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Traumatic Brain Injury

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Open or Closed Head or Brain Injury. Skull fractures, brain concussions, cerebral ... CAT Scans best initially. Later MRI or PET. ICP monitoring via LP ... – PowerPoint PPT presentation

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Title: Traumatic Brain Injury


1
  • Traumatic Brain Injury
  • Professor Deborah Cary,RN,MSN

2
INCIDENCE
  • Open or Closed Head or Brain Injury
  • Skull fractures, brain concussions, cerebral
    contusions/lacerations, and hemorrhage
  • (subarachnoid, subdural, epidural, intracerebral,
    brain stem)
  • Primary or Secondary Injury

3
Types of Insults
  • Intracranial Hemorrhages

4
Causes of Head Injury
  • MVA
  • Sports
  • Cerebral Bleeds
  • Concussions
  • Masses/Lesions

5
  • Whiplash
  • a Coup contre coup
  • injury causes injury
  • to neck/cerebrum

6
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8
  • The leading cause of death in head
  • trauma patients who reach hospital alive
  • is increased intracranial pressure

9
Initial Interventions
  • Cervical collar
  • Assess for bleeding
  • ABCs
  • CVA 6hr window for TPA to minimize
    complications
  • Protect from further injury

10
THE BRAIN FACTS
  • Composed of tissue, blood and cerebrospinal fluid
    (CSF)
  • Encased within a rigid structure (skull)
  • Little room for brain components to increase in
    size/volume, expand

11
AUTOCOMPLIANCE
  • Dynamic process of Accomodation
  • and Compliance----gt
  • ICP maintained at 10-15mm/Hg (Normal)
  • Range maintained despite normal pressure

12
MONROE-KELLY HYPOTHESIS
  • Any increase in the volume of one
  • component must be compensated for by
  • a decrease in the volume of other
  • components

13
Response to Increased Volume
  • CSF shunted to spinal arachnoid space
  • OR
  • The rate of CSF absorption is increased

14
ADDITIONAL RESPONSE
  • If needed a decrease in blood volume occurs
    secondary to the displacement of
  • venous blood into the sinuses
  • Minimal ICP increases as long as brain able to
    compensate

15
FACTS
  • AS ICP increases, Cerebral blood flow
  • decreases (CPP) ---gt tissue hypoxia
  • decrease in serum
    pH
  • increase in CO2
    levels

16
AS THE PROCESS CONTINUES---gt
  • Cerebral vasodilation.
  • Cerebral edema
  • Further ICP

17
IF THE PROCESS CONTINUES-----gt
  • The brain herniates downwards towards the brain
    stem------gt
  • Irreversible brain damage----gt
  • Death

18
Determining CPP
  • CPP pressure gradient that is needed to supply
    adequate blood to brain
  • Difference between MAP and ICP
  • SBP (2x DBP)
  • 3

Norm80-100mmH
19
Clinical Manifestations
  • Level of consciousness (LOC)
  • subtle or rapid
  • Etiology From impaired cerebral flow affecting
    the RAS - the area that wakes you up
  • Seizures

20
VITAL SIGNS
  • Increasing Systolic BP
  • Widening Pulse Pressure
  • Bradycardia
  • Irregular Respiratory Pattern

Cushings Triad or Cushings Reflex
21
Etiology
  • Increasing pressure on the
  • Thalamus
  • Hypothalamus
  • Pons/ Medulla

22
OCULAR SIGNS
  • Etiology Shifting of brain from
    midline---gtcompression of CN III----gtparalysis of
    pupil sphincter
  • Dilation of ipsilateral pupil (one side)
  • Sluggish response to light
  • Inability to move eyes upward
  • Ptosis of eyelid

23
OCULAR 2
  • Blurred vision
  • Diplopia
  • Changes in Extraocular Movement
  • Papilledema
  • Choked Optic Disc

Opthalmoscope
24
NEUROSENSORY
  • Unequal, weak hand grasps
  • Facial asymmetry (drooping)
  • Loss muscle tone, muscle spasticity
  • Absent/weak deep tendon reflexes (DTR)
  • Apraxia, hemiplegia/hemiparesis
  • behavior changes
  • clumsiness, loss of balance
  • Posturing - decerebrate and decorticate

25
Decorticate Posturing
Ominous Sign brainstem injury
26
Decerebrate Posturing
27
SYMPTOMS cont.
  • Flaccidity
  • Headache - due to compression vessels/nerves
  • Vomiting can be projectile

28
Dx cont.
  • Cerebral Angiography use contrast dx AV
    malformations, venous spasm and thrombus
  • EEG
  • EMG
  • Evoked Potentials to detect lesions in cerebral
    cortex might predict
  • coma outcome

29
Diagnosis
  • Neuro exam
  • CAT Scans best initially
  • Later MRI or PET
  • ICP monitoring via LP
  • Intraventricular catheter Gold Standard for
    monitoring ICP

30
Medical
  • Goal decrease ICP and maintain cerebral
    perfusion (CPP) poor prognosis ICP lt3
  • Ventilation - ABCs!!!
  • Monitor cardiac
  • Hypothermia
  • Sedation if extremely agitated (can ICP)

31
Medications
  • Ticlix
  • Plavix
  • Heparin
  • Coumadin antidotes check labs
  • Osmotic diuretics Mannitol
  • Corticosteroids
  • Anticonvulsants
  • Sedatives
  • Antipyretics

32
Nursing Interventions
  • Neurological checks/document - may be q1hr -
    chart on Glascow Coma scale
  • Analysis of vital signs changes?
  • Pad siderails \
  • Eye Care
  • Assess reflexes
  • Assess for nuchal rigidity (stiff neck)
  • Quiet environment
  • Darkened room
  • HOB - some controversy re position recent
  • thought is flat

33
Nursing cont.
  • Observe for otorrhea / rhinorrhea
  • No valsalva maneuvers
  • Suctioning only if necessary
  • 10 and only 2 passes since inc.ICP
  • SCDs
  • Never forcibly restrain ICP increases
  • With TIA sx assess for carotid bruit (bell)
  • Private Room
  • If HOB up 30 degrees
  • If conscious soft diet s caffeine
  • mannitol, requires inline filter

34
Nursing cont.
  • ABGs hypercapnia (CO2 gt45mm Hg) will dilate
    cerebral blood vessels and constrict with levels
    lt21
  • Serum O2 lt50mm Hg dilation
  • gt80mm decrease CBF

35
Brain Attacks
  • Third cause death US and Canada
  • Higher incidence in SE
  • Higher risk with African Americans,
    Japanese,Chinese
  • Risk factors HTN ,AGE - see complet list in
    textbook
  • Decline since 80s
  • 1/3 survivors, 2nd stroke in 5 yrs!
  • Precursor TIAs STAT RX!!
  • TIA reversible, 2-15minutes
  • gt 6hrs can lead to infarcts
  • Sx severe headache, speechlessness,
  • partial vision loss 1 eye,
    weakness,numbness,
  • unexplained dizziness
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