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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Tumour lysis syndrome

Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Electrolyte or renal tumour-lysis emergency

Arrhythmia, ECG change, seizure, tetany, weakness, oliguria, rising creatinine, fluid overload, severe hyperkalaemia or rapidly rising phosphate represents clinical tumour lysis and can be fatal within hours.

Action: Use ABCDE and continuous cardiac monitoring, call paediatric oncology, nephrology and intensive care, stop potassium and phosphate input, give protocol-directed rasburicase and controlled hydration, treat hyperkalaemia immediately and prepare early renal replacement therapy when abnormalities do not rapidly respond.

Overview

Predict tumour lysis before anticancer therapy, recognise its biochemical pattern and clinical consequences, sequence hydration, urate-lowering therapy, electrolyte treatment and renal support safely, and monitor high-risk children closely enough to prevent irreversible organ injury.

TLS assessment begins before treatment. Define malignancy, tumour burden, white count, LDH, organ enlargement, renal infiltration and anticipated treatment sensitivity. Record baseline kidney function, urine output, hydration, sepsis, cardiac function and nephrotoxic medicines. A child with Burkitt lymphoma, lymphoblastic lymphoma or acute leukaemia with high count and renal compromise needs prevention in a unit with immediate oncology, intensive-care and dialysis access.

At baseline and serially measure FBC, potassium, phosphate, calcium including ionised calcium when symptomatic, urate, urea, creatinine, bicarbonate, glucose and LDH. Obtain ECG and continuous monitoring for hyperkalaemia, hypocalcaemia, weakness, paraesthesia, cramps, tetany or seizure. Interpret trends: a rapid 20% rise may be important before a result crosses its reference interval. An unexpectedly high serum potassium in marked leucocytosis should be repeated urgently on a rapidly analysed blood gas while treating any ECG or clinical danger.

Practice

Two practice questions

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Paediatrics and child healthOriginal SBA

Post-rasburicase urate sampling

A child with high-risk lymphoma receives rasburicase. How should the next urate sample be handled to avoid a falsely reassuring result?

Choose one answer, then submit
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Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • BSH Updated Tumour Lysis Syndrome GuidelineCurrent 2025 UK adult and paediatric risk, prevention, diagnosis and management standard.
  • NHS SPS Time-Critical Rasburicase AdviceAvailability within one hour, rapid urate effect and G6PD safety.
  • Sheffield Children's Tumour Lysis Prevention and Management GuidelineCurrent paediatric hydration, biochemical monitoring, rasburicase, allopurinol and renal-escalation protocol.
  • NHSGGC Paediatric Hyperkalaemia Emergency ManagementImmediate ECG monitoring and paediatric oncology and intensive-care escalation for TLS hyperkalaemia.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

Preventive hydration is prescribed by the paediatric oncology protocol, adjusted for age, cardiac function, kidney status and urine output. Use a solution without added potassium or phosphate, begin before tumour-specific therapy where possible, record strict fluid balance and weigh at least twice daily in the highest-risk period. Do not force fluid through oliguria: reassess perfusion, obstruction and renal injury, and involve nephrology before pulmonary oedema develops. Diuretic is inappropriate in hypovolaemia or obstructive uropathy.

Select urate therapy from risk. Allopurinol blocks xanthine oxidase and therefore prevents additional uric acid, but it works slowly and can increase xanthine. Rasburicase converts existing urate to soluble allantoin within hours and is used for established TLS and the highest-risk states. Give time-critical rasburicase through the local paediatric protocol, do not co-administer allopurinol routinely, and never give rasburicase to a child with G6PD deficiency. If risk is foreseeable, establish G6PD status early in at-risk ancestry without delaying other prevention.

Treat abnormalities alongside continued oncology and nephrology review. Hyperkalaemia follows the paediatric emergency algorithm with cardiac monitoring and bridging therapy while definitive clearance is arranged. Restrict phosphate input and consider protocol binders or dialysis for major rise. Do not correct an asymptomatic low calcium simply to normalise the number, because calcium-phosphate precipitation may worsen; give carefully dosed IV calcium with ECG monitoring for tetany, seizure, arrhythmia or clinically important QT change.

Rasburicase remains active after blood is drawn. The urate specimen must be placed on ice immediately and analysed rapidly or the laboratory result will be falsely reassuring. Monitor high-risk children every 4 to 8 hours or more frequently when changing, including potassium, phosphate, calcium, urate, renal function, urine, weight and blood pressure. Continue until tumour burden, treatment phase and biochemical trends clearly place the child at low risk rather than stopping after one normal panel.

Call nephrology before indications become absolute. Oliguria despite adequate hydration, progressive creatinine or urea, volume overload, severe hypertension, persistent potassium above the emergency threshold, rapidly rising phosphate, symptomatic hypocalcaemia or urate rising despite rasburicase may require renal replacement therapy. Explain to families that lysis reflects rapid cell breakdown and effective treatment can trigger it; prevention and monitoring are signs of anticipated safe care, not evidence that therapy has failed.

