Clinical Procedures I Flashcards

test 1

1
Q

Pain

A

Unpleasant sensation with actual or potential tissue injury
- v subjective & depends on factors like anxiety, fatigue, previous experiences, cultural norms
- human nature to try to move away from pain & body tries to prevent more damage
- v hard for pt to quantify pain

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2
Q

muscle guarding

A

protective response in a mm that results from pain or fear of mvmt
- occurs to protect area from further trauma by contracting surrounding mm & providing “exoskeleton”

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3
Q

What factors of mm guarding contribute to continued dysfunction?

A
  • pain may increase mm guarding
  • mm guarding decreases circulation
  • decreased circulation reduces healing
  • pain-spasm cycle: pain- guarding-dysfunction triangle
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4
Q

What is very important to help decrease pain in pt?

A

Education!! Educate on what you’re doing & why you’re doing it - this increases trust and helps them relax their mm, increasing pain threshold

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5
Q

Types of pain producing substances

A

potassium, serotonin, bradykinin, histamine, prostaglandins, leukotrienes, substance p, ACH, ATP, calcitonin gene-related peptide (CGRP), nerve growth factor (NGF), thromboxane, acid environment

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6
Q

What triggers pain producing substances to infiltrate that specific area?

A

injury

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7
Q

Function of pain producing substances

A
  • can directly activate nociceptors to send pain message to CNS
  • sensitize nerve endings
  • lower pain threshold after tissue injury & inflammation
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8
Q

types of pain

A

acute, chronic, referred

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9
Q

Acute pain

A

< 3 months
due to injury/trauma
easiest to understand, dx & rx

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10
Q

How do vitals relate to acute pain?

A

Acute pain often results in changes in HR, BP, RR
take vitals! - they may help know if acute pain present

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11
Q

Function of acute pain

A

Protect against further tissue damage & maintained to allow for proper time of tissue healing

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12
Q

Chronic pain

A

> 3-6 months (can last years)
doesn’t appear correctable or rx-able
could be referred pain
may need lots of modalities to relieve it
associated with physical, emotional, social & financial disability

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13
Q

difference between chronic & acute pain

A

chronic pain is pain that used to be acute but is past expected healing time for injury/insult chronic pain no longer protective mechanism & may be considered a disease itself

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14
Q

what is a characteristic of chronic pain?

A

central sensitization…amplification of neural signaling w/in CNS that underlies pain hypersensitivity

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15
Q

referred pain

A

comes form deep structures but felt at remote site radiating (continues to move) pain is type of referred pain
has patterns to help determine source of pain
Ex. “brain freeze” when you eat something cold, heart attack causing pain in left arm

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16
Q

believed etiology of referred pain

A

convergence of cutaneous, visceral, & skeletal mm nociceptors on common nerve root of SC -> brain interprets afferent input as coming from cutaneous structures bc higher proportion of cutaneous afferents

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17
Q

examples of referred pain

A

MI - pain in jaw, L shoulder/arm, stomach CSP nerve root compression - pain in arm/hand

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18
Q

referred patters for determining source of pain

A

dermatomes - areas of skin innervated by specific nerve root

myotomes - areas of mm innervated by specific nerve root

sclerotomes - areas of bone innervated by specific nerve root

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19
Q

nociceptors

A

“pain receptors”
nerve endings that conduct nerve impulse to CNS
- found in skin, mm, joints, bone & viscera
- high threshold for activation
- types: A-delta & C fibers

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20
Q

A-delta pain fibers

A

small & MYELINATED nociceptors
- respond to high-intensity mechanical (MSK) & thermal (heat) stimuli (immediate response)
- conduct peripheral pain signals very quickly (5-30 m/s)
- FIRST pain sensation & precise localized pain
- generation w/drawl reflexes

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21
Q

How are A-delta pain fibers described?

