Physical Effects, Complications and Effects of Aging Flashcards

1
Q

What are the primary physical effects of a SCI?

A
motor function
muscle tone
sensation
breathing/coughing
bowel and bladder
genital function
cardiovascular 
thermoregulation
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2
Q

What are the hallmarks of a LMN?

A

flaccid paralysis

dennervated atrophy

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3
Q

What are the hallmarks of UMN?

A
paralysis
spasticity
increase DTR
clonus
Babinski
disuse atrophy
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4
Q

How is motor function affected by a SPI?

A

Combination of LMN and UMN d/t disruption of white and gray matter
Paralysis or paresis of voluntary musculature
Anterior horn cells and out are damaged (LMN)
Descending tracts are damaged (UMN)

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5
Q

How is muscle tone affected by a SPI?

A

flaccidity with spinal shock (everything shuts down)

may progress to spasticity

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6
Q

In what SPIs is spasticity more common?

A

cervical, thoracic and incomplete (ASIA B and C)

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7
Q

In what SPIs is flaccid paralysis more frequent?

A

caudal lesions (cauda equina)

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8
Q

What is spasticity?

A

An increase to resistance to movement and is velocity dependent
Hyperactive stretch reflexes and clonus
Gradually increases after 6 months
Varies in level of severity
Can assist or interfere in functional activities

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9
Q

What is spasticity affected by?

A

positional changes, cutaneous stimuli, environmental temperature (cold), tight clothing, fecal impaction/catheter blockage, bladder/kidney stones, UTI, pressure ulcer, and emotional stress

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10
Q

What are the drug therapies for spasticity?

A

diazepam/valium
baclofen
dantrolene
Significant side effects (lethargy) and are non specific so it will decrease tone everywhere

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11
Q

What are the injected agents used for treating spasticity?

A

peripheral nerve block and intafecal catheter (usually more specific but invasive)

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12
Q

What are the surgical options for treating spasticity?

A

Tendon releases

Sever nerves or nerve roots

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13
Q

What is the PT management for spasticity?

A

prolonged stretching
position out of the position that makes it worse
prolonged weight bearing

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14
Q

How is sensation affected with a SPI?

A

impairs body awareness (significant barrier)
makes patient vulnerable to trauma
usually improves overtime

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15
Q

What lesions affect the muscles of respiration?

A

T12 and above will affect muscles but just because it is below T12 doesn’t mean there will be no respiratory problems

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16
Q

What are the muscles of respirations and their innervations?

A
SCM- CN XI, C2-3
Upper Trap- CN XI, C2-4
Diaphragm- C3-5
Scalenes- C3-8
Serratus Anterior- C5-7
Pec Minor- C6-T1
Intercostals T1-11
Abdominals T6-L1
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17
Q

Respiration function with a C1-2 neurological level?

A

Partial SCM and Upper traps
no diaphragm
will need to be on a ventilator
need assistance with forced exhalation or airway clearance

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18
Q

Respiration function with a C3 neurological level?

A

Full SCM, partial Upper Trap, scalenes and diaphragm
may be able to breathe I but will fatigue quickly
ventilator support acutely
need assistance with forced exhalation/airway clearance

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19
Q

Respiration function with a C4 neurological level?

A

Full Upper traps, partial diaphragm and scalenes
may be able to breathe I but ventilation in the beginning because diaphragm will flatten and will be compromised
need assistance with forced exhalation/airway clearance

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20
Q

Respiration function with a C5-8 neurological level?

A

Full diaphragm, partial to full scalenes, serratus anterior and pec minor (most accessory muscles)
breathes I better
need assistance with forced exhalation/airway clearance

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21
Q

Respiration function with a T1-5 neurological level?

A

Partial intercostals but no abdominals
breathes I
needs assistance with forced exhalation/airway clearance

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22
Q

Respiration function with a T6-12 neurological level?

A

Partial to full intercostals and abdominals
Could have some compromise with coughing
L1 and below respiratory muscles are intact

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23
Q

What are the positional factors with respirational problems?

A

Supine will be easier because will increase pressure d/t increase abdominal area
Sitting is harder because abdominal contents lower and diaphragm could flatten and compromise

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24
Q

What is a paradoxical breathing pattern?

A

Upper chest depresses and lower distends in inhalation

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25
Q

What is sleep apnea and who does it affect?

A

Moments in sleep when a person ceases breathing
increased incidence in SPI
associated with obesity and males

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26
Q

What needs to be intact for normal bowel and bladder function?

A

Intact sacral cord

most SCI lead to loss of voluntary bowel and bladder control

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27
Q

What are the implications for loss of voluntary bowel and bladder control?

A
infection
sepsis
skin breakdown
autonomic dysreflexia
death
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28
Q

What is the storage phase in normal bladder function?

A

Sympathetic efferents relax detrusor muscle and contract bladder neck
Somatic control- tonic contraction of external sphincter and pelvic floor muscles

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29
Q

What is the urination phase in normal bladder function?

A

Parasympathetic stimulation contracts detrusor muscle and relaxes bladder neck
Somatic control relaxers external sphincter

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30
Q

What is areflexive bladder?

