Trauma Flashcards
blood brain barrier bbb
Also called BB neurovascular unit
Site of BBB- brain capillary endothelium
Tight intracellular junctions (non-permissive compared to systemic endothelial cells)
Endothelium has low pinocytotic rate and basement membrane, Dynamic interaction of endothelium with astrocytes and pericytes
Small substances and small lipophilic molecules freely diffuse through membrane
Large substances and hydrophilic molecules require active transport
Cerebral edema
Defined as an accumulation of excess fluid in intracellular or extracellular spaces of the brain–> increased intracranial pressure, results from a variety of processes and associated with significant morbidity and mortality
2 forms: Vasogenic edema and cytotoxic edema
The gyri and sulci go awau
Vasogenic edema– extracellular edema
Disruption (increased permeability) of BBB
Results in a shift of fluid from the intravascular to the extravascular compartment
Predominant invloves white matter
Causes- primary or secondary brain tumors, abcesses, contusions, intracerebral hematomas
Machanisms- Newly formed vessels in tumors (deficient in tight junctions), production of vascular endothelial growth factor VEGF by tumor cells, production of inflammatory mediators, chemokines, cytokines, and other growth factor
Often responds dramatically to corticosteroids and to anti vegf antibody (Bevacizumab), flattened gyri, narrow sulci compressed ventricles, brain softening
Cytotoxic edema- intracellular edema
Occurs secondary to cellular energy failure
Results in a shift of water from the extracellular to intracellular compartment
Intracellular sweilling- large amounts of Na enter cells, water follows,
histologically brain tissue vacuolation
More pronounced in gray matter
Most common causes- ischemia/infarct, meningitis, trauma, seizures, hepatic encephalopathy
MOA- dysfunction of neuronal and astrocytic membrane pumps (caused by excess glutamate, extracellular potassium, inflammatory cytokines)
Edema leads to increased intracranial pressure
The brain is in a closed rigid box
Brain volume= Brain and blood and csf (with possible lesions)
Increased volume=increased pressure
Increased pressure leads to decreased perfusion and or herniation syndrome
Rigid dural folds (falx, tentorium) dictate what type of herniation
Subfalcine herniation
Cingulate gyrus herniates under the falx
Caused by asymmetric expanding hemispheric lesions
May cause compression of anterial cerebral artery –> infarct (messes with the leg of homonculus)
Transtentorial uncal herniation
Medial temporal lobe (spc- the uncus) displaced thru the tentorial opening because of asymmetric expanding lesion
Complications- Ipsilateral CN3 nerve compression with pupillary dilatation, compression of brainstem (midbrain peduncle containing corticospinal tracts) against the tentorial edge opposite the direction of herniation (can lead to false localization of motor deficit -ipsilateral hemiparesis (kernohans notch)– Pupillary contrictor fibers (dilatation
Posterior cerbral artery compression (ipsi-bilateral )
Duret hemorrhage
Kernohans notch
With compression of midbrain due to herniation from above the opposite cerebral peduncle is pushed against the opposite free edge of the tentorium (the creasing of the peduncle is called kernohans notch)
Causes weakness and a babinski sign ipsilateral to the cerebral hemispheric lesion (bc of crossing of the corticospinal tracts in distal medulla)
Duret hemorrhage
Fatal brainstem hemorrhage
Secondary to pregression of uncal herniation and resultant tearing of vessels in midbrains and pons
Cerebellar tonsillar herniation
Caused by symmetric expansion of supratentorial contents into posterior fossa OR expanding mass lesion in posterior fossa
Caudal cerebellar structures- tonsils attempt to escape thru the foramen magnum
Medullary compression results in cardiorespiratory arrest
CSF flow
Choroid plexu of the lateral and third ventricles make the CSF, it flows in the lateral ventricles
Then to the third venricle
Cerbral Aqueduct: 3rd ventricle to 4th ventricle
Foramen of luschka: 4th ventricle to subarachnoid space (lateral L for lateral)
Foramen of magendie: 4th ventricle to subarachnoid space (medial)
Arachnoid granulations spit out the excess CSF into the venous sinuses–> circulated in th body and peed out
