A 35-year-old woman is admitted 6 hours after a motor vehicle accident with a crush injury to her left thigh. She has severe pain, marked swelling, and tense compartments. Compartment pressures in the anterior and lateral compartments are measured at 72 mmHg and 68 mmHg respectively. She is oliguric with a urine output of 150 mL in the past 4 hours. Serum creatinine is 1.8 mg/dL (baseline 0.8 mg/dL), and potassium is 6.2 mEq/L. After emergency fasciotomy is performed, which of the following is the most important immediate intervention to prevent acute kidney injury and hyperkalemic complications?

Explanation

## Rhabdomyolysis and Acute Kidney Injury in Compartment Syndrome **Key Point:** Compartment syndrome causes muscle necrosis → rhabdomyolysis → myoglobinuria → acute tubular necrosis (ATN) and acute kidney injury (AKI). The primary mechanism of kidney injury is **myoglobin precipitation in acidic urine** within the renal tubules. **High-Yield:** The cornerstone of preventing AKI in rhabdomyolysis is **aggressive hydration + urinary alkalinization**. This prevents myoglobin precipitation and promotes renal clearance. ### Pathophysiology of Rhabdomyolysis-Induced AKI ```mermaid flowchart TD A[Muscle Necrosis]:::outcome --> B[Release of myoglobin<br/>& intracellular contents]:::outcome B --> C[Myoglobinuria<br/>+ Hyperkalemia<br/>+ Hyperphosphatemia]:::outcome C --> D{Urine pH?}:::decision D -->|Acidic pH| E[Myoglobin precipitates<br/>in tubules]:::urgent D -->|Alkaline pH| F[Myoglobin remains soluble<br/>& filtered]:::action E --> G[Acute Tubular Necrosis]:::urgent F --> H[Renal clearance of myoglobin]:::action G --> I[Acute Kidney Injury]:::urgent H --> J[Prevention of AKI]:::outcome ``` ### Management of Rhabdomyolysis-Induced AKI | Intervention | Mechanism | Timing | | --- | --- | --- | | **Aggressive IV hydration (0.5 L/hr)** | Increases GFR, dilutes myoglobin, promotes urine flow | **Immediate** | | **Urinary alkalinization (target pH > 6.5)** | Keeps myoglobin soluble, prevents tubular precipitation | **Immediate** | | **Sodium bicarbonate** | Alkalinizes urine + shifts K^+^ intracellularly | **Early** | | **Insulin + dextrose** | Shifts K^+^ intracellularly (temporary) | **For acute hyperkalemia** | | **Calcium gluconate** | Stabilizes cardiac membrane (hyperkalemia) | **For ECG changes** | | **Loop diuretics** | Promote urine flow; avoid in hypovolemia | **After hydration** | | **Hemodialysis** | Removes K^+^ and uremic toxins | **If refractory AKI** | **Clinical Pearl:** The urine in rhabdomyolysis is **dark brown or cola-colored** due to myoglobin. Dipstick shows **positive for blood but NO RBCs on microscopy** (myoglobin cross-reacts with heme detection). **Key Point:** Aggressive hydration is the **single most important intervention** in the acute phase. Target urine output is **200–300 mL/hr** until myoglobinuria clears. ## Why This Answer Is Correct Aggressive IV hydration with normal saline achieves two critical goals: 1. **Increases glomerular filtration rate** → promotes myoglobin clearance 2. **Dilutes urine** → prevents myoglobin precipitation in acidic tubules Combined with **urinary alkalinization** (sodium bicarbonate to target urine pH > 6.5), this prevents myoglobin from precipitating and causing ATN. This is the **first-line, immediate intervention** and must be started in the emergency department, even before hemodialysis is considered. **Warning:** Hyperkalemia (K^+^ = 6.2 mEq/L) is present, but calcium gluconate and insulin-dextrose are **temporizing measures** for cardiac stabilization and intracellular shift. They do NOT address the underlying cause (rhabdomyolysis) or prevent AKI. Hydration and alkalinization are the definitive preventive strategy.