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Tumor Lysis Syndrome

Metabolic emergency from rapid tumor cell death releasing intracellular contents into circulation.

Written by: Saygı Hospital Health Guide Editorial Board
Last updated:

This content has been compiled by the Saygı Hospital Health Guide Editorial Board and is periodically reviewed by a specialist physician.

References (5)

This content is for informational purposes only and does not constitute medical advice. You can book an appointment at our Onkoloji department. Book Appointment →

What is Tumor Lysis Syndrome?

Tumor lysis syndrome (TLS) is an oncologic emergency caused by rapid release of intracellular contents (potassium, phosphate, nucleic acids) from tumor cells lysed by chemotherapy, radiation, immunotherapy, or spontaneously. The Cairo-Bishop classification defines laboratory TLS by uric acid 8 mg/dL or 25% increase, potassium 6 mmol/L or 25% increase, phosphate 4.5 mg/dL or 25% increase, or calcium less than 7 mg/dL within 3 days before to 7 days after chemotherapy. Clinical TLS adds organ dysfunction.

Highest risk malignancies include Burkitt lymphoma, T-cell or B-cell acute lymphoblastic leukemia, acute myeloid leukemia with high WBC, high-grade non-Hodgkin lymphoma, and bulky chemosensitive tumors. CD20 monoclonal antibodies (rituximab), Bcl-2 inhibitors (venetoclax), and certain CAR-T cells can precipitate TLS. Risk stratification (low, intermediate, high) guides prophylaxis intensity.

Manifestations include arrhythmias from hyperkalemia, seizures from hypocalcemia, and acute kidney injury from urate and calcium phosphate crystals. Prevention combines aggressive IV hydration, allopurinol for low-intermediate risk, and rasburicase (recombinant urate oxidase) for high risk. Monitoring electrolytes every 4-6 hours, urgent dialysis for severe hyperkalemia or AKI, and ICU admission for high-risk inductions are standard.

Symptoms

Hyperkalemia: muscle weakness, paresthesias, arrhythmias, ECG changes (peaked T, widened QRS)
Hyperphosphatemia: secondary hypocalcemia features
Hypocalcemia: tetany, seizures, prolonged QT, paresthesias
Hyperuricemia: gout-like symptoms, urate nephropathy
Acute kidney injury: oliguria, edema, elevated creatinine
Lactic acidosis with multi-organ dysfunction
Confusion, lethargy
Cardiac arrest in severe electrolyte derangement
Vomiting, abdominal pain
Hematuria from urate crystals
Decreased urine output

Risk Factors

Burkitt lymphoma
Acute lymphoblastic leukemia (especially T-cell with high WBC)
Acute myeloid leukemia with WBC over 100,000/microL
High-grade non-Hodgkin lymphoma
CLL with venetoclax initiation
Bulky tumor mass
High proliferation index
Chemosensitive disease
Pre-existing renal impairment
Dehydration or hypovolemia
Hyperuricemia at baseline
Concurrent nephrotoxic drugs

When to See a Doctor?

If you experience any of the following symptoms, seek medical attention promptly:

  • Symptoms during or shortly after chemotherapy initiation
  • Muscle weakness, palpitations, paresthesias
  • Reduced urine output, edema
  • Confusion, seizures, tetany
  • Severe abdominal flank pain
  • Vomiting and dehydration

Treatment Methods

01
Risk stratify: low, intermediate, high based on tumor type, burden, kidney function
02
Aggressive IV hydration: 3 L/m²/day starting 24-48 hours before chemotherapy, maintain urine output 80-100 mL/m²/hour
03
Avoid potassium and phosphate in IV fluids initially
04
Loop diuretic if fluid overload despite adequate hydration
05
Low-intermediate risk: allopurinol 300-600 mg/day starting 1-2 days before chemotherapy
06
High risk: rasburicase 0.2 mg/kg IV daily for 1-7 days (avoid in G6PD deficiency)
07
Febuxostat alternative if allopurinol intolerant
08
Monitor electrolytes every 4-6 hours during high risk induction
09
ECG monitoring; ICU admission for high-risk cases
10
Hyperkalemia management: calcium gluconate, insulin/glucose, beta-agonist nebulizer, sodium bicarbonate, dialysis
11
Hyperphosphatemia: oral phosphate binders (calcium acetate, sevelamer)
12
Hypocalcemia: replace cautiously due to calcium phosphate precipitation risk
13
Hyperuricemia: rasburicase rapidly normalizes
14
Avoid urinary alkalinization (precipitates calcium phosphate)
15
Renal replacement therapy: severe AKI, hyperkalemia, fluid overload, uremic symptoms
16
Continuous renal replacement therapy for unstable patients
17
De-escalate prophylaxis based on response and post-treatment metabolic stability
18
Prevent rasburicase-induced hemolysis: screen G6PD before high-risk dosing
19
Patient and family education on symptoms
20
Multidisciplinary care: oncology, nephrology, ICU, pharmacy, dietitian
21
Follow-up renal function and uric acid post-treatment

Which Department to Visit?

You can visit our Onkoloji department for these complaints. Our specialist physicians will create the most suitable treatment plan for you.

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