1987 - Infrapatellar contracture syndrome. An unrecognised cause of knee stiffness with patella entrapment and patella infera

Paulos LE, Rosenberg TD, Drawbert J, Manning J and Abbott P. Infrapatellar contracture syndrome. An unrecognised cause of knee stiffness with patella entrapment and patella infera. Am J Sports Med 15:331-341;1987.

This paper, published in 1987, drew attention to the fact that to this date most papers dealing with abnormal fibrotic healing of knees (too much scar tissue) only mentioned management of loss of flexion but ignored the issue of loss of extension. The authors defined in this paper a new syndrome - the infrapatellar contracture syndrome (IPCS) - which they identified as a knee condition with loss of both flexion and extension combined with ‘patellar entrapment’. By this they meant that the patella gets tethered down behind its tendon and above the notch of the femur and can no longer undergo its normal excursion.

They highlighted that IPCS could be either primary (arising on its own) or secondary to one or more of a group of conditions - (immobility, quads insufficiency, poorly positioned cruciate ligament replacements, infection, RSD, an entrapped meniscus, or a neuromuscular disorder (such as polio). These conditions may be associated with a flexion deformity but a mobile patella, but if the condition persists a fibrotic (scarring) process may set in, and the patella may become immobile (entrapped) and then this would be ‘secondary IPCS’.

They discussud a group of 28 consecutive patients with IPCS, from whose outcomes they defined three stages -

• Stage I - a prodromal stage - difficult to distinguish from the normal acute healing response of any injury or surgery to the knee - with inflammation and swelling around the joint, combined with weak quadriceps muscles. This stage usually occurred 2-8 weeks after the initiating incident. But the patients failed to progress with rehabilitation, failed to gain extension and had persistent pain and swelling. The swelling was oedematous ('boggy and swollen') in nature and was most obvious around the patellar tendon and fat pad. There was tenderness around the patellar tendon, and active ROM (range of motion) was painful. A quadriceps lag was demonstrable (could not actively extend the last few degrees, although someone else could help to passively move it through that range), and patellar glide and tilt were restricted but not rigid.

• Stage II - an active stage - in this group, patients in the 6-20 week period after the initiating injury or surgery had slipped over from the prodromal stage into the active stage of IPCS without the problem having been recognised. The authors suggested that in some cases forceful manipulation may have aggravated rather than resolved prodromal problems. The key feature here was significantly decreased patellar mobility, a hardened fat pad and a rigid patellar tendon. The authors identified a ‘shelf sign’ where one compares the profiles of the two knees relaxed in extension - the affected knee has a more steep drop under the patella compared to the normal knee - indicating that the process has moved to the tissues outside the joint. The mobility of the patella was severely decreased in all directions, and the patellar tilt test (trying to tilt the patella by pushing down one of its edges) was found to be zero or negative. The quadriceps lag was no longer
  present - ie both active and passive knee extension were limited. Significant quadriceps wasting (atrophy) was present, with patellofemoral crackling (crepitus) on tracking tests. Also the patella failed to move upwards on voluntary contraction of the quads.

• Stage III - a residual stage - This may be from 8 months to years after the onset of IPCS, when the active process has effectively burned out. The tissues around the patella may be found to be more supple, with a more normal patellar
  glide, although the fat pad may show some residual overgrowth (hypertrophy). But the joint surfaces show damage, with patellofemoral arthrosis (damage to the cartilage surfaces of the joint), crepitus and diminished joint space on X-ray. ‘Developmental’(patella abnormally low) is common (ie patella infera that was not there before). The quads muscles continue to be atrophied and weak, and flexion and extension continue to be restricted, but if a long time has elapsed, most of the signs of IPCS will have disappeared, with the patella infera and
  patellofemoral arthrosis as the only remaining features.

They made the following points and recommendations for treatment -

• For Stage I they recommended aggressive rehabilitation with early motion, and patellar mobility exercises to be taught to the patient. They emphasized getting the quads active, using as needed muscle stimulation, anti-inflammatories, analgesics (pain killers) and TENS (electrical nerve stimulation). If the patient was not achieving extension a drop-out cast or extension board could be used with caution (both physically stress the knee into extension) - but only once the quads were working again. It was suggested that manipulation under anaesthesia (MUA) should also be used with caution and only in the very early stages. They recommend that these forced extension procedures should not be used for more than 3-5 days. In their experience most patients in the early stages would generally respond to this programme, but 5% were still likely to progress to Stage II and require surgery. They considered this 5% to represent ‘primary’ arthrofibrosis.

• Once it is apparent that no progress is being made and that the patient has entered Stage II, they recommended that attempts at forced passive extension be discontinued and that the patient should be treated surgically. They made a point that they did not think arthroscopic surgery likely to be useful, and recommended open intra-articular and extra-articulardebridement (clean up of scar tissue) and release (cutting bands of scar tissue). They felt the timing of this surgery was critical to avoid operating when there was inflammation and the quads were weak - and they felt it valid to wait for some months to achieve this, working meanwhile on regaining strength within the available ROM. Opening the joint on both sides of the patella, their recommendations for surgery included lateral release, debridement of the fat pad and lateral and medial patellomeniscal ligaments, and cleaning out the notch of the femur, removing any cruciate graft if the problem had come on after cruciate reconstruction and the graft had been incorrectly placed. They recommended that adhesions around the patellar tendon and the suprapatellar pouch should be excised, and patellar mobility restored with a patellar tilt test producing at least 45 degrees of tilt. They recommended that the surgeon be prepared to do a tibial tubercle transfer (moving the
  tubercle up) if patella infera was present. They did not mention the use of drains, but did insist that all wounds should be meticulously closed. Prophylactic antibiotics were used, as well as anti-inflammatories. If steroids were to be used, these were avoided until after the wounds had healed.

  CPM was started postoperatively, and the use of epidural for pain relief was encouraged, with a drop-out cast at night for a few days.

• In Stage III surgery was considered ‘salvage’ and included tibial tubercle advancement, patellectomy, Maquet osteotomy, or total knee replacement.