In a patient with tumor lysis syndrome presenting with nausea, palpitations, muscle weakness, and generalized aches, which electrolyte abnormality is most likely responsible?

Hyperkalemia is Causing These Symptoms

In a patient with tumor lysis syndrome presenting with nausea, palpitations, muscle weakness, and generalized aches, hyperkalemia (Answer A) is the most likely culprit—this specific constellation of cardiac and neuromuscular symptoms directly reflects elevated potassium levels and represents a life-threatening emergency requiring immediate intervention. 1, 2

Why Hyperkalemia Fits This Clinical Picture

The symptom triad points unmistakably to hyperkalemia:

• Palpitations arise from cardiac electrical disturbances—including arrhythmias, ventricular tachycardia, and fibrillation—that are directly precipitated by elevated serum potassium levels released from massive tumor cell lysis. 3, 1

• Muscle weakness and aches represent the neuromuscular effects of high potassium concentrations, manifesting as muscle cramps and paresthesias that patients describe as generalized body aches. 3, 1

• Nausea is part of the general clinical manifestations of TLS, but when combined specifically with palpitations and muscle symptoms, it points directly to hyperkalemia rather than other electrolyte abnormalities. 1

Why the Other Options Don't Match

Hypocalcemia (Answer B)

• Hypocalcemia in TLS typically produces tetany and seizures rather than the palpitations and muscle weakness pattern described here. 3, 1
• While hypocalcemia does occur in TLS from calcium-phosphate precipitation, its clinical presentation is distinctly different—characterized by neuromuscular irritability, carpopedal spasm, and Chvostek's/Trousseau's signs. 3

Hyperuricemia (Answer C)

• Hyperuricemia primarily causes renal complications—oliguria and acute renal failure through uric acid crystal deposition in collecting ducts—rather than cardiac or neuromuscular symptoms. 3, 1
• While hyperuricemia is a cardinal feature of TLS, it does not generate the palpitations or muscle weakness characteristic of this patient's presentation. 3

Hypomagnesemia (Answer D)

• Hypomagnesemia is not a cardinal feature of tumor lysis syndrome at all—the syndrome is defined by hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. 3

The Life-Threatening Nature of This Diagnosis

Understanding the mortality risk is critical:

• Clinical TLS with significant hyperkalemia carries an 83% mortality rate compared to 24% in patients without clinical TLS, underscoring why immediate recognition and treatment are paramount. 1

• In a Burkitt's lymphoma cohort, two of four deaths were directly attributable to hyperkalemia, demonstrating that this electrolyte abnormality can rapidly progress from muscle cramps and palpitations to sudden cardiac death. 1, 2

• Hyperkalemia (≥6 mmol/L) is the most hazardous acute complication that can cause sudden death from cardiac arrhythmias and must be treated quickly and aggressively. 4

Immediate Management Required

Once hyperkalemia is identified as the cause:

• Initiate continuous ECG monitoring immediately to detect life-threatening arrhythmias before they cause cardiac arrest. 3, 2

• For severe hyperkalemia (≥6 mmol/L), administer rapid insulin (0.1 units/kg) plus 25% dextrose (2 mL/kg) to shift potassium intracellularly. 3, 1

• Give calcium carbonate (100-200 mg/kg/dose) to stabilize myocardial cell membranes and prevent progression to ventricular fibrillation or cardiac arrest. 3, 1

• Prepare for emergency hemodialysis if hyperkalemia is persistent or life-threatening and unresponsive to medical management—hemodialysis can reduce plasma potassium rapidly and may be lifesaving. 3, 5

Critical Pitfall to Avoid

Do not wait for laboratory confirmation if clinical suspicion is high—the combination of palpitations and muscle weakness in a TLS patient should trigger immediate empiric treatment for hyperkalemia while awaiting potassium levels, as delays can be fatal. 2, 4