CLINICAL FEATURES

Pain is the most common initial symptom. This frequently occurs with motion or activity and is relieved by rest. The source of discomfort is unknown. It may result from chemical mediators and possibly mechanical factors. Joint stiffness typically occurs with rest and improves with activity. The physical findings include crepitus, joint line tenderness, swelling, restriction of motion, and joint enlargement from osteophyte formation. In the hands, these osteophytic overgrowths are termed Heberden’s nodes when they are present at the distal interphalangeal joint and Bouchard’s nodes when they occur at the proximal interphalangeal joint. Pain is usually present on joint motion. Disuse atrophy of the adjacent musculature may develop rapidly, thus increasing the disability and pain. Even though osteoarthritis is not considered an “inflammatory” disease, mild increased temperature with palpable heat is often present. This can be appreciated clinically in a superficial joint (such as the knee) by placing one hand on the front of each knee of the sitting patient and then switching the hands back and forth. Subtle differences in temperature suggestive of synovitis (which indicates an intraarticular problem) may become more apparent. This clinical test is often helpful in the obese patient in whom an effusion may be difficult to visualize.

The roentgenographic findings consist of joint space narrowing, spur formation, sclerosis, and subchondral cyst formation (Fig. 14-1). The laboratory findings and synovial analysis are normal, except for occasional flakes of cartilage in the joint fluid. In most cases, a routine physical examination and plain films are sufficient to establish the diagnosis. More extensive radiographic testing is usually not indicated except in those cases in which the diagnosis is uncertain.

Fig. 14-1 Degenerative arthritis of the hip. Joint space narrowing, sclerosis, and subchondral cyst formation are present.

TREATMENT

The main objectives of treatment are the relief of pain and prevention of progression. As with any joint disorder, the patient should not be told that arthritis is present unless the physical and laboratory findings are consistent with the diagnosis. The stigma of “arthritis” should not be attached to any condition merely to explain vague or nonspecific symptoms. However, once the diagnosis is established, the patient should be made to realize that while miracles cannot be expected, there is almost always something that can be done to relieve the pain and deformity, regardless of the cause. Treatment for osteoarthritis begins with rest of the involved joint. Weight loss and the use of assistive devices for ambulation (cane or crutch) lessen the pressure on the involved lower extremity. Removable splints or braces are also recommended.

Stretching exercises are helpful, and the joint should be passed through a full range of motion several times daily to reduce joint stiffness. The local application of moist heat often relieves discomfort during the acute painful stage and may be especially helpful before exercise. Exercises designed to combat stiffness and restore muscle strength are important, because the weakness contributes to joint instability and disability. The patient may benefit from a short course of formal physical therapy to develop a good home exercise program. All exercise should be low impact. Aquatic exercise programs are generally well tolerated. Nonsteroidal anti-inflammatory drugs (NSAIDs) are traditionally used for osteoarthritis, but may be no more effective than acetominophen for pain relief because the role of inflammation in the condition is uncertain. Mild analgesics may even be indicated on an occasional basis. Intraarticular cortisone injections are often very effective for pain relief. Their effect is usually only temporary, but the benefit may last several months. The injections can be repeated several times per year. Any recommended limits to the number of injections a patient may have per year appears to be arbitrary, although most patients seem to do well with three or four injections per year. Various liniments may be used for their counterirritant effect. Viscosupplementation (a series of joint injections using a hyaluronate-like material) has been tried, but the results are inconclusive. The efficacy of supplements such as chondroitin and glucosamine has not been well proven.

Orthopedic referral is indicated when there is no response to medical management. The most common surgical procedures are arthrodesis and arthroplasty (Fig. 14-2). Each is effective in eliminating the painful articulation. Realignment of faulty weight-bearing joints by osteotomy may also be beneficial.

Fig. 14-2 Total hip arthroplasty (uncemented).

CLINICAL FEATURES

The initial acute attack is usually of sudden onset and occurs in a single joint or area of tenosynovium of the lower extremity (Table 14-2). The metatarsophalangeal (MTP) joint of the great toe is classically the first site of involvement (podagra), although any joint or area of tenosynovium can be involved. The extensor synovium on the dorsum of the midfoot is another common site of acute attack, as is the knee joint (gonagra). In 80% to 90% of cases, the lower extremity is involved. The older patient with gout is more likely to have involvement of the fingers and to develop tophi. Older women may present with polyarticular disease, often involving atypical locations. The pain and inflammation are usually severe and may be precipitated by exercise, dietary indiscretion, and physical or emotional stress. Attacks are common after illness or shortly after surgery, and they typically begin at night. Swelling, heat, redness, and other signs of inflammation are usually present. The physical findings may even simulate cellulitis or infectious arthritis. The area is often tender to even the slightest touch. Fever, tachycardia, and other constitutional symptoms may accompany the attack. The initial episode may be followed later by polyarticular involvement. Eventually, deposits of urate crystals, termed tophi, may form in the subcutaneous tissue.

