Abstract
Aetiology and pathogenesis: The pathogenesis of boutonnière deformity, in the rheumatoid patient is usually quite clear, and is due to either a central slip failure or volar subluxation of the middle phalanx. This subluxation is seen more commonly in the patients with psoriatic arthropathy. The most common cause is a chronic synovitis of the proximal interphalangeal joint leading to attenuation of the sagital fibres between the central slip and the lateral bands and at a later stage disruption or attenuation of the central slip itself.
Synovitis of the pip joint with separation of the lateral bands from the central slip allows the lateral bands to sublux forwards to lie anterior to the axis of rotation thus the intrinsics which extend the proximal and distal joints of the finger come to act as flexors of the proximal joint and continue to act as extensors to the distal joint. The patient will use the intrinsic muscles and they now have a flexion force upon the PIP joint and hyperextension force on the DIP joint, causing a boutonnière deformity. Volar subluxation of the middle phalanx draws forwards the lateral bands and defunctions the central slip creating the same imbalance. Scarring of the volar plate as is seen in volar plate injuries with the production of a pseudo-boutonnière deformity is sometimes seen in psoriatic arthropathy.
In a boutonnière deformity the PIP joint is flexed and the DIP joint is extended. With the joints in this position, the origin and insertion of the intrinsic muscles are closer together, and as a consequence, with the passing of time, the muscles fibres will remodel in a shortened position, creating a lateral band tightness.
Classification: Boutonnière deformity can be classified into four stages.
Type I. The deformity is totally correctable passively, and there is full flexion of the DIP joint when the PIP joint is fully extended.
The patient has a passively correctable flexion deformity of the PIP joint, and can actively flex the distal interphalangeal joint.
The anatomical alterations are the following: elongation of the sagital fibres and volar displacement of the lateral bands but no secondary shortening of musculo-tendinous system.
Type II. Flexion of the DIP joint is limited when the PIP joint is passively corrected.
The patient cannot actively or passively flex the distal interphalangeal joint, when the PIP joint is passively corrected. Secondary shortening of the intrinsic/lateral band system because the intrinsics have remodelled in a shortened position.
Type III. Stiffness of the PIP joint without joint destruction.
There is no passive correction of the deformity but the joint surfaces are sound. The patient can not passively extend the PIP joint nor flex the DIP joint.
Type IV. Stiffness of the PIP joint with joint destruction.
In these cases, stiffness of the PIP joint is not only due to soft tissue remodelling but mainly to joint destruction.
In this type, destruction of the joint cartilage should be added to the previously described anatomical deformities. X-ray examination is needed to confirm the diagnosis.
Treatment: Boutonnière deformities, are both aesthetically and functionally less disabling than swan neck deformities because there is usually little loss of active PIP joint flexion. Some therapeutic options exist, and choosing the most appropriate surgical procedure will depend on the severity of the anatomical deformities which need to be corrected.
Correction of PIP joint flexion. Mobilisation of the lateral bands and transposition of the lateral bands posterior to the axis of rotation of the PIP joint. Release of the volar plate of the PIP joint is often necessary because of secondary contracture.
Improving active DIP joint flexion. The only way to restore loss of active DIP joint flexion is by performing a Dolphin tenotomy or formal lengthening of the conjoined lateral bands over the middle phalanx.
Improving passive PIP joint extension. Passive extension of the PIP joint can usually be obtained by gentle manipulation and serial application of plaster of paris casts, as well as the use of a Capner (or armchair splint)the dorsal structures are usually quite thin and lax. If the joint can not be passively extended, a surgical release of the lateral bands is indicated,. Y-V plasty shortening of the central slip and extensor mechanism is usually necessary. A longitudinal incision at both sides of the central slip, allowing the lateral bands to displace dorsally during PIP joint extension with reefing of the lateral bands to the remnants of the central slip is needed in most cases.
PIP joint arthroplasty. A PIP joint arthroplasty should be considered when the joint is destroyed. A radiological examination is essential in making the diagnosis, as many stiff PIP joints in flexion do not have their joint surfaces preserved because boutonnière deformities are often secondary to PIP joint synovitis. A full soft tissue procedure must be performed at the same time.
DIP joint arthrodesis. Arthrodesis is only indicated for the treatment of uncorrectable deformity of the DIP joint with or without joint destruction, confirmed by radiological examination. The functional results of an arthroplasty are far superior for the treatment of a swan neck than a boutonnière deformity, because of the integrity of the extensor apparatus in the former, allowing for immediate postoperative motion.
7. PIP joint arthrodesis will be the treatment of choice if the finger presents a gross deformity with deteriorating function or failed surgery.
Theses abstracts were prepared by Professor Dr. Frantz Langlais. Correspondence should be addressed to him at EFORT Central Office, Freihofstrasse 22, CH-8700 Küsnacht, Switzerland.