A

Sharp, stabbing or pricking pain

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22
Q

C pain fibers

A

thin & UNMYELINATED nociceptors
- respond to broad range of painful stimuli (including mechanical, thermal or chemical - polymodal)
- longer lasting & slow conduction (0.5-2 m/s)
- poorly localized pain
-help prevent further tissue damage

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23
Q

How are C pain fibers described?

A

They are the “second pain” - dull, burning, throbbing, and aching

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24
Q

Ascending pain pathways

A

nociceptors enter the dorsal horn of the SC for processing
–> send to brain (to thalamus) via tracts where pain is actually perceived

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25
Q

ascending pain tracts

A

spinothalamic tract (STT) - sharp & localized pain (A-delta)
spinoreticulothalamic - diffuse & poorly localized pain, visceral pain (C fibers)

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26
Q

descending pain

A

endogenous opiates released through pain, exercise, laughter, relaxation, meditation, acupuncture, and EStim
*not completely understood

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27
Q

What are endogenous opiates?

A

naturally occurring substances that inhibit perception of pain

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28
Q

Pain theories

A

began in 1965 and constantly evolving - gate control theory & endogenous theory

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29
Q

gate control theory

A

injury activates A-delta & C fibers –> dorsal horn decides whether or not to send signal to brain, depending on noxious stimuli
- dorsal horn contains central transmission cells
- summation of excitatory & inhibitory influences determine if signal moves up the chain

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30
Q

How to close gate, according to gate theory?

A

If you have non-noxious stimuli (modalities) greater than noxious stimuli, gate is closed & pain signal doesn’t go to brain

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31
Q

endogenous opiate theory

A
  • neurotransmitters that are considered descending control mechanisms
  • operate on spinal cord level
  • “block the gate” by interfering w/ A-delta & C fiber signal transmission to T cells
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32
Q

Types of endogenous opiates?

A

enkephalins - activated by rubbing
endorphins - exercise, laughter, unnerving/shaky
serotonin - link to analggesia (lack of feeling pain)
dopamine - pleasure

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33
Q

factors making it hard to close the gate

A

extreme emotions, same previous injury, attention to pain

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34
Q

counter irritation theory

A

counter the noxious stimuli w/ non-noxious stimuli
Ex. other hand squeezes finger that was just smashed in door

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35
Q

use of biophysical agents for pain

A

pain modulation - blocking transmission of pain at the gate or dorsal horn of spinal cord

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36
Q

types of modalities to close gate

A

ice/heat, compression, Estim, massage - get pain assessment to see if effective

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37
Q

What are different pain assessment tools?

A

McGill pain questionnaire - body drawing & pt circles, Xs, etc on body part for type of pain

Visual analogue scale (VAS) 0—-I—-10

Numeric pain rating - “pain on a scale of 0-10?” “4/10”

Baker-Wong scale - smiley faces & numbers 1-10 (peds, HOH, language barrier)

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38
Q

Why and when do we check sensation?

A

Why - looking for gross sensory abnormalities

When - BEFORE rx - always before modality - if pt doesn’t have sensation, modality can injure them

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39
Q

How do you check sensation?

A
  • pain: top of reflex hammer (pointy)
  • light touch: cotton ball, little brush
  • temperature: test tube w/ cold or
    warm water (dif stages of
    cold/heat)
  • vibration: tuning fork (rarely done)
  • proprioception: position of limb or jt in space (eyes closed, able to point out where sensation is)
  • deep tendon reflexes: reflex hammer (patellar tendon, tendoncalcaneus, biceps tendon, triceps tendon)
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40
Q

Other ways to gauge if pt is in pain/if pain increasing?

A

body language, facial expressions, discoloration, not breathing, mm guarding, goni and/or MMT greatly decreased over short period, increased swelling

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41
Q

APTA recommendation of use of modalities

A

passive physical agents should only be used as complimentary to therapeutic exercise and interventions to increase participation in active rx programs (modalities = cotherapies)

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42
Q

What are different types of modalities?

