Can rhabdomyolysis cause lactic acidosis?

Rhabdomyolysis and Lactic Acidosis: Pathophysiological Connection

Yes, rhabdomyolysis can directly cause lactic acidosis through multiple mechanisms related to muscle breakdown and metabolic derangements.

Pathophysiological Mechanisms

• Rhabdomyolysis leads to massive muscle breakdown, releasing cellular contents including myoglobin and creatine kinase into circulation, which can trigger metabolic disorders including lactic acidosis 1, 2
• During rhabdomyolysis, damaged muscle tissue undergoes anaerobic metabolism, producing lactate and contributing to acidosis 3
• Impaired tissue perfusion secondary to rhabdomyolysis-induced hypovolemia can lead to Type A lactic acidosis due to inadequate oxygen delivery to tissues 1
• Myoglobin released during rhabdomyolysis can cause renal vasoconstriction and tubular obstruction, leading to acute kidney injury, which further impairs lactate clearance 4

Clinical Evidence

• Multiple case reports document the co-occurrence of rhabdomyolysis and lactic acidosis, particularly in conditions like:
  • Sickle cell trait with exertional rhabdomyolysis 3, 4
  • Medication overdoses, including metformin 5, 6
  • Strychnine poisoning 7
  • Substance abuse, including legal highs 8

Specific Clinical Scenarios

• In sickle cell trait patients with exertional rhabdomyolysis, a cascade of events can occur including vascular occlusion, endothelial damage, and impaired muscular blood flow, which promotes rhabdomyolysis and subsequently leads to hyperkalemia, lactic acidosis, and impaired cardiac function 3
• Severe cases of rhabdomyolysis can progress to a metabolic insult with lactic acidosis, hyperkalemia, and hypocalcemia, potentially leading to pulseless electrical activity 3
• Malignant hyperthermia, which can cause rhabdomyolysis, also leads to increased metabolic rate and muscle contractile activity, resulting in lactic acidosis 3

Diagnostic Considerations

• Laboratory findings in rhabdomyolysis-induced lactic acidosis typically include:
  • Arterial pH <7.35 3
  • Elevated blood lactate levels (>2 mmol/L) 1
  • Increased anion gap (Na - [Cl+HCO3-] >16) 1
  • Elevated creatine kinase (marker of muscle breakdown) 4
  • Myoglobinuria 3

Management Implications

• Treatment should address both the rhabdomyolysis and resultant lactic acidosis:
  • Aggressive intravenous fluid resuscitation to maintain renal perfusion and prevent acute kidney injury 4
  • Monitoring and correction of electrolyte abnormalities, particularly hyperkalemia 3
  • In severe cases, consideration of renal replacement therapy for both metabolic derangements and myoglobin clearance 5
  • Addressing the underlying cause of rhabdomyolysis 1

Clinical Pitfalls and Caveats

• Rhabdomyolysis-induced lactic acidosis may be misdiagnosed as primary lactic acidosis from other causes, delaying appropriate treatment 6
• The combination of rhabdomyolysis and lactic acidosis significantly increases mortality risk, particularly when accompanied by acute kidney injury 4
• Failure to recognize early signs of rhabdomyolysis (muscle pain, weakness, dark urine) may lead to delayed diagnosis of associated lactic acidosis 1
• In patients with sickle cell trait experiencing exertional collapse, the combination of rhabdomyolysis and lactic acidosis should be considered a medical emergency requiring immediate intervention 3