The Role of Invasive Monitoring in Traumatic Brain Injury

Curr Trauma Rep (2015) 1:125–132 DOI 10.1007/s40719-015-0022-y BLUNT HEAD TRAUMA (M DE MOYA, SECTION EDITOR) The Role of Invasive Monitoring in Traumatic Brain Injury Raphael Arellano Carandang 1 Published online: 11 July 2015 # Springer International Publishing AG 2015 Abstract Severe traumatic brain injury is a complex disease that involves physical injury and distortion of tissues and cell membranes, gross hemodynamic changes including loss of autoregulation, cerebral edema and tissue shifts, changes in pressure and perfusion and multiple secondary cellular processes including electrolyte fluxes, inflammatory mediator release, neurotransmitter mediated excitotoxicity, apoptosis, mitochondrial dysfunction, and alterations in cellular metabolism. The optimal treatment of these patients who have severe neurological dysfunction or require sedation that compromises neurological functional assessment by physical examination requires the monitoring and management of multiple aspects of brain physiology including pressure, perfusion, oxygenation, cellular metabolism, and electrical activity. Invasive monitoring techniques, while still in various stages of development, can and will provide real-time trackable data that informs the management of these patients as well as contributes to our understanding of the pathophysiological processes that contribute to it. Keywords Traumatic brain injury . Invasive multimodal monitoring . Intracranial pressure . Cerebral perfusion pressure . Cerebral blood flow . Oxygenation . Pressure reactivity index . Microdialysis . Near infrared spectroscopy . Laser Doppler flowmetry . Transcranial Doppler ultrasound . PbtO2 This article is part of the Topical Collection on Blunt Head Trauma * Raphael Arellano Carandang 1 Departments of Neurology, Anesthesiology and Surgery, University of Massachusetts Medical School, 55 Lake Avenue North S4-408, Worcester, MA 01655, USA Introduction Traumatic brain injury is all too common and can have devastating consequences and result in severe disability and death. Much research has gone into understanding the numerous gross hemodynamic and physical, biochemical, and cellular processes that occur as the trauma occurs and the consequences thereof that follow [1]. Secondary injury follows cellular membrane damage, resulting in electrolyte fluxes, neurotransmitter release, mitochondrial dysfunction, cytokine and inflammatory mediator release, and apoptotic mechanisms that all contribute to further injury from edema, necrosis, ischemia, metabolic crises, and cell death [2]. Invasive multimodal neurological monitoring is the use of devices to measure, track, and detect pathophysiological changes in the brain after a severe traumatic brain injury with the goal of guiding medical management and therapeutics to help obtain the best possible functional neurological outcome [3]. Many of the principles of management such as the MonroKellie doctrine have been around since the 1800s and from the time of Harvey Cushing, but much of the data following since, until recently, has been slow to accumulate and comes mostly from registries and retrospective database research [4–6]. Given the critical nature of the disease, clinical equipoise for much of the management had been non-existent and guidelines are driven by mostly class II and III level evidence [7, 8•]. Invasive neurological monitoring itself has been on a shifting pendulum in recent years. From measurement of intracranial pressure (ICP) being considered part of the gold standard management and a requirement in the management of patients with severe TBI to being nearly abandoned altogether in some centers because of logistics, cost, perceived risk and lack of evidence. It continues to be surrounded by controversy particularly in light of a recent randomized clinical trial suggesting that it has 126 limited impact above and beyond good conventional neurocritical care [9•]. As with many costly technologies that are in various stages of development, the evidence for its utility continues to grow as does the scrutiny surrounding it. At the current time, it remains largely underutilized [10]. Guidelines [7, 8•] exist, but the impetus for invasive neurological monitoring stems from the physiology of the brain, its sensitivity, and vulnerability to ischemic insults and metabolic crises as well as the need for critical and time-dependent pre-emptive interventions to prevent cell death in the setting of significant brain injury [11]. From a pragmatic standpoint, it is also a necessity given that these patients are often unresponsive, comatose, or require effective sedation to manage their brain injury and whatever accompanying significant polytrauma they suffered in the accident [12]. These patients nearly always require mechanical ventilation and hemodynamic management given their poor airway protection and other organ injuries. Lastly, invasive monitors provide real-time physiological data and help us further understand the various complex pathophysiological processes that occur in brain injury that in turn inform basic, translational, and clinical research and contribute to the development of treatment protocols as well as therapies. It is worth emphasizing that all invasive modalities used in monitoring should always be interpreted in light of a comprehensive synthesis of data available in the context of individualized patient care. ICP Monitoring ICP monitoring makes sense from a pathophysiological standpoint as it affects cerebral perfusion pressures and can precipitate or worsen cerebral hypoperfusion and ischemic injury. Clinical studies have not supported this in terms of benefits for outcome. Data from larger observational studies have suggested a threshold of ICP >20 for harm, and a meta-analysis of studies has shown this to be associated with worse outcome [13•]. Many guidelines have adopted this as class II evidence for ICP monitoring, but recent studies including a re-analysis of the NTDB data from 1994 to 2001 suggested that ICP monitoring was associated with 45 % lower rate of survival and worse functional outcome with ICP monitoring after correcting for other clinical severity measurements [14, 15]. The only randomized clinical trial to study an ICP-based treatment protocol with a treatment threshold of 20 versus a conventional one without ICP monitoring for TBI was conducted in South America because of the lack of clinical equipoise in the USA and showed no difference in functional outcome between both groups [9•]. There were some differences in the intensity of the treatment with the non-ICP treatment group getting more hypertonic saline, mannitol, and Curr Trauma Rep (2015) 1:125–132 hyperventilation and more patients in the ICP treatment group getting pentobarbital. The study was a comparison of two protocols and not ICP values per se. If one wanted to truly test the significance of the ICP threshold of 20, they should have inserted ICP monitor (...truncated)