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Neurology > Traumatic Brain Injuries > Flashcards

Traumatic Brain Injuries Flashcards

1
Q

What is the leading cause of morbidity and mortality following trauma? (3)

A

Head Injury

  • Almost half of all trauma deaths are from head injury
  • Drugs and alcohol are etiologic 70% and confound the examination
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2
Q

What is a primary brain injury?

A

Initial insult. Not much you can do except try to prevent it

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3
Q

What is a secondary brain injury?

A

Examples include: bleeding, edema, movement of the brain. These symptoms can be managed, some are preventable and some are treatable

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4
Q

What are the 3 mechanisms of primary injury?

A
  • Concussion-compression (direct blow)
  • Sudden deceleration (brain squishes into skull)
  • Rotational acceleration (causes axons to tear)
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5
Q

Concussion-Compression

A
  • Directly from localized impact
  • If compressive force exceeds elasticity of the skull, skull will fx
  • Initial force is transmitted to the intracranial contents causing localized tissue damage
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6
Q

Sudden Deceleration (4)

A
  • Abrupt deceleration of a rapidly moving head
  • Sudden halt causes brain to collide with the inner surface of the skull
  • Shearing forces happen d/t acceleration and rebound
  • Contusions and lacerations result
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7
Q

What does tearing of the bridging veins on the side opposite to the area of impact result in?

A

Subdural Hematoma (contrecoup)

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8
Q

Rotational Acceleration (7)

A
  • Parenchymal tearing
  • Axonal disruption
  • Hemorrhage
  • Brain edema
  • Focal shear/strain damage tends to occur in axons btw grey and white matter (common in frontal,temporal, and corpus collosum)
  • Shows up well on MRI, not CT
  • Microhemorrhages may show up as it progresses
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9
Q

“Talk and Deteriorate” Cases

A
  • “Lucid intervals” pt has a temporary moment of improvement and they think they are ok, then they die
  • Can be save with prompt intervention!
  • Cause of deterioration is an expanding intracranial mass lesion (subdural or epidural hematoma)
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10
Q

What are 3 Secondary traumatic brain injuries?

A
  • Systemic insults
  • Intracranial insults
  • Cerebral ischemia-reperfusion injury
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11
Q

What are the 2 most frequent systemic insults causing secondary brain injury?

A
  • Hypoxemia

- Hypotension

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12
Q

What are 6 systemic insults of secondary brain injuries?

A
  • Hypotension
  • Hypoxemia
  • Anemia
  • Electrolyte disturbances
  • Hypo/hyperglycemia
  • Hyperthermia
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13
Q

Hypoxemia (4)

A
  • systemic insult
  • results from hypoventilation
  • Brainstem movement at time of injury causes loss of consciousness and its responsible for respiration
  • other possible causes include: airway obstruction, flail chest, hemo/pneumothorax, pulmonary contusion
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14
Q

Hypotension (5)

A
  • Leads to decreased end organ perfusion
  • Systolic<90
  • Increases mortality
  • Impairment of auto regulation of cerebral blood flow
  • Restoration of arterial blood flow improves neurological status
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15
Q

Intracranial insults (2)

A
  • Subdural hematoma can occur, needs to be operated ASAP, >4hrs increases mortality rate a lot
  • Prolonged elevated ICP is a/w poor outcomes
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16
Q

What happens to ICP if large intracranial hematomas are not removed promptly?

A

Rise rapidly d/t further bleeding and edema

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17
Q

What increases if subarachnoid hemorrhage is seen on CT?

A

Pt developing cerebral vasospasms

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18
Q

Cerebral Ischemia-Reperfusion Injury (4)

A
  • Transmembrane shift of Na & Ca into the cell and K out of the cell
  • Oxygen radical formation
  • Lipid peroxidation
  • All leads to cell death, worse neurological outcomes
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19
Q

Histological and Biochemical Changes in Brain Injuries (4)

A
  • Change in Ca homeostasis
  • Production of free radicals
  • Release of excitatory amino acids
  • Alterations in intercellular magnesium
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20
Q

GSW to the Brain (4)

A
  • Energy dissipated in the brain by a bullet is proportional to the impact velocity squared
  • Rifles are the worst
  • Shell fragments and handgun fragments are not as bad
  • Explosively increased ICP produces direct brainstem damage in experimental models
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21
Q

What are the different types of Primary Traumatic Brain Injuries? (8)

A
  • Scalp injuries
  • Skull fx
  • Penetrating injuries
  • lacerations
  • Concussions
  • Contusions
  • Diffuse axonal injury
  • Intracranial hematoma
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22
Q

Scalp Injury (3)

A
  • Mild bruising to complete avulsion
  • **A major scalp laceration can cause hemorrhagic shock
  • Scalp injuries can overlie a penetrating skull injury that can cause meningitis or a brain abscess
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23
Q

