Myoglobinuria is a pathological condition in which myoglobin is found in the urine. The cause of development are injuries with muscle crushing, electrical injuries, deep extensive thermal burns, CO2 poisoning, gas gangrene, some myopathies, and a significant load on the muscles. Manifested by red or dark brown urine, difficulty urinating, sometimes pain in the lumbar region. Myoglobin is determined by microscopy of urine sediment and by immunoelectrophoresis. Correction is made during the treatment of the underlying pathology.
Myoglobin is a complex pigment protein found in striated muscles (skeletal muscles, myocardium). It plays the role of a temporary depot of oxygen, is responsible for its accumulation and return, which allows for sufficient oxygenation of cells during physical exertion of various intensities. In the urine, it is normally absent, myoglobinuria begins to be determined when the muscle cells are destroyed (rhabdomyolysis) after the concentration of the compound in the blood is more than 3 mg%.
Myoglobin has a low molecular weight, so it quickly enters the kidneys, is excreted in the urine in the first 24 hours after muscle damage. In an acidic environment, it precipitates, clogs the loops of Henle, causes nephrosis and acute necrosis of the renal tissue. Massive myoglobinuria, an increase in the level of potassium leaving the destroyed muscles, secondary hemodynamic disorders provoke the development of acute renal failure.
Prolonged crush syndrome (SDS) develops as a result of prolonged compression of the body or its segments. It is detected in victims of earthquakes, landslides, collapses in mines, accidents during the construction of buildings, logging. It is manifested by pain, dense edema, limitation of movements, decreased sensitivity, massive myoglobinuria. The patient's condition is rapidly deteriorating, necrosis is formed, and renal failure is increasing. There is a high chance of death.
A more favorable variant of SDR is positional compression syndrome (SPS). Pathology is diagnosed with prolonged squeezing of a part of the body during sleep in drug or alcohol intoxication, less often - prolonged anesthesia, loss of mobility due to paralysis or severe somatic diseases. In addition, myoglobinuria is found in patients with myofascial compartment syndrome against the background of extensive skeletal injuries, violation of the rules for using a tourniquet, and other reasons.
With SPS, SDR and compartment syndrome, the clinical picture is formed on the first day, myoglobinuria is determined immediately or some time after admission, rapidly increasing. With extensive burns, electrical injury, a laboratory sign appears several days or weeks after the injury. Caused by necrosis of muscle tissue. Increases gradually.
This type of pathology bears the name marching because it is detected in soldiers after long forced marches. It occurs as a result of prolonged muscle tension, significant muscle overload. Another cause of the symptom is too intense training, especially after a break, the first visits to the gym. In addition, marching myoglobinuria is provoked by epistatus, tetanus, alcoholic delirium, severe muscle spasticity in patients with paresis and paralysis.
Myoglobinuria
Meyer-Betz syndrome or paroxysmal paralytic myoglobinuria is a disease of unclear etiology, accompanied by paroxysmal edema, pain, and muscle weakness. The attack begins as a result of physical activity or spontaneously, the muscles of the lower extremities often suffer. 3 hours after the onset of symptoms, brown or red urine begins to be excreted. Sometimes AKI develops. Myoglobinuria is also observed in the following myopathies:
Paroxysmal-toxic alimentary myoglobinuria, or Haff's disease - food toxicosis caused by harmful substances that accumulate in fat, the insides of fish. The attack occurs a few hours or days after eating fish, potentiated by drinking alcohol, physical activity. It is manifested by pain in the muscles of the whole body, a decrease in the amount of urine, its dark color, fever, nausea, vomiting, diarrhea. After 3-4 days, the condition returns to normal, under the influence of provoking factors, violations appear again.
Sometimes myoglobinuria accompanies the following diseases and pathological conditions:
A characteristic change in the color of urine is a reason for an immediate appeal to a specialist. Diagnosis and treatment of traumatic injuries accompanied by myoglobinuria is carried out by orthopedic traumatologists. Patients with myopathies are consulted by neurologists. When signs of acute renal failure are detected, a nephrologist is involved in the examination. During the survey, the specialist finds out when and under what circumstances the color of urine has changed, whether there are other manifestations (dysuria, muscle pain).
In case of injuries, the doctor detects dense edema, impaired sensitivity and movement, determines the area of the lesion to assess the severity of rhabdomyolysis, and draw up a plan for urgent therapeutic measures. With myopathies, it detects signs of muscle atrophy, conducts a neurological examination, including the determination of reflexes, muscle strength, and various types of sensitivity.
Myoglobinuria is confirmed in the study of urine sediment as part of the OAM. For differentiation with hemoglobinuria, a test with ammonium sulfate is used - the preservation of red or brown urine after the addition of this compound indicates the presence of myoglobin. The most accurate way to detect myoglobinuria is immunoelectrophoresis.
In the urine of patients, proteinuria, a change in the ratio of electrolytes, is also found. The density of urine varies depending on the phase of the disease, the presence and severity of acute renal failure. A characteristic feature is considered to be a violation of the ratio of creatinine and urea in urine and blood tests. To assess the patient's condition, clarify the type of pathology accompanied by myoglobinuria, the following diagnostic procedures are prescribed:
Laboratory study of urine
Elimination of myoglobinuria is carried out by treating the underlying pathology. With a high level of myoglobin in the urine test, urgent hospitalization in the intensive care unit, diuresis control, and a diet low in protein and potassium are necessary. The scheme of drug therapy includes the following areas:
With open injuries, gas gangrene, the formation of necrotic foci, antibiotic therapy is necessary. Patients with Haff disease are prescribed analgesics, anticonvulsants and antihistamines, medicines to improve microcirculation, multivitamin complexes. Sometimes hyperbaric oxygen therapy, transfusion of fresh frozen plasma, platelet and erythrocyte mass are required.
Pathogenetic treatment of myopathies has not been developed. Symptomatic therapy is aimed at activating metabolic processes in muscle tissue. Amino acids, neostigmine, ATP, anabolic steroids, anticholinesterase drugs, calcium, potassium, thiamine pyrophosphate are recommended. Medical methods complement exercise therapy, massage, physiotherapy.
In the early period, surgical interventions are required for patients with myoglobinuria against the background of extensive rhabdomyolysis, severe muscle compression, and the formation of areas of necrosis. In the long term, some patients need to eliminate secondary defects of the musculoskeletal system. Taking into account the stage of the disease and the existing symptoms, the following are carried out:
Minor myoglobinuria after intense muscle tension does not pose a health hazard, it goes away on its own. A pronounced increase in the level of myoglobin in trauma, Huff disease, some types of myopathy is fraught with the occurrence of acute renal failure and the death of the patient. The outcome of acute renal failure is determined by the severity of renal dysfunction, age and health of the patient.