We compared two methods of calcium gluconate infusion to maintain plasma ionized calcium ([Ca ]) during therapeutic plasma exchange (TPE) performed using the Spectra Optia Apheresis System. Method A, our legacy method, consisted of adding 5 mL of 10% calcium gluconate to each 500 mL bottle of 5% albumin replacement fluid. Method B used an accessory IV infusion of calcium gluconate (2 g in 50 mL of 0.9% NaCl starting at 25 mL/h). Plasma [Ca ] was measured at 20-minute intervals, and symptoms of hypocalcemia were recorded during TPE. Baseline [Ca ] was the same (P = 0.616), as was total acid citrate dextrose Formula A used (P = 0.865), with either method. TPE with method A used 2.62 ± 0.52 g of calcium gluconate vs 1.13 ± 0.27 g with method B (P < 0.001). [Ca2+] remained stable with method A (P = 0.251), but fell on average by 5% with method B (P < 0.05). Hypocalcemic symptoms were reported in 0 of 23 TPE with method A and 2 of 24 TPE with method B. We conclude that both methods A and B prevent a symptomatic fall in plasma [Ca ] during TPE. Method B requires significantly less calcium gluconate than does method A.
Hypocalcemic toxicity, because of return of citrate anion to the donor, is the major toxicity of apheresis platelet donation. Oral calcium carbonate, given prophylactically at the start of donation, has shown limited ability to alleviate this toxicity. We examined whether repeated prophylactic doses of calcium carbonate, or of a liquid preparation containing calcium citrate, calcium phosphate, and vitamin D 3 , would be more effective at preventing symptoms of hypocalcemic toxicity. Symptoms were reported by 48% of donors who received no prophylaxis and 60% of donors who received 1000 mg of oral calcium carbonate at the start of, and every 20 minutes during, donation (P 5 0.711). Only 19.2% of donors who received the liquid preparation (1000 mg calcium, 1000 IU vitamin D 3 ) reported symptoms (P 5 0.040 versus no prophylaxis, P 5 0.039 versus calcium carbonate). This difference was not because of gender, weight, age, or blood volume of the donor. Neither calcium preparation prevented a measurable fall in plasma ionized calcium during donation. We conclude that liquid calcium citrate/calcium phosphate/vitamin D 3 provides effective prophylaxis against hypocalcemic toxicity during platelet donation, however it does not prevent a fall in plasma ionized calcium. K E Y W O R D Sblood donor, paresthesia, plateletpheresis, side effects | I NT ROD UCTI ONHypocalcemic toxicity is a common adverse effect of apheresis platelet donation. [1][2][3] It is caused by the return to the donor of plasma carrying a citrate-based anticoagulant, and may limit the blood flow rate and component yield during collection procedures. 3,4 Prophylactic administration of 1-2 g of oral calcium carbonate has been shown to have a distinct but modest effect on plasma ionized calcium ([Ca 21 ]) during platelet donation with only very modest effects on overall symptom development in the donors. 5,6 Gastrointestinal absorption and bioavailability of calcium carbonate is relatively limited compared to some other calcium salts such as calcium citrate, 7-9 and little is known about the effects of repetitive prophylactic dosing of calcium during platelet donation. We therefore undertook to examine alternative approaches to oral prophylaxis for hypocalcemic toxicity in apheresis platelet donation.
We sought to optimize direct intravenous infusion of calcium gluconate (CaGlu) for maintaining plasma ionized calcium concentration ([Ca2+]) and preventing hypocalcemic reactions during 34 consecutive 1‐volume therapeutic plasma exchanges (TPEs) in eight patients. CaGlu, 2 g in 50 mL of 0.9% NaCl, was prepared by our hospital pharmacy and infused at either 1.0 or 1.6 g/h during alternate TPE. Plasma [Ca2+] was monitored at intervals of 20 to 30 minutes. At 1 g/h of CaGlu, plasma [Ca2+] fell by 8.35% after 40 to 50 minutes and then plateaued. At 1.6 g/h of CaGlu, plasma [Ca2+] fell by 6% after 20 to 30 minutes and then plateaued. The difference at 40 to 50 minutes was significant (P = .015). Hypocalcemic reactions were noted in three patients during 5 of 17 TPE at 1.0 g/h (all after 40 to 60 minutes) but 0 of 17 TPE at 1.6 g/h (P = .044). CaGlu at 1.6 g/h stabilized plasma [Ca2+] and appears to prevent hypocalcemic reactions during TPE.
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