Knee Conditions 2

February-12-08 9:40 PM

- Start laterally, work our way in. - Use LCL as the figurehead structure for lateral stability. Its outside the capsule, like the CF lig, therefore when it rips, we get no swelling. Very small lig. - Menisci, PCL, ACL - MCL is a thickening of the capsule, thus we can get swelling. Has 2 portions. Deep - goes to medial meniscus from the fem condyle, then to tib condyle. Deep MCL accounts for how we can damage the medial meniscus in a valgus injury. Superficial MCL - goes femur to tibia.

When we flex the knee: key is that the ACL and PCL become exposed. See that they cross (look from the front or side, make an X pattern) ACL - attaches anteriorly on the tib, and prevents the tib from coming anteriorly on the femur PCL - attaches posteriorly on the tibia, prevents the tib from going posteriorly from under the femur

The intercondylar notch - narrower in females than males. Females get more ACL injuries than males. Why? One theory is b/c the notch is narrower, when they go to rotate, the ligs get bent around the condyle and break. Just know that the intercondylar notch is narrower in females. Also, we have estrogen receptor sites on the ACL, so for 5 days during your cycle, your ACL has a high concentration of estrogen on it, making it weaker. Also, some think females are learning how to play at a higher level, their bodies are becoming exposed to more tension/stress Balance - in proprioception, female's is not as astute as in a male. Aka don't have the same joint sense as males do. Perhaps because they haven't trained at that level yet?

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Menisci and synovial lining ACL and PCL are only painful if the lig is torn where there's synovial lining. If you tear mid-substance where there's not lining, you won't be painful. ACL has ZERO pain fibres in it! So, the pain comes from synovium, which is richly innervated with pain fibres (PCL and LCL have pain fibres). Within 2 days of ACL rupture, you can see vastus medialis getting smaller! (later(

When we flex and extend, that motion takes place b/w the bottom of the femur and the top of the menisci. The menisci move slightly forward and backward (flex - go backward) (extend, go forward). As we flex, they move posteriorly on the tibia. As we extend, the menisci move anteriorly on the tibia. Twisting motion: feet planted, body twisting. This motion takes place b/w the bottom of the meniscus and the top of the tibia. The menisci are wrapped around the femur, so when the femur twists, they go with it, and slide on the top of the tibia.

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Recall from SF - meniscus is something that dissipates force/its a Shock absorber. They're very important! They also make sure equal parts of the femur get equal amts of F

Coronary - goes all the way around the top of the tib, attaches the meniscus to the tibia. You can palpate it, it has pain fibres and blood flow. Why is that important? The fact that it has blood flow - if you get a tear in the outer rim of the meniscus, it will heal - bc it sneaks blood flow from the coronary ligs! Meniscus don't have BF themselves; if you tear the periphery though, it will heal, thanks to the CL Rotation: takes place b/w the top of the tib and the meniscus. Medial doesn't move as much, therefore we know one way to tear the CL or med meniscus is excessive external rotation of the tibia (

Planted, turn body to the LEFT - your RIGHT tib is in excessive external rotationd. Lateral meniscus: the popliteus muscle on the posterolateral corner of the knee pulls the lateral meniscus posteriorly on the tibia during knee flexion. It can only pull it back so far, and if there's excessive flexion, ppl can tear the posterior part of the lat meniscus

Hyper - more than what the person normally has. If you're forced into 'excessive' whatever, you're in 'hyper'

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Recall valgus. X on the femur means its the stationary bone. Most people get a blow from the lateral side of the knee that they don't see coming, forcing a valgus.

Quads - muscle provides stability to the jt, not shown here Medial head of the gastrocs contributes Medial hamstrings - very important ***MCL is number ONE*** its puny in relation to the bones themselves! Meniscus? Does contribute because it makes the jt socket deeper to give it more stability. If you don't have medial meniscus - any test you do for an ACL, the test will increase by 25% if they have no medial meniscus!

