My name is Dr. Laura Black and I am a Pediatric Physiatrist at Riley Hospital for Children, Indiana University Health in Indianapolis, Indiana. Today I will be discussing Pediatric Traumatic Brain Injury. Before we begin, I have nothing to disclose. Another thing that I want to draw your attention to is that none of the medications in this lecture have FDA approval for the indications that I will be discussing. There is one exception, Diazepam or Valium has FDA approval for Hypertonia. We'll start with Epidemiology. When we look at our age 0-14 age group, there are approximately 475,000 traumatic brain injuries per year. Of these, the overwhelming majority, 90% are mild and are discharged home without need for further medical intervention. Like we see in our older population, there is a bimodal incidence of traumatic brain injury that affects the very young, the 0-4 years of age and middle to late adolescence as well. The most common etiologies are falls and motor vehicle crashes. We'll discuss the etiology of traumatic brain injury next. First I'll focus on the primary injury from traumatic brain injury, which is essentially the direct result of the traumatic impact and those forces on the brain. Those can obviously result in skull fracture. As you all probably remember, our brain is bathed in CSF and is inside the skull. You will have movement of the brain and collision between the brain and the inner surface of the skull can result in contusions. The rotational acceleration-deceleration forces can also result in shearing injuries of the long axonal tracks as well as vascular shearing in about 40% of pediatric traumatic brain injuries. The cellular shearing can result in what we call diffuse axonal injury and shearing of blood vessels can result in hemorrhage. Diffuse axonal injury cannot be well imaged on CT, so it's often not picked up in that initial emergent CT without contrast. The optimal imaging in DAI is MRI, particularly using the flare and diffusion-weighted imaging. DAI impacts certain structures in the brain more than others, namely the gray-white matter junction, basal ganglia, corpus callosum, which connects the two hemispheres of the brain, periventricular white matter, parasagittal white matter, as well as the long fiber tracks of the cortex and brainstem. What we see on the molecular level are increased excitatory neurotransmitter release and receptor upregulation, lipid membrane peroxidation, as well as increased intracellular calcium and free radical damage. We also see secondary injury. Secondary injury is defined as the downstream effects of primary injury. Some of this may be cerebral edema, cerebral vasospasm, infarcts due to vasospasm, seizure activity from the primary injury to the brain, as well as there will be periods of time where decreased cerebral blood flow will result in hypotension and hypoxic injury to the brain. No traumatic brain injury is without a component of hypoxic injury. The acute management from our colleagues in the emergency department, in the ICU, and in neurosurgery is really focused on reducing the secondary injury. Intracranial pressure reduction, thinking about hyperventilation, craniectomies to relieve intracranial pressure, as well as seizure management, which can then cause secondary injury to the brain. When we think about our pediatric patients versus our adult patients, I had mentioned before that the patients in the zero to four age group tend to have a higher death rate. We'll talk about some physiologic differences that can result in more vulnerability in these very small children. If you remember, infants have open sutures and less rigid skulls. There's more potential for movement in response to mechanical stress than our older children and adults. The other thing to consider is that infants and very young children have a larger head to body ratio. As children grow, the head to body ratio will decrease gradually, though the younger children are more likely to have head trauma because a greater percent of their body is their head. The other thing to consider is that very young children's neck muscles are weaker. Rather than vertebrae assisting with cranioservical stability, you have more dependence on those ligaments that are much more flexible. The other thing to consider is that myelination, that process does not really finish up until around the age of three. Infant and young toddlers are less myelinated and these unmyelinated regions are more vulnerable to traumatic brain injury. They can transmit forces more easily to deeper structures than myelinated regions. Another thing is because of our biochemical and molecular mechanisms that we talked about earlier with secondary injury, is that children are more likely to have diffused cerebral edema than adults. This is thought to be secondary to more diffusion of excitatory neurotransmitters through the brain in children, as well as impaired cerebral autoregulation. What you are more likely to see in young children is this classically described lucid interval after a traumatic brain injury, and then you see the flare-up of the cerebral edema. This results in a neurologic decline. Another thing to think about is that children are moving targets from a developmental standpoint. We expect them to not only maintain their cognition, but reach developmental and cognitive milestones throughout their childhood. One thing that this means is they can grow into their deficits. If you have a child who was injured in a car accident at the age of nine months, they may after rehabilitation achieve age-appropriate milestones at, let's say, 12 months. But then once they get to maybe third grade, or earlier, or later, they may have difficulty with learning that may have been a result of that early traumatic brain injury. It's difficult to say, though, because they may have had that difficulty with learning even