Traumatic Brain Injury

Species affected: felines, canines, humans, equines

Human Terminology: Inflammatory Bowel Disease, Crohn’s Disease, Ulcerative colitis


Traumatic Brain Injury (TBI) occurs in many species as a response to car accidents, falls, or other sources of traumatic impact that cause injury to the brain. Consequences associated with TBI can be subdivided into primary (immediate) or secondary (delayed) injury. Primary consequences of TBI are injuries directly relating to the impact, penetrating injury, or forces on the head and brain and consist of skull fractures, contusions, hematomas, and vasogenic injury. Secondary consequences occur when hypotension, alterations in blood glucose levels, increased intracranial pressure (ICP), tissue disruption, and systemic inflammation follow the direct injury and can be complicated by the presence of polytrauma. TBIs are often assessed as mild, moderate, or severe based on clinical presentation. Assessment, treatment, and prognosis of human and animal patients have many commonalities, making the canine a promising natural animal model for TBI.

Similarities in Humans and Animals:

The goals in stabilizing, diagnosing, and managing TBI patients – both human and canine – are very similar. When approaching a TBI case, the patient must be initially stabilized and assessed for hypovolemia, hypoventilation, hypoxemia, cerebral perfusion, changes in ICP, and metabolic activity. Patients with TBI may have other injuries that must also be identified early and treated appropriately for best outcomes.  As controlled studies in veterinary patients with TBI are lacking, common treatments in veterinary medicine are drawn from studies and experience in human medicine. In both humans and animals, elevated glucose levels can be an important indicator of severity of TBI, and hyperglycemia therefore influences treatment protocols. To neurologically assess human patients with TBI, the Glasgow Coma Scale (GCS) is used. An adapted version of the GCS, the Modified Glasgow Coma Scale (MGCS), is utilized to assess mentation, motor activity, and reflexes in veterinary TBI patients. Similar diagnostic samples and imaging techniques may be used in both human and veterinary medicine on a case by case basis.

Differences in Humans and Animals:

Differences in TBI occurrence and medical approach in humans and animals include cause of injury, diagnostics pursued and associated costs, and prognosis. Though vehicular trauma is listed as a common external cause of TBI in both human and canine patients, canine patients are more likely to suffer from this trauma both within the vehicle due to lack of seat belts and from hit-by-car incidents. Humans can suffer TBI from athletic activities, and the types of forces suffered in these activities affect the pathogenesis and cause diseases like Chronic Traumatic Encephalopathy (CTE).  Currently, no published studies have demonstrated CTE in a natural animal model. However, the complexity of TBI is highlighted by data indicating that the resultant tissue and cellular damage can vary even among patients with similar mechanisms of injury (Chodobski et al. Blood brain barrier pathophysiology in traumatic brain injury).

Diagnostic imaging availability also varies in humans and veterinary medicine. In human medicine, computed tomography (CT) is the imaging technique of choice for assessing hemorrhage or fractures as a sequela of TBI. In animals, CT and other advanced imaging modalities are not available at all veterinary hospitals, require sedation or general anesthesia of the patient, and can be cost prohibitive. Of note, although CT can aid in identifying structural abnormalities following TBI, studies have also demonstrated that early CT scans in canines have little prognostic value, and magnetic resonance imaging (MRI) may be better suited for assessing prognosis after TBI. Currently, neither imaging modality serves as a valid prognostic indicator in veterinary patients, and these diagnostics should only be pursued if the patient is stable enough to undergo anesthesia. Accordingly, veterinary management of TBI patients is often based on clinical presentation and focused on mitigating consequences of secondary injuries. Importantly, animals have a greater ability than humans to compensate for loss of cerebral function and can often have functional outcomes and good quality of life after suffering TBI (Sharma et. al., Retrospective evaluation of prognostic indicators in dogs with head trauma: (January-March 2011)). Further investigation into the differences between human and canine TBI patients may identify treatments that can improve functional outcomes for all patient types. 


