intro to electrotherapy Flashcards
use for: shockwave Laser TENS heat cold NMES
promote healing promote healing pain relief pain relief + healing reduce swelling + pain relief strengthening
when is it used
Soft tissue injuries/orthopaedics/Rheumatology
Acute, sub-acute & Chronic stages
To provide pain relief
But…
… does this affect the cause of the problem?
… or does it just provide short-term relief?
… is this a problem?
Neuromuscular rehabilitation Neurological deficit (e.g. drop foot) Post-operatively (e.g. ACL) Provide pain relief Influence inflammatory and healing process Increase blood flow which may promote healing and increase soft tissue extensibility Reduce swelling Re-educate & strengthen muscles
Promote return to function
cell membrane transport
Ions and molecules move across cell membrane against conc and electrical gradients
energy needed ATP
30-40% of total energy turnover
electric charge in tissues
All cells are electrically active
Membrane potential approx -70 mV
Critical to normal cell function
Level of cell membrane activity influences the general activity level of the cell
If the membrane is electrically quiet, the cell ‘down regulates’
With increased levels of activity, the general cell activity increases ‘upregulates’
electrotherapy and electric cell activity
By influencing the activity of the cell membrane, it is possible to adjust the ‘excitement’ level in the cell.
Different energy sources in electrophysical agents can affect different tissues
e.g Laser effects collagenous tissues
TENS stimulates nerves
role of electrotherapy
Apply external energy to the tissues
Energy must be absorbed by the tissue to have a physiological effect
Muscle
Nerve
Bone
Other tissues e.g?
inflammatory phase
Immediate response to injury Acute phase lasts approx 24-48 hrs Sub-acute phase lasts 10-14 days Purpose: to remove the debris and dead tissue and to destroy any invading infection before repair Vascular and Cellular changes Associated cardinal signs
vascular changes - the healing process
Bleeding initiates platelet activity and coagulation.
Very brief vasoconstriction (few seconds) where opposing walls are brought into contact resulting in adhesion formation between the 2 surfaces
Coagulation of extravascular blood is due to action of platelets and clotting mechanisms
Prothrombin Thrombin
Fibrinogen Fibrin
Early wound Matrix
Vasodilation
Release of histamine, prostaglandins from injured tissues.
Increased permeability of undamaged vessel walls to plasma proteins (albumin, fibrinogen, globulin)
Increased ‘leakiness’
Increased blood flow through the area
‘Inflammatory Exudate’
cellular changes
Neutrophils and monocytes first the reach to site of injury.
Neutrophils’ function is PHAGOCYTOSIS
Remove dead material and bacteria
Neutrophilic infiltration ends after a couple of days
Monocytes differentiate into macrophages.
Phagocytose and release collagenase and proteoglycan- degrading enzynes
outcome of inflammation
Removal and replacement of injured tissue.
Replacement of injured tissue with early scar tissue
Formation of an abscess (if infection present)
Chronic inflammation
proliferative phase
Lasts approx 3-4 weeks Formulation of granulation tissue Granulation tissue precedes mature scar tissue 2 Processes Fibroplasia Angiogenesis
fibroplasia
Fibroblasts migrate from surrounding tissue
Produce and organise the major extracellular components of granulation tissue
Provides a scaffold
Initially produce Type III collagen
Become Type I collagen when repair matures
Oxygen is critical to formation of collagen
angiogenesis
‘Formation of new circulation’
Extensive vascular system is required for proliferative phase
Appear first as buds of endothelial cells which grow into the damaged area.
Form capillary loops by joining other buds
Increased blood flow and oxygenation through the area
Pink/red hue
remodelling
Can take months
Granulation tissue becomes more fibrous and less vascular
Reduction in number of blood vessels
At 3 weeks, the wound is only approx 15% of strength of original tissue
Final strength will be 70-80% of original tissue
Replacement of Type III collagen with Type I.
Greater tensile strength and increased crosslinks- NB in Physio
factors that delay healing
GENERAL Age Protein deficiency Vitamin deficiency Steroids (inhibitory effect) Colder Temperature Medication Diabetes Compromised Immunity
LOCAL Type and size of injury Poor blood supply to the area Continued inflammation Infection Drying of wound Excessive movement too early
how can electrophysical agents help?
Different modalities have different roles
Role in all 3 phases
Inflammatory phase
Stimulate active cells during Proliferative Phase
Enhance the quality of scar tissue in Remodelling
Pain receptors
Nociceptors= peripheral nerve endings
Activated by thermal, mechanical or chemical stimuli
Release of chemicals e.g. substance P, prostaglandins
Convert the initial stimuli into electrical activity –action potentials
peripheral pathways
Nociceptors give rise to afferent nerve fibres
A -fast, myelinated
C- slow, unmyelinated fibres
Transmit from the peripheral tissue to the grey matter of the Spinal Cord
central pathways
Nociceptive afferents enter SC at dorsal horn
Synapse with second order neurones
Cross midline to ascend in spinoreticular and spinothalamic tracts
Synapse with third order neurones in thalamus
Ascend to the somatosensory cortex
pain modulation occurs at
spinal cord level and brain level
Gate control theory
Severity of pain sensation is determined by
balance of excitatory and inhibitory inputs
A and C fibres are excitatory (pain fibres)
A fibres can inhibit pain at T cells in spinal cord
Close the ‘gate’ to pain
Endogenous opiates
Production of endorphins, enkephalins, dynorphins in the brain
Descending influence on the cells in the Spinal Cord
how can electrophysical agents help pain
Close the gate in the Spinal Cord
Activate the endogenous opoid system in brain
Placebo effect
Non invasive
Non-addictive
No major side-effects
Relatively inexpensive
safety issues - ISPC
Duty of care to patient
Must suffer no adverse effects
Proper Assessment
Indications and Contra-indications for use
Checking skin sensation as appropriate
Checking machine safety before use
Ensure patient understands warnings and instructions
Appropriate preparation of the part to be treated
Application of treatment
Monitoring of treatment
Patient should have a method of contacting physio
Termination of treatment/ inspection of part
Documentation: skin sensation, dosage, time, site of application, response, signature etc
Complete Incident form in the event of an adverse event/accident
Machine should be energised before connecting to patient and patient should be disconnected before switching off
Always turn up current slowly
Never adjust leads, electrodes with current on
Good fixture of electrodes
Proper use of electrode pads and gels
Avoid interference with other machines
Watch water in vicinity of machines
Patient shouldn’t touch machine
physio competent in
Physiological effects Therapeutic effects Contra-indications Precautions Safe application
CI
Those unable to co-operate /comprehend
Over abdomen, low back, pelvis for first 35 weeks of pregnancy
In area of tumour, if active or suspected malignancy, except in palliative care
Areas of recent bleeding tissue/haemorrhage
Active TB in treatment area
(CSP 2006 Guidance on Use of Electrophysical agents)
Other specific Contra-Indications will be covered in each Modality
precautions for all agents
Over anterior aspect of neck
Significant sensory impairment/circulatory impairment
Recent radiotherapy
Acute local skin conditions e.g. eczema, dermatitis
(CSP 2006 Guidance on Use of Electrophysical agents)
Specific Precautions will be covered under each modality
electric shock
Detach person from apparatus, switch off or unplug
Avoid touching person until current switched off.
Use insulating material if possible
Check ABC
Medical attention immediately
adverse effects
CSP Audit 2000 at 83 sites in UK (18 returns)
Audit over a 6-month period
Most unexpected effects occurred with Ultrasound
Most of effects were short lived
