Tumor Lysis Syndrome

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May 30, 2017 by dailybolusoflr

By: Shaughn Keating


Causes

Most often caused by chemotherapy leading to massive cell turnover; often seen with rapidly proliferative hematologic malignancies such as: AML with WBC >50,000, ALL with WBC >100,000, high grade lymphomas (e.g Burkitt, T cell NHL), ALL

Less common in solid tumors – more likely in those with high tumor burden and high chemo-sensitivity (germ cell tumors, bulky SCLC, large HCC)

Can be seen spontaneously – most often in new diagnoses of hematologic malignancies, almost never with solid tumors


Pathogenesis and Pathophysiology

Lysis of of tumor cells leads to massive release of potassium and phosphate

Hyperkalemia is the most acutely dangerous outcome and can lead to death from cardiac dysrhythmias

Hyperphosphatemia can lead to secondary hypocalcemia, potentiating dysrhythmias, myocardial depression, hypotension, bronchospasm, and seizures

Intratubular crystallization which leads obstruction and AKI


Diagnosis

Send: UA, uric acid, phosphorous, magnesium and ionized calcium in addition to standard labs.

Also check EKG for arrhythmias and conduction delays

LDH >2 x upper limit of normal also may suggest a large tumor burden

Given risks of hyperleukocytosis, leukostasis, hyperviscosity syndrome, and DIC as alternative or concomitant diagnoses, also consider sending coagulation studies, type and screen, and plasma viscosity


Laboratory diagnosis: Two of the following 3 days before or 7 days after start of chemo:

  1. Uric acid >8.0 mg/dl
  2. Phosphorus >4.5 mg/dl (or >6.5 mg/dl in children)
  3. Potassium >6.0 mg/dl
  4. Corrected Ca <7.0 or iCal <1.12

Clinical diagnosis: Laboratory features plus one of the following:

  1. AKI (Cr increase by 0.3 mg/dl or Cr 1.5 x the upper limit of normal)
  2. Oliguria (UOP <0.5ml/kg/hr)
  3. Cardiac dysrhythmia (or sudden death from likely dysrhythmia)
  4. Seizures or other signs of symptomatic hypocalcemia (tetany, hypotension, etc)

Treatment

Hydration: D5 1/4 NS for euvolemic patient with a goal urine output of 100 cc/hr

Rasburicase: for all patients with clinical or laboratory TLS; works by converting uric acid into soluble allantoin. In contrast, allopurinol only prevents formation of uric acid. Dose – 0.15-0.2 mg/kg in 50 mL normal saline IV over 30 minutes daily for 5 days

Urine alkalization: Consider if rasburicase is unavailable. Goal urine pH 7-7.5. Avoid higher pH, which can precipitate xanthine or hypoxanthine

Pearls for treatment: Do not treat asymptomatic hypocalcemia; this may precipitate calcium phosphate and induce kidney injury.


References:

Howard SC, Jones DP, Pui CH. “The tumor lysis syndrome.” New England Journal of Medicine. 2011 May 12;364(19):1844-54

 

Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011.

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