Traumatic Brain Injury

Chapter 152 Traumatic Brain Injury






PATHOPHYSIOLOGY


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.




Secondary Injury


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.



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.


The following equation summarizes the “Monro-Kellie Doctrine,” developed in the early nineteenth century to describe intracranial dynamics:



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where V = volume. Sudden increases in any of these volumes as a result of primary and secondary brain injuries can lead to dramatic increases in ICP.


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.

Sep 10, 2016 | Posted by in SMALL ANIMAL | Comments Off on Traumatic Brain Injury
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