Knee Flashcards
What structures likely cause pain in PFPS?
What are not risks for PFPS?
What ARE risks for developing PFPS?
What are the various classifications of patellofemoral pain?
Why is the diagnosis of “patellofemoral pain” insufficient?
Pain Sources:
1. Anterior synovium
2. Retinaculum (often lateral retinaculum)
3. Fat pad
4. Capsule
Not Causes/Risks
1. Age, mass, BMI, height, and WB Q-angle not risk
2. Inconclusive relationship between altered foot mechanics and developing/presence of PFP
3. People with PFP have weakness of hip abd, ER, extensors but no association with this weakness and developing PFPS later
Risks
1. Isometric knee extensor weakness predictive of developing PFPS
2. Athletes who move excessively into dynamic valgus are more likely to develop PFP
3. Physically active women more likely to develop this than men
PFP Impairment/Function-Based Classifications:
1. Overuse/overload without other impairments
2. Muscle performance deficits
-Respond well to hip and knee resistance exercises
3. Movement coordination deficits
- Not likely strength affecting this
- Respond to gait retraining and movement re-education
4. Mobility Impairments
- May have hypermobile or hypomobile structures
- Maybe higher level of foot mobility
- Flexibility deficits of hams, quads, calves, lateral retinaculum, ITB
What PFP Not Sufficient
1. PFP is not a homogenous condition with different impairments and response to intervention varies
How is PFPS Diagnosed?
- This is a diagnosis of exclusion based on a cluster of signs/symptoms after ruling out other pathology
- Anterior knee pain produced by functional tasks of squatting, stair climbing, and sitting with knee flexed is best diagnostic indicator of PFP
- Most accurate diagnostic tests were:
- Retropatellar pain during squatting (+LR 1.8; -LR 0.2)
- Hypomobility with patellar tilt test (+LR 5.4; -LR 0.6)
What is the difference (histologically) between tendinosis and tendonitis?
How would you treat each uniquely?
Histologically
- Studies consistently show the pathology of tendinopathy to be degenerative instead of inflammatory (absence of inflammatory cells), while inflammation is not the primary cause of tendinopathy, some degree may still be present in the early/acute stages
- It is a failed reparative process with progressive tissue degeneration (disorganized vs parallel/organized/wavy)
- Hypercellularity, nerve ingrowth, and neovascularization (all attempts at healing)
- Despite the lack of inflammatory cells, mediators in the inflammatory pathways appear to be involved (higher levels of COX-2 and release of cytokines)
- WIth heavy loading there is tensile failure/microdamage. Tenocytes must increase collagen and matrix production and this is a slow process, with further loading there is progressive microdamage and failed healing attempts
How would you treat each:
- Need to unload the tendon to let it calm (relative rest instead of complete cessation)
- For tendinitis you can initially use ice and NSAID’s, as well as counterforce straps and stretching
- Progress loading based on symptoms
- Try to transfer load to regional areas
- Mechanical loading when able (especially eccentrics)
- Focus on strength/endurance prior to speed
- Steroid injections inhibit collagen synthesis and lead to cell death/tendon atrophy, as well as reduction in load-to-failure
What is posterolateral instability? What structures does in consist of? How does it happen? How can you test it? How is it managed?
- The PLC provides restraint to:
- Posterior tibial translation in near full extension
- ER of tibia
- Varus > at 30 degrees - Comprised of LCL, arcuate complex, posterolateral capsule
- Usually occurs with knee hyperextension but can also happen with blow to anteromedial knee or excessive ER force
- Rule out PCL with negative posterior drawer test in neutral and IR
- Look at PLC with:
- ER at 30 vs ER at 90 (PLC will have >10 degree difference at 30 but not 90)
- Reverse Pivot shift (the knee will clunk in place at 30 when going from 90 flex with ER and applying valgus force/axial compression and extending the leg)
- Posterolateral drawer test (do posterior drawer but in more ER and when you push the tibia ER’s) - Patients may feel unstable with stance phase of gait and walk/stand with hyperextension/varus thrust
- This is usually seen in conjunction with tearing of the ACL or PCL and needs surgical repair
What is unique about articular cartilage healing? How is articular cartilage uniquely created to distribute forces?
- Partial thickness tears do not heal (no blood supply and no undifferentiated cells) but if they involve the subchondral bone they may fill with fibrocartilage.
- Hyaline cartilage is 95% extracellular matrix with sparsely distributed chondrocytes (2% of the cartilage)
- The negative charge on GAG’s creates high affinity for water that helps resist compressive loads and proteoglycans repel each other for maximal volume expansion
- It is low friction to allow joint movement
- Extracellular matrix mostly composed of collagen fibers to provide tensile strength and proteoglycans remain water to absorb compressive forces
After ligament and tendon repair, when is the soft tissue the strongest and when is it the weakest?
