In a chronic myeloid leukemia patient with a white blood cell count of 71 × 10⁹/L and platelet count of 523 × 10⁹/L, what therapy should be administered to prevent tumor lysis syndrome?

Management of Tumor Lysis Syndrome Prevention in CML with Hyperleukocytosis

In a CML patient with WBC 71,000/μL and platelets 523,000/μL, immediately initiate aggressive intravenous hydration (2.5-3 L/day adjusted for cardiac/renal status), continue hydroxyurea for cytoreduction, and use allopurinol (not rasburicase) for TLS prophylaxis while preparing to start definitive TKI therapy once BCR-ABL1 is confirmed. 1

Immediate Hydration Protocol

• Administer 2.5-3 liters of IV fluid per day, adjusting for the patient's individual cardiac and renal function to avoid volume overload 1
• Target urine pH of 6.4-6.8 using sodium bicarbonate to optimize uric acid clearance 1
• Monitor fluid balance closely, as CML patients typically do not have the same acute TLS risk as acute leukemias but still require prophylaxis with elevated counts 2

Cytoreduction Strategy

• Continue hydroxyurea at 40-50 mg/kg/day (or current dose if already started) to rapidly reduce the WBC count before initiating TKI therapy 1, 2
• Hydroxyurea achieves approximately 50% WBC reduction within 1-2 weeks, which is appropriate for CML without organ-threatening leukostasis 2
• Taper hydroxyurea gradually before discontinuation once TKI therapy begins, rather than stopping abruptly 1

Uric Acid Management

• Use allopurinol for hyperuricemia prophylaxis, but restrict to patients with symptomatic hyperuricemia due to risk of xanthine accumulation and renal failure 1
• Rasburicase is NOT typically indicated for CML chronic phase, as the tumor lysis risk is substantially lower than in acute leukemias or high-grade lymphomas 3, 4
• The metabolic derangements in CML occur more gradually compared to acute leukemias, making aggressive uric acid-lowering with rasburicase unnecessary in most cases 3, 4

Critical Monitoring Parameters

• Check electrolytes, uric acid, phosphate, calcium, creatinine, and LDH every 4-6 hours initially to detect early TLS 2
• Assess for signs of leukostasis including neurological symptoms (confusion, visual changes), respiratory symptoms (dyspnea, hypoxia), and priapism in males 2
• Monitor for hyperkalemia, hyperphosphatemia, and hypocalcemia—the classic metabolic derangements of TLS 3, 5, 4

Definitive Therapy Preparation

• Initiate TKI therapy immediately once BCR-ABL1 fusion is confirmed by cytogenetics or molecular testing 1
• First-line TKI options include imatinib 400 mg daily, nilotinib 300 mg twice daily, or dasatinib 100 mg daily, selected based on patient age, comorbidities, and risk stratification 1
• Ensure potassium and magnesium are repleted to appropriate levels before starting TKI, as all TKIs may prolong QT interval 1

Important Caveats

The risk of TLS in CML chronic phase is substantially lower than in acute leukemias or blast crisis, even with elevated WBC counts 1, 3, 4. This patient's WBC of 71,000/μL, while elevated, does not typically cause the massive, rapid cell lysis seen with acute leukemias where WBC >100,000/μL is considered a true emergency 2, 6.

Avoid overly aggressive uric acid management that would be appropriate for acute leukemia—allopurinol is sufficient for CML chronic phase, and rasburicase would be excessive 1. The ESMO guidelines specifically state allopurinol should be restricted to symptomatic hyperuricemia due to xanthine accumulation risk 1.

Do not delay TKI initiation once diagnosis is confirmed—prompt institution of definitive therapy is essential, and hydroxyurea is only a temporizing measure 1. The goal is to taper hydroxyurea as TKI therapy takes effect, not to continue both long-term 1.