Skull Fx

A
  • Most are linear
  • Stellate (star) occur with more force
  • Depressed fx occur with even more force
    • Skull fx greatly increase the likelihood of underlying brain injury
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24
Q

Basilar Skull Fx (3)

A
  • Cause injury to cranial nerves
  • Cause injury to bv’s traversing the foramina at skull base
  • If it extend to the paranasal sinuses or mastoid air cells, it can cause CSF to leak from the nose
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25
Q

Battle’s Sign

A
  • bruising behind the ear

- indicative of basilar skull fx

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26
Q

Penetrating Injuries (4)

A
  • At risk for meningitis or brain abscess
  • Stab wounds to orbit or nasal cavity are prone to enter the cranium
  • Causes vascular injuries
  • And Neurological deficits
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27
Q

Lacerations (2)

A
  • Occur after severe blunt head trauma from a shear/strain injury
  • Pontomedullary junction is prone to this type of injury following hyperextension of the head on the neck (whiplash)
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28
Q

Concussion (4)

A
  • Transient loss of consciousness that may result from temporary dysfunction of either cortical hemispheric neurons bilaterally or reticular activating system
  • Little or no apparent tissue damage but often amnesia
  • Retrograde amnesia
  • Memory of event still intact
  • Decreases in cerebral blood flow for a couple hrs
  • Mild ICP for several days
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29
Q

What are cerebral concussions regarded as?

A
  • Mild head injuries BUT

- there may be extensive subclinical damage

30
Q

Contusions (4)

A
  • Some tissue injury (capillary damage & interstitial hemorrhage)
  • Can produce neurological deficits
  • Usually act as a place for hemorrhage to occur
  • Or a place for swelling/ post traumatic epilepsy to occur
31
Q

What are the 3 types of contusion?

A
  • Coup
  • Intermediate
  • Contrecoup
32
Q

Diffuse Axonal Injury (5)

A
  • Result from strain/shear forces
  • Pathogenesis is poorly understood
  • Magnitude and distribution reflect morbidity of injury, esp. in pts who do not have mass lesion
  • May have petechial hemorrhaging between gray and white matter
  • MRI is preferred but can be seen with CT
33
Q

What is the Triad of Damage in Diffuse Axonal Injury?

A
  • Corpus callosum
  • Dorsal lateral quadrant of the midbrain
  • Microscopic damage w/in subcortical white matter
34
Q

Intracranial Hematomas (4)

A
  • Intracerebral hematoma
  • Subdural hematoma
  • Epidural hematoma
  • Subarachnoid hemorrhage
35
Q

Intracerebral Hematoma (4)

A
  • Hemorrhage in to brain parenchyma
  • Caused by shear/strain forces rupturing bf’s
  • Small ones treated non-surgically (control ICP, maintain perfusion
  • Surgical decompression for: large ones, if pt is severely impaired, deteriorating pts
36
Q

What decreases ICP? (2)

A
  • Hyperventilation

- Mannitol

37
Q

3 Types of Subdural Hematoma

A
  • Acute
  • Subacute
  • Chronic
38
Q

What are subdural Hematomas caused by?

A
  • Tears in the bridging veins

- Limited by the falx!!

39
Q

Acute Subdural Hematoma

A
  • Treated by prompt craniotomy and evacuation

- Poor prognosis d/t underlying brain damage

40
Q

Subacute/Chronic Subdural Hematoma

A
  • Treated with burr hole evacuation
41
Q

What is the magic number for midline shift?

A

3mm

42
Q

What do you do if midline shift is more than 3mm?

A

Call a Neurosurgeon!!

43
Q

Epidural Hematoma Cause

A

Tearing of the middle meningeal artery, usually a/w temporal bone fx. Not limited by the falx!

44
Q

Clinical Picture of Epidural Hematoma (3)

A
  • Loss of consciousness
  • Followed by period of lucidity
  • Followed over several hours by headache, loss of consciousness and progressive neurological deterioration
45
Q

Tx of Epidural Hematoma

A
  • If pt losses consciousness a 2nd time or stays unconscious, neurologic deterioration may progress rapidly
  • Emergency craniotomy and evacuation
  • IV mannitol (buys time)
  • Hyperventilation to PCO2 of 25-35 (buys time)
46
Q

How do you manage cerebral blood flow?

A
  • Elevate head of bed (decreases ICP)
  • Mannitol
  • Hyperventilation
47
Q

How does mannitol manage cerebral blood flow?

