## Acute Kidney Injury in Crush Syndrome **Key Point:** Myoglobinuria is the most common cause of acute kidney injury (AKI) in crush syndrome, accounting for the majority of renal complications in this setting. ### Pathophysiology of Myoglobinuric AKI 1. **Muscle injury** → Release of myoglobin from damaged skeletal muscle 2. **Myoglobin filtration** → Overwhelms renal tubular reabsorption capacity 3. **Acidic urine** → Myoglobin precipitates in distal tubules and collecting ducts 4. **Tubular obstruction + direct toxicity** → Acute tubular necrosis (ATN) 5. **Renal failure** → Oliguria, elevated creatinine, hyperkalemia ### Clinical Features of Crush Syndrome AKI | Feature | Mechanism | | --- | --- | | Dark cola-colored urine | Myoglobinuria | | Elevated CK (often >5000 IU/L) | Muscle necrosis | | Hyperkalemia | Release from damaged muscle | | Hypocalcemia | Precipitation in muscle; later hypercalcemia in recovery | | Acidosis | Lactic acid from ischemic tissue | **High-Yield:** The urine dipstick is **positive for blood** but **no RBCs on microscopy** — this is pathognomonic for myoglobinuria and distinguishes it from hematuria. ### Prevention and Management - **Aggressive IV hydration** (goal urine output 200–300 mL/hr) - **Alkalinization of urine** (sodium bicarbonate) to prevent myoglobin precipitation - **Monitor CK, potassium, and renal function** closely - **Dialysis** if severe hyperkalemia or refractory AKI develops **Clinical Pearl:** Rhabdomyolysis from crush injury is the classic teaching example of myoglobinuric AKI in orthopedic trauma — more common than sepsis or direct thermal injury as a cause of AKI in the acute phase. [cite:Robbins 10e Ch 20]
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