Tumor Lysis Syndrome
Oncology
Illness script · Oncology
Tumor Lysis Syndrome
Metabolic emergency from massive tumor cell lysis releasing intracellular contents, causing hyperuricemia, hyperkalemia, hyperphosphatemia, and hypocalcemia.
This illness script for Tumor Lysis Syndrome covers predisposing factors, classic presentation, mechanism, workup, management, and the clinical pivots that separate it from look-alikes—written for USMLE Step 1 and clerkship reasoning.
01
Predisposing factors
- High-grade hematologic malignancies: Burkitt lymphoma (highest risk), ALL, AML
- Large tumor burden or rapidly proliferating tumors
- Initiated by chemotherapy; rarely spontaneous
- Pre-existing renal insufficiency or dehydration increases risk
- Elevated baseline uric acid or LDH signals high risk
02
Presentation
- Onset within 12–72 hours of chemotherapy initiation
- Hyperkalemia → cardiac arrhythmias, weakness (most immediately life-threatening)
- Hypocalcemia → tetany, seizures, Chvostek/Trousseau signs, QTc prolongation
- Hyperuricemia → oliguria, flank pain, AKI
- Nausea, vomiting, lethargy common early symptoms
03
Pathophysiology
- Tumor cell lysis releases potassium, phosphate, nucleic acids, and proteins
- Nucleic acids catabolized to uric acid → precipitates in renal tubules → AKI
- Hyperphosphatemia chelates calcium → symptomatic hypocalcemia
- Urate and calcium-phosphate crystal deposition worsens renal failure
04
Diagnostics
- Cairo-Bishop criteria: ≥2 of hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia
- Labs: BMP, uric acid, phosphate, LDH, CBC — monitor q6–8h in high-risk patients
- ECG immediately if hyperkalemia suspected (peaked T waves, wide QRS)
- Urinalysis may show urate crystals; urine output monitoring essential
- LDH elevation correlates with tumor burden and TLS risk
05
Management
- Aggressive IV hydration (2–3 L/m²/day) — cornerstone of prevention and treatment
- Allopurinol for prophylaxis in intermediate-risk patients (blocks new uric acid synthesis)
- Rasburicase for high-risk or established TLS — rapidly degrades existing uric acid
- Treat hyperkalemia urgently (calcium gluconate, insulin/dextrose, kayexalate, dialysis if refractory)
- Avoid calcium supplementation unless symptomatic hypocalcemia — worsens calcium-phosphate precipitation
- Hemodialysis for refractory electrolyte abnormalities or severe AKI
06
Clinical pivots
How to separate this script from the look-alikes that show up on exams and on the wards.
Acute Kidney Injury (other causes)
TLS has concurrent hyperuricemia + hyperkalemia + hyperphosphatemia + hypocalcemia in a chemo-treated cancer patient
Rhabdomyolysis
Rhabdo has markedly elevated CK and myoglobinuria; no hyperphosphatemia-driven hypocalcemia pattern or uric acid surge
Addisonian crisis
Addison's has hyponatremia + hyperkalemia but no hyperphosphatemia, hyperuricemia, or oncologic context
Spontaneous tumor lysis
Same metabolic picture but occurs before chemo; rare, seen with Burkitt or bulky ALL — no cytotoxic trigger
Keep reading
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Educational use only. This illness script is a study framework, not medical advice. Confirm decisions with current guidelines and your clinical supervisors.