Tumor lysis syndrome: Difference between revisions
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==Background== | ==Background== | ||
*Associated | *Associated with treatment of acute [[leukemia]], Burkitt [[lymphoma]], NHL | ||
**Rarely observed in solid tumors or without prior therapy | **Rarely observed in solid tumors or without prior therapy | ||
*Rapid turnover of tumor cells (spontaneously or after | *Rapid turnover of tumor cells (spontaneously or after treatment) leading to release of: | ||
**Potassium | **Potassium | ||
**Phosphate | **Phosphate | ||
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===Risk Factors=== | ===Risk Factors=== | ||
*High cell proliferation rate | |||
*Large tumor burden (LDH) > 1500 IU/L, WBC ≥ 50 x 103 cells/L | |||
*Extensive BM involvement | |||
*Tumor infiltration of the kidney | |||
===Cairo-Bishop Definition<ref>Cairo MS and Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br. J. Haematol. 2004; 127(1):3–11.</ref>=== | ===Cairo-Bishop Definition<ref>Cairo MS and Bishop M. Tumour lysis syndrome: new therapeutic strategies and classification. Br. J. Haematol. 2004; 127(1):3–11.</ref>=== | ||
'''Laboratory Tumor Lysis Syndrome''' | '''Laboratory Tumor Lysis Syndrome''' | ||
*Abnormality in 2 or more of the following, occurring | *Abnormality in 2 or more of the following, occurring within 3d before or 7d after chemo: | ||
**Uric acid ≥ | **Uric acid ≥ 8mg/dL or 25% increase from baseline | ||
**Potassium ≥ 6mEq/L or 25% increase from baseline | **Potassium ≥ 6mEq/L or 25% increase from baseline | ||
**Phosphate ≥ 4. | **Phosphate ≥ 4.5mg/dL or 25% increase from baseline (≥ 6.5 for children) | ||
**Calcium ≤ | **Calcium ≤ 7mg/dL or 25% decrease from baseline | ||
'''Clinical Tumor Lysis Syndrome''' | '''Clinical Tumor Lysis Syndrome''' | ||
*Laboratory tumor lysis syndrome plus 1 or more of the following: | *Laboratory tumor lysis syndrome plus 1 or more of the following: | ||
** | **Creatinine > 1.5 times upper limit of age-adjusted reference range | ||
**Cardiac dysrhythmia or sudden death | **Cardiac dysrhythmia or sudden death | ||
**Seizure | **Seizure | ||
==Clinical Features== | ==Clinical Features== | ||
*Hyperuricemia | |||
**[[Nausea/vomiting]], [[lethargy]], [[renal failure]] | |||
*[[Hyperkalemia]] | |||
**Most immediate life-threatening element (due to [[dysrhythmias]]) | |||
*[[Hyperphosphatemia]] | |||
**May combine with Ca to precipiate in renal tubules | |||
*[[Hypocalcemia]] | |||
**Anorexia, cramping, tetany, [[confusion]], [[seizures]], [[V-tach]]/[[torsades]] | |||
*[[Acute Renal Failure]] | |||
**Most common cause of morbidity | |||
**Usually results from uric acid precipitation within renal tubules | |||
== | ==Differential Diagnosis== | ||
{{Oncologic emergencies DDX}} | |||
== | ==Evaluation== | ||
===Work Up=== | |||
*CBC | |||
*Chemistry | |||
**Elevated Cr | |||
*Calcium, phosphate | |||
*Uric Acid | |||
*LDH - >2-3 fold increase stratifies into higher TLS risk<ref>Held-Warmkessel J. Preventing & Managing Tumor Lysis Syndrome. Oncology Times: 25 April 2010 - Volume 32 - Issue 8 - pp 1-7</ref> | |||
*[[Urinalysis]] | |||
*[[ECG]] | |||
**[[Hyperkalemia]], [[hypocalcemia]] | |||
;Avoid IV contrast | |||
===[[Hypocalcemia]]=== | ==Management== | ||
*≤7 or 25% | Aggressive hydration - Goal urine output is 3L in 24hr | ||
