Modalities Final Exam

inflammation phase timeline

1-6 days post injury

proliferative/fibroblastic phase timeline

3-20 days

maturation/remodeling phase timeline

9 days on

inflammation phase

immediate protective response that attempts to destroy, dilute or isolate the cells or agents that may be faulty

inflammation phase causes

soft tissue trauma

fractures

foreign bodies

autoimmune diseases

microbial agents

chemical agents

thermal agents

irradiation

4 cardinal signs of inflammation

1. calor

2. rubor

3. tumor

4. dolor

calor

heat

rubor

redness

tumor

swelling

dolor

pain

inflammatory phase purposes

1. form a fibrin lattice that limits blood loss and provides some initial strength to wound

2. remove damaged tissue

3. recruit endothelial cells and fibroblasts

clot formation

form a fibrin lattice that limits blood loss and provides some initial strength to wound

hyperemia

increase blood flow to area (vasodiliation)

responsible for increased temp and redness

histamines initial reaction

cause vasodilation

increase vascular permeability

responsible for edema

chemotaxis

migration of other cells to the area through the process chemical attraction/recruitment

histamines release chemical to attract leukocytes

phagocytosis

cells involved in the removal damaged tissue

neutrophils

first on the scene

early phases of inflammation clear the injured site of debris and microorganisms

leukocytes

later to the scene (attracted thru chemotaxis)

clear the injured site of debris and microorganisms to set stage for tissue repair

macrophages

specific leukocytes (monocytes) convert macrophages as they exit from the capillaries into the tissue spaces

involved in a wide range of activities including phagocytosis and synthesis of ECM

general goals during inflammatory phase

decrease swelling

decrease pain

improve PROM and AROM

inflammatory phase modalities

cryotherapy and compression

PRICE

proliferative phase

purpose to cover wound and impart strength to the injury site

what is a marker that suggests shift between phases?

the shift from acute neutrophil cells infiltration and the replacement by longer term macrophages correlates to the transition between inflammation to proliferation

proliferative phase four processes

1. epithelization- provides protective barrier to prevent loss of fluid and risk of infection

2.collagen production

3. wound contraction

4. neovascularization- development of blood supply to the injured area

general goals during proliferative phase

improve ROM, function

decrease P!

increase circulation mildly to the area

decrease swelling

protect wound- assist with closure

promote appropriate alignment of collagen fibers- during wound contraction avoid contractures

maturation phase

ultimate goal of this phase of healing is restoration of the prior function of the injured tissue

longest phase of healing process which can last over a year

characterized by the changes in size, form, and strength of the scar tissue

maturation phase PT goals

return the patient/client to activity

general goals for maturation phase

return to activity

increase ROM

increase strength

decrease P!

increase circulation

normal acute inflammatory process

lasts no longer than 2 weeks

subacute inflammation

4+ weeks (normal)

chronic inflammation

last months or years (can be abnormal or age or comorbidity related)

continues as part of the maturation phase (simultaneous collagen tissue destruction and healing)

leads to increased scar tissue and adhesion formation

chronic inflammation methods

1. cumulative trauma or interference w/ normal healing

2. immune response to foreign material or result of an autoimmune disease

local factors affecting healing process

type, size, location of injury

infection

vascular supply

external factors affecting healing process

movement

application of physical agents

systemic factors affecting healing proccess

age

disease

medications

nutrition

other factors affecting healing process

mental/emotional stress

tendons and ligaments inflammatory process

PRICE

tendons and ligaments proliferation/remodeling

immobilization versus early controlled forces for tendons

collagen fibrils->random alignment-> organized

tendons and ligaments maturation process

physiological loading important (promotes realignment)

recover full, normal ROM after injury or surgical repair

normal strength human tissue (40-50 wks post-op)

cartilage physiology

aneural, avascular = limited ability to heal

adolescent cartilage

has some ability to heal

adult cartilage

limited ability to heal

healing occurs by development of fibrous scar tissue or not at all

cartilage with bone injury can form a granulation tissues that acts like articular cartilage

physiology of skeletal muscle

regenerates well

restoration and function depend upon type of injury

skeletal muscle contusion, strains

follow general stages of healing

skeletal muscle severe infections

muscle fibers destroyed

skeletal muscle transection of muscle

muscle fibers may regenerate

growth from undamaged fibers or development of new fibers

bone fractures regeneration and remodeling 4 phases

1) inflammatory

2) and 3) reparative/proliferation

2) soft callus formation

3) hard callus formation

4) bone remodeling

bone fracture soft callus

begins when pain and swelling subside

increase in vascularity

hematoma becomes organized with fibrous tissue cartilage and bone formation

bone fracture hard callus

begins when bony fragments are united by fibrous tissue

pain defined

most common symptom prompting pts to seek medical attention

an experience based on a complex interaction of physical and psychological processes

an unpleasant sensory and emotional experience associated with actual or potential tissue damage

warning to protect body from damage

essential function for survival

pain as a vital sign

in many hospitals, considered 5th vital sign

gives info on pts well being and can indicate underlying disease

many clinics have created comprehensive pain management teams to address pts pain

goals for clinicians in addressing pain

eliminate source of pain

teach pt to fxn within pain limitations

improve pain control thru physical and psychological methods

relieve drug dependency

treat overall well-being

improve family and community support systems

passive medicine

opioid crisis- doctors are now prescribing less

passive modalities

sometimes considered a waste of time to provide short-term pain relief

some clinicians do not use modalities and only restore fxn thru active therapy

types of pain

acute

chronic

referred

subjective pain

most reliable indicator is self-report of pain

objective pain

pain scales: quantitative rating of intensity of pain

objective pain measures

verbal rating scales

numeric rating scales (0-10)

