12 knee

12 knee


Hey everybody, welcome back. We are on
PowerPoint screencast 12 today. This is the knee and related structures, so
hopefully, by now, you’re getting into the groove of the course here and starting
to enjoy the fact that we’re looking at specific body parts. So a lot of that
foundational stuff that we looked at earlier in the course– we’re starting to
to be able to put it to use and look at ways that we can prevent, and then
subsequently evaluate, treat, rehabilitate these specific injuries, so– certainly
there’s no shortage of knee injuries, and– in our day to day, so you can’t turn on
SportsCenter without reading– without seeing– an example of a high profile athlete
that’s sustained a knee injury, so– this photo may be a little dated, but “RG 3”
was– you know, Heisman Trophy winner highly touted draft pick– and his career,
safe to say, has been cut short by the fact that he has sustained a couple of
knee injuries– this one being one of many. So, we’re gonna take a look here at a
number of these injuries, and just like before, we’re gonna always rule out
immediate threats to life, so that primary survey comes first– airway,
breathing, circulation, level of consciousness, severe bleeding. Now, it’s
going to be really rare that a knee injury involves an immediate threat to
life, but the concern here is– is there a knee injury in addition to an immediate
threat to life? We’ll see this sometimes in the case of a
car accident. You know, they slam into the dashboard, they’ve sustained a PCL injury,
but they’ve got other issues that are more pressing, so– we don’t want to treat
the limb at the expense of the life, so that’s where our primary and secondary
surveys come in. Next, we move into our history– where we look at, “What was the
mechanism? Did they land on a flexed knee? “Did they have contact?as there a
non-contact injury involved?” and then we’re also going to look for their chief
complaint– many times that’s going to be pain, or an inability to bear weight. Sometimes it’s gonna be a clicking, or a catching, or popping. Then we get into the specifics of their pain. What type of pain do they have?
Where is it? Sharp or dull? Localized or diffuse? Does it radiate? Does it stay
put? Is it constant? Is it intermittent? Are there things we can do to make it
better or worse? From there, we go to our observation, and this is where we’re,
obviously, looking at the patient, and this can occur before we get to– you know,
we don’t necessarily have to completely finish the history in order to begin the
observation. I’ll begin the observation as soon as the patient walks in, so, in
the case of a knee injury– are they able to walk without a limp? Are there obvious
signs of swelling or discoloration, deformity? Notice I’ve also put pupillary
size here. That’s if we’re doing a head to toe on-site assessment. By the time we
get to the knee– the on-field assessment– we’re not looking at their pupils, okay?
We’ll also check respiration and pulse. How willing are they to move that leg in
the case of a fracture or dislocation? Oftentimes, they won’t want to move it at
all, so that’s– that’s a pertinent, valuable piece of information. And then, what’s their leg
position? If they’re holding it in flexion, then oftentimes that will
indicate a sprain, because that actually offloads the ligament structures in the knee. If it’s locked out straight and they can’t
move it, many times that may be indicative of a fracture or dislocation,
and then we also want to look at their patella, and we’ll take a look at the
patella in a little bit more detail a little bit later in the lesson today. Alright, our neurovascular exam
consists of looking at pulses, looking at sensations and motor function, okay? So in
the case of the knee, we’re going to look at the distal lower extremity pulses–
popliteal, that we’ll find behind the knee. The posterior tibial, that we’ll be
able to feel along the medial aspect of the shin, and then, our dorsalis pedis– and
the best way to palpate dorsalis pedis you may remember from last time. We stick our thumb right in that arch, and then allow our fingertips to wrap over the
foot. Obvious signs of fracture or obvious signs that they’ve got some sort
of nerve injury is– that’s a load-and-go. We don’t mess around with those. We don’t
attempt to manage that ourselves. We may splint it, we may immobilize it– some way,
shape or form— but that’s only in preparation for transport. Okay, when we’re palpating the knee, these
structures are critical. These are kind of the windows, so– I would encourage you
to kind of poke around on your own knee as we talk through this. So, what we see
here– this patient’s left knee. We see the patella, the tibial tuberosity down
here, and if you feel that patellar tendon, it should be a rigid structure–
probably about the size of a finger and a half, maybe even two finger widths–
connecting the tibial tuberosity to the patella. If you’re– if you take your
thumbs and put it right on that patellar tendon and roll your thumbs off, you’ll
feel kind of a fleshy spot on each side– that’s actually your joint line, so– when
we’re palpating, we want to palpate that joint line both medially and laterally.
On the lateral aspect, if we keep rolling out of that joint line, we’re
eventually going to encounter the fibular head– kind of a bony nodule
there. On the medial aspect, we don’t feel that– basically, we just feel the joint
capsule. Okay, if they’ve got obvious provocative
tenderness there in the joint line, then that may indicate a number of
things. That could be meniscus, that could be some sort of inter-articular problem–
say they’ve got a loose body. Could also indicate a cruciate injury. Okay, we’re also going to assess the range of motion. What’s their active flexion and extension look like? Quickest way to check this, grossly, is
roll them over on their belly, have them flex their heel as close to their thigh, or
sure, their glute, as possible, and use your hand to kind of gauge that– can they
get– can they compress your fist between their heel and their glute? Compare that
to the opposite side. For full extension, we roll them back over on their– on the
rear end, and we look to see– can they reach full extension? Okay? Not a whole
lot of special tests we’re gonna go over– your textbook actually covers a lot more,
but for the sake of this course, it’s really not critical that you know them
all. It’s pretty fair mix in the class of folks that are more interested in
coaching, versus those that are more interested in pursuing allied health
care careers, so– I thought it best to kind of split the difference. Some of the
more specific tests we won’t go over, but just like we talked about with the ankle,
there are types of tests that we can do. There are tests that we can do that are pain provocation tests, and there are tests that we can do that are
stability tests, okay? So, all of our ligamentous testing that we’re gonna do
are stability tests– we’ll be able to actually see if one side is looser than
the other. Okay, if we’re doing a sideline assessment, first thing we want to know
is what’s the mechanism of injury.
Have they had a knee injury before? What was the mechanism?
If we saw it, great. If not, have them show us on the non-involved side if
they can– did they feel any collapse? Did they hear or feel anything? Could
they move it or did lock? Did swelling occur? You know, if we’re not there to see that initially, then they may be swollen and
somewhat guarded by the time we get there. You’ll see this, oftentimes– you
may be– I’ll find myself covering a number of athletic events, and by the time I’m
summoned to where that injury occurred, maybe they’ve already started to swell
up. Alright, if we’re dealing with a recurrent or chronic injury, then our
history questions will actually vary just a little bit as opposed to an acute
injury. So first of all, we look at– what was their major complaint? When did they
first notice the condition? Does that swelling come and go? Is it recurrent?
