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The aphorism “Blood Is Life” is likely truer nowhere than within the connes of the operating room. While blood transfusion nally became a life-saving reality in the twentieth century, thereby vastly expanding the range of survivable operations and injuries, it still remains an imperfect science, with both overt and non-overt risks and consequences. Potential safety issues regarding blood transfusion in the operat­ing room range from risks posed by blood products directly and physiological alter­ations resulting from transfusion to the uncertainties that surround transfusion strategies and blood product selection. In this chapter, we will describe the most common safety concerns and measures of mitigation that pertain to blood transfu­sion in the surgical patient. However, it must be noted that this is a very broad topic, and one to which a signicant portion of the eld of transfusion medicine is dedi­cated. Thus, what we present here should be considered an introduction, rather than a comprehensive discussion.

Following a general review of blood transfusion safety practices and risks common to all transfusions, the remainder of the rst portion of this chapter will focus on safety considerations that apply to special scenarios, in particular emergency blood transfusions and massive transfusion events. The second por­tion of the chapter will address safety considerations regarding blood product selection and transfusion strategies, with a particular emphasis on the manage­ment of major hemorrhage. Finally, we will conclude with a brief discussion on transfusion reduction strategies, now widely referred to as patient blood management.

The majority of the fatalities from non-ABO incompatibility events are due to extravascular hemolysis, resulting in the delayed destruction of the incompatible transfused RBCs (typically 3–10days post-transfusion). Less commonly, non-ABO transfusion reactions (typically due to Kell and Kidd antigens) can result in acute hemolytic transfusion reactions that mimic ABO-incompatible transfusion reac­tions, presenting with vasodilatory shock, disseminated intravascular coagulation, and renal failure [7, 9].

The precise nature and mechanisms of TRIM have yet to be fully elucidated or understood though it is thought to be at the root of increased rates of perioperative infections, nosocomial pneumonia, sepsis, and cancer recurrence [13–16]. A com­prehensive systematic review of 20 studies reported an odds ratio of 3.45 for post­operative bacterial infection in transfused trauma patients compared to the non-transfused [17]. Additionally, the number of blood products transfused is also associated with increased infection rates, with a clear dose-dependent correlation between number of RBC units transfused and the risk of development of infection [18, 19]. Unfortunately, various initiatives to mitigate the potential for TRIM, chief among them leukocyte reduction, have generally not been successful [20, 21].

Nevertheless, TRALI incidence in the USA has markedly decreased as the result of mitigation strategies aimed to reduce or eliminate plasma-containing components (plasma, platelets, whole blood) from female donors containing anti-leukocyte anti­bodies that are responsible for the majority of TRALI fatalities. Although not man­dated by the FDA, since 2007, individual blood product manufacturers have been gradually shifting to the use of all-male donor plasma, though exceptions still exist for AB plasma, given its relative scarcity. The Association for the Advancement of Blood & Biotherapies (AABB), formerly known as the American Association of Blood Banks, now requires that all plasma-containing components and whole blood for transfusion must be collected from men, nulliparous women, or women who have tested negative for human leukocyte antigen antibodies [22].

“Computer crossmatch,” also known as “electronic crossmatch,” is a relatively new, more efcient alternative to the serological crossmatch detailed above. This pro­cess allows for a rapid and efcient donor–recipient crossmatching process without the need for contact between donor RBCs and recipient sera. As sensitivity of com­mercially available antibody screens have improved with time, the necessity for tradi­tional serologic crossmatching has declined. The electronic crossmatch has the following steps: rst, the ABO/Rh typing from both donor and recipient are veried twice (two concordant blood samples). Next, recipient serum is screened for the absence of antibodies. Finally, the blood bank computer system compares and veries ABO and Rh D types of the donor and recipient for compatibility. This process is as safe as serological crossmatch and is FDA approved as an alternative to the traditional “type and cross,” provided that the recipient has had their ABO/Rh status tested at least twice and is not known to possess clinically signicant RBC alloantibodies. The major advantage of electronic crossmatch is the rapid availability of RBCs for emer­gency transfusion (under 1 min) vs. conventional serologic testing (45 min). It is important to note that if the recipient has a positive antibody screen or has a history of alloantibodies, then the traditional serologic crossmatch must be performed.

