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
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
3
Q
Common MOIs for SCI
A
- Neurapraxia (in milder injuries)
- Hyperflexion injuries
- Hyperextension injuries
- Crush fractures
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
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
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
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
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
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
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)
11
Q
Difference between complete vs incomplete depends on what
A
- Functional survival of some axons across the lesion
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
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
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
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
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
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
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
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
20
Q
Most common site of syringomyelia
A
- Thoracic spine
- Signs distributed like cape over shoulders & back: progression from distal to proximal extremities
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
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
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
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
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