A

thermal - heat & cold
electromagnetic - electrotherapy, diathermy, light
mechanical - traction, compression
hydrotherapy
acoustic - ultrasound
manual - massage

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43
Q

What are the purposes of modalites?

A

They assist, augment, or complement natural reparative mechanisms of the body (not change how body heals itself) by…
- decreasing pain, edema, and stiffness
- increasing ROM, tissue healing, mm activation

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44
Q

What is a determining factor of which modality to use on a pt?

A

the phase of tissue healing the pt is in - the wrong modality can delay healing (contraindicated)

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45
Q

Function of cryotherapy (cold)

A
  • reduces blood flow (vasoconstriction) & metabolic activity
  • decreases pain (increasing pain threshold), desensitizing peripheral afferent nociceptors
  • reduces swelling
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46
Q

Function of applying heat

A
  • facilitate tissue healing (in proliferative & reconstruction phases)
  • relax skeletal mm, decrease mm spasms & pain
  • promote & increase blood flow (vasodilation)
    -prep soft tissues for stretching, mobilization, and exercise (may be used before a pt sesh)
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47
Q

Function of electrotherapy

A
  • strengthening or relaxing skeletal mm
  • decreasing pain
  • facilitating neuromuscular re-education
  • increasing ROM
  • promoting tissue & wound healing
  • reducing edema
  • increasing local blood flow
  • deliver medicinal ions transdermally
  • attenuating disuse atrophy
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48
Q

function of compression

A
  • prevent, attenuate, or reverse swelling
  • alter or minimize scar formation during proliferative & maturation phases, and reduce hypertrophic scarring
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49
Q

inflammatory/acute phase

A

body’s immediate defense mechanism (days 1-10)

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49
Q

individual factors effecting on the healing of tissues

A

size of the wound, cardiopulmonary disease, severity of wound/injury, active infection, immunosuppressive disorder or drugs

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50
Q

What brief response occurs in the beginning of the inflammatory phase?

A

vasoconstriction of BV & lymph vessels, aggregation of platelets for coagulation - to reduce bleeding & minimize bacteria exposure

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51
Q

What is the second part of the inflammatory phase?

A

vasodilation > edema (fluid released form intracellular space), redness, warm to touch, pain (bc tissues distended & nerve fibers irritated)
- inhibits extra clot formation

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52
Q

Why does fluid build up during inflammation?

A

lymphatic system can’t keep up
- transudate (normal, clear & watery)
- exudate (viscous & cloudy due to plasma protein)
- pus (leukocytes, yellow/green)

53
Q

What is the third part of the inflammatory phase?

A

phagocytosis > macrophages clean up necrotic tissue & recruit fibroblasts
- lack of macrophages & fibroblasts > chronic inflammation

54
Q

Cardinal signs of inflammation?

A

pain (dolor) - stimulation of pain receptors & A delta & C fiber nerve endings triggered by chemicals @ injury site & mechanical pressure of edema

increased tissue temp (calor) - warmth due to vasodilation

erythema (rubor) - redness due to vasodilation

edema - vasodilation & more fluid in extracellular space

LoF - due to all of the above

55
Q

interventions for inflammatory phase

A

COLD ONLY + compression & Estim
- pain relief, decrease edema & local blood flow (vasoconstriction), decrease metabolic activity
- minimizes leakage of proteins into tissue spaces
- lessens duration of inflammation

56
Q

Lack of O2 leads to what during the inflammatory phase?

A

chronic injury/wound!
- macrophages can’t function so no stimulation of fibroblasts

57
Q

Proliferative/subacute phase

A

Fibroblasts lay down collagen & elastin to replace damaged tissue, revascularization (days 3-20)

58
Q

What is the key to the proliferative phase?

A

the presence of fibroblasts (but not too many)

59
Q

Beginning of proliferative phase

A
  • rebuilding > production, organization, infiltration of collagen
  • fibrinogen (blood-borne proteins) come to area & reinforce the collagen and developing scar tissue
  • keratinocytes replace tissue in wound if open
60
Q

End of proliferative phase

A

blood clots dissolve and lymphatic channels open to help reduce edema

61
Q

Why is the subacute phase very O2 dependent?

