Hyperkalemia is the Primary Cause
The answer is A. Hyperkalemia. In a patient with Tumor Lysis Syndrome (TLS) presenting with muscle weakness, palpitations, and body aches after chemotherapy, hyperkalemia is the most likely culprit responsible for this symptom triad and represents the most immediately life-threatening electrolyte abnormality requiring urgent intervention.
Clinical Reasoning
Why Hyperkalemia Explains This Presentation
Hyperkalemia produces the exact symptom constellation described in this patient 1:
- Cardiac manifestations: Palpitations result from cardiac irregularities, arrhythmias, and ventricular tachycardia caused by elevated potassium levels 1
- Neuromuscular effects: Muscle aches, cramps, weakness, and paresthesias occur due to hyperkalemia's effect on neuromuscular function 1
- Body aches: The generalized body ache reflects the systemic neuromuscular dysfunction from potassium elevation 1
The American Society of Clinical Oncology emphasizes that this combination of palpitations and muscle aches with other symptoms in a TLS patient demands immediate assessment and treatment of hyperkalemia before it progresses to life-threatening arrhythmias or cardiac arrest 1.
Why Not Hypocalcemia
While hypocalcemia does occur in TLS, the European Hematology Association guidelines indicate that hypocalcemia typically causes tetany and seizures rather than the symptom pattern described here 1. The clinical presentation of muscle weakness, palpitations, and body aches is not characteristic of hypocalcemia. Additionally, asymptomatic hypocalcemia does not require treatment 1, suggesting it is less clinically significant in this context.
Pathophysiology in TLS
TLS occurs when rapid tumor cell lysis releases massive amounts of intracellular potassium into the bloodstream 2. The syndrome develops when tumor cells undergo rapid destruction, releasing intracellular contents including potassium, phosphorus, and nucleic acids 2. This is particularly relevant in the 12-72 hour window after chemotherapy initiation, when symptoms most commonly appear 3.
Hyperkalemia results from the abrupt release of intracellular potassium from lysed cells, exacerbated by concurrent renal failure 4, which impairs the kidney's ability to excrete the excess potassium load.
Mortality Risk
The evidence demonstrates that hyperkalemia in TLS carries significant mortality risk:
- Two of four deaths in a Burkitt's lymphoma cohort were directly attributable to hyperkalemia 3
- Clinical TLS (which includes significant hyperkalemia) was associated with 83% mortality versus 24% in patients without clinical TLS 3
- Hyperkalemia can progress to life-threatening arrhythmias, ventricular tachycardia, and cardiac arrest 1
Immediate Management Required
The American Society of Clinical Oncology recommends immediate ECG monitoring for cardiac arrhythmias in patients with hyperkalemia 1.
For Severe Hyperkalemia 1:
- Rapid insulin plus glucose to shift potassium intracellularly
- Calcium carbonate to stabilize myocardial membranes
- Sodium bicarbonate to correct acidosis
- Emergency hemodialysis if persistent or life-threatening
For Mild Hyperkalemia 1:
- Aggressive hydration
- Loop diuretics
- Sodium polystyrene sulfonate
Critical Pitfall to Avoid
Do not delay treatment while waiting for laboratory confirmation if clinical suspicion is high. The combination of recent chemotherapy, TLS diagnosis, and this specific symptom triad (palpitations + muscle weakness + body aches) should trigger immediate intervention for presumed hyperkalemia, including cardiac monitoring and preparation for emergent treatment 1. The progression from symptomatic hyperkalemia to fatal arrhythmia can occur rapidly, making early recognition and aggressive management essential for preventing mortality.