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Transfusion of bacterially contaminated blood products may result in no symptoms, bacterial infection, sepsis, or death in the recipient. Bacterial pathogens have emerged as most common cause of transfusion-transmitted infections. Incidence of septic transfusion reactions (STRs) varies with type of platelet product. STR is under recognized and underreported, and high level of suspicion should be maintained in certain patient populations. Significant improvement in bacterial safety of platelets has been achieved since 2004 through implementation of multiple technologies.
Clinical consequences of transfusing bacterially contaminated blood products are influenced by virulence, concentration (STR with ≥5 CFU/mL) and growth rate of bacteria, and immune status of recipient (most fatalities occur in neutropenic patients). Most organisms isolated from contaminated platelet and RBC units tend to be skin-associated contaminants, usually not associated with STR. Historically, gram-negative organisms and high levels of endotoxin, most often achieved with storage times longer than 21 days for RBCs or 3 days for platelets have been associated with more severe reactions and shorter delay between symptom onset and transfusion. In recipient, endotoxin stimulates macrophages and endothelial cells, leading to massive release of proinflammatory cytokines (interleukin [IL]-1β, IL-6, and IL-8), TNFα, and nitric oxide, and also activates complement and coagulation cascades, thereby causing inflammation, intravascular coagulation, hemorrhage, and death. Gram-positive bacteria such as Bacillus cereus , Staphylococcus aureus , and coagulase-negative staphylococci have also been implicated in severe or fatal reactions with S. aureus causing one-third of fatalities over the last 5 years.
Most patients develop fever of ≥39°C (102.2 F) or an increase of ≥2°C (3.9 F) from pretransfusion value, during or within 4 hours of transfusion. Fever might be accompanied by hypotension, rigors, tachycardia, dyspnea, nausea/vomiting, and in rare cases septic shock. Differential diagnosis includes noninfectious transfusion reactions such as febrile nonhemolytic, hemolytic, and transfusion-related acute lung injury.
In 2014, AABB published clinical criteria for investigation of suspected bacterial contamination. When used as part of active surveillance, these criteria demonstrated high diagnostic sensitivity. Active surveillance includes culturing platelets at time of issue and evaluating patients as soon as positive culture results are obtained and with any change in clinical condition during or within 24 hours of transfusion. High level of suspicion should be maintained in patients who are immunosuppressed, neutropenic, transfused during surgery, febrile, or receiving antipyretics.
If sepsis is suspected, transfusion should be stopped immediately and open port capped or tubing clamped. Two sets of blood cultures should be drawn from patient’s arm opposite from transfusion site even if the patient is on antibiotics. Remaining product bag should be returned to transfusion service after placing in plastic-sealed bag, to minimize leakage and contamination risk. Gram stain and optional FDA-approved rapid assay should be performed on remaining product immediately to help guide initial antibiotic therapy. Cultures on remaining product should be done both aerobically and anaerobically. If there is no blood remaining in bag, 10–20 mL of sterile broth should be aseptically injected into bag and mixed thoroughly before sampling. Alternatively, culture can be performed on residual sample from index component prepared at time of issue. Culturing segments yields high rate of false-negative results and should be avoided. Blood supplier should be immediately notified and cocomponents from same donation quarantined or recalled if contamination is likely.
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