Tumour lysis syndrome

• What is Tumour Lysis Syndrome
• Statistics on Tumour Lysis Syndrome
• Risk Factors for Tumour Lysis Syndrome
• Progression of Tumour Lysis Syndrome
• Symptoms of Tumour Lysis Syndrome
• Clinical Examination of Tumour Lysis Syndrome
• How is Tumour Lysis Syndrome Diagnosed?
• Prognosis of Tumour Lysis Syndrome
• How is Tumour Lysis Syndrome Treated?
• Tumour Lysis Syndrome References

What is Tumour Lysis Syndrome

Tumour lysis syndrome is the name given to a collection of metabolic abnormalities that occur following the initiation of cytotoxic chemotherapy.

Statistics on Tumour Lysis Syndrome

This potentially lethal syndrome is most likely to occur in patients with bulky, rapidly proliferating tumours that are responsive to therapy. The most common malignancies it is associated with are leukaemias, high-grade non-hodgkin’s lymphoma and Burkitt lymphoma, although it has been associated with other haematological and solid malignancies. Clinically, tumour lysis syndrome occurs in about 6% of patients being treated for non-hodgkin’s lymphoma, but laboratory parameters consistent with it are seen in up to 42% of patients.

Risk Factors for Tumour Lysis Syndrome

The cells that make up cancer are often numerous and rapidly proliferating. There are therefore large numbers of them to be killed, and chemotherapy aims to do this quickly. As such large numbers are killed at the same time, their contents are rapidly and simultaneously released into the bloodstream. As a result, tumour lysis syndrome may occur and usually does so within 1-5 days of chemotherapy. Very occasionally, tumour lysis syndrome occurs spontaneously, with no exposure to chemotherapy agents.

Progression of Tumour Lysis Syndrome

Tumour lysis syndrome causes a triad of hyperkalaemia, hyperphosphataemia and hyperuricaemia and leads to acute renal failure.

How is Tumour Lysis Syndrome Diagnosed?

Recognition of at-risk patients and the prevention of tumour lysis syndrome are the most important aspects of management. Pre-treatment hyperuricaemia and high lactate dehydrogenase levels represent a high tumour load, and therefore an increased risk for developing tumour lysis syndrome. Patients with pre-existing renal impairment are also at higher risk.
All patients at high risk of tumour lysis syndrome should have electrolytes and kidney function monitored prior to chemotherapy and for 48-72 hours following therapy. This way any abnormalities will be detected early and renal failure may be prevented.

Prognosis of Tumour Lysis Syndrome

Morbidity and mortality are related to acute renal failure, cardiac arrhythmias (due to hyperkalaemia) and metabolic acidosis. Tumour lysis syndrome is often predictable, and close monitoring of at-risk patients usually allows for effective treatment or even prevention.

How is Tumour Lysis Syndrome Treated?

Allopurinol, urinary alkalinisation and aggressive hydration aim to reduce plasma uric acid levels and prevent renal failure. Rasburicase can be used if allopurinol is ineffective. Prophylaxis may also include limiting of potassium and phosphate intake.
Due to the unpredictability of chemotherapy, tumour lysis syndrome may still occur despite aggressive prophylaxis. If signs develop, monitoring should continue at least twice daily. The appearance of renal failure in a patient with cancer does not immediately indicate tumour lysis syndrome. As mentioned earlier, there are many other causes of renal impairment in cancer patients. However, the appearance of all the aforementioned electrolyte disturbances plus renal failure, relatively soon after chemotherapy drugs have been administered, strongly suggests tumour lysis syndrome.
If prevention has been unsuccessful or was not instituted, tumour lysis syndrome requires aggressive treatment. Therapy is aimed at maximising excretion of released intracellular products and minimising production of uric acid. Patients may require treatment in an oncology unit or ICU due to the need for continuous monitoring and specialist treatment. Laboratory results must be given priority and reviewed quickly to allow for rapid detection and correction of electrolyte imbalances. Regular cardiac monitoring using ECG should also be carried out, in order to detect any rhythm abnormalities should they occur. A coagulation profile should also be performed as part of early monitoring.
Each electrolyte imbalance should be corrected individually, and the most important to address is the hyperuricaemia. Allopurinol is used, and can be given intravenously if the patient cannot tolerate it orally. If renal impairment is already obvious, dose reduction may be necessary. Rasburicase may be a useful alternative to allopurinol. It is faster, safe for use in children, and may reduce the need for dialysis.
Urine alkalinisation should be performed to reduce uric acid precipitation. Sodium bicarbonate can be given intravenously to alkalinise urine. This prevents crystallisation of uric acid, and a pH of 7.0 is a reasonable aim. Care must be taken with this treatment, as calcium phosphate crystallises at an alkaline pH and an adjustment too far in that direction should be avoided. Regular urinary pH measurements should be used to guide alkalinisation therapy.
Good urine flow helps prevent uric acid precipitation, but care should be taken not to fluid overload patients whose renal function is deteriorating. Hydration helps to correct electrolyte imbalances by diluting extracellular fluid. It also increases renal blood flow and encourages natural excretion of electrolytes. High-risk patients should be well hydrated prior to and during treatment, using intravenous fluids. This should be continued maintaining urine output of 3L/day unless the patient shows cardiac signs of volume overload. Proper fluid management is vital in preventing fluid overload and hypertensive complications. Diuretics should only be used in well hydrated patients showing signs of volume overload.
Hyperkalaemia should be aggressively treated and monitored. Dietary potassium should be restricted, and potassium immediately removed from all intravenous fluids. Intravenous insulin + glucose helps redistribute potassium into the intracellular space. IV calcium gluconate can be used for cardio-protection if potassium levels exceed 6.5mmol/L. Potassium wasting diuretics should be used with caution as they may worsen renal precipitation. Oral potassium exchange resins should be given immediately, as this will outlast shorter-term treatments. Should all of these treatments fail to reduce potassium levels, dialysis is indicated.
Oral phosphate binders (eg: aluminium hydroxide) should be used to control hyperphosphataemia. Hypocalcaemia usually resolves as phosphate levels are corrected. Hypocalcaemia should not be actively corrected (with calcitriol) unless Chvostek and Trousseau’s signs are positive.
Dialysis may be indicated if the above measures fail to keep uric acid or phosphate levels below 10mg/dL. Haemodialysis is preferred, and may need to be repeated depending on results of ongoing monitoring. Dialysis helps prevent renal failure, and its preparation should be considered early in the course of the syndrome.
The prognosis of tumour lysis syndrome is excellent with adequate treatment, with renal failure returning to normal when uric acid levels drop below 10mg/dL.

Tumour Lysis Syndrome References

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