A

It requires high energy demand due to the epithelization or granulation occurring (pink tissue)
- lack of O2 > HYPOXIC wound, chronic, poor scarring

62
Q

Considerations during the proliferative phase

A
  • collagen is weak, tissues are fragile, because of this it can be easily disrupted/deformed
  • cardiopulmonary issues prolong phase 2 (bc O2 needed)
63
Q

Interventions for subacute phase?

A

Hot packs, ultrasound, diathermy
- enhance local blood flow (vasodilation)
- promote repair of damaged tissue immobilize joint, restrict ROM
- protect fragile collagen formation

64
Q

Why is collagen important?

A

Most abundant protein in the body
tensile strength comparative to steel, when organized

65
Q

remodeling/maturation phase

A

remodeling of scar (starts days 9-10)
- can take 1+ years, depending on severity

66
Q

details of remodeling phase

A
  • modeling, remodeling, organization and maturation of collagen
  • new collagen (fibroblasts) & breakdown of old (fibroclasts)
  • scar tissue reshaped/reogranized to form structure it’s replacing
  • scar tissue at best is only 70-80% strong/functional as og tissue
67
Q

good scars?

A

rosier scar: tissue remodeling occurring, slightly raised
ideal scar: pale, malleable, flat

68
Q

Keloid scar

A

giant scars formed bc not enough tissue breakdown during remodeling phase
- poor blood supply, decreased ROM across jt, decrease organ function

69
Q

Interventions during remodeling phase

A

hot packs, ultrasound, diathermy
- increases pliability of scar & blood flow to area
- scar massage
- mobilize tissue
NOT COLD

70
Q

What is the primary goal of wound healing?

A

to return pt to function

71
Q

Factors negatively impacting healing?

A
  • steroids, immunosuppressive drugs, NSAIDs, blood thinners
  • AIDS, DM, cancer
  • cellular toxicity from betadine or hydrogen peroxide
  • radiation therapy, chemo
  • poor nutrition
  • smoking
  • old age
72
Q

role of PTA in tissue healing

A

promote/aid phases of healing & know when to perform what intervention

73
Q

What is homeostasis?

A

Stable state or equilibrium that the body systems operate optimally

74
Q

Basic principles of temperature

A
  • homeostasis
  • body uses sensory receptors in skin & hypothalamus (body’s therostat) to maintain normal body temp
  • 3 ways to regulate temp –> shivering (increase) –> sweating (crease) –> BV changes (vasodilation increases / vasoconstriction decreases temp)
75
Q

How do we cool the body?

A

By removing heat from it via conduction, convection, or evaporation

76
Q

What reduces the overall metabolism and O2 demand of the living tissues?

A

cold

77
Q

Effects of cold on peripheral nerves

A
  • increases threshold for depolarization
  • slows nerve conduction velocity
  • extreme cold can block nerve conduction
78
Q

Challenging what should be avoided for a period of time after cold modality, due to reduced somatosensory input?

A

balance, proprioception, accuracy, or agility

79
Q

Conduction

A

Direct interaction with the body (transfer of molecules)
- ice pack, cold water immersion, ice massage, controlled-cold units

80
Q

Convection

A

Direct contact between skin & moving fluid particles (circulation molecules)
- cold water whirlpool

81
Q

Why is the convection modality only indicated for distal portions of extremities?

A

Heat loss is 25x greater in water than air at same temp & greater exposure (trunk esp) could lead to hypothermia

82
Q

Evaporation

A

liquid to vapor (energy transfer)
- vapocoolant sprays

83
Q

Basic reasoning to use cryotherapy?