===[[Hypocalcemia]] Treatment=== | |||
*≤7 or 25% decrease in baseline | |||
**Treat only if symptomatic (increased Ca leads to increased Ca/phos deposition), such as widened QRS or ventricular arrhythmias | **Treat only if symptomatic (increased Ca leads to increased Ca/phos deposition), such as widened QRS or ventricular arrhythmias | ||
**Calcium gluconate 50-200mg IV | **[[Calcium gluconate]] 50-200mg IV | ||
{{Hyperphosphatemia treatment}} | |||
* | *Consider sevelamer 800-1600mg PO tid to avoid side effects of aluminum toxicity and hypercalcemia from aluminum hydroxide treatment | ||
=== | ===Hyperuricemia Treatment=== | ||
*≥8 or 25% increase | *≥8 or 25% increase | ||
**[[Allopurinol]] | **[[Allopurinol]] | ||
***Acts slowly; only helpful for preventing future production of uric acid | ***Acts slowly; only helpful for preventing future production of uric acid | ||
***10mg/kg/d PO q8 OR 200- | ***10mg/kg/d PO q8 '''OR''' 200-400mg/m2 IV q12; renally dosed | ||
***Inhibition of xanthine oxidase can last 18-30h | ***Inhibition of xanthine oxidase can last 18-30h | ||
**Urate Oxidase | **Urate Oxidase | ||
***Rasburicase 0.05-0.2mg/kg IV | ***[[Rasburicase]] 0.05-0.2mg/kg IV | ||
***Can be used for BOTH prevention and treatment | ***Can be used for BOTH prevention and treatment | ||
***Uric acid final product of purine metabolism | ***Uric acid final product of purine metabolism | ||
****Urate oxidase converts uric acid to allantoin (5-10x more soluble) | ****Urate oxidase converts uric acid to allantoin (5-10x more soluble) | ||
===[[Hyperkalemia]]=== | ===[[Hyperkalemia]] Treatment=== | ||
*Only give Ca for cardiovascular instability (e.g.ventricular arrhythmias, widened QRS) | *Only give Ca for cardiovascular instability (e.g.ventricular arrhythmias, widened QRS) | ||
**Giving Ca leads to increased Ca/phos deposition which leads to renal failure | **Giving Ca leads to increased Ca/phos deposition which leads to renal failure | ||
*See [[Hyperkalemia]] for treatment options | *See [[Hyperkalemia]] for treatment options | ||
===Dialysis | ===[[Dialysis]] Criteria=== | ||
*Potassium >6 | |||
*Significant renal insufficiency (Creatinine >10) | |||
*Uric Acid >10 | |||
*Symptomatic [[hypocalcemia]] | |||
*Serum phosphorus >10 | |||
*Volume overload | |||
==Disposition== | ==Disposition== | ||
*Admit (often to ICU) | *Admit (often to ICU) | ||
== | ==References== | ||
<references/> | <references/> | ||
[[Category:Heme/Onc]] | [[Category:Heme/Onc]] |
Revision as of 18:58, 1 October 2019
Background
- Associated with treatment of acute leukemia, Burkitt lymphoma, NHL
- Rarely observed in solid tumors or without prior therapy
- Rapid turnover of tumor cells (spontaneously or after treatment) leading to release of:
- Potassium
- Phosphate
- Binds Ca causing hypocalcemia
- Uric acid (converted from nucleic acids)
Risk Factors
- High cell proliferation rate
- Large tumor burden (LDH) > 1500 IU/L, WBC ≥ 50 x 103 cells/L
- Extensive BM involvement
- Tumor infiltration of the kidney
Cairo-Bishop Definition[1]
Laboratory Tumor Lysis Syndrome
- Abnormality in 2 or more of the following, occurring within 3d before or 7d after chemo:
- Uric acid ≥ 8mg/dL or 25% increase from baseline
- Potassium ≥ 6mEq/L or 25% increase from baseline
- Phosphate ≥ 4.5mg/dL or 25% increase from baseline (≥ 6.5 for children)
