The consequent pain and restricted knee motion may lead to a cascade of events which include quadriceps atrophy and weakness, patellar tendon adaptive shortening, and scarring in the tissues around the patella - with an end result of permanent patella infera - where the patella is pulled down into an abnormal position and becomes likely to incur damage to the articular cartilage. In severe cases of arthrofibrosis, the disorder becomes progressive and the whole capsule may become thickened and tight with almost no movement possible in the joint.
Despite this potentially disastrous cascade of events, patients with developing arthrofibrosis and early patella infera may avoid the necessity for surgical intervention by participating in a closely supervised therapy programme. In other cases, surgical excision of the excessive scar tissues followed by a specific in-patient physical therapy program can be successful in regaining significant motion. The key is early recognition and referral to a unit experienced in dealing with arthrofibrosis.
In this course I will try and help delegates understand the precipitating causes, the danger signals, and the early and late management of this potentially disastrous disorder.
When discussing arthrofibrosis, it is useful to refer to the grading system established by Donald Shelbourne. He categorised arthrofibrosis into four types (ref 1):
· Type 1 - < 10 degree extension loss and normal flexion
· Type 2 - > 10 degree extension loss and normal flexion
· Type 3 - > 10 degree extension loss and > 25 degree flexion loss with a tight patella
· Type 4 - > 10 degree extension loss, 30 degrees or more flexion loss, and patella infera with marked patellar tightness
Thus failure to re-establish full range of motion (ROM) after a routine programme of rehabilitation is a key indicator of arthrofibrosis. One must remember, however, that loss of ROM of motion on its own does not mean that arthrofibrosis is necessarily the cause. There may be a different mechanical problem preventing full movement within the knee, for example an unrecognised bucket-handle tear of the meniscus or anterior cruciate ligament graft placed in an improper position in the joint.
In arthrofibrosis the ROM loss is due to disordered healing -
· adhesions stretching across the joint spaces maturing into fibrous tissue
· this fibrous tissue slowly contracting to pull these spaces closed
· the fibrous tissue thickening the joint capsule and slowly contracting to tighten it up.
The loss of range of motion is secondary to this fibrous over-response. As we progress through this course, I will explain to you the set of symptoms and signs which make one suspicious that the cause of a limited ROM is indeed arthrofibrosis and not something else.
Certain conditions tend to make the knee vulnerable to arthrofibrosis -
· the original injury itself - for example a fracture near the joint, injury complicated by haemarthrosis, multiple ligament injury (especially if both ACL and PCL are torn), dislocation of the knee, infection, inflammation (synovitis), associated meniscal tears, disruption of the extensor mechanism (tibial tubercle avulsion, quadriceps rupture, patellar tendon rupture, patellar fracture).
· the treatment - for example arthroplasty, anterior cruciate ligament graft too tight or poorly positioned, poor timing of graft procedure, high tibial osteotomy, prolonged immobilisation in a cast
· post-op complications - for example post-op haemarthrosis (eg after lateral release), inflammation, synovitis, infection, RSD
· the rehabilitation - for example prolonged immobilisation, poor rehabilitation programme, poor adherence to rehabilitation
Arthrofibrosis triggered by such conditions is referred to as secondary arthrofibrosis, as the scarring is a local phenomenon and not part of a generalised healing disorder. However, arthrofibrosis can also be triggered without these predisposing conditions in patients who have a general problem with scar tissue biology, and who tend normally to produce excessive scar tissue in response to any injury or surgery anywhere in the body. In these cases, the arthrofibrosis is termed primary arthrofibrosis. The cause of primary arthrofibrosis is not yet known, but the current assumption is that it is genetically-determined. Investigators are currently studying patients with primary arthrofibrosis to determine if they can identify the guilty gene or genes (eg ref 2). Of course, a person with the primary predisposition may be unfortunate enough to suffer also from one of the high risk conditions.
