Rhabdomyolysis is a clinical and laboratory syndrome characterized by the destruction of muscle tissue and the entry of decay products into the systemic circulation. It can develop with injuries, muscle diseases, infectious diseases and some other conditions. It is manifested by muscle pain, nausea, vomiting, disorientation, cardiac arrhythmias. It is often complicated by acute renal failure. It is diagnosed according to anamnesis and laboratory results. Treatment includes therapy of the underlying disease, detoxification, prevention and correction of acute respiratory infections.
Rhabdomyolysis is an extreme degree of muscle damage, in which a large number of muscle cells are destroyed at the same time. It varies significantly in severity – from subclinical forms, which can be detected only by the results of laboratory tests, to life-threatening conditions. The prevalence of pathology is not precisely defined. In the USA, about 26 thousand cases of rhabdomyolysis are registered annually, but experts believe that this figure does not correspond to the actual occurrence of the disease due to underdiagnosis of erased variants.
All causes of pathology can be divided into two large groups: traumatic and non-traumatic. Traumatic injuries accompanied by muscle destruction include:
- Prolonged Crushing Syndrome (PCS). It is usually observed in natural disasters and man-made disasters. Occurs during prolonged compression of body parts by heavy objects (stones, fragments of a collapsed building, parts of various mechanisms).
- Positional compression syndrome. It is a type of PCS, develops in people who have “laid down” a part of the body in a state of alcoholic or narcotic intoxication. In some cases, rhabdomyolysis is detected after compression of a part of the body during prolonged anesthesia, in patients with loss of mobility.
- Compartment syndrome. It is formed with rapid edema of muscle tissue with compression of the muscle in the fascial case. It can be detected with extensive skeletal injuries, too long use of a tourniquet, etc.
- Other injuries. Most often, extensive deep burns and electrical injuries lead to damage to muscle tissue with the development of rhabdomyolysis.
- Prolonged muscle tension. It is noted with exorbitant physical exertion (too intense training, prolonged marches), epileptic status, alcoholic delirium, pronounced spasticity, tetanus.
Non-traumatic causes of rhabdomyolysis are extremely heterogeneous. Researchers identify the following groups of factors that can provoke the destruction of muscle cells:
- Muscle ischemia: occlusion of arterial trunks, cardiovascular insufficiency.
- Muscle diseases: hereditary and acquired myopathies, polymyositis, dermatomyositis.
- Systemic infections: influenza, chickenpox, leptospirosis, legionellosis, viral hepatitis, AIDS, some bacterial infectious diseases.
- Exogenous intoxication. Alcohol, cocaine, amphetamines and heroin use, carbon monoxide poisoning, snake bites, overdose of medications.
In addition, rhabdomyolysis develops with malignant hyperthermia, gross electrolyte imbalance, hereditary metabolic disorders and diabetes mellitus. In cancer patients, paraneoplastic syndrome (acute myopathy with osteomalacia) becomes the cause of muscle breakdown.
Muscle cells in rhabdomyolysis are destroyed due to direct mechanical pressure, nutritional disorders or exposure to toxins. Inflammation occurs in the necrosis zone, a large amount of fluid accumulates in the tissues (up to 10 liters can accumulate in one damaged limb). Significant hypovolemia leads to the development of shock and acute renal failure at the initial stage of the lesion.
The main number of cases of acute renal failure in patients with rhabdomyolysis is caused by the release of cell breakdown products into the general bloodstream when blood circulation resumes. At this stage, acidosis, hyperkalemia, an increase in the concentration of myoglobin, creatinine and uric acid are observed. Myoglobin and uric acid accumulate in the tubules of the kidneys and clog them. The process is aggravated by dehydration and reflex spasm of the renal vessels.
Diuresis decreases down to anuria. In this case, the fluid from the damaged area enters the bloodstream, but is not excreted by the kidneys, which leads to its exit into the intercellular space. Due to the deterioration of blood supply in the intestine, toxins are intensely absorbed, which further aggravates intoxication and contributes to the development of hemodynamic disorders. Calcinates are formed in the muscles after recovery.
The clinical picture is determined by the volume of necrosis of muscle tissue. Minor injuries are asymptomatic and are detected only according to laboratory tests. With more significant lesions, muscle weakness, pain and muscle swelling are noted. With a rapid increase in swelling, a drop in blood pressure, tachycardia, pallor of the skin, nausea and impaired consciousness are determined.
With the restoration of blood circulation in the affected area and the occurrence of electrolyte disturbances, nausea, vomiting, cardiac arrhythmias are observed. Patients with rhabdomyolysis develop disorders of consciousness from mild disorientation to coma. Due to the presence of myoglobin, urine acquires a dark color (the color of strong tea). With acute renal failure, the amount of urine excreted decreases. Edema, increased blood pressure, tachycardia are detected.
There is an aggravation of arrhythmia or the appearance of cardiac arrhythmias, if they were absent at the previous stage. Uremia provokes increased breathing, increased nausea and vomiting. In the absence of emergency medical measures, the development of multiple organ failure and death is possible. With timely correction of acute respiratory failure, oliguria is replaced by polyuria in a few days. Then the amount of urine gradually normalizes, but full recovery of kidney function takes up to 1 year.
