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TBI Management: Beyond the Resus Room
The document outlines various aspects of intensive care management in neurology, including guidelines, protocols, and surgical interventions. It discusses monitoring techniques such as intracranial pressure (ICP) monitoring, jugular venous oximetry, and brain tissue oxygen tension. Additionally, it highlights current evidence, clinical pearls, and future directions in the field.
TBI Management: Beyond the Resus Room
- 1.
- 2. Guidelines Protocols Surgical interventions Current evidence Clinicalpearls Future directions
- 9. ICP monitoring EVD vs ICP monitor ICP <22
- 10. CBF CPP= MAP - ICP
- 13. Jugular venousoximetry Brain tissue oxygen tension (PbtO2) monitoring Cerebral microdialysis Thermal diffusion flowmetry Pressure reactivity index (PRx)
Editor's Notes
- #2 Thank you for that kind introduction. A quick disclaimer that I am in no way an expert, however I’ve developed an interest in neurointensive care given my clinical exposure to both the neurosurgical and intensive care management of patients with the full spectrum of traumatic brain injury.
- #3 During this talk, I won’t be focussing on guidelines and protocol. Additionally, I won’t focus on the specifics of surgical intervention. Instead, I’d like to highlight some of the latest evidence base, clinical pearls and future directions in the management of our patients with traumatic brain injury.
- #4 TBI patient demographics are changing, with a bimodal age distribution as demonstrated by the CENTRE-TBI group. The previously typical young male (often intoxicated) multitrauma following an MVA is one group, and now elderly fallers are comprising an increasing proportion of patients with TBI requiring ICU admission. Due to the mechanism of injury, each group has separate injury patterns to consider. Apart from sedative infusions and blood products, there is now one more infusion commonly seen on admission to ICU…
- #5 Tranexamic acid (TXA) is a synthetic lysine analogue that blocks plasminogen from being converted to the enzyme plasmin. In doing so, TXA acts as an antifibrinolytic with the recommended dose of 1g infused over 10 minutes, followed by 1g over the next 8 hours. In the setting of TBI, an elevated D-dimer, which may represent enhanced fibrinolytic activity, has demonstrated an association with progressive haemorrhagic brain injury and possibly worse outcomes. A mortality benefit for TXA in patients with moderate TBI was demonstrated in the CRASH-3 trial that randomized 9202 TBI patients with GCS <13 or any evidence of intracranial bleeding on CT scan within three hours of injury to TXA or placebo. Vaso-occlusive events were not increased in those receiving TXA. For those patients with a past medical history of anti-platelet agents or direct and indirect oral anticoagulant therapies, there are reversal protocols, which are being updated as new products (eg andexanet-alpha) become available.
- #6 Injury to the carotid and vertebral arteries most commonly occurs as a result of skull base or vertebral fractures that involve vulnerable segments of those vessels. Whilst blunt cerebrovascular injury (BCVI) may result in stroke at the time of injury, a latency of several hours to several days between the trauma and cerebrovascular event is common. Because antithrombotic therapy during this latent period may prevent subsequent ischaemic strokes, BCVI is important to identify and consideration should be made to commencing aspirin if no contraindications exist; since anticoagulation with heparin is typically contraindicated. Clinical pearl: don’t forget to perform a CTA Arch to COW when there are cervical spinal fractures (especially those adjacent to the foramen transversarium) or if there is a base of skull fracture with concerns regarding the carotid canal!
- #7 After primary brain trauma, modern neuro-intensive care is focused on preventing secondary brain injury, which can significantly impact long-term functional outcomes. Clinical monitoring has traditionally focused on measuring intra-cranial pressure (ICP), and optimizing cerebral perfusion pressure (CPP), more on these two later, but the rest of it relates to good ICU housekeeping. There are several things worth considering and optimising in TBI, for example glucose management and seizure prophylaxis. A word of caution regarding use of therapeutic hypothermia – whilst it does reduce ICP, for example as demonstrated in EUROTHERM3235, it worsened clinical outcomes and increased mortality compared to standard care alone. This finding was reinforced by LTH-1, a multicenter randomized controlled trial just published in the Lancet in January 2021.
