Rheumatologic conditions of the hand and wrist

Etiology

Though much is understood about the pathogenesis of RA, the cause remains idiopathic. That being said, RA is known to have a genetic component. This is demonstrated by the fact that RA has a much higher concurrence rate in monozygotic twins (15–20%) than in dizygotic twins (5%), with susceptibility transferred in an autosomal recessive mode. In addition, there are certain ethnic groups such as the Pima Indians that exhibit a greater incidence of RA than the rest of the population, providing further evidence of a genetic component to RA.

Many studies suggest that a multitude of genes play a role in contributing to susceptibility to RA. These include the class II major histocompatibility complex (MHC) genes and many others. The most well-understood genetic association is with the class II MHC genes, which may contribute up to 40% of the genetic component of RA. One class II MHC gene in particular, human leukocyte antigen (HLA) DR4, is associated not only with increased risk of disease, but also with increased disease severity.

In addition to genetics, gender influences the development of RA. RA is more common in women than in men, with a ratio of 2:1 to 3:1. Multiple laboratory and clinical studies suggest that hormones, and estrogens in particular, affect the development of RA. However, the exact role of estrogen in the development of RA is not known.

Although the mechanisms are not well understood, the environment plays a role in the etiology of RA as well. Smoking is a risk factor for the development of RA, particularly in susceptible men. Coffee intake and exposure to silica have also been associated with RA. In addition, infectious diseases likely act as a trigger in genetically susceptible individuals. Possible triggering agents include mycoplasma, enteric bacteria, Epstein–Barr virus, and other viral and bacterial triggers. In summary, RA is an idiopathic disease, but which is known to have both genetic and environmental components. The genetic susceptibility and environmental triggers are complex and varied, and are not fully understood.

Pathogenesis

The target tissue of RA is the synovium. The disease process begins when an antigen, a trigger for RA, is presented to T-cells within the synovium. A complex interaction between macrophages, B-cells, T-cells, and synoviocytes ensues, orchestrated by systemic inflammatory modulators and local cytokines. The end result is the formation of proliferating inflamed synovium, or pannus ( Figs. 19.1 & 19.2 ). Once initiated, this process becomes systemic and self-sustaining, and does not require the prolonged presence of the trigger antigen. The synovial pannus produces proteolytic enzymes such as metalloproteinases, serine proteases, cathepsins, and aggrecanases that erode cartilage, bone, and supporting soft-tissue structures. Cytokines secreted by the pannus activate osteoclasts in nearby bone, further contributing to bony erosions and joint destruction.

Medical management

The medications used to treat RA include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying antirheumatic drugs (DMARDs). In general, a combination of the above medications, with methotrexate as the basis, is used to control symptoms and the underlying disease. NSAIDs do little to affect the course of the disease and are rarely used in isolation. They are effective, however, in treating symptoms such as joint pain, but must be used judiciously due to their gastrointestinal and renal side effects. Corticosteroids on the other hand are very effective in treating both the symptoms of RA and the underlying disease process. They can be administered systemically or locally, in the form of a joint injection. However, long-term systemic use is associated with substantial morbidity. Because of this, a minimal clinically effective dose is used. Often, corticosteroids are used briefly to control acute symptoms or flare-ups and are then tapered as DMARDs begin to work. DMARDs include a diverse array of medications that can be divided into two groups: conventional DMARDs and biologic DMARDs.

The conventional DMARDs include methotrexate, leflunomide (Arava), azathioprine (Imuran), Plaquenil, and gold. Methotrexate is the most commonly administered DMARD because of its effectiveness and favorable side-effect profile. It is generally taken orally once a week, in combination with folic acid in order to minimize side effects such as hepatotoxicity and bone-marrow suppression. Leflunomide (Arava) is a daily oral pyrimidine antagonist, with side effects that include hepatotoxicity and marrow suppression. Plaquenil, an antimalarial drug that is effective in the treatment of RA, is taken daily and has few serious side effects. Sulfasalazine is another common daily DMARD, and like many of the other conventional DMARDs it can cause leukopenia. Gold is rarely included in the antirheumatic regimen today due to significant side effects and the need for intramuscular injections.