The incidence of arthrofibrosis is fortunately decreasing as clinicians become better at understanding and preventing the full-blown disorder. A survey of the medical literature published over the last twenty years provides us with some idea of the current size of the problem, in at least some of the conditions I have mentioned.
A review of the literature suggests that stiffness after total knee replacement occurs in about 1% of cases (ref 3).
Arthrofibrosis is the most common complication of ACL reconstruction (ref 4). In the 1980's, ACL reconstruction was associated with incidences of arthrofibrosis of approximately 19%, and in some studies was reported to be as high as 35% (ref 5). The loss of motion from the arthrofibrosis was often more disabling than the original instability for which the surgery had been performed. Currently, with improved understanding and changes in surgical timing and technique and rehabilitation, the incidence for this procedure is less than 10%. In our Center, a focus on immediate knee motion and early management of extension and flexion limitations after ACL reconstruction has shown our rate to be less than 1% in major studies conducted on over 600 patients (refs 6-8).
Many early publications reported an unacceptably high incidence of arthrofibrosis after high tibial osteotomy. Windsor and colleagues, for example, in 1988 reported that 80% of their patients developed patella infera following closing wedge high tibial osteotomy with cast immobilisation. Some ten years later Westrich and colleagues were able to show greatly reduced incidences when patients were mobilised early, without a prolonged period in a cast. In our experience, immediate knee motion begun the day following either closing or opening wedge osteotomy has resulted in a 0% incidence of arthrofibrosis (refs 9-11).
It is not easy to determine the incidence of arthrofibrosis triggered purely by immobilisation, as a plaster cast is usually applied in association with another problem, which may in itself be a trigger, eg patellar fracture. Suffice it to say that the trend in knee surgery is to minimise immobilisation to avoid arthrofibrosis.
What is a normal range of motion?
The range of motion (ROM) of a knee is that range (in degrees) from full extension to full flexion.
Take a look at the full flexion and extension of these three healthy university students. You can easily see the amount of variation between them. Note that the middle one is a woman, the outer two are men.
A straight leg is at 0 degrees. A flexed knee is at about 140 degrees. It is a common misconception that 0-140 degrees is a normal range of motion, but most people have some hyperextension, too, taking their ROM into negative numbers.
· normal ROM is usually minus 5 to 143 degrees in women
· normal ROM is usually minus 6 to 140 degrees in men.
Range of motion of the affected knee also needs to be compared to its partner before one can make a judgement on loss of range of motion. Look again at the three NORMAL individuals in the photographs above. There is a wide variabilty between the ROM of the three individuals, but one would find that there would generally be very little difference between the ROM of the two knees of each individual.
You cannot get by with a ten-degree loss of normal knee extension, as this will result in a limp, shortening, and patellofemoral arthrosis.
You use your knee in normal walking from two degrees of flexion to seventy degrees of flexion. That range of motion is what you need to just walk up and down stairs and have a normal gait. If you walk with your knee in ten degrees of flexion (you have lost only eight degrees from the straight position), you will have a limp which can throw off your back because you have a shorter leg. Your limping gait will be very noticeable, not only to yourself, but to other people as well. The most important problem with a loss of flexion and poor gait is that high pressures are placed upon the patellofemoral (kneecap) joint which, over time, will result in damage to the articular cartilage (patellofemoral arthrosis).
Studies of the range of knee motion required for activities of daily living reveal further that -
· 93 degrees of knee flexion is required for rising from a seated position (ref 1)
· 106 degrees of knee flexion is required for shoelace tying (ref 1)
· 135 degrees of flexion is required to properly take a bath (ref 2)
A person can get by with a loss of two to five degrees, where they may not even notice the difference. Obviously, we like zero degrees of difference between knees, or actually less than zero. A normal knee has at least three degrees less than zero (3 degrees of hyperextension), and that is what we really like to see achieved after a knee injury or operation.
