L6 Clinical Presentation after SCI

Question 1

Acute Cardiac Dysfunction after SCI

Answer 1

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

Question 2

Chronic Cardiac Dysfunction after SCI

Answer 2

reduced exercise tolerance
exercise induced hypotension
reductions in cardiac output, can be severe enough to cause atrophy of L ventricle (tetraplegia)
Autonomic dysreflexia

Question 3

PT considerations for acute cardiac dysfunction

Answer 3

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

Question 4

PT Considerations for Chronic Cardiac Dysfunction

Answer 4

physical inactivity is common
this will lead to deconditioning
leads to more functional limitations

Question 5

Impaired Thermoregulation

Answer 5

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

Question 6

Acute Thermoregulation impairments

Answer 6

hypothermia due to unchecked vasodilation from parasympathetic system
after days-weeks, reflexive regulation of vasoconstriction returns

Question 7

Chronic impairments of thermoregulation

Answer 7

loss of ability to sweat below the lesion, does not return

Question 8

Thermoregulation and PT

Answer 8

you may need to assist them with thermoregulation
acute = blankets
Chronic = fans, room temp, etc Education

Question 9

Areflexive or flaccid bladder

Answer 9

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

Question 10

Spastic or Reflexive Bladder

Answer 10

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

Question 11

Bladder Management Program

Answer 11

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

Question 12

During phase of spinal shock (bladder)

Answer 12

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

Question 13

If bladder function is not well managed

Answer 13

can be life threatening __> autonomic dysreflexia, kidney damage, UTI, sepsis
skin breakdown

Question 14

Changes to Bowel Function

Answer 14

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

Question 15

Bowel Programs

Answer 15

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)

Question 16

PT and Bowel Program

Answer 16

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

Question 17

Autonomic Dysreflexia

Answer 17

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

Question 18

Medical Management of Respiratory Impairment

Answer 18

Supplemental O2
Suction
Invasive Mechanical Ventilation

Question 19

Supplemental O2

Answer 19

in early phases of recovery until ventilatory mm strength improves to adequately supprot day to day activities

Question 20

Invasive Mechanical Ventilation

Answer 20

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

Question 21

PT assessment of respiratory function

Answer 21

O2 sats
postural assessment
quality of inspiration
quality of forced expiration

Question 22

Impact of SCI on Ventilation and Coughing

Answer 22

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

Question 23

Ventilation training

Answer 23

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

Question 24

PT Tx of REspiratory Function

Answer 24

strengthening
increase chest wall mobility
address postural alignment
open chest as much as you can

Question 25

Clearing Secretions

Answer 25

Position changes
Strengthening of inspiration and forced expiration
Consultation with resp therapist
manually assisted cough

Question 26

Integumentary System Impairments

Answer 26

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

Question 27

DVT/PE

Answer 27

Common complication after SCI
vasodilation and reduced LE muscle, immobility lead to stasis of blood

can use medication, compression devices, mobilization to treat

Question 28

Pain

Answer 28

common during acute phase
can be chronic or debilitating

pain can be musculoskeletal, visceral, neuropathic

Question 29

Osteoporosis

Answer 29

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

Question 30

Heterotopic Ossification

Answer 30

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

Question 31

Treatment of HO

Answer 31

prevention, using exercise but minimize microtruma to at risk areas (hips, knees, elbows)

Tx includs ROM, meds, surgical resection

Question 32

Causes of decreased ROM in SCI

Answer 32

LMN results in paralysis
Spasticity
muscle strength imbalance
gravity positioning (contractures)

leads to pressure injury, deformity, difficulty with mobility

Question 33

CVD in SCI

Answer 33

high amounts of RF in this population
sedentary lifestyle, higher body fat, lipid abnormalities, altered glucose metabolism, insulin resistance

Question 34

What are the triggers for AD?

Answer 34

bladder issues, most common
bowel (constipation)
back passage/rectal disruption (hemorrhoids)
boils
bones (fractures)
babies

Question 35

What are S/s of AD?

Answer 35

severe HTN
throbbing headache
profuse sweating and goosebumps
flishing of skin
bradycardia
blurred vision, dizziness, anxiety, cognitive impairment

Question 36

Who is at risk for AD?

Answer 36

seen with SCI at T6 or higher
T6-t10 have moderate risk
T10 and below has no risk

complete SCI are 3x more likely

Question 37

How is AD managed?

Answer 37

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