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Clinical Medicine III > Spinal Cord Injury > Flashcards

Spinal Cord Injury Flashcards

1
Q

Overview of spinal cord injury (SCI)

A
  • About 288,00 people living with SCI
  • MVA are currently the leading cause of injury closely followed by falls
  • All patient’s with TBIs should be presumed to have SCIs until proven otherwise
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2
Q

Incidence and risk factors for SCI

A
  • Males > females
  • Average age of SCI incidents have increased from 29 yrs to 43 yrs
  • Catastrophic event within secs, person becomes dependent on others or ADs to perform even most basic ADLs
  • Low incidence rate compared to other disorders but high cost
  • Lengths of stay in hospital acute care unit have declined from 24 days to 11 days
  • Most survivors have incomplete SCI
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3
Q

Common MOIs for SCI

A
  • Neurapraxia (in milder injuries)
  • Hyperflexion injuries
  • Hyperextension injuries
  • Crush fractures
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4
Q

Describe neurapraxia

A
  • Transient neurologic deficits
  • Special concern in athletes with cervical spinal stenosis
  • Hyper ext/flex. injuries cause transient neurologic deficits including tetraplegia
  • Results in temp. conduction block
  • Caused by antero-posterior cord compression
  • Could be a result of temp. ischemia & edema
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5
Q

Describe hyperextension injuries

A
  • Hangman’s fracture: forced distraction & hyperextension of neck, or from whiplash movements, or chin of unrestrained passenger hitting steering wheel, or falls in older adults
  • Causes bilateral fractures of the pars interarticularis of Axis vertebra
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6
Q

Describe crush fractures

A
  • Often result in comminuted fractures
  • Body fragments can put pressure or penetrate spinal cord
  • 75% chance of complete SCI
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7
Q

How are types of SCI classified

A
  • Concussion: temporary loss of function due to blow or violent shaking
  • Contusion: bleeding from local blood vessels due to bruising causes compression from hemorrhages
  • Laceration/maceration: more severe; may cause transection from gunshot or knife wounds
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8
Q

What is the type and degree of spinal lesion dependent on

A
  • MOI: excessive flexion or extension; with or without rotation
  • Determine severity of SCI: incomplete or complete
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9
Q

Describe a complete SCI

A
  • All functions below the injured area are lost, whether or not the spinal cord is severed
  • To be classified as complete there should be absence of all sensory & motor function in the sacral segments supplied by S4-S5
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10
Q

Describe an incomplete SCI

A
  • Involves preservation of some motor and/or sensory function below the level of injury
  • To be classified as incomplete it needs some preservation of sensory or motor activity innervated by S4-S5 (sacral sparing)
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11
Q

Difference between complete vs incomplete depends on what

A
  • Functional survival of some axons across the lesion
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12
Q

Describe pathogenesis of a primary SCI

A
  • In 1-2 days: necrotic death 2ndy to direct trauma to tissue or blood vessels (causing hemorrhage & compression)
    -Important to adequately stabilize injured spine to stop any additional damage: often tissue & axons in the peripheral rim are spared even after severe injuries
  • In paraplegia amount of spread rim correlates to level of ambulation capacity
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13
Q

Describe pathogenesis of secondary SCI

A
  • In the following days/weeks/months: further progression of tissue injury due to biochemical mechanisms (inflammatory processes, oxidative damage, apoptosis)
  • Acute phase: ischemia/hypoxia causing electrolyte imbalance, excitotoxicity, inflammation by immune cells, edema, oxidative damage
  • Sub-acute phase: apoptosis, demyelination, Wallerian degeneration, evolution of glial scar
  • Chronic phase: cystic cavity (Syringomyelia), progressive Wallerian degeneration, maturation of glial scar
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14
Q

Describe general pathogenesis for SCI

A
  • Historical remodeling of the primary spinal cord lesion due to secondary injury mechanisms
  • Progression of injury in both directions from lesion site, can go as far away as 3-4 spinal segments from the level of direct injury
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15
Q

Describe vascular (blood flow) changes following SCI

A
  • Release of NTs like norepinephrine, serotonin, histamine, all cause vasoconstriction
  • Loss of auto regulatory response of spinal cord vasculature
  • Spinal cord edema (from micro hemorrhages) can spread cranially & caudally
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16
Q

Describe demyelination following a SCI

A
  • Direct trauma to oligos
  • Inflammatory response by lymphocytes, macrophages invade lesion site by way of disrupted BBB
  • Loss of myelin may render axon dysfunctional, despite being physically intact
  • Demyelination & inflammation can trigger Wallerian degeneration of axons
  • Cells can die distal & proximal to level of lesion
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17
Q

