is urgently taken to the hospital.
To improve microcirculation, combat shock and acute renal failure, infusion therapy is carried out in the hospital (under the control of diuresis and central venous pressure). To detoxify and compensate for plasma loss, a 5% glucose solution, salt solutions, frozen plasma, phys. solution and albumin solution. To improve microcirculation, heparin (5000 units) and rheopolyglucin are prescribed.
In order to compensate for metabolic acidosis, a patient with crush syndrome is drip-injected with a 4% solution of sodium bicarbonate. Prescribe broad-spectrum antibiotics intramuscularly. Symptomatic therapy is carried out (diuretics, analgesics, antihistamines and antiarrhythmic drugs). In case of prolonged crushing syndrome, extracorporeal hemocorrection (hemodialysis, plasmapheresis, plasma and hemosorption) is performed as early as possible.
While maintaining the viability of muscle tissues and pronounced subfascial edema with impaired local circulation, the traumatologist performs a fasciotomy with revision and excision of necrotized muscle bundles. If there is no suppuration, the wound is sutured for 3-4 days, after reducing swelling and improving the general condition of the patient with crush syndrome.
In cases of irreversible ischemia, the limb is amputated above the place of the tourniquet. In other cases, excision of necrotic areas with the preservation of viable muscle bundles is shown. The viability of the muscles is determined during surgery. The criteria for viability are the preservation of normal coloration, the ability to bleed and shrink. After excision of tissues, the wound is abundantly washed with antiseptics. No stitches are applied. The wound heals by secondary tension.
In the long-term period, patients with long-term crushing syndrome are shown rehabilitation treatment courses (massage, physical therapy) aimed at restoring muscle strength and eliminating contractures.
Literature
- Genthon A. Wilcox S.R. Crush syndrome: a case report and review of the literature. // J. Emerg. Med. — 2014. — Vol. 46. — №2. — P. 313 – 319. link
- Karger AG. The Crush Syndrome (and Lessons Learned from the Marmara Earthquake). S.— 2005.
- Malinoski D.J. , Slater M.S. , Mullins R.J. Crush injury and rhabdomyolysis. // Crit. Care. — 2004. — Vol. 20. — P. 171–189. link
- Sever MS. Rhabdomyolysis. // Acta. Clin. Belg. Suppl. — 2007. — Vol. 2. — P. 350-370.