Trauma Flashcards by Meghan May

Dura mater

appreciate that shit

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subdural vs epidural spaces

Appreciate that shit

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Subarachnoid vs Subdural space

Appreciate everything!!!

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What is responsible for draining CSF in the meningeal layers of brain?

arachnoid granulations

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Be able to recognize the Falx and Tentorium cerebri and sinuses

know these

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Be able to identify Uncus

And uncal herniation

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Appreciate anatomy around tonsil of cerebellum

see image

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“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

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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

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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

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What are the two types of cerebral edema?

What does it look like grossly?

vasogenic and cytotoxic edema

flattened, widened gyri with narrowed sulci

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See disruption and increased permeability of BBB: see a shift of fluid form the INTRAvascular –> Extravascular compartment

Vasogenic edema = Extracellular edema

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What part of brain is effected by vasogenic edema? What are causes?

White matter affected

primary or secondary brain tumors, abscesses, contusions, intracerebral hematomas

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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

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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)

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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

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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

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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

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Occurs secondary to cellular energy failure
Results in shift of water from EXTRA–>INTRACELLULAR compartment

Cytotoxic edema “intracellular”

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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

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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.),

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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

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Increased pressure leads to :

_______ dictate what type of herniation

decreased perfusion and/or herniation syndromes

Rigid dural folds (falx, tentorium)

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_{The cingulate gyrus herniates under the falx d/t an ASYMMETRIC expansion of hemisphere lesions}

Subfalcine Hernation

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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?

1. Ipsilateral IIIrd nerve compression + pupillary dialation 2. Compression of brainstem (midbrain peduncle containing corticospinal tracts) on tentorial edge opposite direction of hernation 3. PCA compression 4. 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, ## Footnote * 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

1. Ventricle system is patent 2. Increased size of ventricles d/t: arachnoid villi obstuction from decreased absorption at arachnoid granulations 3. 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, t**hinned 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

Trauma Flashcards

(74 cards)