Under digital block a curved incision is made over the terminal tendon. The pseudotendon is exposed. There are two methods described to shorten the tendon. The first is a simple plication leaving the tendon intact and the second is to divide the tendon and then to double breast the divided tendon. In both cases once the sutures have been placed the DIPJ should be in full extension. A K-wire is passed across the DIP joint to maintain full extension for 6–8 weeks. After K-wire removal mobilisation of the DIP joint is commenced with night splintage for a further 4 weeks.

This technique was originally described by Brooks in 1961 and later modified by Graner and is therefore sometimes referred to as the Brooks and Graner technique.

The operation is performed under digital block. An elliptical incision is made over the DIP joint and a wedge of skin and subcutaneous tendinous scar tissue is excised. The size of the excised ellipse may be determined by passively extending the DIP joint to produce a dermal fold over the DIP joint preoperatively. The wound edges should come into contact when the DIP joint is extended. The wound is closed using en bloc mattress sutures passing through skin and tendon on both sides of the wound. A K-wire is passed across the DIP joint to maintain full extension for 4 to 6 weeks. The rehabilitation programme is as for tendon plication.

This technique relies on a mature healed but elongated terminal tendon resulting in a persistent extensor lag. At least six months must have passed since the time of injury to allow full maturation of tendon healing. The maximum extensor lag that can be corrected with this technique is 35° [2]. There must also be a full passive range of motion of the DIP and PIP joints. The technique involves dividing the central slip which allows the extensor tendon mechanism to slide proximally thus increasing the tone in the terminal tendon which in turn improves the extensor lag. A boutonnière deformity is not created as the triangular ligament is left intact.

The procedure is best performed under digital block to enable active tendon movement intra-operatively. The tendon is exposed using a mid-lateral incision centred over the PIP joint. An extensor tenolysis may need to be performed over the middle phalanx as the central slip must not be prevented from migrating proximally by distal adhesions. The triangular ligament must not be damaged. The transverse retinacular ligament is divided and the entire extensor mechanism is elevated both proximal and distal to the central slip insertion. The central slip insertion is divided by sliding a scalpel from proximal to distal to take the insertion off the base of the middle phalanx. On active extension there should be improvement of the extensor lag at the DIP joint. If no improvement occurs the surgeon should perform an extensor tenolysis ensuring that the extensor mechanism is not tethered and is able to slide proximally. The finger should then be splinted with the PIPJ in 30° flexion and the DIPJ in full extension.

Post-operatively a dorsal blocking splint is used to maintain at least 20° of flexion at the PIP joint whilst the DIP joint is splinted in full extension. The aim is to maximise the extensor tendon force at the DIP joint. At 2 weeks the PIP joint splint may be discarded and full active mobilisation of this joint may be commenced although hyperextension should not be allowed. At this stage the patient may remove the DIP joint splint several times each day to mobilise the joint. At 4 weeks the DIP joint splint need not to be worn during the day but should be worn at night for a further 4 weeks.

The ORL originates from the flexor sheath on the volar aspect of the PIP joint and inserts into the terminal tendon. During PIP joint extension the ORL tightens and assists in extending the DIP joint.

Reconstruction involves the use of a tendon graft (palmaris or plantaris). The graft is secured dorsally into the base of the distal phalanx which may be done using a pull out suture or bone anchor. The graft is then directed in a spiral fashion around the middle phalanx passing between the flexor sheath and the neurovascular bundle obliquely across the volar aspect of the PIP joint to the opposite side. The graft is then passed transversely through the base of the proximal phalanx and secured in place once the correct tension is achieved. Care must be taken not to over tighten the graft as this may result in a boutonnière deformity.

The primary cause of a chronic Boutonniere deformity is loss of central slip function. This may be due to failure of treatment or a delayed presentation of an acute injury. It may also be caused by a slow attenuation secondary to osteoarthritis, inflammatory arthritis or a prolonged flexion contracture which may be seen secondary to a burn or Dupuytren’s disease.

The pathophysiology of the deformity is that loss of central slip function will result in an extensor lag at the PIP joint and hyperextension at the DIP joint as the extensor force is now concentrated on this joint. Over time the triangular ligament stretches which allows the lateral bands to subluxate palmarly and to then lie palmar to the axis of rotation of the PIP joint. The flexor tendons and lateral bands cause increased force of flexion at the PIP joint and because of the relative shortening of the lateral bands an increased extensor force at the DIP joint. The development of this deformity occurs over time and the initial posture of the finger after division or rupture of the central slip may not be abnormal.

Initially the deformity will be flexible with a full passive range of motion of the interphalangeal joints. However, with time the lateral bands will contract causing a fixed deformity. Consequently a joint contracture may develop secondary to contracture of the collateral ligaments and volar plate.

Burton classified chronic boutonnière deformity into three stages with a fourth stage being added later:

The history should establish the cause of the deformity (as above), treatment to date, and the degree and rate of progression.

The severity of the deformity and whether it is flexible or fixed should be documented. Careful consideration must be given to the functional deficit the patient experiences as most patients with a boutonnière deformity retain full flexion and grip strength. Any treatment aimed at correcting the deformity and gaining extension can jeopardise flexion and therefore impair hand function.

It is important to differentiate a true boutonnière deformity from a “pseudoboutonnière” deformity where there is flexion contracture of the PIP joint without a fixed DIP extension deformity. This is most commonly caused by a hyperextension injury resulting in damage to the volar plate which subsequently scars and contracts and is also seen in Dupuytren’s disease with ORL contracture.

As with chronic mallet deformity the first option may be to advise the patient to have no treatment. This is particularly so if the finger remains flexible at both the PIP and DIP joints and no progression has been noted over time.

If reconstructive surgery is considered it is important that all joints of the finger have a full passive range of movement.

Stage II deformities should be managed with hand therapy using splinting or serial casting to achieve full passive PIP joint extension. Once PIP joint extension is achieved it should be maintained with the use of a splint for 6–12 weeks. During this time active and passive exercises of the DIP joint should be done which help realign the lateral bands and rebalance the extensor mechanism. If full PIP joint passive extension and active DIPJ flexion is achieved and an extensor lag persists then surgery can be considered.

Surgical reconstruction to correct the deformity must never be attempted in the presence of a fixed deformity. The first aim should be to achieve a full passive range of movement and if hand therapy fails then a surgical joint release should be done as a first stage. Following the joint release the patient should undergo appropriate splinting and an exercise program. In some patients the extensor mechanism will rebalance and thus the second stage reconstruction will not be required.

The surgical options for correction of a chronic boutonniere deformnity are shown in Table 3.3. Some of these are discussed below.