A - Hyperkalemia
In a patient with tumor lysis syndrome presenting with nausea, vomiting, palpitations, and muscle aches, hyperkalemia is the electrolyte abnormality responsible for this specific constellation of symptoms. 1
Why Hyperkalemia Explains This Clinical Picture
Cardiac Manifestations
- Palpitations arise directly from hyperkalemia-induced cardiac electrical disturbances, including arrhythmias, ventricular tachycardia, and fibrillation, as the elevated potassium disrupts normal myocardial conduction. 12
- The American Society of Clinical Oncology emphasizes that hyperkalemia is the most hazardous acute complication of TLS, capable of causing sudden death from cardiac arrhythmias. 23
Neuromuscular Effects
- Muscle aches and cramps represent the neuromuscular dysfunction caused by high potassium concentrations affecting skeletal muscle membrane potentials. 12
- These symptoms occur alongside generalized muscle weakness and paresthesias as potassium levels rise. 1
Gastrointestinal Symptoms
- Nausea and vomiting are common manifestations of TLS-related hyperkalemia, though less specific than the cardiac and neuromuscular findings. 2
Why the Other Options Are Incorrect
Hypocalcemia (Option B)
- Hypocalcemia in TLS typically produces tetany, seizures, carpopedal spasm, and positive Chvostek/Trousseau signs—not palpitations or muscle weakness. 12
- The European Hematology Association guidelines specify that asymptomatic hypocalcemia does not require treatment, and symptomatic hypocalcemia manifests as neuromuscular irritability rather than the described symptom pattern. 24
Hyperuricemia (Option C)
- Hyperuricemia primarily causes renal complications through uric acid crystal deposition in tubules, leading to oliguria and acute renal failure. 15
- It does not generate the cardiac arrhythmias (palpitations) or neuromuscular symptoms (muscle aches) characteristic of this patient's presentation. 1
Hypomagnesemia (Option D)
- Hypomagnesemia is not a cardinal feature of tumor lysis syndrome, which is defined by hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. 16
- This electrolyte abnormality does not explain the clinical syndrome described. 1
Critical Clinical Context
Mortality Risk
- Clinical TLS with significant hyperkalemia carries an 83% mortality rate compared to 24% in patients without clinical TLS. 1
- In Burkitt's lymphoma cohorts, two of four deaths were directly attributable to hyperkalemia, underscoring its life-threatening nature. 1
Pathophysiology
- Rapid tumor cell lysis releases massive amounts of intracellular potassium (normal intracellular concentration is 140 mEq/L) into the bloodstream. 17
- Concurrent renal failure impairs potassium excretion, creating a perfect storm for severe hyperkalemia. 14
Immediate Management Priorities
Do not await laboratory confirmation when the clinical picture strongly suggests hyperkalemia—initiate empiric treatment immediately to avoid fatal delays. 1
- Continuous ECG monitoring to detect life-threatening arrhythmias promptly. 24
- Rapid intravenous insulin (0.1 U/kg) with 25% dextrose (2 mL/kg) to shift potassium intracellularly. 12
- Calcium carbonate (100-200 mg/kg per dose) to stabilize myocardial cell membranes and prevent ventricular fibrillation or cardiac arrest. 12
- Prepare for emergency hemodialysis if hyperkalemia persists despite medical therapy or if the patient becomes hemodynamically unstable. 14