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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

Oncology and palliative care · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Life-threatening metabolic tumour lysis

Severe potassium elevation, arrhythmia, symptomatic hypocalcaemia, seizure, rapidly rising phosphate or urate, oliguria or fluid overload around effective cancer treatment indicates established or evolving tumour lysis syndrome.

Action: Use monitored ABCDE care, call oncology or haematology, renal and critical care together, repeat rapidly processed lysis bloods, stop potassium and phosphate delivery, treat dangerous hyperkalaemia immediately, give rasburicase when indicated and arrange early renal replacement if metabolic control or fluid balance is failing.

Overview

Estimate lysis risk before anticancer treatment, prevent avoidable metabolic injury and reverse hyperkalaemia, phosphate accumulation, urate burden and renal failure before arrhythmia, seizure or death.

Tumour lysis syndrome is a predictable mismatch between malignant-cell breakdown and physiological clearance. It is classically associated with acute leukaemia and high-grade lymphoma, but can follow treatment of bulky, rapidly responsive solid tumours, especially with extensive liver involvement or renal impairment. The trigger may be conventional chemotherapy, corticosteroid, antibody, targeted therapy, radiotherapy or spontaneous tumour turnover. A risk assessment tied to tumour biology is therefore more useful than a list of supposedly safe drug classes.

The characteristic direction is simultaneous rising potassium, phosphate and urate, falling calcium and worsening kidney function. Formal Cairo-Bishop-type criteria help classify laboratory and clinical TLS around treatment, but they are not permission to delay. One severely toxic potassium result or symptomatic low ionised calcium requires treatment before a second criterion appears. Trends matter: a rapid change from a normal baseline can be more dangerous than a static borderline result, and apparent hyperkalaemia in extreme leukocytosis needs urgent non-haemolysed confirmation while ECG toxicity is treated.

Practice

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Oncology and palliative careOriginal SBA

High-risk prevention choice

A patient with bulky, highly treatment-responsive lymphoma, markedly raised LDH and impaired kidney function is about to start therapy. Which prevention strategy is most appropriate?

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.

  • British Society for Haematology tumour lysis guidelineUK risk stratification, prevention, urate treatment and established TLS management.
  • UK Kidney Association hyperkalaemia guidelineEmergency cardiac protection, potassium shift, glucose monitoring and renal escalation.
  • Fasturtec rasburicase SmPCLicensed dose, infusion, G6PD contraindication and sample handling.
  • Society for Endocrinology emergency calcium guidanceAdult intravenous calcium regimen and monitoring for symptomatic hypocalcaemia.

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

Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom

Prevention begins before tumour reduction. Correct dehydration, review obstruction and nephrotoxins, choose an appropriately monitored setting and arrange rapid laboratory processing. Isotonic fluid supports renal clearance but must be individualised in heart or kidney disease. Allopurinol inhibits xanthine oxidase and prevents additional urate production, which suits many intermediate-risk situations; it cannot remove urate already present and can allow xanthine accumulation. Rasburicase converts existing uric acid to more soluble allantoin and is used for high-risk or established disease, but G6PD deficiency can lead to haemolysis and methaemoglobinaemia.

Established TLS is managed by treating each threat while continuing control of cell breakdown. Protect the myocardium and shift and remove potassium under the UK Kidney Association algorithm. Stop external phosphate and use renal clearance; severe phosphate burden is often a reason for dialysis. Do not routinely correct asymptomatic hypocalcaemia while phosphate is raised because added calcium can increase precipitation. Give intravenous calcium for seizure, tetany, laryngospasm or electrical danger. Renal referral is early rather than a final step because recurrent potassium, oliguria, fluid overload and phosphate accumulation can require dialysis before traditional uraemic indications.

Key points

  • TLS is rapid release of tumour-cell potassium, phosphate and nucleic acid; phosphate lowers calcium and purines become urate, threatening heart, brain and kidney.
  • Risk is determined before treatment from cancer type and sensitivity, burden, LDH, tumour count, baseline urate, renal function, hydration, obstruction and planned therapy.
  • First-line baseline and serial tests are potassium, phosphate, calcium, urate, creatinine, bicarbonate and LDH with ECG and strict fluid balance when risk is important.
  • Low-risk patients usually need surveillance and hydration; intermediate risk commonly adds allopurinol; high risk needs monitored hydration, rasburicase and frequent blood tests under the current BSH pathway.
  • Allopurinol prevents formation of further urate but does not remove existing uric acid; rasburicase rapidly converts existing urate and is preferred for high-risk prophylaxis or established TLS.
  • Rasburicase is contraindicated in G6PD deficiency because haemolysis and methaemoglobinaemia can occur; post-dose urate samples need pre-chilled tubes and transport on ice.
  • Do not alkalinise urine routinely, add potassium or phosphate to maintenance fluid, or give calcium merely to normalise an asymptomatic low result while phosphate is high.
  • Treat severe hyperkalaemia immediately and involve renal medicine early for oliguria, overload, recurrent potassium, severe phosphate or persistent metabolic rebound.