Does the knee lock or catch on occasion? Is there severe pain? Does it grind or
does it grate? Does that ever feel like it’s giving-way? Lots of times, patients
will actually feel like their knee is collapsing, and they’ll be afraid that
it’s a stability issue, when in fact, it’s a muscular issue. If you were to stand
upright with no muscular activity at all, the first thing you do is collapse, right?
Same holds true for a patient who’s sustained, for whatever reason, chronic
knee pain. If that quadricep is inhibited then it’ll feel like that knee gives way, okay?
Lots of times, we’ll also notice issues if they are ascending or
descending stairs, so that may be of note. And then, what past treatment have they
undergone and did it help? Okay, with our observations, some things we’re going to
want to look at here– how do they walk? Do they walk without a limp? How do they
look when they perform half-squat? How do they look when they go up or down stairs?
Swelling or effusion– we’re going to look at a way to differentiate this, but
basically, just think of swelling as outside the joint capsule– usually will
swell as a result of a contusion, a direct blow, whereas an effusion tells us
that there’s swelling inside the joint, and that’s a sign that there is a more
serious problem in play here, like a meniscus tear or a cruciate injury.
Ecchymosis or discoloration– we can see that. What’s their leg alignment look like? We’ll take a look at at some of these in
just a minute, but– valgum knees, or knock knees, or verum, or bowleggedness.
Hyperextension and hyperflexion– do they have excessive flexion and extension?
What’s the position of their patella? Alta– high riding. Baja– low riding patella.
Are their patellae rotated inward or outward? Patellar malalignment can cause
a whole bunch of different anterior knee pain problems. And then, the shape, size,
length of their tibia and femurs are also important. One thing we can look at
is what’s referred to as “tibial torsion.” Now, torsion always refers to twist, if you
remember way back when we talked about mechanisms of injury, a torsion injury is
when one end is fixed and the other end is rotated in the opposite direction.
Well, that’s precisely what a tibial torsion is. We may have that proximal end
of the tibia square in the knee joint, whereas the distal is rotated outward,
and we can tell that by how that foot is positioned with their knee in a flexed
position, okay? Anything less than 15 degrees is an
indicator of a tibial torsion. Femoral aversion and retroversion– we’ll talk more
about this when we get to the hip, but basically, it’s kind of the same
phenomenon at the hip, where the femur are positioned different relative to the
pelvis, okay? So, we may see a difference from one side to the other. This is not
necessarily something that is equal bilaterally in every patient, and in
many cases it is a unilateral condition. So here we see some examples of these
postural deviations– so valgum, we see here. This kind of knock-kneed appearance.
Verum, we see in the bowleggedness, and then recurvatum, where we actually
extend beyond 0 degrees of extension. So, we’re looking for abnormalities, but
if you look at each of these, they’re actually symmetrical, which is– you know,
the postural malalignment is not idea,l but the fact that they are equal
bilaterally is probably a little better. Is there obvious swelling? Is there
obvious atrophy in the quadriceps? A little harder to see atrophy in the
hamstrings, but we can see calf-swelling as well, or atrophy. Leg length
discrepancy– this may be anatomical, in which case, one leg is actually
physically longer than the other, or functional leg length discrepancy, where
they’re actually the same length, but due to posture, it appears that one is longer
than the other. The biggest concern is anatomical, because we can’t really
change that. We can provide a heel lift, we can do some other modifications, but it
kind of is what it is. Whereas, functional differences, a lot of
times, we can use rehab to train those out. Stretch the concave side, strengthen
the convex side, and pull them back into a neutral alignment. Some things we want
to look at here– the tibial plateaus– that’s been in the news recently, at
least this semester. If you’re watching this in subsequent semesters you’ve
probably heard about it in the past. J.J. Watt sustained a tibial plateau fracture. That is sometimes– what’s that issue? When the ACL remains intact, but it actually pulls off of its bony attachment point. Not sure at this point whether or not
that’s what happened with J.J. Watt, but that certainly can happen. Some other
things we look at– the femoral condyles, the adeductor and Gerdy’s tubercle.
There are pictures of all of these in your textbook, so I would encourage you to to look there and be familiar with the anatomy. Surface anatomy at the knee. In our
athletic training program here, we actually have students draw this out on
one another, so that they can navigate their way
around the knee-joint a little bit easier. But, our vasti group and our
rectus femoris comprise the quad. We’ve got our quadricep tendon and our
patellar tendon. Tendon connects bone to bone. That Sartorius longus muscle in the
body– it’s going to insert immediately. We’ve got what are referred to as the
medial patellar placket– we’ll talk about placa syndrome in a little bit, but a lot
of times someone may be concerned that they’ve got a meniscus injury, because
it’s clicking, it’s catching, it’s popping– thinking that it’s fibrocartilage, when
in fact, it is the plica, which is a fold in the joint capsule. And then on the
lateral aspect, we’ve got the IT band. which a lot of you that train or ride
bikes– you may have had issues with IT band friction syndrome in the past. Some
of the things we look at– the medial and lateral collateral ligaments– Lateral and
medial collateral ligaments. The pes anserine– that is the Sartorius, the
gracilis, and the semitendinosus. Those three muscles insert kind of looks
like a duck foot– if you ever get a chance to see a cadaver being dissected
you can see that PES anserine– it really does look like a duck foot, but over that
medial aspect. On the posterior aspect, we’ve got the hamstrings, the membranosus, the tendinosis, and the gastroc, and then over the posterior aspect of
the knee itself, we’ve got the popliteus. Gastroc being distal– it’s not part of
the hamstring group– but the biceps femoris, the tendinosis and membranosus
are the hamstring group, so– I’m sure you’ve heard of the hamstrings. You
should have had anatomy before you got into this class, so you should have
learned where the tendinosis, membranosus and biceps femoris are, but it’s
worth reviewing the textbook. Alright, so– if we identify the fact
that there is fluid accumulation in the knee, it’s really important for us to
differentiate– is it swelling or is it effusion? If it’s within the capsule, it’s
referred to as a fusion. If it’s outside the capsule– extra capsular– then it’s
just swelling or ecchymosis in some– in some terms. That swelling within the
joint– that fluid accumulation within the joint– is caused by synovial fluid
accumulation. If it’s got blood in it, it’s referred to as a hemarthrosis,
okay? Break that word up. “Hema” refers to blood. If you have a hematocrit issue,
then red blood cell count is a problem. “Arthro” always refers to joint, so
“hemarthrosis” basically means blood within the joint. We can do what’s called
a “sweep maneuver,” where we’ll actually kind of wring the fluid out of one side
of the joint capsule, we’ll place our thumbs– so, there’s a link here. I’m not
going to click it, because anytime I have tried to do this in a screencast, it has–
YouTube has flagged it saying it’s a copyright violation, so– if I mouse over
this, you can see there is a YouTube link
[Click on “i” in upper right corner] there. You can just go to YouTube and
type in “sweep maneuver,” and you should be able to see it. A ballotable patella is
another test we can do for this, and basically, what happens here is– our knee
joint is kind of the floor, the patella rides on top, and with a ballotable
patella test, we’re basically just pressing on that patella to see if we
encounter the bony floor. If we do, then that’s a sign we don’t have effusion. If
we don’t, and it feels boggy or otherwise more fluid, then that would be considered
a positive test. So, extracapsular swelling tends to localize– it’ll stay in
one spot, okay? It may eventually, due to gravity, migrate
down the end of the calf, and eventually even into the foot and ankle.