- #8 Isotonic fluids should be used to maintain euvolaemia. Saline is preferable to albumin as demonstrated by the SAFE clinical trial, which compared saline with albumin for fluid resuscitation in the ICU. While balanced crystalloid solutions (eg Hartmann’s and Plasmalyte) are used to decrease the risk of acute kidney injury in other critically ill patients, normal saline is preferred in TBI, since balanced salt solutions are relatively hypotonic and may worsen cerebral oedema. In the SMART ICU trial, among the TBI patients enrolled, there was no benefit with the use of balanced fluids. With respect to the management of raised ICP – the adult and paediatric literature have now aligned, with a trend towards hypertonic saline rather than osmotic agents such as mannitol.
- #9 Indications for ICP monitoring in TBI have been well established with one of the most widely known being the Brain Trauma Foundation (BTF) guidelines. Types of ICP monitors will vary based on neurosurgeon preference and institutional factors, however the two main types are ICP monitors and external ventricular drains, with the latter being both diagnostic and therapeutic. Placement of the monitor is key, with intraventricular or intraparenchymal positions being preferable. Subdural placement is simply less accurate.
- #10 Importantly, the metal wire in the ICP monitor is MRI safe when coiled in a specific orientation of 6cm loops to reduce resonance and thus probe tip heating, and whilst it may not have become mainstream practice in Australia yet, the manufacturer includes instructions on how to safely perform an MRI with the monitor in situ. Whilst the CT scanner remains the workhorse of radiological investigation for TBI, portable CT scanners are becoming increasingly available with increased image resolution, and have the main benefit that does not require transport of critically unwell patients outside the ICU. Portable MRI scanners are currently too low resolution and the image sequences available and too limited to be of significant clinical utility.
- #11 Cerebral autoregulation is one of the key concepts fir individualised TBI management. Through autoregulation, the normal cerebral vasculature maintains an adequate cerebral blood flow (CBF) across a wide range of mean arterial pressure (MAP). Cerebral autoregulation is disrupted in approximately one-third of patients with severe TBI. In these patients, a rise in MAP can lead to an elevated ICP due to increased cerebral blood volume and hyperaemia, while drops in MAP may be associated with hypoperfusion and ischaemia. Patients with impaired cerebral autoregulation are described as ‘pressure passive’. Whilst optimization of CBF is a foundation of TBI treatment, bedside measurement of CBF is not easily obtained. Cerebral perfusion pressure (CPP), the difference between the MAP and the ICP is a useful surrogate. A goal CPP of 60-70mmHg is recommended to improve survival and favourable outcomes. Efforts to optimize CPP should first focus on the treatment of elevated ICP. Patients with more severely impaired autoregulation and suboptimal CPP are best managed with efforts to lower ICP, rather than by elevating MAP with vasopressors; and similarly hypertension is more likely to worsen cerebral oedema when protective autoregulation is impaired. Multimodal monitoring, including the pressure reactivity index (PRx) may help determine the adequacy of autoregulation and identify the optimal CPP in individual patients.
- #12 How do we determine if autoregulation is intact? This is an example of data available from the ICM+. Pressure reactivity is calculated as the Pearson correlation between MAP and ICP. Mean values are calculated every 10 seconds and then correlation of 30 consecutive values is taken. In this case variations in MAP occur with simultaneous changes in ICP and thus the PRx is impaired (close to 1). Poor pressure reactivity index after traumatic brain injury
- #13 Conversely, In cases when the brain vasculature is healthy, increases in MAP will be associated with decreases in ICP because an increase in MAP will cause cerebral vasoconstriction, decreased cerebral blood volume, and decreased ICP. The correlation between MAP and ICP will be negative (in this case PRx = -0.45). Good pressure reactivity after traumatic brain injury So it’s all about finding =an individualised ‘optimal’ CPP (CPPopt). This value may be different between patients, and may change in time within a patient.