Key points

  • The classic laboratory pattern is hyperkalaemia, hyperphosphataemia, hypocalcaemia and hyperuricaemia with rising urea and creatinine after or even before therapy.
  • Risk-assess every new high-grade haematological malignancy before corticosteroid, chemotherapy or radiotherapy; prevention is safer than treating established lysis.
  • First-line tests are potassium, phosphate, corrected and ionised calcium, urate, urea, creatinine, LDH, bicarbonate, glucose and FBC, with ECG and continuous monitoring when abnormalities or symptoms are present.
  • First-line prevention for high or very high risk is specialist-controlled IV hydration without added potassium or phosphate, strict input and output, frequent weights and protocol-selected urate-lowering therapy.
  • Rasburicase is the treatment of choice for established TLS and very high urate risk because it degrades existing uric acid rapidly; it should be available within 1 hour of prescription.
  • A paediatric treatment regimen is rasburicase 0.2 mg/kg IV over 30 minutes once daily, with duration set by biochemical response and the oncology protocol.
  • Rasburicase is contraindicated in G6PD deficiency because of haemolysis and methaemoglobinaemia risk; assess ancestry and prior results during risk planning and use the specialist alternative when deficient.
  • Allopurinol prevents new uric acid formation but does not remove existing urate; it suits selected lower-risk prophylaxis and requires renal and mercaptopurine interaction review.
  • Do not routinely combine allopurinol with rasburicase or alkalinise urine; alkalinisation promotes calcium-phosphate and xanthine precipitation.
  • After rasburicase, collect urate into the specified tube, place it on ice immediately and transport rapidly, because ongoing ex-vivo urate breakdown gives a falsely low result.
  • Treat symptomatic, not asymptomatic, hypocalcaemia unless a specialist protocol directs otherwise; calcium can worsen calcium-phosphate deposition.
  • Escalate early for dialysis when hyperkalaemia, phosphate rise, symptomatic hypocalcaemia, oliguria, uraemia or fluid overload is refractory.

Aetiology

01

Treatment-triggered cell lysis

Chemotherapy, corticosteroid, radiotherapy and selected targeted therapies can destroy a large chemosensitive tumour burden within hours to days.

02

Spontaneous tumour lysis

Rapidly proliferating leukaemia or lymphoma can outgrow blood supply and break down before any anticancer treatment is given.

03

Tumour risk

Burkitt or lymphoblastic lymphoma, acute leukaemia with high white count, bulky disease and high LDH are especially high risk.

04

Patient risk

Kidney infiltration, pre-existing AKI or CKD, oliguria, dehydration, sepsis and nephrotoxic medicines reduce the capacity to excrete released solutes.

Pathophysiology

  1. 1
    Potassium release

    Intracellular potassium rapidly enters plasma, depolarising myocardium and skeletal muscle and causing weakness, arrhythmia or cardiac arrest.

  2. 2
    Phosphate and calcium shift

    Released phosphate binds circulating calcium, causing hypocalcaemia and calcium-phosphate precipitation in renal tissue and other organs.

  3. 3
    Urate generation

    Purine nucleic acids are metabolised to uric acid, which has limited solubility and can crystallise within distal renal tubules.

  4. 4
    Acute kidney injury loop

    Urate, calcium-phosphate deposition, hypovolaemia and tumour or drug effects reduce filtration, further limiting potassium, phosphate and urate clearance.

  5. 5
    Electrical instability

    Hyperkalaemia, hypocalcaemia and uraemia alter cardiac conduction and neuronal excitability, producing arrhythmia, tetany, seizure and sudden death.

Clinical features and red flags

Laboratory TLS

A coordinated rise in potassium, phosphate and urate with falling calcium around tumour treatment indicates acute cell breakdown.

Clinical TLS

Laboratory abnormalities accompanied by acute kidney injury, arrhythmia, seizure or sudden death define organ-level emergency.

Highest-risk tumour

Rapidly proliferative, bulky and highly treatment-sensitive leukaemia or lymphoma with high LDH carries the greatest risk.

Renal vulnerability

Kidney infiltration, pre-existing injury, dehydration, sepsis, oliguria or nephrotoxic exposure lowers solute-clearance reserve.

Electrolyte symptoms

Weakness, palpitations, paraesthesia, cramps, tetany, nausea, confusion or seizure may be the clinical face of lysis.