Aetiology

01

Rapid treatment response

Highly chemosensitive leukaemia, lymphoma and selected bulky solid tumours can lose a large cell mass within hours of systemic therapy or corticosteroid exposure.

02

Large active disease burden

Bulky nodes, extensive liver or marrow involvement, high circulating tumour count and raised LDH increase the intracellular material available for release.

03

Limited renal reserve

Chronic kidney disease, dehydration, oliguria, obstructive uropathy and nephrotoxic medicines reduce potassium, phosphate and urate clearance during tumour breakdown.

04

Spontaneous cell turnover

Aggressive untreated malignancy can outgrow its blood supply and lyse spontaneously, producing high urate and kidney injury before anticancer treatment begins.

Pathophysiology

  1. 1
    Potassium escapes malignant cells

    Abrupt intracellular potassium release exceeds renal excretion, changing membrane potential and causing weakness, conduction delay, ventricular arrhythmia or arrest.

  2. 2
    Phosphate complexes calcium

    A large phosphate load lowers ionised calcium and promotes calcium-phosphate precipitation in renal tubules and soft tissue when clearance is inadequate.

  3. 3
    Purine catabolism raises urate

    Released nucleic acid is converted through hypoxanthine and xanthine to uric acid, which can crystallise in acidic, concentrated tubular fluid.

  4. 4
    Renal injury drives feedback

    Urate, calcium-phosphate deposition, hypovolaemia and tumour obstruction reduce filtration, accelerating retention of each toxic electrolyte and worsening overload.

Clinical features and red flags

High-risk treatment window

Biochemical change can begin before treatment or within hours to days of an effective first dose, including steroid or targeted therapy.

Potassium membrane toxicityRed flag

Weakness, paraesthesia, bradycardia, broad QRS, absent P waves or ventricular arrhythmia is an immediate resuscitation problem.

Symptomatic low ionised calciumRed flag

Perioral tingling, spasm, tetany, seizure, laryngospasm or QT prolongation indicates clinically important calcium reduction.

Renal clearance failureRed flag

Oliguria, rising creatinine, hypertension, pulmonary oedema, nausea or encephalopathy signals accumulating solute and fluid burden.

Silent laboratory trajectory

Serial lysis tests may show coordinated metabolic change before symptoms, allowing escalation before an irreversible rhythm or kidney event.

Spontaneous pre-treatment lysis

High urate, LDH and kidney injury in aggressive untreated cancer may represent spontaneous TLS even when phosphate change is less pronounced.

Red flags requiring action

  • ECG change, muscle weakness, bradycardia or ventricular arrhythmia with rising potassium requires immediate hyperkalaemia treatment before formal TLS criteria are completed.
  • Tetany, laryngospasm, seizure or QT prolongation with low calcium needs monitored calcium, while asymptomatic hypocalcaemia during high phosphate is usually not corrected.
  • Falling urine output, rapidly increasing creatinine, pulmonary oedema or biochemical rebound despite urate treatment requires urgent renal replacement discussion.
  • Bulky, rapidly proliferating and highly treatment-responsive cancer with high LDH or renal impairment needs prophylaxis before steroids, antibodies, targeted therapy or chemotherapy.
  • TLS can occur spontaneously before treatment or after a first small treatment exposure, so timing alone cannot rule it out.

Investigations

  1. 01
    First-line lysis blood panel and ECGFirst stepFirst line
    Why
    Identify the biochemical syndrome and immediately dangerous electrical effect.
    Interpretation and limitations
    Measure rapidly processed potassium, phosphate, calcium, urate, creatinine, urea, bicarbonate and LDH; obtain ionised calcium when symptomatic or critically ill.
  2. 02
    Pre-treatment risk classification
    Why
    Match location, prophylaxis and monitoring frequency to expected cell death and clearance reserve.
    Interpretation and limitations
    Combine cancer type, burden, LDH, circulating count, treatment sensitivity and previous response with renal function, urate, hydration, obstruction and nephrotoxins.
  3. 03
    Serial metabolic trend
    Why
    Detect early movement and rebound that a single baseline cannot exclude.
    Interpretation and limitations
    For high risk or established TLS, repeat core chemistry commonly every 4 to 6 hours and more frequently for instability or active hyperkalaemia under the local protocol.
  4. 04
    Urgent true-potassium confirmation
    Why
    Separate dangerous hyperkalaemia from haemolysis or leukocyte-fragility artefact.
    Interpretation and limitations
    Use ECG and a rapidly transported, carefully collected plasma or blood-gas sample; treat credible electrical toxicity without waiting for laboratory adjudication.
  5. 05
    Fluid and renal assessment
    Why
    Find oliguria, obstruction and intolerance of preventative hydration.
    Interpretation and limitations
    Record hourly urine, weight, cumulative balance and respiratory findings and use imaging when tumour or stone obstruction is plausible; creatinine can lag acute loss of clearance.
  6. 06
    G6PD status before rasburicase
    Why
    Prevent oxidant haemolysis and methaemoglobinaemia in susceptible patients.
    Interpretation and limitations
    Check status before planned high-risk prophylaxis; in an immediate emergency, make a senior risk decision informed by ancestry and prior results without ignoring the contraindication.