if they didn't have the brain injury. The skills that are developed early in development are most often what's spared. Cerebral atrophy can also be seen in traumatic brain injury. It may be from the brain injury itself or subsequent impairment in growth. One of the most difficult parts of my job in pediatric rehab is non-accidental trauma. When we look at incidents, it occurs in approximately 2.36 per 100,000 children nationally. Because of these physiologic vulnerabilities, infants under the age of one have the highest mortality. NAT, or non-accidental trauma, also has higher mortality than other injuries. When we think about our car accidents or accidental falls, and we'll talk about some reasons for that a little bit later. Risk factors for NAT are delay in prenatal care, low birth weight, as well as socioeconomic stressors. As you know, those three risk factors are often interrelated. I mentioned that outcomes are often worse in NAT. Some of this is because there is a delay in care. These children are often not brought in right away for assessment. They may have more of a hypoxic component than a child who sustained accidental trauma. Some warning signs are that the caregiver account of the history doesn't add up. They may describe a mechanism of a fall that doesn't match up with what a child should be able to do developmentally. For instance, three-month-olds rolling off the couch. Initial presentation may be drowsiness, irritability, vomiting. These patients are more likely to have seizures and apnea than other etiologies of brain injury. When we look at our imaging findings, I have here on my left bilateral retinal hemorrhages, which are pathognomonic for non-accidental trauma, as well as bilateral subdural hematomas. Also, we talked about that increased hypoxic component in these children. When we think about that delay in care, that often results in more hypoxic injury than other etiologies. When we think about our mechanisms of injury of how children are injured in abusive head trauma, shaking comes to mind. That's what we think about classically. We think about our bridging vein tears resulting in subdural hematomas. The other thing, when we talk about those more flexible ligaments, cervical spinal cord injury can also occur by this mechanism. Blunt force trauma can also happen. This is often manifested by subdural hematomas in the brain and spine. We'll move on to talk about prognostic factors in all patients with pediatric traumatic brain injury. Some of the poor prognostic factors that we think about are hypoxic injury, like I mentioned. Subarachnoid hemorrhage is a poor prognostic factor, one, because it's associated with higher energy injuries, and second, because of its association with cerebral vasospasm and downstream secondary injury that can result in more deficits. Basilar skull fractures are also more likely to occur in higher energy injuries. Midline shift, again, suggestive of significant bleed or cerebral edema, autonomic dysfunction, as well as a fixed pupillary reaction. One thing to think about when we compare our pediatric patients to our adult patients is that children with fixed pupillary reactions may do a bit better long-term than adults with fixed pupils. Also, our Glasgow coma scale after resuscitation is an important prognostic factor, length of time in coma, or unresponsiveness. Moving along with this a little bit is the length of time to follow commands, and as well as what we see in our adult population is that duration of post-traumatic amnesia, which is arguably one of the most important prognostic factors after traumatic brain injury. The Glasgow coma scale, or GCS, is widely used in assessing severity of brain injury in adults in the acute setting. This will review back to your adult TBI knowledge, but we have our eyes, motor, and verbal categories. The score is three, the minimum score is three, and the maximum score is 15, with three obviously being the most impaired, and 15 being essentially normal function in those upper three categories. I'll show you on the next slide a modification on the scale for pre-verbal children, so children under two years of age. If you are going to expect an infant to follow commands, that is not a realistic goal. A GCS of eight is indicative of coma and severe TBI in adults, although one study in children ages two to ten, so our toddlers to school age, suggests that a GCS of five should be a cutoff for severe TBI rather than eight, because it seems that according to these authors, the children that are aged two to ten, that between five and eight, they tend to do better than adults in that same category. And GCS has been shown to correlate with cognitive outcomes. In terms of the pediatric for pre-verbal children, so our kids under two, the GCS is modified as follows. The eyes scale or proportion is exactly the same as the adult GCS. I have the adult scale on my left, and the pediatric scale on the right. Essentially, verbal and motor are different. So when we look at getting two points for the verbal, you are getting moans as opposed to incomprehensible sounds. And essentially, you are getting crying to pain, irritability, crying, as well as cooing and babbling to get the full five points, just because, like I mentioned, children under two will not be oriented. For motor, you will see essentially everything looks about the same until you get to the score of five. You should see rather than localization, which you see in adults to pain, is withdrawal to touch or light sensation. And rather than following commands to get the full six points in your motor, you see a spontaneous movement rather than following commands. Post-traumatic amnesia, or I will abbreviate it as PTA, is defined as the period of time where the patient is confused and unable to form new memories. And what we see in school-aged children is that the duration