Soft Tissue Injuries - muscles/tendons, ligaments and hyaline cartilage, meniscus, and tendinopathy

muscle and tendon injuries/strains MOI

eccentric muscle activation (common), excessive passive elongation/stretch or max concentric action

risk factors for muscle/tendon injuries

age, previous injury, lack of flexibility and strength can be associated

grade 1 muscle and tendon injury

minor injury, defined as 10% of fibers injured

grade 1 muscle injury presents with

minimal pain with resisted motion, passive stretch and palpation, mild localized swelling, minimal weakness, no observable or palpable muscle deformation, negative imaging

grade 2 mucle/tendon injury

10-99% of fibers injured, wide spectrum of severity and extent of findings

grade 2 muscle/tendon injury presents with

pain with resisted motion, passive stretching and palpation, mild/substantial weakness (from pain), possible ecchymosis and palpable defect, positive imaging findings

grade 3 muscle/tendon injury

100% of fibers injured (sometimes defined as 80-100%)

grade 3 muscle/tendon injury presents with

minimal pain with resisted motion due to lack of attachment, could be very painful if fibers are still intact or from inflammation, substantial weakness via the muscle itself (other muscles compensate), increased ROM via loose endfeel, swelling and tenderness, possible eccymosis/palpable defect, visible appearance of muscle belly, positive findings with imaging

grade 1 will become asymptomatic in

a few days - not healed as injured fibers still need the 6 week healing process, but protected and guarded

grade 2 will represent a

wide continuum for healing/recovery time

grades 1 and 2 interventions (same progression, differing timelines)

POLICE

optimal loading for grade 1 and 2 injuries

progressive ROM to address the lengthening component of muscle function within pain free range, no stretching in acute phase, do isometrics in shortened length to address the broadening component of muscle function and progress as tolerated

functions of muscles that need to be addressed in intervention of injury

elongation with painfree ROM and broadening with painfree isometrics in a shortened range

muscle injuries will likely "heal" as

intramuscular tendinous/fibrotic tissue, takes up to 6 weeks (3 for repair and healing, 3 for remodeling), questionable if it will ever return to muscle tissue again - just scar tissue

tendons, first and second degree tears can be distinct from muscle when

affecting long tendons - complete healing/maturation takes up to 6 months (5 weeks repair, 6 months remodeling), progressive loading is key

grade 3 muscle/tendon injuries ntervention

varies based on involved muscle/tendon unit - possibilities include no treatment, immobilization followed by progressive rehab, or surgical repair or reconstruction followed by progressive rehab

repair

primary repair of the structure with sutures

reconstruction

use of graft to replace or augment the original structure

classification of muscle/tendon injury based on MRI is based on

severity (0-4) and location (a, b, c)

location a muscle injkury

myofascial injury in the peripheral aspect of the muscle

location b muscle injury

within the muscle belly, most commonly at the muscle tendon junction (most common site of muscle injury and is associated with prolonged rehab)

location c muscle injury

extends into the tendon (poorest prognosis)

muscles have tendons that are

within the muscle belly - intermuscular tendons, slower prognosis when these are affected

ligament injury/sprain MOI

excessive applied load, most commonly from external force

grade 1 ligament sprain

(less than 10% fibers injured) no laxity with stress testing, minimal localized swelling and tenderness, pain on stress testing

grade 2 ligament sprain

(10-99% fibers injured) laxity with stress testing, firm endfeel still present, mild/severe localized swelling, tenderness with palpation and pain with stress

grade 3 ligament sprain

(100% fibers injured) laxity with stress testing, loose endfeel, could have damage of capsule and avulsion fracture, potentially minimal pain with stress testing, severe swelling and tenderness with palpation

classification of sprain injuries based on joint laxity

0 laxity = normal, 1+laxity= 0-5mm, 2+ laxity= 5-10mm, 3+laxity=>10mm

0 laxity

joint opening is equal bilaterally - indicates normal ligament or grade 1 sprain

1+ laxity

mild 2nd degree injury, joint opening 0-5mm greater than contralateral limb

2+ laxity

severe 2nd degree injury, joint opening 5-10mm greater than contralateral limb

3+ laxity

3rd degree, complete ligament tear, joint opening more than 10mm than contralateral limb

grade 1 and 2 ligament sprain healing interventions

POLICE - emphasis on protection

optimal loading with grade 1 and 2 ligament sprains

consider where ligaments get taut in ROM - do ROM exercises to prevent healing in a shortened position, progressive strengthening and adjust load and arc of motion as appropriate

