CNS injury 1-2 Flashcards

1
Q

peak age groups with head injuries

A

24-35 y/o male urban from violence and car acidens

small peak at 0-4 for child abuse
peak over 65 from falls

2/3 before hospitalization

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2
Q

mechanisms of head injuries

A

20-50% transport injuries
20-40% gunshot
falls and nonpentrating assults rest

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3
Q
contact injury (low velocity/blunt) 
causes
A

injury to structures protecting brain –> scalp lac, skull fracture, epidural hematoma, cerebral contusion

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4
Q

contact injury (low velocity/blunt)
linear skull fracture
define
outcome

A

line fracture

good outcome if no underlying

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5
Q
contact injury (low velocity/blunt) 
depressed skull fracture
A

comminuted bone fragments may or may not drive into brain

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6
Q
contact injury (low velocity/blunt) 
basilar fracture
A

skull base from high velocity blunt injurys

may extend thru cribiform plate or petrous bone –> CSF leak causing meningitis

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7
Q

signs of basilar fracture

A
meningitis
CSF rhinorrhoea or otorrrhea
bilateral periorb hematoma (raccoon eyes)
Battle sign 
facial nerve palsy 
subconjunctival hemorrhage
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8
Q
contact injury (low velocity/blunt) 
diastatic skull fracture
A

traumatic separation at suture lines

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9
Q
contact injury (low velocity/blunt) 
growing fracture
A

dural tear and herniation of arachnoid into fracture site–> CSF pulsations cause bone loss over month require surg correction

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10
Q
contact injury (low velocity/blunt) 
epidural hematoma
A

intracranial extradural ARTERIAL hemorrhage from skull fracture rupture middle meningeal artery

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11
Q
contact injury (low velocity/blunt) 
epidural hematoma symptoms

shape on mri

can lead to

A

lucid interval then progressive obtundation and coma as expands

lens shape

can lead to uncal herniation

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12
Q

contact injury (low velocity/blunt)
epidural hematoma
survival rate

treatment

A

low mortality due to damage from bleeding

treat with removal of mass lesion

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13
Q

acceleration/deceleration

describe translation vs rotational forces

A

translation = head move after impact

rotation = head move in more than one plane (MVC, rollover)

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14
Q

acceleration/deceleration

translational mechanism of injury

A

stretch and tear bridging veins causing subdural or cerebral contusions

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15
Q

acceleration/deceleration
subdural hematoma mechanism

assoc with

treatment

A

rupture of bridging veins in subdura

assoc with brain contusions

treat with remove clot, control ICP, restore cerebral blood flow

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16
Q

acceleration/deceleration
cerebral contusion
location

result in

treatment

A

frontal (anterior fossa) and temporal lobe (sharp edge of sphenoid wing)

result in swelling, brain shift, incr ICP, herniation

same tx as subdural

17
Q

rotational injury

mechanism of injury

A

microscopic tear of nerve cells in brain –> not seen on microscope

18
Q

rotational injury
diffuse axonal injury

pathology

location

symptom

A

shear injuries and retraction balls
axonal spheroids

in corpus callosum and brainstem not seen until 24 hr

vegetative with significant recover

19
Q

monroe kellie doctrine

A

volume of CSF + cranial blood volume must be constant

so any incr in intracranial volume decr CSF or CBV for constant ICP

20
Q

mechanism of brain compensation for incr intracranil volume

A

displace CSF but beyond certain point, ICP causes herniation

21
Q

equation for CPP

A

CPP = MAP - ICP

so ICP incr, CPP incr

22
Q

cellular mechanism of injury causing cytotoxic vs vasogenic edema

A

1) injury
2) masive depol and excess K+ extracellular
3) rverses glutamate transport so glutamate incr extracell
4) excess K+ taken up by astrocytes –> swell–> cytotoxic edema
5) excess glutamate –> incr Ca2+ –> activates enzymes for leak BBB –> vasogenic edema

23
Q

after edema happens how does injury occur

A

1) ICP rises
2) herniation of brain
3) can’t clear glutamate and K+ due to lack of blood supply –> more edema, ischemia, damage

24
Q

common symptoms of herniation

A

1) lethargy

2) poor response (obtunded) = hallmark

25
Q

define subfalcine herniation

A

cingulate gyrus herniates beneath falx

can kink anterior cerebral –> stroke

26
Q

define uncal herniation

effects of herniation

A

aka transtenotrial

uncus herniates across tentorial edge into posterior fossa compressing midbrain and ipsil cerebral peduncle

–> ipsil CN 3 palsy and contralateral hemiparesis or hemiplegia

27
Q

describe duret hemorrhage

A

due to uncal herniation if affect ascending reticular activating system

28
Q

describe cerebral herniation

A

with downward pressure –> bilateral uncal herniation

29
Q

describe tonsillar herniation

A

tonsil herniate down to foramen from mass in post fossa –> compress medulla –> Cushing’s reflex (bradycardia and HTN)

30
Q

complication from incr CBF at cell level

A

disrupt autoregulation

can’t constrict vessels so incr vessel diameter –> hyperemia and ischemia

31
Q

goal of treatment of head injury

A

decr ICP by maximize O2 and metab delivery

1) intubation
2) control ventilation
3) osmotic diuretic
4) ventricular catheters
5) drug induced coma

32
Q

reason for control ICP

A

after brain volume rise beyond compressible compartment space, small change in volume = big change in ICP

this incr MAP, blood vessel compressed –> ischemia

33
Q

symptoms of incr ICP

A

lucid interval with HA, n,v, lethargy, LOC

34
Q

glasgow coma scael
13-15
9-12
3-8

A
13-15 = mild 
9-12 = mod
3-8 = severe
35
Q
reflexes, which CN
pupillary 
corneal blink
cold caloric testing, doll's eyes
gag
A

pupillary = 2, 3, midbrain
corneal blink = 5, 7, pons
cold caloric testing, doll’s eyes = 3, 6, 8, pons–> midbrain)
gag (9, 10, medulla)