When I had my stress fracture, my calf was actually swollen for a while. It was
a proximal tibial stress fracture, but I ended up with calf swelling. So our
special tests here for knee instability. We’re going to utilize what’s called the
“endpoint” to determine stability. An MRI can be helpful for assessment– with or
without contrast. If we’re doing these stability tests, then we’re looking for
what’s referred to as “knee laxity,” looseness within the knee joint. We’re
also looking for translation– if the tibia translates, then it is moving
relative to those femoral condyles, and as damage to those stabilizing
structures increases, both laxity and translation increase– we end up with a
loose, sloppy knee joint. Okay? So Varus and Valgus– this is not
ideal positioning, he’s basically doing this for the sake of the camera. Hand
position’s correct, but ordinarily I would teach my students– we want to be nice and
tight, so where that hand is stabilizing at the lateral aspect of the patient’s
left knee, I’m gonna put that right up against my belly, and I’m gonna stabilize
their distal ankle right up against my my left side, and I’m basically gonna try
to open that gate, so to speak. So that’s gonna stress the medial collateral
ligament, so this is a valgus stress test– tests the MCL. And then, what I would
typically do if I were actually doing this test, is lift their leg up, set
inside, and actually sit on the table, hold their medial knee up against my
left belly, and the lateral aspect of their ankle up against my right belly,
and try to open with a Varus force. So that is referred to as a Varus test for
LCL. These are both stability tests.
Particularly, the Varus test is going to open a little bit– normally, that’s
totally normal. The question is, how does it open relative to the opposite side,
okay? The position of the knee is important for these tests, so I’ll do
this at full extension, I’ll also do it at 30 degrees of flexion. If I get much
deeper than 30 degrees– and you can try this on a partner, or your roommate, or
somebody– if you flex more than 30 degrees, and you try to apply that Varus
or Valgus force, their hip will start to rotate in and out, so you end up– it feels
like they’ve got a lot of laxity, but, in fact, you’re not actually testing their
knee, you’re just moving them in internal and external rotation at their hip. Okay,
same thing. Anterior drawer tests– there are a couple of cool ones on YouTube where the
patient is actually under general anesthesia before surgery, and they’ll
have a ton of movement, because under general anesthesia, they’re not gonna be
able to guard consciously or unconsciously, okay? So with our interior
drawer tests, we’re gonna position them in flexion– laying down. We’re gonna sit
on their foot, we’re gonna palpate those joint line windows, palpate the
hamstrings around back– we want to make sure their hamstrings aren’t firing,
because that’s going to give us a false negative, and we’re trying to translate
that knee forward anteriorly. So, the reason why this test is really good for
us is because we’ve got a lot of leverage here. The reason why it’s
actually kind of prone to error is because we’ve put their hamstrings in
prime position to fight against this, so– they may guard against this consciously
or unconsciously, and there’s not really a whole lot we can do about that, so
there are better tests for knee stability– that they’re– they’re harder to
perform correctly. The hand positioning is a little less forgiving, but– so this
test is pretty easy on hand positioning, but the downside of it is their hamstrings can fight against you, okay? So our
alternative here is a Lachman drawer test. If you’ve got large hands, this one
is pretty ideal, because in extension, if the hamstrings fire, basically all
they’re going to do is compress that knee joint– they’re not really in
position to prevent that anterior translation, so they don’t have the
leverage to do that. The problem with this is we have to hold their thigh with
one hand, and their calf with another. Six-four. It’s not a problem for me to be
able to do that on most patients unless they’re just– you know, 350. If you’re 100
pounds, 5 foot 2,– chances are your hands are not large enough to be able to do
this with any amount of control, so you may be kind of stuck with the anterior
drawer test as opposed to the Lachman. Now, this is an example of a modified
Lachman’s, where the patient’s distal extremity is isolated between the legs,
but this is another test for ACL, so anterior drawer and Lachman are both ACL
tests, and there’s a YouTube link to this one too– you can just type in “Lachman
drawer test.”
[Click link in upper right corner] For the PCL, we can use that same positioning for the anterior drawer, and instead of trying to pull forward, we actually push backward. This one is
fairly good. The problem with the drawer test for the posterior, is if they are
already lax, they may sag into near-end range already. So if you notice in this
patient– you notice the contour of their knee, and we see how they have kind of
this dip. That tells me that their their tibia is actually already riding
posteriorally. If I try to push that further, there’s really nowhere else for
it to go, so I may get a false negative, because gravity has already pulled them
into in-range position. Now, to kind of combat against that, I can use what’s
called Godfrey’s test, or the posterior sag sign where I elevate them into a 90 degree knee flexion, 90 degree hip flexion position– I can even put them up on a bench, if need be– and I look to see
what’s the contour of that knee look like. This actually doesn’t look too bad.
I’ll compare this bilaterally– they may have some differences, but if I see this
kind of dip or divot distal to the patella, then that’s an example of a
positive test. For the meniscus, I can’t really do a stress test for this.
