SCI demographics M \_\_ F Mean age? Etiology? Distribution of complete vs incomplete para vs tetraplegia?
SCI demographics 17,000 new SCI each year M (80%) >> F (20%) Mean age? 42yo Etiology? MVA (38%), Falls (30%), violence (14%), recreational sports (9%)
66% of all injuries are INCOMPLETE Incomplete tetraplegia = 45% Complete tetraplegia = 14% Incomplete paraplegia = 21% Complete paraplegia = 20%
Impaired __ capacity is the most common cause of death after SCI.
Describe complications in terms of related PT diagnoses
Any interventions that help?
Impaired RESPIRATORY capacity is the most common cause of death after SCI
Reduced ventilation = microatelectasis
Ineffective cough = unable to clear secretions -> PNA and insufficient respiration
Interventions: respiratory muscle training improves VITAL CAPACITY, EXPIRATORY MUSCLE STRENGTH, and RESIDUAL VOLUME - e.g. singing, coughing, and exercising are good interventions to improve respiratory capacity!
Most severe respiratory complications post SCI occur in high-level cervical injuries. Injuries above __ are likely to require endotracheal intubation & mechanical ventilation. May also need ___ nerve stimulation/direct motor point pacing of the __ (muscle)
Describe changes in FEV & FVC relative to age-predicted values in high vs low cervical injuries
Most severe respiratory complications post SCI occur in high-level cervical injuries. Injuries above C5 are likely to require endotracheal intubation & mechanical ventilation. May also need PHRENIC nerve stimulation/direct motor point pacing of the DIAPHRAGM
C3-C5 = FEV 56%, FVC 53% age-predicted values
C6-8 = FEV 65%, FVC 64% age-predicted values
Describe muscles associated with inspiration and spinal nerve innervation
What about exhalation?
Describe muscles associated with inspiration and spinal nerve innervation
- Diaphragm: C3-5
- Accessory mm (SCM/ scalenes C1-8) - these assist w/respiration and may compensate after paralysis of lower musculature!
- Intercostal mm (innervated by intercostal nerves T1-T11) - these increase and decrease rib cage volume, impact deep breathing and coughing
- Abdominal mm (Rectus, transversus abdominus; innervated at T6-L1) - required for an effective cough
Exhalation is usually PASSIVE, except w/coughing, singing, and exercising
Most common infection post SCI? What are the risk factors for this inherent to SCI?
What may decrease risk of this?
UTI
- Urinary retention
- Bladder over distention
- Urine reflux into ureters
- Kidney and bladder stones
- Intermittent catherization
- Assist required for ADLs/lack of independence
Factors to decrease risk of UTIs:
- Independence w/ADLs
- Engaging in weekly exercise
- Good personal hygiene
- Education
Describe neurogenic bladder/urinary management post SCI. How does this change with higher vs lower injuries (UMN vs LMN management)? At what level does it switch?
Neurogenic bladder = lose supraspinal control of bladder due to SCI
Indwelling/foley catheter usually used until medically stable
Injury above t12 = UMN management = REFLEXIVE bladder. Urine fills bladder - nerves signal to contract bladder, it squeezes and empties reflexively - requires a leg bag. Needs intermittent catheterization (~q4 hrs). May still need a leg bag. Bladder augmentation (surgery so bladder can store larger amounts of urine safely) is an option.
In Injuries below T12 (LMN management = AREFLEXIVE bladder). Doesn’t empty based on a reflex; the sensory signal of bladder fullness won’t get back to spinal cord, bladder will overfill/over stretch = bladder accidents.
Requires intermittent catherization vs condom cath. Areflexive bladder. Usually need a leg bag.