Table 14-2 Joint Swelling—Differential Diagnosis*

ESR, Erythrocyte sedimentation rate; FANA, flurorescent antinuclear antibody; GI, gastrointestinal.

* NOTES: The workup should include aspiration of joint fluid. Fluid is observed for color, and the string test is performed. The fluid is analyzed for cell count, Gram stain, crystal analysis, and culture and sensitivity. The blood work should include complete blood cell count, uric acid, blood cultures if indicated, sedimentation rate, fluorescent antinuclear antibody, and rheumatoid factor. Blood cultures should include aerobic and anaerobic cultures. Roentgenographic evaluation is always performed to evaluate for osteoarthritis and calcific changes in soft tissues.

Early in the disease, roentgenogram findings are normal. Later, erosive changes appear that have a characteristic punched-out appearance (Fig. 14-3). Destruction and degeneration of the articular cartilage frequently follow.

Fig. 14-3 Gouty arthritis. Multiple punched-out lesions are present.

The standard for the definitive diagnosis of gout requires crystal identification on joint aspirate, although a presumptive diagnosis is often established on clinical grounds, especially if associated with hyperuricemia. Laboratory findings include a mild leukocytosis, elevated sedimentation rate, and hyperuricemia, although acute attacks are occasionally associated with a normal level of uric acid. In some patients, the SUA level may decrease into the normal range during an acute attack. Uric acid levels are best checked again after the attack is over. The synovial aspirate is usually cloudy and mildly inflammatory in nature. Because acute gout and infectious arthritis can present identically, the fluid should also be tested for infection. Urate crystals are usually demonstrable. They are needle shaped and negatively birefringent (shine brightly) under polarized light. A 24-hour urinary collection for uric acid may be helpful in determining the appropriate treatment.

TREATMENT

The treatment of gout depends on the stage of the disease. The objectives in management are to terminate or prevent the acute attack, encourage mobilization of tophaceous deposits, and reduce the level of SUA.

Prevention of acute attacks depends on modification of diet and lifestyle. Obese patients should be counseled regarding weight loss, and alcohol intake should be kept moderate (no more than two drinks per day). Hypertension and its management require careful assessment, and nondiuretic drugs may be needed.

Although hyperuricemia is central to gout, it does not always lead to arthritis, and there is no indication to treat asymptomatic hyperuricemia. Most patients with hyperuricemia do not have gout, and fewer than half of those with hyperuricemia will ever develop gout. Thus, the pharmacologic treatment of hyperuricemia can probably be delayed until the patient actually develops symptoms.

Treatment of the acute attack usually involves the use of generic NSAIDs, which have generally replaced colchicine in the management of the acute gout. Colchicine is an alkaloid found in the meadow saffron or autumn crocus. It has been used for gout for 1500 years and is still used on occasion. (Two 0.5-mg tablets are given initially, followed by one tablet every hour, up to 12 tablets, until the symptoms subside or diarrhea ensues.) Disappearance of symptoms with colchicine helps confirm the diagnosis, but its dosing is inconvenient, and the gastrointestinal (GI) side effects can be severe. Intravenous colchicine has been used, but there are some recent reports of serious side effects. Quick-acting drugs such as ibuprofen and indomethacin are often recommended, although most of the NSAIDs are effective. Indomethacin is especially helpful in the young but is poorly tolerated in the elderly. Aspirin may not be as useful. For those who are intolerant of NSAIDs (GI symptoms or renal insufficiency), corticosteroids or adrenocorticotropic hormone can be used. The side effects of steroid use can be minimized by tapering the dose as soon as possible. When oral medication cannot be given (in postoperative patients, for example), intraarticular cortisone injections are valuable. The medical management of the acute attack is accompanied by rest, elevation, moist heat, and narcotics as needed. Full resolution of symptoms may take several days.

The main indication for prophylaxis is frequent (≥3 per year) attacks of gouty joint inflammation. A single attack, or perhaps even two, probably does not warrant prophylaxis, but for protection from further attacks, one of two agents, probenecid or allopurinol, is commonly used. The goal is to reverse the process by lowering the SUA level to below the level at which urate saturates the extracellular fluid (ECF) and to eliminate the excess urate that has accumulated as tophi. This requires that the SUA level be lowered below 6.0 mg/dL. Probenecid is a uricosuric agent; that is, it increases the renal excretion of uric acid and is indicated for hypoexcretors if renal function is normal. It should not be used in the presence of renal insufficiency, which is common in the elderly. Probenecid is also effective in reducing the size of the tophaceous deposits. Allopurinol is a xanthine oxidase inhibitor that prevents the formation of uric acid from xanthine and hypoxanthine. It is especially valuable in the patient who forms urate stones because it directly decreases the production of uric acid. Although rarely required, the 24-hour urine collection may give direction in deciding which agent to use. (Hypoexcretors are given probenecid to block absorption, and overproducers are given allopurinol.) High excretors are not good candidates for probenecid because it could increase the risk of renal stones. Regardless of the etiology of the uric acid elevation, the most popular drug used is allopurinol, mainly because of its efficacy and its convenient once-a-day dosing schedule. As a rule, the start of uric acid–lowering drugs should be delayed for 2 weeks after an acute attack because this intervention may prolong the attack or even precipitate a new one. NOTE: NSAIDs alone are even used by some for long-term prophylaxis.