Biologic DMARDs are those that target tumor necrosis factor-alpha (TNF-α) and interleukin 1 (IL-1), or the cellular components of the immune system. Etanercept (Enbrel) is an anti-TNF-α that requires once-weekly subcutaneous injections. Infliximab (Remicade) is a TNF-α blocker that is administered every 1–2 months, intravenously. Adalimumab (Humira) is a TNF-α blocker that is injected subcutaneously every 2 weeks. All three are very effective in treating RA, especially when combined with methotrexate. However, the long-term toxicity of these new medications is unknown, and all three result in an increased susceptibility to infections. Anakinra (Kineret) is a biologic DMARD that blocks IL-1 receptors and requires daily subcutaneous injections. Like the anti-TNF-α biologics, it is associated with an increased susceptibility to infections. Rituximab (Rituxan) is an intravenously administered monoclonal antibody that targets certain B-cells and lasts from many months up to a year. Abatacept (Orencia) is an antibody that targets T-cells and requires a monthly intravenous injection.

The surgeon must be aware of the potential toxicities and side effects associated with these medications. The preoperative evaluation of patients on DMARDs should include laboratory panels to screen for hepatotoxicity and bone-marrow suppression. In addition, the surgeon must weigh the risk of increased susceptibility to infection with the benefits of surgery.

The perioperative management of DMARDs and other rheumatoid medications is somewhat controversial and should be coordinated with the patient's rheumatologist. The perioperative cessation of DMARDs or corticosteroids can result in an acute deterioration (rheumatoid flare-up) that is poorly tolerated by the patient. In fact, the flare-up may be so severe that it affects the patient's ability to participate in postoperative rehabilitation. In general, methotrexate should be continued throughout the perioperative period at its normal dose. Methotrexate does not appear to increase infection rates in patients with RA undergoing elective surgery. Furthermore, corticosteroids, when used alone or in combination with methotrexate, do not affect wound infection rates and should not be stopped in the perioperative period. Data on the other conventional DMARDs are more limited, and their perioperative dosing should be discussed with the patient's rheumatologist.

The appropriate perioperative management of biologic DMARDs, particularly the TNF-α inhibitors, is less clear. There are few data and no large studies to guide perioperative dosing of the biologic DMARDs. Therefore, a conservative approach is recommended at this time. In general, the TNF-α inhibitors should be held 2–4 weeks before and after surgery. Similarly, few data exist regarding the other biologics, and a similar approach is recommended.

Wrist involvement

Within the wrist and distal radioulnar joint (DRUJ) cartilage is degraded and bony erosions develop. Bony erosions occur first at sites of nutrient vessels and at the joint margins because there is no protective cartilage at these locations, thereby giving the invading pannus direct access to the bone. Radiographic changes are first noted at the scaphoid waist, the ulnar styloid, and the DRUJ ( Fig. 19.3 ). As the arthritis progresses, the radiocarpal joint becomes involved. Bony destruction tends to be more severe at the radiocarpal joint than the mid-carpal joint, although both joints are often involved. In late stages, the volar lip of the distal radius becomes severely eroded, allowing proximal migration, volar translation and volar angulation of the lunate, with compensatory mid-carpal extension ( Figs. 19.4 & 19.5 ).

The ligaments of the wrist and DRUJ are affected as well. As the pannus proliferates, it stretches and then directly invades the intrinsic and extrinsic wrist ligaments. Synovitis occurring at the scaphoid waist weakens the radioscaphocapitate ligament, leading to ulnar translocation of the carpus ( Figs. 19.6 & 19.7 ). Destruction of the scapholunate ligament leads to carpal instability, and further contributes to ulnar translocation of the carpus. At the DRUJ, pannus invades the triangular fibrocartilage complex (TFCC), including the dorsal and palmar radioulnar ligaments, resulting in DRUJ instability and eventually dorsal dislocation of the ulnar head. Pannus also destroys the extensor carpi ulnaris (ECU) subsheath, resulting in volar subluxation of the ECU. The ECU's function as a wrist extensor and ulnar deviator is lost, contributing to supination and radial deviation of the carpus. The combination of dorsal dislocation of the ulnar head, carpal supination, and volar subluxation of the ECU is termed the “caput ulnae” ( Figs. 19.8 & 19.9 ).

End-stage wrist arthritis falls into three different clinical patterns, depending upon the degree of bony destruction and ligamentous instability. These patterns are: (1) ankylosis; (2) arthritic stable; and (3) arthritic unstable (subdivided into ligamentous unstable and bony unstable). In the ankylosing wrist, the carpus undergoes autofusion. Frequently, ankylosis occurs with the wrist in acceptable alignment, although this is not always the case. In the arthritic stable wrist, the arthritis follows a pattern similar to that of osteoarthritis. Ligamentous destruction is limited, and the wrist remains stable over time. In the unstable wrist, there is progressive malalignment. In the ligamentous unstable wrist, bony destruction is minimal, whereas in the bony unstable wrist, there is severe loss of bone resulting in instability and eventually dislocation.

