MSK Week 5 Flashcards
Phases of healing
- Hemostasis
- Inflammation
- Proliferation
- Remodeling
- OCCURS SEQUENTIAL AND SIMULTANEOUS
What are MSK injuries?
- Damage to MSK structures and nearby CT, blood vessels, nerves
- Response to injury occurs sequentially and simultaneously
How do MSK injuries happen?
- Direct trauma
- Compressiong
- Friction
- Repeated over-stretching
- Typically with a mechanical force
Hemostasis
- 0 to up to 6-8 hours
- Stop the bleeding
- Cellular and vascular cascade causes local vasoconstriction
What is clot formation?
Stimulation of platelets and formation of fibrin
Inflammatory phase
- 0 hours up to 2 weeks
- Peak 2-3 hours
- Clean up the wound site - prepare for construction
- Begins as soon as chemical mediators start to move
Prominent inflammatory mediators
- Histamine
- Bradykinin
- Serotonin
- Lymphokines
- Prostaglandins
- Leukotrienes
- Arachidonic acid
What is diapedesis?
Where cells squeeze through gaps in capillary wall to get where they need to go
What is chemotaxis?
Signaled by chemical agents in the area and they follow the train to get to the injury site
External factors that may affect the inflammatory phase - potentially derailing it
- NSAIDs
- Repetitive or forceful tasks
How do NSAIDs impact the inflammatory phase?
- Can delay or hamper healing in MSK tissues (muscle, tendons, cartilage and bone)
- Inflammation is a necessary step for healing and transition to proliferation
How to repetitive or forceful tasks impact the inflammatory phase?
- Cause the acute inflammatory stage to continue, followed by fibrotic and structural tissue changes
- Possibly also CNS reorganization resulting in movement disorders
Clinical signs during inflammatory phase
- Swelling, redness, heat
- Impairment or loss of function
- Pain at rest, or with active motion, or with specific stress of the tissue
- Potential for muscle guarding, self-splinting, protective posturing
- W passive movement, pain is reported before tissue resistance reacher
Protective phase of rehab
- Control pain, edema and inflammation
- Restore full RPOM, prevent atrophy, maintain soft tissue joint integrity
- Enhance function
PRICEMEN
- Protection
- Rest
- Ice
- Compression
- Elevation
- Manual therapy
- Early motion - done safely
- Medications
Proliferative phase
- 4-22 days
- Peak at 2-3 weeks
- Rebuild damaged structures and strengthen the wound
When is the peak of the Proliferative phase?
When bulk of scar material is formed - continues for several months post-injury
What are the two tissue healing processes?
- Regeneration - regrowth of original tissue
- Repair - formation of a connective tissue scar
What are the 4 simultaneous processes of proliferation?
- Epithelialization
- Collagen production
- Wound contraction
- Neovascularization
Epithelialization
- Only when the skin is involved
- Reestablishes the epidermis
Collagen production
- Limited tensile strength
- Type III —> Type I
- Excessive scarring may affect outcome
Wound contraction
If uncontrolled, contractures may result in
Neovascularization
New blood vessels (w/in 4 days)
Clinical signs during the Proliferative phase
- Decrease in pain
- Erythema resolved
- No active effusion, residual swelling may persist
- Increase in pain-free active and passive ROM
- With passive movements, pain is felt at the point of tissue resistance
What is the intervention goal of the proliferation phase?
Create a strong extensible scar
How is a strong extensible scar going to be created during intervention?
- Protection of the forming collagen
- Direct collagen orientation to be parallel to the lines of force it must withstand
- Prevent cross-linking and scar contracture
- Modify faulty joint mechanics
Intervention approaches for Proliferative phase
- Educate patients about signs/symptoms of over stress of healing tissues
- Transition from passive interventions toward progressive stress of tissue - therapeutic exercise progression
How does loading the tissues help them heal?
Mechanotransduction
What is the 3 step process of Mechanotransduction
- Mechanocoupling
- Cell to cell communication
- Effector cell response
Mechanocoupling
Mechanical trigger or catalyst
Cell to cell communication
Distribution of the message
Effector cell response
The tissue factory that produces and assembles
Remodeling Phase
- Longest phase
- Few days - 2 years
- Modify scar tissue into its mature form
Clinical signs during the remodeling phase
- Progression to pain-free function and activity
- Pain is felt at end range of passive movements after tissue resistance met
Local factors affecting healing
- Type, size, location of injury
- Infection
- Vascular supply
- External forces (thermal agents, electromagnetic, mechanical pressure)
- Movement (early, later)
Systemic factors that affect healing
- Age
- Disease or infection (diabetes, autoimmune)
- Medications (antibiotics, corticosteroids)
- Nutrition
- Hormones
- Fever
- Oxygen
Acute, subacute and chronic timelines/additional names
- Acute = 7-10 days; protective phase
- Subacute = 10 days - 6 weeks; controlled motion
- Chronic = 6 weeks - months; return to function
Structural components of muscle
- Endomysium
- Perimysium
- Epimysium
What does the basal lamina serve as?
