Hello, my name is Dionne Spohr, and I'm a neurointensivist at Prometica Toledo Hospital at the University of Toledo. And I'm going to take you through the management of traumatic brain injury in the neuroICU. I have nothing relevant to disclose. The general learning objectives of this talk is to give you a broad overview of the topic of traumatic brain injury with a focus on the most salient management strategies for TBI in the neuroICU. To begin, we will review defining criteria and classification of traumatic brain injury. Then we will illustrate the principles behind the management of TBI, and finally we'll describe clinical strategies for reducing secondary brain injury and their management. Traumatic brain injury is defined as an induced structural injury to the brain as the result of an external force, and it can be divided into two categories. Closed brain injury and penetrating brain injury. Closed brain injury occurs when there is rapid shaking of the brain within the skull, leading to bruising and tearing of brain tissue and blood vessels. These kinds of injuries can be seen in falls, motor vehicle collisions, sports injuries, and assault. Penetrating brain injury occurs when there is a break in the skull, leading to injury to the brain. These sorts of injuries can be seen in gunshot wounds, knives, or a railroad spike through the frontal lobe. Primary brain injury occurs at the time of impact and results in an altered level of consciousness. Unrivaled to the emergency department, once basic stabilization has been done, one of the first tests a patient with TBI will get is a head CT, so I'd like to take a minute to go over some common findings you will see on a head CT in a patient who presents with TBI. Starting on the left-hand side of the slide, the first image shows an epidural hematoma. This is where blood collects between the dura and the skull, respecting suture lines, and is seen as a convex appearance on head CT. This pattern is a little bit different than you'll see in a subdural hematoma, which is in the next image over. This is where blood collects between the dura and the brain and results in a concave appearance on head CT. In the next image, you'll see a traumatic subarachnoid hemorrhage, and traumatic subarachnoid hemorrhage is actually the most common cause of subarachnoid hemorrhage and can occur in up to 35% of TBI patients. As opposed to aneurysmal subarachnoid hemorrhage, where blood is commonly seen in the sylvian fissure and basal cistern, traumatic subarachnoid hemorrhage is typically seen in the cerebral sulci and is usually adjacent to skull fractures or a cerebral contusion. In the next image, you'll see diffuse axonal injury, and this is caused by a shearing injury of axons. And while better visualized on MRI, when there's associated hemorrhage with these injuries, it can be picked up on head CT. And so you'll see these arrows are pointing to small little micro hemorrhages right at the gray-white junction, which is where you typically would see a diffuse axonal injury. In the final image, you'll see a hemorrhagic contusion, and this is the result of a sudden striking of the brain against the skull, which leads to bruising of the brain tissue. They can be seen anywhere in the brain, but are typically seen in the anterior cranial fossa and temporal pool, and take on a coup-contrecoup pattern. They may not be found on the initial head CT, because it takes a little bit of time for them to blossom, and often you can see them in follow-up imaging. When monitoring primary brain injury, it is important to monitor for and treat things that may lead to neurologic worsening and secondary brain injury. Specifically, we want to monitor and avoid things like hypoxia, hypotension, fever, hematoma expansion, intracranial hypertension, cerebral edema, herniation, and seizures. Monitoring for secondary brain injury is perhaps the greatest point of intervention a neurointensivist can offer in the management of TBI patients. The Glasgow Coma Scale, or GCS, is used to assess the severity of patients with traumatic brain injury. The scale assesses behaviors across three domains, eye movement, speaking, and body movement. Higher scores are associated with higher levels of consciousness, and lower scores correlate with lower levels of consciousness. It is assessed initially in the ED and can be used as a measure of who may require ICP monitoring and or intubation. A GCS less than 8 is considered the cutoff for patients who may need these interventions. While GCS is used as a marker of TBI severity, it does not predict outcome and should not be used as such. The GCS score is the primary measure used to classify TBI severity into mild, moderate, and severe categories. The post-resuscitation GCS score should be used when classifying TBI severity, as many compounders such as sedation, paralytics, hypotension, and hypoxia can all alter the GCS score. This next part of the talk will go over the initial management of TBI. The management of TBI and prevention of secondary brain injury begins in the field with emergency medical services. Airway management takes priority. Hypoxia, with oxygen saturation defined less than 90%, is associated with increased mortality in TBI. Normal ventilation is key in preventing secondary brain injury, as hyperventilation reduces blood flow to the brain and can lead to ischemia. In the case of signs of brain herniation, such as a unilateral dilated pupil that is unreactive, transient hyperventilation may be used as a short-term bridge to more definitive treatment for brain herniation. Like hypoxia, hypotension in the field can increase the risk of secondary brain injury and should be addressed in the field. When coupled with hypoxia, hypotension can double mortality in TBI. While addressing the ABCs, placement of a C-collar to restrict spinal motion and prevent spinal injury should be done. Calculating a GCS, performing an exam, and obtaining a history