Thank you for joining us today for a portion of the nine-part TBI series. Today's speaker is Dr. Kian Nasiri, and he's going to discuss some content in our rehab section. Dr. Nasiri is a brain injury medicine attending physician at the Shirley Ryan Ability Lab and assistant professor at Northwestern University Feinberg School of Medicine. Originally from the Bay Area in California, he completed his undergraduate training at the University of California, San Diego, and medical school at the Arizona College of Osteopathic Medicine. He completed both his PMR residency, training, and brain injury medicine fellowship at the Shirley Ryan Ability Lab, McGraw Medical Center of Northwestern University. His academic interests include the full spectrum of traumatic brain injury, non-traumatic brain injury, neuropharmacology, disorders of consciousness, spasticity management, and medical education. I'm excited to now turn it over to Dr. Nasiri. Thank you for that introduction, Nori. So today we'll be reviewing some acute medical complications that can result after a traumatic brain injury. Like Nori had said, my primary clinical practice is working with these patients in the acute inpatient rehabilitation settings, but I do have experience working in the acute medical setting and, you know, anticipating for some of these complications that can occur after a traumatic brain injury. So I have no disclosures or financial disclosures to disclose at this time. So jumping into some objectives for today's talk, we'll really quickly go over some basic epidemiology of traumatic brain injury. Most of this information is available through the CDC website. Next, we'll briefly go over some principles pertaining to acute management of TBI, including pathophysiology, principles of management, and then that's when we'll jump into the real meat of our lecture, where we'll review some of those early complications that can result after a traumatic brain injury and how to appropriately manage those. So with regard to some basic epidemiology, it's just important to review some numbers so we get an understanding of how prevalent it is in the United States. So per the last CDC data that was available to us, it's been estimated that there's roughly 2.5 million TBI-related AD visits. However, we do know that this is likely an underestimation because, number one, the vast majority of traumatic brain injuries fall under that category of mild traumatic brain injury, and the majority of those patients, when an event does occur, don't actually go and seek medical care for that. However, when it comes to more moderate and severe traumatic brain injuries, per the last data that was available, there's been roughly 215,000 TBI-related hospitalizations and roughly 70,000 TBI-related deaths. Risk factors for TBI include being of the male gender, being older does put you at increased risk of hospitalization and death, being of lower socioeconomic status, non-white, or having significant psychological comorbidities. When we look at etiologies of traumatic brain injury, the vast majority of traumatic brain injuries do result after a fall, next blunt force trauma, and then finally motor vehicle accidents. Also, that's important to note that traumatic brain injury-related deaths do include suicide attempts, most likely due to gunshot wounds. Then when we're thinking about the distribution of traumatic brain injury when it comes to age, the vast majority either occurs in the newborn to toddler range, and then those individuals who are greater than 75 years old. So next, jumping into acute management of TBI, we'll briefly review some pathophysiology. So when we think about traumatic brain injury and how it's the result of an external force causing damage to the brain, we can kind of subdivide it into the primary injury and then the secondary injury. That primary injury is usually the direct result of the impact. There's nothing we can really do to treat this, so a lot of our therapies are actually focused on preventing that secondary injury or that metabolic cascade that takes place, which can have devastating consequences for patients. So after, you know, the initial injury, typically what happens is that you'll have disturbed cerebral blood flow, causing an impaired blood-brain barrier. This all ultimately leads to metabolic stress, ischemia, inflammation, excitotoxicity, causing increasing edema, which generates reactive oxygen species, which essentially cause increased cell death and apoptosis, ultimately driving intracranial pressures. And then finally, once our tissues start to heal, that results in, you know, tissue regeneration. So what we're typically targeting is kind of the areas of metabolic stress and excitotoxicity to prevent that increased intracranial pressure. In brief review, just to quickly review some common bleed types after traumatic brain injury, starting from A to F, if we're looking at A, that's just a healthy brain. Next in B, we have what's known as a subdural hematoma, which is that crescentaric, that crescentaric-shaped type bleed that's pretty common in more older, elder individuals and can, that typically results from the sharing of the bridging vessels. Next we'll have the epidural hematoma in C, which is shaped more like a lens, and that's because it's bound by our cranial suture lines. So essentially what happens is the bleeding is concentrated within a fixed space, so it has nowhere to expand but inwards, and those patients are at high risk of severe progression and have to be intervened on pretty acutely. Next we have intraparenchymal bleeds, or bleeding within the brain tissue itself. Then there's intraventricular bleed, which is bleeding within our ventricular system, which is essentially the system that creates the fluid that our brain tissue sits in. And then finally, in more severe cases, we can have what's known as subarachnoid hemorrhage, which is noted in F, and like I said, those types of bleeds are typically associated with more severe traumatic brain injury, and you'll typically see blood within the sulci, within the sulci or grooves of the brain tissue. So when we're thinking about principles of acute care management, one thing to really cover that essentially kind of drives theories behind management is what's known as the Monroe-Kelly hypothesis. Essentially this states that the intracranial volume is essentially fixed and surrounded by the inelastic skull. Therefore, our brain is able to make kind of small volume Therefore, our brain is able to make kind of small volume changes in order to compensate and maintain that intracranial pressure, where a normal person's