Describe glial scarring following a SCI

A
  • Tissue is invaded by reactive astrocytes, microglia, macrophages, & fibroblasts
  • Reactive astrocytes make a physical scar, a physical barrier to axonal regeneration, around an area of cavitation
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18
Q

Describe syringomyelia following a SCI

A
  • Presence of fluid filled cyst (syrinx) after SCI
  • Can continue to develop/extend over several segments
  • Happens 4-9 yrs post-trauma
  • Causes significant additional symptoms due to compression/destruction of the ascending/descending neural pathways & the autonomic nerves
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19
Q

Symptoms of syringomyelia

A
  • Pain
  • Loss of sensation
  • LMN signs
  • Spasms
  • Phantom sensations
  • Autonomic signs: low BP w/ lightheadedness, sweating, sexual dysfunction, loss of bladder/bowel control
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20
Q

Most common site of syringomyelia

A
  • Thoracic spine
  • Signs distributed like cape over shoulders & back: progression from distal to proximal extremities
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21
Q

Describe dural scarring following a SCI

A
  • Cord moves freely within dura
  • Scarring causes sticking/tethering of cord to dura
  • Can cause microscopic injuries to cord during neck flexion
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22
Q

What does clinical manifestations of a SCI depend on

A
  • Depends on the area of injury in the cross section of spinal cord
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23
Q

Clinical manifestations of a SCI

A
  • Damage to cervical spinal cord: tetraplegia/paresis in addition to limbs & trunk, and respiratory muscles
  • Complete cord lesions: complete loss of sensory & motor function below level of lesion
  • Incomplete cord lesions: depends on the SCI syndrome
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24
Q

What are the incomplete SCI syndromes

A
  • Anterior cord syndrome
  • Posterior cord syndrome
  • Central cord syndrome
  • Brown-Sequard syndrome
  • Conus Medullaris syndrome
  • Cauda Equina syndrome
  • Partial cord lesions
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25
Q

Describe brown-squard syndrome

A
  • Damage to one side of spinal cord
  • Common causes = gun shots or stab
  • Complete hemisection is rare
26
Q

Describe partial cord lesions

A
  • Eg: Spinothalamic tract lesion = loss of pain, temp., & touch below lesion on contralateral side
27
Q

Describe changes in muscle tone due to a SCI

A
  • Flaccidity and loss of reflexes (skeletal & autonomic) below lesion level during spinal shock period (few hrs/days/weeks)
  • Spasticity could help with bladder emptying or flexing hip/knee
  • Excess spasticity is triggered by afferent stimuli
  • Spasticity can be exaggerated by noxious stimuli, constipation, infection, pressure sores, and/or emotional stress
28
Q

Describe autonomic dysreflexia due to a SCI

A
  • Common above T6 lesions
    Symptoms: HTN, bradycardia, pending HA, sweating above level, nausea, blurred vision, restlessness/anxiety, nasal congestion
  • Sudden rise in systolic (>20) & diastolic (>10)
  • Triggered by noxious stimuli, problems w/ bladder/bowel emptying, clogged/kinked catheter, UTI, pressure ulcer, sexual activity, menstruation
  • Caused by unbalanced/unrestricted vasoconstriction by sympathetic nervous system blew lesion level
  • Medical emergency
29
Q

Describe heterotypic ossification

A
  • Often develops near large joints like the hip/knee
  • Symptoms: pain, redness, tissue swelling, increased temp., loss of ROM
  • Changes in bony alignment due to weakness, muscle imbalances, scoliosis can develop over time
30
Q

Describe pain related to a SCI

A
  • # of pain sites increases with time
  • Depression associated with increased pain
  • Parasthesia: perceived as pain, pins & needles, burning, tingling
  • MSK pain due to faulty posture, overuse of UE due to dependency for ADLs (protect shoulder joints from overuse injuries)
31
Q

Describe fatigue related to a SCI

A
  • Due to ANS changes with lack of sweating, thermoregulation
  • Due to reconditioning: lack of aerobic activity
  • Increased effort to accomplish basic ADL tasks
32
Q

Describe respiratory complications

A
  • Occurs with cervical/thoracic lesions: can be life threatening
  • > C4 lesions cause diaphragm paralysis due to loss of phrenic nerve function
  • C5-T12 lesions cause respiratory problems due to loss of intercostal & abdominal muscle innervations
  • Absence of abdominals decreases strength of cough, increases risk of aspiration & pneumonia
  • Paradoxical breathing pattern: inspire solely by diaphragm causes chest wall to be sucked inside in the absence of intercostal function
  • Abdominal flaccidity = organs sag forward and down, insufficient diaphragm position, require abdominal binder
  • Respiratory infections/failure: complication, common cause of death
33
Q

