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.^3–5 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.⁶

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.⁷ 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.⁴

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.⁸

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.⁹ Coffee intake and exposure to silica have also been associated with RA.⁴ In addition, infectious diseases likely act as a trigger in genetically susceptible individuals. Possible triggering agents include mycoplasma, enteric bacteria, Epstein–Barr virus, and others viral and bacterial triggers.^10–13 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.^14–16

Fig. 19.1 The erosive synovial pannus consists of hypertrophic synovium and inflammatory cells.

Fig. 19.2 Gross appearance of synovial pannus.

Medical management

The medications used to treat RA include non-steroidal 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.¹⁷ 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 two weeks. All three are very effective in treating RA, especially when combined with methotrexate.^18,19 However, the long-term toxicity of these new medications is unknown, and all three result in an increased susceptibility to infections.²⁰ 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.^21–23 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.^21,22 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.²³ 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.²² 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.²² Similarly, few data exist regarding the other biologics, and a similar approach is recommended.²⁴

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.³³ Radiographic changes are first noted at the scaphoid waist, the ulnar styloid and the distal radioulnar joint (DRUJ) (Fig. 19.3).^34,35 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.³⁶ 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).^35,37

Fig. 19.3 PA radiograph of the left wrist, demonstrating early involvement of the DRUJ, as well as scattered carpal erosions from invasive synovitis.

Fig. 19.4 PA radiograph of the right wrist, demonstrating severe involvement of the wrist.

Fig. 19.5 Lateral radiograph of the right wrist, demonstrating destruction of the volar lip of the radius, with volar subluxation of the carpus.

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 (Fig. 19.6).³⁸ 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.^39,40 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 19.7, 19.8).

Fig. 19.6 PA radiograph of the left wrist, demonstrating ulnar translocation of the carpus. Note that the lunate no longer sits in the lunate fossa.

Fig. 19.7 Caput ulnae, with dorsal dislocation of the ulnar head and carpal supination.

Fig. 19.8 Lateral radiograph of the wrist, demonstrating a dorsally dislocated ulnar head.

End-stage wrist arthritis falls into three different clinical patterns, depending upon the degree of bony destruction and ligamentous instability.⁴¹ These patterns are: (1) ankylosis; (2) arthritic stable, and (3) 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. 19.9). 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 Vaughn–Jackson syndrome (Fig. 19.10).⁴² 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. 19.11).⁴³ Within the carpal tunnel, synovial pannus and tenosynovitis proliferate, creating a space-occupying lesion that results in carpal tunnel syndrome (Fig. 19.12).

Fig. 19.9 Extensor tenosynovitis protruding from under the extensor retinaculum distally.

Fig. 19.10 Patient with Vaughn–Jackson syndrome, demonstrating extensor tendon ruptures associated with a caput ulnae.

Fig. 19.11 Axial cross-section of the radial side of the wrist, demonstrating the Mannerfelt lesion. Note the proximity of the flexor pollicis longus tendon to the sharp erosion on the volar aspect of the scaphoid.

Fig. 19.12 Large proliferative flexor tendon tenosynovitis.

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.^44,45 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. 19.13) and volar subluxation (Fig. 19.14).^46,47 Radial deviation at the wrist creates an ulnar approach of the extensor tendons to the MCP joints, which further contributes to ulnar deviation (Fig. 19.15).⁴⁸ 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.⁴⁹ 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. 19.16).^35,50

Fig. 19.13 Ulnar deviation at the MCP joints (ulnar drift).

Fig. 19.14 Radiograph of bilateral hands, demonstrating flexion and volar subluxation of the MCP joints.

Fig. 19.15 Radial deviation and ulnar translocation at the wrist contribute to ulnar deviation at the MCP joints.

Fig. 19.16 The extensor tendons to displace ulnarly and volarly into the space between the metacarpal heads, making them ineffective as MCP extensors, and adding to ulnar deviation force.

One of two patterns of finger deformity can occur, the swan-neck (Fig. 19.17) or boutonniere deformity (Fig. 19.18). 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. 19.19). 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. 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.

