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.

TREATMENT

Proper management requires close cooperation among primary physician, therapist, rheumatologist, and orthopedist. Early referral to a rheumatologist is especially important because evidence exists that outcomes are improved with early, aggressive medical management. The goals are to maintain function and to halt the irreversible damage that may become visible radiographically. Patient education is of utmost importance. (Information from the physician can be supplemented from outside sources, such as the Arthritis Foundation.) Rest is beneficial in reducing inflammation. When combined with an exercise program, moist heat, and splinting, joint deformities can frequently be prevented or corrected.

Pharmacologic management is beyond the scope of this text, but four types of drugs are commonly used to treat rheumatoid arthritis: NSAIDs, corticosteroids, disease-modifying antirheumatic drugs (DMARDs, including biologic agents), and analgesics. NSAIDs are commonly used as the initial treatment to relieve inflammation. Aspirin remains the drug often used for many patients although other NSAIDs are also popular. Unfortunately, GI side effects are common, and there are concerns that these drugs actually may not alter the course of the disease. DMARDs such as gold and methotrexate are used when the other drugs begin to lose their effectiveness. These are usually slow acting and may require several weeks to become effective. The biologic response modifiers (BMRs) are the newest therapeutic agents to be used in rheumatoid diseases and may offer the best chance to directly target those substances such as tumor necrosis factor that are responsible for the profound inflammatory changes seen in rheumatoid arthritis. These drugs represent one of the most important advances in the treatment of inflammatory joint diseases. Oral and intraarticular steroids are helpful as well, although it is hoped that as other, more specific drugs continue to be developed, reliance on corticosteroids will diminish.

Among the surgical procedures that are commonly used are synovectomy, soft tissue releases, arthroplasty, and arthrodesis. The soft tissue procedures are most beneficial early in the disease before significant fixed deformity or subluxation appears.

CLINICAL FEATURES

Juvenile rheumatoid arthritis is usually one of three types: (1) systemic (20%), (2) pauciarticular (30%), or (3) polyarticular (50%). Systemic or acute febrile juvenile rheumatoid arthritis is characterized by extraarticular manifestations, especially high spiking fevers and a typical rash. The rash frequently appears in the evening and may be elicited by gently scratching the skin in susceptible areas (Koebner’s phenomenon). Splenomegaly, generalized lymphadenopathy, pericarditis, and myocarditis may also occur. The articular findings are often minimal and usually are overshadowed by the systemic symptoms. The morbidity from this form is usually from chronic arthritis, however.

The pauciarticular or oligoarticular form usually involves the larger joints, such as the knees, elbows, and ankles. Girls are affected four times more often than boys. Systemic features are often minimal, and only one to three joints are usually involved. The joint disease rarely causes impairment, but iridocyclitis develops in approximately 30% of cases with this form, and permanent loss of vision develops in a high percentage of these patients. Frequent ocular examinations, early detection, and treatment are therefore indicated. In this form of juvenile rheumatoid arthritis, accelerated growth of the affected limb from chronic hyperemia may result in a temporary leg length discrepancy that is eventually equalized in most cases on control of the inflammation.

Polyarticular juvenile rheumatoid arthritis resembles the adult rheumatoid disease in its symmetric involvement of the small joints of the hands and feet. The knees and wrists may also be involved, and this form in more common in girls. Cervical spine involvement is not uncommon and may produce marked restriction of motion. Early closure of the ossification centers of the mandible may produce a markedly receding chin, a characteristic of this form. Systemic manifestations are similar to the febrile variety but are not as dramatic. Children who develop the disease in adolescence are often seropositive and manifest symptoms and signs similar to adult rheumatoid arthritis.

The roentgenographic findings in juvenile rheumatoid arthritis are the same as those in the adult, except that joint destruction is less frequent (Fig. 14-6). The laboratory findings are also similar, except that the peripheral WBC count may be very high and the rheumatoid factor is rarely demonstrable in the serum of children.

Fig. 14-6 Juvenile rheumatoid arthritis. Osteoporosis is present, but joint destruction is minimal. Multiple erosions and cysts (arrows) are present because of synovial hypertrophy.

TREATMENT

The treatment is similar to that given to the adult.

CLINICAL FEATURES

The foot is usually involved in diabetes, the shoulder and elbow joint in syringomyelia, and the vertebrae and lower extremities in tabes dorsalis (Fig. 14-7). Gradual enlargement and instability of the affected joint are common complaints. Pain is usually present but tends to be relatively mild when compared with the severity of the joint destruction.

Fig. 14-7 Charcot foot deformity with medial dislocation of the medial cuneiform.

The examination is characterized by swelling and hypermobility. Palpation frequently reveals gross deformity of bone and joint and crepitus. Early involvement of the foot because of diabetes is first manifest by painless swelling at the apex of the arch. As weight bearing continues, there is collapse of the arch with frank dislocation and deformity of the mid-foot. Eventually, the arch completely disintegrates, and a reverse arch or rockerbottom foot is formed (Fig. 14-8). There is commonly skin breakdown and ulcer formation where the dislocation has occurred.

