All You Need to Know About Traumatic Brain Injury in Dogs & Cats | VETgirl Veterinary Continuing Education Podcasts
December 2024
In today’s VETgirl online veterinary CE podcast, we’re going to talk about traumatic brain injury (aka head trauma) in small animals. We will discuss the clinical presentation of these patients, important monitoring tools, treatments, and prognostics.
Does thinking about traumatic brain injury make your head hurt? In today’s VETgirl podcast, we are going to help alleviate that as we discuss the workup and treatment of traumatic brain injuries (commonly referred to as TBI) in small animals. TBI can occur from any blunt force trauma to the skull. In dogs the most common cause of TBI is from vehicular trauma, and crush injuries are the most common cause in cats. We suspect TBI in our patients that exhibit external lesions around the head and neck or a history consistent with blunt force trauma like being hit by a car, and having signs of altered mentation, maybe some abnormal pupils, heavy breathing or tachypnea, and they may have an abnormal gait or complete inability to stand or walk.
First let’s start at the initial traumatic event…the direct injury to the brain. This encompasses things like contusions, hemorrhage, and edema, are these are referred to as the “primary injury.” Now, the cranial vault is a fixed space- within it is the brain, blood supplying the brain, and the cerebral spinal fluid bathing the brain. An increase in size or volume of any one of these compartments, causes an increase the intracranial pressure because the other 2 have nowhere else to go. So when the brain swells, the increased pressure collapses the blood vessels in the brain and we lose some of our blood supply to the brain. Then we deal with “Secondary injuries,” which refers to all the damaging changes that occur in the brain as a sequela to the primary injury such as chemical changes, oxidative changes, and changes in blood flow to the brain. These can appear within minutes or hours to days after the initial insult and cause cellular death. So the main goal of managing patients with TBI is to help prevent or at least limit the secondary injury to the brain by closely honing in on changes in the patient’s blood pressure, arterial oxygen and carbon dioxide partial pressures, and electrolyte imbalances. We want to avoid hypotension, hypoxemia, hyperoxemia, hyper- and hypocapnia and electrolyte imbalances.
Starting from the time of triage, animals with TBI often present with a variety of additional injuries from whatever event caused their blunt force or crushing trauma in the first place, so it’s always important to perform a primary survey of these patients first to address any of the life-threatening abnormalities – broken bones can absolutely wait a minute! As a quick refresher of the primary survey, it’s a way of performing your first physical examination of a pet that focuses, in priority order, on the body systems that can present with critical, life-threatening conditions that could cause sudden death if we don’t stop everything and address these concerns in a timely fashion. First, we look at the Airway, then Breathing, then Cardio, and then we get to Dysfunction (neuro). So your patient should be be first assessed and stabilized according to this algorithm before performing a more thorough evaluation of the pet (your secondary survey). In patients suffering from TBI, we will often find they have an altered mentation and are dull, stuporous, or sometimes even in a coma or possibly even exhibiting grand mal seizure activity. Remember the adage, “The pupils are the window to the brain”? Well, you definitely don’t want to skip performing evaluation of the eyes because this can tell us a lot about what’s happening in the brain at that moment. Patients with TBI may or may not have pupil size incongruity, miotic pupils or mydriatic pupils, with reduced or asymmetric pupillary light reflexes and all these ocular abnormalities can reflect on what the brain is experiencing in regards to intracranial pressure and the possible risk for sudden brain herniation from these pressures. Acute pupillary dilation should be emergently addressed as this may represent herniation and compression of the oculomotor nerve. Blood pressure and heart rates are also important pieces of triage information for these patients because if your dog has a low heart rate and concurrent hypertension, this could indicate that the intracranial pressures are dangerously elevated and brain herniation is potentially on the horizon so fast action is needed. The identification of bradycardia and hypertension is called the Cushing’s reflex – and no this has nothing to do with overstimulated adrenal glands. Be careful in cats because yet again they don’t read the book and so the Cushing’s reflex may not be as evident in them as it is in dogs.
