Anemia management after acute brain injury

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.

Keywords: Anemia; Red blood cell transfusion; Subarachnoid hemorrhage; Threshold; Traumatic brain injury.

Fig. 1

In the normal brain, a progressive reduction of hemoglobin (Hb) is compensated for by vasodilation, which results in increased cerebral blood flow (CBF, black line) and a constant cerebral oxygen delivery (DO ₂, grey line). When Hb falls below 5–6 g/dl, DO₂ is progressively reduced; no further vasodilation can occur and maximal CBF values (CBF _max) are obtained. The oxygen extraction rate (OER) then increases to meet metabolic tissue requirements

Fig. 2

In the injured brain, cerebral blood flow (CBF, black line) is lower than in the normal brain at the corresponding Hb levels. As the “cerebrovascular reserve” is compromised in this setting, the maximal CBF (CBF _max) will be possibly obtained at Hb levels around 8–9 g/dl and any further decrease of Hb below these thresholds will contribute to reduce cerebral oxygen delivery (DO ₂, grey line). The oxygen extraction rate (OER) then increases to meet metabolic tissue requirements above these thresholds

Fig. 3

The decision to administer red blood cell transfusions (RBCT) should take into consideration the potential benefits and harms of this intervention, according to different haemoglobin (Hb) levels at which RBCT is initiated. In brain-injured patients, the RBCT strategy should be “restrictive” (if Hb is less than 7.0 g/dl) in awake and conscious patients. For poor-grade comatose patients, systemic (superior vena cava oxygen saturation (ScvO ₂) or high lactate levels) or cerebral triggers (jugular vein oxygen saturation (SvjO ₂) or brain tissue oxygen pressure (PbtO ₂)) could be used to guide RBC administration