ligamentous injuries take how long to heal

up to 6 weeks for repair and healing, 1+ year for remodeling/maturation

grade 3 ligament sprain treatment

address initial swelling/infl./pain related to injury, then manage based on involved ligament

ligaments with expectation of tissue healing for grade 3 sprain

address inflammation/pain, progressive rehab of ROM, strength and function

ligaments without expectation of tissue healing for grade 3 sprain

if noncritical - address inflammation/pain, progressive rehab of ROM, strength and function, if critical - address inflammation/pain and progressive presurgical rehab, surgical reconstruction or repair followed by progressive posturgical rehab for ROM, strength and function

components of hyaline cartilage

chondrocytes synthesize collagen and proteoglycan, matrix formed of GAG and water for volume, collagen fibers for shape

layers of collagen fibers of hyaline cartilage

superficial parallel to joint surface (resist tension, spread load, promote gliding), transitional, deep fibers perpendicular to joint surface (resistance and compression)

role of hyaline cartilage

absorb compression, promote gliding

characteristics of hyaline cartilage

no nerve, blood vessels or lymphatics, nutrition is synovial fluid via milking action with movement, limited/no ability to heal

chondral lesion

lesion limited to cartilage, minimal pain/inflammation (not involving vascularized or innervated tissue), more common in adults

osteochondral lesions

extends into subchondral bone, involves vascularized/innervated tissue activating an inflammatory response, more common in children

osteochondritis dissecans

subchondral bone necrosis and likely trauma, cartilage overlying area remains relatively intact with synovial nutrition, cartilage can become loose as necrotic bone is resorbed and fragments can be displaced into joint space (loose body)

etiology of osteochondritis dissecans

repetitive overuse, trauma, ischemic, idiopathic, hereditary

signs/symptoms for chondral lesions, osteochondral lesions and osteochondritis dissecans

pain increasing with WB, swelling, joint locking/catching, instability feeling secondary to arthrogenic muscle inhibition

arthrogenic muscle inhibtion

clinical impairment caused by ongoing reflex inhibition of musculature surrounding a joint following distention or damage to structures of that joint

increased joint effusion leads to

decreased ability to generate torque

trying to strengthen a painful and/or swollen joint

is unlikely to work

interventions for chondral lesions, osteochondral lesions and osteochondritis dissecans following addressing initial swelling/infl/pain

based on joint involved, size of defect, location of defect in the joint, displacement of the fragment or not

small, nondisplaced, NWB region defects may be addressed with

initial control of weightbearing and functional activity and gentle ROM/strengthening with progressive return to WB and functional activity

larger, displaced, WB area defects will likely require

surgery followed by an initial 6-8 weeks of NWB and progressive rehab for ROM and strengh with progressive return to WB and functional activity

reparative surgical procedures

microfractures of subchondral bone causing healing in the form of fibrocartilage - lasts 5 years, or autologous chondrocyte implantation restoring hyaline cartilage - expensive

restorative surgical procedures

osteochondral autograft transfers, or allograft implanation

injury associated with degeneration and cartilage destruction - OA

4 stage process of softening, fibrillation, fragmentation, then complete cartilage erosion with exposed subchondral bone

OA

most common joint disorder in majority of population >65 years, metacarpals, knees, hips and spine

classic symptoms of OA

pain, joint stiffness, swelling, loss of strength, decreased mobility, and difficulty performing ADLs, joint deformity paarent in more advanced OA

etiology of OA

primary risk is aging causing decreased activity of chondrocytes, number and size of GAGs, water concentration, strength/stiffness of cartilage and progressive surface fraying and softening, otherwise too much or too little mechanical activity, or genetics

interventions for OA

nonsurgical education and exercises, surgical joint arthroplasty followed by rehab

menisci are found in 5 joints

knee, TMJ, SCJ, radiohumeral, ulnotriquetral

characteristics of menisci

no sensory innervation or blood supply except in periphery (deeper in children and decreases with age)

menisci injury associated with trauma

most common at knee, intervene with surgical excision or repair addressing torn portion of meniscus, progressive rehab of ROM, strength and function

menisci injury associated with joint degeneration/OA

degenerative tears most common at knee, intervene with rehab based on optimizing knee ROM, strength and function, surgery if mechanical locking occurs

effect of loading on healthy tendons

increased circulation and collagen synthesis, becomes larger/stronger and more resistant to injury, responds more strongly to greater loads

adaptive response of tendons to loading is

slower than muscle adaptations - quick strength enhancement increases risk because muscle is much stronger then tendons (steroids, BFR risk)

tendon response to exercise

acute exercise is followed by an increase in synthesis and degradation of collagen (metabolically active) - initial net loss of collagen 24-36hrs then a net synthesis of collagen 36-72hrs after exercise