A
  • increases intravascular volume, SBP, CPP
  • ICP decreases
  • Osmotic effects
  • Hemodilution (decreases blood viscosity)
  • Don’t give to rapidly or it can cause hypotension
48
Q

How does hyperventilation manage cerebral blood flow? (5)

A
  • causes alkalosis
  • decreases ICP (constricts arterioles)
  • Have to be careful! Follow ABG’s
  • Can cause increase vessel reactivity which leads to hypoxemia and severe damage
  • prolonged alkalosis can cause decrease in 02 available to tissues
49
Q

Increased ICP (3)

A
  • 10-20 needs careful monitoring
  • over 20 should be treated urgently
  • 30-50 a/w poor prognosis
50
Q

Indications for ICP monitoring (4)

A
  • When its important to determine ICP
  • If there is a chance ICP is elevated
  • When tx is needed for increased ICP
  • When accurate assessment of neurological status is not possible
51
Q

Herniation of the medial portion of the temporal lobe through the tentorium cerebelli causes?

A
  • brain herniation
  • midbrain compression
  • LOC
  • Decerebrate rigidity
52
Q

Herniation of the medulla through the foramen magnum causes? (3)

A
  • brain herniation
  • reduced blood flow to the central medulla
  • Cushing response (systemic HTN, bradycardia, respiratory irregularities)
53
Q

Herniation of the cerebellar tonsils through the foramen magnum can cause? (3)

A
  • brain herniation
  • further brain stem compression
  • medullary ischemia
54
Q

Herniation of the cerebellum upward through the tentorial hiatus can cause? (2)

A
  • Bilateral decerebrate rigidity

- Can be precipitated by release of fluid from the lateral ventricles

55
Q

What is important to assume with major trauma?

A

Assume there is a head injury and a c-spine fx until proven otherwise!

56
Q

Glasgow Coma Scale GCS consists of what categories?

A
  • Eye opening
  • Verbal response
  • Best motor response
57
Q

Eye Opening of the GCS (4)

A 
4= spontaneous
3= on command
2= in response to painful stimuli 
1= closed
58
Q

Verbal Response of the GCS (5)

A 
5= coherent speech
4= confused speech
3= speaks with inappropriate words
2= makes incomprehensible sounds
1= no response
59
Q

Best Motor Response of the GCS (6)

A 
6= obeys commands
5= purposeful movements to painful stimuli
4= withdraws from pain
3= decorticates to painful stimuli
2= decerebrates after painful stimulus
1= no response
60
Q

What are 2 types of ventilatory patterns with brain injury?

A
  • Central neurogenic hyperventilation

- Phasic respiratory patterns

61
Q

Central Neurogenic Hyperventilation happens with? (4)

A
  • severe cerebral acidosis
  • localized hypoxia
  • pontine damage
  • tentorial herniation
62
Q

Types of Phasic Respiratory Patterns (3)

A
  • Cheyne Stokes Variant (no apnea)
  • Cheyne-Stokes
  • Ataxic ventilation
63
Q

Criteria for ventilatory assistance (9)

A
  • Abnormal rate
  • Rate of >30, <10
  • Abnormal ABG
  • Absence of motor response to pain
  • Repeated convulsions
  • Signs of aspiration pneumonia, pulmonary edema
  • Rising ICP
  • Required for potent analgesics
  • Concurrent severe pulmonary, cardiac or abd. injury
64
Q

What do you use to control agitation and seizures? (5)

A
  • Sedatives
  • Paralytics
  • Avoid electrolyte imbalance, hypoxia, fever
  • Dilantin
  • Diazepam
65
Q

Immunizations (2)

A
  • Tetanus toxoid

- If contaminated and deep, tetanus IgG, abx, and cleaning in OR

66
Q

Abx Prophylaxis (2)

A

Opened depressed skull fx and penetrating wounds
- antistaph PCN or 1st generation cephalosporin
GSW
- same as above
- + gram - and anaerobe coverage

67
Q

What do Barbiturates do? (4)

A
  • reduce ICP
  • Reduce cerebral metabolism and O2 requirements
  • prevent intravascular coagulation
  • reduce free radical damage to brain cells
68
Q

“Phenobarb Coma” (2)

A
  • Useful in reducing brain damage in patients with persistently high ICPs despite max therapy
  • Neurologic status is monitored by evoked potentials
69
Q

Complications of Severe Brain Injuries (5)

A
  • Neurogenic pulmonary edema
  • SIRS
  • Cardiac complications
  • GI bleed
  • Coagulopathy
70
Q

Spinal Cord Injury

A
  • From blunt or penetrating trauma
  • Can present with a variety of deficits or none
  • Stable and unstable fx
  • Absence of a distracting injury
  • GCS of 15, not intoxicated or medicated
71
Q

How do you deal with a spinal cord injury?

A
  • Immobilize the spine in trauma patients!!!
  • Clear the C-spine
  • X-ray flexion/extension
  • CT/MRI
  • Careful neurologic exam
  • Tx involves fixation
72
Q

SCIWORA

A
  • Spinal cord injury without radiographic abnormality
  • Results from blunt injury, hyperextension/flexion
  • Normal x-ray and CT
  • May be MRI evidence of injury
  • Most common in children

Neurology (12 decks)

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