How do I manage a blood product shortage?

BACKGROUND: The demand for blood products sometimes exceeds the available inventory. Blood product inventories are dependent upon the availability of donors, supplies and reagents, and collection staff. During prolonged extreme shortages, blood centers and transfusion services must alter practices to meet the needs of patients. STUDY DESIGN AND METHODS: The Association for the Advancement of Blood and Biotherapies Donor and Blood Component Management Subsection compiled some strategies from its blood center and hospital transfusion service members that could be implemented during blood product shortages. RESULTS: Some strategies that blood centers could use to increase their available inventories include increasing donor recruitment efforts, using alternate types of collection kits, manufacturing low-yield apheresis-derived platelets and/or whole blood-derived platelets, using cold-stored platelets, transferring inventory internally among centers of the same enterprise, using frozen inventory, decreasing standing order quantities, prioritizing allocation to certain patient populations, filling partial orders, and educating customers and blood center staff. Transfusion service strategies that could be implemented to maximize the use of the limited available inventory include increasing patient blood management efforts, using split units, finding alternate blood suppliers, trading blood products with other hospital transfusion services, developing a patient priority list, assembling a hospital committee to decide on triaging priorities, using expired products in extreme situations, and accepting nonconforming products after performing safety checks. DISCUSSION: Blood centers and transfusion services must choose the appropriate strategies to implement based on their needs.

Clearance of maternal isohemagglutinins from infant circulation (CME).

BACKGROUND: Non-group O neonates require testing for passively acquired maternal isohemagglutinins for them to receive type-specific red blood cells (RBCs), according to the latest edition of the AABB Standards. A neonate is defined as an infant up to 4 months old in the AABB Standards, and many blood banks tend to stop testing for maternal anti-A and/or anti-B after 4 months of age. In lieu of such testing, group O RBCs are usually transfused to infants up to 4 months of age. This practice can limit the overall supply of group O RBCs available to other patients. STUDY DESIGN AND METHODS: A retrospective study of 1309 infants up to 4 months of age was performed, to assess the age by which passively acquired maternal isohemagglutinins are cleared from infant circulation. Detection of isohemagglutinins was performed by mixing sample sera and observing agglutination, followed by incubation and addition of anti-immunoglobulin anti-human globulin (antiglobulin test phase). RESULTS: The data show that 6.4% of infants up to 1 month of age had maternal isohemagglutinins, while none of the infants ranging from 2 to 4 months of age had maternal isohemagglutinins in their sera. CONCLUSIONS: Maternal isohemagglutinins are rare after the first month of life and patients who are at least 2 months old can safely receive ABO type-compatible RBC units without testing for passively acquired maternal anti-A and/or anti-B.

The effect of argatroban on activated protein C resistance.

Activated protein C (APC) resistance is commonly tested in hypercoagulation evaluations, and argatroban is an anticoagulant therapy used in hypercoagulable patients. The effect of argatroban on APC resistance testing is unknown. We studied 100 ex vivo specimens from 44 patients treated with argatroban. Argatroban increased the APC resistance ratio in all but 1 patient. The effect was seen even in the specimens containing subtherapeutic argatroban levels. For patients without APC resistance, the mean APC resistance ratio significantly increased from 2.43 without argatroban to 3.10 with argatroban. For patients with APC resistance due to factor V Leiden, argatroban significantly increased the mean ratio from 1.73 to 2.13, falsely raising it into the normal range (>2). Argatroban increases the APC resistance ratio, which can mask a diagnosis of APC resistance and, therefore, factor V Leiden. Clinicians should be advised that APC resistance testing for patients receiving argatroban is not valid.

Effect of tramadol use on three point-of-care and one instrument-based immunoassays for urine buprenorphine.

We report that use of the popular analgesic tramadol can cause false-positive urine buprenorphine results. We examined the extent of tramadol cross-reactivity in three point-of-care urine buprenorphine immunoassays (ACON, QuikStrip, and ABMC) and an instrument-based one (Cedia). We tested 29 urine samples from patients known to be taking tramadol. Ten different samples tested positive for urine buprenorphine by at least one immunoassay. Samples with positive buprenorphine screens by immunoassay were tested for total buprenorphine and total norbuprenorphine content by liquid chromatography-tandem mass spectrometry (LC-MS-MS), which confirmed that seven of the 10 positive samples were false-positives. The remaining three positive immunoassay samples had insufficient quantity for LC-MS-MS testing. No false-positives were detected with the ACON (10 ng/mL calibration cutoff) or the Cedia assay (using a 20 ng/mL calibration cutoff). All four false-positive Cedia results (using a 5 ng/mL cutoff) in this study tested negative using the ACON device. Our data suggest that tramadol use can cause false-positive urine buprenorphine immunoassays, and this effect appears to be assay-dependent. Tramadol interference with the Cedia assay is clinically relevant, especially if the 5 ng/mL calibration cutoff is used.