Intro to Physical Agents Flashcards
What are Physical Agents?
Energy and material applied to patients to assist in rehabilitation
Include: Heat Cold Water Pressure Sound Electromagnetic radiation Electrical currents
Categories of Physical Agents
Thermal
Mechanical
Electromagnetic
Thermal
Transfer energy to a patient to increase or decrease tissue temperature
Can be superficial or deep
Examples:
Hot packs, Cold packs, US, Whirlpool or Diathermy
Mechanical
Applies force to either increase or decrease pressure on the body
Examples:
Water, Traction, Compression and Sound
Electromagnetic
Applies energy via electromagnetic radiation or an electrical current
Examples:
UV radiation, infrared, laser, diathermy, and electrical stimulation
History: Why change in use?
Ineffective
-IR lamps for wounds – dried out
Inefficient
-Sunlight for Tuberculosis
Cumbersome
-Diathermy
Excessive risks
-Diathermy
Level at which physical agents have a direct effect…
Impaired body function and structure
Ex) Muscle paresis, hypotonicity, pain, sensory deficits, atrophy, soft tissue tightness
Can modalities be used alone?
NO! it’s not PT
Evaluation and Planning for the Use of Physical Agents
- Physician referral as needed
- Medical Diagnosis
- Precautions/Contraindications
- Examination
Documentation of PA used
Physical agents used
Area of body treated
Patient position during treatment
Intervention duration
Parameters
Outcomes including progress towards goals
Regressions or complications
Precaution
Conditions under which a particular form of treatment should be applied with special care or limitations
Relative
Contraindication
Conditions under which a particular treatment should NOT be applied
Absolute
General Contraindications/Precautions
Pregnancy
Malignancy
Pacemaker or other implanted device
Impaired Sensation or Mentation (lack of communication)
Selection of Physical Agents
Goals and Effects of Treatment
Contraindications and Precautions
Evidence for Physical Agent Use
Cost, Convenience, and Availability
Quality Research
Patient / Population
- Question should apply to a specific population
- More specific = less evidence
Intervention
-Specific
Comparison
-Control
Outcome
-Defined as precisely as possible
Effects of Physical Agents
Modification of tissue
inflammation and healing
Relief of pain
Modification of muscle tone
Alteration of collagen extensibility and motion restriction
3 phases of tissue healing
1) Inflammation (Days 1-6)
2) Proliferation (Days 3-20)
3) Maturation (Days 9+)
Cardinal Signs of Inflammation
Heat = increased vascularity Redness = increased vascularity Swelling = lymphatic drainage blockage Pain = pressure or irritation of pain sensitive areas Loss of function = pain and swelling
Inflammation Phase
1) Vasoconstriction
2) Vasodilation
3) Clot Formation
4) Phagocytosis
Proliferation Phase
1) Epithelialization
2) Collegen production
3) Wound contracture
4) Neovascularization
Maturation Phase
1) Collegen Synthesis/Lysis balance
2) Collegen Fiber organization
Vascular Response
1) Vasoconstriction followed by vasodilation at the capillaries, postcapillary venules and lymphatics
- Vasodilation mediated by chemical mediators
2) Leukocyte Extravasation
- Movement out of the circulatory system and towards the site of tissue damage or infection
3) Accumulation of fluid in the interstitial tissue (outside the vessels) resulting in edema
Hemostatic response
Controls blood loss when vessels are damaged or ruptured.
Retracts and sealing off of blood vessels
Platelets form clots and assist in building of fibrin lattice, which serves as wound’s source of tensile strength
Cellular Response
Phagocytosis
-Neutrophils rid the injury site of bacteria and debris
(24 hrs then disintegrate)
Monocytes
- Predominate for 24-48 hrs
- Convert to macrophages when they migrate from capillaries into the tissue spaces
Macrophages
- Most important cell in inflammation!
- Produce while range of chemicals
- Facilitate the removal of necrotic tissue and bacteria
- Promote cell proliferation
- Influence the number of fibroblastic repair cells - Most effective when oxygen is present.
Resident macrophages
Proliferation Purpose
cover the wound and regain some of it’s initial strength.