should all be done in tandem as part of pre-hospital TBI management. Resuscitation and stabilization efforts continue in the emergency department. Following stabilization, a repeat GCS score should be calculated and pupillary exams should be done to help guide further treatment. All patients with TBI should have CT head imaging done. Patients with moderate to severe TBI should also have CT imaging of the cervical spine. Continued efforts to avoid hypoxemia and hypotension should be done to help decrease the risk of mortality. Consultation neurosurgery and the appropriate ICU team should be done to help coordinate care beyond the emergency department. What to avoid in TBI? As mentioned in previous slides, prophylactic hyperventilation should be avoided in TBI. Hyperventilation induces hypocapnia, which reduces carbon dioxide in the blood, leading to vasoconstriction and reduced cerebral blood flow. This may be beneficial in the short term when there are signs of pending brain herniation, but when continued can lead to brain ischemia and worsening of brain injury. Other things to avoid in TBI include the use of steroids, which have been shown in a randomized control trial to increase mortality in TBI. A separate randomized control trial has also shown that the use of prophylactic hypothermia does not improve outcomes and should be avoided. All patients with TBI should be placed in a cervical collar. How do we assess for C-spine clearance in patients with TBI? In an awake patient, the nexus criteria for clinical clearance can be used for C-spine clearance and removal of the C-collar without the need for imaging. The nexus criteria assesses for intoxication, the presence of focal neurologic deficits, painful distracting injuries, normal level of alertness, and the presence of posterior midline tenderness to palpation. If the answer to all of these criteria are no, then the C-collar can be removed and no C-spine imaging is needed. In most cases of TBI, however, consciousness is altered and patients do not meet criteria for clinical clearance. In the case of moderate to severe TBI, a high-resolution CT of the C-spine is recommended in consultation with a spine specialist is suggested prior to the clearance of the C-spine and removal of the C-collar. Severe TBI often accompanies polytrauma. In 2019, the World Society of Emergency Surgery and Consensus Guidelines published their management recommendations for severe TBI in the setting of polytrauma. A summary of these guidelines can be seen here in this diagram. The main take-home point of these guidelines are that if there is hemorrhage and that hemorrhage is life-threatening, then stabilization of the bleeding takes priority along with concurrent management with osmotherapy if there are signs of impending brain herniation. Once the bleeding is stabilized or if the hemorrhage is not life-threatening, then standard management of brain injury should take place. TBI and burns often occur together in the setting of blast or combat-related trauma. TBI, when combined with burns, is associated with an increased mortality rate. This may be in part related to conflicting management recommendations for these two injuries. Guidelines for the management of TBI and burns differ in key areas, in particular, fluid resuscitation. In TBI, fluid resuscitation is conservative, while in burns it is aggressive. Burn goals tend to be high for TBI to help with management of cerebral edema, but in burns, hypernatremia is associated with poor outcome. Albumin is associated with worse outcomes in TBI, but it is a routine part of the recommended resuscitation guidelines for burn. Overall, treatment recommendations for these concurrent injuries should be individualized and guided by markers of response to treatment. In the next part of the talk, we will be going over the treatment of TBI with the focus of reducing secondary brain injury. Hemodynamic monitoring targets to avoid hypotension and hypoxia in TBI have been shown to improve mortality and improve outcomes. Traditionally, hypotension has been defined as the solid subcluster of less than 90 mmHg. However, new evidence supports a higher, more age-specific threshold. Patients aged 15 to 48 and over 70 years old have a reduced mortality rate if the solid subcluster is maintained at 110 mmHg or greater. And patients aged 50 to 69 years have reduced mortality when their solid subcluster is maintained at 100 mmHg or greater. In general, targeting a cerebral perfusion threshold of 60 to 70 is felt to be associated with better outcomes. Intracranial pressure monitoring is recommended in severe TBI in order to reduce in-hospital and two-week mortality. Severe TBI, defined as a GCS less than eight, along with an abnormal head CT, are indications for placement of an ICP monitor. ICP monitoring can be done either via an external ventricular drain, EVD, or a parenchymal monitor, which is more commonly referred to as a BOLT. An EVD tends to be the preferred monitor, as it has the added benefit of providing therapeutic CSF drainage for elevated intracranial pressures. The Brain Trauma Guidelines recommend treatment of ICP over 22 millimeters of mercury and maintaining a cerebral perfusion pressure target of 60 to 70 millimeters of mercury. Low brain tissue oxygen and hypoxia is associated with poor outcomes in TBI. If brain tissue oxygen monitoring is performed, a brain tissue oxygenation target greater than 20 millimeters of mercury is recommended. BOOST-3 is a randomized controlled clinical trial currently undergoing enrollment. The primary aim of this study is to determine the safety and efficacy of two separate management strategies for TBI. A strategy guided by treatment goals of brain tissue oxygenation monitoring in combination with ICP monitoring versus a strategy guided by treatment goals of ICP monitoring alone. Both of these treatment strategies are currently used in the standard of care. However, it is unknown if