Traumatic brain injury (TBI) is a frequent component of head trauma in small animals. The most common cause is motor vehicle accidents in dogs and crush injuries in cats. In humans, guidelines for TBI treatment are focused on maintaining cerebral perfusion, reducing intracranial pressure, and treating secondary injury. In veterinary medicine, most clinical recommendations are drawn from human studies and clinical experience.<\/p>\n
To maximize the chance of recovery, expedient and aggressive therapy must be initiated. Treatment includes addressing life-threatening injuries first, followed by supportive care, and in some cases surgery. Prognosis can be best estimated using the Small Animal Coma Scale. Hypotension, and thus reduced cerebral perfusion pressure, is a negative prognostic indicator. This article reviews the pathophysiology of head trauma, patient assessment, diagnostic testing, treatment recommendations, monitoring, and prognosis.<\/p>\n
Take-Home Points<\/strong><\/p>\n Traumatic brain injury (TBI) is a frequent component of head trauma in small animals. TBI is associated with high morbidity and mortality in both animals and humans. Etiologies are most commonly motor vehicle accidents in dogs and crush injuries in cats.1<\/sup> Falls from heights, gunshot wounds, bite wounds, and accidental or purposeful attacks from humans are other causes. Recovery is enhanced by early and aggressive therapy. Treatment is focused on maintaining cerebral perfusion pressure (CPP), reducing intracranial pressure (ICP), and treating secondary injury. This article reviews the pathophysiology of head trauma, patient assessment, diagnostic testing, treatment recommendations, monitoring, and prognosis.<\/span><\/p>\n Mean arterial pressure (MAP) minus ICP is the CPP. The Monro\u2013Kellie doctrine states that the volume of brain parenchyma, blood, and cerebrospinal fluid is constant, and any change in volume without compensation leads to an increase in ICP. Usually, there is a high intracranial compliance and a minimal effect on ICP with fluid shifts in the brain vasculature and cerebrospinal fluid.<\/span><\/p>\n When the volume-buffering capacity is exceeded beyond the limits of compensatory mechanisms, the ICP will increase. Increased ICP leads to a decrease in CPP, cerebral ischemia, and neuronal death. Severe increases in ICP trigger a cerebral ischemic response called the Cushing reflex (manifested as hypertension with bradycardia) in an attempt to maintain appropriate CPP. The Cushing reflex occurs with an acute and severe increase in ICP, which results in a decrease in cerebral blood flow and thus an increase in carbon dioxide. The Cushing reflex occurs in terminal stages of brain herniation and is indicative of possible life-threatening elevations in ICP; thus, aggressive treatment should be initiated. Prior to this stage, there is likely failure of other hemostatic mechanisms related to Pco2<\/sub> (partial pressure of carbon dioxide), blood pressure, cerebral metabolic rate, and pressure autoregulation.<\/span><\/p>\n Primary brain injury is the direct physical damage from the traumatic event. Injuries range from mild contusion to severe laceration of the brain parenchyma. Vasculature damage may also lead to intracranial hemorrhage, hematoma formation, and subsequent vasogenic edema. Unstable skull fractures can contribute to primary injury as well.2-5<\/sup><\/span><\/p>\n A complex cascade of biochemical derangements causes secondary injury within minutes to days after the initial trauma. Trauma causes increased release of excitatory neurotransmitters and depletion of adenosine triphosphate. A sudden influx of sodium and calcium into cells leads to a further increase in excitatory neurotransmitters. Increases in sodium lead to cytotoxic edema along with failure of membrane pumps, whereas increases in calcium lead to neuronal damage and death. Local tissue acidosis and hypoperfusion trigger production of reactive oxygen radicals, which damage the neuronal cell membranes. TBI also causes release of inflammatory cytokines, which accumulate in tissues and worsen secondary injury by activating the arachidonic acid and coagulation cascades, thus damaging the blood\u2013brain barrier (BBB). Inflammation leads to release of nitric oxide, which leads to excessive vasodilation and loss of pressure autoregulation. Cerebral perfusion is compromised with systemic changes such as hypotension, hypoxia, inflammation, changes in glucose concentrations, hyperthermia, electrolyte abnormalities<\/a>, acid\u2013base abnormalities, and hypercapnia or hypocapnia.6-9<\/sup><\/span><\/p>\n Life-threatening extracranial injuries are evaluated first (ABCs [airway, breathing, circulation]). An electrocardiogram and blood pressure test are part of the triage exam. If the animal is in shock, the clinician should immediately address hypotension, hypovolemia, and oxygenation\/ventilation. Hypovolemia and hypoxemia strongly correlate with an increased ICP and mortality.6<\/sup><\/span><\/p>\n The Animal Trauma Triage (ATT) scoring system was developed using 6 categories: