Performance characteristics of the PowerFlow apheresis port: Early experience.

We prospectively evaluated the Bard PowerFlow Implantable Apheresis IV Port in four patients undergoing outpatient therapeutic plasma exchange over 18 to 97 days. Three had bilateral internal jugular access ports, and one had a single left internal jugular access port for the inlet line with return via antecubital vein. Two patients receiving 5% albumin as replacement fluid achieved peak inlet flow of 99 ± 5 mL/min and 101 ± 6 mL/min, and peak plasma flow of 53 ± 6 and 47 ± 6 mL/min, respectively. Two patients receiving plasma as replacement fluid achieved peak inlet flow of 46 ± 7 and 85 ± 4 mL/min and peak plasma flow of 27 ± 3 and 35 ± 4 mL/min, respectively. Apheresis nurses accessed the ports on the first attempt in all procedures. Pressure alarms occurred in 6 of 47 procedures and were easily resolved by lowering the inlet rate by 10% in 5 of them. The PowerFlow shows promise as an implantable venous access device for apheresis.

Optimization of infusional calcium gluconate for prevention of hypocalcemic reactions during therapeutic plasma exchange.

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.

Automated red blood cell exchange in preparation for filgrastim mobilization of autologous peripheral blood hematopoietic progenitor cells in a patient with sickle cell anemia.

Increasing survival of patients with sickle cell anemia (SCA) well into adulthood results in a rising likelihood of developing hematological malignancy. High-dose chemotherapy with autologous hematopoietic progenitor cell (HPC) rescue is standard of care for several hematological malignancies, but the risk of severe or life-threatening vaso-occlusive phenomena during filgrastim mobilization of HPC for collection poses a potential barrier to this approach. We report the use of automated red cell exchange in preparation for filgrastim mobilization in a patient with homozygous SCA. Red cell exchange was repeated just prior to high-dose chemotherapy to mitigate the need for red cell transfusion during bone marrow reconstitution. The patient experienced no vaso-occlusive phenomena throughout the entire episode of care and did not become iron overloaded. This approach should be considered for all patients with homozygous or compound heterozygous sickle cell disease who are candidates for auto-HPC rescue therapy.

Dietary citrate and plasma ionized calcium: Implications for platelet donors.

BACKGROUND: Platelet donors receive 40 mmol or more of IV citrate anion during donation. When plasma ionized calcium ([Ca2+ ]) falls by ∼20%, half of the donors report symptoms of hypocalcemic toxicity. Citrus juices contain clinically relevant amounts of citrate anion. We asked whether citrus juice can lower [Ca2+ ] thus potentially contributing to hypocalcemic toxicity. METHOD: Six volunteers were given 20.4 mmol of citrate anion as grapefruit juice or orange juice. Capillary blood obtained by fingerstick was analyzed for [Ca2+ ] using an iSTAT point-of-care blood analyzer. [Ca2+ ] was measured at baseline and then 30, 60, 120, and 180 minutes after drinking juice. Subjects were tested with the alternative juice on a subsequent day. The outcome measure was the percent change in plasma [Ca2+ ] from baseline. RESULTS: [Ca2+ ] fell -2.2% to -11.5% in four of six subjects 30 minutes after drinking grapefruit juice. The effect persisted up to 3 hours. [Ca2+ ] fell -2.1% to -12.2% in four of six subjects 30-60 minutes after drinking orange juice. The effect abated after 2 hours. We could not correlate gender or body surface area to these findings. SUMMARY AND CONCLUSIONS: Citrus juice may lower [Ca2+ ] for 2-3 hours. This could add to the effect of IV citrate infusion during platelet donation, thus worsening the expected fall in [Ca2+ ]. This, in turn, would likely increase the rate and severity of hypocalcemic toxicity. It is prudent to advise platelet donors to avoid high citrate anion beverages, such as citrus juice, for at least 4 hours prior to donation.

Prophylactic infusion of calcium gluconate to prevent a symptomatic fall in plasma ionized calcium during therapeutic plasma exchange: A comparison of two methods.

We compared two methods of calcium gluconate infusion to maintain plasma ionized calcium ([Ca2+ ]) 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 [Ca2+ ] was measured at 20-minute intervals, and symptoms of hypocalcemia were recorded during TPE. Baseline [Ca2+ ] 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 [Ca2+ ] during TPE. Method B requires significantly less calcium gluconate than does method A.

A liquid calcium+vitamin D3 supplement is effective prophylaxis against hypocalcemic toxicity during apheresis platelet donation.

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 D3 , 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 = 0.711). Only 19.2% of donors who received the liquid preparation (1000 mg calcium, 1000 IU vitamin D3 ) reported symptoms (P = 0.040 versus no prophylaxis, P = 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 D3 provides effective prophylaxis against hypocalcemic toxicity during platelet donation, however it does not prevent a fall in plasma ionized calcium.