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Aim for 2 Milliliters Per Kilogram Per Hour of Urine Output in Rhabdomyolysis
Awori J. Hayanga MD
Elliott R. Haut MD
Rhabdomyolysis is a syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulation. The severity of illness ranges from asymptomatic elevations of serum muscle enzymes to life-threatening cases associated with severe electrolyte imbalances, acute renal failure, disseminated intravascular coagulation, and death.
The classic presentation of rhabdomyolysis includes myalgias, pigmenturia due to myoglobinuria, and elevated serum muscle enzymes. The most commonly measured enzyme is serum creatinine kinase (CK), which is typically greater than 10,000 IU/L. It should be noted that serum CK levels may remain elevated in the absence of myoglobinuria since myoglobin is cleared from the serum more rapidly than CK. Since serum and/or urine myoglobin levels often take at least hours (if not days) to obtain results, these should not be relied upon to make the diagnosis. Rhabdomyolysis can be reliably diagnosed with the combination of the urine dipstick that is positive for heme (because of urine myoglobin) and urine microscopy showing an absence of red blood cells. Other abnormal electrolyte findings include hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis.
Rhabdomyolysis has many varied etiologies, which are difficult to categorize. Direct mechanical injury resulting in rhabdomyolysis can be caused by trauma, electrocutions, prolonged immobilization, ischemic limb injury, and crush injuries. Other cases can be caused by heatstroke and exertional rhabdomyolysis following vigorous exercise (e.g., strong-man triathlons). In addition, rhabdomyolysis can be caused by drugs and toxins, which can exert either direct myotoxicity (e.g., statins) or cause indirect muscle damage (e.g., alcohol or cocaine). Infections, inflammatory disorders, endocrine, and metabolic etiologies are also included in the long list of differential diagnoses. Genetic causes must be considered if no other cause is readily apparent.
The most important goal of treatment in rhabdomyolysis is preservation of renal function. Plasma volume expansion with intravenous isotonic saline should be given as soon as possible, even while trying to establish the cause of the rhabdomyolysis. As an example, saline
infusion may be started before reperfusion of the trapped body part in the case of severe crush injury. The time to adequate fluid volume restoration directly influences the rate of renal failure. Massive amounts of fluids (well over 10 L) are often required to compensate for the amount of fluid sequestered by necrotic muscle. Urine output is the most important early marker of adequate hydration and many experienced physicians aim for 2 mL/kg/h.
Controversy still exists about the use of mannitol and alkalinization of the urine as additional possible therapies to help prevent renal failure. While some physicians have very strong beliefs regarding the utility of these maneuvers, most agree that neither approach should be used in patients with oliguria. There is no clear evidence that alkalinization is beneficial and there is a risk that alkalinization may worsen hypocalcemia. Likewise, there is no good evidence of the benefit of mannitol use. Saline diuresis seems to be the primary therapeutic action. Monitoring with serial measurements of serum potassium, calcium, phosphate, and creatinine is recommended. It should be noted that hypocalcemia should not be corrected unless the patient is symptomatic to avoid worsening the common rebound hypercalcemia seen during the recovery phase.
Acute renal failure secondary to rhabdomyolysis is managed expectantly and renal replacement therapy begun to control hyperkalemia and/or volume overload. Rhabdomyolysis-induced renal failure behaves somewhat differently than renal failure from other causes. Serum creatinine rises to a higher level more quickly, yet the patients have a better prognosis for recovery of renal function.
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