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N304 > Spinal Cord Injuries > Flashcards

Spinal Cord Injuries Flashcards

1
Q

What region does tetraplegia involve?

A
  • Cervical region
  • C1 to C8
  • Causes paralysis of all four extremities; most likely to die at a young age d/t complications
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2
Q

What region does paraplegia involve?

A
  • Thoracic section
  • T1 to L4
  • Causes paralysis of lower limbs and trunk
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3
Q

What region does pentaplegia involve?

A
  • Injury C1 to C4 (phrenic nerve)
  • Causes diaphragm dysfunction, causing inability to spontaneously breath, diminished lung compliance, weak coughs and cannot bear secretions, requires mechanical ventilation
  • Fatal
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4
Q

What is spinal cord injury?

A
  • An acute pathologic insult to the spinal cord that interrupts sensory and motor communication within the central nervous system and between the CNS and the peripheral nervous system (PNS)
  • Depending on whether the lesion is complete or incomplete, the individual will experience a wide range of impairments to all body functions.
  • lengthy and difficult adjustments and rehab necessitated by physiological dysfunction
  • social, economic and emotional ramifications of SCI are indeterminable
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5
Q

When does autonomic reflexia typically occur?

A

T6

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6
Q

If C5-T1 is impaired, where will it manifest?

A

Upper limbs

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7
Q

If T1 to L4 is affected, what will be impaired?

A
  • This section likely to be most stable d/t protection by rib cage
  • Sympathetic outflow (e.g. temp control, blood vessels)
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8
Q

Describe how hyperextension damages the CS:

A

Hyper-extension of the neck (backwards) leads to rupture of anterior ligaments

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9
Q

Describe how flexion damages the CS:

A

Ruptures posterior ligaments

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10
Q

Describe how compression damages the CS:

A

Crashes the vertebrae and forces bony fragments into spinal canal

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11
Q

Describe how rotation damages the CS:

A

Flexion-rotation injury causes tearing of ligaments that support the spine

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12
Q

Describe cord concussion:

A

Temporary disruption of cord-mediated functions, short duration (e.g. shock)

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13
Q

Describe cord contusion:

A

Bruising of neural tissue causing swelling and temp loss of cord-mediated function

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14
Q

Describe cord compression:

A

Pressure on cord causing ischemia to tissues, requiring decompression to prevent permanent cord damage

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15
Q

Describe laceration:

A
  • Tearing of neural tissues that may be reversible if damage is minimal
  • May result in loss of cord-mediated functions if spinal tracts are disrupted
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16
Q

Describe transection

A

Severing of spinal cord; permanent loss of function

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17
Q

Describe hemorrhage:

A

Bleeding into neural tissues d/t blood vessel damage; usually no major loss of function

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18
Q

Describe the ASIA Grade A Injury:

A
  • Complete injury

- Total loss of sensory and motor function below level of injury

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19
Q

Describe the ASIA grades B-D injury:

A
  • Incomplete injury
  • Mixed loss of motor and sensory function
  • Degree of loss dependents on level of injury and specific nerve tracts damaged
  • 6 syndromes are associated with incomplete injuries
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20
Q

Describe upper motor neuron injury:

A
  • Presents as spasticity (reflex arc is untouched and can complete its circuit)
  • In this situation, the upper motor neurons are unable to temper the responses and spasticity is seen
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21
Q

Describe lower motor neuron injury:

A

Presents as flaccidity as the reflex arc is broken before it contacts the spinal cord

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22
Q

Describe primary SC damage patho:

A
  • Cord compression d/t bone displacement, tumor or abscess or interrupted blood supply
  • Physical disruption of axons, blood vessels and cell membranes
  • Maximal deficit is observed immediately
  • Neurologic injury that occurs at the time of the initial trauma or mechanical injury
  • Primary is at time of injury, secondary occurs later
  • Because the SC is wrapped in tough layers of dura and rarely torn of transected by direct trauma (except for penetrating) other events occurring at time of injury result in damage
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23
Q

Describe secondary SC damage patho:

A
  • Ischemia, electrolyte imbalance and inflammatory response (damages cell membranes, causes electrolyte imbalances)
  • Excessive release of NT’s (e.g. high influx of calcium causing demyelination)
  • Begins immediately, may extend to days; some processes (apoptosis) may continue for weeks or months!
  • By 24 hours or less, edema develops above and below level of injury and can cause ischemic damage, resulting in permanent damage; requires critical care in initial phase to improve patient prognosis
  • Mechanical re-injury (autodesctruction by pathological processes occurring around cord)
  • Release of endogenous substances at the injury site
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24
Q

Prognosis of SC injury is best determined ______ hours after the injury.

