Trauma Flashcards
Dura mater
appreciate that shit
subdural vs epidural spaces
Appreciate that shit
Subarachnoid vs Subdural space
Appreciate everything!!!
What is responsible for draining CSF in the meningeal layers of brain?
arachnoid granulations
Be able to recognize the Falx and Tentorium cerebri and sinuses
know these
Be able to identify Uncus
And uncal herniation
Appreciate anatomy around tonsil of cerebellum
see image
“Blood-brain neurovascular unit”
- Site of BBB: ___________
- Tight intercellular junctions (non-permissive compared to systemic endothelial cells)
- Endothelium has low _______ & basement membrane
- Dynamic interaction of endothelium with _______
brain capillary endothelium
pinocytotic rate
astrocytes & pericytes
What diffuses freely and what requires active transport to get across teh BBB?
- Small substances & small lipophilic molecules freely diffuse through membrane
- Large substances & hydrophilic molecules require active
Defined as an accumulation of excess fluid in intracellular or extracellular spaces of the brain
Cerebral edema
*see increased intracranial pressure d/t variety of processes & associated with significant
morbidity/mortality
What are the two types of cerebral edema?
What does it look like grossly?
vasogenic and cytotoxic edema
flattened, widened gyri with narrowed sulci
See disruption and increased permeability of BBB: see a shift of fluid form the INTRAvascular –> Extravascular compartment
Vasogenic edema = Extracellular edema
What part of brain is effected by vasogenic edema? What are causes?
White matter affected
primary or secondary brain tumors, abscesses, contusions, intracerebral hematomas
What are the three mechanism for Vasogenic (extracellular) edema
- 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 factors
What features are typical of vasogenic edema?
What therapy does vasogenic edema usually respond to?
Flattened gyri/narrow sulci with compressed ventricles and soft brain
will respond to coticosteroids and anti-VEGF!!!
(picture is glioblastoma with vasogenic edema)
Explain how a brain tumor like glioblastoma results in vasogenic edema
Have extensive angiogenesis w/ microvascular proliferation, poorly formed BBB
end up with extensive vasogenic edema and mass effect
How can we get a clear idea of the extent of cerebral edema in a pt through imaging?
T1 will give us good idea of location of lesion
T2 really highlights extent of edema
What are some consequences of vasogenic edema as it’s responding to insult?
can see right to left or left to right shifts
get mass effect
get herniations
- Occurs secondary to cellular energy failure
- Results in shift of water from EXTRA–>INTRACELLULAR compartment
Cytotoxic edema “intracellular”
Where in brain do we see Cytotoxic edema and what causes the intracellular swelling?
GRAY matter
ntracellular swelling - large amounts of sodium enter cells, water follows
Most common causes of cytotoxic edema and mechanism
Most common causes: ischemia/infarct, meningitis, trauma, seizures, hepatic encephalopathy
• Mechanisms: dysfunction of neuronal and astrocytic membrane pumps (caused by excess glutamate, extracellular potassium, inflammatory cytokines, etc.),
Increased intracranial pressure
The brain is in a closed rigid box
Brain volume =
Increased volume =
Brain volume = Brain + blood + CSF (+ lesion)
Increased volume = increased pressure
Increased pressure leads to :
_______ dictate what type of herniation
decreased perfusion and/or herniation syndromes
Rigid dural folds (falx, tentorium)
The cingulate gyrus herniates under the falx d/t an ASYMMETRIC expansion of hemisphere lesions
Subfalcine Hernation
What vascular stuctures are compromised in a subfalcine hernation?
May compress the anterior cerebral artery–> leading to infarct
Medial temporal lobe displaced through the tentorial opening because of asymmetric expanding lesion
Transtentorial Uncal Herniation
What four complications can we see d/t Transtentorial Uncal Hernation?
- Ipsilateral IIIrd nerve compression + pupillary dialation
- Compression of brainstem (midbrain peduncle containing corticospinal tracts) on tentorial edge opposite direction of hernation
- PCA compression
- Duret hemorrhage
Why do we see Ipsilateral cranial nerve III compression in transtentorial hernation?