intracranial pressure is roughly 10 millimeters mercury. However, after a brain injury, it causes a severe disruption in the system whereby those small volume changes lead to uncontrolled large increases that our normal physiology is unable to compensate for. So that's one of the kind of core principles that drive a lot of the management with regard to the critical care setting. So when we're thinking about how do we initially assess and manage these patients, kind of standard of care is performing serial imaging. Again, it can be helpful in identifying delayed onset edema or hemorrhage. Typically, we're getting CT scans because those are quick to obtain, can easily identify bleeding. Once patients become a little bit more stable, we do consider getting MRI scans, which can be helpful, especially in our setting, in the rehabilitation setting for translating kind of the areas that have been damaged as a result of the traumatic brain injury and giving families an indication of how damage to those certain areas are translating to some of our patient's functional presentations and can also help in terms of prognostication. Next thing to consider is intracranial pressure monitoring that's typically done with an external catheter. There's various different indications for monitoring the intracranial pressures. Typically, any individual that's scoring under a nine on the Glasgow Coma Scale gets intracranial pressure monitoring or meeting two out of the three criteria, which would include age greater than 40, systolic blood pressure under 90, or any sort of motor posturing that's observed. And then finally, we have to balance, you know, managing our intracranial pressures with making sure that we're maintaining adequate cerebral perfusion or maintaining an adequate blood supply to the brain. We obtain that number by subtracting our mean arterial pressure from the intracranial pressure. So as you can see, the intracranial pressure and cerebral perfusion pressure are intrinsically tied. Our typical cerebral perfusion pressure goal is between 50 to 70. So typically what we're trying to do is manage and keeping intracranial pressure volumes roughly under 20 in order to make sure that our brain is getting the appropriate blood supply. As we delve further into critical care management, some of that initial management does include some controlled ventilation in order to kind of help, you know, maintain patient's oxygenation status, make sure that we're maintaining adequate cerebral perfusion pressures, maintaining a head of bed elevation, and then performing serial assessments with obtaining a GCS score as well as pupillometry to potentially help identify any impending herniation. When we're thinking about that initial pharmacologic management for management of intracranial pressures, that does include giving some diuretics that would be more commonly known as like mannitol or hypertonic saline in patients where they are having, you know, questionable seizures. We try to achieve what's known as burst suppression where essentially we're quieting the metabolic activity of the brain, typically managed with barbiturates or propofol, which are different types of infusions or anesthetics that we can give to patients. And then finally making sure we're also maintaining adequate cerebral perfusion by giving our patients fluids and potentially additional medications to help maintain blood pressures. After a traumatic brain injury, that does put increased metabolic stress on the bodies. So it's been roughly estimated that after sustaining a traumatic brain injury by day seven, we're actually operating at 140% of our basal metabolic rate. So making sure our patients are getting adequate nutrition. That also translate to kind of having a little bit looser glycemic control where our target glucose levels are typically between 140 to 80. There's no real guidelines that exist at this point, but the general consensus is avoiding overt hypoglycemia to make sure that our tissues have energy available and nutrients available for them to use. Uncontrolled fever is also associated with worse outcomes. We are also, you know, maintaining normal thermia in our patients. And then with regard to brain oxygenation monitoring and steroids, literature actually shows that neither one of those things have sufficient evidence for either of those things. Next, when we're thinking about indications for surgery, number one, it's important for us to briefly review some terminology that's associated with the different types of surgeries that can take place after traumatic brain injury. So when we talk about craniotomies, that's typically done as, you know, some primary evacuation of hematomas where a portion of the skull will be removed and then immediately replaced. In more severe traumatic brain injuries, if they're using the term craniectomy, that's typically done when a portion of the skull is removed and not immediately replaced and left for a period of time in order to give the significant swelling that might be present time to resolve. Once patients stabilize from that standpoint, that's typically when we'll, you know, discuss cranioplasty, which is essentially where they'll either use native bone or an artificial flap to place and recreate that closed system that had to be open to help manage some of the uncontrolled pressures. But ultimately what we do know is that the benefit and timing of surgery have yet to be identified, so a lot of the decisions whether, you know, providers are determining whether a patient would be appropriate for a craniotomy or craniectomy, it's up to the clinician that's performing that initial assessment. Some things we also know is that hematoma can be one of the strongest predictors of 30-day outcome for our patients, and like I said, there's no specific guidelines at this point for procedure selection, but what we do know is that craniectomy is usually done for patients with refractory or uncontrolled intracranial pressure elevations. Some things to, you know, briefly review when we're thinking about survivorship after traumatic brain injury is there's been several studies that have shown that surgeries have resulted in decreased mortality and increased survivorship. However, when we're thinking about functional outcomes, it has shown an increased proportion of patients staying in unresponsive wakefulness or the vegetative state, so may not necessarily be associated with favorable outcomes. So, just, you know, kind of something to keep in mind that with the advent of some of these surgical interventions, it is increasing the overall number of people that survive after