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Sports Medicine > Week 2 - Overuse Injuries > Flashcards

Week 2 - Overuse Injuries Flashcards

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1
Q

What are overuse injuries?

A
  • Associated with repetitive (micro) traumatic tissue damage
  • repetitive micro trauma exceeds tissue repair capacity
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2
Q

What are 4 challenges to overuse injuries?

A
  1. Insidious onset - difficult to identify what initiated injury
  2. Frequently multifactorial etiology - interactions between extrinsic & intrinsic risk factors
  3. Long recovery common - often recalcitrant to treatment (months to resolve)
  4. Re-injury rates high - complexity of determining correct diagnosis, interacting risk factors, effective treatment
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3
Q

What are the 4 stages of overuse injury?

A
  1. Pain in affected area after exercise
  2. Pain during exercise not restricting performance
  3. Pain during exercise, restricting performance
  4. Chronic, persistent pain, even at rest
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4
Q

What is the failed healing model for overuse injury within a tendon?

A
  • morphology becomes more cartilaginous (instead of collagen)
  • increased prostaglandin E2 in tissues (associated with injury)
  • increased collagenase (degrades collagen) , decreased collagen synthesis
  • upregulation of genes for cartilage
  • down-regulation of genes for tendon
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5
Q

What is overuse tendinopathy?

A
  • Increased matrix remodelling leads to mechanically less stable tendon
  • long term pathology is tendon degeneration not inflammation
  • short term pathology may involve inflammation/paratendinitis
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6
Q

What is the mechanics behind overuse tendinopathy?

A
  • increased collagen disarray
  • increased cell proliferation
  • increased vessels and nerves
  • increased extracellular matrix
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7
Q

What are some extrinsic risk factors for overuse injury?

A
  • training & technique errors
  • surfaces & shoes
  • equipment
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8
Q

What are some intrinsic risk factors for overuse injury?

A
  • previous injury
  • “flexibility”
  • leg Length discrepancy
  • mal-alignment
  • tibial torsion / vara
  • genu valgum / varum
  • mal-tracking (patella)
  • patella Alta / baja
  • q-angle (8-14° males, 11-20° females)
  • pes planus (mobile flat foot)
  • pes cavus (high arch rigid foot)
  • overpronation
  • muscle weakness
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9
Q

What are some examples of over use running injuries?

A

– Patellofemoral pain syndrome (PFP)
- Achilles tendinopathy
– medial tibial stress syndrome (MTSS)
– plantar Fasciitis

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10
Q

What are some potential causes for overuse running injuries?

A
  • over-striding

Can be addressing with reduced step length and increased cadence to create “pose running” - it proven

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11
Q

What are the differences in running injuries between males and females?

A

Female runners have a twofold higher risk of having a bone stress injury compare to male runners

Male runners have an almost twice risk of Achilles tendinopathy as female runners

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12
Q

And what are some anatomical/biomechanical factors to tibial stress fractures that are running related over use injuries?

A

I decreased tibial bone width and decreased tibial bone internal rotation are associated with stress fractures

  • Lower risk “compression” injuries tend to occur in the posterior medial section of the distal tibia
  • higher risk “tension” (anterior) injuries tend to occur mid shaft
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13
Q

What are some typical tendons that may get tendinopathy?

A

– Achilles
– patellar (jumpers knee)
– gluteal
– supraspinatus (rotator cuff)
– extensor carpi radials brevis (tennis elbow)

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14
Q

What is tendinopathy?

A

– Failed healing: long-term pathology is tendon degeneration not information
– chronic painful condition: presence substance P (nociceptor excitation) and calcitonin gene-related peptide (pain sensitisation)

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15
Q

What is stage one of tendinopathy?

A

Reactive tendinopathy
– tenocytes proliferate
– increase in Proteclycans
– MRI mild Fusiformis swelling (increase in bound water)

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16
Q

What is stage two of tendinopathy?

A

Tendon disrepair
– collagen separates. Matrix disorganised
– ingrowth of vessels and nerves
– tenocytes rounded appearance more prominent

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17
Q

What is stage three of tendinopathy

A

Degenerative tendinopathy
– areas of apoptosis
– degenerative matrix and vascular changes hypoechoic areas in ultrasound images
– chronic pain

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18
Q

How do we is clinicians Approach tendinopathy?

A

History, examination and diagnosis
– what’s changed?
– reproduce pain
– assess potential risk factors
– avoid aggravating activities (relative rest)

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19
Q

What type of exercise has been shown to be effective for treating tendinopathy?

A

Eccentric exercise

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20
Q

On the best evidence that we have to date what are the typical results from eccentric exercise therapy treating tendinopathy?

A

results from majority of studies show significant improvement for Achilles and patella tendinopathy at short and long-term follow up - Specifically significant improvements in function and pain

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21
Q

What is overuse injury in Bone?