Tentorium firmly attached to skull, midbrain pushes down from above and compresses 3rd nerve (oculomotor)
**see pupillary dilation bc pupillary constrictor fibers are on the surface of 3rd nerve.
You pt comes in with a Babinski sign on the left side. Your preceptor suspects hernation based on imaging she saw. Where would the herniation be located?
what other symptos would you see?
Why was there a babinski sign
Called Kernohans notch; seen in Transtentorial uncal hernation
babinski shows up IPSI to the lesion and is result of compression of midbrain from hernation aove the opposite cerebral peduncle being pushed against opposite free edge
Pt comes in with Babinski sign and a duret hemorrhage. What blood supply in the brain is vulnerable in this patient?
signs of transtentorial hernation
PCA vulnerable
- Fatal brainstem hemorrhage
- Secondary to progression of uncal herniation and resultant tearing of vessels in midbrain/pons
Duret hemorrhage: seen in transtentorial hernation
- Symmetric expansion of supratentorial contents into posterior fossa or
- Expanding mass lesion in posterior fossa
Cerebellar Tonsillar Herniation
In Cerebellar Tonsillar Hernation,
- Caudal cerebellar structures (“tonsils”) attempt to escape through the ________
- Medullary compression results in ___________
foramen magnum
cardiorespiratory arrest
Enlargement of ventricles associated with increase in CSF volume
Hydrocephalus
Three causes of Communicating (NON-obstructive) hydorcephalus
- Ventricle system is patent
- Increased size of ventricles d/t: arachnoid villi obstuction from decreased absorption at arachnoid granulations
- Overproduction of CSF from choid plexus papiloma
appreciate CSF flow
Where are the major sites for CSF block leading to COMMUNICATINGhydrocephalus
- Obstruction within ventricular system
- Prevents “communication” between the ventricles proximal and distal to obstruction
NON-communicating hydrocephalus
• Tumor in ventricle blocking flow (example: At foramen of Monro)
- Congenital malformation (example: Atresia of aqueduct of Sylvius)
- Thick meninges at base of brain blocking flow (example: fibrosis secondary to meningitis)
All are examples of:
NON-communicating Hydrocephalus
Head trauma
- Leading cause of death of people ________, in developed countries
- In road traffic accidents: head trauma accounts for 50% of deaths
- Two primary types:
< 45 years old
Blunt and Penetrating
Describe Blunt head trauma and what happens as a result
- Associated with acceleration or deceleration forces to the head
- Skull fractures• Parenchymal injury • Vascular injury
What is the difference between Primary and Secondary damage releated to non-missile or blunt trauma to head
Primary: scalp lac, skull frx, cerebral contusions and lacs, intracranial hemorrhage, diffuse axons injury
***primary happens immediately
Secondary: ischemia, hypoxia, cerebral swelling, infection: occurs later
This type of injury cause specific neuro deficiets and eplielpsy
This type causes more coma and vegetative state
Focal
vs
Diffuse
Primary damage in Focal trauma is:
Primary damage in Diffuse trauma is:
Foca: scalp lac/contusions, fractures, brain lacs and contusions and intracramial hemorrhage
Dissuse: Diffuse axonal injury and diffuse vascular injury
_____results in infection
_____results in brain swelling and global brain ischemia
Focal trauma
Diffuse Trauma
_______: single fracture line, through entire thickness of skull
______: multiple linear fractures radiate from point of impact
______: bone fragments displaced inward
Linear
Comminuted
Depressed
*skull fractures occur over the CONVEXITY or base of skull and can be open or closed
Typically seen in motor vehicle crash victim
Has hinge fraxture extending transversly across base of skull anterior to petrosous + displaced circular frx extends through occipital bone
Basilar skull fracture
**end up with a “ring” fracture encircling formen magnum
Pathology of Concussion
Causes
Biochemical/physiologic abnormalities
pathophysiologic process induced by traumatic biomechanical forces (also called mild traumatic brain injury)
- Caused by direct or indirect forces to head
- Biochemical and physiologic abnormalities occur; usually no structural abnormalities on imaging acutely
What are signs and symptosm of concussion and how long do they last?
Immediate transient neurologic impairment
Constellation of physical, cognitive, emotional, and/or sleep- related symptoms that may or may not involve loss of consciousness
• Duration is highly variable: several minutes to days, weeks, months, or longer
superficial bruises of the brain that usually at crests of gyri
• Occur overlying rough area of inner skull (orbital, temporal regions)
Contusion
What is damaged in a contusion, where do we see the damage?
