Leakage of myoglobin from muscle and damaged tissue secondary to a crush injury can result in rhabdomyolysis. Myoglobin at high concentrations precipitates in the nephron, appearing pigmented and causing acute renal injury. The urine can look suspicious for hematuria or have a "tea-colored" appearance. Rhabdomyolysis can be diagnosed by the presence of myoglobinuria, electrolyte disorders, isolated elevated aspartate aminotransferase, and/or increased serum creatine kinase levels. Preventing ARF in these patients is essential because the development of ARF is associated with increased mortality. Treatment in patients with hypovolemia and euvolemia is hydration with large volumes of isotonic crystalloid, resulting in goal urine output as high as 100 to 300 mL/h. In addition, alkalization of the urine, with agents such as isotonic sodium bicarbonate, can help by decreasing the rate of precipitation. Mannitol has also been used to induce osmotic diuresis and flush the myoglobin through the kidneys. The evidence for the utility of bicarbonate and mannitol in the management of rhabdomyolysis is weak. Electrolyte abnormalities, including hyperkalemia, hyperphosphatemia, and hypocalcemia, mimicking a tumor lysis pattern, can develop with crush injury, so this should be monitored.

References

• Bosch X, Poch E, Grau JM. Rhabdomyolysis and acute kidney injury. N Engl J Med. 2009;361:62-72.
• Gonzalez D. Crush syndrome. Crit Care Med. 2005;33:S34-S41.
• Lee GX, Duong DK. Rhabdomyolysis: evidence-based management in the emergency department. Emerg Med Pract. 2020;22:1-20.
• Okusa MD, Portilla D. Pathophysiology of acute kidney injury. In: Yu ASL, Chertow GM, Luyckx VA, Marsden PA, Skorecki K, Taal MW, eds. Brenner and Rector's The Kidney. 11th ed. Elsevier; 2019:906-939.