Traumatic brain injury: keys to success (Proceedings)

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Traumatic brain injury: keys to success (Proceedings)

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Nov 01, 2010

Pathophysiology of Traumatic Brain Injury (TBI):

TBI in the small animal patient may be the result of a variety of traumatic events. Primary brain injury results from a variety of forces (acceleration, deceleration, torsion, etc.) imparted on the cranium and its contents and may range from mass-lesions caused by vascular disruption (epidural hematoma, subdural hematoma, intraparenchymal hemorrhage) to contusions and diffuse axonal injury (most common). Excluding the surgical management of mass lesions (hemorrhage) and depressed skull fractures; there is little that we as veterinarians can do about the primary injury. However, minimizing the incidence or impact of secondary brain injury is the focus of the emergency medical management of the small animal TBI patient.

Secondary brain injury refers to a variety of pathophysiologic processes that culminate in progressive neuronal damage at sites both local and distant from the primary injury. Of greatest importance of the mechanisms of secondary brain injury and that to which therapy can most easily and practically be directed against is decreased global oxygen delivery (DO2). Oxygen delivery to any tissue in the body is dependent on blood flow (Cardiac Output (CO)) and oxygen content of the arterial blood (CaO2). Cardiac output is equal to the product of stroke volume and heart rate. Stroke volume can be depleted in the trauma patient secondary to blood loss, restricted fluid administration, and the administration of diuretics. Blood oxygen content is defined by the following equation: CaO2 = (Hemoglobin X 1.34 X SaO2) + (.003 X PaO2). According to the equation, CaO2 can be depleted through alterations in blood hemoglobin concentration (hemorrhage) and oxygen saturation (pulmonary contusion, pleural space diseases, etc). Insufficient oxygen delivery to neuronal tissue will accentuate the already depleted ATP levels and predispose to the accumulation of lactic acid through anaerobic glycolysis. Aggressive resuscitation of the trauma patient will minimize the occurrence of secondary brain injury from decreased DO2.

Clinical Approach to the Head Trauma Patient:

The approach to the small animal TBI patient should initially address the three major body systems (cardiovascular, respiratory, and CNS) in an effort to identify and institute treatment for immediately life threatening problems. Treatment for problems identified based on the examination of the cardiovascular and respiratory systems should be instituted immediately such that delivery of oxygen to the brain can be maximized. A rapid history including the time of the trauma, clinical signs immediately after the trauma and progression until the present time, medications administered, and previous pertinent medical history should be sought out soon after presentation.

Clinical manifestations and physical and neurologic examination findings in the small animal patient that has suffered TBI may include an altered level of consciousness (agitation/delirium, depression, stupor, coma), seizures, ataxia, proprioceptive deficits, and various cranial nerve deficits including but not limited to head tilt, circling, and nystagmus. The veterinarian may observe obvious wounds to the head and / or neck region, episcleral hemorrhage, hyphema, epistaxis, oral trauma (broken teeth, jaw), blood in the ears, and fractures on palpation of the bones of the head. Inappropriate bradycardia should alert the clinician to the possibility of severely increased intracranial pressure. Identification of any of the aforementioned injuries should prompt the clinician to consider the possibility of a significant intracranial injury and further diagnostic options. Immobilization of the small animal with suspected TBI is important due to the possibility of concurrent cervical spinal injury.



A resurgence of attention is being paid to grading the severity of TBI according to the Modified Glasgow Coma Score (MGCS). The MGCS was developed in 1983 by Shores in an effort to grade the severity of neurologic injury, allow for comparison to that baseline over time, and finally to predict prognosis. The scale was proposed as follows:

A score is given in each of the categories above (motor activity, brain stem reflexes, and level of consciousness) and then the scores are totaled. It has been proposed that a score of 3-8 suggests a grave prognosis, 9-14 suggests a guarded prognosis, and 15-18 suggests a good prognosis. Retrospective evaluation of a series of 38 dogs with head trauma correlated the probability of survival within the first 48 hours with MGCS. A prospective evaluation of 24 dogs with head trauma showed that MGCS predicted length of stay, cost of care, and thus severity of injury but concluded that further studies will be necessary to determine if MGCS is a good predictor of outcome.3 Future studies will also be necessary to determine if MGCS will be a useful predictor of the necessity for CT scan after head trauma in dogs.

Imaging studies (CT or MRI) of the intracranial structures should be considered in any patient with focal clinical signs, moderate to severe clinical signs of TBI on presentation, failure of clinical signs to improve within hours of initiation of treatment, or deterioration in clinical signs. Imaging will allow the clinician to rule in or out a significant mass lesion (epidural, subdural, or intraparenchymal hemorrhage) or depressed skull fractures as contributory to the clinical signs. Mass lesions and depressed skull fractures in patients with moderate to severe trauma and static or progressive clinical signs should be approached surgically. Imaging studies will also allow the clinician a better appreciation for the other injuries (contusion, edema) often present in the head trauma patient.