A 2003 study reported a 2% prevalence of clinically signicant RBC alloanti­bodies in a population of patients at risk for requiring urgent, uncrossmatched trans­fusions [23]. The same study estimated a rate of RBC alloimmunization of up to 4% among patients admitted to the emergency department. While the transfusion of uncrossmatched blood has been well documented in the military setting for decades [24], these results cannot be reliably applied to a non-combat population. More recently, studies from the civilian trauma literature have reported no acute hemo­lytic transfusion reactions (AHTRs), leading to the claim that uncrossmatched transfusions are safe in this setting. A longitudinal single-center study of over 1,000 emergency department RBC transfusions discovered clinically signicant alloanti­bodies in 6% of transfused individuals, resulting in 3% of cases receiving antigen incompatible RBC units, and one case of non-ABO alloantibody-mediated HTR (0.1% of emergency release transfused units) [25]. Several studies have corrobo­rated this nding, demonstrating a 0.02–0.5% rate of detectable hemolysis (acute and delayed) following uncrossmatched RBC transfusions [26, 27].

Overall, the transfusion of uncrossmatched RBC units is a relatively safe inter­vention with a very low risk of signicant adverse reactions although close monitor­ing of recipients with (subsequently identied) clinically signicant antibodies for evidence of hemolysis is recommended.

As a result of this unsustainable demand for AB plasma, some academic hospi­tals have trialed the use of group A plasma as an alternative. In the initial studies, no signicant hemolysis was reported amongst B or AB patients who received “incom­patible” group A plasma. This lack of harm has been further conrmed with wider clinical adoption [28]. There are several potential reasons for the observed lack of harm arising from group A plasma transfusions to the ~15% of the population who are non-A.First, as part of TRALI mitigation strategies, almost all group A plasma units now come from male donors, and group A male plasma typically have low titers of anti-B antibodies. Second, many centers are pre-screening the anti-B titers in A plasma units and selecting only those with low titers of anti-B for emergency use. Third, transfused anti-B antibodies are diluted into much larger recipient total blood volumes, likely reaching clinically irrelevant levels. Fourth, in the setting of

emergent transfusion support, the recipients would be receiving group O RBC units, and consequently, the proportion of B or AB RBC units available for the anti-B to bind to will be progressively reduced. Finally, 80% of B or AB patients are “secre­tors,” with soluble group B antigen in their plasma. As anti-B antibodies preferen­tially bind to free plasma B antigens over RBC membrane-bound ones, in these cases much of the anti-B antibodies will be “neutralized” before they can cause any clinically relevant effects. Consequently, it is a reasonable a priori assumption that group A plasma use is safe for emergency transfusion. This assumption has been borne out in ever more frequent clinical practice [28, 29].

Coagulopathy is also a common occurrence among individuals receiving massive transfusion for numerous reasons, the constitution of the transfused blood products themselves contributing signicantly. Simply, the standard process for producing blood components results in products that are diluted with crystalloid- based preser­vative solutions—a combination of 1 unit of RBC, 1 unit of plasma, and 1 unit of platelets results in a markedly diluted mixture (hematocrit of ~29%, platelet count 85,000/mcL, coagulation factor activity ~62% of normal) as compared to whole blood [30]. Nearly one-third of the volume of a unit of RBC is comprised of preser­vative solutions, and crystalloids may be infused as “carrier” uids as well. Therefore, the clinician must maintain vigilance, as a dilutional coagulopathy is still possible even when transfusing equal amounts of RBC, plasma, and platelets [30, 32].