QuestionSBA
QuestionChoice
Hyponatreamia can be a sign of paraneoplastic syndromes such as syndrome of inappropriate ADH. It is not in keeping with tumour lysis syndrome
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d
Sodium 128 mmol/L
QuestionChoice
This is a normal potassium level. A high potassium level would be associated with TLS
32737
e
Potassium 4.2 mmol/L
QuestionChoice
Breakdown of cells includes the breakdown of their nucleic acid, which has a phosphate group, and therefore a high phosphate is expected in TLS. As phosphate leads to calcium chelation, patients will also have low calcium rather than high calcium. High calcium is associated with malignancy with boney metastasis, for example, lung cancer, breast cancer and renal cancer
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Adjusted Calcium 3.70 mmol/L
QuestionChoice
As rapid cell breakdown releases potassium, a low potassium would be unusual in TLS
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b
Potassium 2.9 mmol/L
QuestionChoice
TLS is a severe metabolic disturbance caused by the abrupt release of cellular components following the rapid lysis of malignant cells upon initiation of treatment. Therefore high potassium, high urea, high phosphate and low calcium are expected.

Lactate, urate and LDH may also be increased and so should be monitored, but are not diagnostic.

It is usually within 1-5 days of starting chemotherapy and can cause seizures, cardiac arrhythmias, kidney injury and even death. Management is through prevention and careful monitoring and treatment of any complications should they occur
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Urea 22 mmol/L
QuestionComment
I know in tumour lysis syndrome there is raised K, PO4 and uric acid with low Ca. But is urea the same as uric acid (ie urate)?
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QuestionComment
innit? i was thinking the samee bc notes say high urate rather than urea idk if they are used interchangeablyyy
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Suture Bradykinin
QuestionComment
They're not the same.
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Financiers 
QuestionComment
the urea is raised due to AKI due to the TLS
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ButtMuncher
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Lueh Chien
QuestionComment
Feel like this is a bit mean and also kind of teaching people that uric acid and urea are the same thing (they're not). The lab criteria of TLS is uric acid, calcium, phosphate and potassium.
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# Summary


Tumour lysis syndrome is a potentially lethal condition caused by the rapid death of tumour cells often following chemotherapy or rapid progression of haematological malignancies, resulting in the massive release of intracellular contents. It is an oncological emergency. Patients commonly present with acute-onset dysuria/oliguria, abdominal pain, or weakness. Key investigations include measurements of U&E (showing raised potassium and phosphate), calcium (typically low), uric acid (raised), and ECG to detect metabolic abnormalities and life-threatening arrhythmias. Initial management involves the correction of electrolyte abnormalities and intravenous fluid administration.


# Definition


Tumour lysis syndrome is a serious metabolic disorder caused by the rapid death of tumour cells in response to chemotherapy. This results in a massive release of intracellular contents into the bloodstream, leading to significant electrolyte imbalances.


Tumour lysis syndrome is most commonly associated with aggressive, rapidly proliferating tumours such as acute leukaemia and high-grade lymphomas, particularly after the initiation of cytotoxic therapy. 


# Aetiology


The syndrome occurs due to the rapid release of intracellular contents from dying tumour cells, often following chemotherapy. It can however also be caused by high-grade lymphomas and acute leukaemias. This leads to hyperuricaemia, hyperphosphatemia, hyperkalaemia, and hypocalcaemia. These metabolic abnormalities lead to the clinical manifestations including acute kidney injury and arrhythmias.


# Signs and symptoms


Patients may present with symptoms related to electrolyte abnormalities and hyperuricaemia, which include:


* Dysuria or oliguria
* Abdominal pain
* Weakness
* Nausea or vomiting
* Muscle cramps
* Seizures
* Cardiac arrhythmias
* Gout/joint swelling


# Differential diagnosis


Differential diagnosis should consider other causes of similar symptoms and laboratory abnormalities, such as:


* **Acute kidney injury**: while tumour lysis syndrome can cause AKI, other causes should be considered. For example, patients may have significant dehydration or have received nephrotoxic drugs contributing to AKI. Careful history-taking and the absence of other features of tumour lysis syndrome should raise suspicion of AKI due to other causes. It is important to note though, that AKI can cause significant electrolyte abnormalities, so careful monitoring is required.
* **Isolated hyperkalaemia**: presents with muscle weakness, fatigue, palpitations, and potentially life-threatening cardiac arrhythmias. Patients may have a history of renal failure or taking potassium-sparing medications. Uric acid, phosphate and calcium levels would be normal.
* **Isolated hyperphosphateamia**: presents with muscle cramps, itching, and perioral tingling or numbness. Uric acid and potassium would be normal.
* **Isolated hypocalcaemia**: presents with numbness and tingling in the hands, feet, and around the mouth, muscle cramps, and seizures. Uric acid, potassium and phosphate would be normal


# Investigations


Key investigations for tumour lysis syndrome include:

* Basic observations
* U&E: Potassium and phosphate are usually raised, raised Cr suggestive of AKI/renal failure.
* Calcium: Typically low in tumour lysis syndrome.
* Uric acid: Usually elevated.
* ECG: To assess risk of arrhythmias caused by electrolyte abnormalities.
* Hyperkalaemia may cause tented T waves, broad QRS, flattened P-wave and a prolonged PR interval. 
* Hypocalcaemia may cause a prolonged QT interval.


# Management


Management of tumour lysis syndrome primarily focuses on:


* Correction of electrolyte imbalances & mitigation of arrhythmia risk.
* For example in severe hyperkalaemia, calcium gluconate is given followed by an insulin-dextrose infusion or nebulised salbutamol. Further management may include calcium resonium to prevent further potassium absorption from the gut.
* Severe hypocalcaemia may require parenteral replacement.
* Dialysis may be required in severe cases.
* Administration of intravenous fluids to help flush out the intracellular contents released by the dying tumour cells.
* Medications: rasburicase (a recombinant form of the urate oxidase enzyme) transforms uric acid into allantoin. Allantoin is more soluble in urine than uric acid, and more easily eliminated by the kidney.


### Prevention 


* Low/intermediate risk patients can be managed with a combination of adequate hydration and allopurinol. 
* Rasburicase (a recombinant form of the urate oxidase enzyme) can be used as a prophylactic agent in adults with hyperuricaemia that is inadequately managed by allopurinol or febuxostat.


# References

[British Society for Haemotology: Management of Tumour Lysis Syndrome in Adults and Children with Haematological Malignancies](https://b-s-h.org.uk/guidelines/guidelines/management-of-tumour-lysis-syndrome-in-adults-and-children-with-haematological-malignancies)

[Patient.info: Oncological emergencies](https://patient.info/doctor/oncological-emergencies#tumour-lysis-syndrome)
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Tumour Lysis Syndrome
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Oncology and Palliative Care
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Tumour Lysis Syndrome
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Tumour lysis syndrome
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Tumor lysis syndrome occurs when cancer cells rapidly die, releasing nucleic acids that break down into uric acid, overwhelming the kidneys, causing hyperuricemia, renal dysfunction, and elevated blood urea levels.
A 24-year-old male is treated for Hodgkin's lymphoma with chemotherapy.

As he has a high tumour burden, he is deemed at high risk of tumour lysis syndrome (TLS); which of the following blood tests would suggest tumour lysis syndrome?
a