Abstract
Anemia is frequent among brain-injured patients, where it has been associated with an increased risk of poor outcome. The pathophysiology of anemia in this patient population remains multifactorial; moreover, whether anemia merely reflects a higher severity of the underlying disease or is a significant determinant of the neurological recovery of such patients remains unclear. Interestingly, the effects of red blood cell transfusions (RBCT) in moderately anemic patients remain controversial; although hemoglobin levels are increased, different studies observed only a modest and inconsistent improvement in cerebral oxygenation after RBCT and raised serious concerns about the risk of increased complications. Thus, considering this "blood transfusion anemia paradox", the optimal hemoglobin level to trigger RBCT in brain-injured patients has not been defined yet; also, there is insufficient evidence to provide strong recommendations regarding which hemoglobin level to target and which associated transfusion strategy (restrictive versus liberal) to select in this patient population. We summarize in this review article the more relevant studies evaluating the effects of anemia and RBCT in patients with an acute neurological condition; also, we propose some potential strategies to optimize transfusion management in such patients.
Highlights
Anemia is a frequent condition among critically ill patients [1] and appears early during their hospital course
In another study on 4892 intensive care unit (ICU) patients in which 44 % received at least one red blood cell transfusion (RBCT) after a median of 3 days, an Hb level below 9 g/dl was associated with poorer outcomes whereas the amount of RBCT transfused was associated with increased ICU length of stay and mortality [3]
In a large retrospective study on 1150 traumatic brain injury (TBI) patients in which 46 % of patients received RBCT when Hb levels were below 9 g/dl, Salim et al [26] found that RBCT was associated with an increased hospital mortality in a logistic regression model, while anemia was not
Summary
Anemia is a frequent condition among critically ill patients [1] and appears early during their hospital course. HIF promotes the secretion of erythropoietin (EPO), which negatively regulates neuronal apoptosis and seems to exert some neuroprotective effects through specific receptors expressed within cerebral tissue [18], and of vascular endothelial growth factor, which stimulates angiogenesis and allows long-term adaptations to tissue hypoxia [19] Overall, these adaptation mechanisms maintain DO2 during anemia in healthy conditions, at least until a critical Hb threshold below which tissue hypoxia and altered brain function may develop. Anemia-induced vasodilation may be limited by other ongoing compensatory mechanisms to maintain adequate brain perfusion induced by the acute brain injury itself, so that the “cerebrovascular reserve”, i.e., the capability of brain vasculature to vasodilate in response to different stimuli (including changes in mean arterial pressure, arterial carbon dioxide tension (PaCO2), or reduced DO2), is significantly limited when compared with healthy subjects [24] This could promote brain tissue hypoxia at hemoglobin levels higher than the hemoglobin thresholds observed in healthy volunteers [25]. As the “cerebrovascular reserve” is compromised in this setting, maximal vasodilation may occur at Hb levels around 8–9 g/dl and any further decrease in Hb below this threshold may contribute to reduced cerebral DO2
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