Page 781 - Clinical Small Animal Internal Medicine

69 Central Nervous System Trauma 749

to hemorrhage or contusion and tearing of neuronal tis- come and can lead to continued death of neurons and
VetBooks.ir sue. The rotational forces have more of an impact on the glial cells. The primary mediators involved in secondary
brain injury include oxygen free radicals, excitatory
deeper white matter of the brain, causing concussive
injuries and axonal damage. The spherical shape of the
skull and the propagation of rotational forces after injury amino acids (i.e., glutamate), and nitric oxide.
direct these forces into the deeper tissues of the brain. Cerebral Edema
Additionally, penetrating injuries can cause direct dam-
age to the brain parenchyma, fractures, and hemorrhage. Edema develops after primary brain injury and continues
to develop as secondary brain injury ensues. Typically,
brain edema is most severe 24–48 hours after injury.
Skull Fractures There are two main types of edema: vasogenic and cyto-
Skull fractures are described based on pattern (depressed, toxic (intracellular).
comminuted, linear), location, and type (open vs closed).
A depressed fracture is one where the inner shelf of ● Vasogenic edema occurs secondary to failure of the
bone is driven into the brain to a depth equivalent to the blood–brain barrier and vasodilation. Vasodilation is
width of the skull. Depressed fractures are most com- frequently secondary to hypercapnia, which is often
mon on the dorsal and lateral aspects of the skull. associated with head injury. Initially, the brain is able
Fractures may also occur at the base of the skull, middle to compensate for this increase in fluid through the
ear, and temporomandibular joint; however, fractures in compliance strategies discussed earlier.
these locations are difficult to evaluate. Bullae fractures ● Cytotoxic edema occurs secondary to failure of cellular
can result in neurologic signs such as vestibular syn- ion pumps and damage to cellular membranes.
drome, facial paresis/paralysis, and Horner syndrome Cytotoxic edema can lead to cellular death.
on the side of the fracture. Fractures of the temporoman-
dibular joint, mandible, and zygomatic arch may require Intracranial Pressure
additional treatment, but are unlikely to cause neuro- The brain is protected within the bony confines of the
logic signs alone. skull, where it exists in equilibrium with cerebrospinal
fluid (CSF) and blood. The pressure exerted between the
Brain Hemorrhage brain and the skull is the ICP, which is normally 5–12
Hemorrhage following trauma may be located in an mmHg in dogs and cats. The skull is relatively inelastic,
extraparenchymal or intraparenchymal location. limiting the volume that can exist within the cranial cav-
Extraparenchymal hemorrhage may occur in the epidural, ity. The space within the cranial vault is occupied pri-
subarachnoid, or subdural space. The most common loca- marily by three components: brain parenchyma, CSF,
tion of hemorrhage following trauma is within the brain and blood.
parenchyma (intraaxial) or subarachnoid space. Epidural The Monro–Kellie hypothesis describes the relation-
hemorrhage is frequently secondary to bleeding from ship between these compartments and their ability to
meningeal arteries, resulting in blood between the skull and compensate for increases in volume within the cranial
dura. Hematomas located in the subdural space (between cavity. After head trauma, the volume of the intracranial
the arachnoid and dura) are typically secondary to venous contents within the skull may increase due to hemor-
bleeding, resulting in slow accumulation of blood. rhage, edema, or CSF accumulation. The brain has the
Hemorrhage into the cranial cavity has several delete- capacity to tolerate small increases in volume by adjust-
rious effects. The presence of hematomas contributes to ing the size of one of the three components, primarily
elevations in ICP and reduction of CBF. Additionally, the CSF compartment. Shunting CSF to the spinal
hemorrhage provides a substrate for oxygen free radical subarachnoid space, decreasing CSF production, and
formation and promotes inflammation. Finally, hemor- increasing CSF absorption can rapidly decrease the CSF
rhage promotes the release of excitatory amino acids compartment. CSF production does not typically affect
exacerbating secondary brain injury. elevations in ICP unless its drainage is obstructed, lead-
ing to obstructive hydrocephalus. Additionally, venous
Secondary Injury blood can be redirected out of the cranial cavity and cer-
After impact, a cascade of biomolecular events occurs ebral blood flow will decrease to compensate for ICP
causing continued and progressive brain pathology. The elevation. The ability of the brain to adjust for increases
presence of hematomas and edema from the primary in intracranial pressure by decreasing the volume of
injury distorts normal brain parenchyma, and decreases CSF and blood is called compliance. During this time of
CBF. Additionally, a series of cellular reactions begins compensation, the patient’s clinical signs will remain rela-
at the time of impact and continues after the injury. This tively normal, unless the trauma primarily injured the
secondary brain injury has a significant effect on out- parenchyma via laceration, puncture wounds, etc. Once