Along with acute renal failure, which is the main cause of death of patients, life-threatening conditions such as hypovolemic shock and DIC syndrome may occur with rhabdomyolysis. Sometimes, against the background of hyperkalemia and renal insufficiency, fatal cardiac arrhythmias are formed. AKI is accompanied by suppression of immunity, which causes the frequent (in 30-70% of patients) development of severe infectious complications, including sepsis.
The diagnosis is made by traumatologists, resuscitators or specialists who supervised patients before the development of muscle necrosis (infectious diseases, rheumatologists, etc.). Clinical diagnosis of rhabdomyolysis in traumatic injuries is usually not difficult due to a combination of a characteristic history and significant swelling of the local lesion area, the tissues of which acquire a woody consistency.
Muscle necrosis of non-traumatic genesis is often difficult to differentiate clinically due to the nonspecific nature of the signs, the prevalence of the process, previous disorders of the patients’ condition and the possibility of developing other complications of the underlying disease. A change in the color of urine is not a specific symptom of rhabdomyolysis, since it can be caused not only by myoglobinuria, but also by hemoglobinuria. In some cases, it is rational to conduct a gene diagnosis. The leading role in the diagnosis is played by:
- Blood test. An increase in the level of myoglobin and creatine phosphokinase is an early specific sign of rhabdomyolysis. The activity of markers gradually increases during the first 12 hours, the concentration of myoglobin reaches a maximum on the first day, the concentration of CK – on 3-5 days. In addition, the tests reveal acidosis, an increase in the amount of creatinine, uric acid, hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia.
- Assessment of diuresis. The development of acute renal failure is indicated by a decrease in diuresis by 8-10%. Subsequently, diuresis decreases by 25% or more, with a severe course, anuria is possible. An increase in the amount of urine indicates the restoration of kidney function, during this period, daily urination can reach 5 liters.
Urine tests. In the urine of patients with rhabdomyolysis, myoglobinuria, proteinuria, and a violation of the composition of electrolytes are determined. The density of urine changes, a violation of the ratio of urea and creatinine in blood and urine, the ratio of sodium clearance to creatinine clearance is revealed.
Ultrasound and MRI are promising methods for assessing the severity of muscle damage in rhabdomyolysis, but in practice these studies are still rarely used. Visual techniques in the early stages indicate edema and destruction of muscle tissue, in the later stages – the formation of calcinates.
Suspicion of rhabdomyolysis is an indication for emergency hospitalization in the intensive care unit, early initiation of infusion therapy, control of diuresis. Patients are recommended a special diet with a limited amount of protein and potassium-containing products. Correction of the underlying pathology that provoked rhabdomyolysis is carried out. The scheme of drug therapy is determined by the stage of the disease and the severity of the patient’s condition, may include:
- Prevention of acute respiratory infections. Upon admission, patients are prescribed diuretics, an intravenous drip solution of sodium bicarbonate is injected to reduce damage to the renal tubules by myoglobin cylinders.
- Correction of hypovolemia. Infusion of saline solutions with rhabdomyolysis should be started within 6 hours from the moment of damage. In the first 2 hours, the volume of the injected liquid reaches 1 liter / hour, in the next 2 hours – 500 ml / hour. Infusion infusions are carried out under the control of diuresis and CBS of blood. The goal is to ensure urination of more than 300 ml/hour.
- Elimination of intoxication and metabolic disorders. Calcium gluconate and sodium bicarbonate are injected intravenously. Beta-adrenergic receptor agonists and insulin with glucose are used. Enterosorbents are used to reduce the absorption of toxins in the intestine.
- Extracorporeal hemocorrection. Hemosorption is considered a promising method of treatment of rhabdomyolysis. In some cases, plasmapheresis is prescribed. With the development of acute renal failure, hemodialysis is performed.
Operations for rhabdomyolysis are of a preventive or curative nature, performed in the first hours after admission or within 1-2 weeks of hospitalization. Apply:
- Decompression fasciotomy. The purpose of the operation is to reduce the pressure in the muscle case with the development of compartment syndrome. The technique allows to reduce the prevalence of necrosis, reduce the likelihood of the development of gross metabolic disorders and acute renal failure.
- Necrectomy. It is performed for deep thermal burns, electrical trauma, prolonged crushing syndrome and other traumatic injuries, vascular diseases. In severe cases, it is performed in the volume of amputation or exarticulation of the limb.
In the long-term period after surgical treatment of rhabdomyolysis, reconstructive plastic surgery may be required: replacement of the defect with a Filatov stem, myoplasty, scar surgery, etc.
The prognosis for rhabdomyolysis is always regarded as serious due to the risk of life-threatening complications. The cause of death of patients most often becomes renal failure or hyperkalemia with the development of severe arrhythmias. Timely initiation of infusion therapy and hemodialysis improves the prognosis. Kidney function after successful correction of acute renal failure is usually fully restored.
Prevention of rhabdomyolysis includes the fight against alcoholism and drug addiction, prevention of excessive physical overload, measures to reduce the level of injuries, compliance with occupational safety and rules of patient care in medical institutions. It is necessary to timely identify and treat pathological conditions that can lead to the development of rhabdomyolysis.
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