Max allowable bladder fillage = 500-600mL. Uses sterile technique in hospital -> clean technique (so they can reuse catheters once clean) at home
Neurogenic bladder complications…
- Leaking
- UTI
- Kidney infection
- LE spasticity
Challenges:
- Men C6-7 level (or lower) may be independent with intermittent catheterization (largely d/t difficult to apply condom cath)
- Women C7 (or lower) may be independent with IC (labia splitter)
Options: intermittent catherization
- Suprapubic catheters
- Bladder augmentation
- Reflex voiding (option for LE injuries/below t12, via essentially “leaking” into leg bag)
Describe how a suprapubic cystostomy works and why this might be a good bladder management option
Suprapubic cystostomy = surgical intervention creating a stoma in the abdomianl wall with a catheter inserted directly into the bladder. Drainage options include free drainage (urine drains freely into bag t/o the day) vs with a catheter valve (drains urine directly into a toilet using a catheter)
This is a secondary option for those who cannot be independent with intermittent catheterization. Very favorable option for individuals with C5-6 level injuries who can’t do intermittent catheterization. Generally good satisfaction rates.
Contributing factors post SCI that makes individuals at high risk for developing skin issues (beyond the obvious)…
- Collagen degradation after SCI
- Decreased peripheral blood flow (low BPs, smoking)
- Immobility and sensory loss
- Muscle atrophy over bony prominences
- Incontinence, moisture
- Dependent mobility = shearing forces
- External pressure > capillary pressure
- Ischemia/necrosis
*Estimated cost to heal 1 pressure sore = >$60k; >%11B spent annually to heal pressure ulcers!
Key features for preventing pressure ulcers…
- Weight shifts q20-30 min
- Regular turns and proper positioning in bed (initially q2-4 hrs, increasing turn times up to 6 hours max as tolerated, monitoring skin) - in supine, keep HOB <15-30 deg to minimize shearing
- Skin checks at least 2x/day
- Good hygiene, keep skin dry
- Proper positioning in w/c, pressure mapping
- Safe transfers (watch that pt isn’t hitting their buttocks
- Shoe tolerance ( need shoes that are 1-1.5 sizes bigger than usual to account for usual LE edema post SCI)
- Pressure reducing DME (cushions and mattresses)
- Good nutrition and adequate fluids
- Decreased prevalence of pressure ulcers in indiduals who:
- maintain normal weight
- return to work/family roles
- no previous hx tobacco use, suicidal behaviors, incarcerations, EtOH/drug abuse
Weight shifting options in SCI for pressure relief
Power: power tilt or power tilt + recline (harder to justify this to insurance; sometimes arguing that it decreases caregiver burden, assists with ADLs/dressing, and can aide individual with doing intermittent catheterization in chair can help w/insurance payout)
Manual:
- Can shift laterally or forward
- Can do chair push up/depression - need triceps! Good for injuries to C7 and below
- Need to weight shift EACH ischial tuberosities for 60 SECONDS (60 sec for each ischial tub, or in a position that you can do both at once!!) every 20-30 MINUTES. Goal is to restore blood flow to that area!
DVT risk in SCI - contributing factors?
- Common in acute phase of SCI
Incidence is 4.5% leading to 3.5% mortality in first 3 months post SCI.
More common in M>F, motor complete, incr weight, longer LOS, pelvic.LE fracture and delayed admission to SCI specialty center
Contributing factors: - Peripheral vasodilation/reduced LE muscle pump
- immobility -> venous stasis
- trauma
- hypercoaguability
Incidence of DVT & PE in SCI (~9% DVT; ~2% PE) is similar to that of trauma (~11.8% DVT; 0.9 PE) patients. IVC filter placed prophylactically in:
- SCI + long bone fx (37% get DVTs!!)
- DVT despite prophylactic anticoag
- If anticoag is contraindicated
- IVC filter placement may actually contribute to increased risk of DVT! So use them only w/particular populations above (esp long bone fx + SCI)
GI complications after SCI
~27% of chronic SCI had significant GI complications:
- Abdominal pain
- 20% difficulty with evacuation
- 74% hemorrhoids (=swollen anal veins; d/t bowel programs)
- 73% abdominal distention
- 43% autonomic hyperreflexia / dysreflexia
- 23% needed at least 1 hospital admission d/t GI complication
Neurogenic Bowel in SCI - damage to the CNS prevents supraspinal control of bowel regulation, determined by the presence of absence of the ___ reflex (BCR). This refers to the contraction of the ___ in response to ___ stimulation. Presence of this reflex = [UMN/LMN] pattern, vs absence of this reflex = [UMN/LMN] pattern. What innervates this reflex?