A

Cheap and proven effective in acute phase of healing

84
Q

Effects of cold therapy

A
  • vasoconstriction, reduces blood flow
  • decrease metabolism
  • reduce inflammation including early edema formation
  • reduce mm spasms IF body has reached analgesic state (remember pain-spasm cycle)
  • reduces PNS conduction, including pain perception (gate control theory) -> increasing pain threshold
  • reduces neuromuscular tone such as spasticity or clonus
  • may increase joint stiffness, decreasing viscosity & elasticity
85
Q

Affects of cold application to MMT?

A

May lead to inaccurate findings…perform MMT B4 cold (or several hrs after)
- after < 5 min of cold, mm may produce more force than uncooled state
- after longer cold application (> 5 min), mm may have reduced force production than uncooled state

86
Q

Factors influencing tissue response to cryotherapy

A
  • temp difference between cold object & soft tissue
  • time of exposure (duration)
  • thermal conductivity of area being cooled
  • type & size of cooling agent
  • total body surface area cooled
  • activity level (increased activity -> increased circulation -> faster rewarming)
  • ability of cooling agent to maintain its temperature
87
Q

thermal conductivity & consideration

A

measure of efficiency of material or tissue to conduct heat

consider when cooling areas where cutaneous or subcutaneous metal (piercings, arthroplasty, shrapnel, etc) is present & also over scars that have compromised circulatory response!

88
Q

Thermal conductivity of materials/tissues: good to poor

A

silver > aluminum > titanium > ice water @ 69F > bone > mm > fat/adipose > air @ 32F

89
Q

Implications of thermal conductivity of adipose tissue

A
  • less conductivity than tissues with high water content
  • acts as insulator, resisting heat transfer (gain or loss)
  • mm usually underneath varying depths of adipose tissue -> affects rate of intramuscular cooling & rewarming
  • 6x the amount of time needed to produce 12.5F
89
Q

clonus

A

rhythmic, oscillating, stretch reflex due to upper motor neuron lesion –> hyperreflexia (usually in extremties)

90
Q

clinical indications of cold therapy

A

cold is modality of choice for acute phase (new MSK trauma or s/p swelling) used w/compression & elevation

acute MSK trauma, pain & mm spasm, myofascial pain syndrome, migraines

91
Q

PRICES

A

Protect
Rest
Ice
Compression
Elevation
Stabilize

92
Q

What is the goal of cold therapy?

A

Pain relief for 30 min to 2 hrs after rx

93
Q

What must be considered before applying cryotherapy?

A
  • accessibility of body part (where to apply modality)
  • is compression & elevation needed?
  • size of area to be cooled
  • contraindications & hypersensitivity to cold
  • cold only reaches 1-3cm or 1 in depth (can’t use for deep mm)
  • if cooling important, avoid activity right after application of it
94
Q

What must we inform pt of before applying cryotherapy?

A

Cold perception (pt education!)
CBAN - cold -> burn -> ache -> numb/analgesia (ask pt feeling)
skin may be red & that’s okay (unless it stay that way)

95
Q

CONTRAINDICATIONS for cold

A
  • cold urticaria (skin rash/hives w cold)
  • cold intolerance (awful pain after - 1 min of cold)
  • Raynaud’s disease (poor circulation to fingers/toes -> white/blue & feel cold)
  • over areas of compromised circulation
  • impaired cognition
  • lack of sensation in area of rx
96
Q

PRECAUTIONS for cold

A
  • hypertension (check BP, meds?)
  • open wounds
  • poor sensation
  • very young & very old
  • aversion to cold (dislikes cold but can tolerate it)
97
Q

Measurable outcomes for documentation

A
  • edema-girth & volumetric (measuring tape!)
  • pain (pain scales)
  • ROM (goni, best for vapocoolant spray)
  • function (observe movement - iffy, no activity, or stiff after)
  • mm guarding & tone (palpation & mm flexibility)
98
Q

Checking for sensation w cold

A

Pain: sharp & dull
- clean end of sharp edge
- demo beforehand
- ask pt to close eyes

Light touch
- cotton ball or small brush

Temperature
- test tube with ice water

99
Q

Documentation of cryo/thermotherapy

A

S: pain rating (before & after rx, how pt feels
O: type of modality, pt position, site of application, duration of rx, good and/or adverse responses (edema, ROM, skin appearance), use of concurrent compression or elevation
EX: CP x 20 min to CSP supine, tolerated without complaint or pain 2/10 after, normal skin responses noted

100
Q

Which type(s) of cold modality is best for application around bony prominences?

