4.

Rheumatology

Arthur N. Steinhart, DPM

Evaluation of the Patient with Joint Pain

Musculoskeletal (rheumatic) pain is a common presenting complaint. Rheumatic diseases (rheumatism) are those diseases in which some part of the musculoskeletal system is affected. Enthesopathy is a condition in which there is inflammation and degeneration at the sites of ligament or tendon insertion into bone. Arthralgia is a condition of pain associated with a joint. There is no actual disease of the joint unlike arthritis in which there is actual disease of the joint. Evaluation of these patients requires a history and physical examination. Additional testing such as x-rays, blood tests, and synovianalysis may also be needed. Even biographic information regarding the patient may provide clues as to the diagnosis. For example, rheumatoid arthritis (RA) tends to have its onset between the ages of 20-65 with peaks at 35 and 45 while systemic lupus erythematosus (SLE) has its onset between the ages of 15-25. Many disorders tend to predispose to one gender: SLE affects women eight times more frequently than men, Reiters syndrome tends to affect men more frequently than women, and premenopausal women generally do not develop primary gout. Occupation may also play a role such as occupational trauma contributing to the development of osteoarthritis. When eliciting the history of the chief complaint it is necessary to determine the nature of the discomfort, its location, its duration, the mode of onset, its course, any alleviating or aggravating factors, and past treatment. Pain character is often suggestive of its etiology so that: Throbbing and aching- musculoskeletal origin Burning, numbness, and lightning (lancinating)- neurologic Nocturnal pain- bone tumor, early ankylosing spondylitis, carpal tunnel syndrome, cord tumor In considering pain location, attention must be paid not only to the actual site of discomfort but to the number of joints affected. Because an articular nerve may be responsible for sensation of many joints, joint pain in many cases is poorly localizable by the patient. Thus: Disease of the lower lumbar spine may produce pain in the thighs and outer leg below the knee. Sacroiliac joint involvement may produce pain encircling the thigh Hip joint pathology may be manifest in the buttocks, groin, greater trochanter area, thigh, above and in the knee, and in the lower leg to the ankle Ankle and subtalar joint disease may produce diffuse rearfoot pain Midtarsal joint disease may produce discomfort diffusely in the forefoot In many cases conditions tend to affect specific joints more frequently than others. For example, acute gout tends to commonly affect the first metatarsophalangeal joint; ankylosing spondylitis affects the nonsynovial articulations of the back; intermittent hydrarthosis affects large joints. The number of joints affected is described as monarticular or polyarticular and should be considered along with whether the condition is inflammatory or not.

Inflammatory Monarthritis
Crystal induced Gout Pseudogout Oxalosis Infectious Bacterial Fungal Lyme

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 Mycobacteria Viral HIV Hepatitis B Systemic Psoriasis RA SLE Reiters syndrome Reactive arthritis Inflammatory bowel disease Other Osteoarthritis (although usually non-inflammatory) Osteonecrosis Trauma Foreign body reaction

Non-inflammatory Monarthritis
Osteoarthritis Amyloidosis Osteonecrosis Benign tumor Osteochondroma Osteoid osteoma Pigmented villonodular synovitis Fracture Internal derangement Hemarthrosis Trauma Hemophilia Anticoagulant therapy Scurvy Malignancy

Polyarticular
Reiters syndrome Reactive arthritis Arthritis of ulcerative colitis Psoriatic arthritis RA Determining the duration of the problem helps assess whether the problem is acute or chronic. It is also felt that in cases of musculoskeletal pain of less than six weeks duration rest and simple analgesics are all that is necessary UNLESS: There was acute onset of a monarticular problem Risk of fracture, dislocation, etc. exists Constitutional symptoms (fever, malaise, fatigue, etc) are present Associated neurologic abnormalities are present

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The mode of onset, whether acute, or gradual also provides information helpful in establishing a differential and working diagnosis.

Acute Onset
With trauma Sprain/strain Fracture Dislocation Hemarthrosis Gout Without trauma Gonococcal arthritis Rheumatic fever RA Gout Pseudogout Hematogenous pyarthrosis Reiters syndrome SLE Psoriatic arthritis Palindromic rheumatism Leukemia Foreign protein reaction Arthritis of ulcerative colitis

Gradual Onset
Osteoarthritis SLE Reiters syndrome Tuberculous arthritis Hypertrophic osteoarthropathy RA Sarcoidosis Ankylosing spondylitis Psoriatic arthritis Arthritis of ulcerative colitis Viral Arthralgia In addition to determining whether or not the condition is improving, the pattern of joint involvement should also be determined. Those conditions involving bacterial infection tend to increase in severity while viral Arthralgia tends to resolve spontaneously. The discomfort associated with osteoarthritis will change with activity. In some conditions joints become symptomatic one at a time so that at first a single joint is symptomatic, then a second and a third and so on. This pattern is referred to as additive and is exhibited by RA and rheumatic fever in adults. Another pattern, described as migrator,, is demonstrated by rheumatic fever in children, Lyme disease, Gonococcal arthritis, and meningococcal arthritis. Joints in these cases become symptomatic one at a time, the second joint becoming active after the first resolves. In some cases, the joints may become symptomatic in a cyclical pattern as exemplified by palindromic rheumatism.