On the dorsal aspect of the wrist, synovitis develops within the extensor tendon compartments ( Fig. 19.10 ). Depending upon the extent of the synovitis, there may be a bulge protruding beyond the distal and proximal margins of the extensor retinaculum, creating an hourglass appearance. Direct invasion of extensor tendons, combined with attritional wear over sharp bony edges at the ulna and DRUJ can lead to tendon ruptures. The extensor tendons to the small finger are usually affected first. Extensor tendon ruptures often progress radially, eventually affecting all digits. This ulnar to radial progression of extensor tendon ruptures is called the Vaughan–Jackson syndrome ( Fig. 19.11 ). Tendon ruptures are sudden and may not be painful. They can be difficult to identify in patients with severe deformity and must be differentiated from volar subluxation of the MCP joint, radial nerve palsy, and extensor tendon subluxation at the MCP joint. On the volar aspect of the wrist, sharp erosions on the scaphoid can result in attritional rupture of the flexor pollicis longus (FPL) tendon, known as a Mannerfelt lesion ( Fig. 19.12 ). Within the carpal tunnel, synovial pannus and tenosynovitis proliferate, creating a space-occupying lesion that results in carpal tunnel syndrome ( Fig. 19.13 ).

Finger and thumb involvement

In the fingers the MCP and PIP joints are primarily affected, with relative sparing of the DIP joints. As cartilage is degraded, joint space narrowing is seen. Pannus invades at the margins of the joints, resulting in marginal bony erosions. The joint capsule and collateral ligaments are initially stretched and then directly invaded by the synovial pannus, resulting in instability and deformity.

At the MCP joints, the typical pattern of instability is volar subluxation and ulnar deviation, and is the result of multiple forces. Synovitis at the MCP joint erodes the dorsoradial portion of the joint capsule early in the disease process, creating an early tendency towards ulnar deviation ( Fig. 19.14 ) and volar subluxation ( Fig. 19.15 ). Radial deviation at the wrist creates an ulnar approach of the extensor tendons to the MCP joints, which further contributes to ulnar deviation ( Fig. 19.16 ). In addition, ulnar deviation forces during oppositional and key pinch stretch the dorsoradial portion of the capsule and the radial collateral ligament, particularly in the index and long fingers. Finally, continued dorsoradial invasion of the pannus weakens the radial sagittal bands, causing ulnar subluxation of the extensor tendons between the metacarpal heads, which further increases ulnar deviation force on the MCP joints, and weakens extension power at the MCP joints ( Fig. 19.17 ).

One of two patterns of finger deformity can occur: the swan-neck ( Fig. 19.18 ) or boutonnière deformity ( Fig. 19.19 ). Although swan-neck deformity is more common, either deformity can occur, and both can occur in the same hand. Swan-neck deformity can originate from pathology at the MCP joint, the PIP joint, or the DIP joint ( Fig. 19.20 ). At the DIP joint, the terminal tendon insertion attenuates or erodes, resulting in a mallet finger. This causes an imbalance in the extensor mechanism, with increased extension force at the PIP joint. MCP flexion also contributes to increased pull of the central slip at the PIP joint. When these increased extension forces are combined with synovial disruption of the PIP volar plate, PIP hyperextension occurs, resulting in swan-neck deformity. Swan-neck deformity can originate at the PIP joint as well. Pannus stretches and erodes the volar plate and capsule, allowing hyperextension. Flexor tendon rupture may also contribute to a loss of flexion force at the PIP joint. The lateral bands slide dorsally, limiting PIP flexion. DIP joint flexion is a secondary phenomenon in this scenario and is due to slack in the extensor mechanism combined with tightening of the flexor digitorum profundus (FDP) from PIP hyperextension. MCP pathology can initiate the development of swan-neck deformity as well. The flexed MCP position results in excessive pull through the extensor mechanism. The intrinsics also tighten over time, thereby hyperextending the PIP joint when MCP extension is attempted. The lateral bands also migrate dorsally, contributing to the deformity. The most debilitating result of swan-neck deformities is loss of flexion at the PIP joints, resulting in an inability to flex the fingers for pinching and grasping.

