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tumor lysis syndrome

overview, ddx, ttt, follow up, conclusion

razan alamoudi

on 7 June 2011

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Transcript of tumor lysis syndrome

Chemotherapy Target Cell Death Breakdown of malignant cells 2ry to cell death resulting in a variety of biochemical abnormalities most of which are electrolyte in origin Definition: Epidemiology Incidence is unknown. Prevalence varies among different malignancies. Frequency Patients with intermediate-grade or high-grade non-Hodgkin lymphomas
TLS (42%) occurred much more frequently than the symptomatic clinical syndrome (6%). Children with acute leukemia receiving induction chemotherapy, silent laboratory evidence of TLS occurred in 70% of cases, but clinically significant tumor lysis syndrome occurred in only 3% of cases. examples for studies of frequency Risk Factors for TLC Large Tumor Burden Hyper Leukocytosis Increased LDL Increased Uric Acid Chemosensitive Tumor Pre-existing Renal Dysfunction Massive Organomegaly Age Advanced age → IR function → TLS IC ION released with cell destruction
First abnormality to occur
12 hrs after chemotherapy begins
Can be aggravated by Acidosis & hypocalcemia • 12-24 hrs after chemo begins.

• Most common abnormality associated with RF during induction.

• Metabolic acidosis Follows hyperphophatemia
Believed to result in tissue precipitation of Calcium-phosphate Goal of Therapy Reduce morbidity and prevent complications. CONTROL OF HYPERURICEMIA
DIALYSIS CONTROL OF HYPERURICEMIA Uricosurics Allopurinol Rasburicase Hydration Volume depletion is a major risk factor for TLS & must be corrected vigorously.
Aggressive IV hydration helps correct electrolyte disturbances by diluting extracellular fluid, and increases intravascular volume.
Increased volume enhances renal blood flow, GFR, and urine volume to decrease the concentration of solutes in the distal nephron and medullary microcirculation. Urinary Alkalinization Sodium Bicarbonate Acetazolamide Promotes alkaline diuresis with potential benefits of solubilizing and minimizing, intratubular precipitation of uric acid.
It increase urinary pH to 7 maximizing uric acid solubility in renal tubules and vessels Urinary alkalinization is not achieved with bicarbonate solutions
Dose 5 mg/kg/d IV Alkalinizing agents Diuretics Reserved for well-hydrated patients with insufficient diuresis
Not proven to be beneficial as front-line therapy in TLS CONTROL OF ELECTROLYTE DISTURBANCES Dextrose (D-glucose) Plus Insulin IV Infusion Promotes redistribution of K from extracellular to intracellular space.
Stimulates cellular uptake of K within 20-30 min.
Glucose should be administered along with insulin to prevent hypoglycemia.
Monitor blood sugar levels frequently. Used as cardioprotection for potassium levels >6.5 mmol/L or for patients with ECG alterations. Moderates nerve and muscle performance, and facilitates normal cardiac function. Calcium Gluconate (Kalcinate) IV Managed with oral phosphate binders and the same solution of glucose plus insulin used for control of hyperkalemia.
It may lead to hypocalcemia, which usually resolves as phosphate levels are corrected. Hyperphosphatemia: Considered if the previously mentioned methods failed
Prevents irreversible renal failure and other life-threatening complications.
Indicated in persistent hyperkalemia or hyperphosphatemia despite treatment, volume overload, uremia, symptomatic hypocalcemia, and hyperuricemia.
Hemodialysis is preferred over peritoneal dialysis because of better phosphate and uric acid clearance rates. Dialysis Uremia and oliguric RF due to tubule precipitation of uric acid, calcium phosphate.
Cardiac Arrhythmia.
Life Threatening Pulmonary Edema. Complications For cancer survivors staying well includes maintaining a healthy lifestyle and following healthcare standards. In addition, it is important to keep in mind that special health needs may apply depending on the type of cancer they have had and the types of treatments they have received. Tumor Lysis Syndrome
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