Differential diagnosis

01

Sepsis with acute kidney injury

Sepsis can cause hypotension, acidosis, oliguria and potassium rise and may coexist during cancer treatment; cultures and antibiotics proceed with lysis management.

02

Pseudohyperkalaemia

Haemolysis and fragile extreme leukocytosis can artefactually raise laboratory potassium; ECG and an urgently handled plasma or blood-gas sample clarify without delaying true-toxicity treatment.

03

Rhabdomyolysis or haemolysis

Muscle and red-cell breakdown also release potassium and phosphate; creatine kinase, haemolysis tests, urate pattern and treatment timing help identify overlap.

04

Drug or renal electrolyte failure

Renin-angiotensin blockade, potassium-sparing therapy, acidosis and pre-existing kidney failure may create hyperkalaemia without the coordinated lysis trajectory.

Management

01Before therapyAssign risk and prevent lysisFirst stepA responsive malignancy is about to receive systemic therapy, corticosteroid prephase, radiotherapy or another rapid tumour-reducing intervention.+
  1. 1Classify tumour and patient risk from diagnosis, burden, LDH, tumour count, renal reserve, urate, hydration, obstruction and planned treatment.
  2. 2Correct volume depletion, stop avoidable nephrotoxins and potassium or phosphate supplements and choose ambulatory, ward or higher-acuity monitoring appropriate to risk.
  3. 3Use surveillance and hydration for selected low risk, add renal-adjusted allopurinol for intermediate risk and use rasburicase with close monitoring for high risk under the BSH pathway.
02Established TLSRemove urate and preserve clearancePotassium, phosphate or urate rises with falling calcium or renal function around tumour reduction.+
  1. 1Call oncology or haematology, renal medicine and critical care, start continuous ECG when indicated and reassess neurological, respiratory, fluid and urine status.
  2. 2Give rasburicase when indicated and carefully titrated isotonic fluid without potassium or phosphate, balancing ongoing tumour control against current instability.
  3. 3Repeat lysis chemistry at least every 4 to 6 hours and arrange renal replacement early when potassium, phosphate, uraemia or fluid cannot be controlled.
03HyperkalaemiaProtect, shift and remove potassiumSevere potassium, ECG change, muscle weakness or arrhythmia occurs during suspected TLS.+
  1. 1Follow the UK Kidney Association algorithm, giving intravenous calcium to stabilise the myocardium when ECG toxicity is present with continuous monitoring.
  2. 2Give intravenous soluble insulin with glucose and use nebulised salbutamol as an adjunct when appropriate, monitoring glucose for delayed hypoglycaemia.
  3. 3Remove potassium by recovering renal excretion or urgent dialysis and recheck early because intracellular shift is temporary while lysis continues.
04Low calciumTreat clinical toxicity rather than a target numberIonised or adjusted calcium falls as phosphate rises during TLS.+
  1. 1Assess symptoms and ECG and stop non-essential phosphate and calcium delivery while restoring renal phosphate clearance.
  2. 2Withhold routine calcium in asymptomatic hypocalcaemia because increasing the calcium-phosphate product can worsen renal and tissue deposition.
  3. 3Give monitored intravenous calcium gluconate for seizure, tetany, laryngospasm or arrhythmia while urgently reducing phosphate and arranging renal support.
Key medicines and prescribing safety4 treatments · regimens, roles and cautions+
Prevents generation of additional uric acid in many intermediate-risk patients by inhibiting xanthine oxidase.

Allopurinol

Give 300 mg orally once daily, or 100 mg three times daily, commonly starting 24 to 48 hours before tumour-reducing treatment and continuing through the defined lysis-risk period, with renal dose adjustment.

It does not lower urate already present and may increase xanthine load. Stop for serious rash or hypersensitivity and avoid or drastically reduce azathioprine or mercaptopurine because exposure rises.