Results at point of impact from fall or from direct blow to head
Small blood vessels, neurons, and glia are damaged
(deficits correlate with size and location of injury )
- Wedge-shaped
- Superficial hemorrhage in cortex and meninges
- Microscopically: Perivascular accumulation of blood and after hours, brain edema
Acute Contusion
- Orbital surfaces of frontal +/or temporal lobes
- Gyri indented, cavitated, with brown/orange discoloration
• Macrophages with hemosiderin, fibrillary astrocytes
Old contusion
What would you expect to find histologically in a patient with an old contusion?
Cavitation (loss of tissue) and hemosiderin laden macrophages with pigment form old hemorrhage
• Contusion occurs at point of impact
Usually secondary to blow to stationary head and May occur at point of impact from fall
COUP CONTUSION
Contusion directly opposite the point of impact
Usually occur withfall
As head hits ground a sudden deceleration occurs that causes brain to “bounce” back and hit skull 180o opposite the point of impact with ground
Counter Coup Contusion
What is another theory for Counter Coup contusion damage?
: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
Most common locations of Contrecoup contusions
Bilateral contusions of frontal and temporal poles; opposite the point of impact
Deceleration/acceleration injury and/or angular acceleration
• Loss of consciousness at onset WITHOUT lucid interval
• Unconscious or disabled till death
Diffuse Axonal injury
- Lesser degrees may be compatible with varying severity of neurologic deficits
- Widespread damage to the axons :Mechanical forces disrupt axons
DAI
What areas of the brain are susceptible to diffuse axonal injury?
White matter:
• corpus callosum, paraventricular white matter, superior cerebellar peduncle,
superior colliculi
What Acute and Chronic changes do we see in DAI?
• Acute changes: clusters of petechial hemorrhages and soft hemorrhagic foci
• Chronic changes: hydrocephalus ex vacuo, thinned corpus callosum, gray discoloration of white matter
This pt died of sudden deceleration injury. Fellow passenger in car that survived said friend was unconsious right away and never came to. What did pt die from?
Acute Diffuse axonal injury: see cluster of petichaial hemorrhage and there we no lucid interval
What must be present to confirm Dx of acute DAI?
Microscopic exam:
Axons are disrupted; axonal transport continues and causes axonal
swellings
Your attending points out axonal swellings in a brain tissue specimen. It is positive for B amyloid protein and silver stains. What caused the pt death?
You are looking over histolgy slides and case studies. A resident points out microglia and axonal swellings. YOu state this is typically seen in what type of DAI?
seen in Subacute DAI
__in chronic we have degeneration of fiber tracts
Epidural and Subdural hematoma
Epidural: outside of dura; often MMA ruptured, get LENS shape
Subdural: under dura and pools iwth venous blood
- Associated with skull fx & middle meningeal artery tear
- LUCID INTERVAL between trauma & clinical symptoms
- Slow accumulation because of adherence between skull & dura
Epidural hematoma
- -Most often nonlocalizing signs: headache, confusion
- -Tear of bridging veins extending from subarachnoid space to dura –More common in elderly people with brain atrophy
Acute Subdural hematoma
What are some concerns with chronic subdural hematomas?
susceptible to recurrent bleeds from friable vessesl in granulation tissue,
often happen while back and see well organized membrane enclosing hematoma and compression of the underlying hemisphere
How would you get a subarachnoid space hemorrhage?
–Occur from contusions, lacerations skull base fractures, escape of blood from ventricular system
In Post-traumatic hydrocephalus we see obstruction of CSF resorption due to
subarachnoid space hemorrhage
Chronic traumatic encephalopathy is associated with
mild repetitive traumatic brain injury • Described in athletes (football, hockey) and veterans
Symptoms of chronic traumatic encephalopathy
Initially impulsivity, aggression, depression, short-term memory loss
Eventually dementia, gait, speech abn, parkinsonism
extensive deposition of tau in form of neurofibrillary and glial tangles and TDP-43 inclusions
pathology for seqeulae of chronic traumatic encephalopathy