traumatic brain injury, but sometimes those patients might not have, you know, an ideal outcome, especially for family members. So, I do think it is important to be upfront with families that, you know, while some of these procedures might be taking place, it might not necessarily mean that they'll, you know, return to how they were functioning before the injury had taken place. In patients that do undergo decompressive hemicraniectomy or, you know, that removal of the skull, an important complication to know is what's known as sunken flap syndrome, also known as trephonation syndrome or syndrome of trephonade. Essentially, what happens is that over time, because we're taking a closed system and making it open system, because of the significant swelling and pressure that's present, the tissues expand past the borders of the skull, but as things start to heal, we lose that pressure and our pressures start to normalize. But because of that event, there'll be a point where, because this, you know, turns into what I like to call an open box system, eventually the atmospheric pressure will start to compress on the brain tissues, which will cause the sinking of the flap, which, you know, in some of the more severe scenarios will cause mass effect, suckle effacement, or pushing of the brain tissues away from the craniectomy site, which essentially leads to, you know, kind of an atmospheric-related herniation system. When we're thinking about treatment for this, ultimately these patients do have to have the skull replaced in order to restore that closed box system, can typically done as early as one month. However, kind of up to the providers, we're typically, you know, performing cranioplasties at around the three-month mark, but there's several temporizing means that you can do to correct sunken flap, which can include, you know, lying patients flat or lying them in Trendelenburg, where essentially you're tilting them back and allowing for increased blood supply to the brain. So we're essentially, you know, filling up the tank, as I like to say, and causing, you know, swallowing of the tissue so that we can overcome the atmospheric pressure. You could also clamp an external drain if they have one, increasing the shunt settings so that it requires, so that if the shunts are draining fluid, it requires more force to drain the fluid off, or giving our patients IV fluids. This is a very common complication that we do see in the rehabilitation setting, so just for everyone to be aware of if it were to happen, how to appropriately manage it. Next, I'll be talking about post-traumatic seizures. So when we're defining seizures, this is sudden or transient alterations in consciousness, abnormal motor, sensory, autonomic, or psychic events that are usually due to abnormal or excessive electrical discharges of a set of neurons within the brain. We can further delineate seizures as, you know, being seizures, wherein it's usually just a single event, or recurrent seizures occurring after a traumatic brain injury. We start to term it epilepsy, where patients will have recurrent late seizures that are not attributable to other causes outside of the traumatic brain injury that occur after that initial seven-day period. And then there's also psychogenic non-epileptic seizures, or pseudo seizures, which is essentially episodic behavioral events that aren't associated with any sort of abnormal electrical activity. When we classify seizures, we can classify it in several different ways. The kind of first way that we'll typically classify seizures is when they were to occur. So if it's occurring within that first 24-hour period, those are termed immediate seizures. Early, if it's within the first seven days, and then late, when it's after the first seven days. Next, we can classify it based on type, where focal seizures can include essentially very specific motor, somatosensory, or autonomic, or psychic events, such as lip smacking, limb shaking, can be further subdivided in patients that have impaired consciousness, where it'll be termed complex versus no impaired consciousness. And then those seizures do have potential to evolve into bilateral convulsive seizures. Next, when we think about generalized seizures, that can be classified as generalized motor seizures, where you can kind of further classify it based on the movements, where they can be termed myoclonic, where you'll kind of see brief synchronous bilateral jerking of the extremities. Atonic versus tonic, where tonicity essentially refers to muscle tone. So in an atonic, our patients will look flaccid, versus tonic, where they'll have intermittent flexion and extension of extremities. And then tonic-clonic seizures, where patients will initially be stiff and then jerk. And then finally there's also non-motor seizures or what's also known as absence or absence seizures which are abrupt onset impaired awareness where patients will usually have fairly immediate return to kind of their normal cognition afterwards. There's various different risk factors and precipitants that can be associated with seizures but ultimately any sort of dural injury or injury to the tissue that's overlying the brain that can put patients at higher risk of having any sort of seizures. Also patients that are in a prolonged coma or have prolonged post-traumatic amnesia greater than 24 hours at increase of seizures. Anyone that has any sort of foreign body such as a gunshot wound is at increased risk of seizures. Any history of alcohol abuse, use of tricyclic antidepressants or increased age are also at increased risk of seizures. There's various different precipitants of seizures that can include hydrocephalus, sepsis, hypoxia or decreased oxygen. Any sort of metabolic abnormalities and potentially any significant mass occupying lesions which would include hemorrhages which is as we all know fairly common after traumatic brain injury. So when we're thinking about epidemiology in patients with non-traumatic brain injury roughly four to seven percent may have a seizure in the hospital, roughly 17 percent in the rehabilitation setting. It's much higher for patients with a penetrating traumatic brain injury and like I said patients with any sort of you know dural injury or loss of dural integrity which is that tissue that overlies the brain does have increased risk of seizures. Then roughly 50 to 66 percent of patients will experience a seizure within the first year which does increase to roughly 80 percent by the end of the second year and after five years patients that have sustained a moderate to severe cbis do remain at risk. When we think about seizure