STRAIGHT VALGUS - no twisting. Single plane. The force can stop at any time, tearing any number of structures IF the MCL tears: then the ACL is next. Force continues? PCL. Then dislocate. MCL --> ACL --> PCL --> dislocate

65 - 70% of injuries occur in practice!

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Order of support provision: Biceps femoris IT band Popliteus Capsular ligaments (posterolateral capsule thickenings) Lateral collateral lig (not part of the capsule!)

Rarely see disruption of the lateral complex, because you need a varus to get it - you get hit from the inside, you usually see it coming and can avoid it. Whereas valgus is often a blindside hit (you can also do it by yourself ie skiing and catch an edge) LCL --> ACL --> PCL

ACL - is tight in extension (there's primarily 2 bundles, one part is tight all the time) but the majority: gets tight in extension and internal rotation. Combo of both creates the most tension, worst case scenario

Hyperextension - knee forced into a position its not used to, cause damage within the jt itself

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Cleated footwear: debate in soccer, how many cleats/shoe, and how long should they be? Issue because of knee safety, especially in soccer and football. Long cleats are unsafe. Shoes are too good? Aka too much friction between the shoe and the floor in bball - you go to stop, your shoe stops and your body keeps going! Hearing squeaks means the shoe is sliding on the floor, dissipating force so it doesn't go up into the leg saving knees!

When we test the ACL, we'll get different results depending on whether they have MCL damage.

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Major MOI for PCL. Can be a hyperflexion (PCL tight in flexion) but the majority: strike their knee on the floor/hard surface Worse if they have/had osgood shlatters disease (larger tibial tuberosities) - Forced hyperflexion - Hit knee on floor

Positive posterior drawer: push knee back. When we push on the front of the tib, the whole tib will go back.

ACL is like a twist tie when the tib is in internal rotation. The ACL and PCL wrap around each other and tighten each other up Therefore - one common MOI for ACL and PCL is internal rotation! ACL - int rot and hyper extension PCL - int rot and hyper flexion

Valgus with External Rotation of the knee MCL Deep, Superficial, and ACL.

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MOI MCL major MOI is a valgus: that's why its important to take histories (what happened). We can immediately create an index of suspicion ACL - valgus after you tear the MCL. Internal rotation tightens up both cruciates.internal rotation + extension, hyperextension. Varus after the lateral complex/LCL (but its uncommon) PCL - 3rd in line in either a valgus or a varus - lots has to rip in order to get to the PCL. This is a dislocated knee** - Hyperflexion with internal rotation (feel pain in popliteal fossa). Blunt trauma to tib tub - land hard on knees, pushes the knee posteriorly. If you can think of any kind of force that pushes the tibia excessively anteriorly or posteriorly - these are MOI for ACL and PCL! The list below aren't the only way we can injure...

FCL - figurehead structure, if you don't have it, you've done major damage! MM - external rotation (coronary ligs tighten up) or valgus to the knee: the deep portion of the MCL attaches to the meniscus. With valgus, knee in slight flexion (takes the tension off the superficial portion of the MCL) - get a valgus, the deep part of the MCL gets very tight (its attached to the MM) Severe external rotation - can just tear meniscus MCL + MM + ACL = unhappy triad of the knee. Common!

LM - hyperflexion. In the LM, as we knee flex, the popliteal muscle pulls the meniscus posteriorly - just can't pull it far enough

***the ACL mid-substance where there's no synovial may not hurt! Most ACL are painful, MCL is very painful. PCL has pain fibres in the same distribution as the ACL (not in the middle) If athletes say they felt something/something's not right - they know Unusual sounds - that's the ACL

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Feeling of 'giving way' - the knee buckling, you feel like its going to give way Loss of function of the joint Watch out for painful-not-painful. The lig that's totally torn may not be painful anymore (ie grade 3 MCL) ***don't need to have all of these!***

This was a safety net - now we say if a person has a torn ligament (grade 2 MCL) its advisable to get them off NWB You don't want them to slip and turn the grade 2 into a 3 Posivite Lachman's on the field? NWB!!! Any torn ligament - NWB When you tear the MCL, it will continue to weaken for the next 5 days before it gets stronger! So if you have a grade 1, for 5 days after that its more prone to injury because its getting weaker. Other ligaments don't do that!

