Rheumatoid arthritis is a chronic, progressive, systemic autoimmune inflammatory disease that primarily affects the synovium. Synovium is a thin layer of tissue that lines the articular surface of joints and tendon sheaths. It has two main functions: first, it acts as a selectively permeable membrane to control entry and exit of factors to the joint; second, it produces substances that lubricate the joint, e.g., synovial fluid. In certain disease processes, such as rheumatoid arthritis, there is an abnormal inflammatory response within the synovium. The synovium produces matrix metalloproteinases, collagenases, and cathepsins, which in turn cause damage to the cartilage, bone, and periosteum. The end result is a thickened, inflamed synovium called pannus, with erosion of adjacent soft tissues such as tendon, joint capsule, ligament, and bone.1–3
The risk for females developing rheumatoid arthritis is two or even three times that of males. The diagnosis of rheumatoid arthritis requires that four of seven key criteria are met and that symptoms have been present for at least 6 weeks. The criteria are as follows: 1. Morning stiffness in joints 2. Soft-tissue swelling at three or more joints 3. Symmetrical involvement of joints 4. Involvement of metacarpophalangeal (MCP), proximal interphalangeal (PIP), or wrist joints 5. Rheumatoid nodules 6. Seropositive for rheumatoid factor (RF) 7. Typical radiographic findings Therefore, although she has three of the key symptoms, she would need one further feature for the diagnosis, and her symptoms would need to persist for at least another 2 weeks. Note that a patient being rheumatoid factor negative does not exclude a diagnosis of rheumatoid arthritis. Only 70 to 80% of patients are seropositive, and some may develop positivity later in the disease. In some cases, patients become seropositive prior to experiencing any symptoms.1,2 There does appear to be an epidemiologic association between smoking and caffeine intake and rheumatoid arthritis, although the latter is not uniformly observed in all studies, and actually decaffeinated coffee may itself be a risk factor. Tea drinking seems to be inversely related to risk of developing rheumatoid.3 Joint space narrowing is one of the radiologic features of rheumatoid arthritis, but this is also seen in other forms of arthritis and joint spaces are sometimes increased because of swelling in early disease.1–3
3. Mikuls TR, Cerhan JR, Criswell LA, et al. Coffee, tea, and caffeine consumption and risk of rheumatoid arthritis: results from the Iowa Women’s Health Study. Arthritis Rheum 2002;46(1):83–91 Some of the common features of established rheumatoid arthritis in the hand are: • Attenuation or rupture of the radial sagittal bands of the extensor digiti communis (EDC) mechanism over the MCP joint • Radial deviation of the wrist • Ulnar deviation at the MCP joints • Volar (not dorsal) subluxation of the MCP joints • Rheumatoid nodules around the olecranon and ulnar proximal forearm or other pressure points • Swan neck and boutonniere finger deformities • • Synovitis with visible swellings from pannus (e.g., around extensor compartments at the wrist) Firm subcutaneous swellings over the DIP joint are more characteristic of Heberden’s nodes in osteoarthritis. It is important to understand the underlying mechanisms for rheumatoid hand deformities. Pannus generally starts to erode supporting soft tissues around joints and the tendency is for the wrist to drift into radial deviation and palmar subluxation. This alters the line of pull of the extrinsic extensor tendons to the digits, which in turn tends to lead to ulnar deviation of the digits at MCP joint level. The radial joint soft tissues are friable from inflammation and as such the dorsoradial joint capsule, radial sagittal bands, and radial collateral ligaments start to give way under this additional mechanical strain quite early in the disease process. The extensor tendons eventually drop into the sulcus between the metacarpal heads to the ulnar aspect of each joint, preventing active extension at the MCP joint and further exacerbating volar subluxation and ulnar drift at this level. Swan neck and boutonniere deformities in the digits follow suit due to the deranged mechanics of the intrinsic and extrinsic tendon mechanisms.1–3
Early sites of involvement around the wrist in rheumatoid arthritis include the scaphoid waist, scapholunate ligament, ulnar styloid, and distal radioulnar joint (DRUJ). Late changes occur at the radiocarpal joint and midcarpus. Other late findings include erosion of the volar rim of radius, volar subluxation of the carpus, ulnar translocation and radial deviation of carpus, and dorsal prominence of the ulna with carpal supination (caput ulnae).1,2