recurrence patients that have had an immediate seizure carry no or little risk of recurrence. Patients that have had early post-traumatic seizures or seizures within that initial seven day period may experience a late seizure in 20 to 30 percent of cases and then those individuals that have late seizures or seizures after that seven day period are also at higher risk of seizure recurrence. Usually 33 percent of patients with a first unprovoked seizure can be expected to have a second one within three to five years of that event. So when we're thinking about medical management of seizures after traumatic brain injury I do want to reference this landmark trial that was done which essentially looked at administration of an anti-seizure agent for prevention of post-traumatic seizures and what this study showed us is that phenytoin which was the drug that was used in this study could be effective in preventing seizures during that first week post-injury period. However no benefit was seen with continuation of prophylaxis beyond that initial first week period. So when we're thinking about how those results were translated to clinical practice typically what's you know standard of care now is to give patients a week of prophylaxis. If they don't have a seizure event then it's typically discontinued. Now Keppra is usually the preferred agent just due to better tolerability and ease of administration. However there's other agents that can be considered such as carbamazepine which can be helpful in preventing partial seizures or valproic acid which could be helpful in preventing generalized seizures. In patients that have had you know multiple seizures after traumatic brain injury if they do have a two-year seizure-free period it is reasonable to consider withdrawal of pharmacologic agents for those patients and then in patients where seizures might be refractory to medication management um can potentially consider can potentially consider some surgical options such as resection of the seizure focus vagal nerve stimulation or deep brain stimulation but that would be kind of in the more chronic setting. An important thing to also discuss since we're on the topic of seizures especially in my setting a lot of patients and their family members do want to know if it's safe for them to drive. States, different states and state regulations do vary so there is no kind of general consensus regarding a set seizure-free period. Usually it varies somewhere between 3 to 12 months however the American Epilepsy Society does recommend a seizure-free interval of at least three months prior to return to driving and then if adjustments are being made to the medication regimen or if we're considering tapering patients off of medications we typically recommend no driving within kind of the first three months of that initial like medication adjustment. Next we'll review acute endocrinopathies that can result after a traumatic brain injury. So briefly going over incidents um can occur in 80% of traumatic brain injuries but usually it's transient um when we're thinking about you know more chronicity um 15 to 60% of adults can have chronic endocrine um abnormalities and 42% of pediatric patients can have chronic endocrine abnormalities. Usually 30% of individuals will have some sort of endocrinopathy at around the one year mark. It's usually associated with increased morbidity and mortality um when we're thinking about predominantly acute issues that are most common to occur that's typically involving ACTH or the cortisol or our stress hormones or the posterior pituitary but initial abnormalities within you know these two systems don't necessarily predict chronic insufficiencies and what's thought of being you know the driving factor behind this is just due to the vascular axonal injury that results from the sharing forces after traumatic brain injury versus potentially being a side effect of some of the medical treatments that we do administer in this initial acute period. So next I'm going to kind of further subdivide our pituitary into the anterior pituitary and then the posterior pituitary and review kind of the most common endocrinopathies that are associated at least in the acute period. So starting with our anterior pituitary, our anterior pituitary is responsible for secretion of various hormones that include growth hormone, our sex hormones, our thyroid hormones, ACTH and cortisol, our stress hormones, and then prolactin. The number one you know insufficiency that we can see is alterations in our stress hormone which essentially supports our blood pressures in times of stress. What commonly occurs is what's known as adrenal insufficiency which can manifest as lower labile blood pressures and can be fatal if untreated. We test the integrity of this axis with provocative testing usually administering cosentropin where we're looking for a cortisol response greater than 18. Next can be alterations in thyroid hormone which is responsible for our body's metabolic activity. Typically what does occur is what's known as euthyroid sick syndrome where you'll essentially just have altered thyroid levels during periods of critical illness. However we actually do defer testing until after the period of acute illness because in the vast majority of cases it does self-correct. So my rule of thumb is usually potentially checking the integrity of the system or checking levels anywhere between that initial three to six months and then again at the year mark. Next kind of the big hormone that our posterior pituitary is responsible for is antidiuretic hormone which is important for regulating our physiologic water balance. Essentially it can be classified as either you know syndromes of hypernatremia or increased sodium levels or hyponatremia or low sodium levels. When we're thinking about higher sodium levels that's usually the result of central diabetes insipidus which is reduced ADH secretion. So typically how that how that'll clinically manifest is that our patients will have increased urine output. If we're looking at specific numbers that's greater than 200 cc's per hour for a period of two hours they'll have you know significant polyuria and will have very dilute urine. Can potentially develop transient SIADH which I'll delve into next but how we manage this is by giving them replacing the fluid that's lost as well as potentially administering desmopressin or you know synthetic ADH. The next two syndromes that are associated with hyponatremia or low sodium levels can be SIADH which is essentially an excess of ADH secretion. What we'll see is that our patient's plasma osmolarity will be more dilute