Neurological: TBI, SCI, seizures

Question 1

TBI: mechanism of injury, acceleration vs. deceleration

Answer 1

acceleration- occurs when a moving blunt object strikes the head (ex. hit in head with bat) site of impact with skull causes brain injury
deceleration- occurs when person head strikes an immovable object like dashboard and brain moves until it hits skull, rapid deceleration causes brain injury as it hits bony wall of cranium

Question 2

TBI: mechanism of injury, coup vs. contrecoup

Answer 2

coup- injury affects cerebral tissue directly under the point of impact (acceleration)
contrecoup- injury occurs in a line directly opposite of point of impact (deceleration)

Question 3

TBI: mechanism of injury, rotational

Answer 3

occurs when force impacting head transfers energy to brain in a nonlinear fashoin so head rotates on neck resulting in shear fores being exherted
ex. boxing (punch side of head)

Question 4

TBI: mechanism of injury, penetrating injury

Answer 4

a foreign object invades brain
ex. knife
may pass completely through brain and exit opposite side or just bounce around cranium causing multiple injuries in brain

Question 5

primary brain injury

Answer 5

occurs from direct injury caused by force of impact from traumatic event = immediate damage of neurons

Question 6

secondary brain injury

Answer 6

occurs in response to primary injury that arises from tissue and system responses to primary injury
involves ischemia, neuronal death, inflammation, cerebral swelling
can lead to worsening outcomes

Question 7

skull fractures : types

Answer 7

linear- minor injury, not seen to naked eye, need CT scan, can heal without intervention, not life threatining
depressed- force depresses skull inward usually causing fragments tearing through brain tissue, surgical repair and evacuate hematomas beneath fracture
open- where scalp has been lacerated, can expose brain to environment = r/f infection, surgical repair + debridement of contamination, antibiotics
basilar- develops at base of skull with high force, results in rhinorrhea (CFS draining from nose), or otorhea (CFS draining from ear), bruising around eyes, facial nerve paralysis, mastoid bruising. test drainage for glucose (will test positive if CSF), and check for halo sign(ring will form around drop of CSF indicating tear in meninges). drain CSF then dura closes itself

Question 8

what conditions can cause increased ICP

Answer 8

increase in brain volume (cerebral edema, space occupying lesions like hematoma)
increase in cerebral blood volume (hypercapnia, hypoxia)
increase in CSF

Question 9

what can happen when there are severe increase in ICP

Answer 9

it impairs cerebral perfusion and oxygenation to brain cells and may cause intracranial hypertension which is life threatening

Question 10

what are 2 processes that lead to increase in brain volume

Answer 10

1) space occupying lesions- develop as result to tumors, abscesses, hemorhages, hematomas (aka lesions that increase in size)
2) cerebral edema- due to abnormal accumulation of fluid in brains extraceullar space which increases brain tissue volume. can occur after any intracranial insult (trauma, surgery, cerebral anoxia, ishchemia) it doesn’t impair brain function until it results in increased ICP

Question 11

what are three circumstances that increase serebral blood volume?

Answer 11

hypoxemia or hypercapnia - results in cerebral vasodiilation and increased cerebral blood volume. any systemic process that effects blood levels of oxygen/CO2 directly affects cerebral blood flow, perfusion pressure and blood volume
cerebral venous outflow obstruction- increases with any process that impedes cerebral venous outflow, ex. impeding jugular venous drainage from head (neck/head flexion/rotation, devices too tight like trach ties) also things that increase intrathoacic or intraabdominal pressure (valsava maneuver, use of posititve pressure vent)
loss of cerebral autoregulation- becomes ineffective in prolonged ischemic conditions, sustained increases of ICP and/or states of hyperemia. when autoregulation lost, blood vessels dilate and insult homeostasis by increasing CBV and ICP

Question 12

what is autoregulation

Answer 12

process where cerebral vessels have capacity to dilate or constrict in response to changes in perfusion pressures
it maintains adeqaute cerebral blood flow by altering cerebral vascular tone
As CPP increases, compensatory vasoconstriction occurs
as CPP decreases, cerebral vasodilation occurs
Requires: CPP within 50-150mmHg + MAP within 60-130mmHg , if this lost, autoregulation is lost

Question 13

CSF: cause of increase

Answer 13

when CSF increases its circulation or flow is blocked, or its absorption decreases causing a increase in CSF amount
obstruction to CFS outflow can be due to mass lesions or infections
decreased absorption can result from subarachnoid hemorrhage or meninigitits
loss of autoregulation
hypercapnia, hypoxemia

Question 14

what is hydrocephalus

Answer 14

condition involving increased volume of CSF particularly in ventricles of brain
this can increase ICP

Question 15

what is a focal brain injury

Answer 15

localized to the area of direct injury
include: contusion to a hematoma
may be result from a concentrated collection of blood from a blunt trauma or intracerebral bleed, or an object

Question 16

Focal brain injury: subdural hematoma

Answer 16

accumulation of blood between dura and arachnoid layers of meninges
developes secondary to venous injury from tears in the bridging veins
S+S onset = slower
may occur as result of mild brain trauma (elderly/alcoholics), or spontaneously
three catagories:
1) acute (S+S onset <48hrs after injury, drowsy or comatose following injury, headache, confusion, agitated, slow thinking)
2) subacute (develop 48hr-2weeks after injury, headache, mild contralateral hemiparesis, drowsy, confusion occur onset for days or weeks)
3) chronic (S+S onset over weeks after injury, S+S vague, lethargy, vomiting)
Manage: surgical removal of hematoma if shift of brain present on CT or symptomatic + 1cm in size, use burr holes or craniotomy or subdural drain