A scaffold for healing
What are satellite cells?
Muscle stem cells for regeneration and rebuilding
What is the myotendinous junction?
Where muscle proper is merging with the tendon proper - we get junction transition tissue
What are the contractile units of muscle?
Myofibers
Factors affecting muscle performance under load
- Age
- Temperature
- Immobilization or disuse
Muscle phases of healing
- Destruction phase
- Repair phase
- Remodeling phase
Destruction phase
- Necrosis of damaged muscle tissue
- Factors released, start hemostasis and inflammatory response
- Vascular disruption - hematoma and edema begin
- Leukocytes infiltrate and activation/proliferation of satellite cells (myoblasts)
Repair phase
- Hematoma formed
- Inflammatory cells arrived and satellite cells proliferation continues
- New myofibers are formed
- Neuromuscular junction reestablished
Remodeling phase
- Regenerated tissue matures and tensile strength increases
- Scar contracts and is reorganized
- Type I returns to normal proportion over Type III
Contusion
- Blunt trauma
- Hematoma (inter or intra muscular)
- Myositis ossificans (calcified hematoma)
Risk factors of strain
- Inadequate flexibility
- Inadequate strength or endurance
- Muscle imbalances
- Insufficient warm-up or fatigue
- Inadequate rehab from past injury
What is a distractive strain?
Excess pull, overstretch
What tissues are impacted during eccentric motions that are not damaged during concentric and isometric motions?
- Damage to sarcomere
- Disrupt ECM
- Intramuscular edema
- Increased creatine kinase
Grade I strain (First Degree)
- Tear only a few musculotendinous fibers
- Pain only with limited swelling
- No loss of function
Grade II Strain (2nd Degree)
- Disruption of moderate number of fibers
- Increased pain
- Some loss of strength and function
Grade III strain (3rd Degree)
- Complete rupture of some musculotendinous units
- Loss of function with little pain
- MT junction site
When is pain most pronounced in muscle injury?
Eccentric activation
Muscle injury management
- Protective phase
- Controlled motion phase
- Return to function phase
- Re-injury prevention
Protective phase management
- PRICEMEN, patient education
- PROM, AAROM, AROM
Controlled motion phase management
- AAROM, AROM, flexibility
- Submaximal isometrics —> multiangle submaximal isometrics —> multiangle max isometrics —> PREs
- Simple/safe balance, proprioception activities
- corrective exercise of associated biomechanical deficiencies
Return to function phase management
- Endurance and maximizing strength, concentric —> eccentric training
- General return to activity - 80% strength of unaffected contralateral
- Speed, power, agility exercises
Re-injury prevention management
- Education on proper warm-up
- Holistic conditioning
- Maintenance of flexibility, strength
Complications of muscle injury management
- Immobilization/disuse - less force, less tolerance to lengthening
- Reinjury
- Fibrosis
- NSAIDs induce impairment in functional capacity and histology when administered at later points
Anatomy of Tendon
- Glistening white
- Collagen fibers in tightly packed bundles
- Elastin
- ECM: proteoglycans, GAGs
- Parallel fibers
- Avasular
- Aneural
Tissue tendon properties
- Transmit force from muscle to skeleton
- Store and release elastic energy
- High tensile strength
- Respond and adapt to loading, Mechanotransduction
- Low metabolic rate —> very slow healing after injury
Tendon mechanisms of injury
- Loading
- Overuse loads
- After activity
Loading mechanism of injury - tenodn
- Sudden overload
- Repetitive loading
- Rapid unloading
Overuse loads mechanism of injury - tendon
- Tension + Compression
- Shearing and friction
- Fascicle on fascicle
- Paratenon, retinacula, bone
After activity mechanism of injury - tendon
- Catabolism (24-36 hrs; break down)
- Anabolism (24-80 hours; build up)
- Adequate rest between exercise bouts
Intrinsic factors for tendon injury risk factors
- High body weight
- Malalignments, imbalances, weakness, poor flexibility, poor form
- Age
- Gender
Extrinsic factors for tendon injury risk factors
- Excess volume, speed, magnitude of loading
- Abrupt change to amount or type of load
- Poor environmental conditions (like temperature)
- Poor equipment
- Medications
- Prolonged immobilization
Tendinopathy
- Blanket term for tendon conditions arising from overuse
- Absence of PG-mediated inflammation
- Persistent, recalcitrant
- Poor healing potential
Specifics of tendinopathy - Blanket term for tendon conditions arising from overuse
- Cumulative trauma
- Weaken collagen cross-links
- Degrade ECM and vascular elements
- Does not follow the traditional phases of healing
- Except vascular, proximal 1/3
Chronic tendon injury stages
- Stage I tendinitis
- Stage II tendinosis
- Stage III complete rupture
- Stage IV tendinosis with other changes such as fibrosis or calcification
Tendinitis
- Pain, swelling, dysfunction of tendon
- Broad term
Tendinosis
- Degeneration of tendon structures
- Not well correlated with clinical symptoms
- Pain not always present
- Lower resistance to strain
4 main histological changes of tendinosis
- Angiofibroblastic hyperplasia
- Disorganized and immature collagen
- Hypercellularity and increased ground substance
- Vascular hyperplasia and neo vascularization
- Increase of neurochemicals
What is angiofibroblastic hyperplasia?