and then our urine will actually appear to be more more concentrated. This is a diagnosis of exclusion is typically transient and treatment does usually include restricting the amount of fluids that our patients do intake potentially giving them salt tablets to help raise sodium levels and then in severe cases you can also give them dimeclocycline which essentially blocks the action of the antidiuretic hormone within our renal system. And then finally there's what's known as cerebral salt wasting which is a situation that can occur fairly commonly after traumatic brain injury where our patients are unable to resorb sodium so it causes renal overexcretion. So how these patients will typically look is that they'll look dehydrated clinically but then when you check the labs their sodium levels will be low. So usually just giving them a normal saline infusion can resolve those low sodium levels. The next common syndrome that I'll cover is what's known as paroxysmal sympathetic hyperactivity also known as sympathetic storming, autonomic dysfunction syndrome, paroxysmal autonomic instability with dystonia or paid syndrome. Again various different names however all generally referring to kind of the same clinical entity. So in order to understand this and you know kind of like ways that I like to describe it to family members is that when we're thinking about our autonomic nervous system that's typically what's responsible for our fight or flight response so as well as our rest and digest so you know activating in periods of stress and then and then calming down in periods of rest. So what's thought to happen after a traumatic brain injury is that essentially it causes a disconnection within this system so when patients are presented with you know potentially a threat or a noxious stimulus it throws our sympathetic nervous system into overdrive so you know increasing our heart rate, increasing our blood pressure, causing sweating and then usually our cortex can you know take in that information process that information and then release inhibit inhibitory signals to calm that down however after a traumatic brain injury our brain loses that ability to send those inhibitory signals so we remain in overdrive. But ultimately when we think about autonomic dysfunction syndromes there's a full spectrum of autonomic disorders that can range in severity and symptoms even after mild traumatic brain injury patients can develop autonomic dysfunction such as heart rate variability, abnormal tilt testing, feigning episodes, postural orthostatic tachycardia syndrome so not necessarily only present in patients with moderate to severe TBIs but when we're thinking about PSH this refers to paroxysmal transient increases in sympathetic activity after traumatic brain injury usually with the result of you know persistent catecholamine elevations which causes severe hemodynamic alteration and motor activity in response even to minor environmental or physical stimuli so like I said earlier patients are presented with you know a noxious stimuli it causes it causes our sympathetic nervous system to go into overdrive and because we can't fully process that information we're unable to downregulate those signals so typically what you'll see is increased heart rate, increased ejection fraction, increased blood pressure, redirection of blood flow from the GI system to our muscles, sphincter and muscle tightening it can happen up to 33% of patients after a traumatic brain injury and then usually when it does occur 80% of cases are usually after a traumatic brain injury and are more likely with patients that have sustained deeper brain injuries. When we're thinking about imaging findings it's usually associated with scattered lesions, diffuse axonal injury especially when we're looking at evidence of DAI in the corpus callosum or the interconnecting white tract matter between the two cerebral hemispheres or lesions within the posterior limb of our internal capsule or basal ganglia. How we'll see this clinically is potentially agitation, restlessness, diaphoresis, hyperthermia, tachycardia, hypertension, tachypnea or increased breathing, hypertonia and potentially posturing. I do have a star on tachycardia because I do want to specify and make a clear distinction with patients with spinal cord injuries because concomitant traumatic brain injury and spinal cord injury can occur. PSH has potential to seem very similar to autonomic dysreflexia which is essentially a similar situation that many spinal cord injury patients do have. However, the main distinction between the two syndromes is the heart rate wherein PSH you'll actually see tachycardia but in autonomic dysreflexia you'll actually see bradycardia and that's you know important to note just because the pharmacologic management of the two is different so we just want to make sure that we're giving the patients the appropriate medications especially in instances where patients may have a concomitant brain and spinal cord injury. When we're thinking about differential diagnosis, essentially episodes of paroxysmal sympathetic hyperactivity can be attributed to various different causes and can mimic various different types of syndrome so it's just important to be aware of that if it does occur it doesn't necessarily mean that it's solely due to PSH or overdrive of the sympathetic nervous system and it's important to rule out potential other causes first. But a way that we have of you know more definitively identifying PSH if it were to occur is what's known as the PSH assessment tool where essentially it's you know subdivided into a clinical feature scale and then a diagnosis likelihood tool where within the clinical feature scale you'll score patients based on how they're presenting and then in the diagnosis likelihood tool you'll you know take into account kind of all of the additional factors that the patients are presenting with. You'll add up the two scores together and based on the total score it can essentially identify as PSH being unlikely, possible, or probable. So not perfect but you know an assessment tool that we do have for potentially more accurately identifying this when it does occur. So when we think about management you know number one is you know getting an appropriate differential diagnosis and ruling out potential other causes, making environmental adjustments to minimize occurrence of avoidable secondary morbidity. We want to target the drivers of the paroxysms so ensuring appropriate patient positioning, making sure that our patients aren't constipated and having regular bowel movements, making sure that pain is controlled, and