Jessica Frankenhoff and Jonathan Isaacs

To understand the problem, one must determine the etiology of the SND and then choose the best of the available treatment options based on the patient’s needs and disabilities.

The term SND refers to a finger with a posture of hyperextension at the PIPJ and concomitant flexion at the DIPJ. Although the appearance of the finger is the same in all instances of SND, the etiology varies. The functional loss associated with this deformity is related to the loss of PIPJ motion. In some patients, the deformity has only minor clinical consequences, and it is mostly a cosmetic issue. Some may only be bothered by a mechanical snapping into flexion. For others, it can adversely affect function, decrease grip strength, and cause pain.

SND is caused by an imbalance in this extensor mechanism. That imbalance originates in one, or sometimes more, of three areas: (1) extrinsically, at the level of the forearm, wrist, or MCP joint; (2) intrinsically, from the intrinsic extensor tendon system; or (3) at the articular level of the PIPJ or DIPJ themselves. For example, a wrist or MCP joint flexion contracture increases extrinsic EDC tension. This increased tension is transmitted to the base of the middle phalanx via the central slip insertion and can result in hyperextension of the PIPJ. Alternatively, contracture or spasticity of the intrinsic system can flex the MCP joint and hyperextend the PIPJ (via the lateral bands) resulting in the same deformity. A loss of PIP flexion tone from a disruption to the superficialis tendon (which inserts onto the volar base of the middle phalanx) can have the same result though by creating an intrinsic extension/extrinsic flexion force imbalance that allows the PIPJ to hyperextend. Finally, proximal migration of the extensor mechanism due to terminal tendon disruption at the DIPJ (mallet finger) can increase extensor force to the central slip and hyperextend the PIPJ by yet a different mechanism, while laxity (or stretching) of the volar plate of the PIPJ can independently contribute to the SND.

The diagnosis of SND is based just on physical appearance of the digit and functional complaints. The pathophysiology of the tendon imbalance, the presence of arthritis in the joints, and the quality of the soft-tissue envelope and tendency for tendon adhesions must all be considered in designing a successful treatment strategy. A history of known disease states (e.g., rheumatoid arthritis, cerebral palsy) or trauma (e.g., mallet deformity, volar plate avulsion fracture) can direct the workup, and radiographic evaluation of the joints should reveal degenerative and posttraumatic joint conditions.

The passive and active range of motion of the wrist, MCP, and IP joints should be evaluated both with the hand in its resting posture and with the SND passively corrected. This can allow the identification of a chronic mallet injury from either traumatic disruption or gradual attenuation of the terminal slip insertion. Extrinsic tightness can be assessed by evaluating changes in extrinsic extensor tendon tension related to wrist position. Extension of the wrist would allow more finger flexion in the presence of extrinsic tightness. Intrinsic tightness, on the other hand, can be determined utilizing the Bunnell test. The Bunnell test is performed by holding the MCP joint in extension and then in flexion while actively or passively flexing the PIPJ. Decreased passive PIPJ flexion with the MCP joint in extension is compatible with intrinsic tightness (lateral bands run volar to MCP joints and dorsal to the IP joints).

The SND can be classified into one of four types as devised by Nalebuff and Millender:

• Type I: full range of motion of the joints with no significant functional limitations.

• Type II: intrinsic tightness as shown by a positive Bunnel test; the PIPJ can be ranged fully with MCP joint held in flexion only.

• Type III: the PIPJ is stiff both actively and passively irrespective of the position of the MCP joint.

• Type IV: the same as type III, but with radiographic arthritic changes at the PIPJ.

Type I

For a type I deformity, only the PIPJ hyperextension needs to be addressed. This can be done by decreasing the amount of skin volarly with a dermodesis or by creating a mechanical restriction to extension with an FDS sling, an oblique retinacular ligament (ORL) reconstruction, or a lateral band rerouting procedure. Excising and closing an ellipse of skin from the volar aspect of the PIPJ is only helpful for very mild deformity (and can stretch out with time). A stronger restraint to hyperextension can be achieved using the FDS to create a restraint sling known as the “sublimis sling.” This was performed on our patient, and is described later under the section “Technique.” These strategies only address the PIP hyperextension and not the DIPJ extension lag. If this appears to be a persistent problem even with the PIP passively corrected than one of the following reconstructions can be used. In the ORL reconstruction, the ulnar lateral band is freed from the extensor mechanism proximally at the level of the MCP joint, passed volar to Cleland’s ligament and volar to the PIPJ axis of rotation, and sutured radially either to the flexor tendon sheath or passed through the proximal phalanx via a bone tunnel. Alternatively, a palmaris free graft can be used, sutured to the terminal tendon, then following the same path as the ulnar lateral band as described earlier. Finally, one or both lateral bands are freed from their dorsal attachments, translocated palmarly, then either sutured to the ipsilateral FDS slip and volar plate or placed into a flap made in the flexor tendon sheath at the PIPJ level.

Type II

For a type II deformity, the same procedures as in type I are available for the PIPJ deformity, but the MCP joint needs to be addressed as well. Often, this is done with just an intrinsic release. However, any MCP joint or wrist disorder that aggravates the imbalance of the finger such as subluxation or deviation must be corrected as well.

Type III

For a type III deformity, in addition to the intrinsic release, the PIPJ needs to be released. There is often a paucity of skin dorsally that may need to be addressed. A formal joint release with transection of the collateral ligaments, volar translocation of the lateral bands, and possible step-cut lengthening of the central slip may be necessary. Also, due to the prolonged lack of range of motion, there may be flexor tendon adhesions, which need to be freed simultaneously. This approach is obviously more complex and the results tend to be less predictable.

Type IV

For a type IV deformity, the PIPJ needs to be addressed most commonly with an arthrodesis.

The Presented Case

Our patient had a type 1 SND, complicated by the proximal phalanx malunion and extensor tendon adhesions. His biggest problems were initiating flexion and keeping his small finger from catching on objects in its resting swan posture. Dermodesis was unlikely to be sufficient or lasting in a young laborer. This left the superficialis sling surgery, the lateral band translocation procedure, and the ORL reconstruction. The final option also helps correct DIP flexion deformity. His DIP flexion deformity was not severe enough to warrant correction especially in the small finger and because of the crush nature of his initial injury, there were concerns about the propensity for adhesions and stiffness with a more complex procedure.

The patient was taken to the operating room after administration of regional anesthesia and placed in the supine position on the operating table. An upper extremity tourniquet was inflated to 250 mm Hg. Wide-awake surgery local anesthesia without tourniquet (WALANT) is also an option and is normally the author’s preference as it allows for visualization of the range of motion in real time and allows for any necessary modifications at the time of surgery. However, this was not possible in this case due to the necessity of performing several concomitant procedures.

There are multiple approaches to exposing the flexor tendon sheath, and many variations in technique for creating the sling (e.g., using one or both slips of FDS, securing the tendon through the A1 or the A2 pulley or to the proximal phalanx).