Traumatic Brain Injury Flashcards

1
Q

What are the Mechanisms of Injury

A

Acceleration/Deceleration
Rotational
Penetrating
Contrecoup

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2
Q

What are the types of Fractures?

A

Linear
Depressed
Open
Basilar

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3
Q

What is Basilar Sign?

A

Battle sign (Behind ear)
Racoon Eyes
Otorrhea (CSF in ears)
Rhinorrhea (CSF in nose)
Positive halo signs (fluid on gauze, if turns yellow, CSF present)

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4
Q

What are the 3 points that increases Intracranial Pressure?

A
  1. Increased Blood volume (tumours/edema) - Increased bleeding that occupies space, decreases cerebral perfusion
  2. Increased Cerebral Blood Volume Dilution occurs which CPP less than 50 - auto regulation fails
  3. Increased Cerebrospinal Fluid (CSF) = Increased ICP, flow blocked = absorption decreased
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5
Q

What is Focal Brain Injury?

A

Local injury, range from small contusion to severe hematoma

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6
Q

[Focal Brain Injury]
What are the 3 types of Subdural Hematoma?

A
  • Blood between dura and arachnoid

Acute: manifest <48hrs after (drowsy/coma, progress rapidly, unilateral h/a)
Subacute: manifests 48hrs-2wks, h/a, drowsy, contralateral hemiparesis
Chronic: over course of weeks, h/a, absent minded

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7
Q

[Focal Brain Injury]
Subdural Hematoma Interventions and Nursing Care?

A

Those that bleed more easily: alcoholics, anticoag users

Interventions: Surgical removal, drain
Nursing: LOC, and focused neuro assessment

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8
Q

[Focal Brain Injury]
What is Epidural Hematoma?
s/s & Interventions?

A
  • Blood between dura and skull

S/s: Fixed and dilated pupils on ipsilateral side
I: Surgical removal, ICP monitoring, osmotic diuresis (to decrease ICP), airway protection, and mechanical ventilation

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9
Q

[Focal Brain Injury]
What is intraparenchymal Hematoma?
s/s? Interventions?

A
  • Blood in brain tissue

S/s: h/a, decreased LOC, pupil dilation, contralateral hemiplegia
I: No surgical evacuation, treat ICP, management of CPP
(MAP-ICP)

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10
Q

What is Contusion?

A

Bruising of cerebral soft tissue

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11
Q

What is Diffuse Brain Injury? (3 parts)

A

Widespread involvement of the brain, difficult to detect and treat
- Concussion (mild TBI but blunt trauma)
- Diffuse axonal injury (shear force disrupts structure of neurons by vessels)
- Subarachnoid Hemorrhage (blood between arachnoid & pia mater – from ruptured cerebral aneurysm l/t uncontrolled HTN)

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12
Q

S/s of DAI? Subarachnoid? and Concussion?

A

DAI: Decreased LOC, Increased ICP, decerebrate or decorticate posture, cerebral edema

Subarachnoid: thunderclap h/a, contralateral hemiplaegia, pupil dilation

Concussion: [Rest, tylenol] Post-Concussion - h/a, short term memory loss, decreased concentration, fatigue, difficulty sleep, irritable, sensitive to light and noise

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13
Q

What are the Assessments?

A
  • ABCs
  • V/s
  • Neuro assessments (LOC, motor function, Pupillary response, GCS)
  • Secondary assessment (mech of injury, past mx hx, allergies, sx, comorbidities)
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14
Q

What is the 3 levels for severity of Injury?

A
  • Mild TBI (GCS 13-15 with or w/o loss of LOC for 6 hrs)
  • Moderate TBI (GCS 9-12 w loss of LOCL for 6 weeks)
  • Severe TBI (GCS <= 8 on initial assessment or deterioration after 48 hours)
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15
Q

What are the diagnostics? (Lab, Imaging, Other)

A

Lab: ABGs, CBC, Coag, electro, BUN, CR, Liver, Osmolarity, u/a, urine osmolarity, drug toxicity

Imaging: CT Scan, MRI
Other: Tomography, transcranial doppler, EEG

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16
Q

What is Level One Collaborative Management?

A

Level One:
Analgesics/sedatives (in intubated patients)
Normothermia maintenance,
HOB 30
Intermittent ventricular drainage
If ICP >20-25: Go to level 2

17
Q

What is Level Two Collaborative Management?

A

External Intermittent ventricular drainage
Intermittent CSF drainage
Hypertonic saline + Mannitol (Goal: PaO2 >100, PaCO2 30-35)
If autoregulation is absent - increase CPP to 50 to decrease ICP
Repeat CT and neuro exam
If ICP remains 20-25: Go to level 3

18
Q

What is Level Three Collaborative Management?

A

Neuromuscular blockade if positive response to loading dose
Barbiturate if ICP is responding well to loading dose
Craniectomy

19
Q

TBI Goals?

A
  • Limit ischemic Injury
  • Cerebral Perfusion Pressure
20
Q

How to decrease secondary TBI?

A
  • Ongoing monitoring and assess
  • Identify neuro compromise and report
  • Maintain adequate oxygenation
21
Q

What is Supportive Treatment?

A
  • Decrease stimulation
  • Normothermia
  • HOB 30 degrees
  • Intermittent ventricular drainage
22
Q

What is Aggressive Treatment?

A
  • Mannitol
  • Eurovolemia (isotonic)
  • Hypertonic
  • Hyper Ventilation (PaO2 manipulation)
  • Neuromuscular blockage
  • Drug induced coma
  • Decompressive craniectomy
23
Q

What the surgical approaches? (3)

A

Evacuation
ICP monitoring/CSF drainage
Craniectomy

24
Q

What are the complications of Increased ICP?

A

Antidiuretic Hormone Challenges (DI, syndrome, cerebral salt wasting)

Other (seizures, herniation, brain death)

25
Q

What is Syndrome of Inappropriate SIADH?

A

Excess ADH secretion l/t water retention
<400ml/ day, increased urine gravity
Decreased serum sodium
Systemic/intracerebral edema
Fluid Restriction

26
Q

What is Cerebral Salt Wasting?

A

Neurogenic Salt wasting, hypovolemia
Decreased Na