of PTA is the strongest predictor of outcome in TBI. And there are a few ways to measure this. Serial assessment, essentially you need to assess orientation and ability to form memories of new events over several days until somebody can consistently do it. So one of the more commonly used PTA assessments is the COAT, or the Children's Orientation and Amnesia Test. And it was developed for hospitalized children. But one thing that you need to use caution with is that if a child had some pre-morbid intellectual disability or cognitive impairment, you may see that reflected on the COAT rather than the impairment secondary to the traumatic brain injury. So that's something you have to be very aware of the child's pre-morbid cognitive functioning. The other scale that is used was initially developed for adults. It's called the Westmead Post-Traumatic Amnesia Scale. And that has been translated for use in school-aged children. So complications of TBI, a lot of this is going to parallel our adult population. So when we think about our disorders of consciousness, agitation and aggression, motor impairment, cognition communication problems, dysphagia, neuroendocrine abnormalities, autonomic instability, post-traumatic epilepsy, and heterotopic ossification. And we'll go into a few of these topics in more detail. So first of all, we'll talk about autonomic dysfunction. There are a few different names for this. Paroxysmal sympathetic hyperactivity, or PSH, central autonomic dysfunction. And what you'll often hear on the inpatient rehab unit is autonomic storming or neurostorming. And we see this phenomenon in approximately 13 to 14% of children with severe TBI. And remember, this is a poor prognostic feature. And what we notice is increased sympathetic activity. Potential to see tachycardia, hypertension, hyperthermia. You may see diaphoresis. And a patient may appear extremely uncomfortable. Increased motor posturing as well, you may see. So the etiology of why kids with brain injury have central autonomic dysfunction is unclear. It may be because they're, due to the brain injury, there's an imbalance between sympathetic and parasympathetic nervous system activity. It may also be because there's increased circulation of catecholamines in the bloodstream. So managing PSH, what you first wanna do unless you have a child that's storming every night and has had a extensive workup for infection recently, is you want to rule out infection. So often doing a CBC with differential to see if they have an elevated white count and neutrophilia can be very helpful. If possible, really doing, working with your nursing colleagues and identifying the trigger. It may be they need suctioning. It may be GI distress, so gas pains, constipation. Pain may also be a problem. They may also get better with repositioning, and this could be pain-related. The other thing to keep in mind is if they are hyperthermic or diaphoretic, you wanna start out using environmental cooling measures for hyperthermia. So thinking about fans, ice packs, particularly in the axillary area, and taking off any sort of blankets. Medications that we've used for central autonomic dysfunction include propranolol. That one's particularly helpful with patients who have high heart rate. Bromocriptine as well. There's anecdotal evidence that it can address hyperthermia. And diazepam, which is helpful if there's a tone component, and clonidine, which is helpful for tachycardia and hypertension. Post-traumatic epilepsy is another complication that is often seen after brain injury in kids, and it's more common in children with TBI than adults. And we classify it into three different categories. So we see the immediate post-traumatic or post-seizures, and these are the majority of seizures in pediatric TBI, and they occur within 48 hours after brain injury. Early seizures are defined as seizures that occur within the first week after injury. So the incidence is somewhere between 20 and 39%, and we really see the highest risk of early seizures after TBI in age under two. Late seizures may occur anytime from weeks to years post-injury. The incidence is generally lower, seven to 12%, and the highest risk is in the infant age group, so under one year of age. There's no evidence to suggest that AED, or anti-epileptic drug prophylaxis, prevents development of late seizures. So it's important to note that early seizures and late seizures don't necessarily correlate with each other in children. We talked about how children are at higher risk for epilepsy in adults, and we also talked about how AED prophylaxis, it's difficult to tell if it's helpful. There's not much evidence for it at this point in time. It's important to obtain an AEG prior to weaning an AED. To look to see if the patient is either having subclinical seizures or is at risk for epileptic discharges. So the other thing, and this is similar to adult brain injury, are considering regulation of sleep-wake cycles. So not only is sleep potentially helpful in neuro-recovery and reducing inflammation, it's also important for brain maturation, which is occurring rapidly as children grow. Patients with acquired brain injury are noted to have difficulty with initiating sleep and maintenance compared to controls. And it can be difficult, particularly in the hospital environment, to determine whether this is secondary to brain injury and disorientation, poor regulation of sleep-wake cycles, or worsened by the hospital environment, particularly in the ICU. And those things can be definitely more difficult to tease apart, especially in the acute phase. So agitation and aggression in traumatic brain injury, you see different phases during recovery. So in early recovery, when you think about your Rancho Fours, you can see that physical agitation and motor restlessness. Later on in recovery, you can see aggression and irritability, but