The characteristic finding at the MCP joints in rheumatoid arthritis is ulnar deviation with volar subluxation. Tightness of the flexor tendons is not usually implicated in this deformity. If, however, an A1 pulley release is considered for triggering, it should be borne in mind that the flexor tendon angle of approach may drift ulnarward and further exacerbate the ulnar deviation deformity already caused by other factors. Tightness of the intrinsics is implicated in the volar subluxation, rather than the flexor tendons, and this is the rationale for releasing the intrinsics at the ulnar aspect of each MCP joint and transferring them to augment the weaker radial aspect of each joint during reconstructive surgery. There are a number of contributory factors in ulnar deviation at the MCP joint. All of factors A through D are important. Radial deviation of the carpus alters the angle of approach of the extensor tendons to the MCP joints, while pinch forces between the thumb and fingers also push them in an ulnar direction. Pannus stretches and erodes the joint capsule (which tends to erode most dorsoradially because of the other forces in action); and the same factors similarly damage the radial sagittal bands and collateral ligaments. The extensor tendons then subluxate ulnarward into the valleys between the metacarpal heads, further increasing the deforming forces and pulling the digits ulnarward.1,2
The index PIP joint really has only one option for surgical management in severe rheumatoid arthritis and this is arthrodesis rather than arthroplasty. This joint is subject to significant lateral loading during normal activities such as key pinch and grip, and the surrounding soft-tissue support is inadequate in RA for arthroplasty to succeed. In contrast, the long, ring, or small finger PIP joints can be effectively treated with either arthrodesis or arthroplasty. Arthrodesis can be more predictable with fewer complications, but sacrifices joint motion. Arthroplasty can be less predictable with higher complication rates, but preserves motion. The PIP joints are frequently affected by RA; so, surgery is commonly required. The surgical access is straightforward using a dorsal approach. When arthrodesis surgery is performed to the PIP joints, the joint surfaces are prepared by removing cartilage and subchondral bone, exposing cancellous bone before being stabilized with the surgeon’s preferred methods which may include K-wires, a headless compression screw, or (the most common approach) tension band wiring. When PIP joint arthroplasty is performed, cartilage and subchondral bone are removed, the medullary canals are reamed to accept implant stems and a silicone prosthesis is inserted. Pyrocarbon or surface replacement arthroplasties are not good options in RA because of poor soft-tissue support.1,2
When stiff or fixed, swan neck deformities are much more debilitating than boutonniere deformities. With a boutonniere, patients can grip and pinch. With a swan neck, these motions are difficult or impossible. The swan neck deformity involves PIP joint hyperextension with DIP joint flexion (Fig. 98.1). It can occur secondary to joint abnormalities of the DIP, PIP, or MCP joints. This is in contrast to a boutonniere deformity, which involves PIP joint flexion with DIP joint hyperextension and is always secondary to an abnormality at the level of the PIP joint. Both boutonniere and swan neck deformities can occur secondary to pannus erosion that weakens joint support. The swan neck deformity can occur from extensor tendon rupture at the DIP joint (leading to a mallet deformity), rupture of the volar plate at the PIP joint, or rupture of the flexor digitorum superficialis (FDS) tendon insertion. Alternatively, a swan neck deformity can begin at the MCP joint secondary to volar subluxation and intrinsic muscle tightening. Central slip attenuation (resulting from pannus erosion) with lateral band subluxation describes the process underlying a boutonniere deformity in RA. Initial treatment for a swan neck deformity is with a splint, and rebalancing surgery is considered only if this fails, and the PIP joint remains supple. Surgical interventions include using a slip of the FDS tendon or one lateral band to prevent PIP joint hyperextension and may require intrinsic muscle release. PIP joint fusion in a more functional position may also be helpful.1–3