preventing significant pressure areas or areas that are at higher risk for pressure sores. We'll also check for potential sources, number one again looking at the environment, looking at the urine, making sure there's no you know potential infection, making sure our patients are having regular bowel movements, or making sure that our patients aren't developing new wounds or old wounds aren't being aggravated. Once we're able to make those environmental modifications and you know the episodes are still occurring, it's important to kind of have a tool that can help you determine which medications may be appropriate. When I'm initially you know managing these patients, typically I'll consider using Tylenol which is effective at you know helping manage elevated temperatures as well as giving some adequate pain control. Propanolol is a non-selective beta blocker that actually does decrease catecholamine levels post-traumatic brain injury and has been shown to be quite effective in managing PSH when it does occur. However, if it is refractory to increasing doses of Propanolol, it would be reasonable to add Bromocryptine which is essentially a D2 agonist that we frequently use in our patient population that can be helpful in managing some symptoms. If we do believe that the primary driver is pain related, we can potentially consider opiates or gabapentin. If one of the manifestations is manifesting as like posturing, spasm, muscle spasms, or increased tone, we can consider Dencholine, Baclofen, or benzodiazepines. And then if we're having a harder time regulating heart rates as well as blood pressures, we can potentially consider Clonidine. And then in those refractory cases, it would be reasonable to consider placing an intrathecal baclofen pump in those patients, which has been shown to help decrease rates of storming episodes, because ultimately uncontrolled storming does predispose our patients to worse outcomes if it's uncontrolled. Next, we'll just briefly review some vascular complications that can occur after traumatic brain injury. So two things that can be related are either traumatic aneurysms or blunt cerebral vascular injury. Both are fairly rare, can be subdivided into various types. We'll both essentially have variable clinical presentations. Typically when we're identifying that, we'll use MRI scan with and without contrast or angiography, and both can potentially include, when we're thinking about treatment, would include endovascular treatment, potentially surgical treatment, or in less severe cases, just antithrombic therapy. Next, what can occur is what's known as a carotid cavernous fistula. When we're thinking about our internal carotid artery, it's unique because it's a large artery that passes through a large venous space. So after injury, it can result in a direct fistula between the two symptoms. There's various different nerves that do pass within that cavernous sinus. So typically how that'll clinically manifest in patients is that they may have delayed visual loss, usually a month after the trauma. And typically when it is identified, it's usually an endovascular intervention involving a coil or balloon. Next is what's known as cerebral venous sinus thrombosis, which is uncommon. It's poorly understood, but generally just thought to occur because we are in a hypercoagulable state after traumatic brain injury. But patients with skull fractures and intracranial hematomas close to the sinus are at increased risk for development of this. But overall treatment is controversial, usually can either be antithrombic therapy versus full dose anticoagulation. Here's just a schematic of how the internal carotid artery passes through the cavernous sinus and the various nerves that are next to it that are at high likelihood to be injured if a fistula were to form between the two the two systems. And again, just demonstrating that a lot of the nerves that are next to it are nerves that are responsible for vision or eye movement, more specifically. The next complication that we can see after traumatic brain injury is what's known as post-traumatic hydrocephalus. It's, you know, the most common treatable neurosurgical complication that can occur and we do an overall treatment of this can have a dramatic effect on overall outcome of our patients in the rehabilitation setting. So it's important to be aware of this clinical entity when it does arise. So what is post-traumatic hydrocephalus or just hydrocephalus? So essentially it is the dynamic imbalance between the formation of absorption of CSF resulting in accumulation of CSF within our ventricular system causing dilation or enlargement. There's various different risk factors of this that include intracranial hemorrhage, specifically any sort of subarachnoid or interventricular hemorrhage, meningitis, or even potentially craniectomy. Ventriculomegaly or enlargement of the ventricles can be common after traumatic brain injury and doesn't necessarily translate to true post-traumatic hydrocephalus. Usually what's, you know, being referred to is ex-vacuo changes where there's a relative enlargement of the ventricular spaces, but that's simply due to the result of the tissue atrophy that results after traumatic brain injury. But incidence of true post-traumatic hydrocephalus is roughly an 8% of patients and its enlargement of the ventricles due to abnormalities in production flow or absorption of CSF. We can further subdivide this into communicating versus non-communicating where communicating essentially means that there is patent flow throughout the ventricular system, so you'll see uniform dilation throughout versus a non-communicating or obstructive where you'll have, you know, a focal blockage within kind of the various spaces of our ventricular system where you'll see dilation above the area of the obstruction, so it won't present as like a uniform dilation on imaging. When we think about symptoms in early post-acute, or in early post-injury acute hydrocephalus, we'll typically see signs of elevated intracranial pressure that can include headache, nausea, vomiting, lethargy, decreasing mental status. The classic triad of normal pressure hydrocephalus is typically ataxia or gait disturbance, urinary incontinence, urinary incontinence or dementia. However, in traumatic brain injury, we're not limited to those triad of symptoms, especially in the rehabilitation settings. It is important to consider in patients that aren't making, you know, adequate functional progress or beginning to plateau in therapy or having a sort of, you know, progressive decline, so it is important to screen these patients when