A

Bone stress injuries
Repetitive stress – cumulative (micro) damage
50 to 66% of runners have a history of Phone stress injuries

Continuation of bone damage:
– stress reactions
– stress fractures
– complete fracture

22
Q

What are the ways to investigate brain stress injuries?

A

– x-rays: not sensitive to early changes
– Bone scans: high sensitivity poor specificity. Picks up activity in bone through a die injection but will pick up any activity not just stress injuries also moderately high in radiation
– CT: radiation issues, better in later stages. Higher levels of radiation then bone scans
– ultrasound: needs further development
– MRI: gold standard

23
Q

What are the grading sequences of bone stress injuries using MRI based systems?

A

0 - normal
1 - Periosteal edema no bone marrow abnormalities
2 - periosteal edema with mild bone marrow edema
3 - periosteal edema extensive bone marrow edema
4a - periosteal edema, extensive bone marrow edema multiple foci of intracortical signal change
4b - periosteal edema, extensive bone marrow edema, fracture line

24
Q

What are the return to sport estimates with each grading of bones stress injuries?

A

Grade 1–3 weeks
Grade 2 –3 to 6 weeks
Grade 3 –12 to 16 weeks
Grade 4–16+ weeks

25
Q

What is the type of loading related to bone stress injuries?

A

– Bending (tibia)
– compression (calcaneum)
– tension (femoral neck)

26
Q

What are the locations and types of low risk bone stress injuries?

A

– Commonly heal without complication

– pelvis
– femoral shaft (compression)
– fibula/lateral malleolus
– posterior medial tibia
- Calcaneous
– diaphysis 2nd to 4th metatarsals

27
Q

What are the implications of using NSAIDs with bone stress injuries?

A

– Can mask the pain which will lead to excessive loading
– they have been shown to have the potential to impede a tissue healing especially in bone

I discourage the use of NSAIDs beyond several days

28
Q

What are some locations and injury types for high-risk bone stress injuries?

A

Require specific treatment
Generally bending and tension
Risk of delayed non-union
Risk of progression to complete fracture

– femoral neck(Specifically superior section, tension injury)
– Anterior tibial cortex (bending type)
– Talus (lateral, tension)
– medial malleolus (bending)
– navicular
– sesamoid
– base of the 2nd to 5th metatarsals

29
Q

What is the strength of bones?

A
  • compression strength ~ 170 MPa
  • tensile strength ~ 100-120 MPa
  • shear stress strength ~ 50 MPa
30
Q

What’s the difference in injury healing in cortical and cancellous bone?

A

BSIs in cortical bone (80% skeletal mass) heal quicker than cancellous (20% skeletal mass) or “mixture” injuries

31
Q

What are 2 risk factors for bone stress injuries?

A
  1. Factors modifying load applied to bone (biomechanics and external loading)
  2. Factors modifying ability of bone to resist load without damage accumulation (internal strength of the bone, health of bone, nutrition etc)
32
Q

What are some factors that may modify the load applied to a bone?

A

– Static (external hip rotation, pes cavus - high arch & planus - low arch)
– dynamic (peak hip abduction, knee internal rotation moment)
– muscle factors (weekend, fatigued)
– Training areas
– equipment and playing services
– shoes and insoles

33
Q

What are some factors that influence the ability of bone to resist load?

A

– Phone mineral content and distribution
– energy availability
– vitamin D, calcium
- RED’s (relative energy deficiency in sport - menstrual function, Phone health, and crying, metabolic, immunological, gastrointestinal, cardiovascular, physiological, growth and development

34
Q

What is our role when suspected Bone stress injury early stages

A

– Relative rest (maintain fitness)
– avoid precipitating activity
– modify weight-bearing
– assess (modify) risk factors

35
Q

What are osteochondroses?

A

Overuse injuries of growth areas in bone (apophyseal) places where tendons or ligaments attach, you get pulling of the growth sites and accumulative micro damage occurring
- little leaguer’s elbow

Address with rest, activity modification, reassurance

36
Q

What is osteitis pubis?

A

Inflammation of bone or surrounding areas of bone

  • painful, overuse condition affecting pubic symphysis & parasymphyseal bone
  • MRI shows bone edema
  • abnormal muscle forces and pelvic instability

Address with rest (activity modification), referral (diagnosis, potential causes), retraining (strengthening), return disport (pain-free)

37
Q

What are the three classifications of osteochondroses?