one strategy is more effective than the other. Recognizing the signs of brain herniation and providing early intervention is key to preventing secondary brain injuries. Brain herniation is the result of brain swelling, bleeding, or both. As pressure from the injured brain builds, the brain tissue translocates to other compartments of the brain, leading to compression of cranial nerves, blood vessels, which results in decreased blood flow, strokes, and eventually death. Early signs of brain herniation include a unilateral dilated non-reactive pupil, worsening neurologic exam marked by a decline in GCS more than a year after the initial diagnosis, a decline in GCS more than two points, extensor posturing, and eventually Cushing's triad, which is marked by bradycardia, hypertension, and an irregular breathing pattern. Treatment of elevated ICP above 22 millimeters of mercury is recommended in adults to avoid secondary brain injury and improve outcomes in TBI. In children, treating ICP above 20 millimeters of mercury is recommended. Initial management strategies include things that can be done at bedside, such as raising the head of the bed to 30 degrees to help promote venous drainage, correcting hyponatremia, treating fevers, maintaining a CPP of 60 to 70, and providing sedation. The next steps in managing elevated ICP include short-term hyperventilation to target an untitled PCO2 of 30 to 35, initiation of hyperosmolar therapy with either mannitol or hypertonic saline, and placement of an EVD to provide CSF drainage. If these initial management strategies fail to control ICP, more aggressive measures can be taken. Additional boluses of hyperosmolar therapy, such as 23.5% hypertonic saline, can be given to target a higher sodium goal of over 155. Increasing sedation with continuous propofol infusions can also be done. And decompressive craniectomy can be considered. If ICP remains elevated and is recalcitrant to these efforts, then a pentobarbital infusion can be started to induce coma and target burst suppression on EEG. Moderate hypothermia can also be considered, noting that hypothermia, while it may reduce ICP, has not been shown to improve outcome. Targeting a higher CPP goal above 70 can be trialed. However, this too has not been shown to improve outcome and may have adverse effects of causing pulmonary edema. Osmotherapy is the mainstay of treatment for elevated ICP. Hypertonic saline and mannitol can be used separately or together and are considered equivalent in terms of efficacy and safety for long-term management of acute TBI. Hypertonic saline and mannitol should be administered as bolus dosing and not continuous infusions in order to avoid rebound cerebral edema. A sodium goal of 145 to 155 is targeted for hypertonic saline dosing. And a serum osm goal of 310 to 320 is targeted for mannitol dosing. Some adverse effects of using osmotic agents to be aware of. Both of these agents can be associated with renal failure and rebound cerebral edema, though less so when bolus dosing is used. Hypertonic saline can cause metabolic acidosis and hypokalemia and should be monitored for and corrected. When ICP is refractory to osmotherapy, then decompressive craniectomy can be considered. Two trials, which I will discuss on the next two slides, investigated the utility of craniectomy and TBI in order to determine whether there was an improvement in outcomes. The first trial, DECRA, reported in 2011, investigated whether a bifrontal craniectomy versus standard of care improved outcome in TBI. What they found was that patients receiving a craniectomy had decreased ICU stays and a decrease in ICP. However, they had worse functional outcomes when compared to the standard of care group, and there was no difference in mortality. The next trial, RESQ-ICP, was reported in 2016. In this trial, they investigated whether a decompressive hemicraniectomy versus medical therapy improved outcome in TBI. In this study, they found lower mortality rates in patients undergoing hemicraniectomy, but no improvement in outcome. The bottom line for these studies is that though hemicraniectomy in TBI may be lifesaving, it does not appear to improve outcome. Post-traumatic seizures in TBI occur in approximately 30% of patients with moderate to severe TBI. The use of benotone for seizure prophylaxis has been shown in a randomized double-blind study conducted in the early 90s to reduce early post-traumatic seizures down from 14% to 3.6%. Since that time, new anti-seizure medications, namely levotriacetam, or Keppra as it's commonly known, which has a safer side effect profile, have emerged and have replaced the use of benotone for seizure prophylaxis in TBI. The efficacy of Keppra for seizure prophylaxis in TBI, however, has not been determined, and its role in reducing post-traumatic epilepsy is unclear. Post-traumatic vasospasm is rare and occurs at a variable incidence rate in patients with TBI. It is more commonly seen in penetrating head traumas and occurs earlier in the course than what is typically seen in vasospasm associated with subarachnoid hemorrhage. Endovascular therapy is the mainstay of treatment for post-traumatic vasospasm. Standard management strategies used for vasospasm and subarachnoid hemorrhage differ in traumatic vasospasm. Hemodynamic augmentation, like what is done in subarachnoid hemorrhage, may actually worsen cerebral edema in TBI and should be avoided. Nemotipine, which improves outcome in subarachnoid hemorrhage shows no difference in outcome when used in patients with TBI. As we wrap up, I wanted to share with you a summary slide with all the physiologic targets for TBI management, as well as the secondary brain injury prevention recommendations that we went over during the talk. I'm hoping this will be a nice reference guide for you as you're studying. Thank you.

traumatic brain injury

neuroICU

closed brain injury

penetrating brain injury

Glasgow Coma Scale

secondary brain injury