Complications
The aetiology of acute kidney injury (AKI) in TLS is multifactorial, but the main mechanism is uric acid nephropathy. Calcium phosphate deposition due to hyperphosphataemia may contribute. Without appropriate management, TLS may cause AKI in up to 25% of patients.[14][59]
Regular monitoring of renal function and electrolytes is essential.
Treatment of hyperuricaemia and hyperphosphataemia, volume repletion, and avoidance of nephrotoxic agents can help prevent AKI.
Once established, attention to fluid balance and adequate hydration is essential. Phosphate-binding agents (e.g., aluminium salts) have no place in the management of TLS after the development of AKI.[56][57]
Renal dialysis may be required in some patients, but the need for this seems to have reduced since the introduction of rasburicase.[55]
The most serious manifestation of clinical TLS. ECG changes are characteristic, and continuous cardiac monitoring is necessary when any cardiac arrhythmia is diagnosed and throughout treatment.
Treatment depends on the type of arrhythmia and may include pharmacological therapy or cardioversion.
Recognition of early ECG changes and prompt treatment of electrolyte abnormalities (e.g., correction of underlying hyperkalaemia, hyperphosphataemia, or hypocalcaemia) is crucial.
Seizures are usually secondary to severe hypocalcaemia or hyperphosphataemia.
Symptomatically, seizures may be managed with anticonvulsants in a similar manner to seizures of any other aetiology. Development of seizures is a definitive indication for treatment of underlying hypocalcaemia with calcium gluconate (infused intravenously and cautiously repeated if necessary).
Lactic acidosis is thought to be the end result of massive cell chemotherapy-induced apoptosis in combination with acute kidney injury. Acidosis can worsen most of the metabolic abnormalities already present in the syndrome, including uric acid insolubility and phosphataemic shift to the extracellular space.
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