Recognizing, diagnosing, and treating rhabdomyolysis

Abstract

Rhabdomyolysis is an acute and potentially fatal syndrome characterized by striated muscle breakdown and subsequent release of muscle cell contents into the systemic circulation. The sudden release of large quantities of potassium, calcium, organic acids, and myoglobin into the bloodstream can cause renal tubal toxicity, cardiac dysrhythmias, and death. Complications can be managed and minimized if predicted and treated early, but patients may not have classic symptoms of rhabdomyolysis and may even be asymptomatic on presentation. This article reviews the pathophysiology, causes, diagnosis, and treatment of acute rhabdomyolysis.

Rhabdomyolysis in Critically Ill Surgical Patients

“…Patients who developed AKI in our study had serum CK levels above 3000 U/L ( 14 ). Regardless the cause, the treatment of rhabdomyolysis is identical, and the treatment goals are directed towards maintaining adequate tissue perfusion and oxygenation, thus preventing hypo perfusion and hypoxia, eliminating the products of rhabdomyolysis and maintaining urine output, preventing acute kidney injury, as well as eliminating the primary cause of rhabdomyolysis ( 2 , 3 , 10 , 15 ). Main goal of the treatment is to prevent acute kidney failure by maintaining urine output of 200-300 ml/hour ( 3 ).…”

“…Acquired causes of rhabdomyolysis are: trauma and crush syndrome, surgery, extreme physical activity, influence of extreme temperatures, metabolic disorders of water and salts, vascular ischaemia, surgery, various drugs (statins, corticosteroids, antidepressants, neuroleptics, barbiturates, benzodiazepines, salicylates, theophylline, aminocapronic acid) and anesthetics, alcohol abuse, cocaine abuse, neuroleptic malignant syndrome, seizures, toxins, infections or sepsis, prolonged immobilization, carbon monoxide (CO), endocrine disorders, malignant hyprtermia, electrical current and connective tissue disorders ( 2 - 6 ). Despite the vast variety of causes of rhabdomyolysis, the pathogenesis follows common pathway that ultimately leads to destruction of myocytes and release of its components into circulation ( 2 , 3 , 7 - 10 ). Clinical manifestations of rhabdomyolysis are myoglobinuria, myalgia, muscle weakness, swelling, electrolyte imbalance and often, acute kidney injury as severe complication.…”

“…Tea colored urine is a classical manifestation of rhabdomyolysis. The severity of clinical manifestations of rhabdomyolysis can vary from mild and subclinical cases, to severe cases with acute kidney injury and other complications that include disseminated intravascular coagulopathy, changes in micro and macrocirculation, hyperkaliemia, metabolic acidosis, hypocalcemia, hyponatriemia, hyperphosphatemia, cardiac dysrhythmia, changes in mental status, hypotension and shock ( 2 , 3 , 7 - 10 ). Definitive diagnosis of rhabdomyolysis should be made upon laboratory tests that include serum CK, urine and serum myoglobin.…”

Acute kidney injury pathology and pathophysiology: a retrospective review

“…Rhabdomyolysis causes ARF in 7–15% of all AKI cases in the USA and affects 13–50% of hospitalized patients, with worse prognosis and greater mortality in critically ill patients [ 8 ]. In our recent study of renal biopsies accrued from 2011 through June 2014 among 27 850 renal biopsies in our search, 249 biopsies (∼1%) were positive for myoglobin casts [ 9 ].…”

T-cell lymphoma with rhabdomyolysis: case report and literature review

“…This syndrome is characterized by muscle breakdown and necrosis, resulting in the leakage of intracellular muscle constituents into the circulation and extracellular fluid. Rhabdomyolysis ranges from an asymptomatic illness with elevated creatine kinase (CK) levels to a life-threatening condition associated with extreme elevated levels of CK, electrolyte imbalance, acute renal failure (ARF), and disseminated intravascular coagulation ( 1 ). The cause of rhabdomyolysis is usually easily identified.…”