Search

Introduction Metabolic derangements are common after traumatic brain injury (TBI), but few studies have used multi-tracer positron emission tomography (PET) to interrogate underlying pathophysiology. We examined relationships between glucose metabolism (measured using 18F-fluorodeoxyglucose (FDG) PET) and cerebral blood flow (CBF; measured using H215O PET). Methods Twenty-six TBI patients with median (range) pre-intubation Glasgow Coma Score of 6 (3-12) underwent combined 15O and FDG PET on 34 occasions; 10 and 18 healthy volunteers (controls) underwent 15O and FDG PET respectively. FDG rate constants were determined with an irreversible two-compartment model: transport across BBB (K1,k2), hexokinase activity (k3), and influx rate (Ki). Regions of interest (ROIs) were defined for haemorrhagic lesion (core), hypodense tissue (penumbra), 1 cm border zone of normal appearing tissue (peri-penumbra), and remote normal appearing tissue (normal). Results K1 was significantly reduced within core, but was comparable to control values in peri-penumbra and normal ROIs. While k3 and Ki were lower than control values, regional increases were found in the vicinity of lesions and some structurally normal areas. Glucose delivery (measured by K1) was unrelated to CBF when values were above 30ml/100ml/min, and was significantly below 95% confidence intervals for control values when CBF was below 25ml/100ml/min. There was a clear linear relationship between K1 and CBF in core ROIs (R²=0.75, p

Background: Metabolic derangements are common after traumatic brain injury (TBI) (Abate et al., Neurocrit Care, 2008), but few studies have combined 18F-fluorodeoxyglucose (FDG) and multi-tracer oxygen-15 (15O) positron emission tomography (PET) to interrogate underlying pathophysiological mechanisms (Hatori et al., J Nucl Med, 2004). We examined how derangements in FDG kinetic parameters within injured brain relate to cerebral blood flow (CBF), blood volume (CBV), oxygen metabolism (CMRO2) and oxygen extraction fraction (OEF).

Search strategy and network meta-analysis figures. (DOC 117 kb)

Methodology of systematic review on incretins in peri-operative and intensive care (PDF 88 kb)

BACKGROUND: Optimal glycaemic targets in traumatic brain injury (TBI) remain unclear. We performed a systematic review and meta-analysis of randomised controlled trials (RCTs) comparing intensive with conventional glycaemic control in TBI requiring admission to an intensive care unit (ICU). METHODS: We systematically searched MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials to November 2016. Outcomes of interest included ICU and in-hospital mortality, poor neurological outcome, the incidence of hypoglycaemia and infective complications. Data were analysed by pairwise random effects models with secondary analysis of differing levels of conventional glycaemic control. RESULTS: Ten RCTs, involving 1066 TBI patients were included. Three studies were conducted exclusively in a TBI population, whereas in seven trials, the TBI population was a sub-cohort of a mixed neurocritical or general ICU population. Glycaemic targets with intensive control ranged from 4.4 to 6.7 mmol/L, while conventional targets aimed to keep glucose levels below thresholds of 8.4-12 mmol/L. Conventional versus intensive control showed no association with ICU or hospital mortality (relative risk (RR) (95% CI) 0.93 (0.68-1.27), P = 0.64 and 1.07 (0.84-1.36), P = 0.62, respectively). The risk of a poor neurological outcome was higher with conventional control (RR (95% CI) = 1.10 (1.001-1.24), P = 0.047). However, severe hypoglycaemia occurred less frequently with conventional control (RR (95% CI) = 0.22 (0.09-0.52), P = 0.001). CONCLUSIONS: This meta-analysis of intensive glycaemic control shows no association with reduced mortality in TBI. Intensive glucose control showed a borderline significant reduction in the risk of poor neurological outcome, but markedly increased the risk of hypoglycaemia. These contradictory findings should motivate further research.