A difficult situation arises in patients who have a loss of extension of between five and ten degrees. We notice, even at seven to eight degrees, that the patient will say "I've got a limp and I don't like this". So we do everything possible in all of our patients to regain full knee motion. If I have a patient who lacks only five degrees from full extension, I am not happy with them.
Any loss of extension is a problem. In the last few degrees of extension, something called the 'knee-lock' or 'screw-home' mechanism occurs, and the leg is able to support the body weight despite the quads being completely relaxed. This lock-back or screw-home cannot properly occur if there is an extension lag, that is, if the last few degrees of extension are missing. The quads - and the hamstrings, too - are put under enormous strain. The body has to rely on muscle and ligament considerably more for support and stability, resulting in fatigue, biomechanical problems, pain and increased risk of injury or re-injury.
Screw-home Mechanism
The two rounded ends (condyles) of the femur do not have the same radius - the medial one has to turn through a longer distance than the lateral one. After the lateral condyle has completed its excursion, the medial one continues a bit longer - a process known as 'screwing-home'.
In this final phase of extension (as the knee goes into its final few habitual degrees of extension or hyperextension) the anterior cruciate ligaments are taut and so are both collaterals, and the knee is in its maximally stable position, with the leg able to support the body weight despite the quads muscles being completely relaxed.
So the important principle to remember is that this lock-back or screw-home cannot properly occur if the knee cannot fully extend.
The classification of Shelbourne (see Part 1) is important because it defines how much knee flexion and extension has been lost. It is also useful because it identifies two major categories 'III and IV' where a very significant loss of knee motion exists.
There is a second classification system which is really the basis of all of arthrofibrosis, and that is the anatomic classification. This system identifies where the scar tissue has developed, which is what needs to be surgically addressed. I believe this anatomic classification is the most important. In some patients, the scar tissue only develops in limited areas while in others, it is present throughout the entire knee joint.
I have taught many surgeons and physical therapists about arthrofibrosis, and I always start from the anatomic basis. While anatomy is difficult to learn, it is the key to the whole understanding of the diagnosis and treatment of arthrofibrosis. I plan on always educating health professionals in that area.
First, I will provide you with an overview of general anatomy so that we have a common starting point. Then I will discuss the anatomy as it directly relates to arthrofibrosis.
There are two separate areas of bony articulation in the knee -
· the articulation (joint) between the femur and tibia bones (tibio-femoral joint)
· the articulation between the patella and femur bones (patello-femoral joint)
Both can be involved in the arthrofibrotic process.
The patella is particularly important as it is housed within the tendon of the quadriceps muscle. It can be pulled downwards if there is scarring and contraction of the structures below it, thus destroying the normal mechanics of the patellofemoral joint and the entire extensor mechanism.
The term 'extensor mechanism' implies the unbroken chain of anatomical structures which cause the leg to extend -
· the quadriceps muscle group, stretching from the pelvis down to the tibia bone
· the tendon above the patella (quadriceps tendon)
· the patella itself within the tendon
· the tendon below the patella (patellar tendon or patellar ligament)
· the tibial tubercle where the tendon attaches to the tibia (the bony bump below the patella)
The whole of this chain can be affected by the arthrofibrosis process.
The fat pad under the patella is critically important regarding the subject of arthrofibrosis.
Note the relationship of the fat pad to the patellar tendon, and hence the extensor mechanism. It fills the space from the patellar tendon all of the way to the cruciate ligaments. In fact, it also extends sideways, making the bulge that one can often see in a normal knee on either side of the patella (red arrow). Normally the fat pad is not attached to either the meniscus or the patella, and is separated from the patellar tendon by the deep infrapatellar bursa.
With arthrofibrosis fat pad the fat pad becomes thickened and fibrosed, and the deep infrapatellar bursa can be obliterated. The fat pad can become adherent to the anterior horn of the meniscus and to the patella, and via the obliteration of the deep infrapatellar bursa it becomes adherent to the patellar tendon also. This thickened fat pad may also become tethered to the intercondylar notch where the cruciate lies.
