Chapter 152 Traumatic Brain Injury
Traumatic injuries (TBIs) are common in dogs and cats, with motor vehicle accidents, animal interactions, and unknown etiologies being the most common causes seen in a multicenter study of 1099 dogs and 191 cats.1 In that study, 26% of dogs and 42% of cats had evidence of head injury. Other common causes of head injury in dogs and cats include falls from heights, blunt trauma, gunshot wounds, and other malicious human activity.2 The overall prevalence and incidence of head injury in veterinary medicine has not been well studied, but a retrospective study from a large, urban veterinary hospital reported an average of 145 cases of confirmed TBI per year from 1997 to 1999.3
When treating a patient with an acute head injury, both extracranial and intracranial priorities must be acknowledged and evaluated. Identification of life-threatening extracranial injuries such as hemorrhage, penetrating thoracic or abdominal wounds, airway obstruction, and compromise of oxygenation, ventilation, or volume status is of paramount importance. Once life-threatening extracranial factors have been identified, intracranial priorities should include maintenance of adequate cerebral perfusion pressure (CPP), ensuring adequate oxygen delivery to the brain, and treatment of acute intracranial hypertension, as well as continued monitoring of neurologic status.
The underlying injuries that result from head trauma can be separated into two categories: primary injury and secondary injury. Primary injury occurs as an immediate result of the traumatic event. Secondary injury occurs during the hours to days after trauma and is caused by a complex series of biochemical events, including release of inflammatory mediators and excitatory neurotransmitters, and changes in cellular membrane permeability.
The least severe primary brain injury is concussion, characterized by a brief loss of consciousness. Concussion is not associated with any underlying histopathologic lesion.4 Brain contusion consists of parenchymal hemorrhage and edema. Clinical signs can range from mild to severe. Contusions can occur in the brain directly under the site of impact (“coup” lesions), or in the opposite hemisphere (“contrecoup” lesions), or both, as a result of displacement of the brain within the skull. Although mild contusion can be difficult to differentiate from concussion, unconsciousness for more than several minutes is most consistent with contusion.2
Laceration is the most severe of primary brain injury and is characterized by physical disruption of the brain parenchyma. Axial hematomas within the brain parenchyma and extraaxial hematomas in the subarachnoid, subdural, and epidural spaces can occur, causing compression of the brain and leading to severe localizing signs or diffuse neurologic dysfunction.5 The literature suggests that extraaxial hemorrhage is rare in dogs and cats after head injury; however, there is mounting evidence that this type of hemorrhage occurs in up to 10% of animals with mild head injury and more than 80% of dogs and cats with severe head injury.5,6
TBI triggers a series of biochemical events that ultimately result in neuronal cell death. Box 152-1 is a list of the most common types of secondary injury. These secondary injuries are caused by a combination of intracranial and systemic insults that occurs in both independent and interrelated ways.
ATP, Adenosine triphosphate.
Systemic insults that contribute to secondary brain injury include hypotension, hypoxia, systemic inflammation, hyperglycemia, hypoglycemia, hypercapnia, hypocapnia, hyperthermia, electrolyte imbalances, and acid-base disturbances. Intracranial insults include increased intracranial pressure (ICP), compromise of the blood-brain barrier, mass lesions, cerebral edema, infection, vasospasm, and seizures. All of these factors ultimately lead to neuronal cell death.7
Immediately after injury, there is massive release of excitatory neurotransmitters that causes influx of sodium and calcium into neurons, resulting in depolarization and further release of excitatory neurotransmitters. Increased influx of calcium overwhelms mechanisms for removal, causing severe intracellular damage and ultimately neuronal cell death.8 Excessive metabolic activity also results in depletion of adenosine triphosphate (ATP) stores.
Several factors favor the production of reactive oxygen species after TBI, including hypoperfusion and local tissue acidosis. Hemorrhage provides a source of iron, which favors the production of hydroxyl radicals. Catecholamines may also contribute to the production of free radicals by direct and indirect mechanisms. These reactive oxygen species then oxidize lipids, proteins, and deoxyribonucleic acid (DNA), resulting in further destruction of neurons. Because the brain provides a lipid-rich environment, it is particularly susceptible to oxidative injury.
Nitric oxide has been associated with perpetuation of secondary brain injury after trauma, most likely due to its vasodilatory effects and its participation in free radical reactions, but the exact mechanism is not well understood.8
TBI is associated with production of inflammatory mediators.9 These mediators perpetuate secondary brain injury via a number of mechanisms, including inducing nitric oxide production, triggering influx of inflammatory cells, activating the arachidonic acid and coagulation cascade, and disrupting the blood-brain barrier. Because studies have shown both neuroprotective and neurotoxic effects of inflammation, research is focusing on the development of targeted antiinflammatory agents that preferentially affect the more acute, destructive inflammatory processes.9
Primary and secondary intracranial injuries, in combination with systemic effects of the trauma, ultimately result in worsening of cerebral injury as a result of a compromised CPP, the force driving blood into the calvarium and providing the brain with essential oxygen and nutrients. CPP is defined as the difference between mean arterial blood pressure (MAP) and ICP.
Blood flow to the brain per unit time, or cerebral blood flow (CBF), is a function of CPP and cerebrovascular resistance. The normal brain is capable of maintaining a constant CBF over a wide range of MAP (50 to 150 mm Hg) via autoregulatory mechanisms. However, the traumatized brain often loses much of this autoregulatory capacity, making it susceptible to ischemic injury with even small decreases in MAP.
Initially, increases in ICP will trigger the Cushing reflex, or central nervous system ischemic response, a characteristic rise in MAP and reflex decrease in heart rate (see Chapter 100, Intracranial Hypertension). The central nervous system (CNS) ischemic response in a patient with head trauma is a sign of a potentially life-threatening increase in ICP and should be treated promptly.