Boutonnière deformities are usually less debilitating than swan-neck deformities because pinch and grasp are usually preserved. Unlike swan-neck deformities, boutonnière deformities always begin with pathology at the PIP joint ( Fig. 19.21 ). The initial insult is stretching, erosion, and rupture of the central slip insertion on the base of the middle phalanx. Attenuation of the dorsal capsule, transverse retinacular ligament and triangular ligament allows the lateral bands to sublux volar to the joint axis of rotation, becoming PIP flexors. The volar position of the lateral bands makes them even more effective extensors of the DIP joint, resulting in secondary DIP hyperextension.

Synovitis also develops within the flexor tendon sheath and can lead to triggering or rupture of the flexor tendons. Trigger digits associated with RA are distinct in mechanism and pathology from non-rheumatoid trigger digits and occur secondary to synovitis or small rheumatoid nodules in the flexor tendon. The specific location of the synovitis or rheumatoid nodules determines the presentation of the rheumatoid trigger finger. A nodule located proximal to the A1 pulley may present like a typical non-rheumatoid trigger finger with locking in flexion, or triggering during extension. A nodule just distal to the A2 pulley can result in the finger locking in extension or triggering during flexion. Diffuse tenosynovitis or multiple nodules can result in swelling and loss of flexion and extension.

The rheumatoid thumb deformity can be organized into five categories. Type I, the most common, is a boutonnière deformity with MCP flexion, IP hyperextension, and radial abduction of the metacarpal ( Fig. 19.22 ). Deformity begins when synovial pannus at the MCP joint erodes dorsally, attenuating and eventually rupturing the extensor pollicis brevis (EPB) tendon insertion, and displacing the extensor pollicis longus (EPL) ulnarly and volarly. Because of the loss of dorsal capsule and the loss of the EPB, the MCP joint flexes and subluxates volarly. Hyperextension at the IP joint occurs secondarily and can be exacerbated in patients with an FPL rupture. Type III rheumatoid thumb deformity is a swan-neck deformity, and is the second most common deformity, presenting with MCP hyperextension, IP flexion, and metacarpal adduction contracture. This deformity begins at the carpometacarpal (CMC) joint, with attenuation of the volar beak ligament. As the CMC joint subluxates or dislocates, metacarpal adduction occurs in a similar fashion to non-rheumatoid CMC arthritis. MCP joint hyperextension occurs secondarily as the thumb compensates for the adducted metacarpal and is exacerbated by volar plate attenuation or erosion from pannus invasion.

Types II, IV, and V are less common, but do occur. Type II rheumatoid thumb includes MCP flexion and IP extension, but unlike a type I boutonnière deformity, there is dislocation or subluxation at the CMC joint. Type IV is a gamekeeper's deformity secondary to synovial pannus destruction of the ulnar collateral ligament. Type V is MCP hyperextension, and compensatory flexion at the IP joint, similar to a swan-neck deformity (type III) but without metacarpal adduction contracture.

Perioperative considerations

Care must be taken during the preoperative workup of RA patients, because many unique problems can impact the safety and timing of surgery. Airway management can be quite difficult. Temporomandibular joint arthritis can limit oral opening, making intubation difficult. Glottic narrowing can also occur due to inflammation or arthritis of the cricoarytenoid joints, creating further difficulty with airway management. Atlantoaxial instability is another concern, and is quite common in patients with RA. Flexion of the neck during intubation in patients with significant instability can cause spinal cord injury or death. Therefore, preoperative cervical spine flexion–extension radiographs should be obtained in all rheumatoid patients preoperatively. Fiberoptic intubation with the patient in a cervical collar is recommended in patients with atlantoaxial instability.

Cardiac function can be affected as well. Pericardial effusion, constrictive pericarditis, or conduction block can occur secondary to RA. In addition, RA patients are at increased risk for coronary artery disease. Pulmonary involvement may include rheumatoid nodules, pleural effusion, and interstitial disease. Patients with long-standing disease are at risk for Felty's syndrome, a combination of splenomegaly, neutropenia, and secondary thrombocytopenia. For the above reasons, RA patients undergoing surgery should have a thorough preoperative anesthesia evaluation including an EKG, metabolic panel, complete blood count and differential, chest and cervical spine radiographs.