those things do occur. On imaging, if we are, you know, trying to diagnose hydrocephalus on CT imaging, we'll typically see periventricular lucency or shadowing of the ventricles as a result of impaired, you know, CSF flow within the cells that line the edges of our ventricular system because those are responsible for both production and reabsorption. We'll also see sulfo-effacement or flattening of the gyri and then uniform ventricular dilation. How we do diagnosis, we can, you know, diagnose this in various ways, whether that's just a CSF tap test, so essentially we'll just remove roughly 50 cc's of CSF from the patients, and then we'll see an improvement in their cognitive status, or we can potentially place an external lumbar drain, which will provide continuous drainage for roughly a three to five day period, and then monitor how our patients do during the period where the CSF is being drained out. It can potentially have greater sensitivity and predictive value of shunt success ultimately, so it is something to consider in patients where potentially a shunt is being considered. When we're thinking about definitive treatment of hydrocephalus, that's typically with shunt placement, most commonly ventricular peritoneal shunts, however there can be shunts to other spaces such as our atria, pleural spaces, again all up to the surgeon that's performing the procedure as well as that patient's presentation, but shunts can potentially come with complications can potentially come with complications such as, you know, shunt failure or obstruction. It is a foreign body, so they are at risk for infection, can potentially cause seizures, can potentially cause over drainage of the system, which can result in chronic subdural hematoma, so it is important to have a regular follow-up and regular scans to ensure that the VP shunt is doing its job every so often in the more kind of like chronic period. Next, our cranial nerves are at increased risk of injury after a traumatic brain injury, mostly because these nerves do traverse over bony provinces and through bony canals. When we're thinking about the most common nerve that's affected after traumatic brain injury, that's usually our olfactory nerve or the nerve that's responsible for our sense of smell, but next would be our facial nerve or what's responsible for our facial movements, and then our vestibulocochlear nerve, which is responsible for hearing as well as our vestibular system or that system that helps, you know, regulate our sense of balance. Here's just the various different ways that we can perform cranial nerve testing. I won't, you know, belabor these, but this is here. Again, you know, testing smell identification, visual acuity, looking at eye movements, facial sensation and movement, assessing their hearing, looking for potential nystagmus, assessing a patient's swallow, seeing our ability to shrug our shoulders, rotate our head, and also looking at tongue movements. In patients that aren't, you know, cognitively intact and are more comatose, there's also ways that we can, you know, test the integrity of their cranial nerves by testing various different reflexes, so assessing like a visual threat reflex, a pupillary reflex, corneal reflex, oculocephalic reflex, potentially performing caloric testing, looking at a gag and assessing a cough, and that can pretty much give, you know, the majority of cranial nerves, the majority of the integrity of the cranial nerves that we're looking for. And then finally, last to note is that movement disorders are very common after traumatic brain injury and can be seen in up to 20% of survivors. Typically, when we're thinking about the various types of movement disorders that can occur, it can either be classified as slowness or poverty of movement, otherwise known as hypokinesia or excessive involuntary movements, known as hyperkinesia, can be seen in up to 22.6% of traumatic brain injury patients, are usually transient in 10% of cases, but usually have a more delayed onset. When we're thinking about the brain areas that are responsible for movements and causing movement disorders, that's usually seen in basal ganglia damage, damage to the superior cerebellar peduncles, and potentially secondary injury. Deep brain stimulation is typically the last line of treatment for all movement disorders, so if you're having difficulty controlling with pharmacologic management or, you know, it's refractory, something to consider for these patients. But tremor is actually the most common after traumatic brain injury, and it is an involuntary rhythmic oscillatory movement of a body part. Treatment can either be propranolol or that nonspecific beta blocker that I discussed before in management of PSH or storming, potentially carbidopa levodopa. Next is dystonia or sustained intermittent muscle contractions that cause abnormal positions or movements. Uncontrolled dystonia can put patients at increased risk for development of plantar flexion contractures. Usually treatment includes medications more directly, um, more effective at managing tone such as baclofen, dantroline, tizanidine, chemo-denervation, so that can include botulinum toxin injections, phenol nerve blocks, or potentially even intrathecal baclofen pump placement. Parkinsonism, which essentially refers to bradykinesia or slow movements. Rigidity, resting tremor, postural instability is usually associated with multiple head injuries. Treatment of choice for this is typically levodopa carbidopa. And then finally myoclonus, which is sudden or involuntary muscle movements caused by muscle contraptions and muscle tone lapses are very common after hypoxic ischemic brain injury and can predispose patients to what's known as Lance Adams syndrome or chronic post-hypoxic myoclonus, where you'll see, um, epileptiform activity that's associated with those abnormal movements. It's typically action-based and or appendicular, meaning that if patients are trying to initiate a movement, um, the myoclonus does get worse, so can be pretty functionally impairing to patients. So when we're thinking about treatment, it is important to be aggressive with treatment where, you know, initial choice of treatment can either be with Depakote or valproic acid, clonazepam, or Keppra. Um, I think Dr. Nasiri, I do have a couple of questions, uh, to see if you can comment on. One of which is when a patient is storming, so PSH like we've talked about today, uh, or has a TBI, what I commonly see happening is the utilization of Haldol in those patients, um, due to behavior. And I'm curious on your thoughts on Haldol for that population. Yeah, so very good