I basically do a pain provocation or a symptom reproduction test, and this is
probably one of the hardest tests for new clinicians to learn– it’s called the
McMurray’s Meniscal test, and with this test, I’m basically moving the knee
throughout its range, flexion and extension, I’m loading it up in internal
and external rotation, and I’m trying to see if I can reproduce a click, a catch,
or a pop. Fibrocartilage is kind notorious for being prone to clicking, catching, popping– when it is torn, so what I will see here is internal rotation, deep
flexion. Move them passively out into extension– the patient should be
totally relaxed. Another downside of this test is it can be painful, so they’ll
tend to guard against you. Also repeat this test with the tibia externally
rotated, and move through flexion extension. And I’m just looking to see– do
I cause pain? Do I cause clicking, catching, popping? The Plica, as we said,
folds in the joint capsule. Notice they are right superficial to the medial
meniscus, so– they’ll click and they’ll pop, they’re right in the joint line, so a lot
of times, this structure may kind of masquerade as a meniscus tear, when in
fact, it’s not as serious, okay? It’s not really a structural pathology. So there’s
a couple of different tests we can do for this. The plical stutter– we basically
have them extend the knee with light palpation– a couple of fingers over the
patella– and we look to see if that patella tracks smoothly, or whether it’s
stutters– it kind of catches and grabs. With the Houston Plica test, we put them
in supine with their knee flexed to 90, and then we internally rotate their
tibia, passively extend their knee, and glide their patella medially, looking to
see if we can reproduce that pop. Aplay’s Compression test– this is for
meniscus. Kind of a useless test, quite honestly. It’s in your textbook, we still
use it, but the specificity is not very good on this test. if I have a patient
with a meniscal injury, more than likely I’m gonna use the McMurray test– I
probably– I don’t see orthopedic surgeons really use this test at all– they’ll use
them in the McMurray’s test in exclusivity. but basically, we just try to
compress the joint. We’re gonna rotate tibia internally and externally to see
if we’re reproducing pain. It’s not a stability test, it is a pain provocation
test. And then the opposite– we basically take our knee, put it over
their thigh, and we try to distract and internally and externally rotate. This
may be indicative of a capsular injury. Some other things we can look at here–
girth measurements. Here we’re just looking to check bilaterally, and then
we’re looking to trend their girth measurements over time. Take it at the
joint line, the level of the tibial tubercle, and then 2 centimeters above
the superior border of the patella, and then some will also do a mid-thigh, 8 to 10
centimeters above the joint line. We’ll also use the subjective rating– on a scale of one to ten, what’s your pain? 10 being the worst pain you’ve ever felt, one being no pain, or zero being no pain. Alright, some other assessment strategies we might use involve a functional exam, where we assessed walking, running, turning, cutting. This can be completely unorganized, or just kind of spur of the
moment, where we have them jog back and forth on the sideline. Or this can be
highly organized, where we actually do something like a triple hop for distance– where– on one leg, we have them hop as far as they can, we measure that, we compare it to the non-involved side. Some other things we might do are
resistive strength tests, where we assess the function of the muscles across the
knee joint. Another thing we might want to assess is the athlete’s– what’s
referred to as their “Q angle,” and the Q angle is determined by two different
lines– first, a line from the ASIS, the anterior superior iliac spine, usually
round about the belt line, down to the patella– that’s one of the legs of the
angle. And then the second leg of the angle is from the tibial tuberosity to
the patella, and the greater this angle, basically the more varus that patient
has, so we tend to see a greater Q angle in females than males, because their hips
are relatively wider for giving birth. Normal angle for males is around 10
degrees, for females is around 15. If we have a greater than normal Q angle, then the line of [inaudible] the quadriceps starts to become increasingly laterally
directed, so the patella is less likely to move up and down, and it’s more likely
to glide out, which can cause knee pain. The A angle, on the other hand– we use the
line of the tibial tubercle to the patella again, but instead of going
patella to the ASIS, we go inferior pole of the patella to the tibial tubercle.
This is just an alternative that we can use, but more often than not, that Q angle is
gonna be used– much more likely. We can palpate the patella all the way around.
We can actually glide it quite a bit medially, and actually palpate the under surface of the patella. If we get grinding or compression or apprehension
with movement, then that may be an indicator that the patella is at least somewhat involved in the pain that your patient’s feeling.
Now, preventing the injuries really does depend on a number of factors: posture,
muscular strength, coordination, the motor patterning to keep the knee in a
protected position is important. Lots of times we’ll see non-contact knee
injuries and patients that are underdeveloped musculoskeletally, or
neuromuscularly, more specifically. And what happens there is they tend to
land with their knees in more extension, rather than in flexion, and just like we
talked about with the anterior drawer test, if I land in flexion, my hamstrings
can actually fire to prevent the ACL from being loaded or from being loaded
as much, whereas if I land an extension, then I don’t have that primary– that
dynamic restraint of the hamstrings, and it’s pretty much all up to the static
restraints of my ligaments, okay? In an effort to prevent injury, extensibility
of the hamstrings, the– I don’t know why that says “quadpoliceps,” should be
“quadriceps.” And the gastroc is important. So, training the muscles of the joint to
provide that dynamic restraint is really important, okay?
ACL prevention programs are really focused on enhancing that neuromuscular
control. There have been a lot of theories as to why female athletes are
more likely to sustain– on the order of two to one– a non-contact knee injury
than their male counterparts, and there are a lot of reasons– that Q angle
difference is one, the notch width of the distal femur is another, but for us as
clinicians, not a whole lot I can do about those things. The only research that
has shown any kind of alterable risk factor is the tendency for females to
lack the neuromuscular control– the proprioceptive ability, the
strength of their male counterparts. So, there have been a number of studies that have actually looked at this and focused on improving this in female athletes, and
have shown a significant decrease in the likelihood of injury after those
athletes have done that type of training, okay? Another thing we can do to prevent
any injuries is look a shoe type, so the length of the cleat is actually
important, believe it or not. Shoes with shorter cleats don’t allow the foot to
become fixed in the turf– they’re more likely to slip, and on the surface that
sounds bad, but it’s actually not. We’re less likely to send forces up these
lower extremity if our traction is not quite as good. The athlete is also more
likely to keep their center of mass closer to their base of support. They’re
less likely to get out of position if they know they can’t trust the playing
surface– if you’ve ever played on a wet or muddy field, you kind of know what I’m
talking about there. So, while the risks of slips may be greater, the risk of
significant knee injury is actually less with a shorter cleat. We can also utilize
knee braces. There have been a number of studies looking at knee bracing and
whether or not it’s essential. We’ve talked about braces in this class before.
Data is really lacking to support the use of a knee brace to protect the ACL
following surgery. One of the– one of recent changes in years– or, one of the changes we’ve seen in recent years, rather– is where quarterbacks have
started wearing a knee brace on the knee opposite their throwing arm, and the
reason for that– if you think about a quarterback who’s dropping back to pass,
that lead leg– if I’m right handed, my left knee is exposed to all of that, you know,
300 plus pounds or 200 and however many pounds of defensive lineman, and they’re
headed my way. So that the lead leg is far more exposed to potential trauma
than the trail leg. So you’ll see a lot of quarterbacks who have have started even using this preventatively– they haven’t had
a knee injury, but they’re wearing a brace to protect their vulnerable knee from
that risk. Something as simple– this is just an off-the-shelf, strap-on,
collateral knee brace– important for a lot of offensive lineman.