sometimes they can have similar triggers. The first thing you wanna do with managing either agitation or aggression is our environmental measures. So thinking about reducing light, noise, any other noxious stimuli. So not only turning down the volume of voices, but minimizing the number of people in the room. The other thing is if there are known triggers that set off agitation, trying to avoid them as possible, because it's much easier to avoid than to try and deescalate the situation. The other thing is thinking about sources of discomfort that may be making this person agitated. So perhaps it's pain from a fracture. It could be discomfort from constipation or nausea. Thinking about those potential triggers. And part of this is if there is an environmental measure that can reduce agitation or aggression, you're avoiding the risk of sedation as well as impairment of neuro-recovery with medication management. In terms of medication management for agitation, there really is limited evidence for what works in children. We often have to extrapolate based on what works in adults. There was a meta-analysis in adults with traumatic brain injury done in 2017 that noted some improvement in agitation with the following agents. So propranolol, methylphenidate, valproic acid, and olanzapine. The agents that showed mixed results were sertraline and amantadine. And one of the things to consider, so anecdotally, there's a potential to see some increased agitation with methylphenidate as well as sertraline because both are activating agents. Also, diazepam is often used in pediatric populations, particularly when there is tone involved, increased hypertonia. Heterotopic ossification, or HO, can also occur during any period of immobility, and TBI is one of these. And it's defined as the formation of bone at any extra-oscious site. And it's most often seen in the connective tissue. In pediatric TBI, it's most seen in the hip and knee, and it often occurs in the one month after traumatic brain injury. We see it more often in children over 11 years of age. HO is managed differently after it matures, and in general, the transition from immature to mature HO occurs around one and a half years after TBI. In immature HO, bisphosphonates can be used as well as indomethacin. There's also some evidence for radiation therapy as well during this stage. For surgical management of HO, you really have to wait for the HO to mature. And even then, you can see a recurrence in about a third of patients with mature HO that undergoes surgical excision. It appears that some combination of prophylactic bisphosphonates, radiation therapy, and surgical resection reduces recurrence risk. It's also very important after HO is identified as well as patients that do not have HO is to continue with range of motion exercises because you really want to prevent contracture in the area as well as preserve joint function. So thinking about cognitive and academic outcomes, academic skills, not shockingly, are impaired in children six months after TBI, and they persist up to five years post-injury. With cognitive recovery and neurologic recovery, you can see some improvement in the first year after injury. Children with severe TBI are most likely to need school support. So when we think about needing an IEP or an individualized education program, that refers to any sort of modification of the curriculum. And that may be getting extra supports or tutoring within a typical classroom or a self-contained classroom for children with disabilities. Children with mild to moderate TBI were less likely to have school services early on, but what's interesting is that they often had similar school support needs as children with more severe TBI at six years post-injury. Part of this could be because their deficits were more subtle. The other thing to think about is, are these children growing into their deficits? So what's so important are meeting academic needs after TBI, is transitioning information between healthcare professionals and the school. Many inpatient pediatric rehab units have a school teacher, they are invaluable members of the rehabilitation team because they can help facilitate this communication and transition back to school. So I'll briefly discuss pediatric stroke. So the etiology of stroke in children is very different. The incidence is also much lower in children than adults. You're more likely to see congenital diseases and vascular malformations contributing to stroke. So when we think about our hemorrhagic stroke, you have the potential for arteriovenous malformation resulting in that. With ischemic stroke, sickle cell disease can contribute to that as well as congenital heart disease. About 50 to 80% of children after stroke have hemiplegia and have impact on their language function, as well as executive functioning. The conventional wisdom is that children make better recoveries than adults do after stroke. But again, we see this concept of children growing into their deficits, i.e. they're not reaching milestones rather than losing function. There's also limited evidence. This is a common theme in pediatric rehab in general for rehabilitation interventions in pediatric populations, though much is extrapolated again from studies in adult stroke. So we see many of similar upper extremity interventions, so constraint-induced movement therapy, which has significant evidence based in the adult population as well as children with congenital hemiplegia, as well as forced use. And gait training is commonly used in lower extremity interventions as in many rehabilitation neurologic diagnoses. So thank you very much for your time and attention. I am going to briefly go through my references.

pediatric traumatic brain injury

TBI epidemiology

skull fractures

diffuse axonal injury

cerebral edema

non-accidental trauma

rehabilitation interventions