- #14 In order to supplement ICP monitoring, several technologies have been developed for the treatment of severe TBI. These techniques allow for the measurement of cerebral physiologic and metabolic parameters related to oxygen delivery, cerebral blood flow (CBF) and metabolism, with the goal of improving the detection and management of secondary brain injury. Whilst observational data suggest that these monitoring tools provide unique information that may help to individualize the management of patients with severe head injury, clinical trial data demonstrating improved outcomes with use of these multimodality advanced neuromonitoring approaches are awaited.
- #15 Such techniques include: ● Jugular venous oximetry – Retrograde cannulation of the internal jugular vein that allows measurement of oxygen saturation in the blood exiting the brain. Normal jugular venous oxygen saturation (SjVO2) is approximately 60 percent. SjVO2 <50 percent for 10 minutes is considered a "cerebral desaturation" and implies a mismatch between oxygen delivery and demand in the brain. These desaturation episodes are associated with unfavorable neurologic outcomes in this setting. Jugular venous oximetry protocols that specify stepwise escalation of therapy to improve cerebral perfusion when desaturations occur have been used at several institutions; however, randomized clinical trials have not been performed.
- #16 ● Cerebral microdialysis – An intraparenchymal probe placed in a manner similar to a PbtO2 probe that allows measurement of extracellular glucose, lactate, pyruvate, and glutamate. A lactate:pyruvate ratio >40 is suggestive of anaerobic metabolism, which is believed to exacerbate secondary brain injury.
- #17 ● Thermal diffusion flowmetry – Intraparenchymal probe placed in a manner similar to a PbtO2 probe that allows continuous measurement of CBF, usually in the white matter. Correlation with CBF from neuroimaging and outcome data is very preliminary at present.
- #18 However the one that might be of most interest to the local audience is ● Brain tissue oxygen tension (PbtO2) monitoring – Intraparenchymal oxygen electrode placed in a manner similar to a fiberoptic ICP probe that measures PbtO2 in the white matter. Normal PbtO2 is >20 mmHg; duration and depth of PbtO2 below 15 mmHg are associated with worsened outcomes. Some studies have shown improved outcomes in patients managed with treatment protocols directed at optimization of PbtO2 as compared with historical controls. A phase 2 randomized clinical trial (BOOST-2) demonstrated the feasibility of a goal-directed management protocol for the optimization of PbtO2 following TBI; a phase 3 trial (BOOST-3) is underway. From an local ICU perspective, BONANZA (Brain Oxygen Neuromonitoring in Australia and New Zealand Assessment Trial) is a phase III clinical trial with a goal of improving outcomes post severe TBI and reduce long-term healthcare costs, by conducting a large (n=860), pragmatic, patient-centred randomised controlled trial of a neuro-intensive care management protocol based on early brain tissue oxygen optimisation.
- #19 Whatever combination of advanced neuromonitoring is used, one of key parts remains the old adage: location, location, location! The data will be difficult to interpret if the monitors are placed incorrectly (eg infarct or contusion), and to change your clinical management based on possibly flawed data means things still need to be interpreted subjectively. In practice, the clinician must ultimately decide whether or not to “believe” the number in combination with the clinical examination findings! Depending on your unit, there are other modalities eg TCD, cEEG, and these will add to your clinical accumen.
- #20 Putting it all together… Even as we begin 2021, it’s clear that our knowledge of TBI, or even neurophysiology is still growing. The future direction of TBI management will be patient centric, involve multi-modal monitoring with individualised targets. Emerging areas of research include biomarkers and genomics… and perhaps, one day we will have things such as immunotherapy as an adjunct in our arsenal to achieve neuroprotection. Either way, I’m excited and look forward to the future! Thank you for listening.