Red Blood Cell Transfusion in Sepsis: A Review

Sepsis is very common and lethal. Sepsis is the leading cause of death in non-coronary Intensive Care Units, and the tenth leading cause of death overall. Red blood cell transfusion is one of the most commonly used interventions in the ICU to treat severe anemia, which often occurs in sepsis. Several problems were documented with RBC transfusions and will be reviewed, such as infection, pulmonary complications such as TRALI and Transfusion-Associated Circulatory Overload (TACO), Transfusion-Related Immunomodulation (TRIM) and multiorgan failure, and increased mortality. Most of these complications are partially explained by volume of the unit of blood as well as pathogenic factors of stored RBCs related to 2,3 BPG concentration, inflammatory mediators, nitric oxide, ATP concentration and RBC rheology, and RBC adhesion characteristics. These same factors are present in RBCs of septic patients as well. Until better evidence is available, a “restrictive” strategy of RBC transfusion (transfuse when Hb < 7 g/dL) is recommended except in acute hemorrhage, or in patients with acute myocardial ischemia when a hemoglobin trigger of 8 g/dl is reasonable. Complications of RBC transfusion (Table 1) ISSN: 2155-9864 JBDT, an open access journal Sepsis: Pathophysiology & Management J Blood Disord Transfus Transfusion-related acute lung injury (TRALI): TRALI is defined as Acute Lung Injury (ALI) that occurs within 6 h of transfusion (may happen up to 72 hours) and is not related to other risk factors for ALI or Acute Respiratory Distress Syndrome (ARDS) [17,18]. ALI and ARDS were defined by the North American-European Consensus Conference in 1994 as acute hypoxemia (PaO2/FIO2 ≤ 300 mm Hg for ALI or < 200 for ARDS), bilateral pulmonary infiltrates on chest radiograph, and no evidence of left atrial hypertension [19]. TRALI is the most common cause of major morbidity and mortality after transfusion [18,20]. The risk of TRALI is estimated at 1 case per 5,000 units PRBCs. The estimated mortality rate for TRALI is 5-8% [21]. The leading hypothesis of pathogenesis is a “two hit” hypothesis, with the first which point DO2 is highest at the lowest energy cost to the individual. This occurs around a hematocrit of 30% [14]. Decreases in hematocrit from this “optimal” level must be compensated by active increases in cardiac output to maintain DO2. For instance, Cardiac output peaks at 180% of control at a hematocrit of around 20%. Below this “optimal” level, the maintenance of tissue oxygen consumption (VO2) and aerobic metabolism at decreasing levels of DO2 is principally provided by increased oxygen extraction. In the critical care environment, there have been several studies examining the interrelationship between hematocrit, DO2 and VO2. Shoemaker et al. [15] and Boyd et al. [16] initially defined the optimal hematocrit at around 30% since, below this level, oxygen delivery and consumption were decreased in critically ill patients and mortality was increased. Above this level, there was no change in these variables or outcome. This line of reasoning led to the common practice of maintaining this “10/30 rule” as the transfusion triggers. Journal of Blood Disorders & Transfusion J o u r n al o f B loo d DisordersTransf u s i o n ISSN: 2155-9864