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
Describe brown-squard syndrome
- Damage to one side of spinal cord
- Common causes = gun shots or stab
- Complete hemisection is rare
26
Describe partial cord lesions
- Eg: Spinothalamic tract lesion = loss of pain, temp., & touch below lesion on contralateral side
27
Describe changes in muscle tone due to a SCI
- 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
Describe autonomic dysreflexia due to a SCI
- 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
Describe heterotypic ossification
- 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
Describe pain related to a SCI
- # 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
Describe fatigue related to a SCI
- Due to ANS changes with lack of sweating, thermoregulation
- Due to reconditioning: lack of aerobic activity
- Increased effort to accomplish basic ADL tasks
32
Describe respiratory complications
- 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
Describe bladder/bowel control changes due to a SCI
- 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
Look. at slide 18, 19, and 21 on teachers version
35
Describe a lesion at the conus medullaris/cauda equina
- Flaccid bladder
- Sensory & parasympathetic connections are disrupted
- No external sphincter control
- Overflow incontinence
36
Describe a lesion above the conus medullaris
- Spastic bladder
- Voids reflexively
- Urge incontinence
- Voiding difficulties due to loss of muscle coordination (dyssynergistic bladder) can cause kidney damage by backflow
37
Describe sexual/reproductive changes due to a SCI
- 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
Describe the differences between UMN and LMN type sexual responses due to SCI in men
- UMN/Reflexogenic: higher level lesions, reflexive erection (parasympathetic) without ejaculation (sympathetic)
- LMN/Flaccid: no erection or ejaculation
39
Metabolic changes due to a SCI
- 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
Describe sleep disorders related to a SCI
- 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
Describe pressure ulcers related to a SCI
- 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
Imaging diagnosis of a SCI
- 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
Describe the physical assessment of neurological level of SCI
- 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
ASIA impairment scale components
- 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
Grading classification for the ASIA impairment scale
- 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
Describe prehospital management (by EMS) for SCI
- 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
Describe medical management for critical/acute care phase of SCI
- 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
Management of pulmonary dysfunction
- 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
Management of spasticity
- Prevent contractures
50
Management of pain
- Opioids
- NSAIDs
51
Management of bladder bowel dysfunction
- Catheterization
- Prevent UTI
52
Management of pressure ulcers
- Skin care
- Wound care
- Follow turning protocols
53
What percentage of SCI patients visit clinicians from complications arising from immobility, bladder/bowel dysfunction, pathologic fractures, skin breakdown, pain, spasticity, & AD
- 58% of individuals with SCI
54
Future directions for medical treatment for SCI
- 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
Until future directions of medical management become reality critical components of care are
- Protection of neural tissue
- Limitation of 2ndy injury
- Recovery of function by driving neuroplasticity through activity based therapy
- Compensatory approaches
56
What does recovery for SCI patients depend on
- Level of injury
- Initial ASIA impairment scale
- Complete vs incomplete
- Age
- Other complications
- Pre-existing comorbidities
57
What is the primary concern related to SCI prognosis
- Ability to ambulate
58
Describe prognosis of SCI patients based on ASIA scale grade
- 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
Describe SCI prognosis
- 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
Goals for PT in SCI patients in intensive care setting
- Respiratory management
- Maintaining ROM
- Positioning/repositioning for prevention of pressure ulcers
- Maintaining optimal muscle activity
- Early mobilization if cleared
61
Goals for PT in SCI patients in inpatient rehab setting
- 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
Goals for PT in SCI patients in outpatient setting
- Continue task-oriented tx
- Cardiovascular fitness
- Strength training
- Spasticity management
- Pain management
- Contracture management
- Integumentary management