A
  1. Non-articular - outside joint
    – osgood-schlatter’s (anterior tibial tuberosity)
    – Sinding Larsen Johansson (inferior pole patella)
    – Severs (calcaneal apophysis)
  2. Spinal - physeal
    – scheuermann’s (commonly associated with smalls nodes through vertebral body endplate into adjacent vertebra - can cause alteration in curvature of spine
  3. Articular - inside joint
    – legg-calve-perthes (rare childhood hip disorder initiated by a disruption of blood flow to head of femur osteonecrosis or avascular necrosis due to lack of blood flow)
38
Q

What are the four stages of osteitis pubis?

A
  1. Unilateral pain - inguinal region may radiate to adductors - pain alleviates after warm up, exacerbated after training
  2. Bilateral pain - inguinal & adductors - pain exacerbated after training
  3. Bilateral pain - groin, adductors, suprapubic, abdominal - during training, kicking, sprinting
  4. Generalised - generalised, lumbar region - ADL’s
39
Q

What is osteoarthritis?

A

– Degenerative disease involving breakdown of joint Cartlidge and underlying bone
– multifactoral pathophysiology
– multiple joints, fingers, hips, knees
– Has been associated with acute injuries
– Can also be idiopathic (cause unknown)

40
Q

What is knee osteoarthritis?

A

– Prevalence increases with age
– Females have higher incidence than males
– Classification system looks at joint space narrowing and boney spurs, osteocyte within the joint - grade 1-4

41
Q

What are the risk factors for knee OA?

A
  • strong risk factors for females and obesity, heavy work activities, previous joint injury
  • moderate risk factor for knee malalignment
  • weak risk factors for knee extensor muscle weakness
42
Q

How are knee OA and ACL rupture related?

A
  • ACL injury increases knee OA risk with symptomatic OA appearing in around 50% of individuals 10 to 15 years after ACL rupture
  • 50 to 90% of ACL injuries progress to post traumatic OA (lifetime risk)
  • around 50% ACL injuries have articular cartilage damage of medial & lateral femoral condyle
  • 25%-66% ACL injuries have concomitant meniscal damage: patients with meniscal tear more likely to develop radiographic OA compared to patients with isolated ACL injury
  • 80%-90% patients show signs subchondral bone injuries after ACL injury: may cause osteocyte necrosis in bone marrow, prosteoglycan loss, chondrocyte injury and matrix degradation in overlying cartilage
43
Q

What is soulder OA?

A
  • OA affects both acromioclavicular (more common) and glenohumeral joint
  • Glenohumeral joint more debilitating including significant dysfunction and pain
  • Various non-traumatic and traumatic factors involved
44
Q

How are anterior shoulder dislocation related to OA?

A

– 55% of patients first time anterior shoulder dislocation before 40 years old had some degree of arthropathy on radiographs after 25 year follow-up
– symptomatic glenohumeral OA detected in 22.7% of patients at average of 15 years after initial instability event

45
Q

What are the risk factors for developing OA after shoulder dislocation?

A

– Current or former smoker
– hyper laxity
– labourer occupation
– body mass index
– age at initial instability

46
Q

What can cause bone spurs and where are some common sites & other related info

A

– Chronic impingement due to over use leads to development of bony spurs
– anterior talus (footballers ankle)
– posterior talus
– calcaneous Postolateral corner (Haglunds)
– Associated with chronic conditions which may restrict movement or be painful
– Neck, stiffness in Neck, radiating pain in shoulders arms and fingers
– Rugby front rowers, sumo wrestlers, jockeys
Can lead to chronic bony impingement – FAI (Femoro acetabulum impingement) in the hip joint, cam lesions (head neck region), pincer lesions (acetabulum), mixed

47
Q

What is periosteitis?

A

– Inflammation of the periosteoma associated with chronic muscle activity
– medial tibial stress syndrome (MTSS)
– solea’s, tibialis posterior attachment at the medial border of the tibia along the periosteum

48
Q

What is chronic compartment syndrome?

A

– Exercise raises intracompartmental pressure
– leads to swelling and accumulation of fluid in interstitial spaces which leads to impaired bloodflow
– creates pain/compression of neural structures
– And example includes pain and foot slap after a fixed time of running

49
Q

What is chronic Groin pain?

A

– Repetitive sheer forces across the hemipelvis involving abdominal and thigh muscles
– adductor longus
– rectus abdominis
– conjoint internal oblique and transversus abdominis muscle

50
Q

What is bursitis?

A

– Chronic bursa inflammation
– comorbid with tendinopathy’s, impingement syndrome
– various sites: olecranon (students elbow), pre-patella (carpet layers knee), pes anserine (medial hamstring tendons)
– wrestlers, surfers, cyclists, swimmers
– mostly self limited, often result with the rest, ice, compression (Conservative management)

Olecranon site *
– Corticosteroids often inadvisable can lead to infection, skin atrophy, potential triceps rupture
– benefits of aspiration may not outweigh risks
– excision of olecranon bony spare considered (with failed Conservative management)

Sports Medicine (20 decks)

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