Assessment and Management Flashcards
(21 cards)
Symptoms of sprains
- MOI that fits overstretching of particular structure
- Any age group, but often in early adulthood
- Focal joint pain
- +/- h/o clicking, popping, giving way, locking
- Swelling developing > 24 hours for extra-articular ligs <24hrs for intra-articular ligs or intra-articular damage
- TOP of lig
- Positive on appropriate stress test(laxity +/-pain)
- In Grade III injuries will have laxity at neutral
Tendons Management
Tendons - Modify load, strengthen (loading), progress to plyometrics if applicable, RTP
General Management
Load Management for most conditions, esp overuse injuries (POLICE)
Increase muscle strength/co-ordination
Restore ROM (soft tissue or Joint)
Progressive rehab
Graded exposure for central and peripheral sensitization (pain)
Treat the person not the tissue
Continue Maintenance regime (overuse conditions)
Joint/OA management
Joint/OA – Modify load, ROM (improve shock absorption prior to strength), Strengthen, Progress function back to normal
Passive Physiological movements to encourage arthrokinematics of joint
Ligament management
Ligaments- Modify load (POLICE), ROM (sprains involve joint injuries), balance (LL and shoulder dislocations), strength (around joint), Neuromuscular control (MOI: start in neutral, progress to activities requiring more control than MOI)
Unlikely to be isolated - Consider Rx of other structures
Rehab +/- reconstruction
Functional bracing - early stages to aid recovery
Restoration of function - ROM, strengthening exercises (isometric -> isotonic), progression into high-speed exercises (proprioception)
Joint mobs/MWM for pain modulation
Fractures and Joint replacement management
Fractures and joint replacements – ROM, strengthen (close chain), rehab function
Joint mobs to encourage arthrokinematics + pain modulation
What other thing to include in management
Always remember the person
Soft tissue Assessment includes:
Length
Strength
Isometric - pain provocation
Palp for tenderness (Inc TrP searching)
If tendon:
Plyometrics (SSC) - energy recoil capacity
If ligaments, sports specific or functional goal involved: Endurance Power - often relevant to tendons Proprioception and balance Motor control/patterning
Overuse injuries, stress #, tendinopathies all occur by:
An active degenerative process involving inflammatory pathways.
Correct amount of activity/load will trigger tissue adaptation which in turns will make tissue stronger increasing level of stress tissue can withstand.
Too much activity will lead to loss of homoeostasis and tissue changes with pain occurring when the tissue has to rapidly adapt. Rested tissue (too little activity) causes tissue to become unloaded causing tissue to become structurally weaker and if then normal or excessive load is suddenly applied tissue failure occurs through an active inflammatory process and degrades. If tissue degradation is allowed to continue for an excessive length of time with excessive loading this leads to significant alteration to tissue structure
Ligament Assessment
PROM
ACC movements (special tests)
Proprioception
Muscles tests (to check if muscles are injured)
How does strengthening exercises help tendinopathy
Strengthening muscles causes neuromuscular adaption to increase neuromuscular capacity in turn increasing shock absorption capability of muscles which reduces load through tendon
Muscle strain management
Activity modification (POLICE), Stretching/lengthening to maintain length and prevent contracture, strengthening, neuromuscular control (MOI), RTS if applicable
How is tissue capacity/tolerance improved
Mechanotherapy:
Load tissue, stimulate cellular activity for tissue adaptation which overtime improves tissue resilience or robustness so tissue can maintain homeostasis
How does length of MTU occur
Creep - uncrimping of collagen by providing sustained low load to tissue. Effect is transient thus stretching needs to be done regularly
Hysteresis - heat produced from energy loss of lengthened tissue returning back to normal length. Reduces tissue stiffness
How does ROM improve
Improved glide, roll and slide (arthrokinematic motion) and increased synovial fluid production
How does pain relief occur
Neuromodulation - altering neural input that modulated pain perception at a central or peripheral level, reducing pain for person
Descending pain modulatory pathway
Pain gate theory
General health conditions affecting assessment:
- Age (not a health condition but gives a big clue!)
- Diabetes – peripheral neuropathies. High risk of capsulitis in shoulder. Poor healing. Tendinopathies. Type 1 vs type 2
- Inflammatory arthropathies – joint pain and tendinopathies
- Smokers – poor healing / circulation. Tendinopathies
- HTN, High cholesterol, obesity, general deconditioning
- Steroid use - tendinopathies
- HIV, IVDU, recent surgery – infection risk
- Anxiety / stress / psychosocial factors - chronicity
- History of Ca – risk of secondary metastases
Peripheral nerve entrapment conditions:
- Thoracic outlet syndrome
- Radial tunnel
- Pronator syndrome
- Cubital tunnel
- Carpal tunnel
- Guyons canal
- Piriformis syndrome
- Fibular head
- Tarsal tunnel
Routine Assessment
Observation •AROM •PROM •MMT •Palpation – tissue tenderness •Accessory movements •“Special” tests •Functional tests - relate to AGGs
Explain Pain Gate Theory
Low threshold, large diameter, myelinated Aβ fibres (mechanoreceptors) are stimulated by innocuous stimuli (touch)
Mechanoreceptors enter into spinal cord stimulate inhibitory interneuron within spinal cord, stopping transmission of nociceptive fibres A delta and C fibres.
There are multiple gates in the dorsal horn of the spinal cord. Closing one gate reduces some pain transmission. Relatively impossible to close all the gates
Explain descending pain modulatory pathway
Manual techniques, i.e. joint mobilisations, SSTMS, nerve flossing that elicit some pain (noxious stimuli) is thought to activate the descending pain modulatory pathway. Peri-aquaductal grey matter (PAG) receives input from the frontal lobe, amygdala and the hypothalamus. Neurones either project to the dorsal horn, having a descending control of nociception and/or neurones project upwards to the medial thalamus and orbital frontal cortex, having an ascending control of nociception. The PAG has two distinct regions, the dPAG and vPAG. Stimulation of the dPAG (noradrenergic system) causes the release of the neurotransmitter nor-adrenaline at the spinal cord level causing inhibition of substance P in response to noxious mechanical stimuli. Stimulation of the vPAG (serotonergic system) causes the release of neurotransmitter serotonin at the dorsal horn inhibiting the release of somatostatin, produced by noxious thermal stimuli.
It is suggested that nerve mobilisations almost immediately stimulate the dPAG to cause hypoalgesia and a few minutes later vPAG is stimulated