A

72 hours

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25
Q

Describe cellular changes occurring within the first few minutes:

A
  • microscopic hemorrhage in central grey matter
  • vasospasm
  • hypotension
  • loss of autoregulation
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26
Q

Describe cellular changes occurring within 2 hours:

A
  • Edema on white matter

- impaired microcirculation of spinal cord

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27
Q

Describe cellular changes occurring within 4 hours:

A
  • Disruption of myelin
  • axonal degeneration
  • endothelial cell ischemia
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28
Q

Describe cellular changes occurring within 24 hours:

A

Necrosis – 70% of cross section of spinal cord

29
Q

Describe cellular changes occurring within first few days:

A
  • Progressive axonal degeneration

- cavitation and coagulation necrosis at the site

30
Q

Describe cellular changes occurring within 3-4 weeks:

A

Traumatized cord replaced by acellular collagenous scar tissue

31
Q

Describe spinal shock:

A
  • 50% of people with SCI
  • Complete, temporary loss of motor, sensory, reflex and autonomic function (e.g. reflexes, loss of sensation and flaccid paralysis)
  • Occurs immediately after injury
  • Usually lasts 48 hours, but can last weeks
    and visceral sensation
  • Resolution—anal reflex, spastic muscles
32
Q

Describe neurogenic shock:

A
  • Temporary loss/disruption of autonomic nervous system below level of injury
  • Occurs with cervical or upper thoracic injuries (above T6)
  • Occurs soon after the injury
  • Can last 3 days to 3 weeks
  • Triad of symptoms (hypotension, bradycardia, inability to regulate body temp)
  • Loss of sympathetic innervation causes peripheral vasodilation, venous pooling and decreased cardiac output
33
Q

What are the characteristics of spinal shock?

A
  • Decreased reflexes
  • Loss of sensation
  • Flaccid paralysis
34
Q

What are characteristics of neurogenic shock?

A
  • Characteristics at T5 or above
  • Hypotension
  • Bradycardia
  • Inability to sweat (dry, warm skin)
  • NB: masks signs and symptoms of hypovolemia
35
Q

What are priorities of care?

A 
- Pre-hospital resuscitation: 
Communication with EMS is key
- ER resuscitation: Primary survey/ Resuscitation and Secondary survey
- Definitive care/operative care
- Critical care phase
- Rehabilitation phase
36
Q

What does surgery focus on in the definitive care phase?

A
  • Stabilizes, realigns and decompresses the spinal column
  • Achieved by:
    laminectomy with fusion, Harrington Rods, spinal fusion
37
Q

What does non-surgical treatment focus on in the definitive care phase?

A
  • Focus is on stabilization and realignment of injured spine.
  • Achieved by: Cervical traction (ex. Halo), Immobilization of the neck in neutral position (ex. Halo vest), Brace Tongs—ie.. Gardner Wells.
38
Q

What is autonomic dysreflexia?

A
  • Can occur anytime after resolution of spinal shock
  • An acute episode of exaggerated sympathetic response to a noxious stimuli below the level of injury
  • Results from a lack of control from higher brain centers
  • Associated with those with T6 or higher injury
  • Those with lower injury usually have enough sympathetic outflow to control visceral reflexes
  • Considered a medical emergency
39
Q

What are the manifestations of anterior cord syndrome?

A
  • Paralysis in lower extremist
  • Loss of pain and temp sensation below level of injury
  • Position, vibration and touch remain intact
40
Q

What pathways are disrupted in anterior cord syndrome?

A
  • Direct injury, compression or vascular compromise
  • Damage to anterior spinal artery
  • Ventral and lateral motor tracts
41
Q

What are the manifestations of central cord syndrome?

