Acute lymphoblastic leukaemia – tumour lysis syndrome

Cite this article as:
Tessa Davis. Acute lymphoblastic leukaemia – tumour lysis syndrome, Don't Forget the Bubbles, 2014. Available at:
https://doi.org/10.31440/DFTB.6185

Treating leukaemia produces its own complications. The most common time to have complications is during induction. For any new presentations of tumours, or for patients at the start of treatment, be aware of tumour lysis and how it can present.

View all our Acute Lymphoblastic Leukaemia Week posts

Tumour lysis syndrome is most commonly seen at the start of treatment as this is when there is the highest tumour load.

What is tumour lysis syndrome (TLS)?

TLS results from cell death and the subsequent release of chemicals from these cells.

It can be triggered by steroids, chemotherapy, fever, or dehydration.

What are the chemical abnormalities in TLS?

When cells die, they release their intracellular potassium and phosphate. Calcium then binds to the phosphate in the tissues. Urate is also deposited in the kidneys. The usual order of detected abnormalities is:

  1. High potassium
  2. High phosphate
  3. Low calcium – this can also be associated with kidney calcification
  4. High urea and creatinine  – this is due to renal failure and if this happens then the renal team need to be involved and the patient will likely require dialysis.

How do we treat TLS?

Treatment is through three main ways:

  • Hydration
  • Allopurinol – aiming to reduce the urate
  • Rasburicase – a medication that converts uric acid to allantoin which is water soluble and excreted in the urine.

Also, beware that if the patient has a high potassium, they are at risk of cardiac arrest so may also need standard hyperkalaemia management.

What are the other potential complications of ALL?

Anaemia – often the presenting complaint and result of treatment. Most patients require platelet & red cell transfusions.

Febrile neutropenia – most patients will have an episode of febrile neutropenia during induction. This can be due to life-threatening sepsis. Find your hospital guideline and if you suspect febrile neutropenia, talk to your consultant early.

Hyperviscosity syndrome – can be a presenting complaint, associated with WCC >100×109/L 

Acute lymphoblastic leukaemia – risk factors and prognosis

Cite this article as:
Henry Goldstein. Acute lymphoblastic leukaemia – risk factors and prognosis, Don't Forget the Bubbles, 2014. Available at:
https://doi.org/10.31440/DFTB.6182

 We suspect that Hamish has ALL – how do we confirm this, and more importantly, what is his prognosis?

View all our Acute Lymphoblastic Leukaemia Week posts

What are the initial investigations?

  • Repeat FBC & send group & hold; coagulation profile; blood cultures if febrile; electrolytes, including PO4-, Mg+, Ca++ as high WCC at risk of tumor lysis syndrome; liver function tests; Hep B, C, HIV, EBV, CMV, herpes simplex, HHV6, syphilis & toxoplasma serology
  • Blood film must be reviewed & reported by a consultant haematologist
  • ECG – sinus tachycardia, normal axis
  • Chest radiograph – to check for mediastinal mass
  • Urinalysis
  • Official height & weight – for chemotherapy & body surface area calculations (standard scales/measure, sighted by two staff)
  • Pregnancy test in females of childbearing age

Once clinically stabilised (including meeting minimum platelet counts), they will have a GA lumbar puncture (usually with intrathecal chemotherapy) a bone marrow aspirate, and if there is no contraindications, insertion of a tunnelled central line.

What are the risk factors for ALL?

  • Family history
  • Immunosuppression
  • Alkylating agents (more commonly linked to AML rather than ALL)
  • Trisomy 21
  • Neurofibromatosis
  • Ataxia telangiectasia
  • Bloom syndrome

What are good prognostic factors for ALL?

1. Age  >1yo and <10yo at diagnosis

2. White cell count <50×109/L at presentation

3. No testicular involvement at presentation

4. Not a child with Down Syndrome

5. No prior steroid exposure – this is important, as steroids are themselves chemotherapeutic and can put a child into remission as a single agent. If there has been a history of URTI or wheeze, they may have been prescribed (or been given a sibling’s) steroids. There are reports of spontaneous tumour lysis syndrome in undiagnosed patients as a result of steroids. Steroid exposure will move the child to a high-risk protocol.

6. No CNS disease – established with first CSF examination

In recent years, cytogenetics & minimal residual disease (MRD) has added a further layer to prognosis and treatment. This analysis requires CSF & bone marrow samples.

What do remission, relapse, and cure mean?

For diagnosis – a patient has to have over 25% blasts in the peripheral blood film

For remission – a patient has to have <5% blasts in the peripheral blood film

For cure – a patient has to have no evidence of leukaemia over 5 years from diagnosis

Bone marrow is the most common site for relapses and 10% of relapses are central nervous system only. In boys, testes are a known site of relapse and present as a hard testicular lump – so make sure you examine the tests during follow-up appointments.

Using the most up to date study outcomes, the 5 year survival is 85%

Once the child gets further through the initial treatment and is given a standard risk, then the 5 year survival is 97%