## Rhabdomyolysis and Acute Kidney Injury Following Compartment Syndrome ### Pathophysiology of Crush Injury Complications **Key Point:** Crush injuries cause massive muscle necrosis with release of intracellular contents (myoglobin, potassium, phosphate, uric acid) into the circulation, leading to **rhabdomyolysis** and **acute tubular necrosis (ATN)**. ### Clinical Features of Rhabdomyolysis | Feature | Finding in This Case | |---------|----------------------| | **Muscle damage** | Crush injury + compartment syndrome | | **Myoglobinuria** | Dark brown (cola-colored) urine | | **Serum myoglobin** | Elevated (not routinely measured) | | **Creatine kinase (CK)** | Markedly elevated (typically > 5,000 U/L) | | **Acute kidney injury** | Creatinine rise from 0.9 to 2.8 mg/dL in 24 hours | | **Mechanism** | Myoglobin precipitation in renal tubules + direct tubular toxicity | **High-Yield:** The dark urine (myoglobinuria) is pathognomonic for rhabdomyolysis. Myoglobin is a small molecule that is freely filtered by the glomerulus and precipitates in acidic urine within the tubules, causing ATN. ### Prevention and Management of Rhabdomyolysis-Induced AKI **Mnemonic:** FLUSH — **F**luids, **L**oop diuretics, **U**rine **S**tatus, **H**yperkalemia management #### 1. Aggressive IV Hydration - **Goal:** Maintain urine output **200–300 mL/hour** (or 1 L/day minimum) - **Fluid choice:** **Normal saline (0.9% NaCl)** — isotonic, maintains intravascular volume without diluting serum osmolality - **Mechanism:** High urine flow dilutes myoglobin concentration in tubules, reducing precipitation and tubular obstruction - **Rate:** Often requires 1–1.5 L/hour initially; titrate to urine output **Warning:** Hypotonic saline (0.45% NaCl) is NOT recommended — it can worsen myoglobinuria by increasing urine flow but diluting serum osmolality, potentially worsening rhabdomyolysis. #### 2. Urine Alkalinization - **Goal:** Maintain urine pH > 6.5 (ideally 7–8) - **Method:** Add **sodium bicarbonate** to IV fluids (target serum HCO~3~^−^ 20–25 mEq/L) - **Mechanism:** Myoglobin is less soluble in acidic urine; alkaline urine prevents precipitation in tubules - **Monitoring:** Check urine dipstick (myoglobin) and urine pH hourly initially #### 3. Loop Diuretics (Furosemide) - **Indication:** If fluid overload develops or urine output plateaus despite hydration - **Mechanism:** Increases urine flow, further diluting myoglobin - **Caution:** Use only *after* adequate hydration; diuretics alone worsen dehydration and AKI #### 4. Hyperkalemia Management - **Risk:** Massive K^+^ release from muscle necrosis - **Interventions:** Calcium gluconate, insulin + glucose, beta-2 agonists, diuretics - **Dialysis:** Reserved for severe hyperkalemia (K^+^ > 6.5 mEq/L) or refractory AKI ### Why Hemodialysis Is NOT First-Line **Clinical Pearl:** Hemodialysis is indicated for: - **Refractory hyperkalemia** (K^+^ > 6.5 mEq/L unresponsive to medical management) - **Severe metabolic acidosis** (pH < 7.1) - **Fluid overload** with pulmonary edema - **Uremia** (BUN > 100 mg/dL, creatinine > 10 mg/dL) In this case, the patient has early AKI (creatinine 2.8 mg/dL) and no mention of hyperkalemia or pulmonary edema. Aggressive medical management with fluids and alkalinization is the appropriate first step; dialysis is reserved for progression or complications. ### Management Algorithm ```mermaid flowchart TD A[Crush injury with rhabdomyolysis]:::outcome --> B[Dark urine + elevated CK + rising creatinine]:::outcome B --> C[Aggressive IV hydration with normal saline]:::action C --> D[Target urine output 200-300 mL/hour]:::action D --> E[Add sodium bicarbonate for urine alkalinization]:::action E --> F{Urine output adequate + pH > 6.5?}:::decision F -->|Yes| G[Continue hydration + monitoring]:::action F -->|No| H[Add furosemide if fluid overload]:::action H --> I{Hyperkalemia or refractory AKI?}:::decision I -->|Yes| J[Hemodialysis]:::urgent I -->|No| K[Continue medical management]:::action ``` 
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