Goals of surgery

The goals of surgery in RA patients are pain relief, improvement of function, prevention of progression, and improvement of appearance. In general, pain relief can be accomplished reliably by arthrodesis or arthroplasty. Because of this, pain is the primary indication for surgery in the rheumatoid patient. Improvement of function is less reliably accomplished, and although important, is a secondary indication for surgery. It is important to remember that deformity does not equal loss of function. Many patients have little pain and are able to function quite well in spite of severe deformity. These patients may not benefit from surgery. Slowing the progression of disease is a third priority and is less often required in the era of effective DMARDs. However, in some situations, surgery is required to prevent progression of disease. For example, a Darrach procedure (resection of the distal ulna) and dorsal tenosynovectomy in the setting of an extensor tendon rupture can prevent or delay additional extensor tendon ruptures. Appearance is considered a last priority. However, aesthetic considerations should not be discounted as these issues are important to RA patients.

Sequence of surgery

In general, proximal problems within the upper extremity should be corrected first, particularly if they affect more distal problems. For example, wrist surgery should be performed prior to finger surgery, because the deformity at the wrist exacerbates the finger deformity. In practice, however, the sequence of surgery may be dictated by patient preference. For example, a patient with severe swan-neck deformities and a pain-free but ulnarly subluxated wrist may not accept the idea of wrist surgery before correcting the finger deformity. Another consideration is the mobility of the patient. Many RA patients use crutches or canes for ambulation, or may even be confined to a wheelchair, resulting in a loss of mobility during the recovery period after hand surgery. The surgeon should discuss these issues with the patient preoperatively so that preparations can be made.

Operations at the wrist level

Wrist synovectomy/dorsal tenosynovectomy

A minority of patients will have persistent wrist synovitis or dorsal tenosynovitis that is painful and unresponsive to at least 6 months of maximal medical treatment. Wrist synovectomy and/or dorsal tenosynovectomy may be effective in improving pain in these patients. Whether this significantly slows the progression of disease is unknown.

A midline longitudinal incision is made over the dorsal wrist, and skin flaps are elevated at the level of the extensor retinaculum, preserving the radial and ulnar sensory nerves that lie within the subcutaneous tissue. If there is a large amount of synovitis, it can be seen deep to the attenuated extensor retinaculum ( Fig. 19.23 ). The extensor retinaculum is incised along the radial border of the first extensor compartment, leaving enough substance intact for later closure. The retinaculum is elevated in an ulnar direction to, but not into the sixth extensor compartment, exposing the extensor tendons. The extensor retinaculum is often very attenuated, and care should be taken to preserve its integrity during elevation. Extensor tenosynovectomy is then performed. Working systematically, each extensor tendon is retracted individually, and synovium is excised with curved tenotomy scissors ( Fig. 19.24 ).

Clinical tips

• Always be prepared to perform tendon transfers when you are doing a tenosynovectomy.

• Ruptured tendons may be held together by thick pannus and adhesions.

• Be sure to talk to tenosynovectomy patients about the possibility of tendon transfer.

After completing the extensor tenosynovectomy, a posterior interosseous neurectomy may be performed to improve pain relief. The posterior interosseous nerve is identified on the floor of the fourth extensor compartment and a 2-cm segment is excised, with cauterization of the proximal stump.

If painful wrist synovitis is present, a ligament-sparing capsulotomy is made. Synovial pannus is identified at the radiocarpal and mid-carpal joints. With the wrist flexed and distracted, a synovial rongeur is used to remove all synovium within the radiocarpal and mid-carpal joints. Any sharp edges are smoothed with a curette or rongeur. If DRUJ synovitis is present, a longitudinal incision is made over the DRUJ, in the floor of the fifth extensor compartment. This incision can be extended 90° ulnarly just proximal to the TFCC if necessary for additional exposure. Pronation also improves exposure of the DRUJ. Synovial pannus is removed with a synovial rongeur. Sharp bony edges are smoothed with a rongeur to prevent tendon ruptures. The capsulotomy incisions are closed with 3-0 absorbable suture.

If any rough bony surfaces remain exposed after closure of the capsule, the retinaculum can be divided transversely, creating two ulnarly based retinacular flaps. One flap is sutured deep to the extensor tendons, covering the exposed bony surfaces. The other retinacular flap is closed dorsal to the extensor tendons, leaving the EPL transposed ( Fig. 19.25 ). Alternatively, if the ECU tendon is subluxated volarly, the retinaculum can be used to stabilize it. The ECU tendon synovium is debrided, and the ECU is then relocated to its normal position dorsal to the ulna. Half of the retinacular flap is placed deep to the ECU tendon, then wrapped back dorsally and radially and sutured to itself at the border of the fifth extensor compartment, securing the ECU dorsal to the wrist axis of rotation.

