What are the key clinical signs and laboratory findings that indicate the onset of Tumour Lysis Syndrome (TLS) in a patient undergoing chemotherapy?

Key clinical signs indicating the onset of tumour lysis syndrome (TLS) in a patient undergoing chemotherapy include symptoms related to electrolyte imbalances and acute kidney injury, such as nausea, vomiting, muscle cramps, tetany, seizures, cardiac arrhythmias, and sudden onset of oliguria or anuria. These clinical manifestations arise due to rapid cell lysis releasing intracellular contents into the bloodstream, overwhelming the body's homeostatic mechanisms ¹ (Yarpuzlu, 2003).

Laboratory findings critical for diagnosing TLS include hyperuricaemia, hyperkalaemia, hyperphosphataemia, and hypocalcaemia. Specifically, elevated serum uric acid results from nucleic acid breakdown, increased potassium and phosphate levels reflect intracellular release, and secondary hypocalcaemia occurs due to phosphate binding calcium. These biochemical abnormalities can precipitate acute kidney injury and cardiac complications ¹ (Cairo et al., 2010; Wilson and Berns, 2012).

Early recognition relies on serial monitoring of these laboratory parameters before and during chemotherapy, especially in high-risk patients with bulky or rapidly proliferating tumours. The consensus recommends defining laboratory TLS by the presence of two or more metabolic abnormalities within three days before or seven days after chemotherapy initiation, accompanied by clinical signs such as renal impairment or cardiac arrhythmias ¹ (Cairo et al., 2010).

In summary, the onset of TLS is indicated by a constellation of clinical symptoms related to electrolyte disturbances and acute kidney injury, supported by laboratory evidence of hyperuricaemia, hyperkalaemia, hyperphosphataemia, and hypocalcaemia occurring in close temporal relation to chemotherapy.