From the Guidelines
Rhabdomyolysis treatment should prioritize aggressive intravenous fluid resuscitation with normal saline at rates of 200-300 mL/hour initially, aiming to maintain urine output above 200-300 mL/hour, as recommended by recent guidelines 1. The goal of treatment is to prevent complications like acute kidney injury, electrolyte abnormalities, and compartment syndrome. Key aspects of management include:
- Monitoring creatine kinase (CK) levels, renal function, and electrolytes (particularly potassium, calcium, and phosphate) is essential 1.
- Addressing the underlying cause is crucial, whether it's medication discontinuation, treating infections, or managing other triggers.
- Bicarbonate administration may be considered to alkalinize urine if the pH is below 6.5, though this remains controversial 1.
- Patients should avoid NSAIDs and other nephrotoxic medications during recovery.
- Severe cases may require kidney dialysis if acute kidney injury develops.
- In patients with severe limb(s) trauma, the risk of developing compartment syndrome should be assessed, and clinical signs such as pain, tension, paraesthesia, paresis, and increased compartmental pressure should be monitored 1.
- The use of diuretics, such as loop diuretics, is not recommended for the prevention of AKI, and their use in patients with AKI and rhabdomyolysis should be cautious 1. In terms of fluid resuscitation, the volume to be administered remains debated, but most retrospective studies report that patients who eventually developed acute kidney injury had a longer time to initiate volume resuscitation compared to those who did not 1. Overall, the management of rhabdomyolysis requires a multifaceted approach that prioritizes prompt fluid therapy, monitoring, and addressing the underlying cause to prevent complications and improve outcomes.
From the Research
Definition and Pathophysiology of Rhabdomyolysis
- Rhabdomyolysis is a clinical syndrome of muscle injury associated with myoglobinuria, electrolyte abnormalities, and often acute kidney injury (AKI) 2.
- The pathophysiology involves injury to the myocyte membrane and/or altered energy production that results in increased intracellular calcium concentrations and initiation of destructive processes 2.
- Myoglobin has been identified as the primary muscle constituent contributing to renal damage in rhabdomyolysis 2.
Causes of Rhabdomyolysis
- Rhabdomyolysis can be caused by various factors, including crush injuries, trauma, prescription and over-the-counter medications, alcohol, and illicit drugs 2.
- Other possible causes include excessive muscular activity, infections, and varied metabolic, connective tissue, rheumatologic, and endocrine disorders 3.
Diagnosis of Rhabdomyolysis
- The diagnosis is confirmed by elevated creatine kinase levels, but additional testing is needed to evaluate for potential causes, electrolyte abnormalities, and AKI 2.
- Serum potassium levels must be obtained and electrocardiograms must be evaluated to identify life- and limb-threatening complications of hyperkalemia 3.
Treatment of Rhabdomyolysis
- Early and aggressive fluid resuscitation to restore renal perfusion and increase urine flow is agreed on as the main intervention for preventing and treating AKI 2, 4.
- Aggressive intravenous fluid resuscitation (IVFR) has been shown to decrease the incidence of acute renal failure (ARF) and need for dialysis in patients with rhabdomyolysis 5.
- There is little evidence to support the routine use of bicarbonate-containing fluids, mannitol, and loop diuretics 2, 5.
- Hyperkalemia and compartment syndrome are additional complications of rhabdomyolysis that must be treated effectively 2, 3.
Management and Prognosis
- The systemic impact of rhabdomyolysis ranges from asymptomatic elevations in bloodstream muscle enzymes to life-threatening acute kidney injury and electrolyte abnormalities 6.
- Early vigorous fluid resuscitation with ≥12 l daily intravenous infusion of alkaline solution started at the scene of injury can stabilize the circulation and mobilize edema fluids sequestered in the injured muscles into the circulation, correct hyperkalemia and acidosis, and protect against the nephrotoxic effects of myoglobinemia and hyperuricosuria 4.