perfusion, cardiac, respiratory, eye\/muscle\/integument, skeletal, and neurologic. Each category is scored on a scale of 0 to 3, with 0 indicating mild to no injury and 3 indicating severe injuries. The score for each category is added to give a maximum total ATT score of 18. The ATT was initially developed in 1994, and it was found that each point on the scale resulted in a 2.3 to 2.6 decreased likelihood of survival.10<\/sup> Since then, several studies have validated this scoring system.11-14<\/sup><\/span><\/p>\n A newer veterinary trauma score, VetCOT (Veterinary Committee on Trauma), has been developed that uses 4\u00a0predictive variables: blood ionized calcium and plasma lactate concentration within 6 hours of admission, and presence or absence of head and\/or spinal trauma. However, further validation studies are needed for this scoring system.15<\/sup><\/span><\/p>\n Neurogenic pulmonary edema can develop rapidly following a TBI, causing dyspnea, hypoxemia, and hypercapnia, and therefore potentially increased ICP. The pathophysiology is not well understood, but it is thought to be due to a marked peripheral vasoconstriction secondary to an increase in sympathoadrenal activity. The vasoconstriction is then thought to lead to systemic hypertension and pulmonary capillary hypertension with subsequent edema. Neurogenic pulmonary edema is typically self-limiting and resolves within hours to days. Early intervention and aggressive supportive therapy are important. This consists of employing therapies that improve oxygenation<\/a> and support of respiratory function (e.g., oxygen mask, oxygen cage, oxygen via nasal catheter), minimizing stress with use of light sedation as needed, and administering diuretics (furosemide 2 to 4 mg\/kg IV q4h to q12h) in the acute phase. Intubation and positive-pressure ventilation are recommended for critically dyspneic animals.16-19<\/sup><\/span><\/p>\n Hyperthermia may be noted as a result of trauma to the thermoregulatory center, iatrogenic causes, stress, seizures, or pain. Hyperthermia should be addressed immediately as it increases cellular metabolism <\/span>and vasodilation, which may lead to an increase in ICP.20<\/sup><\/p>\n After addressing life-threatening injuries, the patient should be fully evaluated for other injuries (e.g., fractures<\/a>, thoracic or abdominal injuries).<\/span><\/p>\n A full neurologic exam and a Small Animal Coma Scale (SACS) evaluation, also known as the modified Glasgow Coma Scale (MGCS), should be performed next (<\/span>FIGURE 1<\/b><\/span>).21<\/sup> The SACS evaluates motor activity, brainstem reflexes, and level of consciousness, with a total score of 18. A lower score is associated with a poorer prognosis. The idea of a SACS was derived from the work of Teasdale and Jennett, who developed the Glasgow Coma Scale (GCS) in humans. Although much of the GCS relies on verbal responses in humans, the SACS delivers scores based on physical and neurologic responses that are evaluated or observed. The result is an objective measurement of the patient\u2019s status. SACS assessment helps the clinician assess severity of neurologic status and initial prognosis; it also allows the clinician to perform serial SACS scores to monitor for improvements or deteriorations.2<\/sup><\/span><\/p>\n Figure 1. Small Animal Coma Scale. Evaluations are made of each category and the composite score can be used to estimate patient outcome.<\/p><\/div>\n Hyperosmolar therapy (mannitol, hypertonic saline) is the treatment of choice for reducing ICP in patients with TBI. Hypertonic saline may be favored over mannitol because it significantly decreases ICP to a greater degree and for a longer duration compared with mannitol22<\/sup>; however, the Brain Trauma Foundation guidelines in human medicine still consider mannitol as first-line treatment in patients with TBI if the patients are euvolemic and preferably normotensive.23<\/sup> Hypertonic saline may also be a better choice for hypovolemic patients, although hypernatremia is a contraindication for use. Dose recommendations for hypertonic saline are 3 to 4\u00a0mL\/kg (7.5% sodium chloride [NaCl]) and 5.3 mL\/kg (3% NaCl). The dose recommendation for mannitol is 0.5 to 1.5 g\/kg as a bolus over 15 to 20\u00a0minutes; however, one study in humans showed that a higher dose (1.4 g\/kg) showed significantly better outcomes when compared to a lower dose (0.7 g\/kg).24<\/sup> The lower concentration of hypertonic saline (3%) is preferred when using a peripheral vein because the higher concentration (7.5%) usually causes a severe vasculitis.