A 28-year-old male marathon runner presents to the emergency department with severe muscle pain, dark urine, and a serum lactate of 8.2 mmol/L (normal: 0.5–2.2 mmol/L) after completing a 42 km race. His liver function tests are normal, and blood glucose is 95 mg/dL. Arterial blood gas shows pH 7.28 with HCO₃⁻ of 14 mEq/L. What is the most appropriate immediate next step in management?

Explanation

## Clinical Context: Exertional Rhabdomyolysis with Type B Lactic Acidosis This patient presents with **exertional rhabdomyolysis** — a Type B lactic acidosis (tissue hypoxia/hypoperfusion during intense exercise) complicated by myoglobinuria (dark urine). ### Pathophysiology of Lactate Accumulation **Key Point:** During intense exercise, anaerobic metabolism in skeletal muscle overwhelms the Cori cycle's capacity to clear lactate. Lactate produced in muscle exceeds hepatic gluconeogenic clearance, causing lactate accumulation and metabolic acidosis. **High-Yield:** The Cori cycle normally recycles muscle lactate → hepatic glucose → muscle glycogen. In exertional rhabdomyolysis, this cycle is **overwhelmed**, not dysfunctional. The liver is intact; the problem is **volume depletion and renal hypoperfusion** from myoglobin precipitation in renal tubules. ### Why Aggressive IV Fluid Resuscitation is the Best Next Step | Intervention | Rationale | Outcome | |---|---|---| | **IV fluid resuscitation (normal saline)** | Restores circulating volume → improves renal perfusion → prevents acute kidney injury from myoglobin precipitation | Prevents progression to acute tubular necrosis | | Dextrose bolus | Lactate is NOT due to hypoglycemia (glucose = 95 mg/dL); dextrose will worsen hyperglycemia and osmotic stress on kidneys | Harmful in this context | | Sodium bicarbonate | Alkalinization increases myoglobin solubility in urine, reducing tubular precipitation | Secondary measure after volume repletion; not first-line | | Glucagon | Lactate clearance depends on hepatic perfusion, not gluconeogenic stimulation; liver function is normal | Ineffective; does not address the underlying problem | **Clinical Pearl:** The immediate threat in rhabdomyolysis is **acute kidney injury**, not lactate metabolism per se. Aggressive hydration (target urine output 200–300 mL/h) is the cornerstone of management. Monitor: - Serum creatinine and urine myoglobin - Urine output (catheterization if needed) - Electrolytes (hyperkalemia risk from muscle breakdown) **Key Point:** Lactate will clear spontaneously once tissue perfusion is restored and anaerobic metabolism ceases. The Cori cycle will resume normal function once the patient is rehydrated and rhabdomyolysis is halted. ### Mnemonic for Type B Lactic Acidosis Management **FLUIDS** — Fix perfusion, Limit myoglobin precipitation, Urine output monitoring, Identify complications (AKI), Dextrose only if hypoglycemic, Support organ function.