The likelihood of being struck from the outside of algis force– these are used to
protect the MCL. These can be custom molded and designed to control
rotational forces as well, so– if you watch high-level college football, NFL–
you’ll see a lot of the offensive linemen will wear prophylactic knee
braces. Just everybody wears left and right, whether they’ve had an injury or
not. So that leads us to injuries. First is a tibial femoral dislocation.
Now, sometimes people will say, “Oh, I dislocated my knee.” It’s real critical to determine– are we talking about the knee joint itself, or are we talking about the
patella? Both are, certainly, serious injuries, but a tibia femoral dislocation
far more so, because there is a risk for amputation. There’s a risk they will lose
their limb. Depending on the study you look at, anywhere from five to as– almost 60 percent,
where the suggestion is if if a patient dislocates the true knee joint– the
tibia femoral joint– there’s a risk of amputation. If there– and the reason for
that is because we’re disrupting blood flow to the distal extremity. These
oftentimes will reduce on their own, but just because they reduce doesn’t mean
the vascular disruption is fixed. When it dislocated, it potentially damaged the
nerve function to the distal foot, and it also disturbed the blood flow to the
distal foot, so as long as that vascular repair is made within the first eight
hours of injury, the risk, according to studies looking at basically post-hoc
analyses, 10 percent, so, I mean, there’s still a risk. If that vascular repair is made
after eight hours, that risk jumps to 86 percent. More likely than not, that patient’s gonna
lose that limb. Peroneal nerve injury we see in anywhere from 11 to 40% of cases.
We actually had a case of this when I was working at UTEP– non-contact drill,
our defensive back over-strided during a a simple past protection– I’m sorry, a
defensive drill against receivers, and he over-strided, dislocated. It’s like the
first or second day of fall camp. He had to be airlifted back to El Paso, he had
surgery right away. He had a– he never lost, never had a compromise in the pulse,
but he did lose neurologic function, so he ended up with a foot drop, he ended up
with some pretty significant atrophy, and after months and months of
rehabilitation, he had surgery, obviously. But after months and months of
rehabilitation, he was finally able to walk again without a brace– he never
played again. A third of these cases will recover completely. Another study indicated that up to half
would have a permanent complete deficit, which means the remaining little portion
there would have a– a permanent minimal deficit. So you see why this is such a big deal in the case of a posterior
dislocation– we got that popliteal artery, our peroneal nerve– we see the branch
here, and when it moves out of position, we’re actually stretching it beyond its
normal amount of movement. Now, we know that the the nerves, arteries and the
veins do move somewhat, but they don’t– they’re usually tethered and held in
position enough that a location like this can disrupt their
function significantly. Now, in the case of the football player I’m talking about,
he had what’s referred to as a “taffy injury,” or a stretch injury to his perennial nerve.
If you think about– like a big stick of Laffy Taffy. This only works in
the summer, when it’s warm. If it’s cold, it doesn’t work. But if you take
that taffy and you pull it when it’s warm, what happens? It thins out in the
middle. It doesn’t necessarily break unless you keep stretching it, but it
will definitely thin out in the middle, and that’s what happened his perennial
nerve. When it was stretched, it was traumatized and it didn’t rupture, but it
did stretch, and it was injured. Now, MCL sprains are more likely than LCL sprains, just simply because– kind of like we talked about with the quarterback, the
lateral aspect of the knee is far more likely to sustain an impact, okay? The– in
order for a defender to deliver a varus force– would mean they have to cut all
the way across the body, miss this leg, and hit the in– the outside leg, okay? So,
medial collateral ligaments are more likely. We grade these just like we do
any sprain or strain– grade one through three. With a grade one, there’s little to
no macroscopic trauma. Usually they’ll be pretty stable on a valgus test. Little to
no effusion, and relatively normal range of motion– these just kind of hurt, but
they’re not terribly unstable. Crutches if necessary on these. Here you see that
laterally-developed delivered force– that valgus force– results in the tearing or
injury of the medial collateral, okay? Grade one, usually they’ll recover from
this in a couple of weeks– three– three weeks at the most.
With more severe MCL sprains, this becomes a question of whether or
not this is going to be handled surgically or not. Lots of times, these
will scar down appropriately, and won’t lead to long-term
disability. With a grade 2, they’ve got a partial tear, so what we see here would
actually be indicative of a grade two sprain, not a grade one.
No gross instability, but some laxity as we valgus test them. They may have some
swelling, maybe even a light effusion. That MCL is actually a thickening of the
joint capsule, so– it can swell inside the joint, or out. They’ll have pain along
that medial joint line. We want to protect, optimally load– ice, compression,
elevation for the first two or three days. Crutch use until that acute phase resolves. They may do modalities for pain
control. We’ll start them out with just quad exercises. We know that effusion of
any sort will start to shut down the quads, and that’s the last thing we want–
we want those dynamic stabilizers to remain online and ready to go. Then we
progress them to closed kinetic chain exercises and functional activities. With
a grade three, this is a complete tear. Minimum to moderate swelling– just can’t
necessarily depend on swelling or effusion to tell you the grade of the
sprain. This is really dependent on the athlete to determine how we’re going to
manage this. Even with a grade three sprain, we may choose to handle this
conservatively– just let it scar down. Some of the exceptions to that– if they
are a very elusive athlete, lots of lateral movement– then surgery may be the
way to go we’ve seen this in runningbacks, wide receivers, skill position
players– they’re likely surgical candidates. Baseball, volleyball– same
thing. Whereas, if they’re a cross-country runner– not so much cross country– a
distance runner, they might be able to get away with
conservative management. Rehab’s gonna be similar to a grade one or grade two, it’s
just gonna take longer, okay? With a LCL sprain, we don’t see these as often
because varus force is harder to get in athletics. Usually, the tibia is going
to be internally-rotated. More often than not this is going to be a non-contact
varus force where they step awkwardly. That’s why I kind of back cut a little
bit on cross-country– because of the rough terrain, they can encounter a varus
or valgus load fairly regularly. They’re usually gonna have pain and tenderness
over the LCL, swelling and effusion, joint laxity with varus testing. They may also
get some perennial nerve involvement that’s going to impair their ability to
actively dorsiflex. We’re gonna basically manage this much the same as the MCL,
depending on the severity. Not a tremendous difference there. Where we do see differences with the cruciates[?], okay? 75% of ACL injuries are
non-contact, so, this is not often a result from a collision with an opponent,
something like that. Females are at least twice as likely, and some studies would
say as high as eight times more likely to sustain a non-contact ACL injury as
their male counterparts, and we’ve already talked about some of the reasons
for that. There’s lots of research that has been done here to look at– why the
difference between males and females, but as we said, it’s that neuromuscular
component that’s trainable. That’s really the only way I can intervene. Frankly, I
don’t care what the intercondylar notch width or femoral notch width is in my
patient– I can’t change that. I can’t change the size of their ACL. I can’t
directly impact their Q angle to a tremendous degree, but I can improve
their biomechanics, okay? So, their conditioning, their motor
skill– those kinds of things– that’s what I’m after.