Clinical tips

• In some cases, the extensor retinaculum is attenuated and cannot be used to pad rough surfaces.

• Be sure to have acellular dermal matrix (dermal allograft) available for padding if needed.

Postoperative care

The wrist is immobilized for 2–3 weeks, followed by initiation of motion. If the DRUJ was debrided, a sugar-tong splint should be used to prevent forearm rotation. If the wrist or DRUJ is unstable prior to surgery, a longer period of mobilization may be required.

Outcomes, prognosis, and complications

Synovectomy of the wrist or DRUJ usually relieves pain, but recurrence of synovitis is the rule rather than the exception, although the rate at which synovitis recurs is variable. Whether wrist synovectomy significantly alters the course of the disease is not known. Dorsal tenosynovectomy, on the other hand, likely prevents or delays the occurrence of extensor tendon ruptures.

Secondary procedures

If the patient develops recurrent painful synovitis after wrist joint synovectomy, a definitive wrist procedure such as arthrodesis may be indicated.

Hints and tips

• Allow at least 6 months of maximized medical treatment prior to considering surgery.

• Concomitant posterior interosseous nerve (PIN) neurectomy may improve pain relief.

• Ensure that all rough bony surfaces are smoothed and ­covered with soft tissue.

Distal ulna resection (Darrach procedure)

Distal ulna resection may be indicated for painful DRUJ instability, painful destruction of the DRUJ, or caput ulnae syndrome with extensor tendon ruptures. It can be performed in isolation, but is often combined with extensor tenosynovectomy, extensor tendon repairs or tendon transfers, wrist arthrodesis, or wrist arthroplasty.

If performed in isolation, a 3-cm longitudinally oriented chevron incision is made over the dorsal aspect of the ulnar head ( Fig. 19.26 ). If combined with another wrist procedure, skin flaps and retinacular flaps are elevated, and extensor tenosynovectomies are performed as described above. A longitudinal incision is made in the floor of the fifth extensor compartment, with a 90° extension ulnarly just distal to the head of the ulna, and just proximal to the TFCC. Although it is often destroyed, when the TFCC is present, it should be preserved. The capsule is elevated off the ulnar head, and the ulnar head and neck are dissected subperiosteally with a 15-blade and Freer elevator ( Fig. 19.27 ). The ECU is usually subluxed volarly and is elevated off the ulna during subperiosteal dissection. Hohmann retractors are used to provide exposure of the neck and head of the ulna. Once the ulnar head and neck have been exposed circumferentially, a sagittal saw is used to create a transverse osteotomy at the neck of the ulna, at the level of the proximal margin of the sigmoid notch of the radius. Any remaining soft-tissue attachments are released, and the ulnar head is removed ( Fig. 19.28 ). The dorsal edge of the ulnar stump is then beveled with the sagittal saw and rasped smooth to prevent tendon abrasion and rupture. Any remaining synovial pannus can now be easily accessed and is debrided with a synovial rongeur.

Prior to closure, the ulnar stump should be stabilized and the normal relationship between the ulna and the carpus should be re-established or improved. The pronator quadratus is elevated subperiosteally from the volar ulnar aspect of the ulna, leaving its attachment to the radius intact. It is important to keep the periosteum attached to the pronator quadratus. It is then delivered through the interosseous space and draped dorsally over the ulnar stump. The ulna is reduced volarly. While maintaining the ulnar stump in reduction, the pronator quadratus and its periosteum are sutured securely to the dorsal aspect of the ulnar stump, using bone anchors if necessary ( Fig. 19.29 ). In this position, the pronator quadratus serves as a buffer against impingement between the radius and ulna, and also helps prevent dorsal subluxation of the ulna.

Alternatively, a distally based slip of the ECU is elevated. The DRUJ capsule and periosteal flaps are closed with non-absorbable sutures, and are imbricated tightly with the ulna reduced volarly. The slip of ECU is then woven through the capsule at the distal end of the ulna and is then sutured to the dorsal ulnar aspect of the radius. This sling helps stabilize the ulnar stump and also reduces carpal supination ( Fig. 19.30 ). Pre- and postoperative radiographs are shown in Fig. 19.31 .

Clinical tips

• Darrach stabilization using the ECU tendon is particularly useful when a wrist fusion has been performed.

• The ECU tendon is divided at the muscle/tendon junction.