A

LMN at or below T12
lose parasympathetic stimulation
bladder is flaccid and large volumes remain d/t lack of reflexive emptying
overflow or dribbling incontinence

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31
Q

What is reflexive bladder?

A

UMN C/T-spine injuries
S2-4 reflex arc intact
descending (sympathetic) input lost
bladder empties reflexively (parasympathetic control) because there is no voluntary control

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32
Q

What is detrusor-sphincter dyssynergia?

A

involuntary external sphincter contraction occurs at the same time as detrusor contraction (can’t get urine out)
high post void residuals
can be present with reflexive bladder

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33
Q

What are the possible causes of detrusor-sphincter dyssynergia?

A

UTI
sepsis
autonomic dysreflexia
renal damage

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34
Q

What are the bladder management goals?

A

complete bladder emptying at appropriate intervals
low pressure voiding and storage of urine
prevention of urinary incontinence

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35
Q

What is normal bowel function?

A

Intrinsic- control of smooth muscle in gut, internal sphincter
Autonomic- sympathetic dampens peristalsis and parasympathetic excites peristalsis
Somatic- external anal sphincter and pelvic floor (S2-4)

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36
Q

What is the intrinsic defecation reflex?

A

mediated by intrinsic system
relaxes internal anal sphincter and peristalsis
not strong enough to produce bowel movement alone

37
Q

What is the parasympathetic defecation reflex?

A

relaxation of internal anal sphincter and intensification of peristalsis

38
Q

What is areflexive bowel function?

A

Sacral reflex arc not intact
can become impacted or incontinent
manual evacuation techniques needed

39
Q

What is reflexive bowel function?

A

Sacral reflex arc intact
bowels function reflexively
digital stimulation needed

40
Q

How is genital function affected by SPI?

A

innervated from thoracolumbar and sacral region
disrupts sexual response
men are likely to be infertile

41
Q

What are the early cardiovascular effects?

A
at or above T6
bradycardia
bradyarrhythmia
hypotension
orthostatic hypotension
42
Q

What are the lasting cardiovascular effects?

A
at or above T6
decrease exercise tolerance
exercise-induced hypotension
decrease venous return, stroke volume and CO
autonomic dysreflexia
43
Q

How can you manage postural hypotension?

A

common early on
slow progression to vertical
monitor BP
compression hose or abdominal binder may help

44
Q

How is thermoregulation affected by SPI?

A

tendency toward hyperthermia
lose sympathetic control of sweat glands (no sweating below excessive sweating above)
higher lesions are more problematic (can’t go in hot tub)

45
Q

What are some physical complications in SPI?

A

autonomic dysreflexia, pressure ulcers, contractures, HO, respiratory, osteoporosis/fractures, pain, GI, urinary tract, DVT/PE, and CV disease

46
Q

What is autonomic dysreflexia?

A

pathological autonomic reflex produced by noxious stimuli below LOL
usually in at or above T6 complete or incomplete lesion
considered a medical emergency because it triggers excessive sympathetic response (could lead to CP failure, LOC, seizures, stroke, coma or death)

47
Q

What are the symptoms are autonomic dysreflexia?

A
hypertension
bradycardia
HA (severe and pounding) usually first symptom
increase sweating
increase spasticity
flushing above LOL
nasal congestion/ constricted pupils
goose bumps
blurred vision
anxiety
48
Q

What are possible initiating stimuli of autonomic dysreflexia?

A
bladder distention
bowel distention
tight clothing/orthotics/straps
pressure sores
urinary stones
bladder infection
49
Q

What is the intervention for autonomic dysreflexia?

A

Sit pt up
search for noxious stimuli and correct (question pt if needed)
call for help or code
monitor BP and keep head up
document event
usually removal of stimuli will fix problem

50
Q

Pressure ulcers in SCI?

A

more vulnerable
up to 85% will develop at least 1
serious medical complications
can lead to osteomyelitis/infection/sepsis/death

51
Q

What are the factors associated with pressure ulcers?

A
excessive pressure
prolonged unrelieved pressure
shearing or dragging
exposure to moisture
local or systematic temperature elevation
skin collagen degradation
compromised peripheral blood flow
52
Q

What are the stages of a pressure ulcer?

A

1: non-blanchable erythema
2: partial thickness
3: full thickness skin loss
4: full thickness tissue loss

53
Q

What is stage 1 of a pressure ulcer?

A

Non-blanchable erythema
intact skin
can keep from progressing
harder to see on darker patients

54
Q

What is stage 2 of a pressure ulcer?

A

partial thickness
partial loss of dermis
shallow open wound

55
Q

What is stage 3 of a pressure ulcer?

A

full thickness skin loss

eaten through subcutaneous fat

56
Q

What is stage 4 of a pressure ulcer?

A

full thickness tissue loss

eaten through muscle, tendon and down to bone

57
Q

What are the most susceptible areas for pressure ulcers?

A
sacrum
heel
ischial tuberosity
scapula
malleolus
occiput
spinous process
58
Q

What is the treatment of pressure ulcers?