visual analogue scales

picture of face scales

measuring pain

when selecting a measure consider symptom duration, pts cognitive abilities, and time needed

also, consideration for complexity of measure to be sensitive to change

pain assessment

describe your pain

how much

where is it

nonverbal pain indicators

signs, gasps, moans, groans, cries

facial grimaces/winces

bracing or guarding against movement

restlessness

rubbing the area

vital sign response (inc HR, RR, and/or BP)

anterolateral spinothalamic pathway

primary sensation for nondiscriminative/crude touch, pain, temp

receives signals from: mechanoreceptors, nociceptors, thermoreceptors

C fibers (peripheral nerve): small, unmyelinated

nociception

neural process of encoding a noxious stimuli

pain is not nociception

the transmission of nociception can be facilitated or inhibited along the way before it reaches the brain

modalities can inhibit this transmission

pain definition

output of the brain triggered by the action potential of a nociceptor and converted to conscious understanding of that stimulus

the perception of nociception by the cerebrum

3 dimension of the experience of pain

sensory-discriminative

motivational-affective

cognitive-evaluative

sensory-discriminative

where the pain is felt and the sensation type

motivational- affective

how the patient feels about the pain

cognitive- evaluative

what the patient thinks about the pain and what they expect

nociceptors

type of sensory receptor that responds to noxious stimuli and result in the perception of pain

where are sensory receptors located

at the distal ends of an afferent nerve

what are sensory receptors specific for

type of stimulus for which they are designed to "sense"

free nerve endings

type of nociceptor/mechanoreceptor that "sense" pain

nociceptors are triggered by

intense thermal, mechanical, or chemical stimuli

exogenous source: brick, acid or bleach, fire

endogenous source: fractured bone, inflammatory response

nociceptors are nerve endings for

afferent neurons (c fibers and A-delta fibers)

what percent of afferent neurons transmit pain

80% C fiber

20% A-delta

C-fibers

small and unmyelinated

respond to noxious levels of mechanical, thermal, and chemical stimulus

pain described: dull, throbbing, aching, burning

slow onset, long lasting symptoms and diffusely localized

may be emotionally difficult to tolerate

blocked by opioid medication at receptors

A-Delta fibers

larger, myelinated

most sensitive to high intensity mechanical stimulus

pain described: sharp, stabbing, pricking

quick onset, short duration

localized to where stimulus arose

not associated with emotional involvement

not blocked by opioids

pain matrix

group of structures in the CNS that collaborate to respons to nociceptive stimulus

pain matrix mulifaceted preprogrammed response

1. conscious perception of the pain

2. motor responses (physical reaction)

3. homeostatic system response (ANS, endocrine and immune systems)

two theories of pain modulation

gate control theory

endogenous opioid systems

gate control theory

stimulating non-nociceptive fibers simultaneously

A-beta fibers overtrump slower signals from C-fibers (slow, dull pain)

"closes the gate" to the pain signal

how do modalities use gate control theory?

thermoreceptors send signal on A-beta fibers to brain

electrical stimulation causes electrical impulse to be felt instead

examples of gate control you have unknowingly performed

rubbing a contusion, strain, sprain

applying moist heat

massaging sore muscles

endogenous

"having an internal cause or origin"

bodies internal, natural way of masking pain

opioids

endorphins are released in body, bind to specific opioid receptor sites in the CNS and PNS to decrease pain perception

PNS: opioids and opiopeptins have inhibitory actions causing presynaptic inhibition of nociceptive signal

CNS: endorphins relieve pain naturally as they attach to reward centers in the brain

endogenous opioid systems theory

act as neuromodulators and have inhibitory action on normal pain pathways

the release of endorphins is thought to play an important role in controlling pain during times of emotional stress

peripherally: act on C Fibers but not A-Delta

Endogenous opioid systems modalities

explains the paradoxical pain-relieving effects of painful stimulation like acupuncture and TENS (e-stim)

these feelings of different pain trigger the release of opiopeptins which provide systemic pain relief

pain management goals

control inflammation

altering nociceptor sensitivity

increase binding to opioid receptors

modifying nerve conduction

modulating pain transmission at the spinal cord level

altering higher-level aspects of pain perception

management of psychological and social aspects

pharmacological agents and pain management

primary method for alleviation of pain

patient education and pain management

most important nonpharmacological acute pain management technique

modalities and pain management

nonpharmacological management using

pharmacological agents drawbacks

adverse side effects

may not be sufficient

risk of dependence

may need multi-disciplinary treatment (psychological, physical agents)

patient adherence (personal, cultural)

systemic analgesics

primary method of pain management

NSAIDs

acetaminophen

opiates

antidepressants/sedative

spinal analgesia

epidural or subarachnoid space of spinal cord

opioids, local anesthetics, corticosteroids

bypass blood brain barrier

reduces systemic side effects

local injection

into structures or painful/inflamed areas

short-term pain relief are used primarily for procedures or diagnostically

pharmacological agents control pain by

modifying inflammatory mediators at the periphery

altering pain transmission from the periphery to the cortex

altering the central perception of pain

opioid examples

morphine, codeine, fentanyl, methadone, hydromorphone, oxycodone, hydrocodone, herion, meperidine

non-opioid examples

acetaminophen, NSAIDs

pt education should include

info about neurophysiology of pain

reassurance that pain with movement is not necessarily a sign of further tissue damage

reassurance that pain is normal after trauma or surgery

complete elimination of pain is usually not achievable in short term

pain is multifactoral in nature

pain almost always resolves with time

time spent applying modalities is a good opportunity to educate the patient

psychosocial aspects of pain

specific heat

the amount of energy required to raise a temp of a unit of mass of material by 1 degree celsius