Doesn't feel right - best diagnosis in the world

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After rehab return to play Physicians often 'underdiagnose' (screw up) We have more musculoskeletal training than med school students!

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MRI of the knee: underneath the patella there's an infrapatellar bursae and a fat pad. They measure the height of the patella and the length of the patellar tendon. If we have the tendon longer than the height of the patella - called a high riding patella (or a patella alta - altitude, high)very common, especially in females. Means that you patella doesn't sit in between the fem condyles, sits above them. These people dislocate their patellas a lot Baja - the patellar tendon is really short, shorter than the height of the patella. Most of us are equal lengths or alta - not many people are Bajas.

gastrocs The back of the patella. The patella is not in contact with the femur until 20 degrees of knee flexion. At 20 degrees, the inferior pole of the patella is in contact. Then there's a transition. At 45 degrees, the mid-portion of the patella is in contact (the inferior part isn't anymore!). Same thing applies for 90 and 135 degrees. When you're in full squat, there's only 2 little parts of the patella in contact with the femur! Not additive, the patella passes through zones

Person with patella alta gets more medial and lateral movement of the patella (dislocaters) So, with rubbing back and forth, they also wear out the cartilage behind their patellas more quickly - get more patella-femoral pain. Condromalasia patella - diagnosis can only be made through a scope, its the actual wearing of the cartilage. Back of patella looks like a can of crab meat

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Baja - when the person goes into flexion, get lots of problems with the inferior pole - bone compression pain with the top of the tibia.

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Very common! Can be caused by a number of things, and unless its visualized by a surgeon you can't call it anything else. Otherwise, we'll just call it PFP syndrome Imaginary line indicating the quadriceps angle. Greater = pulls laterally w/ pronation, we get an internal rotation of the lower extremity (leads to greater Q angle). These ppl tend to have more PF pain (doesn't mean you WILL have it) TP is primarily responsible for STOPPING the pronation that occurs in the foot. Its responsible for stopping the internal rotation of the leg. If they're weak (test them), then must show how to strengthen Tight hams - the tighter the hams, the harder the quads have to work to overcome the tightness. Go to extend your knee and your hams are tight? Quads attempt to extend your knee, have to contract harder. Increases the PF compression force. Tight RF - quads are tight and you flex your knee? Greater PF compression forces 5. Number one cause of PF pain! Weak muscles in the pelvis. If you can't stabilize your pelvis, your femur can't work properly. (aka core stability, lower abs, etc). If their femur's not able to track in the proper position, get problems!

2 pics of Barb: This is called a 'squinting patella' - one looks at the other! She also has scars under her knee caps - her Q angle was so bad that they surgically tried to correct it (Houser's procedure = they cut the tib tuberosity out from under the tibia, took a piece of bone, and screwed the tib tuberosity onto a more medial position! Doesn't work! But they need to try it in cases like this. Genu (knee) Recurvatum (hyperextending) - looking from the side. Patella becomes more lax, because you're taking the femur and moving it back, away from the patella. She's dislocated many times - also has patella alta (high riding patella). She was a ballet dancer, had a lot of pain. Probably should have looked at weak pelvo-femoral muscles.

Ideally, when you flex your knee, the patella should come straight down over the second toe. Knee whip = the knee whips in towards midline then comes out. In running, when motion is so fast, that knee just whips in and hits the midline. Recall the video - repeated knee flexion Can't tell by looking at someone standing! Must make them flex

If patella is coming towards midline, pulling this line over Females have a wider pelvis, and thus a greater Q angle ASIS to mid patella; tib tuberosity to mid patella

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If someone has a high riding patella and a large Q angle: its going to sublux/move back and forth laterally and wear out. Plant, cut and turn - increases the Q angle. Then push off? That really increases the tendancy for the patella to dislocate

