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35 Cards in this Set
- Front
- Back
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Why are SCI pts more prone to skin breakdown?
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Sensory impairment = prolonged pressure
Skin collagen degradation Dec peripheral BF Shear forces (transfers) Prolonged exposure to moisture Atrophy |
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3 components of skin care after SCI
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Procedural
Education Coordination |
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What type of procedural interventions will you perform for skin care?
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Skin inspection
Pressure relief Exercises to enhance CV fitness |
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What will you educate a pt on for proper skin care post SCI?
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Avoiding shear, friction, blunt trauma, and exposure to heat
Clothes, shoes, orthoses fit properly Skin clean and dry Balanced diet B&B |
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How/who/what will you coordinate with for skin care?
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Equipment to relieve pressures and disperse force
Communicate wiht primary physician |
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Etiology and time frame of osteoporosis post SCI
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Loss of collagen and Ca from bones, most evident in the first few months after SCI and lasting for about 4 years
Due to loss of mm action and WB, as well as circulatory, endocrine, and immune changes |
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What type of pt is most likely to develop severe osteoporosis?
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ASIA A and B with flaccid paralysis (as opposed to spasticity)
Amt. of loss is proportional to their disuse |
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Location of osteoporosis post SCI?
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Distal femur and proximal tibia
NOT SPINE |
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S/S of fractures?
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Redness, swelling, bruising, displacement/deformity
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Difference in bone mass between Paras and Quads?
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Para = inc in UE bone mass
Tetra = inc or dec in UE bone mass depending on use |
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Can osteoporosis be prevented or reversed in the SCI pt?
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No, prolonged standing, treadmill trng, and FES make be helpful later on to slow the progression, but early on nothing has been effective in reversing/preventing the devolopment
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Tx for osteoporosis?
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WB, treadmill trng, FES
Balanced diet with adequate protein Biphosphonates (Fosamax) |
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What does the SCATS exmaine that the MAS and Tardieu do not? Why is this important?
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Multijoint flexor and extensor spasms, which makes it a more comprehensive clinical scale for spastic hypertonia in SCI = more fxt measure
Imp b/c dif types of spasm interfere with functional mobility in dif ways. |
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How are clonus, flexor and extensor spasms triggered?
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Clonus = rapid stretch (stretch reflex)
Flexor = cutaneous withdrawl reflex Extensor = EXT at the hips: inc excitability of the interneuronal circuitry normally used for inc limb stiffness during standing/AMB |
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How does clonus, and flex/ext spasms interfere with function?
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Clonus - W/c and transfers
Flexor - Sleep, bed mobility, transfers Extensor - most discomfort and greatest interference with fxt during transfers and W/c propulsion |
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How can tx be altered for pts with clonus, flex/ext spasms>
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Equipment prescription (W/C)
Prescibing footwear based on forces on foot (withdrawl reflex) Alternative transfer techniques Pharmacological interventions |
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How do you perform the SCATS for each type of spasticity?
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Clonus - rapid DF
Flex - pin prick supine Ext - Flex hip/knee 90 deg and EXT hips |
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2 types of resistance to motion
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Myoplastic hyperstiffness
Spasticity (neural) |
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How do you perform the Tardieu?
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3 speeds, slower than gravity, gravity, faster than gravity
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How do you perform MAS?
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Only at speed of gravity
Looking at where there is a catch and resistance |
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What is the Penn Spasm Frequency Scale?
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Self report measure of frequency of reported mm spasms used to quantify spasticity
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Conclusion of PRISM measure
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Spasticity-related interventions need to be aimed at what matters most to the pt
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Interventions to treat spasticity (nothing proven for long term benefit)
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1. Positioning (maintenancy of mm length)
2. ROM/stretching (possible plastic changes of CNS or mm) 3. WB (decreased excitability due to influence of cutaneous and joint receptor input) 4. Strengthening (balance of agaonist/antagonist) 5. ESTIM (to contralateral mm = reciprocal inhibition) 6. Cold/heat (slow nerve conduction) 7. Slinting/orthoses (long-term stertch) |
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Difference in acute vs. chronic pain in SCI in terms of origin
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Acute is usally due to MSK or visceral pain
Chronic pain often lasts once the injurious stimulus is no longer present |
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What is neuropathic pain caused by?
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Direct damage to the NS. Constant, unrelenting, burning, shooting, electric pain.
Due to N and N root issues (dermatological pattern) or actual SC, pathway, or tracts Usually below the lesion |
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Common causes of pain ABOVE lesion?
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Typical things - MSK, visceral (if viscera exists above lesion), CRPS
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Common causes of pain BELOW lesion?
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MSK
Syringomyelia Neuropathic pain |
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Common causes of pain BELOW lesion?
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Central pain syndrome
Visceral or neuropathic |
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Drugs for spasticity? And pain...
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Baclofen, valium, zanoflex, gabapentin (neurotin), dantrium
All CNS depressants except dantrium! |
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Tx for pain post SCI?
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Treat what you can
Psychological tx |
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What is syringomyelia?
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Cyst that can develop in cavity where original lesion occures - central symptoms. Effects crossing STT first = changes in pain/temp in segmental region of inj. Can progress to compress A-mn and maybe even dorsal columns
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How do we manage UE injury after SCI?
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Mechanics, ROM/stretching, Strengthening
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What type of injury reports greater dec in fxt due to spasticity?
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Incomplete injuries b/c they have more function in the first place... so they notice it more
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When is stiffness/spasticity the msot for 1. C-sp complete 2. Th-sp either 3. C-sp incomeplete
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1. Worse at night (spasticity)
2. same all day 3. Worse in morning (stiffness) |
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How do you get clonus to stop? Ext spasm?
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Clonus - slowly WB thru limb or lift limb up
EXT - Get into flexion or gentle rocking in IR and ER |
