This program is available until December 31, 2019.
Director: Jason Acker Moderator: Philip Spinella, MD Speakers: Jason Acker; Jennifer Muszynski, MD; Neil Blumberg, MD Intended Audience: Medical Director, Nurse, Physician, Research Scientist, Residents/Fellow, Student (MD, MT, SBB), Supervisor, Technologist, Transfusion Safety Officer
Evaluate the evidence for and against the presence of transfusion-related immune modulation.
Explain the potential biological mechanisms for TRIM.
Discover how modification of blood component manufacturing or secondary processing may reduce the risk of TRIM.
Discuss how to better define TRIM.
Description: There is an emerging interest in the risks posed by the ability for blood transfusion to modulate the recipient immune system. Transfusion Related Immune Modulation (TRIM) is implicated in multiple adverse clinical outcomes such as increased infection, acceleration of cancer growth, multiple organ dysfunction and short-term mortality after transfusion. Purported mechanisms for TRIM include the release of immunosuppressive prostaglandins, activation of T lymphocytes by exosomes, inhibition of cytokine production (IL-2), suppression of monocytes and cytotoxic T-cells and increase in T-cell suppressor activity. These varied mechanisms span the spectrum from potently immunosuppressive to highly pro-inflammatory effects, which hampers the ability to precisely define what TRIM is. Similarly, in-depth reviews of epidemiologic and clinical studies present conflicting evidence for the existence of clinically relevant TRIM in the era near-universal leukocyte reduction.
What is the definition of TRIM? The answer is likely complex, as there are undoubtedly both pro-inflammatory and immune-suppressive mediators present within transfused blood products, and the balance of how (or whether) these factors influence an individual patient will depend on the underlying physiology, age and comorbidities of the patient, the timing of transfusion, and the individual blood product(s) used. Understanding these interactions is important because transfusion of leukoreduced red cell concentrates represents a potentially modifiable factor among the many mediators of immunologic dysregulation encountered by hospitalized and critically ill patients.
This session will provide a summary of the evidence for and against the presence of TRIM in different transfusion recipient populations and a review of the candidate biological mechanisms for TRIM. The impact of blood product manufacturing and component modifications, such as leukoreduction, cell washing, cryopreservation, irradiation, and pathogen reduction on the risk of TRIM will be presented.
Department of Laboratory Medicine and Pathology, University of Alberta
Transfusion Medicine, University of Rochester Medical Center
The Research Institute at Nationwide Children's Hospital; Nationwide Children's Hospital
Washington University in St. Louis, Pediatrics Critical Care Dept.
- General Continuing Education (GEN)
- Florida Lab Personnel (FLP)
- California Nurse (CN)
- California Lab Personnel (CLP)
- Physician (PHY)
You must be logged in and own this session in order to