Complications
The etiology of acute kidney injury (AKI) in TLS is multifactorial but the main mechanism is uric acid nephropathy. Calcium phosphate deposition due to hyperphosphatemia 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 hyperuricemia and hyperphosphatemia, 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., aluminum 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 pharmacologic therapy or cardioversion.
Recognition of early ECG changes and prompt treatment of electrolyte abnormalities (e.g., correction of underlying hyperkalemia, hyperphosphatemia, or hypocalcemia) is crucial.
Seizures are usually secondary to severe hypocalcemia or hyperphosphatemia.
Symptomatically, seizures may be managed with anticonvulsants in a similar manner to seizures of any other etiology. Development of seizures is a definitive indication for treatment of underlying hypocalcemia 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 the uric acid insolubility and phosphatemic shift to the extracellular space.
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