Refers to the breakdown of muscle fibers resulting in the release of muscle fiber contents, myoglobin, into the bloodstream.
Characterized by muscle injury that leads to the release of intracellular muscle contents into the systemic circulation.
Refers to the rapid breakdown of striated muscle caused by multiple processes including: drugs, trauma, viruses, and metabolic disorders.
Can because by muscle compression.
Most cases are caused by trauma due to crush injuries, prolonged immobilization or confinement, or less commonly post surgical ischemia.
Myoglobin is released into the bloodstream and filtered out of the body by the kidneys and it may block the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure.
Dead muscle tissue may cause a large shift of fluid into the muscle.
Damage to muscle results in fluid filling muscles with sodium and chloride, and the resultant swelling may lead to destruction of of the muscle cells.
Injured muscle cells exchange calcium for sodium (sodium-calcium exchanger) with the accumulation of calcium in the sarcoplasmic reticulum leading to sustained muscle contraction and ATP depletion.
Outcomes variable, ranging from asymptomatic elevations creatine phosphokinase to life-threatening electrolyte abnormalities to acute kidney injury requiring dialysis or continuous renal replacement therapy.
Potentially fatal process with a mortality rate of 8% and long-term survival of approximately 80% (Bosch X et al).
Risk factors for muscle damage include: alcoholism, crush injuries, genetic disorders, heat intolerance, heatstroke, necrosis of the muscle, hypophosphatemia, seizures, severe exertion, rigors, trauma, use of cocaine, amphetamines, ((statins)),heroin and PCP
Causes classified as physical or non-physical.
Physical rhabdomyolysis can be confined to a particular area of the body, or affect all muscle simultaneously.
Crush injuries damage muscle directly, and by impairing blood supply.
Exertional causes of rhabdomyolysis include heavy exercise, heat exposure, seizures and a hyperkinetic state.
Recurrent non-physical rhabdomyolysis can be associated with intrinsic muscle enzyme deficiencies.
Non-physical causes include:
Nontraumatic causes of rhabdomyolysis include electrolyte abnormalities, inflammatory myopathies, endocrinopathy, Alcoholism, drugs, infections, toxins, metabolic myopathies, mitochondrial myopathies, malignancy hyperthermia and neuroleptic malignant syndrome.
Infections-Coxsackie, influenza A, B, Epstein-Barr viris, HIV, Plasmodium Falciparum, herpes infections, Salmonella, mycoplasma, tick- borne infections including ehrlichia, babesiosis, Lyme disease Rocky Mountain spotted fever, and tularemia.
Electrolyte and metabolic disturbances-hyperglycemic hyperosmolar state, hyponatremia, hypernatrenia, hypokalemia, hypocalcemia, hypophosphatemia, ketoacidosis, and hypothyroidism.
Toxic exposure-to poisons, venoms.
Autoimmune muscle damage-polymyositis, dermatomyositis.
Drug abuse agents-include alcohol.
Medication-statins, fibrates, antipsychotic medications, neuromuscular blocking agents, and agents that cause hypokalemia.
Genetic-McArdle’s disease, mitochondial disease, G6PD.
Most common complication is renal failure.
Accounts for 7-10% of all cases of acute kidney injury.
Acute kidney injury occurs in 13-50% of patients, with an associated mortality rate as high as 59 % in critically ill patients.
CPK elevation is poorly correlated with disease severity.
The risk of renal replacement therapy or in-hospital mortality was found to be associated with initial CPK levels in excess of 40,000 units per liter (McMahon GM et al).
Symptoms include dark urine, weakness, myalgias and muscle tenderness, muscle weakness, fatigue, arthralgias, seizures, and fluid retention.
Skeletal muscles may be tender.
CPK leves may be very high.
Release of muscle tissue components leads to nausea, vomiting, confusion, coma, cardiac arrhythmias, and electrolyte disturbances.
Serum and urine myoglobin tests are positive.
Serum potassium may be very high.
Swelling of muscles may lead to compartment syndrome.
DIC may be a complication of rhabdomyolysis.
Urinalysis may reveal casts and be positive for hemoglobin without evidence of red blood cells on microscopic examination.
Early and aggressive fluids may prevent kidney damage by rapidly flushing myoglobin out of the kidneys.
Aggressive fluid repletion reduces the accumulation of toxic cellular contents related to rapid breakdown of muscle.
Fluids may need to be given intravenously and some patients may need dialysis.
The risk of renal failure is directly related to the elevation of creatinine kinase levels.
No standardized second line treatment is advocated.