- Hyperleukocytosis: WBC count > 100,000/μL (typically in AML)
- Leukostasis: intravascular accumulation of WBCs/blasts in vascular lumen (+/- fibrin) resulting in end-organ damage
Posted 11/16/16 10:53:02 AM by Matthew Cummings
Leukostasis: Clinical Overview
- End-organ damage results from vascular occlusion
- Eyes and lungs most common sites for vascular obstruction
- Extremities, kidneys, heart, can also be affected.
- Diagnosis? AML patient p/w dyspnea or AMS w/ WBC is > 100,000/μL in the absence of a clear etiology
- Common ddx: PNA/neutropenic sepsis, TRALI/TACO (if recent products)
- Emergent management: Cytoreduction w/ leukopheresis +/- hydroxyurea (may also consider steroids for TRALI, broad-spectrum abx)
- Indication for leukopheresis: clinical leukostasis OR asymptomatic w/ markedly elevated WBC to prevent sx
- Leukopheresis: Typically two sessions (12-24 hours apart, each session 4-5 hours long)
- Complications: hypotension (volume shifts), allergy to citrate (anti-coagulation in circuit), catheter-placement related
Posted 11/16/16 11:02:20 AM by Matthew Cummings
Pancytopenia w/ suspected leukemia? More likely to be AML > ALL
Posted 11/16/16 11:03:52 AM by Matthew Cummings
Tumor Lysis Syndrome Diagnosis
- Primary: onset prior to initiation of rx due to high turnover of malignant cells
- Secondary: shortly after the beginning of treatment (more common)
- Diagnosis: 2+ abnormal values of uric acid (high), potassium (high), phosphorus (high), or calcium (low) at presentation OR 25% change in values from the pre-treatment values.
- Increased risk w/ high tumor burden, potential for rapid cell lysis (steroids), and underlying renal dysfunction
Posted 11/16/16 11:19:10 AM by Matthew Cummings
Tumor Lysis Management = Aggressive hydration, electrolyte correction, and reduction of uric acid levels
- IVF to maintain UOP typically 80 to 100 ml per hour (can add loop diuretics if low UOP, urinary alkalinization not needed)
- HyperK/hyperPO4 = typical mgmt (latter add sevelamer)
- AVOID administering calcium UNLESS symptomatic hypocalcemia (risk increasing Ca-PO4 product = CaPO4 renal crystallization)
- Reduce uric acid
- Allopurinol: xanthine oxidase inhibitor = prevents the formation of uric acid (takes 1-3d to lower) --> does not decrease the level of uric acid already present
- Rasburicase ("Recombinant urate oxidase") = reduces the level of uric acid by promoting the catabolism of uric acid to allantoin
- Typically used in established TLS (not as prevention) w/ presence of AKI, UA>9, or if not responding to allopurinol.
- G6PD deficiency is contraindication to rasburicase: H2O2 (rasburicase byproduct), cannot be broken down --> hemolysis/methemoglobinemia
Posted 11/16/16 11:19:44 AM by Matthew Cummings
For further reading...
Posted 11/16/16 11:21:29 AM by Matthew Cummings
Created by Christopher Kelly
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