So, my injury prevention programming for this consists of a lot of jumps, consists
of hops, single-leg work, but with good form, okay? So, it’s actually kind of rare
that the ACL is going to occur in isolation. Usually, if they’ve got an ACL,
they’ve probably also got a meniscus tear, potentially a joint capsule injury, and
an MCL, in many cases– kind of the unhappy triad. Lots of times, they’ll describe an
immediate pop with severe pain and disability. They’ll have swelling at the joint line, and effusion that follows. Positive
anterior drawer test, positive Lachman’s test. Other ACL tests may also be
positive, but we didn’t really go over any other than the anterior drawer and
the Lachman’s, but there are others that you can see in your textbook. Tore
my ACL in high school– it was due to a hyperextension injury, non-contact, and it– it really didn’t hurt when it happened. I actually continued to play. Didn’t really
notice it till later that night, when it started to stiffen up on me, and that’s
pretty typical. I didn’t know it then, but I know it now. More often than not, this
is going to be a surgery. The only time it wouldn’t be a surgery is maybe if
they’re [an] older patient, sedentary. The problem with ACL injury is the rotary
component– the rotary stability can lead to chronic joint irritation, arthritis.
It’s just not going to heal, it’s not gonna get better, okay? Usually, this is
going to be– if they’ve done– gone the surgical route, we’re looking at six
months, maybe seven in some cases. They may do this outpatient. Historically,
they’ve done this inpatient, but we’ve kind of got into a time where the likelihood
of that has actually gone down quite a bit. They may be in a brace or a long leg
immobilizer, and there are some options as far as where they’re gonna source
the raw material, so to speak, for that graft. Bone, tendon, bone, out of the
patellar tendon. Hamstring tendon, cadaver graph, there are a lot of different options here. PCL sprains– we see this from a direct blow. You see an
example here of a patient suffering a hyperextension trauma, but, actually a lot
of times, it’s not from a direct blow like this,
it’s from landing on a flexed knee, and we get that same posteriorally-directed
force. One of the reasons this is referred to as a “dashboard tear”– we’re
sitting in a flexed position, come to a sudden stop due to an automobile
accident, and that tibia is forced posteriorally, femur’s still
moving forward, and we end up with a PCL. We feel a pop in the back of the knee,
tenderness, and a little swelling. They may have some laxity, and they may have a
sag sign, okay? These can actually be managed non-surgically as well.
Surgery will require up to six weeks of immobilization, but then we’re looking at
four to even six months of rehab after the fact. So here you see that mechanism–
flexed knee. Same holds true– it doesn’t have to be the dashboard. I’ve seen this occur
and basketball and volleyball players who have gotten crossed up or tangled up with– in case of basketball, an opponent. In the case of volleyball, maybe they just
tripped, or stubbed their toe, and they land forcefully on the hardwood with
that flexed knee, and suffered that– that same injury. Okay, with meniscal
lesions, this is fibrocartilage in the knee, shock absorbers of the knee. We can have
an injury to them isolated, but lots of times, we’ll have other things going on. If the patient’s presentation doesn’t
really add up or make sense, think meniscus. This is actually what I thought I had when I had my stress fracture, because I
can tell you precisely where I was when I first noticed the pain, and I have a
history of meniscus tear. My ACL also resulted in a meniscus tear.
So, I was thinking meniscus, and usually, it’s really just a question of, “can you
push through it?” So, if it’s an overuse condition, I know– do less, okay? If
it’s meniscus, it’s– “do what you can do, “and if it hurts too much, stop doing it.
If it doesn’t hurt too much, keep going.” So, I actually kind of ran myself into a more severe stress fracture, because I
misdiagnosed it as a meniscus, but usually, the symptoms are gonna be
clicking and popping, which I had. Effusion. You get a big, fat, swollen knee,
developing over a three to four day period. Usually pain with a deep squat. So,
I had all these symptoms, okay? So it– honestly, it didn’t make sense that it
was a stress reaction. So here we see the menisci can be injured in a couple of
ways– that’s one of the reasons why you’ll see– people talk about, you know,
“a catcher has bad knees”– it’s because they’re in this deep-squat position for an extended
period of time, for years of their career, and this can result in a cincher
tear, whereas if it’s a cutting mechanism, it’s the condyles of the femur that are
actually– kind of pinching the structure, and tearing it. If the knee isn’t locked,
but the indications of a tear are there, then we may need some further diagnostic
testing. If they are locking, it may be necessary to do this under anesthesia. Menisectomies are actually pretty
straightforward procedures if we’ve got a meniscus tear. Basically, the physician
will just go in and try to clean out as little as possible. We don’t want any
clicking or catching, but we don’t want to remove this. Decades ago, they would
go in and just cut the whole thing out. My dad had this– had a motorcycle accident, and he had a complete menisectomy. Solved the problem in the short-term, but in the long-term,
guess what happened? Take the shock absorbers out, you get bone-on-bone wear
over time, so he’s now got a knee replacement. So they don’t cut out the menisci in their entirety anymore, they cut out as little as possible to
prevent the symptoms, but provide some relief, okay? Now, an alternative is a meniscus
repair. That’s a different surgery altogether. If I have a menisectomy, I
can be back in as little as two weeks. I’ve seen football players return to
play seven days post-op, six days post-op, actually, in one case. Whereas with the
meniscus repair, we can’t return to play nearly as quickly, so instead of cutting
this thing out, they’ll actually go in and suture it up, and hope that it heals.
Now, some meniscus tears are more responsive to a repair than others. It just
really depends on how much vascularity there is– how much blood flow there is in
that area, but that repaired meniscus may take upwards of three months, okay?
