MDM Templates

Tumor Lysis Syndrome

Patient presents with *** in the setting of recent chemotherapy (last treatment ***). Presentation is concerning for tumor lysis syndrome. Patient’s malignancy (***) carries significant risk for TLS. Labs demonstrate electrolyte derangements consistent with cell lysis — the hallmark pattern of hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia.

History, exam, and workup lower suspicion for sepsis, disease progression, and other chemotherapy-related complications as the primary etiology.

Plan: Aggressive IV fluid resuscitation initiated. Electrolyte abnormalities addressed individually — hyperkalemia management per severity, calcium repletion for symptomatic hypocalcemia. Rasburicase administered for significant hyperuricemia. Oncology consulted regarding further management and disposition. ECG monitored for changes related to hyperkalemia or hypocalcemia.

Disposition: Admit to ICU for continuous monitoring, serial lab rechecks, and assessment for need for hemodialysis.

Indications for emergent hemodialysis: Refractory hyperkalemia, severe symptomatic hypocalcemia, uric acid nephropathy with oliguria/anuria, volume overload refractory to diuretics.

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TLS — Mild/Incidental Lab Findings

Patient presents with *** in the setting of recent chemotherapy. Labs show early electrolyte derangements suggestive of tumor lysis (***) without evidence of end-organ dysfunction. Patient is well appearing and asymptomatic.

Plan: Aggressive IV hydration initiated. Allopurinol started for uric acid prophylaxis. Oncology consulted regarding disposition — may be appropriate for admission to monitored floor bed with serial labs every 4–6 hours. Return precautions for muscle cramps, weakness, palpitations, decreased urine output, or any new symptoms.

Clinical Education

Pathophysiology and Diagnosis

TLS results from massive cell lysis releasing intracellular contents: potassium, phosphorus, uric acid, and nucleic acids.^[1] Phosphorus binds calcium → hypocalcemia. Uric acid precipitates in renal tubules → AKI. Typically occurs 12–72 hours after initiation of cytotoxic therapy, though it can rarely occur spontaneously in high-burden tumors.

Cairo-Bishop criteria define the diagnosis:^[2] Laboratory TLS requires 2 or more abnormal values. Clinical TLS = laboratory TLS + end-organ dysfunction (seizures, arrhythmias, or AKI).

Lab Value	Cairo-Bishop Criteria
Uric acid	≥8 mg/dL or 25% increase from baseline
Potassium	≥6 mEq/L or 25% increase from baseline
Phosphorus	≥4.5 mg/dL or 25% increase from baseline
Calcium	≤7 mg/dL or 25% decrease from baseline

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Risk Stratification

High-risk malignancies: NHL (especially Burkitt — near 100% risk), ALL, AML with WBC >100k. Approximate TLS rates by malignancy: NHL 30%, solid tumors 20%, AML 19%, ALL 13%.^[4]

Key risk factors: High tumor burden, elevated baseline LDH and uric acid, pre-existing renal dysfunction, dehydration.

TLS with AKI carries 21% in-hospital mortality versus 7% without AKI. This underscores the importance of aggressive volume resuscitation and early recognition.

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ED Management

Problem	Treatment
Volume depletion	Aggressive isotonic crystalloid (200–300 mL/hr goal) — cornerstone of management
Hyperuricemia	Rasburicase 0.2 mg/kg IV (first-line if significantly elevated); allopurinol 300–800 mg/day for prophylaxis/mild
Hyperkalemia	Calcium gluconate (membrane stabilization), insulin/dextrose, kayexalate; dialysis if refractory
Hypocalcemia	Treat only if symptomatic (tetany, seizures, QTc prolongation) — calcium repletion can worsen Ca-PO₄ precipitation
Hyperphosphatemia	Phosphate binders (sevelamer); dietary restriction; dialysis if severe

Key pearl: Do NOT aggressively correct asymptomatic hypocalcemia — calcium-phosphate product precipitation in tissues and kidneys can worsen renal injury. Treat only if symptomatic or ECG changes present.^[3]

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Rasburicase vs Allopurinol

Rasburicase is a recombinant urate oxidase that converts uric acid to allantoin (soluble, renally excreted). Works within hours versus allopurinol which takes days. First-line for established TLS with significant hyperuricemia.^[1]

Allopurinol (300–800 mg/day) is appropriate for prophylaxis or mild cases. Prevents new uric acid formation but does not break down existing uric acid.

CONTRAINDICATED in G6PD deficiency — rasburicase causes methemoglobinemia and hemolytic anemia in G6PD-deficient patients.

Lab pearl: Send uric acid level BEFORE administering rasburicase and transport on ice. Rasburicase continues to break down uric acid in the tube at room temperature, giving falsely low results.

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Hemodialysis Indications

Indications for emergent dialysis in TLS: Refractory hyperkalemia despite medical management, severe symptomatic hypocalcemia with hyperphosphatemia, uric acid nephropathy with oliguria/anuria, volume overload refractory to diuretics, and rapidly deteriorating renal function.^[5]

Early nephrology consultation is key. Don’t wait until the patient crashes — if the trajectory is worsening despite aggressive medical management, get nephrology involved early for dialysis planning.

References

1. Howard SC et al. The tumor lysis syndrome. N Engl J Med. 2011;364(19):1844-1854. PubMed
2. Cairo MS, Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br J Haematol. 2004;127(1):3-11. PubMed
3. Coiffier B et al. Guidelines for the management of pediatric and adult tumor lysis syndrome. J Clin Oncol. 2008;26(16):2767-2778. PubMed
4. Wilson FP et al. Tumor lysis syndrome: new challenges and recent advances. Adv Chronic Kidney Dis. 2014;21(1):18-26. PubMed
5. Mirrakhimov AE et al. Tumor lysis syndrome: a clinical review. World J Crit Care Med. 2015;4(2):130-138. PubMed