Rhabdomyolysis is a syndrome that develops as a result of damage to the skeletal muscle, resulting in the appearance of free myoglobin in the blood (myoglobinemia). Blood myoglobin is filtered by the glomeruli of the kidneys and appears in the urine (myoglobinuria), which can lead to the development of acute renal failure. Genetic Aspects

    • Acute recurrent rhabdomyolysis (familial paroxysmal myoglobinuria,
    • 268200, p)
    • Hypoglycemia hypoketotic (#255120, llq, carnitine palmitoyl transferase I gene CPT1,
    • 600528, p)
    • Myopathy with deficiency of carnitine palmitoyl transferase II (-#255110, gene carnitine palmitoyl transferase II CPT2, 600650, p).

Dominant age

    • Depends on the etiology of acute skeletal muscle necrosis
    • At a younger age, hereditary disorders lead to acute necrosis of skeletal muscles.
    • Other causes (trauma, infection) can cause rhabdomyolysis at any age. Etiology
    • Hereditary metabolic disorders (see Genetic Aspects)
    • Electrolyte disorders (hypokalemia, hypophosphatemia)
    • Myopathies
    • Polymyositis, dermatomyositis
    • Malignant hyperthermia
    • Malignant syndrome when taking certain drugs (anesthetics, phenothiazines, MAO inhibitors)
    • Muscle tension (physical, secondary to spasticity or heatstroke)
    • Injury
    • Muscle ischaemia due to arterial occlusion or cardiovascular failure
    • burns
    • Repeated muscle injury (for example, during sports), prolonged pressure on the muscles
    • Epileptic status
    • Infectious diseases
    • Viruses (influenza A, Epstein-Barr, chickenpox)
    • bacteria
    • Toxic muscle damage
    • Alcohol
    • Snake venom (for bites)
    • Carbon monoxide (carbon monoxide)
    • cocaine, heroin, amphetamine
    • Overdose of drugs
    • Theophylline
    • Isoniazid
    • Malignant neoplasms (acute necrotic myopathy of tumors)
    • Diabetes.


    • Muscle necrosis
    • The picture of kidney damage by myoglobin resembles acute tubular necrosis of another etiology.

clinical picture. Pain, muscle weakness, and muscle swelling may occur early on (physical examination may not reveal muscle abnormalities despite myoglobinuria)

    • Symptoms and signs of renal failure are similar to those of acute renal failure of other etiologies.

Differential Diagnosis

    • Diseases that cause necrotic changes in the tubules of the kidneys
    • Kidney damage by hemoglobin pigments.

Laboratory research

    • Increased blood levels of muscle enzymes (CPK, aldolase, LDH)
    • Elevated levels of potassium and phosphorus due to muscle damage
    • Hypocalcemia during oliguria, sometimes hypercalcemia during recovery from acute tubular necrosis
    • Urinalysis – a positive result of a urine test for blood without detecting red blood cells in the sediment
    • There may be high hyperuricemia, which can cause acute uric acid nephropathy
    • Vitamin D levels are reduced during oliguria
    • Sometimes there is reversible liver dysfunction. Special Studies
    • Hypocalcemia during the period of oliguria is a useful diagnostic feature, but does not give the likelihood of establishing a diagnosis of acute skeletal muscle necrosis.
    • High hyperkalemia, hyperphosphatemia and hyperuricemia are a weighty argument in favor of acute skeletal muscle necrosis.


Tactics of conducting

    • Mandatory hospitalization (see also Acute Renal Failure)
    • With skeletal necrosis

flight muscles caused by pinching, surgery is sometimes indicated

    • Dialysis required for severe kidney failure
    • Treatment of hypocalcemia – see Hypocalcemia

Physical activity—Exercise can lead to acute necrosis of skeletal muscle, especially in those with metabolic myopathies. Diet—Acute kidney failure will require dietary restriction of protein (to reduce blood urea nitrogen) and potassium-containing foods.

Drug therapy

    • In acute skeletal muscle necrosis to prevent the development of renal failure – increase urine output to 150 ml / h (3 ml / kg / h)
    • Mannitol (mannitol) 12.5–25 g IV
    • Infusion of sodium bicarbonate (up to a urine pH of 7–7.5) to reduce myoglobin damage to the tubules
    • For severe hyperkalemia, see Hyperkalemia.


    • The disease can start spontaneously
    • Some cases (damage with tissue crush) are accidental, do not recur and do not require further long-term follow-up after treatment. Prevention
    • Prevention of exposure to certain etiological factors before the onset of acute skeletal muscle necrosis
    • Prevention of metabolic disorders (hypokalemia) and combinations of drugs leading to acute necrosis of skeletal muscles.


    • Unfavorable, death often due to hyperkalemia or renal failure
    • The prognosis improves with dialysis and replacement therapy.

Synonym. Myoglobinuria with renal insufficiency R82.1 Myoglobinuria


  • 232600 McArdle disease
  • 255110 Myopathy with carnitine palmitoyl transferase II deficiency
  • 255120 Hypoglycemia, hypoketotic
  • 268200 Acute recurrent rhabdomyolysis

Leave a Comment

Your email address will not be published. Required fields are marked *