• A hole is made in the dorsal cortex of the ulna 2 cm proximal to the Darrach osteotomy using a bur.

• The ECU tendon passed into the medullary canal of the ulna stump, and withdrawn out the hole in the cortex.

• The tendon is then pulled distally, cinched tight, and sutured to itself.

• In the setting of a wrist fusion, the ECU can be tensioned tightly without concern for creating ulnar deviation of the wrist, resulting in excellent ulna stump stability.

Postoperative care

The patient is placed in a sugar-tong splint in supination for 2–3 weeks prior to allowing wrist motion and forearm rotation. If a tendon transfer is done, the patient should be splinted for 4 weeks.

Outcomes, prognosis, and complications

One potential complication after distal ulna resection is extensor tendon rupture due to attrition over the sharp dorsal edge of the osteotomy. This is prevented by beveling and rasping down the dorsal edge of the osteotomy, and by performing a soft-tissue stabilizing procedure at the time of the Darrach procedure in order to minimize dorsal subluxation of the ulnar stump. Another potential complication is painful radio­ulnar convergence and impingement, which tends to occur during loading. Again, stabilization and/or padding of the distal ulna at the time of Darrach procedure as described above helps to minimize this.

Secondary procedures

Persistent painful instability or radioulnar impingement may be treated with a soft-tissue stabilization procedure using the ECU as described above. Alternatively, ulnar head implant arthroplasty may be considered to salvage the failed Darrach procedure complicated by painful radioulnar impingement.

Hints and tips

• Create a dorsal bevel after making the transverse osteotomy, and smooth with a rasp to prevent attrition ruptures.

• Distal ulna resection should be performed at the time of extensor tendon transfers if the distal ulna was the source of extensor tendon rupture.

• A stabilizing procedure should be performed to decrease recurrent dorsal subluxation, minimize radioulnar convergence, and reduce carpal subluxation.

Partial wrist arthrodesis (radioscapholunate arthrodesis)

In some rheumatoid wrists, the radiocarpal joint becomes arthritic with relative preservation of the mid-carpal joint ( Fig. 19.32 ). In these patients, radioscapholunate arthrodesis may be indicated to treat refractory pain secondary to radiocarpal arthritis. Patients should understand that they will lose approximately 60% of wrist flexion–extension, depending upon the quality of the mid-carpal joint. In addition, patients should be consented for the possibility of complete wrist arthrodesis if the mid-carpal joint is found to be substantially arthritic at the time of surgery.

The skin and retinacular incisions are the same as described above. Extensor tenosynovectomies are performed if required, and a posterior interosseous neurectomy is performed. An H-shaped capsulotomy is made, exposing the radiocarpal and mid-carpal joints. Radiocarpal and mid-carpal synovectomies are performed. The quality of the mid-carpal joint is assessed, and the decision to proceed with radiocarpal fusion versus complete wrist fusion is made. The radiocarpal joint is assessed as well. In some cases, the radioscaphoid articulation is preserved, allowing the surgeon to perform a radiolunate fusion, although in most instances the entire radiocarpal joint is arthritic. With the wrist flexed and distracted, a rongeur is used to remove the remaining articular cartilage and subchondral bone from the distal radius and the proximal articular surfaces of the lunate and scaphoid. The articular surfaces are prepared in this manner until bleeding cancellous bone is encountered. During joint surface preparation, the matching concave–convex surfaces of the radiocarpal joint should be preserved. The carpus is then reduced by maneuvering the lunate into neutral flexion–extension, correcting any scapho­lunate gap, and correcting ulnar translocation if present. The use of 0.062-inch Kirschner wires as joysticks may be necessary for reduction. The scaphoid and lunate are temporarily held in reduction with 0.062-inch radiocarpal K-wires, and a mini C-arm is used to confirm carpal alignment. Next, the distal pole of the scaphoid is resected in order to improve mid-carpal motion. A transverse osteotomy is made at the proximal margin of the distal pole of the scaphoid using a reciprocating saw. The distal pole is then removed piecemeal with a rongeur.