Question 17

Focal brain injury- epidural hematoma

Answer 17

occurs in space between dura mater and skull
high impact to temporal areas induce these
S+S: brief loss of consciouness right after injury followed by episode of lucidity then recurrent loss of consciousness, fixed and dilated pupil on same side as impact
manage: cauterizing vessel to evacuate hematoma and placing ICP monitor, osmotic diuretic (to decrease ICP), mechanical ventilation

Question 18

Focal brain injury- intraparenchymal hematoma

Answer 18

accumulation of blood between parenchyma or tissue of brain rather than between meningeal layers
results from: uncontrolled HTN, ruptured aneurysms, trauma
vary according to location: headache, ALOC, ipsilateral pupil dilation, contralateral hemiplegia
manage: treat increased ICP and optimize CPP, cannot do surgery bc hematoma ais deep within brain

Question 19

Focal brain injury- contusion

Answer 19

bruising of cerebral soft tissue
commonly seen in traumatic brain injury
cause macroscopic tissue and vessel damage- detectable via CT/MRI
associated with longer periods of unconsciousness

Question 20

what is diffuse brain injuries

Answer 20

injury occurs in several areas of brain
include concussion and diffuse axonal injury, and subarachnoid hemorrhage

Question 21

what is concussion

Answer 21

mild traumatic brain injury caused by blunt trauma to head
cerebral damage occurs at microscopic level, not detectable through radiographic or other tests
includes: immediate period of unconsciousness (lasting up to 20 min) and short term amnesia
if mild- will not lose consciousness but appear confused, dazed, stunned
Reports: loss of consciousness, post traumatic amnesia, altered mental status, focal neuro deficits, deterioration
CT ordered
Post concussion syndrome- where concussion symptoms persist for 3 months or more after injury

Question 22

what is diffuse axonal injury

Answer 22

occurs when shearing forces disrupt structure of neurons and vessels
may be present without bleeding (hard to see on CT/MRI)
results from high speed acceleration/deceleration or rotational injury
present- multiple small hemorrhages
mild DAI- result in comatose state for hours to days followed by recovery with minimal residual neuro damage
severe DAI- high morbidity/mortality

Question 23

what is subarachnoid hemorrhage

Answer 23

accumulation of blood between meningeal arachnoid and pia mater layer
results in blood leaking into CSF
bleeding can be focal “+ minor or massive and diffuse with intracranial HTN
results from - ruptured aneursysm, uncontrolled HTN, TBI
S+S: acute onset of severe headache (worst headache ever) accompanies with ALOC, diplopia, seizures, photophobia

Question 24

assessment with TBI

Answer 24

Initial: ABC, vitals then neuro, body for signs of injury
second: hx, meds, allergies, surgeries, comorbid conditions
general systems assessments with interventions to ensure adequate ventilation/oxygen/perfusion
priorities = ABC, neuro assessments to detect deterioration

Question 25

determining severity of injury

Answer 25

using GCS- scale to measure patients ability to interact with environment
score GCS when initial resus is finished and before any sedation given
mild TBI = GCS 13-15 with or without loss of consciousness , monitor within home for 24 hours, no hospital stay needed
moderate TBI = GCS 9-12 accompanied with loss of consciousness for up to 6 hours, required an admission in hospital. high risk for increased ICP from edema, monitor neuro + hemodynamic status and CT performed
severe- GCS < 8 , or if GCS deteriorates to that level within 48 hours of admission, may need ventilator, ICP monitoring, treat ICP

Question 26

what is included in bedside neurologic assessment

Answer 26

LOC, motor function, pupil response, respiratory function, vital signs, GCS
identify intracranial HTN:
decreasing GCS
vitals change: bradycardia, SBP HTN with wide pulse pressure, irregular resps, ICP S+S (N/V, headache, lethargy, restless, ALOC)
fluid status
monitor respiratory system- O2, RR, rhythm, depth, sounds, cyanosis, hypoxia, ABGs, effort, distressed, accessory muscle use

Question 27

what is jugular venous oximetry (SjO2)

Answer 27

measure of cerebral oxygen sats to assess relationship between oxygen supply and demand and it assist in determining if CPP is sufficient to satisfy cerebral metabolic demand
maintain PbtO2 greater then 15mmHg

Question 28

what are lab tests used for and which ones for TBI

Answer 28

monitors to early detect cerebral hypoxia and impending ischemia
ABgs, CBC, coag profile, electrolytes, BUn, Creatinine, Liver function, serum osmolality, urinalysis, urine osmolality, panel of blood for alcohol and/or illicit substances

Question 29

what imagine studies are used for TBH

Answer 29

CT (first line) - detects fractures, soft tissue injuries (lacerations, contusions, hemorrhages, masses)
MRI- used for DAI
Doppler- detect changes in CBF
EEG- detect abnormalities in brain electrical impulses like seizures/brain death

Question 30

managing cerebral tissue perfusion

Answer 30

decreased cerebral tissue perfusion is due to cerebral edema and intracranial HTN
goal- limit ischemic injury by treating hypoxia and hypotension to minimize secondary injury
include: increase MAP and reduce ICP

Question 31

managing cerebral perfusion pressure