hydrocephalus: communicating (non obstructive
Enlargement of ventricles associated with increas in CSF volume
Ventricular system is patent- increased size of ventricles may be due to: arachnoid villi obstruction due to decreased absorption at arachnoid granulation, causes of decreased absorption: meningitis, hemorrhage in subarachnoid space, or sinus thrombosis
OR over production of CSF from a choroid plexus papilloma
non- communicating hydrocephalus
Obstruction within ventricular system
Prevents Communication between the ventricles proximal and distal to obstruction
Examples of causes- tumor in ventricle blocking flow (at the foramen of monro), congenital malformation (atresia of aquduct of sylvius)
Thick meninges at base of brain blocking flow (fibrosis secondary to meningitis)
Normal pressure hydrocephalus and hydrocephalus ex vacuo
Normal pressure hydrocephalus: idiopathic condition associated with urinary incontinence, gait apraxia, and dementia (wet, wobbly, wacky), responds to shunt placement
Hydrocephalus ex vacuo- Occurs when there is loss of brain tissue due to stroke, trauma, or degenerative contions, no increase in CSF pressure and no obstruciton
head trauma
Leading cause of death of people<45
2 types: Blent and penetrating
Blunt- most common, associated with acceleration or deceleration forces to the head, Results in skull fractures, parenchymal injury, vascular injury
Penetrating missle- penetration by external object bullet
Characterization of trauma- open vs closed (referring to skull), focal vs diffuse, primary damage vs secondary damage
Primary vs Secondary damage related to non missle head injury
Primary damage- scalp laceration, skull fracture, cerebral contusions, cerebral laceration, intracranial hemorrhage, diffuse axonal injury
Secondary damage- ischemia, hypoxia, cerebral swelling, infection
Skull fractures
3 patterns-
linear :single fracture line, through entire thickness of skull
Comminuted- multiple linar fractures radiate from point of impact
Depressed: bone fragments displaced inward
Occur over convexity or base
Skin may be open or closed
Parenchymal damage- focal (concussions)
Concussion- pathophysiologic process induced by traumatic biomechanical forces (mild tramatic brain injury)
Caused by direct or indirect forces to head: biochemical and physiologic abnormalities occur, usually no structural abnormalities on imaging acutely, immediate transient neurologic impairment, constellation of physical, cognitive, emotional, and or sleep related symptoms that may or may not involve loss of consiousness, duration is highly variable- several minutes to days weeks, months or longer
Parenchymal damage- focal (contusions)
Wedge shaped superficial bruises of the brain, occur at any point of impact from fall or from direct blow to head
Usually at crests of gyri overlying rough area of inner skull
(oribital surfaces, tips of temporal lobes, occipital poles)
Small blood vessels, neurons, and glia are damaged
(Grossly- hemorrhage in meninges and superficial cortex), microscopically corresponds to subarachnoid space blood, perivascular accumulation of blood, after hours, necrosis, brain edema
Clinical correlations- deficits correlate with size and location of injury
coup vs contrecoup contusion
coup contusion- contusion occurs at at point of impact, usually secondary to blow to stationary head, may occur at point of impact from fall
Contrecoup contusion- contusion directly opposite the point of impact (usually occur with fall, as head hits groud a sudden decelration occurs that causes brain to bounce back and hit skull 180 opposite the point of imapct with ground
Another theory is brain in motion lags behind skull and with deceleration or impact of skull, it keeps moving the tensile strength of vessels at the site opposite of impact is exceeded producing damage
Parenchymal damage- diffuce
Diffuse axonal injury (DAI)- deceleration/acceleration injury and or angular acceleration, loss of consciousness at onset without lucid interval, unconscious or disabled till death, lesser degrees may be compatible with varying severity of neurologic deficits, axons are disrupted axonal transport continues and causes axonal swellings (acute and subacute - axonal swellings reactive macrophages, chronic degeneration of involved fiber tracts
Damage to white matter mostly
