Abstract
BackgroundCerebral regional microcirculation is altered following severe head injury. In addition to tissue disruption, partial pressure of tissue oxygenation is impaired due to an increase in the oxygen tissue gradient. The heterogenic distribution of cerebral microcirculation is multifactorial, and acute anemia challenges further the delivery of oxygen to tissues. Currently, a restrictive transfusion threshold is globally applied; however, it is unclear how anemia modifies regional cerebral microcirculation; hence, it is unclear if by aiming to a global endpoint, specific anatomical regions undergo ischemia. This study aims to quantify the temporal changes in cerebral microcirculation after severe head injury, under the effect of anemia and transfusion. It also aims to assess its effects specifically at the ischemic penumbra compared to contralateral regions and its interactions with axonal integrity in real time. Twelve ovine models were subjected to a severe contusion and acceleration-deceleration injury. Normovolemic anemia to a restrictive threshold was maintained after injury, followed by autologous transfusion. Direct quantification of cerebral microcirculation used cytometric count of color-coded microspheres. Axonal injury was assessed using amyloid precursor protein staining.ResultsA mixed-effect regression model from pre-transfusion to post-transfusion times with a random intercept for each sheep was used. Cerebral microcirculation amongst subjects with normal intracranial pressure was maintained from baseline and increased further after transfusion. Subjects with high intracranial pressure had a consistent reduction of their microcirculation to ischemic thresholds (20–30 ml/100 g/min) without an improvement after transfusion. Cerebral PtiO2 was reduced when exposed to anemia but increased in a 9.6-fold with transfusion 95% CI 5.6 to 13.6 (p value < 0.001).ConclusionsAfter severe head injury, the exposure to normovolemic anemia to a restrictive transfusion threshold, leads to a consistent reduction on cerebral microcirculation below ischemic thresholds, independent of cerebral perfusion pressure. Amongst subjects with raised intracranial pressure, microcirculation does not improve after transfusion. Cerebral oxymetry is impaired during anemia with a statistically significant increase after transfusion. Current transfusion practices in neurocritical care are based on a rigid hemoglobin threshold, a view that excludes cerebral metabolic demands and specific needs. An RCT exploring these concepts is warranted.
Highlights
Cerebral regional microcirculation is altered following severe head injury
An additional contributor to cerebral ischemia is partial pressure of tissue oxygenation (PtiO2) with a series of studies focussing on the relevance of cerebral oximetry [4,5,6,7]
While current evidence-based practice attempts to minimise the use of allogenic blood transfusions, amongst critically ill patients [8, 9] by establishing a restrictive transfusion threshold [10,11,12,13]; controversy still remains regarding the safety of these measures, when facing sustained low Partial pressure of tissue oxygenation (PtiO2) levels, during the acute phase of head injury [4, 7, 14,15,16,17,18,19]
Summary
Cerebral regional microcirculation is altered following severe head injury. In addition to tissue disruption, partial pressure of tissue oxygenation is impaired due to an increase in the oxygen tissue gradient. This study aims to quantify the temporal changes in cerebral microcirculation after severe head injury, under the effect of anemia and transfusion. Secondary patho-physiologic processes may result in areas of ischemia and cerebral infarct These changes are commonly found in regions where cerebral microcirculation (RMBF) has been critically reduced [2, 3]. An additional contributor to cerebral ischemia is partial pressure of tissue oxygenation (PtiO2) with a series of studies focussing on the relevance of cerebral oximetry [4,5,6,7]. The absence of clinical equipoise as well as the lack of methodological feasibility in designing a study that focuses on cerebral RMBF during anemia and severe head injury, leads to the need of experimental models, to further challenge this question. In the absence of clinically available measures of cerebral microcirculation, physiological markers of cerebral ischemia and hypoperfusion rather than global metrics such as mortality outcomes may be more appropriate endpoints [21]
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