Nursing care
Why tumour lysis syndrome causes hyperkalaemia and what to monitor
Written and reviewed by Dana Whitfield, RN, MSN · 4 min read · Updated October 2026
Short answer
When treatment kills large numbers of cancer cells quickly, their contents spill into the blood. Cells hold most of the body's potassium and phosphate, and their DNA breaks down into uric acid. The kidneys can be overwhelmed, and crystals may damage them further. The result is rising potassium, phosphate and uric acid, falling calcium and a risk of arrhythmia.
Follow the cell contents into the bloodstream
Potassium is mainly an intracellular ion; cells keep far more inside than the blood carries. Phosphate is also concentrated inside cells, and nucleic acids from DNA and RNA are broken down through purine metabolism into uric acid. When a large, fast-growing, treatment-sensitive tumour is destroyed rapidly, all of these are released at once, faster than the kidneys can excrete them.
This is why tumour lysis syndrome is most often seen soon after starting therapy for high-grade lymphomas and acute leukaemias with high white cell counts, although it can occur with other cancers. Patients with a large tumour burden, raised baseline uric acid or LDH, or existing kidney impairment are at higher risk. Hyperkalaemia can develop within hours to a few days of treatment starting.
Why calcium falls and the kidneys suffer
Excess phosphate binds calcium in the blood, forming calcium phosphate. As calcium is bound and deposited, the serum calcium falls, producing secondary hypocalcaemia. Low calcium can cause tingling, muscle cramps, tetany, seizures and arrhythmias. Phosphate rises typically a day or two after treatment starts, so the calcium fall may lag behind the potassium rise.
The kidneys are both the exit route and a target. Uric acid and calcium phosphate can precipitate as crystals in the renal tubules, causing acute kidney injury. Once kidney function drops, potassium, phosphate and uric acid are excreted even less, so levels climb faster. This feedback loop is why prevention focuses so heavily on keeping urine flowing and lowering uric acid before it accumulates.
Read the lab pattern and the warning trend
The typical laboratory pattern is high potassium, high phosphate, high uric acid and low calcium, often with rising creatinine. Some patients have these changes without symptoms, and others develop clinical complications such as arrhythmia, seizure or kidney failure. Because hyperkalaemia often causes no symptoms until it affects the heart, waiting for the patient to feel unwell is unsafe.
Watch the trend between draws rather than a single number. Rising potassium alongside falling urine output is a dangerous combination. ECG changes from hyperkalaemia include peaked T waves, a widening QRS complex and, at worst, life-threatening rhythms. Muscle weakness, palpitations, nausea and reduced urine output are clinical clues that should prompt immediate review of the latest results.
Turn the mechanism into nursing monitoring
For at-risk patients, the plan often starts before chemotherapy, with intravenous hydration and a medicine to reduce uric acid, such as allopurinol or rasburicase, as prescribed. The nurse checks electrolytes, uric acid and kidney function at the frequency ordered, measures intake and output carefully, weighs the patient daily and reports falling urine output promptly.
Use cardiac monitoring when ordered and report ECG changes immediately. Do not give potassium or phosphate supplements, or fluids containing them, without confirming with the prescriber. Assess for signs of low calcium and fluid overload during aggressive hydration. Emergency treatment of hyperkalaemia, such as intravenous calcium or insulin with glucose, follows prescriber orders and local protocol.
Work through a hypothetical exam-style scenario
Picture a hypothetical patient with a high-grade lymphoma who started chemotherapy yesterday. Today urine output has fallen over several hours, he reports muscle weakness, and a new potassium result is high. The options are to encourage oral fluids and recheck tomorrow, to give a scheduled potassium supplement, or to place him on cardiac monitoring and notify the provider now. Monitoring and notifying is the strongest answer.
Encouraging fluids alone delays treatment of a rising potassium with falling kidney output, and the supplement adds to the problem. The question tests whether the candidate links timing after chemotherapy with cell breakdown and recognises that hyperkalaemia, not discomfort, is the immediate threat. Holding the supplement and reporting the falling output belong in the same call.
Sources and further reading
PMC: Tumor lysis syndrome in patients with hematological malignancies. Release of potassium, phosphate and nucleic acids, timing of hyperkalaemia and hyperphosphataemia, secondary hypocalcaemia, crystal-related kidney injury, risk factors, hydration, allopurinol and rasburicase.
MSD Manual Professional: Hyperkalemia. Acute tumour lysis as a cause of potassium shift out of cells, ECG progression and emergency treatments.
The next step on this is the same as on everything else here: answer questions and read the rationales. Our med-surg practice questions are the closest set to what this page covers.
One question from the med-surg set
A client with chronic obstructive pulmonary disease has an oxygen saturation of 88% on 2 L/min via nasal cannula and is alert with no distress. What should the nurse do first?
Rationale
In COPD a saturation of 88–92% is the therapeutic target, not an emergency, and this client is alert with no distress. The first action is the independent nursing intervention that is least invasive and most likely to help: sit them up and reassess. Turning the oxygen up to 6 L/min risks blunting the hypoxic drive, and calling rapid response or drawing an ABG escalates ahead of an assessment you have not finished.
Answer: B
Common questions
Why does tumour lysis syndrome cause high potassium?
Cells hold most of the body's potassium. When treatment destroys many cancer cells quickly, that potassium enters the blood faster than the kidneys can remove it.
Why is calcium low in tumour lysis syndrome?
Released phosphate binds calcium, forming calcium phosphate that can deposit in tissues and kidneys, so the free calcium in the blood falls.
Why is urine output monitored so closely?
The kidneys clear potassium, phosphate and uric acid, and crystals can injure them. Falling output means levels may rise faster, so it should be reported promptly.
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