A
  • Greater motor/sensory deficits in upper limbs than lower limbs
  • Bowel and bladder control is preserved
42
Q

What pathways are disrupted in central cord syndrome?

A
  • Centrally located nerve tracts innervating upper extremities are disrupted
  • Contusion or lesion in the central portion of spinal cord
43
Q

What are the manifestations of Brown-Sequard syndrome?

A
  • Ipsilateral motor, position and proprioception loss

- Contralateral loss of pain and temp

44
Q

What pathways are disrupted in Brown-Sequard syndrome?

A
  • Lateral and corticospinal tracts

- Damage to lateral half of spinal cord (hemisection)

45
Q

What are the manifestations of Conus-Medullaris-Cauda Equine injury?

A
  • Motor and sensory impairment
  • Bowel and bladder dysfunction
  • Sexual dysfunction
  • Neurological deficits vary
  • Dependent on area of lesion
46
Q

Describe the population most at risk for SC injuries:

A
  • 15 to 25 years old
  • Males more likely compared to females (4:1)
  • Most injuries are associated with the C spine and have the most devastating neurological impairments
  • Shorter life span by 15-30 years (d/t compromised resp function, impaired renal function and impaired skin integrity, especially in tetraplegics)
  • Requires nearly 3x as many HCP contact
  • Requires 30x more hours of home care services
  • Re-hospitalized 2.6 times more often
47
Q

Why is SC trauma a significant issue?

A
  • Disrupted individual growth and development (think young age)
  • Altered family dynamics
  • Economic loss d/t absence
  • High cost of rehab and long-term health care (up to $3 million a person!)
  • Nearly 46,000 to 60,000 live with SC injury in Canada!
  • Indirect costs to gov’t d/t lost employment earnings, lost contribution to economic, and tax base and loss of productivity of family caregivers
48
Q

Describe the pathophysiological map of how hemorrhage can lead to tissue hypoxia of the SC:

A
  • Hemorrhage = RBC and plaelete aggregation and breakdown of RBC’s > SNS vasoconstriction hormones released > Vasoconstriction, thrombosis formation and increased free radical formation by RBC breakdown > secondary injury > decreases blood flow to SC > hypoxia
  • Hemorrhage = neutrophilic action > production of inflammatory mediators > vasospasm and edema > decreased SCBF > hypoxia
49
Q

Primary injury causes damage to _______ and secondary injury causes damage by ______________.

A

1) Actual physical disruption of axons

2) Ischemia, hypoxia, micro-hemorrhage and edema

50
Q

What are the different mechanisms of injury?

A
  • Flexion
  • Hyper-extension
  • Flexion-rotation
  • Extension-rotation
  • Compression
51
Q

What is the difference between skeletal and neurological level of injury?

A
  • Skeletal = vertebral level where damage to bones and ligaments are most extensive
  • Neurological = lowest segment of spinal cord at which sensory and motor function of both sides are normal
52
Q

What is the difference between complete and incomplete SC injuries?

A

COMPLETE: total loss of sensory and motor function below level of the injury
INCOMPLETE: mixed loss of motor and sensory function

53
Q

What six syndromes are associated with incomplete lesions?

A
  • Central cord syndrome
  • Anterior cord syndrome
  • Brown-Sequard syndrome
  • Posterior cord syndrome
  • Conus medullaris syndrome
  • Cauda Equina syndrome
54
Q

Describe how to care for complications of the respiratory system:

A
  • C4 and above major problem d/t total loss of respiratory function (mech ventilation necessary)
  • Trach care and suctioning
  • Oral hygiene
  • Prevention of infection (e.g. pneumonia)
  • Chest physiotherapy
  • CXR to evaluate fluid and infections
55
Q

Describe what to expect of a patient’s resp system with SCI:

A
  • Phrenic nerve involvement (above or below C4, esp. if hemorrhage and edema present)
  • Hypo-ventilation d/t decrease in vital capacity and tidal volume
  • Impairment or paralysis of intercostal muscles
  • Decreased ability to cough and clear secretions (may need trach or endotrach)
  • Pulmonary edema
56
Q

Describe what to expect of a patient’s cardiovascular system with SCI:

A
  • Any injury above T6 decreases influence of SNS = vasodilation causing hypotension and bradycardia
  • Hypovolemia
  • Hypovolemic shock (e.g. associated injury at time of accident)
  • Decreased CO
  • Low venous return
  • Hemorrhaging and clotting
57
Q

How do we care for patient’s with CV complications?