Note also from the MRI that the fat pad is truly in contact with the bony lower edge of the patella. If that fat pad is scarred and contracted, can you imagine how it can pull the patella downward?
The cruciate ligaments, by their complex position of the knee, anchor the femur to the tibia. Superimpose in your mind eye the photograph above upon this illustration of the intercondylar notch and the cruciate ligaments. Imagine how the fat pad tucks into the femoral notch, and how easily it and the cruciates can both be involved in the arthrofibrotic scarring process.
The two menisci can also be seen in the illustration, which are located between the tibia and femur. They are held in position around their outer edges by the coronary ligaments, which attach them to the tibia.
Both the cruciate and coronary ligaments may become involved in arthrofibrosis.
Now that we have some common anatomical terminology, I will try to illustrate for you those structures which are most influential in the early progression of arthrofibrosis - the soft tissue spaces.
The soft tissue spaces become directly involved in the production of fibrous scar tissue, and this may include the following -
Starting from the top of the knee joint, the first soft tissue space I want to discuss is the suprapatellar pouch. This is the fold of the normal joint space which creates a pouch above the kneecap.
On the left, the inset MRI scan shows the extent of the suprapatellar pouch (yellow). In the large image, it shows up as white. Note how far this pouch extends above the patella. The fat pad is touching the patella and anterior part of the meniscus but is normally not adherent to these structures.
On the right is a three-dimensional illustration which shows the extent of the joint cavity and suprapatellar pouch when expanded with fluid.
When the suprapatellar pouch scars down, the patient will have a limitation of flexion. I want to make a few important points about this region -
· The scar tissue can be very dense and it can form underneath the muscles. The surgeon has to remove the scar tissue that is actually underneath the muscles of the quadriceps.
· In the suprapatellar pouch, a band may form which extends from the top of the patella (kneecap) to the top of the femoral condyles. It is a very dense band of scar tissue that has to be removed. This band or scar tissue may produce what we call a 'patellar clunk', where the kneecap clunks as it goes through flexion. The question is often asked if this represents actual damage to the joint. And the answer is - it may be damage to the joint, but it also may be just from the scar tissue located in that location. This same clunk may be present after total knee replacement, for the same reason.
· The knee joint also has a pouch on both the medial and lateral sides. I tell my patients these pouches are like your cheeks in your mouth - like the cheeks, they have a normal extensibility or flexibility and they are usually not really very tight.
These pouches are anatomically called the 'capsular pouches' and during arthrofibrosis, they will scar down to the point of where they become adhesive to the side of the femur on both the medial and lateral aspects. Patients often complain that as they are trying to move their knee they feel tremendous stiffness - and they have - because their capsular pouches are adhesed down (adhered) to the side of the joint. The surgeon must open up those pouches to restore the normal gliding.
The patellar retinaculum is the fibrous tissue located on both sides of the patella -
· on the medial side, this includes the medial patello-femoral ligament that provides medial stability to the patella
· on the lateral side, the retinaculum is also part of what is termed the iliotibial band. With arthrofibrosis, this region always gets tight and patients have what we call 'limited patellar mobility'. The patient cannot glide their kneecap to the inside or the outside (which we call 'medial glide' or 'lateral glide').
Scar tissue in this region produces tremendous stiffness and blocks flexion. This scarring must be released nearly one-hundred percent of the time by the surgeon to restore a normal glide to the patellofemoral joint in a medial-lateral direction. It is very important if a patient does not have normal patellar glide, that they do not try to go past 100 degrees of flexion. This is because the tightness present in those tissues binds down the kneecap - forcing flexion may produce permanent damage to the joint.
One of the most important things that we do in our clinic is carefully stretch a knee joint, but with the recognition that in some patients, we will not be able to stretch out excessive scar tissue that is very firm and inelastic. To do so would be at the expense of the joint.
...
fizjo_kamila