Hematology Oncology · Year 2 · from Hematology Oncology

Case 2: Tumor Lysis Syndrome

Patient Presentation

Demographics: 24-year-old male

Chief Complaint: Muscle weakness and palpitations 24 hours after starting chemotherapy

History of Present Illness: The patient was diagnosed with Burkitt lymphoma with high tumor burden (large abdominal mass, elevated LDH). He started chemotherapy yesterday with R-CHOP. Today he reports progressive muscle weakness, cramping, and palpitations. He has had decreased urine output despite IV fluids.

Past Medical History:

  • Burkitt lymphoma (newly diagnosed)
  • Previously healthy

Pre-chemotherapy Labs:

  • Creatinine: 1.0 mg/dL
  • Potassium: 4.2 mEq/L
  • Uric acid: 9.8 mg/dL
  • LDH: 2,450 U/L

Workup and Results

Current Laboratory Studies:

  • Creatinine: 3.2 mg/dL (was 1.0)
  • Potassium: 7.1 mEq/L (severely elevated)
  • Phosphorus: 8.4 mg/dL (elevated)
  • Calcium: 6.8 mg/dL (low)
  • Uric acid: 14.2 mg/dL (elevated)
  • LDH: 4,200 U/L

ECG:

  • Peaked T waves
  • Widened QRS

Urine Output:

  • 0.3 mL/kg/hour (oliguria)

Clinical Image

Diagram illustrating tumor lysis syndrome pathophysiology: rapid cell death releases intracellular contents (potassium, phosphate, nucleic acids converted to uric acid) leading to hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, and acute kidney injury.

Diagnosis

Tumor Lysis Syndrome (Laboratory and Clinical)

Cairo-Bishop Criteria for Laboratory TLS (≥2 of the following within 3 days before or 7 days after chemotherapy):

  • Uric acid ≥8 mg/dL or 25% increase ✓
  • Potassium ≥6 mEq/L or 25% increase ✓
  • Phosphorus ≥4.5 mg/dL or 25% increase ✓
  • Calcium ≤7 mg/dL or 25% decrease ✓

Clinical TLS: Laboratory TLS + AKI, seizures, arrhythmia, or death

Discussion

This case illustrates tumor lysis syndrome:

  • Mechanism: The lecture describes TLS as occurring when rapid tumor cell death releases intracellular contents. Potassium and phosphate are released directly; nucleic acids are metabolized to uric acid.
  • High-Risk Tumors: The lecture identifies Burkitt lymphoma, ALL, and rapidly proliferating tumors with high tumor burden as highest risk. High LDH reflects rapid cell turnover.
  • Hypocalcemia Mechanism: The lecture explains that hypocalcemia results from calcium phosphate precipitation as phosphorus rises dramatically.
  • Uric Acid Nephropathy: The lecture describes how uric acid crystals precipitate in renal tubules, causing acute kidney injury. Maintaining high urine output is critical for prevention.

Treatment Plan

  1. Emergent Hyperkalemia Management:
  • IV calcium gluconate (cardiac protection)
  • IV insulin + glucose (shift potassium)
  • Sodium bicarbonate if acidotic
  • Kayexalate or patiromer
  • Emergent hemodialysis if refractory
  1. Rasburicase (Recombinant Uricase):
  • Rapidly converts uric acid to allantoin
  • Contraindicated in G6PD deficiency
  1. Aggressive IV Hydration:
  • Target urine output 80-100 mL/m2/hour
  • Monitor for fluid overload
  1. Phosphate Management:
  • Phosphate binders
  • Avoid calcium-containing binders if hypercalcemic
  1. Dialysis:
  • If refractory hyperkalemia, severe AKI, or fluid overload
  1. Prevention for Future Cycles:
  • Pre-hydration
  • Allopurinol or rasburicase prophylaxis
  • Monitor labs every 6-8 hours during high-risk period

Teaching Points

  1. TLS: Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia
  2. High-risk: Burkitt, ALL, high tumor burden, high LDH
  3. Prevention: Aggressive hydration + allopurinol/rasburicase
  4. Rasburicase contraindicated in G6PD deficiency
  5. Dialysis for refractory hyperkalemia or severe AKI

All cases for this lecture as Markdown