Tumour lysis syndrome and oncologic emergencies: Case

Framing the case

This seven-year-old boy with the Burkitt lymphoma sits at the very top of the tumour lysis risk. The large abdominal mass, the lactate dehydrogenase of three thousand, and the elevated urate together mark a high tumour burden and a high cell turnover, and the start of the chemotherapy will release a torrent of the intracellular contents. The framework that organises the case is the recognition that the tumour lysis is predictable and preventable, and the first decision is to put the prophylaxis in place before the first dose of the chemotherapy. [3]

The risk assessment and the prophylaxis

The boy is high risk by the Cairo stratification, because the Burkitt lymphoma has the very highest cell turnover of any childhood tumour, with a doubling time of around twenty-four hours. The prophylaxis is the foundation of the management, and it begins before the first dose. The hyperhydration with an isotonic fluid that contains no potassium is run at two to three litres per square metre per day to maintain a urine output above two millilitres per kilogram per hour. The fluid is potassium-free because the child is at risk of the hyperkalaemia. [1]

The rasburicase, a recombinant urate oxidase that converts the existing uric acid into the soluble allantoin, is given at zero point one five to zero point two milligrams per kilogram, and the glucose-six-phosphate-dehydrogenase status is checked first, because the rasburicase is contraindicated in the deficiency and causes a severe haemolysis and a methaemoglobinaemia. The biochemistry of the potassium, the phosphate, the calcium, the creatinine, and the urate is monitored every four to six hours for the first twenty-four to forty-eight hours, and the renal replacement therapy is kept on standby. [1][9]

The recognition and the management if it declares

Should the tumour lysis declare, the recognition rests on the Cairo-Bishop definition. The laboratory tumour lysis syndrome is two or more of the urate over four hundred and seventy-six micromoles per litre, the potassium over six millimoles per litre, the phosphate over two point one millimoles per litre in the child, and the corrected calcium under one point seven five millimoles per litre, within three days before to seven days after the cytotoxic therapy, each or a twenty-five percent change from the baseline. The clinical form adds the acute kidney injury, the cardiac arrhythmia or sudden death, or the seizure. [2]

The management of the declared syndrome is staged. The hyperkalaemia is the immediate killer, and the calcium gluconate is given the moment the ECG shows the peaked T waves and the widened QRS, to stabilise the cardiac membrane within minutes, followed by the insulin with the glucose and the salbutamol to shift the potassium into the cell. The asymptomatic hypocalcaemia is not corrected in the high-phosphate state, because the correction drives the calcium-phosphate deposition and worsens the kidney injury. The refractory hyperkalaemia, the oliguria, and the volume overload are the indications for the renal replacement therapy. [5]

The structural emergencies

Should the boy instead present with a progressive leg weakness and a bowel or bladder change, the malignant spinal cord compression would be assumed until the magnetic resonance imaging proved otherwise. The intravenous dexamethasone would be started early to reduce the cord oedema, the urgent whole-spine magnetic resonance imaging would define the level and the cause, and the definitive management would be the emergency decompression, the radiotherapy, or the chemotherapy. The ambulation at the presentation is the strongest predictor of the ambulation at the outcome, and the window to preserve the walking is twenty-four to forty-eight hours. [7]

Should the boy develop a fever with a neutrophil count under zero point five times ten to the nine per litre, the febrile neutropenia would be managed empirically with an antipseudomonal beta-lactam such as the cefepime or the piperacillin-tazobactam within one hour after the blood cultures, because the fever in the neutropenic child is a bacterial emergency. [5]

Communication and the family

The family is counselled honestly on the high tumour lysis risk, on the rationale for the hyperhydration and the rasburicase, and on the need for the close biochemical monitoring in the first days of the therapy. The glucose-six-phosphate-dehydrogenase check is explained, and the family is taught the warning signs of the fever and the new symptom and the need to return at once. The boy is prepared in an age-appropriate way, and the multidisciplinary team is assembled around the family. [4]