Fig. 14-8 Radiograph showing the common rocker deformity (arrows).

Variable degrees of joint destruction and disintegration with exuberant osteophyte formation are usually present on roentgenographic examination. Later, subluxation and deformity may be seen (Fig. 14-9).

Fig. 14-9 Diabetic neuroarthropathy of the midfoot. Destruction, debris, dislocation, and density (4 Ds) are usually present in neuropathic joints. The medial cuneiform is dislocated.

In questionable cases, sepsis may need to be ruled out by aspiration, sometimes with biopsy. Usually, 2 to 3 hours of elevation relieves the redness of neuropathy but not sepsis. In addition, the patient with infection usually feels sick, but systemic signs are usually absent in the Charcot foot.

TREATMENT

Once the full-blown neuropathic joint has developed, treatment can be difficult. In the lower extremity, effu sions, sprains, and fractures should be well protected until all hyperemic response has subsided. Braces, special shoes with molded inserts, and elevation of the extremity are helpful. A “rockerbottom” shoe allows an improved walking pattern. Surgery is generally limited to debridement of bony prominences and local ulcer care.

CLINICAL FEATURES

The condition is rare before the age of 50, with an average age of 70 years at onset. Females are affected twice as often as males. Symptoms are frequently of sudden onset but have often been present for months before the diagnosis is made. Neck, shoulder, low back, and thigh pain are common complaints. Morning stiffness, lasting 2 to 3 hours, is typical, and patients often have difficulty getting out of bed. Malaise, depression, weight loss, and a low-grade fever are common constitutional symptoms and may suggest a systemic inflammation. Shoulder pain is the presenting symptom in the majority of cases and is typically bilateral.

Physical findings are usually limited. Some restriction of shoulder motion may be present. Synovitis may be present in peripheral joints and may also be responsible for the proximal girdle symptoms despite the fact that they appear to be “muscular” in origin. Patients may have difficulty raising their shoulders overhead. Hip range of motion may also be limited. Mild soft tissue tenderness may be present. The temporal arteries should be carefully examined because of the strong relation of polymyalgia rheumatica with temporal or giant cell arteritis.

Laboratory findings are usually normal, except for a typically elevated erythrocyte sedimentation rate (ESR) over 45. C-reactive protein levels are also sensitive to the disease. A mild anemia may be present. Muscle biopsies are always normal. Synovial biopsy may show mild inflammation. Some patients have a vasculitis similar to that seen in giant cell arteritis, one of the several manifestations that the two disorders have in common. (Giant cell arteritis may rarely present as a medical emergency with headache and variable degrees of blindness.) Any patient with cranial signs or symptoms should have a temporal artery biopsy.

TREATMENT AND PROGNOSIS

Low doses of predisone (10 to 20 mg per day) have traditionally been used. The response is often so dramatic that it can be used to confirm the diagnosis. Improvement is usually noted within a few days. Steroids are gradually tapered as symptoms permit, but small doses (5 mg/day) may be needed for more than 2 years. NSAIDs may be effective in mild cases. Physical therapy is unnecessary. If there is no response to steroids, other diagnostic possibilities may have to be considered.

The prognosis is usually favorable. Relapse occasionally occurs in several years but again responds well to prednisone.

CLINICAL FEATURES

The female-to-male ratio is 9:1, and the prevalent age range is 30 to 50 years, although a juvenile form has been described. The patient is frequently depressed. There may have been some recent trauma, such as a motor vehicle accident. Complaints of spinal pain are common. The patient may occasionally present with a list of other vague symptoms, such as headache, stiffness, sleep disorders, chronic fatigue, and even abdominal complaints. Tender “nodules” and trigger points may be present, and when palpated, regional referral of the pain may occur. (These tender sites may simply represent normal variations in muscle density or fatty deposits.) There are never any objective physical findings. The usual roentgenographic and laboratory assessments are always normal.

Subsets of this disorder are often described if symptoms develop in conjunction with other conditions or after motor vehicle accidents, but the primary disorder is often suggested by the following criteria from the American College of Rheumatology:

TREATMENT

Before making this diagnosis, rule out other more likely causes for the pain. Then, the treatment is mainly empiric and symptomatic. Physical therapy, NSAIDs, acupuncture, transcutaneous nerve stimulation, sympathetic blockade, muscle relaxants, trigger point injections, and antidepressants are among the many treatments used, all with uncertain success rates. An aerobic fitness program can be very helpful. The patient needs to be actively involved with the exercise program, and prolonged passive care should be avoided.

