Knee Arthroplasty - Science topic

What do you think about delayed physiotherapy in the outcome of knee arthroplasty?

Interpositional arthroplasty has gained in success and popularity in non load bearing joints in recent years. All of the joints that have had great success have been sheer force joints and not in load bearing joints. Any thoughts or experience in performing this procedure in load bearing joints as to integration of graft or graft breakdown due to loads. Is there any graft that is more durable with load than others?

The rationale of the new cruciate (ACL and PCL) sparing TKR seems feasible but I cannot find any clinical data on this.

Sometimes during the surgical procedure for TKR, one comes across hypertrophied synovium especially in suprapatellar pouch. I have only occasionally excised the synovium. Should it be excised as a routine or not, or what is the indication to remove it?

As in the majority of the hospitals, we use a blood management program. We use postsurgery blood recovery system in some situations: low presurgery Hb level, tranexamic acid contraindication..., but, if the surgeon practices an intraarticular infiltration of local anesthetic, within a fast recovery system, we won't be able to use it, . What is more important in your opinion, faster recovery or lower possibility of blood transfusion?

I've been using for a long time an association of Marcaine, Morphin and steroids with rather good results. Any other opinion or better results?

Thank you in advance for your advices...

I have edited the guidelines of AAOS in a tabular form for a ready referral. The opinion of arthroplasty surgeons, please.

Does the chronological age really matters in this decision making?

Is CT or MRI based technology  better for the making of patient specific instruments? 

Are there longitudinal studies on the medium and long-term events (outcome) post total knee arthroplasty TKA? In long-term studies, are there any relationships between outcome and nature of TKA rehab received by TKA clients?

Every year a lot of studies are published on tourniquet time and blood loss and outcome after TKA. I do not use a tourniquet at any time of the TKA procedure. I am interested in conducting a study to assess quad muscle function and outcome of TKA without using a tourniquet.

Currently several landmarks are used to identify the joint line level in revision knee arthroplasty. However, I wonder which one is a suitable method? Does anyone have an idea? Thank you for your contributions.

Detection of beginning infection in the early postoperative period is important for the adequate treatment ? There are controversies about the issue which are the reliable markers for early detection of infection.

Material Chemical and Mechanical Properties.

It is very probably a child with a form of arthrogryposis-syndrome. After serial casting and prolonged traction, reduction of the knee is not possible. Surgery will be necessary, but probably not before 3-6 months of age. I don't know if there is a good idea for a splint or cast in the mean time in order not to lose to much length.

Recently BJM published an article about effectiveness and safety of tranexamic acid in total hip and knee arthroplasty. Are there any institutional protocol in your hospital? How do you use it? Dose, interval, exclusion criteria, thromboembolic prophylaxis?

Is this necessary? What is the rationale? Is not the spacer another foreign body that could maintain the infection?

Synovial Fibrosis

Does anyone have experience in synovial fibrosis in surgically-induced OA rat knee or mouse or other animal model? Has anyone tried to reduce synovial fibrosis while trying to treat OA by any means (like stem cells etc)? Any comments on fibrosis vs OA in induced OA reference?

How should a medical doctor attempt to reduce arthrofibrosis? What are any of the latest treatments besides mild exercises to reduce stiffness?

I like this old study by Hubbard from the JBJS. It is a well designed study with a clearly defined patient cohort and they showed a clear benefit to debriding focal osteoarthritic lesions of the medial femoral condyle.

Since this study there have been three sham surgical trials on knee arthroscopy, each greeted with a media fanfare, the problem for me is that despite these studies being interesting to a degree, I am not convinced that knee arthroscopy is as dead in the water as some physicians seem to want it to be. Why?

Well, there are some serious flaws in all these studies in terms of patient groups (heterogeneity/symptoms/stage of OA/type of OA lesions etc), outcome measures and study power. For example in the trials of Moseley and Kirkley they took heterogeneous groups of patients with diffuse OA of different stages and showed that a general bit of non-specific debridement (ie no chondroplasty/microfracture etc) did not improve outcome. While in the recent study by Sihvonen patients had no mechanical symptoms, and isolated knee pain with no arthritic lesions.

From what I can see we have learnt some interesting things from these sham surgical trials, for example we know that a general bit of non-specific debridement is probably not a good thing for people with knee pain related to diffuse osteoarthritis and no mechanical symptoms, and we have also learnt that a meniscectomy is not a good thing in terms of relieving pain in patients with an isolated degenerate meniscus, no osteoarthritis and no mechanical symptoms.

It will be interesting in the years ahead to see the role of knee arthroscopy become better defined, in my opinion the baby should not be thrown out with the bath water at this stage. We know focal osteoarthritis lesions respond better with surgery, and the role of modern treatments like chondroplasty/MACI/ACI needs to be better determined. The problem is I don't think that knee arthoscopy is of no value in the treatment of knee pain as a result of more diffuse osteoarthritis, I just think the evidence is not good enough to tell us the answer yet, it all depends on what one does once inside the knee and in which specific patient groups one intervenes.........

Do you know of any recent research on this topic?

The extension ROM after TKR has been reported as a negative value, i.e. - 3.2 or -2 in some articles and in some other articles it has been reported as a positive value, i.e. 3.56 , 3.58 . What should we interpret? The authors have not mentioned anything.

Does it tell that passive range of motion is checked by CPM? Or manually or something else?

Do you have a specific diagnostic algorithm? Please specify what to do and when. What kind of imaging modalities do you include?