Describe bladder/bowel control changes due to a SCI

A
  • Always affected regardless of level of injury
  • Parasympathetic center for voiding control is at conus medullar is (S2-S4)
  • During spinal chock = flaccid bladder
  • Bowel mimics bladder pattern
  • UTI: most common 2ndy complication due to catheterizations & urinary retention
  • Increased concentration of Ca in urinary system leads to kidney stones
34
Q

Look. at slide 18, 19, and 21 on teachers version

A
35
Q

Describe a lesion at the conus medullaris/cauda equina

A
  • Flaccid bladder
  • Sensory & parasympathetic connections are disrupted
  • No external sphincter control
  • Overflow incontinence
36
Q

Describe a lesion above the conus medullaris

A
  • Spastic bladder
  • Voids reflexively
  • Urge incontinence
  • Voiding difficulties due to loss of muscle coordination (dyssynergistic bladder) can cause kidney damage by backflow
37
Q

Describe sexual/reproductive changes due to a SCI

A
  • Control centers are at the same sacral level as bladder/bowel
  • 2 types of sexual responses in men depending on lesion level: UMN type and LMN type
  • Occurrence of AD during bladder/bowel care is a predictor of AD during sexual activity
  • Menstruation stops for 3-6 mo post-SCI: can cause AD when restored
  • Fertility is unaffected but pregnancies need to be observed closely as labor may cause AD
38
Q

Describe the differences between UMN and LMN type sexual responses due to SCI in men

A
  • UMN/Reflexogenic: higher level lesions, reflexive erection (parasympathetic) without ejaculation (sympathetic)
  • LMN/Flaccid: no erection or ejaculation
39
Q

Metabolic changes due to a SCI

A
  • Abnormal carb metabolism
  • In chronic SCI increased body fat to muscle ratio due to muscle wasting/atrophy & sedentary lifestyle
  • Decreased BMD due to lack of WBing, alterations in ANS, & circulatory systems (osteoporosis & increased Fx risk)
40
Q

Describe sleep disorders related to a SCI

A
  • Obstructive sleep apnea hypopnea syndrome (OSAHS): repeated O2 desaturation during sleep, high risk after cervical SCI
  • Signs of OSAHS: frequent awakening during sleep, daytime sleepiness, obesity
  • Changes in cardiac rhythm: arrhythmia, bradycardia, ventricular tachycardia (can lead to sudden death)
41
Q

Describe pressure ulcers related to a SCI

A
  • Common complication after SCI
  • Due to sensory loss & persistent pressure on bony prominences below lesion
  • Common acute phase sites: sacrum, heel, scapula (due to bed bound)
    -Common sites with w/c mobility: trochanter & ischium
  • Follow selfceare schedules, repositioning schedules, skin checks (Braden scale) during acute/subacute phases
  • Moisture, poor nutrition, complete lesions, cigarettes smoking, alcoholism, depression increase risk
42
Q

Imaging diagnosis of a SCI

A
  • X-rays are rapid & effective for diagnosing SCI from vertebral Fx
  • CT scan if lateral and AP x-ray views are inadequate
  • MRI can detect intra/extra dural hematoma & differentiate contusion from hemorrhage
  • MRIs show tissue damage/impingement of spinal cord
  • MRI can help in detecting syringomyelia early
  • fMRI can track implanted stem cells to track migration & success of implantation
  • Neurophysiological studies can help determine if lesion is progressing or resolving using evoked potentials & EMG
43
Q

Describe the physical assessment of neurological level of SCI

A
  • Use ASIA Impairment Scale (AIS) made by ASIA (American Spinal Injuries Association)
  • Indicates most caudal unimpaired spinal level with respect to both sensory & motor function (≥3/5 MMT)
  • 28 dermatomes assessed bilaterally (pinprick & light touch)
  • 10 key muscles assessed bilaterally (MMT)
  • Anal sensory & sphincter function assessed
    -Results of sensory & motor scores are summed & used in combination of anal assessment to determine level of injury & AIS category
44
Q

ASIA impairment scale components

A
  • Determine sensory levels for right & left sides
  • Determine motor levels for right & left sides
  • Determine the neurological level of injury (NLI)
  • Determine whether the injury is complete or incomplete
  • Determine ASIA impairment scale grade
45
Q

Grading classification for the ASIA impairment scale

A
  • A = Complete SCI
  • B = Motor complete & sensory incomplete SCI
  • C = Motor incomplete: less than half of key muscle functions below the single NLI have a muscle grade ≥3
  • D = Motor incomplete: at least half of key muscle functions below the single NLI have a muscle grade ≥3
  • E = Normal
  • Using ND
46
Q

