Recent advances in traumatic brain injury

Abstract

Traumatic brain injury (TBI) is the most common cause of death and disability in those aged under 40 years in the UK. Higher rates of morbidity and mortality are seen in low-income and middle-income countries making it a global health challenge. There has been a secular trend towards reduced incidence of severe TBI in the first world, driven by public health interventions such as seatbelt legislation, helmet use, and workplace health and safety regulations. This has paralleled improved outcomes following TBI delivered in a large part by the widespread establishment of specialised neurointensive care. This update will focus on three key areas of advances in TBI management and research in moderate and severe TBI: refining neurointensive care protocolized therapies, the recent evidence base for decompressive craniectomy and novel pharmacological therapies. In each section, we review the developing evidence base as well as exploring future trajectories of TBI research.

Keywords: Critical care; Monitoring; Neuroprotection; Neurosurgery; TBI; Therapy; Traumatic brain injury.

Conflict of interest statement

The authors have no conflicts of interest relating to this manuscript to declare.

Figures

Fig. 1

Multi-modality monitor in neurocritical care—illustrating cerebral microdialysis, intracranial pressure and brain tissue oxygenation monitoring. The microdialysis catheter allows sampling of the brain extracellular fluid by recovering molecules of interest that diffuse across the catheter tip and are recovered within a microvial

Fig. 2

Summary of the mechanisms of energy failure in traumatic brain injury that lead to increased brain lactate: pyruvate ratio (LP ratio). The conversion of lactate to pyruvate is an oxygen-independent step, whereas oxidative phosphorylation and the tricarboxylic acid cycle are oxygen-dependent. Of note, reduced cerebral blood flow and increased oxygen extraction fraction, which characterize classical ischemia, are typically not seen in microvascular ischemia. Mitochondrial dysfunction in the TBI context can arise from multiple pathological processes, often concurrently (most common shown). Ca2+ ionized calcium, CBF cerebral blood flow, iNOS inducible nitric oxide synthase, LDH lactate dehydrogenase, NAD+ nicotinamide adenine dinucleotide (oxidised form), NADH nicotinamide adenine dinucleotide (reduced form), NO nitric oxide, O2 oxygen, O2·−, superoxide radical, OH· hydroxyl radical, pO2 tissue oxygen saturation, ROS reactive oxygen species, TCA tricarboxylic acid cycle

Fig. 3

Bar chart of RESCUE-ICP trial outcomes at 6 months [47]. Outcomes are displayed using the Extended Glasgow Outcome Scale (eGOS) on the horizontal axis. eGOS at 6 months represents the primary outcome measure of this trial. The percentage of patients falling within the respective outcome category is displayed in the figure table and illustrated in the corresponding graph. “Favourable” outcomes were defined as upper severe disability or better in the RESCUE-ICP trial. “Unfavourable” outcomes comprise of lower severe disability and vegetative state

Fig. 4

a Bifrontal decompressive craniectomy with the dotted line on the dura representing durotomy site and the red line illustrating an area of falxotomy. b Decompressive hemi-craniectomy with the dotted line representing durotomy incision. Adapted with permission from Timofeev et al. (2012) [43]

Fig. 5

Bar chart of RESCUE-ICP trial outcomes at 6 months (47). Outcomes are displayed using the Extended Glasgow Outcome Scale (eGOS) on the horizontal axis. eGOS at 6 months represents the primary outcome measure of this trial. The percentage of patients falling within the respective outcome category is displayed in the figure table and illustrated in the corresponding graph. “Favourable” outcomes were defined as upper severe disability or better in the RESCUE-ICP trial. “Unfavourable” outcomes comprise of lower severe disability and vegetative state