So, the long-term outcome, no question– the repair is going to be better. Short-term–
it may be the difference between a player returning to play that season, and
being done for the year, so– lots of things to weigh. This was
actually a criticism, not long ago, of Derrick Rose. He injured his meniscus, he
opted for the repair over the menisectomy, and a lot of people questioned that, you know? “Hey, this guy’s not tough. He’s more concerned about his career than he is about helping his team.” and I’m not saying whether that was right or wrong. I know in my career, athletes have been pressured away– by team physicians and
coaches alike– from the repair, but, are they more likely to have problems down
the road with the repair? No, they’re gonna have a better outcome with the repair. it’s just gonna take them longer to get
there. Alright, with the plica, you can kind of think about these like pleats– we
don’t see pleated pants much anymore. Look at– Google some pictures from the
80s of dress pants, and you’ll see plenty of pleated pants, pleated skirts. You can
think of these plica as pleats in the joint capsule, and what happens is those
pleats actually kind of stick together and we get localized inflammation.
Generally, that’s on the medial side. They’ve usually got a history of knee
pain and injury. They’ve got some painful– I call it “pseudo-locking,” because there’s
not actually anything in the joint– it’s pain that that is inhibiting motion. So
if you look at these signs and symptoms, they all look a lot like meniscus. The
only difference is usually, with meniscus, we’ve got a mechanism, okay? So if they’ve
got no mechanism and these symptoms– in particular, if it’s medial, then I can’t
necessarily rule plica out. Treatment for plica is much different than
meniscus, though. These can be injected with a corticosteroid, we can treat this
with anti-inflammatories, and usually these will resolve. If not, then surgery
can be done relatively easily. Alright, we’re getting there. Osteochondral knee fractures– next up on the list. Same mechanism as a collateral or cruciate
ligament, or meniscal injury. A twist, or a sudden cut, or direct blow. Lots of times,
they’ll describe a sensation of giving way– hearing a snap. This can only be
confirmed through– usually, through an X-ray. This injury will require
surgery to replace that fragment, to avoid joint degeneration and arthritis.
Related to that– a Osteochondritus Dissecans is basically a loose body.
This is fibrocartilage instead of hyaline cartilage. Here we get that articular cartilage and
maybe a little chunk of subchondral bone that breaks free and makes its way into
the joint space. Sometimes, this can be due to trauma, but sometimes it just
starts, okay? And we basically get this degenerative condition. Lots of times,
they’ll have aching pain– there’s that “quadraPOLICE” again. I think it should be–
I did a find and replace for “RICE,” and it changed a couple of “RICE”s and
quadriceps– I apologize for that. Atrophy and point tenderness– arrests and
immobilization for children, lots of times because they are skeletally
immature. This will resolve on its own. In older patients, this may be a
surgical case. Okay? And related to that– any type of loose body, whether it’s OCD or
something else. This can be a result of fragments of the menisci, chunks of
synovial tissue, part of the cruciate can be– really any number of things. These can
become lodged in the joint space, resulting in a lock or a pop. If these
aren’t surgically removed, they can lead to chronic degeneration. Joint contusions–
relatively minor, so we’re kind of making our way away from the the more surgical
cases, and into things that are more conservatively managed. Here, usually
we’ll get a blow to the vastus medialis– one of the quadricep’s muscles. We may be
concerned if this is a sprain– whether or not this is something more severe They’re
usually gonna have tenderness, swelling, discoloration. This may actually involve
the capsule, depending on what struck the patient. If swelling doesn’t resolve
within a week, they may have a more severe condition– it may be a synovitis– the joint capsule itself is inflamed, or the bursitis may be inflamed,
requiring more rest or an alteration of treatment. With peroneal nerve contusion,
this can be a little unsettling for the patient,
because they start to lose muscular function. But, the the fact is, this can
oftentimes be a very temporary set of symptoms and signs. Local pain, they may
have some shooting pain. Added pressure may make this worse, so if they try to
tighten their brace, or– even tightening their shoes. Usually it’s not shoes
because it’s gonna be more at the knee joint. This will usually resolve pretty
quickly. If it doesn’t, it could result in foot drop, because they’re gonna lose
some of the ability of their tibialis anterior to function. We may need to pad
that fibular head for a few weeks, just to protect them against re-injury
Bursitis– talked about this elsewhere in the body, and we will definitely talk
about it more as we make our way toward the shoulder, for instance. Here we get
acute, chronic, or recurrent swelling. They can have a bursitis this would be a pre-patellar bursitis– it’s right in front of the knee. So even though their knee looks
huge, it’s not effusion, it’s not a joint capsule problem– it’s tissue
anterior to the knee or superficial to the knee. We have to figure out what
caused this. Something like this was probably a traumatic pre-patellar
bursitis– they landed on on their knee, or they took a direct blow to the knee, and
it swelled up like this. If it’s non-traumatic, then we got to figure out
what’s causing it, okay? these can be aspirated and injected.
That’ll calm them down and treat them pretty readily. And then you notice the
Ace bandage here. Once it’s been drained and injected, we’re gonna wrap it to
prevent it from swelling back up. Patella fracture– these aren’t terribly common,
but they are debilitating. This can be the result of a direct blow. These can
also be indirect, where a forceful quad contraction and a patella that maybe is a little– I want to say “diseased,” but– is not
completely healthy, has had some problems with anterior knee pain. You can actually
pull it apart. Indirect fractures like that can cause the capsule to tear, they
can cause separation of the bone fragments and quad-tendon tearing.
There’s that “POLICE” again, I apologize. This may or may not result in a– here
we see this, you know, massive defect. It may not be that severe. You may want to
splint this if the fracture suspected– basically, we’ll treat it like a fracture
until an X-ray tells us otherwise. This may need to be immobilized for upwards
of three months. Okay, patellar dislocation. Here we see–
you know, that laterally-directed force from a high Q angle may result in a
laterally deviated patella. Dislocation is usually going to result in a total
loss of function. Patellar dislocation is not the same as a tibial femoral
dislocation. We already said, the risk of amputation can run as high as in the 80
percentile– 80% if we don’t get the vascular compromise dealt with soon. No
risk of amputation with a patellar dislocation, but it does results in a
total loss of function. No question, it’s terribly painful, and it’s gonna take
some time for them to recover. So once it’s been reduced, they’re gonna be
immobilized for about a month. Put on crutches. Start with isometric
exercises just to maintain the muscle. After that, we may put them in a brace–
some sort of pad that helps keep that patella in position. We may need a
surgery to release the tight lateral structures, help them track more
immediately, and we want to do things to improve their posture and their
biomechanics. Injury to the Infrapatellar fat pad is kind of common. It can be
wedged between the tibia and patella. Direct blow can cause this. Can be
worsened with chronic kneeling pressure, or trauma to the structure. They’re gonna
have pain, but it’s going to be mostly superficial– it’s going to be just below
the patellar ligament. They may be weak, and that’s because of the pain– they’re
getting some inhibition there. We wanna figure out what’s causing it, stop what’s
causing it, use ice to minimize the inflammation. During extension, we may
want to use a heel lift, because full extension actually further compresses
that infrapatellar fat pad, so we want to avoid that. And then our knee
hyperextension taping will keep them out of that extended position too, until this
can calm down. Chrondro– Chrondromalacia patella. This is
the cracking and popping you will hear probably in your parents, grandparents.
