Does Rhabdomyolysis Cause Hyperkalemia?
Yes, rhabdomyolysis directly causes hyperkalemia through the release of intracellular potassium from damaged muscle cells into the circulation, and this can be life-threatening. 1, 2
Mechanism of Hyperkalemia in Rhabdomyolysis
The pathophysiology is straightforward and well-established:
Muscle cell breakdown releases massive amounts of intracellular potassium into the bloodstream, as mechanical stresses on skeletal muscle membranes lead initially to loss of potassium ions from muscle cells, followed by larger molecules like myoglobin and creatine kinase. 1
Potassium shifts from the intracellular to extracellular compartment because 98% of the body's potassium is normally contained within cells, so even small shifts during muscle destruction result in major changes in serum potassium concentrations. 1
Acute kidney injury compounds the problem by impairing renal potassium excretion, which occurs in 13-50% of rhabdomyolysis patients and is the principal cause of mortality. 2, 3
Clinical Severity and Cardiac Risk
The hyperkalemia from rhabdomyolysis can be severe and immediately life-threatening:
Cardiac arrest from hyperkalemia has been documented in multiple case reports of rhabdomyolysis, with potassium levels reaching 9.2 mmol/L causing wide QRS complexes and asystole. 4, 3
Reperfusion injury after vascular procedures in patients with traumatic rhabdomyolysis and compartment syndrome can trigger life-threatening hyperkalemia requiring emergency treatment. 3
The combination of rhabdomyolysis-induced acute renal failure and hyperkalemia creates a dangerous cycle where impaired kidney function prevents potassium elimination while ongoing muscle breakdown continues releasing potassium. 5, 2
Specific Clinical Contexts
Malignant Hyperthermia
- Rhabdomyolysis from malignant hyperthermia causes hyperkalemia through muscle membrane breakdown, with mechanical stresses leading to potassium ion loss from muscle cells. 1
- This can progress to acute hyperkalaemia severe enough to produce cardiac arrest, though more commonly presents as myoglobinuria postoperatively. 1
Exercise-Related Rhabdomyolysis
- Exertional rhabdomyolysis can trigger a cascade leading to hyperkalemia, lactic acidosis, worsening hypoxia, impaired cardiac and renal function, and lethal arrhythmias. 1
- Metabolic insult with hyperkalemia can lead to pulseless electrical activity where external defibrillation effectiveness is unpredictable. 1
Drug-Related Rhabdomyolysis
- Severe hyperkalemia (9.2 mmol/L) has been documented after drug abuse causing rhabdomyolysis, requiring immediate cardiopulmonary resuscitation and transcutaneous pacing. 4
Paradoxical Presentation
A critical pitfall: hypokalemia can cause rhabdomyolysis, which then causes hyperkalemia, creating a diagnostic challenge where the initial hypokalemia may go unrecognized due to the counteracting effect of rhabdomyolysis on serum potassium. 6 This emphasizes the need for vigilance, as failure to detect rhabdomyolysis promptly may prove fatal. 6
Treatment Implications
When hyperkalemia occurs from rhabdomyolysis, standard hyperkalemia management applies:
Cardiac membrane stabilization with calcium chloride (500-1000 mg IV over 2-5 minutes) or calcium gluconate (15-30 mL IV over 2-5 minutes) for immediate cardioprotection. 1
Shift potassium intracellularly with insulin plus glucose (25g glucose with 10U regular insulin IV over 15-30 minutes), sodium bicarbonate (50 mEq IV over 5 minutes), or nebulized albuterol (10-20 mg over 15 minutes). 1
Promote potassium elimination through diuresis (furosemide 40-80 mg IV), potassium binders, or dialysis for refractory cases. 1, 3
Continuous Renal Replacement Therapy may be required for severe cases with acute kidney injury, though mortality remains high despite aggressive treatment. 3