L6 Clinical Presentation after SCI Flashcards
Acute Cardiac Dysfunction after SCI
occurs days to weeks
SCI at T1-L1 or higher will block communication of brainstem and sympathetic nervous system
-PNS is still intact, vagnus nerve
-the disruption results in bradycardia, bradyarrhythmia, peripheral vasodilation, hypotension
Usually most present in lesions above T6
Chronic Cardiac Dysfunction after SCI
reduced exercise tolerance
exercise induced hypotension
reductions in cardiac output, can be severe enough to cause atrophy of L ventricle (tetraplegia)
Autonomic dysreflexia
PT considerations for acute cardiac dysfunction
must monitor vitals
will need supportive measures when changing positions
progress to upright slowly
assistive clothing
TED hose is good for DVT, not much else
PT Considerations for Chronic Cardiac Dysfunction
physical inactivity is common
this will lead to deconditioning
leads to more functional limitations
Impaired Thermoregulation
SCI above L1 interrupts communication between hypothalamus and sympathetic
-the more rostral the injury, the more SCI will affect this
-shivering will be absent below the LOI
Acute Thermoregulation impairments
hypothermia due to unchecked vasodilation from parasympathetic system
after days-weeks, reflexive regulation of vasoconstriction returns
Chronic impairments of thermoregulation
loss of ability to sweat below the lesion, does not return
Thermoregulation and PT
you may need to assist them with thermoregulation
acute = blankets
Chronic = fans, room temp, etc Education
Areflexive or flaccid bladder
T12 or below injury, usually S2-S4 or cauda equina
the bladder remains flaccid
the cells bodies of S2 to S4 preganglionic are damaged, resulting in no parasympathetic innervation to the detrusor muscle
The detrusor muscle will not contract even when stretched
Bladder can’t empty, and will overflow or dribble
High risk for medical complications w/out medical program
Spastic or Reflexive Bladder
Injury above T12
Reflexively functioning bladders
S2-S4 reflex arc is intact
descending input from cortex and pontine miturition centers are disrupted
bladder empties reflexively when full, voluntary control is lost
Bladder Management Program
Can include the following, depending on the impact on S2 to S4
Indwelling catheter, intermittent catherter, suprapubic cather, reflexive bladder empty, valsalva voiding, medications to control spasms
During phase of spinal shock (bladder)
Options are:
indwelling catherization, which increases risk of infection or Intermittent catherterization (4-6 hours)
reflexive bladder may still be intact, which can cause unintential bladder emptying with abdominal pressure
If bladder function is not well managed
can be life threatening __> autonomic dysreflexia, kidney damage, UTI, sepsis
skin breakdown
Changes to Bowel Function
similar to bladder function changes
T12/higher = loses voluntary control
S2/4 intact = reflexive emptying
peristalsis will be slowed
make sure they are up on their fluids
Bowel Programs
during spinal shock, manual evacuation of stool is required
Bowl retraining involves emptying at scheduled times. Nutrition, hydration, abdominal massage, helps with this process.
Patient may have to manually remove stool (areflexive) or stimulate removal (reflexive)
PT and Bowel Program
Bowel program is required
Constipation or impaction can trigger autonomic dysreflexia
help them minimize bowel incontinence, because it increases skin breakdown and decreases community reintergration
Autonomic Dysreflexia
an abnormal, overreaction of the autonomic nervous system to pain or discomfort below the nerologic LOI after SCI
Emergency situation if not addressed. Has serious complications like stroke, seizure, organ damage, brain injury, death
Medical Management of Respiratory Impairment
Supplemental O2
Suction
Invasive Mechanical Ventilation
Supplemental O2
in early phases of recovery until ventilatory mm strength improves to adequately supprot day to day activities
Invasive Mechanical Ventilation
used with high cervical SCI
typically achieved using intermittent positive pressure ventilators
Causes inhalation either by delivering a set pressure, set volume of air
Can be stationary or portable models
PT assessment of respiratory function
O2 sats
postural assessment
quality of inspiration
quality of forced expiration
Impact of SCI on Ventilation and Coughing
LOI is going to impact muscles of inspiration/expiration and postural muscles
Higher lesions interrupt innervation to muscles of both inhalation and expiration
Lower lesions impact mm of expiration
Ventilation training
encourage diaphragmatic breathing during quiet breathing. Can use visual and verbal cues.
Supine is easier than sitting after SCI, abdominal binder can support sitting
Compensatory = cueing, strengthening intact muscles
PT Tx of REspiratory Function
strengthening
increase chest wall mobility
address postural alignment
open chest as much as you can
Clearing Secretions
Position changes
Strengthening of inspiration and forced expiration
Consultation with resp therapist
manually assisted cough
Integumentary System Impairments
Pressure injury, which localized area of tissue necrosis due to prolnged unrelieved pressure
life time risk with SCI
motor, sensory, and urinary impairments all increase risk
DVT/PE
Common complication after SCI
vasodilation and reduced LE muscle, immobility lead to stasis of blood
can use medication, compression devices, mobilization to treat
Pain
common during acute phase
can be chronic or debilitating
pain can be musculoskeletal, visceral, neuropathic
Osteoporosis
below LOW leading to increased fracture risk due to decreased weight bearing forces on skeletal system
Tx: meds that inhibit bone resportion, ambulation or prolonged standing
Heterotopic Ossification
formation of new bone within soft tissue
occurs in 10-53% of all SCI
located below LOI
can lead to decreased ROM, pain, activity limitations, pressure ulcers, incrased spasticity
Treatment of HO
prevention, using exercise but minimize microtruma to at risk areas (hips, knees, elbows)
Tx includs ROM, meds, surgical resection
Causes of decreased ROM in SCI
LMN results in paralysis
Spasticity
muscle strength imbalance
gravity positioning (contractures)
leads to pressure injury, deformity, difficulty with mobility
CVD in SCI
high amounts of RF in this population
sedentary lifestyle, higher body fat, lipid abnormalities, altered glucose metabolism, insulin resistance
What are the triggers for AD?
bladder issues, most common
bowel (constipation)
back passage/rectal disruption (hemorrhoids)
boils
bones (fractures)
babies
What are S/s of AD?
severe HTN
throbbing headache
profuse sweating and goosebumps
flishing of skin
bradycardia
blurred vision, dizziness, anxiety, cognitive impairment
Who is at risk for AD?
seen with SCI at T6 or higher
T6-t10 have moderate risk
T10 and below has no risk
complete SCI are 3x more likely
How is AD managed?
immediately take BP
if HTN is found, sit patient upright with feet dangling
continue to minotr
check for offending stimulus (bladder, clothing, bowel)
document it
