![]() ![]() Blood oxygen content is defined by the following equation: CaO2 = (Hemoglobin X 1.34 X SaO2) + (.003 X PaO2). ![]() Stroke volume can be depleted in the trauma patient secondary to blood loss, restricted fluid administration, and the administration of diuretics. Cardiac output is equal to the product of stroke volume and heart rate. Oxygen delivery to any tissue in the body is dependent on blood flow (Cardiac Output (CO)) and oxygen content of the arterial blood (CaO2). 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). 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. However, minimizing the incidence or impact of secondary brain injury is the focus of the emergency medical management of the small animal TBI patient. 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. 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). TBI in the small animal patient may be the result of a variety of traumatic events. Pathophysiology of Traumatic Brain Injury (TBI): ![]()
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