A
  • Careful monitoring of BP, MAP, HR, CWMS
  • Monitor lab values (e.g. INR, PTT, electrolytes, CBC’s)
  • ECG monitoring
  • In bradycardia, increase with drugs that act as vasopressors (atropine) and IV fluids
  • Maintain MAP of 85 mmHg to perfuse SC
  • Assess for S&S of bleeding (active)
58
Q

Describe what to expect of a patient’s urinary system with SCI:

A
  • Above T12
  • Urinary retention in acute SCI and shock
  • Atonic and over-distended bladder during shock
  • Hyper-irritable after shock, with loss of inhibition (reflex emptying)
  • Possible UTI associated with catheter (long-term possibly)
  • Possible AKI (retention, reduced blood volume to kidneys during shock)
  • Neurogenic bladder
59
Q

How do we care for a patient’s urinary system with SCI?

A
  • Assess risk for infection
  • Assess for changes in reflexivity of bladder
  • Insert catheter and remove as appropriate (once hemo-dynamically stable)
  • Intermit cath use to maintain bladder tone and decrease infection risk
60
Q

Describe what to expect of a patient’s GI system with SCI:

A
  • Occurs with damage above T5
  • Hyper-motility = paralytic ileus and gastric distention
  • Stress ulcers in stomach d/t certain drugs
  • Intra-abdominal bleeding
  • Neurogenic bowel (injury below T12 or during shock, lost sphincter tone and reflexes)
61
Q

How do we care for a patient’s GI system with SCI?

A
  • NG tube to relieve distention
  • Anti-emetics
  • Meds to reduce acidity of stomach
  • Assessment for S&S of intra-abdominal bleeding (look for further drops in BP and blood in stool, unable to tell if pain)
  • Regular bowel program
62
Q

What is a leading cause of death in this population?

A

Pulmonary embolism

63
Q

What is a consequence of paralysis to the integ system?

A
  • Potential for skin breakdown over bony prominence’s in areas of decreased or no sensation, causing pressure ulcers to quickly develop and cause major infection or sepsis
  • Perform freq skin assessments and reposition
64
Q

What is Poikliothermism?

A
  • Adjustment of body temp to room temp
  • Altered in SCI’s d/t interruption of SNS, preventing temperature sensations from reaching the hypothalamus
  • Ability to sweat or shiver will also be decreased below level of lesion, further affecting ability to regulate temp
65
Q

Describe the immediate interventions while working with SCI patients after the injury:

A
  • Assessment of possible injury to SC (e.g. pain adjacent to spine; paraesthesias; alterations in sensations; change in limb movement; spinal shock; incontinence; difficulty breathing)
  • Ensure patency of airway
  • Stabilize CS
  • Admin O2 via NP or NRM
  • Establish IV access with two large-bore catheters and infuse NS or RL
  • Assess for other injuries (likely to have multiple d/t high likelihood of associated trauma)
  • Control external bleeding
  • Insert foley cath
  • Monitor VS, LOC, O2 sat, cardiac rhythm and urinary output
  • Keep patient warm
  • Anticipate need for intubation if gag reflex absent or resp function declines
66
Q

Describe collaborative care in rehab and home care:

A
  • Physiotherapy (ROM exercises; chest physio; mobility training; muscle strengthening)
  • Occupational therapy for ADL training
  • Bowel and bladder training
  • Prevention of autonomic dysreflexia
  • Prevention of pressure ulcers
  • Recreation therapy
  • Patient and caregiver education
67
Q

What are the signs and symptoms of autonomic dysreflexia?

A
  • Sudden onset of headache
  • Elevation in BP and reduction in HR
  • Flushed face and pale extremities
  • Sweating above level of lesion
  • Nasal congestion
  • Apprehension
68
Q

What interventions do we do for autonomic dysreflexia?

A
  • Raise patient to a sitting position
  • Remove stimulus (distended bladder, tight clothing)
  • Call MRP if actions do not relieve S&S

N304 (16 decks)

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