A

ice bag or ice massage

101
Q

Cold Pack / ice bag procedures

A
  1. prep cold pack w/ insulating layer
  2. orient pt to procedure (what you’re doing & where, consent)
  3. position & drape pt comfortably (elevation required?)
  4. explain stages of cold perception (CBAN, pt understand?)
  5. check sensation (sharp, light touch, cold)
  6. apply cold pack
  7. leave call system in place!! (bell), set timer for 5 min
  8. check pt response in first 5 min
  9. normal application 10-15 min
  10. dry & inspect skin after
102
Q

ice massage procedure

A
  1. gather ice & towels
  2. orient pt to procedure (what & where, get consent)
  3. position & drape pt comfortably (is elevation required?)
  4. explain stages of cold perception (CBAN, pt understand?)
  5. check sensation (sharp, light touch, cold)
  6. apply ice massage for 5-10 min
    (no more!) over 10-15 cm area (4x6 card)
  7. continually check pt response (CBAN stage?)
  8. dry & inspect skin after
103
Q

Methods of heating

A

conduction, convection, radiation, conversion

104
Q

heat conduction

A

direct contact w/ tissue, kinetic motion of molecules of one object passed on to another object (best when one hotter than other)
- hot pack, heating pads, paraffin

105
Q

heat convection

A

circulation of moving molecules in liquid or gaseous form
-fluidotherapy, warm whirpool

106
Q

radiation

A

conversion of heat energy to electromagnetic radiation
- infrared lamp (not in clinics)

107
Q

conversion

A

ultrasound

108
Q

Effects of thermotherapy

A
  • arteriolar vasodilation, increases blood flow
  • increase metabolism & O2 uptake by tissues
  • mild inflammation including edema formation
  • reduces mm spasms
  • reduces PNS conduction, including pain perception
  • reduces localized spasms pain relief
  • facilitate tissue healing in proliferative & remodeling phase
  • increase elasticity of tissues (alters collagen)
  • increase jt & mm flexibility
109
Q

Clinical indications for heat therapy

A
  • modality of choice beyond acute phase
  • especially used before stretching & joint mobilization
  • to increase ROM
  • scar mgmt
  • pain relief
110
Q

Guidelines for heat therapy

A
  • consider accessibility of body part & size of area to be healed
  • contraindications & hypersensitivity to heat
  • inform pt of mild-mod heat sensation (feel warm & happy) > never feel burning!
  • superficial - only 1-3 cm/1 in depth
  • deep - US, diathermy 1-5cm depth
111
Q

How long will it take for well-vascularized tissue to get optimal heating affect?

A

8-10 min

112
Q

mild heating temp

A

less than 104F, subj feeling of surface temp = hot

113
Q

Therapeutic heating temperature

A

104-113 (40-45C)
- anything above 113F causes tissue damage -> burn

114
Q

Four main considerations for physiological changes from increasing tissue temperature

A
  1. intensity of heat application
  2. time allowed for heat exposure
  3. thermal conductivity of tissue
  4. temperature difference between tissue & applied agent
115
Q

How does temp of heated tissue react when therapeutic heat reached & modality removed?

