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Calcium and Other Electrolyte Management in Patients Undergoing Leukocytapheresis Collections: Review and
Lance A Williams1, Kristin Gray1, Elizabeth A Godbey2
1Department of Laboratory Medicine and Pathology, Mayo Clinic, Phoenix, Arizona, USA.
Collection of hematopoietic progenitor cells and mononuclear cells by leukocytapheresis is a critical step of procuring cellular starting materials for future therapeutic use. Leukocytapheresis requires use of anticoagulant to prevent blood clotting in the extracorporeal circuit during collection. A commonly used anticoagulant is Acid Citrate Dextrose Solution A (ACD-A). ACD-A primarily prevents blood clotting by reversibly chelating free ionized calcium, which is essential for the clotting cascade. Electrolytes frequently affected by ACD-A include calcium, magnesium, potassium, phosphate, and bicarbonate. Risks for development of electrolyte derangements include procedure-related parameters as well as patient comorbidities. Symptoms range from mild paresthesias to life-threatening cardiac arrhythmias. Recognition of related signs and symptoms is important for prompt intervention with procedure modification and electrolyte replacement to optimize patient safety. This paper will provide an enhanced understanding of the underlying pathophysiology and assist in timely identification and management of electrolyte abnormalities associated with cellular therapy collections.
Collection of hematopoietic progenitor cells and mononuclear cells by leukocytapheresis is a critical step of procuring cellular starting materials for future therapeutic use. Leukocytapheresis requires use of anticoagulant to prevent blood clotting in the extracorporeal circuit during collection. A commonly used anticoagulant is Acid Citrate Dextrose Solution A (ACD-A). ACD-A primarily prevents blood clotting by reversibly chelating free ionized calcium, which is essential for the clotting cascade. Electrolytes frequently affected by ACD-A include calcium, magnesium, potassium, phosphate, and bicarbonate. Risks for development of electrolyte derangements include procedure-related parameters as well as patient comorbidities. Symptoms range from mild paresthesias to life-threatening cardiac arrhythmias. Recognition of related signs and symptoms is important for prompt intervention with procedure modification and electrolyte replacement to optimize patient safety. This paper will provide an enhanced understanding of the underlying pathophysiology and assist in timely identification and management of electrolyte abnormalities associated with cellular therapy collections.
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