repeated training with rest periods that are too short can result in

net degradation of matrix and lead to overuse injuries/"stress fractures" of tendons

optimal tendon response is obtained with

high loads, slow movements and sufficient rest

tendons are not uniform structures

stiffness can change along its length or depth - each tendon has a unique distribution of compliance

effect of offloading on healthy tendons

smaller, weaker, less stiff and more prone to injuries (a good tendon is stiff)

primary tendinopathies

no predisposing medical condition for the occurrence of tendon pathology other than mechanical factors or advancing age

classic features of tendinopathies

localized pain exacerbated by tendon loading, with palpation of tendon, or on loading tendon (history, physical exam)

contributing factors for tendon injuries

direct trauma, excessive repetitive training/work, repetitive microtrauma (excessive compression/friction internally by soft tissue pulleys/ligaments or bones or externally by footwear/braces), previous injury, rapid change in activity/intensity, poor biomechanical function or ergonomic conditions or insufficient recovery

tendons are designed to resist

tensile forces not so much compressive forces (want neutral joint positions)

systemic risk factors for tendionpathies

aging (tendons decrease stiffness beyond age 40), obesity, smoking, genetics

pathological features of acute tendinopathies

tendon cells detect overload and cellular response of tendon occurs - similar to inflammatory response and more fluid/cells are between cartilage fibers

the cellular response of tendons results in

short term adaptive thickening of the tendon reducing stress via increased CSA (not for force, just fluid), collagen intensity and neurovasculature emains the same (makeup of tendon is normal), tendon can convert

clinical features of tendinopathies

tendon with brief history of symptoms related to acute tendon overload, large fluctuations in amount of pain, pain 1-2 days later, patient perceived stiffness (nothing changed with the structure of the tendon so no stretching is necessary)

direct correlation between load on tendons and

pain and swelling (cellular response related directly to loading)

progression of acute tendinopathies

stiffness following activity but gone quick - some stiffness with initial activity then relieved during and sore after - initial soreness and minimal pain with activity and sore after - pain during activity severe enough to alter activity and mild pain with ADL - need to alter activity, pain before during and after - pain at rest and disrupting ADL - pain at night

intervention for acute tendinopathies

address cellular response and reduce excessive load, relative rest (not appropriate for high loads or energy storage/release), long duration isometrics for analgesic effect, EPA, NSAIDs, address technique for wrong load, assess amount of training for excessive load

address technique for wrong load

efficiency of mechanics

assess amount of training for excessive load

reduce volume of work on tendon

prognosis of tendinopathy

recovery time of days to weeks - never months

acute tendinopathy timeline

4-6 weeks

acute tendinopathies are also called

reactive tendinopathies due to the pain fluctuation proportional to load

the acute phase tendinopathy appears physically as

larger tendon but cellular makeup of matrix is the same and can return to normal

subacute tendinop[athy

6 weeks - 3months, continued increased cellular activity and protein production

cellular changes in subacute tendinopathy

increasing amount of type 3 collagen instead of type 1 (more compliant and less stiff), islands of nodules/disruptions in matrix, increased neovascularization in islands of fibrotic tissue

neovascularization is not

the source of nociception with tendinopathy (unknown what the source is)

subacute tendinopathies are still

reversible with load management and exercise to stimulate matrix structure (sooner rather than later)

clinical features of subacute tendinopathy

chronically overloaded tendon, localized thickness with palpation

chronic tendinopathy

substantial extracellular matrix breakdown and collagen degeneration - tendon is more compliant (even though patient may report stiffness, stretching will not help)

with chronic tendinopathy, the cellular response is

resolved, tendon is normally sized with areas of fibrotic tissue within the tendon, cell death, little capacity for reversibility

what do we treat with chronic tendinopathy

treating the healthy part of the tendon to increase strength and allow sheilding of weak regions`

clinical features of chronic tendinopathy

chronically overloaded tendon (middle aged most common), focal areas of tendon thickening and pain noted with palpation, history of repeated bouts of tendon pain, symptoms do not fluctuate (if aggravated, settles down in a short time)

intervention for subacute/chronic tendinopathies

reloading program with eccentric high load exercises and heavy slow resistance training - optimize adaptation of the healthy portions of the tendon, assess wrong load and excessive load (not much evidence supporting adjunct treatments)

prognosis of subacute/chronic tendinopathies

recovery time of weeks to months (pain will become manageable but the islands dont really reverse)

acute on chronic tendinopathy

structurally normal portion of the tendon drifts in and out of an acute response - accidental overload on healthy portion of tendon - treat as acute for short term and chronic for long term