Traumatic Head and Spinal Cord Injury & Raised Intracranial Pressure Flashcards
What are secondary effects of traumatic brain injury?
Ischaemia - can be acute Hypoxia - can be acute Cerebral swelling (raised ICP) Infection Epilepsy
Epi/extradural haematoma is caused by
rupture of MMA
Epi/extradural haematoma is less likely in
old age; dura increasingly adheres to skull with age
Subdural haematoma is caused by
subdural veins; can be acute or chronic
Subdural haematoma is more common in
old age; as the brain shrinks there is stretch put on the subdural veins where they enter the sagittal sinus and they can rupture w/less force than that causing an extradural haematoma
Contusion is what type of necrosis?
Haemorrhagic
Where can contusions occur?
Coup (impact site), contrecoup (opposite), and inferior lobes (frontal, lateral temporal)
How do cerebral contusions heal?
macrophages remove dead tissue and blood, leaving collapsed gyri that are orange in colour (haemosiderin)
Where is the cerebral tissue vulnerable to tearing?
ponto-medullary junction (pons and medulla in brainstem), results in instant death
What is traumatic/diffuse axonal injury (TAI/DAI)?
damage to individually axons in cerebral tissue, not necessarily with contusions, haemorrhaging, or tearing; the corpus callosum is particularly susceptible
What is diffuse vascular injury?
Tearing of small vessels, give spotty haemorrhages; usually occurs with TAI/DAI
What is an axonal spheroid?
indicator of axonal injury/transsection; axoplasm continues to send proteins down axon, get a buildup of neurofilaments and axonal material
What are the long-term effects of DAI?
brain atrophy, enlargement and dilation of the ventricles, thinning of the corpus callosum and white matter relative to cortical tissue
What are the long-term sequelae of brain trauma?
infection - especially in open skull fracture; hydrocephalus (dilated ventricles compress brain tissue, occurs to blockage of CSF drainage or overproduction); epilepsy; chronic traumatic encephalopathy (brain atrophy due to neuronal loss, deposition of proteins and plaques - ie in boxers, footballers)
What is the initial response to expanding brain lesions?
expulsion of CSF to decrease ventricular size, gyral-sulcal flattening, and expulsion of venous blood - then ICP starts to rise
As ICP approaches arterial pressure
brain perfusion ceases
How can CSF caused raised ICP?
overproduction, obstruction to absorption or flow
What are the two types of cerebral oedema?
vasogenic and cytotoxic
Vasogenic cerebral oedema
due to BBB disruption with increased vascular permeability; predominantly involves white matter; responsive to steroids and other tx
Cytotoxic cerebral oedema
increased intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury - occurs in strokes and infarcts; does not respond to tx; affects grey and white matter
What is subfalcine herniation?
cingulate gyrus is pushed underneath the falx
What is transtentorial/medial herniation?
medial temporal lobe is pushed through tentorium cerebelli
What is tonsilar herniation?
cerebellar tonsils pushed into spinal canal due to pressure on brainstem from herniating cerebral tissue
What are Duret haemorrhages?
Secondary to raised ICP pushing the brainstem downwards, tearing of blood vessels in the brainstem occurs because they are fixed relative to the cerebral tissue; causes further brainstem damage