Red flags requiring action

  • Potassium rise or ECG change demands immediate hyperkalaemia treatment; the absence of ECG change does not make important hyperkalaemia safe.
  • Oliguria despite adequate perfusion, rising creatinine, fluid overload or severe hypertension requires urgent nephrology and critical-care involvement.
  • Paraesthesia, cramps, carpopedal spasm, tetany, seizure or prolonged QT indicates symptomatic hypocalcaemia and requires carefully monitored calcium treatment.
  • Rapidly rising phosphate, calcium–phosphate burden or persistent hypocalcaemia can cause nephrocalcinosis and dialysis-requiring renal failure.
  • High-burden leukaemia or lymphoma, renal infiltration, pre-existing kidney injury, dehydration, high LDH or marked leucocytosis predicts lysis before treatment begins.
  • Unexpectedly low urate after rasburicase may be a sample-handling artefact unless blood was chilled immediately and analysed rapidly.

Investigations

  1. 01
    First-line serial TLS biochemical profileFirst stepFirst line
    Why
    Detect potassium, phosphate, calcium, urate and renal changes before and during cytoreductive therapy.
    Interpretation and limitations
    Interpret direction and speed as well as thresholds; coordinated abnormalities are more convincing than one isolated value.
  2. 02
    ECG and continuous cardiac monitoring
    Why
    Identify conduction effects of hyperkalaemia or hypocalcaemia and guide immediate treatment.
    Interpretation and limitations
    Normal ECG does not exclude dangerous hyperkalaemia, while peaked T waves, QRS widening or prolonged QT accelerates emergency care.
  3. 03
    Rapid blood-gas potassium
    Why
    Confirm a discordant high laboratory potassium quickly in marked leucocytosis or sample-haemolysis risk.
    Interpretation and limitations
    A lower rapidly analysed value supports pseudohyperkalaemia, but treat clinical or ECG instability before confirmation.
  4. 04
    Strict urine output and fluid balance
    Why
    Detect falling renal clearance and prevent harmful underhydration or fluid overload.
    Interpretation and limitations
    Oliguria despite adequate perfusion and hydration is an early nephrology trigger, not an invitation to give unlimited fluid.
  5. 05
    G6PD activity before anticipated rasburicase
    Why
    Prevent rasburicase-induced haemolysis and methaemoglobinaemia in a susceptible child.
    Interpretation and limitations
    A deficient result contraindicates rasburicase; plan testing early because recent haemolysis or transfusion can complicate interpretation.
  6. 06
    Reference-standard chilled post-rasburicase urate
    Why
    Measure true in-vivo urate response after recombinant urate oxidase treatment.
    Interpretation and limitations
    Immediate icing and rapid transport are essential; room-temperature handling causes ongoing degradation and falsely low urate.

Differential diagnosis

01

Pseudohyperkalaemia

Extreme leucocytosis or traumatic sampling can cause ex-vivo cell lysis; an urgent blood-gas potassium helps clarify a discordant result.

02

Sepsis-related acute kidney injury

Shock, nephrotoxic antimicrobials and inflammation can raise creatinine and potassium without the characteristic phosphate, calcium and urate pattern.

03

Drug or obstruction-related renal injury

Cisplatin, methotrexate, aminoglycoside, contrast exposure or urinary obstruction can cause AKI and may coexist with tumour lysis.

04

Rhabdomyolysis or haemolysis

Muscle or red-cell breakdown raises potassium and LDH; creatine kinase, haemolysis markers and the phosphate–urate context separate mechanisms.

Management

01Before tumour therapyRisk-stratify and preventFirst stepA new malignancy or cytoreductive treatment has potential for rapid cell lysis.+
  1. 1Classify tumour burden, proliferation, sensitivity, LDH, white count, renal function and hydration risk.
  2. 2Start protocolised potassium- and phosphate-free hydration with strict balance and weight monitoring when indicated.
  3. 3Use allopurinol for selected lower-risk prophylaxis or rasburicase for the highest-risk plan after G6PD assessment.
  4. 4Locate the child where frequent laboratory testing, intensive care and dialysis are accessible.
02Laboratory changeEscalate before organ injuryEscalationPotassium, phosphate, urate or creatinine rises or calcium falls during the risk window.+
  1. 1Increase monitoring frequency, obtain ECG and review fluid and urine output immediately.
  2. 2Give rasburicase for established TLS under the oncology protocol unless G6PD deficient.
  3. 3Stop potassium and phosphate input and treat hyperkalaemia through the paediatric emergency algorithm.
  4. 4Call nephrology early for rising phosphate, creatinine, oliguria or fluid overload.
03Symptomatic electrolyte emergencyStabilise electricity and clear soluteArrhythmia, ECG change, seizure, tetany, severe weakness or major biochemical derangement occurs.+
  1. 1Use ABCDE, continuous monitoring and intensive-care support while emergency hyperkalaemia treatment begins.
  2. 2Give IV calcium only for symptomatic hypocalcaemia or specified ECG danger under the protocol.
  3. 3Prepare renal replacement therapy when abnormalities are refractory or renal and fluid status worsens.
04After rasburicaseMeasure response correctlyUrate oxidase has been administered and biochemical follow-up is due.+
  1. 1Notify the laboratory and collect urate using the specified local tube.
  2. 2Place the sample on ice immediately and transport for rapid analysis.
  3. 3Continue full TLS monitoring because a low urate does not resolve potassium, phosphate or renal risk.
Key medicines and prescribing safety2 treatments · regimens, roles and cautions+
Rapidly degrades existing uric acid and is the treatment of choice for established TLS and selected highest-risk prevention.