<\/span><\/p>\n In addition to hyperosmolar therapy, elevating the head at a 15\u00b0 to 30\u00b0 angle with the head and neck extended helps reduce cerebral blood volume by increasing venous drainage from the brain. This helps decrease the ICP and increase the CPP. Care must be taken to avoid compression of the jugular veins, which leads to an increase in ICP.2,25<\/sup><\/span><\/p>\n If the patient is actively having seizures, diazepam or midazolam is the first-line treatment for rescue (diazepam 0.5 to 1 mg\/kg IV or midazolam 0.3 to 0.5\u00a0mg\/kg IV or intranasally). The dose can be repeated up to 4 times in an hour. For prevention of further seizure activity, a maintenance anticonvulsant medication should be started after a seizure. Levetiracetam is a good option. It has low sedative properties and is less likely to interfere with serial neurologic assessments. The loading dose of levetiracetam is 60 mg\/kg IV, followed by 30 mg\/kg IV q8h. Levetiracetam should be administered diluted as per the package insert and given slowly over 15 minutes to avoid possible severe and life-threatening adverse reactions.26<\/sup> Prolonged seizure activity can cause hypoxemia secondary to noncardiogenic pulmonary edema or aspiration pneumonia.19<\/sup> It can also cause cerebral edema and hyperthermia. Prompt and aggressive treatment of seizures<\/a> is very important.<\/span><\/p>\n During triage, emergency diagnostic testing should include blood pressure, packed cell volume, total protein, blood glucose, electrolytes, coagulation screening, and urine specific gravity. Point-of-care thoracic ultrasound is recommended to identify pleural effusion, pneumothorax<\/a>, and pulmonary contusions. After life-threatening abnormalities are addressed, a full complete blood count, chemistry panel, and thoracic and abdominal radiographs are indicated. If available, a full-body computed tomography (CT) scan can be considered in lieu of other imaging modalities for evaluating limbs, the vertebral column, and thoracic and abdominal cavities.1,2,27-29<\/sup><\/span><\/p>\n When evaluating head injury, noncontrast CT is the gold standard diagnostic test in humans because it helps clinicians identify fractures, damage to brain parenchyma, hemorrhage\/hematomas, and signs of brain herniation.3<\/sup> A helpful feature of CT is 3-dimensional reconstruction, which helps with visualization of the extent of the fracture and aids in surgical planning (<\/span>FIGURE 2<\/b><\/span>). A magnetic resonance imaging (MRI) scan is typically more sensitive for subtle lesions, but it requires general anesthesia, images bone poorly, and is often not available in general practices.30<\/sup> CT is faster, less expensive, and better at visualizing fractures and peracute hemorrhage; in addition, it requires sedation rather than anesthesia.4<\/sup> Chai et al developed the Koret CT score (KCTS), which is a 7-point prognostic scale using CT scan findings. The score includes points for hemorrhage, midline shift or lateral ventricle asymmetry, cranial vault fracture, depressed fracture (1 point each), and infratentorial lesion (3 points).31<\/sup> If advanced imaging of the head is not available, skull radiographs may be helpful in identifying skull fractures, but they are not helpful in evaluating the brain parenchyma.2<\/sup><\/span><\/p>\n\n
Pathophysiology of Head Trauma Patients<\/h2>\n
Increased Intracranial Pressure<\/h3>\n
Primary Brain Injury<\/h3>\n
Secondary Brain Injury<\/h3>\n
Assessment of Head Trauma Patients<\/h2>\n
Primary Assessment and Extracranial Stabilization<\/h3>\n
Neurologic Assessment and Intracranial Stabilization<\/h3>\n
![\"\"](\"https:\/\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2023\/02\/ShoresDanel_TVPMarApr23_TBI_Fig1.png\")
<\/a>Diagnostic Testing for Head Trauma Patients<\/h2>\n
![\"\"](\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2023\/02\/ShoresDanel_TVPMarApr23_TBI_Fig2A.png\")
Figure 2. Noncontrast computed tomography (CT) images of a 2-year-old spayed female miniature pinscher with a history of head trauma. There are multiple fractures of the right aspect of the calvarium, including comminuted fractures of the right parietal bone, right temporal bone, and right occipital bone. Most of these fracture fragments are displaced outwardly from the brain; however, there is slight depression of one of the caudodorsal fragments of the parietal bone. Variable swelling of the subcutaneous tissues at the fracture is heterogeneous and contains multiple patchy regions of fluid-dense material. There is a large amount of hypodense tissue within the brain deep to the right calvarial fractures. The hypodense regions within the brain may be hemorrhage of various stages and\/or edema, causing a mass effect. (A) Transverse soft-tissue window of the skull and brain showing the hypodense area representing hemorrhage and edema and creating a mass effect (asterisk).<\/span><\/a><\/div><\/div>![\"\"](\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2023\/02\/ShoresDanel_TVPMarApr23_TBI_Fig2B.png\")
Figure 2B. (B AND C) 3-dimensional reconstructions of the CT scan showing the extent of the fractures.<\/span><\/a><\/div><\/div>![\"\"](\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2023\/02\/ShoresDanel_TVPMarApr23_TBI_Fig2C-604x1024.png\")
Figure 2C. (B AND C) 3-dimensional reconstructions of the CT scan showing the extent of the fractures.<\/span><\/a><\/div><\/div>
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![\"\"](\"https:\/\/navc.sitepreview.app\/todaysveterinarypractice.com\/wp-content\/uploads\/sites\/4\/2023\/02\/ShoresDanel_TVPMarApr23_TBI_Fig2E.png\")