- Calcium ≤ 7mg/dL or 25% decrease from baseline
Clinical Tumor Lysis Syndrome
- Laboratory tumor lysis syndrome plus 1 or more of the following:
- Creatinine > 1.5 times upper limit of age-adjusted reference range
- Cardiac dysrhythmia or sudden death
- Seizure
Clinical Features
- Hyperuricemia
- Hyperkalemia
- Most immediate life-threatening element (due to dysrhythmias)
- Hyperphosphatemia
- May combine with Ca to precipiate in renal tubules
- Hypocalcemia
- Acute Renal Failure
- Most common cause of morbidity
- Usually results from uric acid precipitation within renal tubules
Differential Diagnosis
Oncologic Emergencies
Related to Local Tumor Effects
- Malignant airway obstruction
- Bone metastases and pathologic fractures
- Malignant spinal cord compression
- Malignant Pericardial Effusion and Tamponade
- Superior vena cava syndrome
Related to Biochemical Derangement
- Hypercalcemia of malignancy
- Hyponatremia due to SIADH
- Adrenal insufficiency
- Tumor lysis syndrome
- Carcinoid syndrome
Related to Hematologic Derangement
Related to Therapy
- Chemotherapy-induced nausea and vomiting
- Cytokine release syndrome
- Chemotherapeutic drug extravasation
- Differentiation syndrome (retinoic acid syndrome) in APML
- Stem cell transplant complications
- Catheter-related complications
- Tunnel infection
- Exit site infection
- CVC obstruction (intraluminal or catheter tip thrombosis)
- Catheter-related venous thrombosis
- Fracture of catheter lumen
- Oncologic therapy related adverse events
Evaluation
Work Up
- CBC
- Chemistry
- Elevated Cr
- Calcium, phosphate
- Uric Acid
- LDH - >2-3 fold increase stratifies into higher TLS risk[2]
- Urinalysis
- ECG
- Avoid IV contrast
Management
Aggressive hydration - Goal urine output is 3L in 24hr
Hypocalcemia Treatment
- ≤7 or 25% decrease in baseline
- Treat only if symptomatic (increased Ca leads to increased Ca/phos deposition), such as widened QRS or ventricular arrhythmias
- Calcium gluconate 50-200mg IV
Hyperphosphatemia treatment
- Treat the underlying cause
- Restrict calcium phosphate intake
- IV Normal Saline (if normal renal fx)
- Acetazolamide (500mg IV q6hr) - if normal renal function
- Phosphate Binder - Aluminum hydroxide (50-150mg/kg PO q4-6h) - limited effect
- Dialysis if refractory
- Consider sevelamer 800-1600mg PO tid to avoid side effects of aluminum toxicity and hypercalcemia from aluminum hydroxide treatment
Hyperuricemia Treatment
- ≥8 or 25% increase
- Allopurinol
- Acts slowly; only helpful for preventing future production of uric acid
- 10mg/kg/d PO q8 OR 200-400mg/m2 IV q12; renally dosed
- Inhibition of xanthine oxidase can last 18-30h
- Urate Oxidase
- Rasburicase 0.05-0.2mg/kg IV
- Can be used for BOTH prevention and treatment
- Uric acid final product of purine metabolism
- Urate oxidase converts uric acid to allantoin (5-10x more soluble)
- Allopurinol
Hyperkalemia Treatment
- Only give Ca for cardiovascular instability (e.g.ventricular arrhythmias, widened QRS)
- Giving Ca leads to increased Ca/phos deposition which leads to renal failure
- See Hyperkalemia for treatment options
Dialysis Criteria
- Potassium >6
- Significant renal insufficiency (Creatinine >10)
- Uric Acid >10
- Symptomatic hypocalcemia
- Serum phosphorus >10
- Volume overload
Disposition
- Admit (often to ICU)