Early ischaemia after severe head injury. Preliminary results in patients with diffuse brain injuries.
ABSTRACT Ischaemic brain lesions still have a high prevalence in fatally head injured patients and are the single most important cause of secondary brain damage. The present study was undertaken to explore the acute phase of severely head injured patients in order to detect early ischaemia using Robertson's approach of estimating cerebral blood flow (CBF) from calculated arterio-jugular differences of oxygen (AVDO2), lactates (AVDL), and the lactate-oxygen index (LOI). Twenty-eight cases with severe head injury were included (Glasgow Coma Scale Score below or equal to 8). All patients but one had a non-missile head injury. All the patients had a diffuse brain injury according to the admission CT scan. ICP measured at the time of admission was below 20 mmHg in 17 cases (61%). All patients were evaluated with the ischaemia score (IS) devised in our center to evaluate risk factors for developing ischaemia. Mean time from injury to the first AVDO2/AVDL study was 23.9 +/- 9.9 hours. According to Robertson's criteria, 13 patients (46%) had a calculated LOI (-AVDL/AVDO2) value above or equal to 0.08 and therefore an ischaemia/infarction pattern in the first 24 hours after the accident. Of the 15 patients without the ischaemia/infarction pattern, in three cases the CBF was below the metabolic demands and therefore in a situation of compensated hypoperfusion. No patient in our series had hyperaemia. Comparing different variables in ischaemic and non-ischaemic patients, only arterial haemoglobin and ischaemia score (IS) was significantly different in both groups. The ischaemia score had mean of 4.3 +/- 1.7 in the ischaemic group and 2.7 +/- 1.4 in non-ischaemic patients (p = 0.01). It is concluded that ischaemia is highly prevalent in the early period after severe head injury. Factors potentially responsible of early ischaemia are discussed.
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ABSTRACT: Lactate and the lactate-pyruvate index (LPI) are two hypoxia markers widely used to detect brain tissue hypoxia in patients with acute traumatic brain injury. These two markers have a more complex behavior than expected as they can be abnormally high in circumstances with no detectable brain hypoxia. This condition must be considered in the differential diagnosis because it also reflects an alteration of brain energy metabolism. Objectives 1. To describe cerebral energy metabolism characteristics observed in the acute phase of traumatic brain injury (TBI) based on two traditional indicators of anaerobic metabolism: lactate and LPI, 2. To determine the concordance between these two biomarkers in order to classify the incidence of anaerobic metabolism and 3. To classify the different types of metabolic abnormalities found in patients with moderate and severe TBI using both lactate and LPI. Materials and methods Twenty-one patients were randomly selected from a cohort of moderate or severe TBI patients admitted to the neurotraumatology intensive care unit. All of them who underwent both cerebral microdialysis and brain tissue oxygen monitoring (PtiO2). We analyzed the levels of lactate and the LPI for every microvial within the first 96 hours after head trauma. These data were correlated with PtiO2 values. Results Lactate levels and the LPI were respectively increased during 49,5% and 38,4% of the monitoring time. The incidence and behavior of high levels of both markers were extremely heterogeneous. The concordance between these two biomarkers to determine episodes of dysfucntional metabolism was very weak (Kappa Index = 0,29; IC 95%: 0,24–0,34). Based on the levels of lactate and the LPI, we defined four metabolic patterns: I: L > 2,5 mmol/L and LPR > 25; II: L > 2,5 mmol/L and LPR ≤ 25; III: L ≤ 2,5 mmol/L and LPR ≤ 25; IV: L ≤ 2,5 mmol/L and LPR > 25). In more than 80% of cases in which lactate or LPI were increased, PtiO2 values were within the normal range (PtiO2 > 15 mmHg). Conclusions Increased lactate and LPI were frequent findings after acute TBI and in most cases they were not related to episodes of brain tissue hypoxia. Furthermore, the concordance between both biomarkers to classify metabolic dysfunction was weak. LPI and lactate should not be used indistinctly in everyday clinical practice because of the weak correlation between these two markers, the difficulty in their interpretation and the heterogeneous and complex nature of the pathophysiology. Other differential diagnoses apart from tissue hypoxia should always be considered when high lactate and/or LPI are detected in the acute injured brain.Neurocirugia (Asturias, Spain) 08/2010; 21(4):289–300. DOI:10.1016/S1130-1473(10)70120-2 · 0.32 Impact Factor
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ABSTRACT: L’anémie est une complication fréquente chez les patients cérébrolésés. Elle est souvent considérée comme un facteur aggravant le développement de lésions cérébrales secondaires. Néanmoins, le niveau optimal d’hémoglobine à maintenir dans ce contexte est actuellement inconnu, et les effets des transfusions de globules rouges chez les patients atteints de traumatisme crânien grave, d’hémorragie sousarachnoïdienne ou d’accident vasculaire cérébral sont discutés: ils peuvent améliorer le transport local d’oxygène mais aussi être grevés de différentes complications. Le but de cette revue est de décrire les connaissances actuelles dans le domaine de l’anémie et des transfusions chez le patient cérébrolésé.Réanimation 11/2013; 22(6). DOI:10.1007/s13546-013-0728-1
Neurocirugia (Asturias, Spain) 01/2010; 21(4):300–301. DOI:10.1016/S1130-1473(10)70121-4 · 0.32 Impact Factor