Clinical signs:
- Granulation tissue is generated which is characterized by red, beefy, shiny tissue with a granular appearance
- Wound begins to fill
Proliferation at the cellular level
Cell activity consists of macrophages-stimulated collagen synthesis, capillary formation, wound contraction and wound epithelialization
Epithelialization
The reestablishment of the epidermis
Early with superficial wound
Later with deeper injury
-After collagen production and neovascularization
Components Involved in Tissue Healing
Fibronectin
Prteogylcans
Elastin
Collagen
Collagen Production
Fibroblasts make collagen
Fibroblasts migrate to the injured area and fibroplasia (fibroblast growth) occurs
Fibroblast initially produce type III collagen
- Thin, weak, and no consistent organization.
- By day 12, immature type III starts to be replaced by type I which is more mature and strong.
Fibronectin
Tensile strength
“Glue” substances together
Proteoglycans
Secreted by fibroblasts early in tissue repair
Bind to fibronectin and collagen and help stabilize tissue
Retain water to assist in hydration
Elastin
Protein that is cross-linked to provide elasticity
Collagen
Most important protein, provides structural support and tensile strength
3 chains of amino acids coiled around each other in a triple helix
27 types identified
Wound Contraction
Pulls the edges of the injured site together and in effect shrinks the defect
Begins at day 5 and peaks at 2 weeks
Myofibroblasts are primary cells responsible
Speed of contraction
Linear > Square/rectangular > circular
Neovascularization
Development of new blood supply or the growth of new vessels = angiogenesis
Healing cannot occur without it
Supplies oxygen and nutrients to injured/healing tissue
Forms capillary loops
Gives scar it’s pinkish to bright red hue
These loops cease as the wound heals leading to more mature scars
Whitish appearance.
Maturation
Stop here for Quiz#1
Day 9 up to 2 years
Clinical Signs:
Shrinking and thinning of scar and loss of redness
Maturation at the Cellular level
The collagen fibers remodel, mature, and gain tensile strength
Outcomes of Acute Inflammation
Complete resolution and replacement of injured tissue with like tissue
(Most beneficial)
Healing by scar formation
(Most common)
Formation of abscess
Progression to chronic inflammation
Chronic Inflammation
Months to years
Occurs in 1 of 2 ways:
1) Cumulative trauma
- Interference of healing process
2) Immune response to altered host tissue / foreign material or the result of an autoimmune disease (RA)
Normal Acute Inflammatory Process
no more than 2 weeks
Sub acute Inflammation
if more than 4 weeks
Local Factors that Effect Healing
Size, type and location of injury
- Small vs. Large
- Surgical incision vs. blunt trauma
- Scalp vs areas of ischemia – excessive pressure
Infection
-Affect collagen metabolism reducing production increasing lysis.
Vascular supply
- Muscle vs. Tendon
- Meniscus
External forces
-Physical Agents
Movement
-Immobilization vs CPM
Systemic Factor that Effect Healing
Age
-Pediatrics vs Geriatrics
Disease
-Diabetes
-Problems with circulatory system
(Atherosclerosis, sickle cell disease, hypertension)
Medications
-Corticosteriods – at time of injury can decreasing inflammatory response at this stage delays subsequent phases of healing and increases the incidence of infection
(Prednisone, dexamethasone)
-NSAIDs are less likely to impair healing
(Ibuprophen)
Nutrition
-Deficiency in AAs, vitamins, minerals, water
(Protein-calorie malnutrition more than depletion of a single nutrient)
Specific Tissue Healing: Cartilage
Limited ability to heal because it lacks lymphatics, blood vessels and nerves
Cartilage itself does not form clots healing fails
Different if subchondral bone is involved
Specific Tissue Healing: Tendon and Ligaments
Inflammation occurs in the first 72 hours
Collagen synthesis occurs in the first week
Intrinsic and extrinsic cells participate in repair
Orientation of cells/collagen are perpendicular to tendon early
- Changes to parallel around day 10 and last up to 2 months
- Ultimate maturation depends on sufficient physiological loading
Specific Tissue Healing: Skeletal Muscles
cannot proliferate once injured
However stem or reserve cells can form new skeletal muscle cells
-Satellite cells
After severe contusion, a calcified hematoma may develop
-Myositis ossificans
Specific Tissue Healing: Bone
Heals with “like-tissue”.