For the most part, our physical exam is going to tell us enough information to raise our suspicion for traumatic brain injury, but if you have access to advanced imaging, this can help us diagnose, localize, and describe the brain injury, which can be useful information in determining next steps and prognosis for TBI patients. While skull radiographs are easier to perform and more readily available, these only show us defects in the skull bones, so if we want more information about what’s happening to the actual brain, a CT or an MRI is going to be more helpful. If a CT is readily available, these are fast nowadays and can be done with little or perhaps even no sedation depending on your patient’s condition. CTs can identify both skull fractures and brain damage, and they don’t cost as much as an MRI. But MRIs are superior in identifying with higher imaging detail the soft tissue structures of concern such as brain bruises or edema, nerve injuries, and bleeding around or in the brain. The main setbacks of MRIs are their cost, and the requirement for anesthesia which can be challenging in these critical patients. So, while both CT and MRI have their strengths, CT is usually the first pick for quick and detailed brain images in pets immediately following head trauma.
If anesthesia is required for the patient with TBI, it can absolutely be done! We just have to consider some important physiologic concerns in the body and how our anesthetic agents and pain medications may affect these. Even outside of the realm of anesthesia, pain control is crucial for these patients, not only for patient comfort to alleviate that massive headache, but also to help avoid increasing the cerebral metabolic rate which can potentially increase our secondary brain injuries. So don’t shy away from giving these patient pain medications even though they may have an altered mental state. Getting back to anesthesia considerations, it’s important to be aware of how analgesia and anesthetics can affect cerebral blood flow, respiratory rates, and blood pressure. If we think of what’s happening inside the skull of a patient with TBI, their brain is swelling from inflammation from the impact, but it’s trapped inside a skull that won’t expand. So swelling of the brain trapped inside a fixed space causes compression of the blood vessels in the brain resulting in poor circulation and blood supply to the brain tissue. The body responds by increasing systemic blood pressure to try to push the blood up to the compressed brain, so these patients can often be hypertensive, but for a very good reason. We have to be careful with our anesthetics not to cause hypotension or this will further decrease the brain’s blood supply. Propofol and opioids are typically good choices as they cause only minimal changes in cerebral hemodynamics. However, do be careful not to push Propofol too fast as this can cause hypotension. Inhalant anesthetics can increase intracranial pressure and should be avoided when possible in patients with TBI, and instead opt for total intravenous anesthesia (TIVA). Ketamine has neuroprotective properties that may be advantageous in TBI patients, so has been recommended in recent years which overrides our original concern of ketamine’s potential to increase systemic blood pressure and therefore intracranial pressure. Nausea is expected in patients with TBI secondary to the elevated intracranial pressures and opioids may also cause some nausea, so ALL brain trauma patients should receive injectable anti emetic medications as a standard treatment for this condition. Fluid therapy must be carefully monitored so as not to exacerbate cerebral edema or intracranial pressure with high fluid rates and volumes – titrate your fluid therapy carefully to the patient’s needs and do not try to over-hydrate them. During anesthesia and recovery, it’s crucial to keep pets from vomiting, coughing, or sneezing as these actions cause spikes of increased intracranial pressure that could cause sudden death if the brain herniates from these spikes in pressure.
Most of our treatments utilized in the management of TBI center around preventing and limiting secondary brain injury by reducing intracranial pressure, maintaining cerebral perfusion pressure, and preventing free radical production. It is recommended to avoid both hyper- and hypoventilation. Hyperventilation will cause lower arterial CO2 pressures, causing vasoconstriction in the brain, and although this does lower intracranial pressure slightly it’s at the cost of reducing blood supply to brain. Hypoventilation causes increased arterial CO2 pressures, producing both vasodilation of the blood vessels and subsequent increase in intracranial pressures. While oxygen supplementation is good to provide to these patients, patients intubated with 100% oxygen can develop superoxide free radicals that increase secondary injury so best not to have patients intubated on 100% oxygen for long. Nasal oxygen catheters should be avoided as well as jugular venipuncture to prevent any sneezing, coughing, or compression of the neck that can lead to increased intracranial pressure.