Rapidly removes existing uric acid for high-risk prophylaxis and established TLS by converting it to soluble allantoin.

Rasburicase

Give rasburicase 0.2 mg/kg intravenously once daily over 30 minutes for up to 7 days, with actual duration determined by risk, tumour response and serial urate under the current BSH and product protocol.

Do not use in G6PD deficiency because severe haemolysis and methaemoglobinaemia can occur. Keep post-dose urate samples cold from collection to analysis to avoid falsely low ex-vivo results.

Temporarily shifts potassium intracellularly while ongoing lysis is controlled and definitive renal removal is organised.

Soluble insulin with glucose for hyperkalaemia

For severe adult hyperkalaemia, give 10 units soluble insulin intravenously with 25 g glucose under the UK Kidney Association algorithm, adding the recommended glucose infusion when pretreatment glucose is below 7 mmol/L.

Check capillary glucose before treatment and serially for at least 6 hours because delayed hypoglycaemia is common; a temporary potassium fall is redistribution, not removal.

Complications

01

Sudden cardiac death

Potassium toxicity and severe calcium disturbance can cause conduction block, ventricular tachyarrhythmia, fibrillation or pulseless arrest before other lysis symptoms appear.

02

Neuromuscular calcium toxicity

Reduced ionised calcium causes paraesthesia, cramp, carpopedal spasm, laryngospasm, seizure and electrical instability, especially while phosphate remains high.

03

Acute kidney failure

Crystal and calcium-phosphate injury, low circulating volume and tumour obstruction can lead to oliguria, uraemia, overload and dialysis.

04

Cancer-treatment disruption

Metabolic instability and renal failure can interrupt a curative regimen, alter drug clearance and create avoidable mortality from both cancer and treatment.

Monitoring and follow-up

  • Before therapy, record tumour and patient risk, potassium, phosphate, calcium, urate, creatinine, bicarbonate, LDH, weight, fluid status and planned monitoring location.
  • In high-risk or established TLS, repeat core lysis chemistry commonly every 4 to 6 hours and shorten the interval for unstable potassium or renal decline.
  • Use continuous ECG for severe hyperkalaemia, calcium symptoms or arrhythmia and check capillary glucose for at least 6 hours after insulin-glucose treatment.
  • Measure hourly urine and cumulative balance and reassess weight and lungs; oliguria with rising fluid or oxygen need triggers immediate renal escalation.
  • After rasburicase, use pre-chilled urate collection and rapid cold transport and continue testing until metabolic rebound is no longer plausible.
  • Before the next cancer cycle, document the trigger, maximum abnormalities, dialysis exposure and an upgraded prevention plan.

Special situations

Biology outranks drug label

Any intervention that kills a large responsive tumour mass rapidly can provoke TLS, including steroid, antibody, small molecule and radiotherapy.

One lethal result is enough

Formal classifications support communication, but severe hyperkalaemia or symptomatic hypocalcaemia is treated before additional criteria accumulate.

Allopurinol cannot clear urate

Xanthine oxidase inhibition is preventive; established high urate needs a removal strategy rather than simply more allopurinol.

The sample remains enzymatic

Rasburicase continues degrading urate after blood is drawn unless the specimen stays chilled, creating falsely reassuring laboratory values.

Dialysis can be early

Recurrent potassium, severe phosphate or overload may justify renal replacement before conventional late uraemic thresholds are met.

Common pitfalls

  1. 01

    Considering TLS only after conventional chemotherapy and missing spontaneous lysis or response to steroid and targeted treatment.

  2. 02

    Using one normal baseline to avoid serial tests in a biologically high-risk cancer.

  3. 03

    Giving allopurinol as though it rapidly removes an already elevated urate.

  4. 04

    Giving rasburicase without assessing G6PD risk or transporting subsequent urate samples warm.

  5. 05

    Correcting asymptomatic low calcium while phosphate is markedly high.

  6. 06

    Using urinary alkalinisation routinely and increasing calcium-phosphate or xanthine precipitation risk.

  7. 07

    Waiting for refractory uraemia before involving renal medicine despite recurrent potassium, oliguria or overload.

Treats dangerous tetany, seizure, laryngospasm or electrical instability while phosphate burden is reduced.

Calcium gluconate 10%

For symptomatic hypocalcaemia, give 10 to 20 mL of 10% calcium gluconate intravenously diluted in 50 to 100 mL of 5% glucose over 10 minutes with continuous ECG monitoring, repeating by symptoms and ionised calcium.

Do not correct asymptomatic hypocalcaemia routinely during marked hyperphosphataemia; avoid extravasation and use specialist caution with digoxin and persistent high calcium-phosphate product.