Surgery is usually limited to excision of large tophi and, occasionally, arthroplasty.

CLINICAL FEATURES

The clinical presentation is variable, but the symptoms are similar to those of chronic gouty arthritis. The age of onset is 60 to 70 years. Intermittent acute episodes occur, but the joint most commonly involved is the knee rather than the great toe. The attacks are usually monoarticular. The condition is frequently familial and is occasionally associated with diabetes, renal disease, and other systemic conditions. Like gout, acute attacks may be triggered by a variety of surgical or medical events. In addition to the goutlike symptoms, calcification of the cartilage of the knee, especially the meniscus, is common (Fig. 14-4). Calcification of the anulus fibrosus, radioulnar disc, and symphysis pubis may also be seen. Stippled calcification in bands running parallel to the subchondral bone margins may be present. Synovial fluid analysis reveals typical rhomboid-shape crystals that exhibit weakly positive birefringence under polarized light. There are no specific changes in blood or urine. The American Rheumatism Association criteria are often used for diagnosis:

Fig. 14-4 Calcification of the meniscus (arrow).

Categories: pseudogout is definitely present if criteria I or II(a) plus (b) are present, probably if II(a) or (b) is fulfilled, and possibly if III(a) or (b) is present.

TREATMENT

Aspiration and cortisone injections are often effective in the acute phase. NSAIDs and colchicine are also helpful. Structural joint damage requiring surgery is rare. In contrast to gout, there are no drugs available to deplete these crystals.

CLINICAL FEATURES

The onset is usually gradual although acute cases may occur. Weakness, fatigue, and anorexia are common prodromal symptoms. Eventually, joint involvement becomes apparent, with stiffness, swelling, heat, and redness. Stiffness is most pronounced in the morning because of the “gelling” effect of the excess fluid. Most cases initially present with multiple symmetric joint involvement, most often in the hands and feet (Table 14-3). The MCP, metatarsophalangeal (MTP), and proximal interphalangeal (PIP) joints are usually involved, but the distal interphalangeal (DIP) joints are not. Eventually, most of the major joints become involved as well. Remissions and exacerbations are common, but the condition is chronically progressive in the majority of cases. The disease shortens life expectancy from 10 to 15 years.

Table 14-3 American Rheumatology Revised Classification of Rheumatoid Arthritis (American College of Rheumatology)

The physical signs are caused by the inflammation of the synovial membrane. Joint effusions, warmth, tenderness, and restriction of motion are usually present early in the disease. Eventually, characteristic deformities appear that consist of subluxations, dislocations, and joint contractures.

In addition to the joint manifestations, extraarticular findings are common. Tendon sheaths and bursae are frequently affected by the chronic inflammation. Tendon rupture may even occur, especially in the hand and often involving the finger extensors. Involvement of synovial bursae may lead to considerable enlargement, especially the Baker’s cyst, which often reaches enormous size. Rupture of this cyst is not uncommon and may lead to a local reaction in the calf, simulating thrombophlebitis. Subcutaneous rheumatoid nodules develop in 25% of cases and are most common over bony prominences such as the elbow and shaft of the ulna. Chronic flexor tenosynovitis may eventually lead to carpal tunnel syndrome in many cases.

Involvement of other organ systems may lead to pulmonary fibrosis, pericarditis, and vasculitis as well as Felty and Sjogren syndromes.

The roentgenogram usually reveals soft tissue swelling and osteoporosis early in the disease. Eventually, joint space narrowing, erosion, and deformity become visible as the result of continued inflammation and cartilage destruction (Fig. 14-5).

Fig. 14-5 Rheumatoid arthritis of the knee. Osteoporosis and severe joint space narrowing are present. Hypertrophic spurring is typically absent.

The laboratory findings consist of a mild anemia, leukocytosis, and elevated sedimentation rate and C-reactive protein levels. The rheumatoid factor is positive in approximately 75% of cases. The joint fluid is usually turbid and forms a poor mucin clot. The cell count is elevated, with an increase in polymorphonuclear leukocytes.