Motion loss after ligament injuries to the knee. Part I: Causes.
Millett PJ, Wickiewicz TL and Warren RF. Am J Sports Med. 2001;29:664-675.
An 'interpretation' of a medical article from 2001 detailing the various causes of diminished range of motion in the knee after ligament injuries.
Millett PJ, Wickiewicz TL and Warren RF. Am J Sports Med. 2001;29:664-675.
This paper, published in 2001, reviews the concepts at that time on terminology, incidence and risk factors for motion loss of the knee after ligament injury or surgery. The authors then outline the published opinions regarding diagnosis, treatment and prevention.
They explain that most normal knees have 5 degrees (women) to 6 degrees (men) hyperextension. That is, full extension is usually beyond the 0 degrees often assumed. This extra few degrees allows to mechanically lock back when standing still, and lets the quads muscles relax.
According to them, flexion in the normal knee is about 143 degrees (women) to 140 degrees (men).
They say that most people find the loss of extension more disabling that the loss of flexion, as even a few degrees loss of extension strains both the quads muscle and the patellofemoral joint, while a small loss of flexion is less disabling in normal activities.
The authors point out that true incidence of motion loss after ACL injury is not known, as the published literature is not consistent in its definition of motion loss. Some authors defined the loss of motion compared to the good leg (the 'contralateral' limb); others defined it according to the normal range of motion. Authors differed in the degree of loss which they defined as significant - from 5 degrees to 10 degrees. Nonetheless, the consensus is that motion loss after ACL injury or surgery has decreased with better understanding of the risk factors, proper surgical technique and early, aggressive rehabilitation. Motion loss continues, however, to remain prevalent where there are multiple ligaments involved or where the knee has suffered dislocation.
The authors point out that risk factors have been clearly shown to be related to -
but there also seems to be a genetic predisposition in certain individuals where they are more sensitive to these triggers:
They highlight that an increased risk is associated with -
The authors continue to discuss the details of surgery and point out that there are a number of factors to consider -
By 2001 prolonged immobilisation was no longer advocated for the uncomplicated ligament injury, and instead rehabilitations programmes emphasised early motion and weightbearing, as this was associated with less motion loss. The authors identify risk factors for motion loss as -
The authors of this paper then went on to explain what anatomical changes might be present to result in this motion loss. They identified the following anatomical possibilities -
Diffuse scar tissue or fibrous adhesions forming within the joint.
A proliferative fibrous nodule, located to the front and side of where the graft exits from the drill hole (tunnel) in the tibia and crosses the joint towards the femur. This was associated with pain in the last few degrees of extension, crepitus (crackly noises) and a grinding sensation. This was thought to be the abnormal tissue response to debris in the tunnel, remanant of the stump of the original ACL or, more rarely, broken graft fibres. In some patients a bony outgrowth, or osteophyte, and in others a narrow notch in the femur contributed to the anatomical disturbance in this region.
Exaggerated scarring around and below the patella can lead to the patella becoming immobile and eventually being pulled into an abnormal low position ('patella infera').
Errors in surgical technique can lead to motion loss in cases where the graft is poorly positioned (tibial tunnel placed too far forward) and/or the notch in the femur inadequated widened (notchplasty) to allow free passage of the new ligament. The issue of the notchplasty is quite complicated as there may be joint cartilage degeneration if it is widened too much, and also the notch may close again by itself and lead to a later loss of motion.
If the graft is well positioned, the authors believe that excessive tensin is not a major issue. However, if positioning is not fully anatomic, then too much tension can lead directly to motion loss.
Motion loss can also be the result of the tissues - ligament or capsule, or both - becoming calcified. In an extreme form of this - 'myositis ossificans' - the tissues of the quadriceps muscle become calcified.
Scarring of the posterior capsule behind the knee can cause flexion contracture, and this may be caused by prolonged immobilisation or faulty meniscal suture (stitching) in this region.