A

tissue will remain at the temperature it was heated to and then plateau, remaining warm for about 30 min

116
Q

CONTRAINDICATIONS for thermotherapy

A
  • area of acute inflammation (increases swelling & inflammatory response)
  • existing fever - check (within past 48 hrs)
  • malignancies (increases activation & spreading of CA cells)
  • over areas of compromised circulation/vascular insufficiency/disease
  • radiation rx effects (burn)
  • lack of sensation (burn)
  • areas of recent or potential hemorrhage (inc bleeding)
  • patient deemed unreliable by practitioner (language barrier, cog deficits)
  • 1st trimester of pregnancy
  • infected area (spreads infection to other areas or causes cross-contamination)
117
Q

precautions for thermotherapy

A
  • open wounds (contraindicated for paraffin!!)
  • poor sensation
  • very young or very old (can’t dissipate heat)
  • during menses (inc bloodflow, pt education)
  • during 2nd-3rd trimester pregnancy (never over abdomen or TSP-LSP)
118
Q

metabolic reaction to heat

A

50F increase in temperature = 2-3x cell activity & metabolic rate

119
Q

Why is the risk of thermal damage increase in older people (40+)?

A

Due to less blood flow in skin to dissipate heat

120
Q

Wet heat vs. dry heat

A

Dry heat can elevate surface temp to greater degree but moist heat can elevate temp to slightly deeper level

121
Q

3 factors resulting in vasodilation of heated skin

A
  1. axon reflex
  2. release of chemical mediators secondary to temp elevation
  3. local spinal reflexes
122
Q

principle of (axon) reflex vasodilation

A

When one area of body heated, increases in skin blood flow occur in distal extremities that aren’t directly heated
- safe for pts c PVD but not usual rational for heat in clinical practice

123
Q

neuromuscular effects of heat

A

elevate pain threshold - increasing firing rate of thermoreceptors in cutaneous tissue blocks input from primary nociceptors to dorsal horn of SC (gate control theory)

alter sensory nerve conduction velocity - esp in subcutaneous tissue during first 2.7-3.6F temp inc.

change mm spindle firing rates - decreased stretch on mm spindle -> decreased afferent firing from spindle -> decreased mm spasm

124
Q

How does elevating mm temps alter strength & endurance?

A
  • decreased endurance due increased O2 uptake by tissues
  • deep heating modality > isometric strength decreased first 30 min post rx & increased during next 2 hrs
  • heat before NM estim (NMES) may lower amt of current intensity needed to achieve desired lvl of mm contraction for strengthening
125
Q

What tissue depth experiences greatest dgree of temp elevation?

A

0.5 - 2 cm

126
Q

moist heat pack advantages & disadvantages

A

advantages:
- ease of prep & application
- variety of shapes & sizes available
- moist, comfortable heat
- relatively cheap to buy & replace
disadvantages:
- no method of temp control once applied to pt
- doesn’t readily conform to all body parts
- sometimes awko to secure on pt
- doesn’t retain heat for more than ~20 min
- passive intervention (pt can’t exercise @ same time)
- may leak & then must be discarded

127
Q

outcome measures for heat

A

pain - pain scales (not v reliable) (S of SOAP)
ROM- goni (O of SOAP)
function - observe movement (A of SOAP)
mm guarding & tone - palpate & mm flexibility (A of SOAP?)
- always perform measurements prior & post rx

128
Q

Paraffin wax advantages & disadvantages

A

advantages:

  • low specific heat allows for application @ higher temp than water w/o risk of burn
  • low thermal conductivity allows heating of tissues to occur more slowly, reducing risk of overheating tissues
  • molten state allows even distribution of heat to areas like fingers & toes
  • first dip traps air & moisture to create more even heat distribution
  • oils used in wax add moisture to skin
  • wax remains malleable after removal, allowing for use as exercise tool (gripping exercises)
  • paraffin provides comfortable, moist heat
  • replacing wax is relatively cheap (if bath owned)

disadvantages:

  • effective only for distal extremities in terms of ease of application
  • most effective method is bath method, limiting accessibility for other body parts to be rx effectively
  • no method of temp control once applied
  • heating only lasts ~20min
  • passive intervention (pt can’t exercise @ same time)