question and definitely something that, um, you know, we do commonly see in the acute care setting. For the majority of, you know, brain injury providers, anytime we hear Haldol, that's like a big no-no for any of us. Um, so kind of jumping into kind of pathophysiology of traumatic brain injury. So the main neurotransmitter that, you know, we believe that's implicated in traumatic brain injury is an overall decrease in dopamine. And Haldol is one of the strongest antidopaminergic agents. So we generally recommend against use of, um, against use of Haldol in kind of all cases, whether or not that's for storming or behavior management in patients with traumatic brain injury, because it can put them at significantly, like, increased risk of, um, neuroleptic malignant syndrome. And it has also been shown to be associated with worse functional outcome. Like I said, like I kind of alluded to earlier, um, in patients where, you know, there is that concern about, you know, storming or PSH, it is important to rule out other causes. So making sure you're doing a comprehensive workup. Once that workup is negative, identifying potentially environmental causes that might be attributing to that, making those environmental modifications, and then really just going through the flow sheet and, you know, starting with ropanolol, potentially starting next to the romocriptine, and then your other medications to treat that. But I'm a strong advocate against Haldol and definitely don't recommend that for any patient after traumatic brain injury. Sure. Um, in a previous webinar within the series, uh, we got to hear from a family's point of view regarding, um, their family member stay and specifically around storming at that time too. And I think I'm kind of hitting storming a little hard just because it's a hot topic. Everybody wants to know more about it. And then you throw out the acronym PSH and everyone says, what is that? So I think it's something that, you know, we're shining a light on, especially with your presentation today. But with that question, you know, from a family's point of view, how do you explain to them in layman's terms, what's happening to their, their loved one, their child, you know, their spouse, whoever it may be, how do we explain to them in layman's terms about NARA storming? Yeah. Um, so I, I think, I think you alluded to a great point is that storming PSH pain syndrome has various different names and can be kind of very overwhelming and confusing for families. And I think there are, you know, various kind of like different work groups that are, you know, kind of looking for giving kind of that entity a singular name so that there can be more consistency when it is identified, but just knowing that essentially it's all referring to kind of the same thing. So if I do have a patient where, um, I'm concerned that storming is going on, um, how I, you know, kind of described it earlier is essentially that our body can't process, you know, stressful, um, information. So essentially what's happening is that, you know, our body is going into overdrive or, you know, having a stress response. And typically, you know, in you or me, um, our brain is capable of, you know, sending, um, sending those signals that can help calm, calm, calm us down, um, after we encounter a stressful response, but because of the traumatic brain injury, our brain can't send those signals that tell the rest of our body to quiet and calm down. So that's essentially kind of how I describe it to our patients is that they're essentially just on overdrive and their body isn't capable of telling itself to calm down. Yep. I think that's a great explanation. And, and going back to, you know, this is something that they don't have control of at this point, you know, it's not a voluntary thing for them that this is happening. It's chemical and, you know, the damage to the brain. So I think you explained that very well. And another question, I guess, too, from a provider standpoint, and even a family standpoint, when we're educating them is our pediatric population and kind of that teenage year where, when do we relate it to just typical age appropriate behavior versus something to be more cautious on the verge of going into that storming, uh, kind of symptom? Yeah. Um, so I think that's a good question. Um, you know, and, you know, good to address. I think it kind of depends on how the, um, the syndrome is, you know, manifesting in, in, in more comatose patients. We do, um, we do in more comatose patients, we do see kind of like that sympathetic overdrive and it, and it is more common in those patients. Um, so we're not necessarily seeing it in, in, in, in pediatric patients that are more, you know, cognitively, like intact. However, in like those instances where, you know, patients do have symptoms such as, you know, the tachycardia increased, um, increased heart rate, it's very important to approach that in a very like comprehensive multidisciplinary way. So in some of the patients that I see in the outpatient setting that are having symptoms of, um, of, you know, potentially storming or tachycardia or potentially even anxiety, I like to involve, you know, having like our psychologists work with them, you know, potentially discussing various like medications and then even having them work with therapists and giving them, you know, specific behavioral techniques, as well as, um, therapeutic techniques to help them overcome those episodes when they do occur. And just providing them with, you know, a comprehensive amount of like clinical support to help them overcome those symptoms when they do occur. I think that's a great answer. And kind of going back to the beginning of it, when you said it's kind of case dependent, honestly, you know, of what are they presenting as, and I think going back to, of, of what you've said in terms of, you got to rule everything out to determine we're storming, you know, make sure that it's not a UTI being discovered or anything like that, get a chest x-ray on them, those kinds of things to rule things out. So I think you hit the nail on the head. Great presentation, greatly appreciate your time and support for this large TBI series that we've been able to do through TCAA. So again, thank you. Thank you so much for having me.

Traumatic Brain Injury

TBI Rehabilitation

Acute Medical Complications

Epidemiology

Intracranial Pressure

Seizures

Cerebral Perfusion

Sympathetic Storming

Post-Traumatic Hydrocephalus

Multidisciplinary Approaches

post-traumatic complications

Monroe-Kelly hypothesis

hydrocephalus

paroxysmal sympathetic hyperactivity

seizures management