Brain Trauma (Gianani( Flashcards
Mechanisms of brain injury
Direct impact (cerebral contusion and laceration). Movement of the brain inside the skull (subdural hematoma and diffuse axonal injury).
Direct impact on the brain–>
can cause laceration or contusion in areas close to or remote from the impact (kinetic energy transmitted through the brain).
This motion stretches axons, tears blood vessels, and damages the surface of the brain as it bounces against bony ridges at the base of the skull.
Classification of traumatic brain injury
Skull fractures.
Parenchymal injury.
Traumatic vascular injury.
Skull fractures classification.
- Linear skull fracture (breaks in bone that transverse the full thickness of the bone from inner to outer table).
- Depressed skull fracture (a fracture displaced by a thickness equal or larger than the thickness of the bone).
- Diastatic skull fracture.
- Basilar skull fracture .
skull fracture in general
- does not necessarily indicate underlying brain damage.
- may create a communication between the intracranial compartment and septic areas such as air sinuses, nasal fossae, and middle and external ear, –> infection of the brain and meninges.
- Linear fracture - usually not clinically significant unless they transverse or parallel in close proximity a suture or involve a vascular structure. may –> suture diastasis, venous sinus thrombosis or epidural hematoma.
Depressed skull fracture usually result from
blunt force trauma.
usually a comminuted fracture in which small bone fragments are displaced inward.
Compound depressed fractures- usually soft tissue laceration above the fracture.
- Depressed skull fracture can be complicated by parenchymal hemorrhage or injury, esp. if associated with torn dura (Complex depressed fracture).
Parenchymal injury.
Concussion. (not actual tissue damage)
Direct parenchymal injury (transmission of kinetic energy to the brain).
1. Contusion (bruising of the brain). 2. Laceration (tearing of the tissue).
Diffuse axonal injury.
CEREBRAL CONTUSIONS
= hemorrhagic necrosis of brain tissue.*
When the head is abruptly brought to a stop against a solid object, such as the dashboard or the ground, the brain continues to move for an instant, hitting the inside the now stationary skull.
The soft brain is easily contused and lacerated by the hard bony ridges at the base of the skull or by the tentorium cerebelli and falx cerebri.
Contusions usually involve the surface of the brain, especially the crowns of gyri, and are ** more frequent in the orbital surfaces of the frontal lobes and the tips of the temporal lobes.
Contre -coup contusions
Contusions that develop opposite the impact.
DIFFUSE AXONAL INJURY
(TRAUMATIC AXONAL INJURY)
a special traumatic lesion, which occurs most frequently in motor vehicle accidents and following blows to the unsupported head.
In the course of such injuries, the cerebrum goes into a back and forth gliding motion, pivoting around the upper brainstem.
The brainstem, together with the cerebellum, is held firmly fixed by the tentorium, and the falx prevents side-to-side motion.
Axons are stretched but do not snap from this injury.
what is prone to diffuse axonal injury?
** Deep white matter is most prone to acceleration-deceleration injury.
Can be mild to severe (shearing injury)
Moderate to severe axonal injury results in Wallerian degeneration.
CNS myelin made by oligodendrocytes, not Schwann cells (PNS)…they don’t come back like Schwann cells.
Traumatic vascular injury (types)
Epidural hematoma.
Subdural hematoma.
Traumatic sub-arachnoid hemorrhage.
Vessels that bleed
(brain)
Middle meningeal artery (R or L) runs in the epidural space
Bridging veins that go across the dura (meningeal layer) to the skull and bleed in the subdural space between the arachnoid layer and meningeal layer of dura.. [cause subdural hematoma]
Cerebral arteries in subarachnoid space.
Key factors in an epidural hematoma
Usually impact injury with tear of middle meningeal artery
the MMA Is a branch of external carotid artery…supplies dura…does not go into brain parenchyma
Lens shaped
Biconvex on CT
Epidural hematoma- blathering
- Rapidly expanding hemorrhage under arterial pressure
- peels the dura away from the inner surface of the skull,–> lens-shaped biconvex hematoma
- no spread past the cranial sutures where the dura is tightly apposed to the skull
- Initially may have no symptoms (lucid interval).
- Within hours hematoma –> compress brain tissue, –> elevated intracranial pressure–> herniation and death unless treated surgically.
- no epidural space normally; dura is adherent to the skull.
- Fracture of the inner table of the skull can tear arteries and veins that run between the dura and the skull.
- blow to the head may cause instant deformation of the skull without a fracture–> vascular tears. Bleeding from these vessels lifts the dura off of the skull forming an epidural blood clot.
- Epidural hematomas develop most commonly with fractures of the squamous portions of the temporal and parietal bones that tear the middle meningeal vessels. Less commonly, they result form tears of diploic veins and dural sinuses.