Neurogenic Bowel in SCI - damage to the CNS prevents supraspinal control of bowel regulation, determined by the presence of absence of the BULBOCAVERNOSUS reflex (BCR). This refers to the contraction of the ANAL SPHINCTER in response to GENITAL STIMULATION. Presence of this reflex = UMN pattern, vs absence of this reflex = LMN pattern (AREFLEXIVE BOWEL). Reflex is innervated by the PUDENDAL NERVE (S2-S4)
Complications of neurogenic bowel
- Bowel accidents
- (“involuntaries”)
Constipation - Impaction
- Diarrhea
- Rectal bleeding
Describe bowel management programs for UMN (lesion above __) pattern.
UMN: Lesion at or above T12
- +BCR
- Good sphincter tone
- Reflexive bowel
- Daily (or every other day) bowel program
- Bristol Stool Scale: Type 5
- Management: digital stimulation (dil stick or finger in rectum to activate reflex), suppository
Describe bowel management programs for LMN (lesion below __) pattern
LMN: Lesion below T12 (L1 & lower) - rectum fills with stool, pushes on sensory nerves, but that signal can’t get back to spinal cord to cause that reflective activity d/t injury, so anal sphincter stays open and loose
- -BCR (so DON’T rely on this reflex for bowel mgmt program!)
- Lacks sphincter tone
- FLACCID bowel
- BID bowel program (aim for 30-60 mins after eating)
- Bristol Stool Scale: Type 2-3
- Management: timing, fiber (needs 25-35g fiber daily to create bulky stool), fluids (gastrocolic reflex); manual evacuation; valsalva maneuver
Role of colestomy vs sacral nerve stimulation in SCI bowel management?
Long story short, traditional bowel programs take a LOT of time during the day!! These can help from a time perspective, but aren’t common largely because they’re invasive.
Historically colestomy is used only as a last resort if bowel complications persist; only 2.4% of SCI pts have a colostomy, but it significantly improves QOL, reduces time spent on bowel care (2hrs vs 12 mins!), reduces # hospitalizations i/s/o chronic bowel dysfunction, increases independence with bowel routine, easier to manage!
Sacral nerve stimulation: anterior sacral nerve root stimulatory implanted at level of cauda equina. Increases frequency fo left colon defication, perianal sensitivity, and deliberate retention. Decreases time for bowel regimen and amount of fecal incontinence, but it can be costly and invasive.
Autonomic dysreflexia occurs in SCI due to loss of supraspinal regulation of the autonomic function of ___. High risk for SCIs above ___ level.
Triggered by noxious stim below the level of injury such as ….
Results in an exaggerated [ sympathetic / parasympathetic ] response, which in turn triggers the __ receptors in the aortic arch, resulting in a [ sympathetic / parasympathetic ] response.
Symptoms?
Autonomic dysreflexia occurs in SCI due to loss of supraspinal regulation of the autonomic function of BLOOD PRESSURE. High risk for SCIs above T6 level.
Triggered by noxious stim below the level of injury such as ….
- Ingrown toenail
- Full bladder/blocked catheter
- Fecal impaction
- Constipation
Results in an exaggerated SYMPATHETIC response BELOW level of lesion, which in turn triggers the BARORECEPTORS in the aortic arch, resulting in a PARASYMPATHETIC response BELOW level of lesion
Symptoms include:
- Increased BP
- Headache
- Flushing
- Anxiety
Autonomic dysreflexia in SCI results in a sympathetic response [above / below] the level of the lesion with related vaso [constriction/dilation] as a compensatory mechanism. Symptoms include [tachy / brady] cardia and [diaphoresis / goosebumps] above the level of the lesion.
