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.

This is the editor's interpretation of a paper published in the orthopaedic literature in 2001 - our attempt to make relevant medical articles accessible to lay readers. If you wish to read the original it is easy to ask your librarian to obtain a reprint for you from any medical library.


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.

 

Terminology

The authors feel that people need to use precise terminology when describing motion loss, and recommend that -

  • the terms 'extension loss' and 'flexion loss' refer to loss of motion compared to the normal side. They are descriptive and do not imply any cause.
  • 'arthrofibrosis' may be associated with extension loss or flexion loss, or both, but this term is specific and should only be used where the cause of such motion loss is known to be due to abnormal scarring of the joint.
  • 'flexion contracture' means that there is a loss of extension specifically due to shortening of the tissues behind the knee. The cause is not specified and may be scarring or muscle shortening.
  • 'ankylosis' is another term which is used where there is flexion and extension loss of the joint, but it is non-specific in terms of causation - and the stiffness may be due to abnormal bony, cartilagenous or scar tissue.

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.

 

Incidence

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.

 

Risk factors

The authors point out that risk factors have been clearly shown to be related to -

  • 1 the injury itself
  • 2 the surgical treatment of the injury
  • 3 the rehabiliation process














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but there also seems to be a genetic predisposition in certain individuals where they are more sensitive to these triggers:

1 The injury itself

They highlight that an increased risk is associated with -

  • multiple ligament damage
  • knee dislocation
  • infection
  • synovitis (inflammation of joint lining)














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2 The surgical treatment of the injury

The authors continue to discuss the details of surgery and point out that there are a number of factors to consider -

  • timing of surgery - in 2001, when this paper was published, this was one of the most controversial issues, some influential surgeons stressing that surgery should not be undertaken too early after injury, particularly in the first week or two when the tissues were still inflamed and the knee swollen, and more particularly in those patients who show an excessive inflammatory response. The authors of the paper stressed that the timing of surgery needs to be a carefully considered clinical decision.
  • preoperative motion - as swelling and inflammation reduces, motion should be restored prior to surgery, as prolonged immobilisation has been shown to aggravate scar formation.
  • malpositioned grafts - if improperly positioned the graft may impinge on the notch, with motion loss consequences.
  • excessive graft tension - if a graft is too tight it will not be possible to regain full range of motion without risking damage to the new ligament.
  • associated extra-articular procedures - medial collateral ligament surgery done at the same time may lead to loss of motion for a number of reasons. Also concurrent reefing ('tucking in') of the posterior oblique ligament is associated with motion loss.
  • associated meniscal repairs














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3 The rehabilitation process

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 -

  • prolonged immobilisation
  • poor rehabilitation - particularly failure to achieve the few degrees of hyperextension which are normal for most people. A number of authors were advocating that the knee be braced in full extension and movement initiated within 24 hours.
  • reflex sympathetic dystrophy (RSD) - this important condition, associated with swelling and increased sensitivity to pain, needs to be identified and managed by a multispeciality team, and surgery may need to be delayed if RSD is diagnosed. If not, there may be an exacerbation of symptoms and consequent motion loss.
  • infection and synovitis- similarly infection and synovitis need to be dealt with promptly and surgery delayed if necessay, as operating in the presence of these conditions may lead to a complicated rehabilitation and motion loss.














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Anatomy of the motion loss

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 -

Arthrofibrosis

Diffuse scar tissue or fibrous adhesions forming within the joint.

ACL nodule ('cyclops lesion')

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.

Infrapatellar contracture syndrome

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').

Malpositioned graft

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.

Excessive graft tension

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.

Tissue calcifications

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.

Flexion contracture

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.

 

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