In today’s VETgirl online veterinary continuing education blog, Dr. Garret Pachtinger, DACVECC reviews the underlying pathophysiology of head trauma (e.g., brain/spinal injury), neurologic evaluation, and Modified Glascow Coma scoring. Make sure to check back next week to read Part 2 for more information on treatment and management of head trauma in your feline and canine patients!
Severe brain and spinal cord injury are challenging cases to treat in small animal medicine. With trauma severe enough to result in neurologic injury, it is important to recognize the potential for other serious injuries including pneumothorax, pulmonary contusion, traumatic hemoabdomen, uroabdomen, and fractures. As a result, rapid patient assessment and treatment is critical to reduce morbidity and mortality. Many veterinary patients can recover from CNS injuries with rapid patient assessment and treatment.
PATHOPHYSIOLOGY OF BRAIN/SPINAL INJURY
Brain and spinal injury can be divided into primary injury and secondary injury. Primary injury refers to the events that occur immediately at the time of trauma and include direct damage to the parenchyma and vasculature. Examples of primary brain injury include contusions, lacerations, hemorrhage, and vasogenic edema. Secondary injury results from a cascade of physiologic and biochemical events that occur in the subsequent hours to days following the primary injury. Events resulting in secondary brain and spinal injury include depletion of neuronal ATP levels (worsened by hypoxemia or hypovolemia), intracellular accumulation of calcium and sodium ions, oxygen free radical formation, increased cytokine production, elevated extracellular glutamate levels, nitric oxide accumulation, lactic acid accumulation, and activation of other cell-damaging pathways (e.g., kinin, complement, coagulation/fibrinolytic pathways). Primary and secondary injuries to the brain and spinal cord can result in increased morbidity and mortality if not rapidly assessed and treated.
Classifications of primary head trauma include concussion, contusion, laceration, intra and extra-axial hematomas, and skull fractures. These are specific and direct abnormalities of the brain parenchyma that occur at the time of the trauma.
Examples of primary spinal trauma include vertebral fracture, intervertebral disk herniation, spinal cord contusion, and extra-axial hemorrhage. The severity of the spinal trauma will depend on the severity of the underlying abnormality. With vertebral fractures, the extent of the spinal trauma will depend on the instability and degree of trauma to the actual vertebral process. Similarly, with intervertebral disk herniation may be more damaging with Hansen’s Type I intervertebral disk disease as compared to a type II disc herniation.
Secondary injury results from a series of biochemical events following the primary injury including excitotoxicity, ischemia, inflammation, and production of reactive oxygen species, accumulation of intracellular sodium and calcium, nitric oxide accumulation, ATP depletion, and cerebral lactic acidosis. Following the primary trauma, there is an increased release of excitatory neurotransmitters (i.e. glutamate and aspartate). These neurotransmitters activate other receptors, resulting in an increased intracellular sodium and calcium concentration. This increased concentration leads to excessive depolarization and further release of excitatory neurotransmitters. Ultimately, this is a viscious cycle of excitatory stimulation resulting in intracellular damage. Other important cytokines and factors in secondary injury include nitric oxide (NO), Interleukin-1β (IL-1β), Interleukin-6 (IL-6), and Tumor Necrosis Factor α.
INTRACRANIAL PRESSURE (ICP) AND CEREBRAL PERFUSION PRESSURE (CPP)
The skull is a rigid compartment containing the brain, blood and cerebrospinal fluid (CSF). If any of the individual components change, the end result is going to be a change in ICP. Since measurement of intracranial pressure is practically impossible in most clinical settings, it is important to for the clinician to recognize changes in the patient consistent with changes in ICP. Such changes may include pupil changes, ocular position, mentation, breathing pattern (apneustic breathing, or Cheyne-Stokes breathing) or via Cushing’s reflex .
When we evaluate CPP, this is done via the equation:
Cerebral perfusion pressure = Mean Arterial Pressure–Intracranial Pressure (CPP = MAP–ICP)
Ultimately, if ICP rises, MAP must also increase in order to maintain CPP. If there is continued elevation of the ICP without therapy, there will be a decreased CPP and poor perfusion of the pons and medulla. The result is an accumulation of CO2 and sympathetic stimulation to increase systemic blood pressure. Sympathetic stimulation and increased blood pressure triggers a baroreceptor-mediated bradycardia. Hypertension and bradycardia associated with elevated ICP is known as the Cushing’s reflex and suggestive of markedly elevated ICP and impending brain herniation.
One of the most important concepts to remember when approaching any emergency patient is a rapid primary survey, keeping in mind the ABCDs of evaluation and resuscitation. Briefly, “A” refers to Airway or Arterial Bleeding. Even if the patient is presenting for seizures, if they seizure to the point of an upper airway obstruction, the “A” of airway may need to be addressed. “B”, Breathing is equally important assessing the character of the patient’s respirations. “C” refers to Circulation and the overall perfusion status of the patient. Finally, “D” refers to Disability notably the patients mental status. Regardless of the presentation, a triage patient assessment is imperative to evaluate patient stability. In patients such as this, severe trauma has the potential for abnormalities in all of these assessment parameters.
Following the triage examination and patient assessment, a more specific neurologic assessment can be made. Neurological assessment should include the patient’s level of consciousness, pupil size and responsiveness, ocular position and eye movements and skeletal motor responses. If there are abnormalities or concerns, this assessment should be repeated every 30–60 minutes. Other examination findings that may indicate possible head trauma include blood within the external ear canals, wounds to the head and / or neck region, episcleral hemorrhage, hyphema, epistaxis, broken teeth, and/or fractures on palpation of the bones of the head.
NEUROLOGICAL EVALUATION AND THE MODIFIED GLASGOW COMA SCALE
In trying to develop a more objective scale when evaluating the patient with neurological injuries, the Modified Glasgow Coma Score (MGCS) may be a useful indicator of prognosis in the patient with traumatic brain injury (TBI). The MGCS will give not only an initial objective assessment of the neurological status, but this will allow for more objective serial neurologic assessment of the patient with TBI. This scale evaluates three primary areas: level of consciousness, brain stem reflexes, and motor activity/posture. Each category is scored 1-6 with 6 being normal in all categories and 1 being abnormal. The three scores are added and the total provides an objective number for initial and serial patient assessment as well as a 48 h survival prognosis: 3-8 grave, 9-14 guarded, 15-18 good.
Important ASSESSMENTS AND DEFINITIONS OF THE HEAD/SPINAL TRAUMA PATIENT
We’ll discuss specific treatment for head trauma in Part 2 next week in our VETgirl blog, so stay tuned!
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