Autologous cancellous bone graft is packed into the fusion site. This should be obtained from the iliac crest, or from the resected distal pole of the scaphoid and from the distal ulna if a Darrach procedure has been performed. Bone graft should not be harvested from the distal radius, as this reduces the stability of the radioscapholunate fixation. Fixation is achieved with headless compression screws that are inserted into the dorsal aspect of the distal radius and driven distally and volarly into the scaphoid and lunate. Three or four compression screws are used, with two passing from the radius into the scaphoid, and one or two passing from the radius into the lunate ( Fig. 19.33 ). It is usually necessary to back out the temporary fixation K-wires in order to achieve compression. In addition, in order to achieve even compression when two screws are placed across one articulation, the screws should be simultaneously advanced. After screw placement, final C-arm views are used to confirm carpal alignment and screw position. The mid-carpal joint is directly examined to ensure that there is no screw penetration. If there is any concern about the stability of the fixation, supplemental K-wires can be placed. If the bone quality is too poor to support compression screws, as it often is in patients with rheumatoid arthritis, fixation can be performed with K-wires alone ( Fig. 19.34 ). Other alternatives for fixation include staples or a T-shaped plate. The capsule is closed, and the extensor retinaculum is closed with the EPL transposed.

Postoperative care

The wrist is immobilized until bony union occurs. Active and passive range of motion (ROM) and strengthening exercises are initiated after bony union occurs.

Complete wrist arthrodesis

Complete wrist arthrodesis is an effective treatment for the painful and unstable wrist. However, the loss of wrist motion after complete arthrodesis can cause significant functional difficulty, particularly if the patient has a stiff contralateral wrist. Because of this, it should be reserved for patients with recalcitrant pain or debilitating instability or malalignment, in spite of maximum medical management, steroid injections, and wrist splinting.

In patients with high-quality bone, a dorsal wrist fusion plate or headless compression screws can be used ( Figs. 19.35 & 19.36 ). However, if bone quality is poor, Steinmann pin fixation may be performed. The wrist is exposed as described above for radioscapholunate fusion. If indicated, a Darrach procedure is performed as described above. The radiocarpal and mid-carpal joints are exposed. With the wrist flexed and distracted, a synovial rongeur is used to debride synovial pannus, allowing access to the articular surfaces. A rongeur is then used to remove articular cartilage and subchondral bone from the opposing articular surfaces, until bleeding cancellous bone is encountered ( Fig. 19.37 ). A small Steinmann pin is drilled retrograde into the radius in order to create a track for the final Steinmann pin. The starting point on the radius is chosen carefully, in order to allow the Steinmann pin to pass directly into the isthmus of the medullary canal without any angulation. The correct starting point is usually in the dorsal half of the radius articular surface, and near the interval between the scaphoid and lunate fossae. Fluoroscopy is used to confirm the position of the Steinmann pin. The small Steinmann pin is removed and exchanged for the largest diameter Steinmann pin that will fit into the medullary canal of the radius. The large Steinmann pin is removed from the radius and then it is drilled antegrade through the carpus, exiting the carpus at the second or third intermetacarpal space, and exiting the skin between the MCP joints. With the radius and carpus reduced, the Steinmann pin is tapped retrograde back into the radius, and through the isthmus of the medullary canal ( Fig. 19.38 ). It is cut distally at the skin, and then tapped 2–3 cm proximal to the level of the skin. If necessary, additional fixation with temporary K-wires can be used. Cancellous autograft is packed into the radiocarpal and mid-carpal joints. The capsule is closed with 3-0 absorbable sutures, and the retinaculum and skin are closed as described above. The wrist is immobilized until union occurs.

An alternative is to use two smaller Steinmann pins. The technique is similar to that described above, except that one pin passes through the second intermetacarpal space, and one passes through the third intermetacarpal space. An oblique K-wire can be added to augment the fixation. The pins are cut deep to the skin and can be removed after bony union is achieved ( Figs. 19.39 & 19.40 ). If future MCP arthroplasty is planned, and there is no reason to preserve the articular surface of the metacarpal head, one pin can be advanced through the medullary canal of the long finger metacarpal, exiting the metacarpal head distally, and then tapped proximally into the radius after reduction. If a Steinmann pin is placed in the medullary canal of the long finger metacarpal, it should be tapped proximally to allow enough room for future MCP arthroplasty ( Figs. 19.41 & 19.42 ). As noted above, in patients with high-quality bone, a dorsal wrist fusion plate can be used. These plates allow compression across the wrist, and result in very stable fixation.

Clinical tips

• When using a wrist fusion plate, it is important to compress the arthrodesis site.

• Eccentric drilling and serial compression using two screw holes helps augment the compression.

• Do not rely on the plate and screws to do all the work of compression.

• Manually compress the arthrodesis as much as possible as the compression holes are drilled and the screws advanced.

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