Disease Etiology:

Traumatic Brain Injury occurs as a response to external impacts such as blunt or penetrating trauma.  Though the impact itself causes the initial mechanical brain injury, the disease process of TBI can encompass many secondary or subsequent issues.  The secondary injuries depend on the area of the brain affected, severity of impact or trauma, other traumatic injuries, and the following inflammatory processes. Fluid accumulation, i.e. hemorrhage and cerebral edema, occur commonly due to impact-induced vascular disturbances. Fluid accumulation within a rigid skull leads to increased ICP, which can impair blood flow and delivery of oxygen to the brain as well as drainage of fluid from the brain leading to herniation and cell death.  Additionally, with these disturbances a pathologic process known as excitotoxicity can create further damage to the patient. After trauma, an excess of excitatory neurotransmitters such as glutamate are released in the central nervous system leading to an imbalance of ions as calcium floods into cells and activates enzyme cascades capable of damaging cell components. Eventually, neurons must trigger apoptosis (programmed cell death) to end this energy-depleting cascade. Furthermore, as inflammatory cytokines and molecules travel through the blood to the site of damage, potentially aided by a disrupted blood-brain barrier, increased nitric oxide production by the arachidonic acid pathway and other responses lead to detrimental effects such as vasodilation and decreased blood pressure. This pathway also triggers the release of reactive oxygen species, which can damage cells, proteins, and DNA in the brain.  Ultimately, the cause of morbidity and mortality in many patients with TBI is brain tissue necrosis due to increased ICP.

Clinical Presentation:

Patients presenting with evidence of head injury or TBI must be thoroughly assessed in order to inform the diagnosis and case management. After stabilizing the patient, the GCS (human) or MGCS (animal) can be used to assess motor activity, brainstem reflexes, and level of consciousness of the patient. Utilizing the GCS/MGCS in combination with a thorough neurological exam once the patient is stable will inform the prognosis of the TBI. In humans, brain injuries are classified as mild, moderate, or severe based on the GCS score in the first 24 hours after injury, duration of loss of consciousness, duration of alteration of consciousness, imaging results, and post-traumatic amnesia (PTA). Affected humans and animals should also be assessed and treated for possible polytraumas or comorbidities. 


Upon clinical presentation, treatment guided by a primary assessment and triage focuses on stabilizing the patient and assessing all organ systems that may be affected. At this time, a clinician may pursue primary diagnostics to quickly assess affected body systems. Common tests in this phase include packed cell volume, total solids/proteins, blood glucose, lactate, liver enzymes, blood pressure, electrocardiography, pulse oximetry, and abdominal and/or thoracic focused assessment with sonography for trauma (AFAST/TFAST). After the initial assessment, testing is repeated serially or assessed by continuous monitoring to note changes in patient condition over time and in response to therapy.

Current treatments for TBI are often supportive and balanced to try and avoid secondary complications: restoring and maintaining adequate ventilation and blood volume, controlling seizure activity, nutritional support, glucose control protocols, pain management, and positioning to allow adequate blood flow and fluid drainage from the brain.  Hypothermia and treatment with medications such as mannitol, hypertonic saline, and naloxone may also be used when indicated. 

In human medicine, there is greater emphasis on examining the neurobehavioral effects of TBI, where changes in cognition, personality, and memory can be more readily observed. Diagnostic imaging such as CT or MRI may be pursued, especially in cases where need for surgical intervention is suspected. Information from the initial and repeated clinical and diagnostic assessments can inform prognosis and guide next steps in treatment. 

Unfortunately, there are limited evidence-based guidelines for the treatment of veterinary TBI, and clinical treatments aim to improve patient mentation and responsiveness while avoiding secondary complications. Many therapies for canine traumatic injury are guided by treatments performed in human medicine. In a recent internet-based survey of veterinarians (Evans et. al., 2019), common therapeutics for patients with TBI included mannitol, hypertonic saline, crystalloid fluids, elevated head positioning, oxygen therapy, and analgesics. 

Further research is needed in both human and veterinary medicine to help provide therapies and protocols that achieve the best outcomes for TBI patients. A 2020 consensus statement published by the human European Society of Intensive Care Medicine in order to provide guidance for the care of patients admitted to the intensive care unit with acute brain injury noted that evidence was “generally insufficient or lacking and research is needed to demonstrate the feasibility, safety, and efficacy of different management approaches.” (Robba C, et al. Intensive Care Medicine 2020. doi: 10.1007/s00134-020-06283-0)

Several evidence-based parameters exist in human medicine that inform prognosis: GCS score, presence or absence of pupillary light reflexes, hemorrhage on CT scan, and laboratory values for secondary injury such as glucose and prothrombin time. Prognosis in animals suffering from TBI is variable and difficult to predict, but loss of consciousness and loss of brainstem reflexes are the most valid prognostic indicators. Whereas some studies report that MGCS and early MRI can have prognostic value, other systematic reviews highlight the gap in veterinary literature for such prognostic tools in TBI. Continued research to improve assessment and treatment of naturally occurring TBI in dogs may help inform and improve treatment and outcomes in human patients. 


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