Stages of fracture healing
-Impaction, induction, inflammation, soft callus, hard callus, remodeling
Types of Pain
Acute
Chronic
Referred
Trigger Points
Acute Pain
-Is experienced when tissue damage is impending and after injury has occurred
(Calor, rubor, tumor)
-Underlying pathology can be identified
Chronic Pain
-Persists beyond normal time for tissue healing
(3-6 months)
- Result of activation of dysfunctional neurological or psychological responses
- Continue to experience pain even when no damaging or threatening stimulus is present
Pain Reception and Transmission: Nociceptors
- Free peripheral nerve endings
- “String-of-beads” appearance
- Present in almost all types of tissues
- Activated by intense thermal, mechanical (brick / broken bone), or chemical (acid/bleach / histamine) stimuli
- Convert stimulus to electrical impulses (action potentials) through transduction along afferent nerves towards the spinal cord.
- Peripheral sensitization
Peripheral Sensitization
Release chemicals to increase the response to noxious stimuli
Resulting in activities and stimuli are perceived as painful even though they are not damaging
Nociceptors are the terminals of what two types of primary afferent neurons?
C-fibers
A-delta fibers
Mechanical trauma activates both!
C-Fibers
Small, Unmyelinated, Slow (1-4 m/s)
“Dull, throbbing, aching, burning”
Slow onset after initial noxious stimulus
Long lasting, diffusely localized – emotionally difficult
A-delta Fibers
Small-diameter but myelinated, Fast (30 m/s)
Sensitive to high-intensity mechanical stimulation but also respond to heat/cold.
“Sharp, stabbing, prickling”.
Quick onset, last a short time, localized – not emotional
Spinal Cord Pathway
C and A-delta nerves –> interneurons (T-cells) –> neurons in the superficial dorsal horn of the grey matter of the spinal cord
T-cells (Transmission cells)
- Integrate info from nociceptive and non-nociceptive (A-beta) primary afferent fibers, other T-cells, and supraspinal sites (brain stem and cortex)
- This balance from excitatory (nociceptors) and inhibitory (sensory nerves) and descending fibers from the brain influence whether or not the person feels pain and how severe it is
- Can cause muscles spasms through efferent anterior horn cells…Result in pain-spasm-pain cycle
Pain-transmitting neurons
Cross midline and ascend to thalamus via lateral or anterospinalthalmic tracts
Referred Pain
At a location distant from its source
From one joint to another
Peripheral nerve to a distal area of innervation
Internal organ to an area of musculoskeletal tissue
Gate Control Theory
Melzack and Wall in 1965
Severity of pain sensation is determined by the balance of excitatory and inhibitory inputs (A-beta) to the T-cells in the spinal cord
PA and interventions for pain relief
- Inhibit activation of pain transmission cells
- Pre-synaptic inhibition of T-cells
- Closing the gate to the transmission of pain
The Endogenous Opioid System / Theory
Control pain by binding specific opiate receptors in the nervous system
Paradoxical pain-relieving effects of painful stimulation and acupuncture
Noxious TENS (Acupuncture like)
Measuring Pain
Visual Analogue Scale (VAS)
Numeric Scale (NPRS)
(Best for quick estimating pain)
Verbal Pain Intensity Scale
Thermometer Scale
Wong-Baker FACES Rating Scale (poor communication population)
McGill Pain Questionnaire (MPQ) [takes a long time!]
Documenting Pain
Pain location Quality Severity Timing Better/worse Setting How pain affects function, activities and participation
Pain Management Approaches
Pharmacological
Physical Agents
Physical Agents for pain management
Stimulate large diameter afferent fibers
- TENS
- Massage
- Analgesic balms
Decrease pain fiber transmission velocity
- Cold
- Ultrasound
Stimulate small diameter afferent fibers
- Acupressure
- Deep massage
- TENS
Stimulate a release of endorphins
-`TENS
Other useful Pain Strategies
Cognitive process and encouragement
- Motivation
- Tension diversion
- Focusing
- Relaxation techniques
- Positive thinking
Minimize tissue damage by application of proper first aid and immobilization
Maintain line of communication with the patient and let them know what to expect
All pain, even psychosomatic, is very real to the patient
Encourage supervised exercise