Alternatively, the sympathetic response triggers baroreceptors in the aortic arch to subsequently trigger a parasympathetic response [above / below] the level of the lesion. Symptoms of this include [ diaphoresis / goosebumps] [ above/ below] level of lesion.
Treatment?
Autonomic dysreflexia in SCI results in a sympathetic response ABOVE the level of the lesion with related VASODILATION as a compensatory mechanism. Symptoms include BRADYcardia and DIAPHORESIS above the level of the lesion.
Alternatively, the sympathetic response triggers baroreceptors in the aortic arch to subsequently trigger a parasympathetic response BELOW the level of the lesion. Symptoms of this include GOOSEBUMPS BELOW level of lesion.
Treatment? UPRIGHT POSTURE to manage HTN while finding the NOXIOUS SOURCE - can be life threatening, as BP will continue to increase until noxious source is removed
Heterotrophic Ossification (HO)
- What is it?
- Where does it occur/impact? (structures? location relative to SCI level?)
- Pathophysiology?
- Prevalence post SCI?
- Factors significantly correlated with HO?
- How do we find/diagnose it?
- How to prevent it?
- How to treat it? (meds? surgery? role of ROM?)
Heterotrophic Ossification (HO)
- What: ectopic bone formation in the soft tissue surrounding a joint
- Where: typically CAUDAL to level of injury in SCI, often in hips
- Why? Pathophysiology isn’t well understood, but thought that bone morphogenic proteins act on mesenchymal stem cells causing them to differentiate into osteoblasts i/s/o decreased WB post SCI.
- Prevalence: as high as 53% post SCI, with clinically significant HO ~27% (clin significant = areas w/bone formation that limits ROM & impacts positioning/ mobility)
- Factors correlated w/HO: Motor complete paraplegia, spasticity, and pressure sores
- How to diagnose? ~50% show elevated levels of alkaline phosphatase in the blood (but that’s not a lot) - often picked up by therapist during regular ROM, then refers to imaging/XR to confirm.
Prevention: regular ROM; NSAIDs, when given early, showed greatest efficacy to prevent HO.
Treatment: Continual ROM is important!
- Medication: Etidronate
- Surgical resection (after bone has reached maturity) - ROM exercise may maintain joint ROM in the presence of immature ectopic bone (just don’t be crazy aggressive)
Spasticity post SCI consists of 2 components:
- Hyperexcitable __ reflex
- Hypertonia: soft tissue changes due to limb immobilization leads to increased muscle ___ to passive movement
Spasticity results from both disordered spinal mechanisms and disordered supraspinal mechanisms.
Spinal mechanisms: altered __ activity, imbalance of __ and __, inactive __ cell.
Supraspinal mechanisms: hyperexcitability of __ [afferents / efferents] of the stretch reflex.
Spasticity post SCI consists of 2 components:
- Hyperexcitable STRETCH reflex
- Hypertonia: soft tissue changes due to limb immobilization leads to increased muscle RESISTANCE to passive movement
Spasticity results from both disordered spinal mechanisms and disordered supraspinal mechanisms.
Spinal mechanisms: altered SYNAPTIC activity, imbalance of NEUROTRANSMITTERS and ELECTROLYTES, inactive RENSHAW cell.
Supraspinal mechanisms: hyperexcitability of GAMMA EFFERENTS of the stretch reflex.
Treating spasticity?
- Stretching
- EStim
- Standing
- Vibration
- Anti-spasmodic meds (may decrease reflex activity accentuate paresis in motor incomplete SCI, so consider in the setting of fxn!)
Osteoporosis in SCI
- Why?
- Increases likelihood of __
Osteoporosis in SCI
- Why? Decreased Ca2+ and collagen in bone immediately following SCI (most significant loss in first 1-2 yrs post injury then plateau ~4-5 yrs post injury. Loss is particularly proximal tib & distal femur = WB surfaces) d/t neurogenic osteoporosis
- Increases likelihood of FRACTURES (incidence of fractures increases as a function of time)
