Hyperkalemia is the Most Likely Cause
In a TLS patient presenting with nausea, vomiting, palpitations, and muscle aches, hyperkalemia (Option A) is the most likely culprit, as this specific constellation of symptoms directly reflects the cardiac and neuromuscular toxicity of elevated potassium levels.
Pathophysiology of Hyperkalemia in TLS
The rapid lysis of tumor cells releases massive amounts of intracellular potassium into the bloodstream, which is further exacerbated by concurrent renal failure that impairs potassium excretion 1.
Elevated potassium levels produce cardiac irregularities including arrhythmias, ventricular tachycardia, and fibrillation, which manifest clinically as palpitations 1.
High potassium levels also cause neuromuscular effects including muscle cramps and paresthesias, explaining the muscle aches in this patient 1.
Nausea and vomiting are part of the general clinical manifestations of TLS that can occur with multiple electrolyte abnormalities, but when combined with palpitations and muscle aches, they point specifically to hyperkalemia 1.
Why Not the Other Options?
Hypocalcemia (Option B) typically presents with tetany and seizures rather than this symptom pattern 2. While hypocalcemia does occur in TLS as a secondary consequence of hyperphosphatemia, it does not produce palpitations and muscle aches as its primary manifestations 1.
Hyperuricemia (Option C) primarily causes renal complications through uric acid crystal precipitation in renal tubules, leading to renal insufficiency 1. It does not directly produce the cardiac or neuromuscular symptoms described in this patient.
Hypomagnesemia (Option D) is not a characteristic metabolic abnormality of TLS. The classic tetrad includes hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia 3.
Clinical Significance and Mortality Risk
Clinical TLS with significant hyperkalemia carries an 83% mortality rate compared to 24% in patients without clinical TLS 2.
In a Burkitt's lymphoma cohort, two of four deaths were directly attributable to hyperkalemia, underscoring its life-threatening nature 1, 2.
This symptom constellation demands immediate ECG monitoring to assess for cardiac arrhythmias before progression to cardiac arrest 2.
Immediate Management Priorities
For severe hyperkalemia, treatment includes rapid insulin (0.1 units/kg) plus glucose (25% dextrose 2 mL/kg) to shift potassium intracellularly 1.
Calcium carbonate (100-200 mg/kg/dose) stabilizes myocardial cell membranes and prevents life-threatening arrhythmias 1, 2.
Sodium bicarbonate corrects acidosis, which worsens hyperkalemia 1, 2.
Emergency hemodialysis is indicated for persistent or life-threatening hyperkalemia unresponsive to medical management 1, 2.