Rasburicase

Give 0.2 mg/kg IV over 30 minutes once daily for established paediatric tumour lysis or protocol-defined very high risk; the paediatric oncology consultant sets duration from urate, tumour burden, renal function and ongoing lysis.

Contraindicated in G6PD deficiency and previous rasburicase-related haemolysis, methaemoglobinaemia, anaphylaxis or hypersensitivity; do not routinely combine with allopurinol, monitor infusion reaction, and chill every post-dose urate specimen immediately to avoid a falsely low result.

Prevents formation of new uric acid in selected lower-risk situations but does not remove urate already present.

Allopurinol

For protocol-defined paediatric prophylaxis, give 100 mg/m² orally every 8 hours, maximum 100 mg per dose, usually starting 1 to 2 days before therapy and continuing until tumour burden and laboratory values indicate low risk.

Adjust or avoid in renal impairment according to the oncology pharmacy protocol, stop for significant rash or hypersensitivity, review the major mercaptopurine interaction and required dose reduction, and do not give routinely on the same day as rasburicase.

Complications

01

Malignant arrhythmia

Hyperkalaemia and hypocalcaemia produce conduction delay, ventricular arrhythmia and sudden cardiac arrest before renal results necessarily peak.

02

Seizure and tetany

Falling ionised calcium and uraemia increase neuromuscular excitability and can cause cramps, carpopedal spasm or convulsion.

03

Acute kidney injury

Crystal deposition, phosphate nephropathy, hypoperfusion and direct tumour effects can produce oliguria, fluid overload and dialysis dependence.

04

Fluid overload

Aggressive prevention fluid becomes harmful when renal output falls or cardiac function is limited, worsening hypertension and respiratory status.

05

Delayed anticancer therapy

Uncontrolled metabolic abnormalities postpone definitive treatment and can permit disease progression, creating a balance requiring senior oncology coordination.

Monitoring and follow-up

  • Measure potassium, phosphate, calcium, urate, urea, creatinine, bicarbonate and LDH before therapy and every 4 to 8 hours in high risk, more often when unstable.
  • Use continuous cardiac monitoring for electrolyte abnormality or symptoms and repeat 12-lead ECG after treatment changes.
  • Record strict intake and output, hourly urine in critical risk, twice-daily weight and frequent blood pressure.
  • Review every fluid prescription for added potassium or phosphate and adjust rate for renal, cardiac and age-specific tolerance.
  • Chill and rapidly transport all urate specimens after rasburicase and document correct handling with the result.
  • Monitor for rasburicase hypersensitivity, haemolysis, methaemoglobinaemia and falling oxygen saturation that does not correct as expected with oxygen.
  • Continue surveillance until the potassium and phosphate peaks have passed, renal function and urine are stable and tumour burden is clearly low risk.

Special situations

TLS can precede treatment

Spontaneous biochemical lysis may be the first sign of a rapidly proliferating lymphoma or leukaemia.

One normal value is not a trend

Rapid relative rises within the reference interval can announce lysis before threshold-based definitions are met.

A low urate may be laboratory treatment

Rasburicase continues working in the tube unless the sample is immediately chilled and processed.

Calcium can worsen the kidney problem

Correct asymptomatic hypocalcaemia cautiously because added calcium can precipitate with abundant phosphate.

More fluid is not always more renal protection

Oliguria and overload require nephrology assessment, not escalating hydration without a clearance plan.

Common pitfalls

  1. 01

    Starting steroid or chemotherapy before documenting TLS risk and baseline biochemistry.

  2. 02

    Adding potassium or phosphate to high-risk hydration fluid.

  3. 03

    Assuming tumour lysis occurs only after chemotherapy.

  4. 04

    Using allopurinol as treatment for already severe hyperuricaemia.

  5. 05

    Giving rasburicase without checking known or anticipated G6PD risk.

  6. 06

    Sending a post-rasburicase urate sample at room temperature.

  7. 07

    Treating asymptomatic hypocalcaemia simply to normalise the result.

  8. 08

    Delaying nephrology until refractory arrhythmia, anuria or pulmonary oedema.

  9. 09

    Flooding an oliguric child with fluid instead of reassessing clearance and obstruction.

Authoring stateComplete draft
Clinical stateAwaiting review
JurisdictionUnited Kingdom