A

prevent by turning patient every 2 hours or pressure relief every 10 mins if in sitting
local wound care
diet (protein for healing)
surgical management is really progressed

59
Q

What are the respiratory problems for SCI?

A

most common cause of death
reduction in inspiratory/expiratory ability
ineffective cough

60
Q

What can respiratory problems in SCI lead to?

A

atelectasis
pneumonia
respiratory insufficiency

61
Q

How can contractures occur in SPI?

A

inability to move and muscle imbalance
spasticity
habitual postures

62
Q

What are some complications for contractures?

A

significantly affect function
increase likelihood of skin breakdown
higher the lesion the more debilitated by contractures

63
Q

What are the common contracture sites?

A

shoulder flexion
elbow flexion
wrist flexion
knee flexion

64
Q

What is heterotopic ossification?

A

deposition of bone in soft tissue around peripheral joints (extra articular/ extracapsular)
usually stronger than older bone
almost always below level of lesion

65
Q

What are the common sites of HO?

A

hip
knee
shoulder
elbow

66
Q

What are the signs and symptoms of HO?

A

1-6 months after SCI
joint swelling/warmth
joint p! if intact sensation
decrease ROM

67
Q

What must be differentiated from with HO?

A

thrombosis
cellulitis
infection
hematoma

68
Q

How do you diagnose HO?

A

plain film is most common
bone scan for early detection and monitoring growth (best way but expensive)
MRI/CT shows relationship to blood vessels, nerves and muscles

69
Q

What is the drug treatment for HO?

A

Prophlactic (NSAIDS)
prevention d/t inhibits osteogenic cells and suppresses prostaglandin-mediated response
Bisphosphonates: inhibit CA phosphate precipitation (prevents progression)

70
Q

What is the surgical management of HO?

A

lesions are removed but must be mature (12-18 months) or will return
bone scan to determine metabolic activity

71
Q

What is PT management of HO?

A

ROM (aggressive could restart process)
strengthening
post-op control of edema, and scar management

72
Q

Osteoporosis in SCI?

A

rapid bone loss in the first few months
25% in hip and 50% in knee 2 yrs after
more common with motor complete than incomplete
UE in tetraplegia

73
Q

What is the fracture risk in SCI?

A

2x more likely than able-bodied
distal femur/proximal tibia most common
associated with increase morbidity: non-union, delayed healing, pressure ulcers
LOS is 7x longer than other health problems

74
Q

What are the common causes of fractures in SCI?

A

fall from WC
transfer from WC
rolling over in bed
(weakest in shearing/twisting)

75
Q

What are the PT interventions for fractures?

A

WB exercise acute (dynamic, duration but not sustained) and chronic
low magnitude vibration (delays bone loss)
FES (acute and chronic but only bones muscle cross)
bisphosphonates
anabolic agents (parathyroid)

76
Q

What are the sources of pain in SCI?

A

traumatic events (fx, ligaments, muscle, sx)
nerve root
dysesthesias (diffuse p)
musculoskeletal (posture, overuse)

77
Q

What are the effects on gastrointestinal in SPI?

A
2-22% develop stress ulcers in stomach/duodenum
paralytic ileus (gut shuts down)
other: fecal impaction/ bowel obstruction, gallstones, hemorrhoids)
78
Q

What are the urinary tract complications in SPI?

A
urinary retention
kidney/bladder stones
kidney failure
septicemia 
increase risk of bladder cancer
79
Q

What are the chances of DVT/PE in SCI?

A

highest incidence 72 hours to 2 weeks after SCI
rare in chronic SCI
consequence of decreased muscle function and mobility and hypercoagulability
PE is leading cause of death in first year after SCI

80
Q

What are the chances of cardiovascular disease in SCI?

A

higher than general population
contributing factors: sedentary lifestyle, increased body fact, lipid abnormalities, altered glucose metabolism and diabetes

81
Q

What is syringomyelia?

A

development of an abnormal cyst or cavity within spinal cord that compresses spinal cord and decreases neurological level
unknown cause months to years after SCI

82
Q

Where are the areas of occurrence of syringomyelia?

A

most common is lower c-spine (cerebrobulbia)
brainstem (CN problem, dysarthria, nystagmus)
lumbosacral segments (less common, B&B problems)

83
Q

What is the treatment for syringomyelia?

A

drain cavity

place shunt

84
Q

What are the effects of aging in SPI?

A

increase rick of pressure ulcers (decrease thickness, decrease blood supply, decrease movement)
increase risk of respiratory complications
increase incidence of sleep apnea
urinary tract complications
GI (slows down, constipation, hemhroid)

85
Q

What are the neurological effects of aging in SPI?

A

overuse
nerve entrapment
decrease neurons
brachial plexus

86
Q

What are the endocrine effects of aging in SPI?

A

increase body fat
distribution of fat changes
increase obesity
increase diabetes

87
Q

What are the musculoskeletal effects of aging in SPI?

A

RTC tears
overuse injuries
shoulder impingements

88
Q

What are the cardiovascular effects of aging in SPI?

A

increase risk for CV disease

quit smoking, lose weight, control cholesterol, and be active