The most common thumb abnormality in a rheumatoid patient is a boutonniere deformity, which is also termed a Z-deformity. This involves MCP joint flexion with IP joint hyperextension and radial abduction of the metacarpal. It occurs because of dorsal pannus erosion leading to rupture of the EPB insertion and volar subluxation of the extensor pollicis longus (EPL). Swan neck deformity is commonly seen in rheumatoid patients, although less frequent in the thumb. This involves MCP joint hyperextension, IP joint flexion, and adduction contracture of the metacarpal secondary to CMC joint subluxation. This process occurs secondary to volar pannus erosion through the joint capsule and MCP joint volar plate (see Fig. 98.1)1,2 Fig. 98.1 Characteristics of swan neck and boutonniere deformities. A, Normal. B, Swan neck. C, Boutonniere deformity. (Adapted from Smith P, ed. Lister’s The Hand, 4th ed. London: Churchill Livingstone, 2002.) DIP flexion PIP hyperextension PIP flexion DIP hyperextension A B C
Pharmacologic agents used in rheumatoid arthritis can be broadly classified as nonsteroidal anti-inflammatory drugs (e.g., naproxen and indomethacin), steroids (e.g., prednisolone) and disease-modifying antirheumatoid drugs (DMARDs). DMARDs are further subdivided into conventional (e.g., methotrexate, sulfasalazine, and gold) and biologic (e.g., etanercept and infliximab). As a general guide, most medications used in rheumatoid arthritis can be continued safely during the perioperative period for relatively small procedures like MCP joint replacement. However, there is an exception with the biological DMARDS. These should be stopped for 2 to 4 weeks before and after surgery (depending on the half-life of the drug). The injectable biologic agents are anti-tumor necrosis factor-alpha agents, and their use is associated with increased gram-positive infection.1 If in doubt, you should discuss the perioperative management of rheumatoid medications with the patient’s rheumatologist, because stopping medications can lead to a rheumatoid flare.1,2
The most important and predictable indication for surgery in rheumatoid arthritis is pain management. Improved function is also clearly important and therefore an indication in many cases, but is less predictably achieved than pain relief. Neither deformity nor aesthetics alone are strong indications for surgery. For example, deformity can be severe, yet there may be absent pain and good function. Surgery to correct a visible deformity might risk downgrading function. When considering surgery, it is good practice to ensure all nonoperative measures have been explored. It is generally accepted that 6–12 months of medical therapy is adequate time to try before embarking on surgery. There are always exceptions, some of which include transfers for or repair of spontaneous tendon ruptures, nerve decompressions, or early synovectomy to prevent tendon destruction. The involvement of joints in the head and neck region has significant impact on surgical management of the hands in rheumatoid arthritis, because limited movement at the temporomandibular or atlantoaxial joints can make airway management and safe intubation a challenge in general anesthesia.1,2
A Mannerfelt lesion is a spontaneous rupture of the FPL tendon observed in the rheumatoid hand.1 It is usually caused by osteophytes around the scaphoid, which must be debrided at the time of reconstruction to reduce the risk of recurrent attrition. The FPL is usually reconstructed with an index FDS transfer, tendon graft, or arthrodesis of the thumb IP joint. Trigger finger and carpal tunnel syndrome are treated differently in rheumatoid patients, because the underlying cause is usually tenosynovitis and there can be adverse mechanical side effects from standard surgical management of these conditions. Carpal tunnel syndrome can result from the compressive effect of thick tenosynovitis/pannus within the carpal tunnel and should generally be treated with an extended carpal tunnel release and synovectomy. Trigger finger results from focal tenosynovitis or a rheumatoid nodule within the sheath or tendon. It should also be treated with synovectomy. Division of the A1 pulley will increase the likelihood of ulnar deviation at the MCP joints, and should be avoided where at all possible. Although early tenosynovectomy can reduce the risk of tendon rupture, it is less commonly required nowadays because of the improved medical control of rheumatoid arthritis. The term Vaughn-Jackson syndrome refers to spontaneous attrition rupture of the extensor tendons, starting with the little finger (not the thumb) and progressing with sequential rupture from ulnar to radial.2 Isolated EPL rupture may be treated with EIP transfer, but again it is vital that the underlying friction points are excised and covered with capsular flaps where possible to prevent recurrence.3,4
