Oncologic Emergencies — Written Clinical Reasoning

SAQ 1 — Concurrent Febrile Neutropenia and Tumour Lysis Syndrome (20 marks, 30 minutes)

Prompt: Outline your integrated management plan for this patient, who has two simultaneous oncologic emergencies. Address: (a) the immediate life-threats and your triage decisions; (b) the management of the hyperkalaemia and the cardiac risk; (c) the empiric antibiotic regimen, the cultures, and the timing; (d) the management of the tumour lysis syndrome, including the choice between allopurinol and rasburicase and the reasons; (e) the supportive care in the first 48 hours, including fluid management and renal replacement therapy thresholds; and (f) the common exam trap in this scenario. ^[1]

Model Answer

(a) Immediate life-threats and triage (3 marks): ^[1]

This patient has two concurrent, immediately life-threatening oncologic emergencies: severe symptomatic hyperkalaemia with ECG changes (the peaked T waves are pre-arrest), and established clinical tumour lysis syndrome with acute kidney injury (laboratory TLS (two or more of hyperuricaemia, hyperkalaemia, hyperphosphataemia and hypocalcaemia) plus clinical TLS (AKI) ^[3]) ^[3]. He is also profoundly neutropenic and febrile, at high risk of septic shock. The triage order is: treat the hyperkalaemia first (it can kill in minutes), then begin the tumour lysis syndrome protocol and the empiric antibiotics in parallel, and admit to a high-dependency or intensive care bed for cardiac monitoring, frequent electrolyte checks and the likely need for renal replacement therapy.

(b) Management of the hyperkalaemia and the cardiac risk (4 marks): ^[8]

The peaked T waves mandate immediate membrane stabilisation with intravenous calcium gluconate 10 mL of 10 per cent for membrane stabilisation, repeated if the ECG changes persist. This does not lower the potassium but stabilises the myocardium to prevent ventricular fibrillation. Immediately afterwards, give intravenous insulin (10 units of Actrapid) with 25 g of 50 per cent dextrose to shift potassium intracellularly; the effect begins within 15 to 30 minutes and lasts 4 to 6 hours, with close blood glucose monitoring. Salbutamol nebulisers or intravenous salbutamol are an adjunct. These are temporising measures — the potassium will continue to rise from the ongoing tumour lysis — so the definitive treatment is renal replacement therapy, which I would arrange immediately with the intensive care and nephrology teams. Do not give calcium for the hypocalcaemia unless the patient is symptomatic from it (tetany, seizure, arrhythmia from the hypocalcaemia rather than the hyperkalaemia); correcting calcium in the presence of severe hyperphosphataemia worsens calcium phosphate deposition and renal injury ^[3].

(c) Empiric antibiotic regimen, cultures, and timing (3 marks): ^[1]

Take two sets of blood cultures — one from each lumen of his central line and one peripheral — plus urine culture and swabs of any obvious source, then give the first dose of antibiotic within one hour. The IDSA standard is an antipseudomonal beta-lactam as monotherapy; I would give intravenous piperacillin-tazobactam 4.5 g every 6 hours. I would add vancomycin because he is unstable and at risk of line infection; the IDSA guideline recommends adding vancomycin for haemodynamic instability, a suspected catheter-related infection, severe mucositis, or known MRSA colonisation ^[1]. The antibiotic must not be delayed for the cultures, the count, or any review. I would not use G-CSF routinely — it is reserved for severe or prolonged neutropenia unresponsive to standard therapy, or as secondary prophylaxis in a subsequent cycle.

(d) Management of the tumour lysis syndrome — rasburicase, not allopurinol (4 marks): ^[1]

This patient already has established clinical TLS with hyperuricaemia (620 micromol per litre), so the agent is rasburicase 0.20 mg/kg/day intravenously, not allopurinol. Rasburicase is a recombinant urate oxidase that converts existing uric acid to the soluble allantoin, lowering the serum uric acid within hours; allopurinol only prevents the formation of new uric acid by inhibiting xanthine oxidase and does not lower uric acid that has already formed ^[4]. The GRAAL1 trial established rasburicase as rapidly and reliably urate-lowering in adult high-grade lymphoma ^[4]. I would send a G6PD screen before the dose if there is any possibility of G6PD deficiency (African, Mediterranean, South-East Asian ancestry), because rasburicase is contraindicated in G6PD deficiency — the hydrogen peroxide generated causes haemolysis and methaemoglobinaemia. If the screen is positive or pending, continue hydration and arrange renal replacement therapy while the uric acid is managed supportively. Alkalinisation of the urine is not recommended.

(e) Supportive care in the first 48 hours, including fluid management and dialysis thresholds (4 marks): ^[1]

• Aggressive intravenous hydration and diuresis — the cornerstone of TLS prophylaxis and treatment. With established AKI and oliguria, fluid is guided by volume status; involve nephrology early.
• Vigilant electrolyte monitoring — potassium, phosphate, calcium, urate, urea and creatinine.
• Cardiac monitoring — continuous ECG for the hyperkalaemia and the arrhythmia risk.
• Renal replacement therapy thresholds — I would dialyse for refractory hyperkalaemia (potassium above 6.5 despite medical therapy, or persistent ECG changes), severe metabolic acidosis (pH below 7.1), volume overload unresponsive to diuretics, and symptomatic uraemia. Continuous renal replacement therapy is preferred in the haemodynamically unstable patient; intermittent haemodialysis is effective if the patient is stable.
• Avoid nephrotoxins — no NSAIDs, no aminoglycosides unless essential, no contrast unless essential. ^[1]

(f) The common exam trap (2 marks): ^[1]

The cardinal trap in this scenario is treating the tumour lysis syndrome with allopurinol instead of rasburicase. Allopurinol is prophylaxis for low-risk patients and does not lower uric acid that has already formed; in a patient with established TLS and hyperuricaemia it is the wrong agent and the uric acid will continue to crystallise in the renal tubules. The second trap is correcting the hypocalcaemia with intravenous calcium in an asymptomatic patient — this worsens the calcium phosphate deposition and the renal injury. The third trap is delaying the antibiotic while attending to the metabolic emergency; the febrile neutropenia and the TLS are managed in parallel, and the door-to-antibiotic time of one hour is non-negotiable. ^[1]