Hyperosmolar therapy such as mannitol and hypertonic saline are used to help shift water out of the brain thereby reducing intracranial pressure. Presently there is no consensus in human or veterinary literature to support the use of one over the other; however there are some notable differences. Hypertonic saline is best in patients with a normal sodium, or only slightly elevated sodium levels, because prolonged hypernatremia can be detrimental in TBI patients. Hypertonic saline has immunomodulatory benefits such as suppressing cytokines and reactive oxygen species formation. There’s another theorized benefit that when it is unknown if there could be a brain bleed, hypertonic saline may be safer than mannitol owing to the ability of sodium to cross the blood brain barrier out of the brain, whereas mannitol being a larger molecule will leak with the blood into the brain and get stuck there, thus pulling fluid with it and exacerbating swelling inside the brain. Hypertonic saline is also preferred over mannitol in hypotensive and hypovolemic patients and those with kidney disease. The main benefit of mannitol is that as a larger molecule, its effects will last much longer. Some have tried hypertonic saline CRI’s for a longer duration of effect, but this has not proven to create the desired effect and is not recommended at this time. Mannitol also has free radical scavenging properties and produces cerebral vasoconstriction which reduces intracranial pressure. Hypertonic saline is typically bolused at 2-5 mL/kg over 10-20 minutes (personally I use 2ml/kg in cats and 4ml/kg in dogs both over 10 minutes, but use whatever dose in published reference ranges are easy for you to remember on the fly!). Mannitol is typically dosed at 0.5-1 g/kg IV over 15-20 minutes and must be administered with an inline filter. Steroids and furosemide should be avoided in TBI. Patients should be positioned on a slanted board to elevate their head 15-30 degrees- the board technique is safer than rolled towels under the head just because the rolled towels can compress the jugular veins and increase intracranial pressure. Seizures can be caused by TBI in the acute phase, or can develop weeks to months after the traumatic brain injury, or never develop at all. Presently there is no recommendation to prophylactically start anticonvulsant therapy, but honestly leviteracetam isn’t contraindicated to just start either. Any active seizures should absolutely be treated – this isn’t one where you want to wait and see if more seizures occur because these seizures associated with TBI can be incredibly refractory to anticonvulsants.
Prognosis of TBI patients varies. Monitoring trends in Modified Glasgow Coma Scale (MGCS) scores may be predicative of survival in both dogs and cats within the first 48 hours after head trauma, and hyperglycemia in dogs and persistent hypernatremia in dogs has been associated with a worse prognosis. Neurologic recovery can take time and some neurologic deficits or abnormalities can persist months or even lifelong. But these patients can also do really great! So I always tell owners that although these patients may look severely affected at first, you have to see how their neuro status changes with time, get them through the first 48hrs of swelling and bruising if you can, and then see how they respond after this.
So what can we take away from today’s VETgirl podcast? While TBI can feel like a scary and overwhelming condition to manage, it’s more of a “do no harm”, watch, and wait. So do no harm with your physical restraint and positioning of the patient (no jug sticks!), watch your patient with serial heart rate and blood pressure monitoring for trends that might suggest increasing intracranial pressure, and serial Modified Glasgow Coma Scale scores to help with prognostics and also for the patient’s response to your treatments like hyperosmolar therapies. I also like to make a pupil position chart to have my techs or doctors fill in every 2-4hrs where they color in the relative pupil size and position because if the eyes are changing, it’s a pretty good indication that the brain is changing too! And then the rest is just a waiting game as the patient’s body needs time to heal. Remember no matter how bad these patients look after the initial injury, we don’t need our dogs and cats to be able to read the newspaper, we just need them to eat/drink and have good quality of life snuggling and interacting with their pet parents.
Reference:
1. Sande A, West C. Traumatic brain injury: a review of pathophysiology and management. J Vet Emerg Crit Care (San Antonio). 2010;20(2):177-190.
2. Cameron S, Weltman J, Fletcher DJ. The prognostic value of admission point-of-care testing and modified Glasgow Coma Scale score in dogs and cats with traumatic brain injuries (2007–2010): 212 cases. J Vet Emerg Crit Care. 2022;32:75–82.
3. Her J, Yanke AB, Gerken K, et al. Retrospective evaluation of the relationship between admission variables and brain herniation in dogs (2010–2019): 54 cases. J Vet Emerg Crit Care. 2022;32:50–57.
4. National Institute of Neurological Disorders and Stroke. Traumatic Brain Injury (TBI). https://www.ninds.nih.gov/health-information/disorders/traumatic-brain-injury-tbi. cited 2024 Jan 18.
5. Carney N, Totten AM, O’Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury, Fourth Edition. Neurosurgery. 2017;80(1):6-15.
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