Education and self-management are important. Social and environmental factors may need to be addressed, especially stress and pending litigation. Simply establishing a diagnosis (giving it a name) can be helpful to the patient to learn that the condition is not progressive or fatal. A compassionate and reassuring approach is important. Support groups are also beneficial. The prognosis is uncertain. Symptoms may come and go for years, despite an aggressive, multifaceted approach to treatment.

CLINICAL FEATURES

The findings are usually bilateral and symmetric. A typical clubbing of the fingers and toes usually develops first, although early pain over the shafts of the bones of the extremities is common. Joint stiffness, swelling, and pain are usually later in onset and may simulate rheumatoid arthritis. Thickening of the arms and legs is often present. The ESR and alkaline phosphatase levels may be elevated.

ROENTGENOGRAPHIC FINDINGS

Periosteal new bone formation is usually present. The long bones of the extremities are most often involved. The bone scan may show increased activity. A chest radiograph should be obtained to rule out underlying lung disorder.

TREATMENT

Treatment is strictly symptomatic. NSAIDs are helpful. The signs and symptoms usually subside when the underlying pulmonary disease is successfully treated.

TREATMENT

Antibiotics (usually penicillin or tetracycline) given for the disease can prevent the chronic arthritis. Even after the arthritis is established, antibiotic therapy (for 4 weeks) may be curative. In cases of “refractory” arthritis, IV antibiotics may be indicated. Children rarely have any long-term joint complications, and even in adults, the arthritis usually resolves without any significant destruction. NSAIDs are useful for their analgesic and anti-inflammatory effects. Intraarticular steroids can provide excellent symptomatic relief and do not appear to cause any adverse local effects. Chronic cases may require synovectomy.

If patients are active in tick-infested areas, sprays containing diethyl toluamide or permethrin may be effective in prevention. Long pants and shirts with long sleeves should be worn. Patients should check clothing and exposed areas carefully for the tick; it takes 24 hours of attachment for infection. Showers after being outdoors are helpful. Attached ticks should be removed with tweezers. If not engorged, the tick rarely causes Lyme disease. Any mouth parts should be left behind.

CLINICAL FEATURES

The disorder is eight times more common in females. The true prevalence is unknown. Early symptoms are often nonspecific. Polyarthritis, polyarthralgia, myalgia, Raynaud’s phenomenon, hand and finger swelling, sclerodactyly, esophageal hypomotility, and muscle weakness are among the common initial complaints. Pericarditis, facial erythema, and psychosis are even noted in some patients. Pulmonary involvement may lead to pulmonary hypertension and even death in rare cases.

Rheumatoid factor is often demonstrated in low titers, and if myositis is present, creatine phosphokinase levels will be increased. The sedimentation rate is usually elevated, and the antinuclear antibody may be positive with a speckled pattern. Anti-ribonucleoprotein antibodies may be present. Leukopenia and anemia caused by chronic inflammation are common.

The response to oral corticosteroids is excellent in most cases, except for pulmonary and scleroderma-like symptoms. Other antiinflammatory agents are used, but the best therapeutic options remain uncertain.

USES

The benefits of this class of drugs to patients with inflammatory joint diseases are enormous. They are front-line medications in the treatment of rheumatoid arthritis, gout, and the spondyloarthropathies. In these diseases, they offer not only pain relief but the ability to actually alter the progression of the disease process. They are also used for a wide variety of other conditions, most of them associated with pain, such as tendinitis, osteoarthritis, and degenerative disc disease. And though the diagnostic terms commonly used for these disorders would imply inflammation, concepts regarding the underlying pathology of these latter conditions continue to evolve. The idea that chronic inflammation is the cause of them is being questioned because more precise information has become available that shows very little inflammatory reaction on histologic examination. Tendinitis, for example, may begin as overuse, leading to inflammation, but chronic pain is more often associated with neovascular changes in the local tissue without typical cellular findings of inflammation. Even the terminology used to describe these disorders is changing (from tendinitis to tendinosis or tendinopathy). Some studies suggest that they are beneficial, and some report no effect. Unfortunately, the outcomes that are measured, such as pain, are based mainly on subjective data, which may be influenced by the analgesic properties of these medications. Whether or not these drugs are appropriate for these disorders is a question that remains unanswered.

NSAIDs have also been recommended in the treatment of acute ligament and muscle injuries. It was thought that suppressing the local inflammation could allow for faster recovery. The use of antiprostaglandins under these circumstances has been the source of considerable debate, mainly because prostaglandins play important roles in the normal healing process, and NSAIDs could actually block rather than enhance the healing of these injuries. Results at this time are inconclusive. NSAIDs may be helpful in some ways, such as restoring circulation, but may have negative effects on other aspects of the soft tissue healing response.

SIDE EFFECTS

Because of their common mechanism of activity, many of these agents have similar side effects. Most of them are reversible when the drug therapy is discontinued. Although most physicians consider them to be safe, more than 16,500 deaths occur each year as a result of anti-inflammatory drug use.