The typical deformity at the MCP joint level in rheumatoid is ulnar deviation, with volar subluxation. This can be corrected with the following maneuvers: • Intrinsic muscle release to allow MCP joint extension • Cross-intrinsic transfer: The tight intrinsic tendon on the ulnar side is sutured to the radial side of the adjacent digit to relieve ulnar-deviating forces and strengthen corrective radially deviating forces. • Ulnar-side sagittal band (which is tight) is released: This helps centralize the subluxed extensor tendon • The radial-side sagittal band (which is attenuated) is tightened: This helps centralize the subluxed extensor tendon • The radial collateral ligament is tightened or reconstructed: This helps correct the ulnar deviation If the joint surface is preserved, an arthroplasty is not required. However, if the joint surface requires replacement, it is important to complete careful soft-tissue rebalancing, since typical flexible silicone prostheses will not be strong enough to realign the joint alone and deviating forces across a prosthesis will also encourage erosion of arthroplasty stems through soft bone. Silicone prostheses are preferred to pyrocarbon in rheumatoid MCP joints due to poor soft-tissue stability.1,2
correct? The Sauve-Kapandji procedure fuses the detached ulnar head to the distal radius, with the aim of relieving pain from a degenerative DRUJ and restoring pro/supination, while stabilizing the triangular fibrocartilage complex (TFCC) and ulnar wrist joint and reducing the risk of ulnarward carpal translocation1 The Darrach procedure involves excision of the ulnar head and may increase the risk of carpal translocation, despite preservation of the TFCC remnants and ulnar collateral ligament of the wrist.2 Since there is no element of fusion or fixation in a Darrach procedure, bone stock is not as important as in many other wrist procedures in rheumatoid arthritis. The distal ulna stump may be unstable following both, potentially leading to pain. During wrist fusion, a common technique is to insert a Stanley or Steinmann pin (with a single trochar tip) through from the third metacarpal head, along the shaft, through the carpus, and into the radius. This technique has been in use since the 1960s, and a variety of different pins have been used. The original general purpose Steinmann pins have been modified by Stanley et al.3 Some surgeons insert the pin between, rather than through, the metacarpals, although this is less common. Although plating techniques (often using precontoured compression plates) are also available for wrist fusion, these generally require good bone stock for adequate purchase and are less frequently used in rheumatoid arthritis than in osteoarthritis. Locking plates can ameliorate this problem to a degree. Radioscapholunate arthrodesis is only of use in scenarios where the midcarpal joint surfaces are preserved.
Nail pitting is a feature of psoriatic arthritis, which is a seronegative arthropathy. The skin may be minimally affected, with some patients reporting only mild scalp psoriasis rather than florid plaques. The arthritic changes can be severe, with marked dissolution of bone leading to arthritis mutilans. The DIP joints are more often involved than in rheumatoid arthritis. Nail pitting is not a feature of the other conditions listed. Systemic lupus erythematosus is a multisystem disease found in young women. Hand findings include joint problems without cartilage destruction and with normal joint spaces retained. The hallmark of this condition is ligamentous and volar plate laxity with tendon subluxation. The visual deformity is similar to rheumatoid arthritis but with preservation of joint surfaces. Scleroderma is another multisystem disease that can affect the hand. Key features include fingertip ulceration, Raynaud’s phenomenon, and sclerodactyly. The small vessel vasculitis can result in fingertip ulceration, chronic wounds, and amputations. Contractures usually result from skin and soft-tissue changes, with MCP joint hyperextension and PIP joint flexion contractures both common. Osteoarthritis tends to present with pain, swelling, stiffness, and deformity in the small joints of the hand. Characteristic findings include Heberden’s nodules near the DIP joint and Bouchard nodes near the PIP joint.1