- New growth of blood vessels, fibroblast infiltration
What is neurogenic inflammation?
Inflammation response caused by release of neural chemicals
Clinical signs of tendon injury
- Well localized with little referral beyond the tendon
- Strong but painful (unless full rupture) in proportion to resistive load
- Painful with stretch or palpation
- Pain resolves quickly when load withdrawn
- Unusual to be painful w/o load, at night or at rest
What do opioid analgesics do?
- Relieve moderate to severe pain
- Act on CNS receptors in spinal cord and brain
What pain receptor signals do opioid analgesics reduce?
- Mu
- Kappa
- Delta
- Sigma
How do NSAIDs decrease inflammation?
- Block PG/thromboxane/leukotriene synthesis —> inhibit cycle-oxygenate (COX) and PG synthase enzymes
- Block vasodilation and inflammatory response
How are NSAIDs anti-pyretic (fever reducer)
- Block PGs that would elevate hypothalamic temperature control
How do NSAIDs act as anti-thrombotic medication (anti-coagulant/blood thinner)?
Block COX —> thromboxanes that stimulate platelet aggregation
How do NSAIDs relieve pain (mild-moderately)?
- Don’t bind to opioid receptors
- Block prostaglandins (PGs)
COX-1 (+)
- Helpful
- Normal constituent of cells in hemostasis
- GI mucoprotection
- Regulate normal platelet activity
- Renal and vascular homeostasis
- Uterine function, embryo implantation
- Regulation of sleep-wake cycle and body temp
COX - 2 (-)
- Produced by injured cells
- Produces prostaglandins that mediate pain, inflammation, pyresis
- Vasodilation and inhibition of platelet aggregation
- Modulation of platelet aggregation
Non-selective NSAIDs
- COX-1 and COX-2 inhibitors
Selective NSAIDs
Cox-2 inhibitors
High potency opioid
Low does required for desired response
Low potency opioid
High dose required for desired response - higher the dose, the more side effects
What determines the dosage of over the counter NSAIDs?
Half-life
Corticosteroids
Natural hormones produced by adrenal glands under control of hypothalamus - maintain fluid and electrolyte balance
Cushing’s syndrome complications of excess use
- Integ - delayed healing, velvet skin of the neck
- Hypokalemia - K+ deficiency —> muscle weakness
- MSK - myopathy and osteoporosis
- Endocrine - hyperglycemia - high glucose levels, increased risk of infection neurological —> vertigo, headache, convulsions
- Sensory - ophthalmic - glaucoma risk
- Growth suppression
What are DMARDs?
Disease specific modifying drugs - they inhibit immune system
How do local aesthetics work?
By blocking peripheral nerve transporting the pain signal
Neuropathic pain agents
- Developed for treatment of seizure and depression
- Increasingly used in management of chronic pain in place of opioids
Muscle relaxers
- Antispasmodic agents
- Reduce muscle guarding and spasm due to MSK injury
How can anticoagulants impact PT care?
Increased risk of bleeding/bruising; caution with manual therapy
How would Hyperlipidemia meds impact PT care?
- Myalgias
- Myositis
- Weakness
- Paresthesias
- Mimic MSK conditions
How would cardiac medications impact PT care?
- Suppression of normal HR, BP response to exercise
- Require HR and BP throughout treatment
How can anti-diabetic medications impact PT care?
- Lower blood glucose levels
- Synthetic insulin - supplement deficiency
- Monitor blood glucose levels
Symptoms of hypoglycemia
- Sweating
- Shaky
- Irritability
- Confusion
- Rapid heart rate
- Maybe hunger
What do you do if a patient becomes hypoglycemic?
Provide glucose
How do antidepressants impact PT care?
- Time lag to effects
- Increased depression during initial treatment
- Mood changes
How do antianxiety medications impact PT care?
Treat symptoms, not cause —> sedation