Symptoms of increased intracranial pressure in epidural hematomas with arterial rupture usually develop within hours after the injury. With venous bleeding, they take longer. There is a natural epidural space around the spinal cord. Spinal epidural hematoma may occur as a result of trauma, but may also develop spontaneously in patients with bleeding disorders.
Subdural Hematoma- key facts
- Subdural space is not connected to arachnoid space where the CSF is.
- half moon shaped/ crescent shaped
Large subdural hematomas raise the intracranial pressure and compress the brain. With arterial bleeding, symptoms develop rapidly. In many instances, especially with venous subdurals of infants and old people, there is an interval between trauma and the onset of symptoms. Sometimes the preceding injury is insignificant, or no history of trauma can be elicited.
how do you know an epidural hematoma is there?
CT scan
Subdural Hematoma- Epidemiology and etiology
Head trauma is the most common cause of SDH, with the majority of cases related to motor vehicle accidents, falls, and assaults
subdural hematoma- common risk factors (blathering)
Patients with significant cerebral atrophy are at high risk for SDH.
- elderly
- history of chronic alcohol abuse
- previous traumatic brain injury.
In such patients, trivial head trauma or even pure whiplash injury in the absence of physical impact may –> SDH.
Thus, SDH, particularly chronic SDH, is seen in older adults more commonly than younger adults.
SDH may be more common than epidural hematoma.
The use of antithrombotic agents increases the risk of SDH,
acute subdural hematoma info
for acute- impact velocity must be quite high.
usually associated with other serious injuries, such as traumatic subarachnoid hemorrhage and brain contusion. –> worse prognosis than with chronic subdural hematoma or even epidural hematoma.
coma is present from the time of injury half the time.
Posterior fossa SDH, like most space-occupying lesions in this location, presents with symptoms of elevated intracranial pressure including headache, vomiting, anisocoria, dysphagia, cranial nerve palsies, nuchal rigidity, and ataxia.
In some instances of SDH, cerebral hypoperfusion due to increased intracranial pressure or mass effect may –> cerebral infarction, esp in the posterior fossa, where the posterior cerebral arteries are vulnerable to compression along the edge of the tentorium cerebelli.
Radiological appearance of subdural hematomas
crescent shaped, spread over a large area
Density depends on the age of the blood.
- acute blood is hyperdense, bright on CT scan.
- After 1 to 2 weeks, the clot begins to liquefy and may appear isodense.
- If no further bleeding, after 3 to 4 weeks the hematoma will be completely liquefied and will appear uniformly hypodense
- if continued occasional bleeding, there will be a mixed density appearance resulting from liquefied chronic blood mixed with clotted hyperdense blood.
Chronic subdural hematoma
insidious onset of headaches, light-headedness, cognitive impairment, apathy, somnolence, and occasionally seizures, may occur as a consequence of chronic SDH, and symptoms may not become evident until weeks after the initial injury. Global deficits such as disturbances of consciousness are more common than focal deficits after SDH.
Focal deficits may be either ipsilateral or contralateral to the side of the SDH. Contralateral hemiparesis can occur as a result of direct compression of cortex underlying the hematoma, whereas ipsilateral hemiparesis can occur with lateral displacement of the midbrain caused by the mass effect of the hematoma. Such midbrain displacement results in compression of the contralateral cerebral peduncle against the free edge of the tentorium. Symptoms due to chronic SDH may be transient or fluctuating.
Bitemporal chronic SDH may present with intermittent paraparesis that is proximal and painless.
where SDH comes from
Subdural haemorrhages occur more frequently than EDHs
less likely to be associated with skull fracture.
SDHs may be preceded by head injury, or no history of trauma
- Those at the extremes of life, chronic alcoholics–> greatest risk (anatomy of the subdural space, cerebral atrophy and an increased propensity for falls etc.)
SDHs may be ‘acute’, ‘sub-acute’ or ‘chronic’.
Bleeding - from torn bridging (‘communicating’) veins crossing the subdural space from the cerebral cortex to the dural sinuses,
- thought to be due to rotational and/or ‘shear’ strains which are often a result of impact.
- impact may not be necessary; frequently encountered in infants who have allegedly been ‘shaken’.
- usually 35- 100 mls blood–> ‘irritant’ or space occupying lesion.
Chronic SDHs- yellow/brown ‘membrane’ on the under-surface of the dura, may be an incidental finding in the elderly, the effects of which may have been confused clinically with dementia or a stroke.
the look of SDH on CT with continued occasional bleeding
there will be a mixed density appearance resulting from liquefied chronic blood mixed with clotted hyperdense blood. Sometimes, with mixed-density hematomas, the denser acute blood settles to the bottom, giving a characteristic hematocrit effect.