Tumour Lysis Syndrome

Take home messages

• This is an oncological emergency
• Remember steroids, allopurinol and rasburicase
• Prevention and hydration are key

A case

Details altered for confidentiality as always.

An independent 52 year old man presents to the emergency department with nausea and vomiting.

No significant previous medical history or regular medications, non smoker and non drinker, but had noticed a loss of weight of around 10 kg over the last month or so.

No respiratory symptoms or chest pain.

What is it?

By definition, tumour lysis syndrome is a metabolic syndrome, featuring a tetrad of:

• Hyperuricemia
• Hyperphosphatemia
• Hyperkalemia
• Hypocalcemia

Caused by insanely fast cell destruction and reproduction by an overexcited tumour.

Because the fragile cancer cells are much easier to break, they then release - en masse - all of their intracellular contents into the lymphatics and bloodstream.

For tumour lysis syndrome to be diagnosed, you need two or more of the above, generally between 2 days and one week after starting chemo or radiotherapy.

But it can happen all by itself.

Tell me about urate

When malignant cells explode as a result of hurried construction, poor design or the treatment designed to destroy them, everything on the inside is now on the outside.

This includes all the DNA responsible for encoding the wretched things.

The nucleic acids that make up this death-helix are metabolised mainly in the liver by xanthine oxidase and the end product is urate.

This needs to be cleared out by the kidneys, which is fine as long as there isn't too much, at which point the urate crystallises in the tubules causing catastrophic renal failure.

Hence one of the things that haematology might advise is giving allopurinol to the patient, to inhibit xanthine oxidase for a while and allow the kidneys to recover.

The ideal scenario, which is seen in many other animals but not primates, is to have an abundance of urate oxidase which breaks the urate down further into allantoin, which is more soluble and less renodestructive.

Since we don't have this, we'll have to settle for the recombinant form, a drug called rasburicase.

A note about potassium

We've all had a weirdly high potassium come back on a tricky VBG that we then reluctantly had to go and repeat, only for the next sample to be fine.

This largely occurs because of the turbulent blood flow through a tiny vein exposed to an angry vacutainer or SHO pulling a syringe plunger causing shear stress on the cells in the blood.

Because the intracellular potassium concentration is around 80 mmol/l, it doesn't take all that much cell damage to cause the sample to have a ridiculously high reading.

If you have a haematological cancer, you're churning out enormous quantities of poorly constructed cells of a particular lineage, and these are exceptionally fragile, meaning even the slightest shearing will cause mass cell damage and efflux of potassium into the ABG machine.

This is sometimes called pseudohyperkalaemia of malignancy.

Phosphate

Angry belligerent tumour cells can contain much more intracellular phosphate than a normal cell, and as they explode they release all of this into the blood.

Phosphate levels are defined as high if above 1.45 mmol/L or if it's risen more than 25% from the patient's usual baseline.

This rapidly overwhelms the kidneys' ability to handle phosphate effectively and it precipitates out (particularly as calcium phosphate).

Management:

• Phosphate binders
• Haemofiltration or dialysis

Calcium

Yes we want to keep ions within their usual homeostatic ranges, and you certainly should replace calcium in patients with symptomatic hypocalcaemia.

However.

There is a risk of precipitation of calcium phosphate in the kidneys that can cause or worsen renal failure, so it doesn't come without risk.

What do I do about it?

As with many problems in our world, it's mainly prevention and then supportive care.

Useful Tweets and Resources

References and Further Reading

Tumour lysis syndrome

Tumour lysis syndrome is a metabolic disorder characterized by hyperuricemia, hyperphosphatemia, hyperkalemia and hypocalcemia. These abnormalities are brought about by rapid tumor cell turnover. A good NEJM review article is available for the time-rich exam candidate. The current classification system demands at least two of the abovementioned electolyte abnormalities 2-7 days after the commencement of cancer therapy.

Deranged PhysiologyAlex Yartsev

Tumour Lysis Syndrome

Tumour Lysis Syndrome: oncological emergency due to turnover of high cell mass malignancies resulting in severe metabolic derangement

Life in the Fast Lane • LITFLChris Nickson

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