Remember this! We only have one tiny little muscle that pulls the patella medially (VM) - everything else in our thigh tends to pull the patella laterally. The rest of the quads, the IT band all pull the patella laterally. Ask about their digestive functions! IBS, chrones, etc - you must ask them about digestive problems. The nerve that innervates the lower bowel innervates the IT band! If a person is in a bad phase (have IBS or something) - you're also going to have a lot of PF pain, because the IT band automatically gets so much tighter when the bowel is irritated

Patella comes into contact with the femur at 20 deg of flexion! As soon as you start flexing, it tracks a little better. Some people will chronically sublux - pops out every times she straightens her leg!

Articular cartilage, hyaline cart is different from the meniscus cartilage. Hyaline can regenerate! The body can repair it/make more of it. The back of our patella is coated with hyaline cartilage. It also has NO pain fibres - so when hyaline cart wears away, it doesn't hurt us. However there are LOTS of pain fibres in the periosteum of the patella (bone) - so when we fully wear through the cart, that's when people start to get pain. Every night when we sleep, body works to build hyaline cart back up. Hyaline cart gets its nutrition from inbibition (drinking) - from being compressed and relaxed. Sucks the fluid in and out.

Bad PFP? Consider taking 2 aspirin 4 times a day for 2 days with milk or meals. Why? Cathepsin - an enzyme in our body that goes around and eats up dead cartilage. What aspirin does is lower the level of cathepsin in our body (along with treating pain, anti-inflam) So, when people are in the acute phase - try this. Coated is better for sensitive stomachs (digests in the gut)

Should see an equal distance b/w the patella and the femur (skyline x-ray) Situations like the above - develop problems over time due to malnutrition. Right side - + side has too much compression, squeezing the cart and not letting go. The synovial fluid is squeezed out - like holding a sponge and not letting go. Can't suck up nutrients, hyperpressure. On the other side is the sponge that never gets squeezed (-). On the hypopressure side, it TOO gets malnourished! Cart starts to get soft. When we get active after that, the cart starts to wear away. We call it 'overuse' - a relative term, whatever the person is not accustomed to **key thing is to look at what the cause is!! Don't just give them quad exercises.

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Don't have to have them all! Knees crunch going up stairs - roughened patella sliding over the femur Swelling - ppl with PFP will swell with days of low atm pressure. We have a positive pressure inside of our joint - need that pos pressure to send the synovial fluid around the joint. Low atm comes in, less air pushes on our body. What happens? The joint gets larger! We know that ppl who damage their ACL - the quads will actually lose bulk in 2-3 days. Can't be pain, cause there's no pain fibres in the ACL. So what causes the atrophy? Study - injected saline into the joint, then stimulated the femoral nerve. Measured how hard the quad contracted - when they got to 30cc saline - CRANKED the stimulator, turned it to max, and the quad did NOTHING. No contraction. Then when they started to take the saline out in 5cc increments, started to draw it off - the quads started to come back. Round 2: injected freezing along with the saline, anesthetized the sensory component of the knee. Same result (so you know there was no pain causing the quads to not work). There's a sensory nerve ending in the knee capsule called the Mazzoli-Golgi end organ: it is senstive to capsular distension (swelling) that's the ONLY time it fires!! When stimulated, it blocks the messages getting into the quads at the spinal cord level. It censors it! The brain percieves there's something wrong with the knee when its swollen - sends a message to weaken the quads. Often if you suck the fluid out of the knee, their leg will feel a ton better! Thus, lower pressure = swollen knee, quads weaken, bad day! Knee hurts more, feels like it might buckle. High pressure - pushes the fluid out of the body, good.

MUST get it down!!

Hoffman reflex - the curve that occurs after a muscle contraction Continued...icing, massage, whatever it takes to get the swelling down, because we now know about M-golgi Activity - rubs the patella on the femur, makes it worse

Reduce pronation - tape feet! Works? Look into orthotics Best way to stretch hams is in the seated position!

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