| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Letters to the Editor |
1 Department of Internal Medicine
2 Department of Nephrology
3 Clinical Laboratory
4 Department of Pathology, University of Arkansas for, Medical Sciences, Little Rock, Arkansas 72205
aAddress correspondence to this author at: University of Arkansas for Medical Sciences, College of Medicine, Department of Pathology, 4301 W Markham St, Little Rock, AR 72205, Fax 501-526-4621, e-mail jabornhorst{at}UAMS.edu
To the Editor:
Hyperkalemia is a potentially fatal electrolyte abnormality that must be differentiated from pseudohyperkalemia, which can occur when potassium is released from ruptured platelets or blood cells during the clotting process in serum specimens (1)(2). We describe a case of "reverse" pseudohyperkalemia in a patient with chronic lymphocytic leukemia (CLL) in whom potassium concentrations in plasma specimens exceeded concentrations observed in serum by more than 1.3 mmol/L (3).
A 49-year-old woman with stage IV CLL was admitted for chemotherapy. Her white cell count (WBC) was 364 x 109 cells/L (96% lymphocytes) and 100 x 109 platelets/L. The patient was treated with rituximab, cyclophosphamide, and fludarabine and received bicarbonate and allopurinol. After therapy, the potassium concentration obtained from a lithium-heparin specimen with separator gel was 10.7 mmol/L on a Beckman LX-20 chemistry analyzer (Beckman Coulter). A second lithium-heparin plasma specimen yielded a potassium concentration of 11.2 mmol/L. Results were similar on a different analyzer. Specimens were transported by pneumatic tube, and the time from phlebotomy to analysis was approximately 60 min. No hemolysis was observed. All specimens were obtained using 5-mL Griener Vacuette tubes (GrienerBio-One) unless otherwise noted.
The patient exhibited no acidosis, renal failure, or tumor lysis syndrome; phosphate, calcium, and uric acid were not increased. Calcium chloride, albuterol, dextrose-insulin, furosemide, and sodium polystyrene sulfonate were administered to decrease the patient’s potassium concentrations. Emergent dialysis was considered as a treatment option. The patient denied symptoms attributable to hyperkalemia (fatigue, muscle weakness, or palpitations), and an electrocardiogram revealed no abnormalities associated with hyperkalemia.
The possibility of pseudohyperkalemia was investigated. Additional venous blood specimens were simultaneously obtained 2 h after potassium-lowering treatment (Table 1
). These specimens were lithium-heparin tubes lacking (specimen A) or containing (specimen B) a separator gel; a heparinized blood gas syringe (Portex® Line Draw Plus blood sampling kit; Smiths Medical) (specimen C) for immediate potassium measurement in whole blood (Rapid Laboratory 1200 series, Siemens); and a red-top tube without anticoagulant (specimen D). All specimens were immediately transported to the laboratory via pneumatic tube (<5 min transport time), promptly centrifuged (7 min at 1915g, samples A, B, and D), and analyzed within 5 min of centrifugation.
|
Both the whole blood (C) and serum (D) specimens indicated severe hypokalemia, and the plasma specimens (A and B) exhibited significantly higher potassium concentrations (Table 1
). Examination of specimens A and B revealed a distinct buffy coat layer of packed WBCs on top of the erythrocyte layer. In specimen B, the buffy layer appeared to span the separator gel. No buffy layer was apparent in specimen D. To eliminate the possibility of potassium from lysis of residual platelets and WBCs present in the serum or plasma supernatant, cellular counts were performed using a Sysmex SE-2100 blood analyzer. Few remaining leukocytes or platelets were observed in the supernatant of specimens A, B, and D after centrifugation (0.02–0.07 x109 WBC/L and <0.01–16 x 109 platelets/L).
We hypothesized that potassium might be diffusing out of the packed buffy coat layer into the plasma supernatant. Because the serum and whole blood potassium values correlated with the clinical assessment of the patient, no dialysis was performed, and potassium supplements were administered. Specimens submitted 3 days later (WBC of 264 x 109 cells/L) also exhibited a similar reverse pseudohyperkalemic pattern.
Because of the potential of pseudohyperkalemia in serum, plasma has been recommended as the preferred sample type for determinations of potassium in patients with leukocytosis, thrombosis, or erythrocytosis (1)(4). In this patient, the observed plasma potassium concentrations appeared to be falsely increased, and the use of serum or whole blood specimens provided results that were consistent with clinical findings. Previously observed relative increases of potassium in plasma specimens have been attributed to preanalytical factors including centrifugation delays or heparin-mediated cell membrane damage (3)(5).
Susceptibility to heparin-mediated cell membrane damage during processing and centrifugation may have contributed to diffusion of potassium into the supernatant from ruptured leukocytes. The presence of gel separator material may have reduced the leeching of potassium from the buffy layer (specimen B). Heparinized whole blood (specimen C) was used in blood gas analysis, but testing was performed immediately after the blood was drawn.
We conclude that the potential for reverse pseudohyperkalemia exists in plasma specimens in the setting of leukocytosis. Further investigation of the frequency of this effect in different specimen containers may be warranted. Clinicians should be aware of this phenomenon to avoid inappropriate therapeutic measures.
Acknowledgments
Grant/funding Support: None declared.
Financial Disclosures: None declared.
Acknowledgment: The authors thank Wren Clingan for monitoring the phlebotomy procedures.
References
Read all eLetters
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
