Where can I as an orthopedic surgeon find a report on postarthroscopic glenohumeral chondrolysis?

Q: I am an orthopedic surgeon and thought you might be able to help me out. I saw a report on postarthroscopic glenohumeral chondrolysis somewhere recently but can't find it again. I seem to recall there were some specific recommendations for surgeons to help prevent this condition. I'd like to review those again. Can you help me out?

A: You may be referring to a recently published report from surgeons at the well-known Kerlan-Jobe Orthopaedic Clinic in Los Angeles. The topic was postarthroscopic glenohumeral chondrolysis or PAGCL. The authors explore this condition covering risk factors, causes, and signs and symptoms.

Chondrolysis develops when the chondrocytes (cartilage cells) suddenly stop working. They are no longer able to make new cartilage cells to replace the old or to maintain the healthy state of the joint cartilage.

The main risk factor is the arthroscopic surgery itself. But many people have arthroscopic shoulder surgery without developing chondrolysis afterwards. There must be other factors at play here. In fact, the authors suggest there is likely a multifactorial etiology. Several or even many risk factors combined together result in postarthroscopic glenohumeral chondrolysis (PAGCL).

A review of studies with reported cases of PAGCL shows a list of potential risk factors. These etiologic factors include direct trauma to the joint during surgery, shoulder instability before surgery, the use of bioabsorbable sutures and other implants, heating the joint with radiofrequency to shrink the tissues, and the placement of sutures (anchors and knots) on the joint (articular) surface.

The authors explore the details of potential mechanical, thermal, and chemical causes. Mechanical causes include direct injury to the fragile cartilage when the arthroscopic probe or other surgical instruments come in contact with the cartilage surface.

As already mentioned, the use and placement of certain types of sutures may contribute to the development of chondrolysis. Loose or prominent sutures/knots rub against the cartilage causing severe wear and tearing. In some patients, the suture material may set off an immune response called a foreign body reaction. The body sets up a massive inflammatory response in an effort to get rid of the sutures or anchors.

Thermal causes (heating the joint) to stimulate a healing response may actually have the opposite effect of killing the chondrocytes. The use of pain pumps (chemical cause) placed inside the joint may help control postoperative pain but may also contribute to chondrolysis and PAGCL. Anyone with a combined set of risk factors (e.g., foreign-body reaction plus thermal or chemical factor) may be at increased risk for this type of rapid joint destruction.

With this information about potential risk factors and causes in mind, the authors make the following recommendations:

Surgeons must always be mindful that arthroscopic surgery can injure the joint surface. Care must be taken when inserting the arthroscopic probe or surgical instruments. Gouging and scuffing the joint surface must be avoided.
Bioknotless sutures are available and should be used, especially when the sutures must sit right on top of the joint surface.
There are also anchors designed to resist pulling out because even a slight pull-out creates suture prominence that can rub against the articular cartilage.
Do not use thermal devices such as radiofrequency energy.
Avoid bathing the joint with local anesthetics. Infusion of numbing agents to reduce pain can be placed in the subacromial space rather than directly inside the joint.
Once the various risk factors and potential causes have been identified, the next step is prevention. When the destructive process begins, there is no going back. And without effective treatment, prevention is absolutely essential.

Reference: Peter C. Yeh, MD, and F. Daniel Kharrazi, MD. Postarthroscopic Glenohumeral Chondrolysis. In Journal of the American Academy of Orthopaedic Surgeons. February 2012. Vol. 20. No. 2. Pp. 102-112.