- The ligament is strongest the day it is harvested
- Its strength diminishes to 50% during the first 4-8 weeks after surgery and is weakness at about 12 weeks after surgery
- In the 3-6 months after there is slow transformation of collagen type and revascularization of the graft tissue
- At the 1 year mark it is about 82% of its original strength
What surgeries for articular cartilage damage are intended to allow an athlete to return to sport? Which are not?
- Debridement and levage
- Removes particle of cartilage and cleans
- Cochrane Review: Probably doesn’t do much for pain/function - Micro fracture
- Poke holes through tide mark (bottom layer of cartilage that is somewhat calcified)
- Hyaline cartilage is replaced with fribrocartilage though (fibrocartilage is less resilient)
- WB has to be controlled
- Advocated as 1st line of intervention
- Decent short term data but less optimal medium/long-term
- LIkely not appropriate for athlete - Autologous osteochondral transplantation (AOT)
- Harvest bone plugs from non-weight bearing areas on femoral condyle and transplant them in - Autologous chondrocyte implantation (ACI)
- 2 step process
- 1st surgery you go in and harvest chondocytes and grow them in a Petrie dish
- Then you go back in and implant then and put a periosteal flap over it
- Mixed reviews on outcomes - Osteochondral Allograft Transplantation System (OATS)
- Implant cadaver graft of subchondral bone and overlying hyaline
Critical defect size is suggested to be 2 cm
Small Lesions (<2.5 cm) For Athletes
1. Micro fracture
2. Autologous osteochondral transplantation
Medium Lesions (2.5-4.0) for athletes
1. Autologous osteochondral transplantation
2. Autologous chondrocyte transplantation
3. Osteochondral allograft transplantation
Large Lesions (>4.0 cm) for athletes
1. Autologous chondrocyte transplantation
2. Osteochondral allograft transplantation
What will rehab look like for the first 6-8 weeks after femoral micro fracture? When back to sports?
NWB for 2-4 weeks and full WB delayed until 8 weeks. Need to wait for sports 4-6 months for small lesions and up to 8 months for larger lesions.
What are the best tests for ruling out a meniscus tear? Ruling in?
Ruling Out:
Joint Line Tenderness
Ruling In:
Thessaly’s and McMurray’s have good specificity but horrible sensitivity
Can also use 3/5 or more positive from the following 5 tests:
1. History of catching/locking
2. Joint line tenderness
3. Pain with forced hyperextension
4. Pain with maximal knee passive flexion
5. Pain or audible click with McMurray test
What would the first 6-8 weeks look like after meniscus repair? Return to sport?
WB is left up to the discretion of the surgeon but often begins either immediately in full extension or by 2 weeks, progressing to full weight bearing by 4 weeks. For the first 4 weeks there is no WB in angles greater than 45 and none greater than 90 for 8 weeks. 90 degrees flexion by 2 weeks, 120 by 4 weeks, full ROM by 6 weeks.
Return to sport about 5 months.
What is the differential diagnosis for exertional compartment syndrome?
- Shin splints
- Periostitis
- Tibial stress fracture
- Fibular stress fracture
- Peripheral neuropathy
- Popliteal artery entrapment syndrome
- Claudication due to peripheral arterial disease
- Muscle strain
- Venous insufficiency
- Diabetes
What is and how to deal with young athlete with Osgood-Schlatters?
This is enlargement and micro fractures of the apophysis of the tibial tubercle, usually in girls 11-12 and boys 13-14.
You usually want to relieve the symptoms with ice or heat, changing activity, using knee pads, and giving NSAID’s. It usually resolves after the apophysis fuses. Flexibility training and isometrics for the quads/hamstrings can be helpful.
Symptoms of an irritated plica? What causes it? Treatment?
Most common symptoms along medial knee and if connected from patella to femoral condyle will mimic PFPS. It causes symptoms with prolonged sitting or kneeling and may give pseudolocking with a “pop” beneath the patella when extending the knee.
Caused by trauma directly or indirectly with repetitive knee bending and straightening that thickens it. It can can pinched in the inner knee joint or patella and has many nerve endings.
Treatment can be PT, modifying activity, injecting with steroids, or surgery.
How will you decide if someone with acute, traumatic knee pain needs radiographs to rule out possible fracture?
Pittsburgh Knee Rules
- Less than 12, older than 50
- Inability to walk 4 steps
Ottawa Knee Rules
1. 55 or older
2. TTP fibular head
3. Isolated TTP of patella
4. Can’t flex knee to 90
5. Can’t take 4 steps (2 on each side)
What impairment is often seen in those with ITB Syndrome? What is the current theory of how pain is produced?
- Weak hip abductors
- There is compression of an innervated local adipose tissue. Studies have shown an “impingement zone” at about 30 degree knee flexion during foot strike. There is eccentric contraction of TFL and glute max during foot strike that causes compression.
