What is the likely cause of nausea, vomiting, palpitations, and muscle aches in a patient with Tumor Lysis Syndrome (TLS)?

Hyperkalemia (Answer A)

The most likely cause of nausea, vomiting, palpitations, and muscle aches in this TLS patient is hyperkalemia, which produces this exact symptom constellation and represents an immediate life-threatening emergency requiring urgent ECG monitoring and treatment. 1, 2

Why Hyperkalemia is the Answer

Pathophysiology in TLS

• Rapid tumor cell lysis releases massive amounts of intracellular potassium into the bloodstream, particularly in the 12-72 hour window after chemotherapy initiation 1
• This potassium overload is exacerbated by concurrent renal failure, which impairs the kidney's ability to excrete the excess potassium load 1, 3

Clinical Manifestations Match Perfectly

• Palpitations: Elevated potassium produces cardiac irregularities including arrhythmias, ventricular tachycardia, and potentially cardiac arrest 2, 3
• Muscle aches: High potassium causes neuromuscular effects including muscle cramps and paresthesias 2, 3
• Nausea and vomiting: These are common gastrointestinal manifestations of TLS-related hyperkalemia 2
• The American Society of Clinical Oncology specifically emphasizes that this combination of palpitations and muscle aches with gastrointestinal symptoms in a TLS patient demands immediate assessment and treatment of hyperkalemia before it progresses to life-threatening arrhythmias or cardiac arrest 1, 2

Mortality Risk

• Clinical TLS with significant hyperkalemia carries an 83% mortality rate versus 24% in patients without clinical TLS 1
• In Burkitt's lymphoma cohorts, two of four deaths were directly attributable to hyperkalemia 1, 3

Why Not the Other Options

Hypocalcemia (Option B) - Wrong Symptom Pattern

• The European Hematology Association guidelines clearly state that hypocalcemia typically causes tetany and seizures rather than the symptom pattern described here 4, 1, 2
• Asymptomatic hypocalcemia does not require treatment 4
• The clinical presentation described does not match hypocalcemia's characteristic neuromuscular irritability pattern 4

Hyperuricemia (Option C) - Wrong Clinical Picture

• Hyperuricemia primarily causes acute oliguric renal failure and anuria through uric acid crystallization in collecting ducts 4
• It does not directly produce the cardiac (palpitations) and neuromuscular (muscle aches) symptoms described 4

Hypomagnesemia (Option D) - Not a Primary TLS Feature

• Hypomagnesemia is not listed among the cardinal metabolic derangements of TLS (hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia) 4, 5, 6

Immediate Management Required

Severe Hyperkalemia Treatment

• Rapid insulin (0.1 units/kg) plus glucose (25% dextrose 2 mL/kg) to shift potassium intracellularly 4, 3
• Calcium carbonate (100-200 mg/kg/dose) to stabilize myocardial cell membranes and prevent life-threatening arrhythmias 4, 3
• Sodium bicarbonate to correct acidosis 4
• Emergency hemodialysis for persistent or life-threatening hyperkalemia unresponsive to medical management 4, 3

Mild Hyperkalemia (<6 mmol/L) Treatment

• Aggressive hydration with loop diuretics 4
• Sodium polystyrene sulfonate 1 g/kg orally or by enema 4

Critical Monitoring

• Immediate ECG monitoring for cardiac arrhythmias is mandatory 4, 1, 2
• Careful continuous ECG monitoring should be performed in all hyperkalemic patients 4

Clinical Pitfall to Avoid

Do not delay treatment while waiting for laboratory confirmation if clinical suspicion is high—the combination of symptoms in a TLS patient warrants immediate empiric hyperkalemia management given the high mortality risk 1, 2