The underside of the patella will start to soften and deteriorate over time.
Abnormal tracking will make this worse, but age causes it, regardless of whether
or not the tracking is good. I’ve had this since I was in college, and it
definitely isn’t getting any better. Another reason why the stress fracture
diagnosis didn’t make sense initially, I thought it was probably my Chrondro
flaring up. As it continued, I thought it was meniscus, but it turned out it was
actually something quite different, okay? With surgical possibilities, usually
we’ll try to manage this conservatively as long as we can with activity
modification, and usually we can keep it under control that way. If it gets too
severe– it starts really cutting into training time– then a physician will go in, actually drill into the patella until it bleeds. There’s some other
things we can do for chondromalacia patella surgically, but
none of them are definitively better than the others.
Okay, patella femoral stress syndrome. This is kind of loosely-characterized,
anterior knee pain. We’ll get lateral deviation of the patella, tracking in
that groove. We’ll have some of the symptoms of Chrondro. We’ll have some of the
symptoms of even– maybe even Plical syndrome, some some medial pain. They’ll
have this kind of dull ache in the center of the knee. The more they
compress the patella, the worse it hurts, so deep squats are not something they
really like. When we force that patella laterally, they don’t like that either.
McConnell taping can be beneficial for this, because it helps address that
tracking. If those conservative measures fail, they’ll do what’s called a “lateral
retinacular release,” and this basically freeze that patella so that it can track
centrally, instead of going out laterally. Just a couple other conditions here.
Ssgood-Schlatter’s is basically an irritation of the tibial tubercle.
Sinding Larsen-Johansson, or “Larsen-Johansson” in your textbook. Disease is kind of the same thing, but instead of the tibial tubercle, it’s the inferior
pole of the patella. And what happens here is we end up with attraction
apophysitis. In other words, the soft tissue is actually good. It’s maybe
even, you know, completely healthy, but it’s being put under tension.
We’ll see this oftentimes in in the case of a growth spurt, where the long
bones are essentially stretching the soft tissue structures because the rate
of growth in the long bones is exceeding the rate of growth in the soft tissue. So
we end up with traction across these structures. Now, you usually won’t see
this concurrently, so this picture– this guy’s in– or this person is in really bad
shape, because they’ve got both going on– usually it’s gonna be one or the other.
This diagram is just showing you where these two conditions manifest,
okay? So– far more commonly you’ll see Osgood-Schlatter’s disease. If you’ve had a
big growth spurt, you’ve probably got a big prominent tibial tubercle, and what
happened there is– and it’s usually opposite your dominant hand, so I’m
right-handed, I have a big prominent left tibial tubercle, because that’s the leg I
tend to jump off of due to handedness patterns. If you’re throwing,
you’re pushing off that left leg, so, due to to your dominance patterns, one
leg is probably more likely to have this than the other, but it can’t happen
bilaterally. So we end up with tenderness, swelling, and degeneration at that
attachment point. Your body will start to chase this injury with bone– that’s the
reason you’ll end up with that big, boney tibial tubercle, okay? Something like this. Because the
soft tissue is kind of stretched taut, and now we’ve got a bony prominence, the–
the patient isn’t gonna like to kneel. Running and jumping or gonna cause
problems for different reasons, but they’re still gonna be problematic. This
will usually kind of come and go on its own if we can modify activity
appropriately. Okay, couple more slides and we’re done. Patellar tendonitis–
“jumper’s knee,” or “kicker’s knee.” You may have seen these straps before. Some
people will use prewrap several laps, and then they roll it up. Basically, all
that does is spread the tension across the structure to a greater extent than
if they don’t have it. Three phases of this tendonitis condition. Pain after
activity, pain during and after, and pain during and after and possibly even
constant. If it’s just during, or after, rather, usually we can modify that
activity and it’ll go away, but the problem with this is, lots of times, the
athlete can’t afford to stop doing it. They’re a high jumper, they need to jump.
They’re a cyclist they need to to put in reps. So, something like this is basically just symptomatic relief– it’s not going to
solve the problem, so we need to figure out what’s causing it,
address the mechanical issues if there are any. Okay,
patellar tendon rupture. Here you see that patellar tendon has ruptured, so the
patella, as a result, it’s on tension. It migrates superiorly. We kind of talked
about how that happens with Achilles tendon already. How it’s on tension, if
it’s if it’s suddenly ruptured, then it’s like a rubber band. If I stretched a
rubber band and snapped it, it ends would recoil, that’s essentially what’s
happening here. In the case of a patellar tendon rupture, they’re gonna have a
palpable defect. They’re not going to be able to forcefully extend the knee. Lots of
pain, lots of swelling– not effusion– and initial pain. This is a surgical
case. If we manage jumper’s knee appropriately, we can minimize a chance
of this occurring, because the problem with tendinitis is improperly managed
tendinitis turns into tendinosis, and tendinosis is degradation of tissue, so
we end up with a diseased patellar tendon– it’s way more likely to
actually tear and rupture. If they’re using steroids of any sort, then intense
knee should be avoided due to the weakening of collagen. And that doesn’t
just mean anabolic steroids, maybe they’ve had a high-dose steroid due to a– a medical condition, okay? In the case of MS,
a lot of MS patients will take high-dose steroids. In the case of a patient that’s
had a chronic inflammation, they might take some longer medrol– dose pack a high-dosage, short-term steroid. But during those times, we want to protect the the
collagen by not loading it heavily. Alright, last one.
Runner’s knee, or cyclist’s knee. This could be at the IT band it could be at the Pes
anserine, but basically that repetitive flexion and extension causes a friction
problem as those structures cross over either the lateral condyle, in the case
of ITB and friction syndrome, or the medial condyle in the case of Pes
anserine– the irritation. So the key here is to correct those malalignments. We
can treat this symptomatically with ice before and after, a proper warm-up and
stretching, but, the mobility is going to be the key here, so foam rolling
aggressive static stretching– can be a real salvation here. We can also
adjust the saddle height if they are, truly, a cyclist. If it’s a runner, we
might want to look at their footwear. We might want to look at the surface that
they’re running on and see if we might be able to make things better there. Alright, well that’s it for knee. Next up, we’ve got the thigh, hip, groin and pelvis. So, we
are making our way up the body, so stay tuned. We’re getting close. I think
we got a total of five more lessons, and we will be ready for the final, so hang
in there. Dr. Brooks signing out.

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