Describe prehospital management (by EMS) for SCI

A
  • Goal is basic life support: monitor/maintain ABCs, O2 support & meds as indicated
  • If SCI suspected: immobilize spine with a rigid collar & spinal board, incomplete SCI can be made worse with mishandling
  • Log roll into spinal board or lift with 4-6 people while kepeping the head steady
47
Q

Describe medical management for critical/acute care phase of SCI

A
  • High cervical injuries may need ventilation (monitor/maintain ABCs = airway/breathing/circulation)
  • Imaging may need to wait if other life threatening injuries (pneumothorax, hemothorax, int/ext bleeding)
  • Prevent/manage hypovolemic (due to blood loss) & neurogenic shocks (due to ANS dysfunction)
  • Maintain MAP b/w 85-90 mmHg for good perfusion
  • Minimize 2ndy injury
  • Imaging confirms SCI: may need orthopedic surgery to re-align spine, de-compress cord, & re-establish vertebral stability
  • Surgery within 24 hrs is associated with better outcomes
  • Early mobilization with lines, leads, drainage tubes in place
48
Q

Management of pulmonary dysfunction

A
  • Cervical/thoracic injury but not requiring mechanical ventilation: normalize breathing with mechanical ventilation (IPPB), bronchodilators, mucolytics
  • Diaphragmatic breathing when phrenic nerve diaphragm unit is functionally intact
  • Prevent infections
49
Q

Management of spasticity

A
  • Prevent contractures
50
Q

Management of pain

A
  • Opioids
  • NSAIDs
51
Q

Management of bladder bowel dysfunction

A
  • Catheterization
  • Prevent UTI
52
Q

Management of pressure ulcers

A
  • Skin care
  • Wound care
  • Follow turning protocols
53
Q

What percentage of SCI patients visit clinicians from complications arising from immobility, bladder/bowel dysfunction, pathologic fractures, skin breakdown, pain, spasticity, & AD

A
  • 58% of individuals with SCI
54
Q

Future directions for medical treatment for SCI

A
  • Spinal cord neuromodulation by implanted electrodes
  • Transplantation of stem cells to replace lost cells: embryonic/adult stem cells; survival of cells & functional recovery cause challenges
  • Producing regenerative growth factors, expression of scar-breaking substances, modulating immune system
55
Q

Until future directions of medical management become reality critical components of care are

A
  • Protection of neural tissue
  • Limitation of 2ndy injury
  • Recovery of function by driving neuroplasticity through activity based therapy
  • Compensatory approaches
56
Q

What does recovery for SCI patients depend on

A
  • Level of injury
  • Initial ASIA impairment scale
  • Complete vs incomplete
  • Age
  • Other complications
  • Pre-existing comorbidities
57
Q

What is the primary concern related to SCI prognosis

A
  • Ability to ambulate
58
Q

Describe prognosis of SCI patients based on ASIA scale grade

A
  • AIS score of A: most will not show motor recovery but functional improvements happen; muscle grades 1-3 have potential to recover motor function
  • Incomplete: show some recovery of function; AIS D recovers better than C
59
Q

Describe SCI prognosis

A
  • Most motor recovery happens in the first year after injury, most rapid during first 3 mo (window of maximal neuroplastic recovery)
  • Preserved pain sensation in sacral or extremities increases likelihood of motor return
  • Generally: L1 or below injuries will likely be able to walk home or community with AD; T1-T12 likely to walk around the house with AD; C7-C8 likely to live independently using manual w/c
60
Q

Goals for PT in SCI patients in intensive care setting

A
  • Respiratory management
  • Maintaining ROM
  • Positioning/repositioning for prevention of pressure ulcers
  • Maintaining optimal muscle activity
  • Early mobilization if cleared
61
Q

Goals for PT in SCI patients in inpatient rehab setting

A
  • Continue respiratory therapy
  • Use of abdominal binder
  • Pressure relieving techniques
  • Initiate functional mobility as tolerated using orthotics as needed
  • Task-oriented tx
  • FES assisted exercises to improve endurance
  • BMD (FES cycle)
  • Whole body vibration thechniques
  • Teach compensatory techniques to max functional independence if quick D/C is needed
  • Recommend home modification & leave patient with good HEP
62
Q

Goals for PT in SCI patients in outpatient setting

A
  • Continue task-oriented tx
  • Cardiovascular fitness
  • Strength training
  • Spasticity management
  • Pain management
  • Contracture management
  • Integumentary management

Clinical Medicine III (20 decks)

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