Fig. 19.17 Classic swan-neck deformities of all fingers, with MCP flexion, PIP hyperextension, and DIP flexion.

Fig. 19.18 Boutonniere deformity of the right ring and small fingers, and left small finger. Left ring finger demonstrates very early boutonniere deformity.

Fig. 19.19 (A) Swan-neck deformity originating from a mallet finger, with subsequent increased extension force at the PIP joint. (B) Swan-neck deformity originating at the PIP joint, with volar plate attenuation and possible FDS rupture due to PIP synovitis, and subsequent dorsal subluxation of the lateral bands.

Boutonniere deformities are usually less debilitating than swan-neck deformities, because pinch and grasp are usually preserved. Unlike swan-neck deformities, boutonniere deformities always begin with pathology at the PIP joint (Fig. 19.20). 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.

Fig. 19.20 Boutonniere deformity secondary to synovitis at the PIP joint, with attenuation of the central slip, and subsequent volar subluxation of the lateral bands.

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 nonrheumatoid trigger digits, and occur secondary to synovitis or small rheumatoid nodules in the flexor tendon.⁵¹ 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 nonrheumatoid 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.^52,53

Thumb deformity can be organized into five categories. Type I, the most common, is a boutonniere deformity with MCP flexion, IP hyperextension, and radial abduction of the metacarpal (Fig. 19.21). 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 nonrheumatoid 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.

Fig. 19.21 Boutonniere deformity of the thumb.

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 boutonniere 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.⁵⁴ 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.⁵⁵

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 anaesthesia evaluation including an EKG, metabolic panel, complete blood count and differential, chest X-ray, 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

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.^56,57 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. 19.22). 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. 19.23). In some cases, it becomes clear during tenosynovectomy that an extensor tendon rupture has previously occurred, and that the ruptured extensor tendon or tendons are held together by a mass of adhesions and synovial pannus. This situation should be discussed preoperatively with the patient, as tendon transfers will be required. 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.

Fig. 19.22 Extensor tenosynovitis of the right wrist, with severely attenuated extensor retinaculum.

Fig. 19.23 The extensor tenosynovitis has been partially removed. Note the redundancy of the extensor tendons, which have been stretched by the long-standing tenosynovitis.

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. 19.24). Alternatively, if the ECU tendon is subluxated volarly, the retinaculum can be used to stabilize it. The ECU tendon is synovectomized and 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.

Fig. 19.24 One retinacular flap (the distal half of the retinaculum) has been placed deep to the extensor tendons to protect them from rough bony surfaces. The other flap (the proximal half of the retinaculum) has been sutured dorsal to the extensor tendons to prevent bow-stringing.

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

Wrist synovectomy/dorsal tenosynovectomy

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

• Concomitant 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 ulna 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. 19.25). 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. 19.26). 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. 19.27). 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.

Fig. 19.25 Chevron incision made directly over the ulnar head, with skin flaps elevated and extensor retinaculum exposed.

Fig. 19.26 The DRUJ and ulnar head have been exposed through an incision in the floor of the fifth extensor compartment.

Fig. 19.27 The ulnar head has been removed. The distal end of the stump will be beveled dorsally.

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. 19.28). 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.

Fig. 19.28 The pronator quadratus is released from the volar aspect of the ulna, passed through the interosseous space, and sutured to the dorsal aspect 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. 19.29). Pre- and postoperative radiographs are shown in Figure 19.30.

Fig. 19.29 Distally based slip of ECU is used to stabilize the ulnar stump.

Fig. 19.30 Pre- and postoperative radiographs demonstrating resection of the ulnar head.

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 radio-ulnar 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 radio-ulnar 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 complicated by painful radio-ulnar impingement.

Hints and tips

Distal ulna resection

• 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.

Related posts:

Technology innovation in plastic surgery Cleft and craniofacial orthognathic surgery Managing the cosmetic patient TMJ dysfunction and obstructive sleep apnea Fractures and dislocations of the wrist and distal radius Repair of bilateral cleft lip

Stay updated, free articles. Join our Telegram channel

Join