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

Hyperkalemia is the Most Likely Cause

In a patient with Tumor Lysis Syndrome (TLS) presenting with nausea, vomiting, palpitations, and muscle aches, hyperkalemia (Option A) is the most likely culprit and represents the most immediately life-threatening metabolic derangement requiring urgent intervention. 1, 2

Clinical Reasoning and Symptom Correlation

The symptom constellation described maps directly to hyperkalemia's clinical manifestations in TLS patients:

• Cardiac symptoms (palpitations) result from potassium-induced cardiac dysrhythmias, ventricular tachycardia, and potentially cardiac arrest 1, 2
• Neuromuscular symptoms (muscle aches) occur due to elevated potassium causing muscle cramps, paresthesias, and neuromuscular irritability 1, 2
• Gastrointestinal symptoms (nausea, vomiting) are common manifestations of TLS-related hyperkalemia 3, 2

This specific combination demands immediate assessment and treatment before progression to life-threatening arrhythmias or cardiac arrest. 1, 2

Why Not the Other Options?

Hypocalcemia (Option B) typically presents with tetany and seizures rather than this symptom pattern, and asymptomatic hypocalcemia does not require treatment. 3, 1 The muscle symptoms from hypocalcemia are characterized by tetany and carpopedal spasm, not the generalized muscle aches described here.

Hyperuricemia (Option C) primarily causes renal complications through uric acid crystal deposition in renal tubules, leading to acute kidney injury rather than the cardiac and neuromuscular symptoms presented. 3, 4

Hypomagnesemia (Option D) is not a characteristic metabolic abnormality of TLS. The classic TLS electrolyte disturbances are hyperkalemia, hyperphosphatemia, hypocalcemia, and hyperuricemia. 3, 4, 5

Pathophysiology and Mortality Risk

• TLS occurs when rapid tumor cell lysis releases massive amounts of intracellular potassium into the bloodstream, particularly within 12-72 hours after chemotherapy initiation 3, 1
• The abrupt potassium release is exacerbated by concurrent renal failure, which impairs the kidney's ability to excrete the excess potassium load 1
• Clinical TLS with significant hyperkalemia carries an 83% mortality rate versus 24% in patients without clinical TLS 3, 1
• In one Burkitt's lymphoma cohort, two of four deaths were directly attributable to hyperkalemia 3, 1

Immediate Management Algorithm

Step 1: Immediate ECG monitoring for cardiac arrhythmias in all patients with suspected hyperkalemia 1, 2

Step 2: Severity-based treatment approach:

For severe hyperkalemia (>6 mmol/L or symptomatic):

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

For mild hyperkalemia (<6 mmol/L, asymptomatic):

• Aggressive hydration with goal urine output ≥100 mL/hour 3
• Loop diuretics 3, 1
• Sodium polystyrene sulfonate 1 g/kg orally or by enema 3

Critical Pitfalls to Avoid

• Do not delay treatment while waiting for laboratory confirmation if clinical suspicion is high based on symptoms and ECG changes 1, 2
• Avoid calcium administration in the presence of hyperphosphatemia unless the patient has symptomatic hypocalcemia with ECG changes or tetany, as this can precipitate calcium-phosphate crystal deposition 3
• Maintain continuous cardiac monitoring as hyperkalemia can cause sudden death from arrhythmias 3, 5