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Most patients with joint disorders will experience stiffness produced by rest. This is generally of short duration in osteoarthritis, lasting less than 30 minutes. The stiffness is of longer duration in the inflammatory arthritides, such as RA, lasting from 1-2 hours to improving but never completely resolving. Gentle activity often relieves the pain of inflammatory disorders but not of osteoarthritis or fibromyalgia. Previous treatment should be evaluated not only as to success but also to adequacy of dosage of and duration on medications, compliance, and reason for stopping treatment. Did the patient stop taking 200 mg ibuprofen tablets after taking one tablet because he did not receive the relief he expected or because he developed severe gastrointestinal discomfort? Did the patient with acute onset pain and swelling of the first metatarsophalangeal joint experience increased pain after drinking cranberry juice as someone advised him to (cranberry juice will increase uric acid levels in the blood - black cherry juice lowers it)? A review of systems will also provide valuable information. Some examples include:

Eyes
Dryness Sjgrens syndrome Ulceration RA Redness Reiters syndrome RA Behets syndrome Ankylosing spondylitis

Mouth
Ulceration Reiters syndrome Behets syndrome SLE Dryness Sjgrens syndrome

Skin
Psoriasis Reiters syndrome SLE Scleroderma Sarcoidosis Inflammatory bowel disease

Gastrointestinal
Reiters syndrome Ulcerative colitis Enteropathic arthritis

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Vascular
Vasculitis Collagen vascular diseases Teleangectasias SLE Scleroderma Raynauds phenomenon Collagen vascular diseases A family history should also be obtained since conditions such as gout and collagen vascular diseases may be familial in nature.

Patient Examination
While a complete general evaluation should be performed looking at/for: Gait Posture Body position Body movement Skin lesions Cardiac abnormalities Lymphadenopathy Hepatosplenomegaly Discussion will be limited to evaluation of the involved joint. Examination of the joint involves looking (for swelling, deformity, muscle wasting, and erythema), feeling (to evaluate tenderness, local temperature, and texture), and moving the joint (active and passive motion and presence of crepitus). Effusion of the joint is the result of an increased amount of fluid in the joint. Only a small amount of fluid is present in normal joints. The knee and hip joint normally have approximately 3-5 cc of fluid in them. The additional fluid producing the effusion may be synovial fluid or blood. Other conditions giving the appearance of swelling of the joint include synovial hypertrophy, bony enlargement, and the presence of an enlarged bursa, tenosynovitis, and the presence of a fat pad. Swelling of the digits may be described as fusiform (swelling is greatest at the joint and tapers proximally and distally- as in RA) or sausage (affecting the entire digit equally as in psoriatic arthritis). Swelling due to the presence of an enlarged bursa tends to be localized and fluctuant while swelling resulting from tenosynovitis tends to be linear and follow the course of the tendon. Hypertrophied synovium tends to have a doughy texture easily felt; the firmness of bony enlargement is easily recognized on palpation. Both are easily differentiated from a fat pad. In the normal joint passive motion (the motion performed by the examiner) will be slightly greater than active motion (the motion performed by the patient). When passive motion is significantly greater than active motion the patient is either guarding or cannot perform the motion due to weakness or paralysis. Active motion greater than passive motion is the result of guarding. The presence of joint disease is demonstrated by both active and passive motion being equal and reduced (this may also occur in cases of guarding due to marked muscle spasm as in peroneal spastic flatfoot). While putting the joint through a range of motion attention should also be given to the presence or absence of crepitus (grating, rubbing sound and/or feeling when the joint is moved). Denuding of articular cartilage from the joint surfaces in osteoarthritis results in rough bone moving across rough bone resulting in coarse crepitus. The presence of pannus over the joint surfaces in RA produces fine crepitus. Squeaking may be the result of motion of an inflamed tendon and snapping the result of tendon or ligament slipping over a bony prominence.

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Laboratory Tests in Arthritis

ESR
The Erythrocyte Sedimentation Rate (ESR) is the rate of settling of red cells in a column of blood. The rate is affected by the sizes of aggregates of red blood cells known as rouleaux. The test is non-specific, an increase usually, but not always, an indication of inflammation. The test is useful in differentiating early mild from more severe rheumatic disorders, estimating the activity of inflammation, following the course of therapy, and differentiating between disorders. Several techniques have been use in the past. These include Linzenmeyer, Rourke-Ernstene, Cutler (uses a short tube), Wintrobe (uses a 100mm tube), and Westergren (uses a 200mm tube, the most accurate of the techniques). Normal values vary with age and gender: Males < 50 = 0-15 Males > 50 = 0-20 Females < 50 = 0-25 Females > 50 = 0-30 Since rouleaux formation is dependent upon plasma proteins, particularly plasma fibrinogen and to some extent alpha and gamma globulins, any conditions affecting these substances will affect sedimentation rate. Thus, newborns tend to have low rates due to low fibrinogen amount, as will patients with liver disease. The ESR will be normal in patients with osteoarthritis (although some may have a slight to moderate increase), traumatic synovitis, neurogenic arthropathy, fibrositis, pychogenic rheumatism, and in those between attacks of gouty arthritis. The ESR will be kept low in patients with polycythemia vera, malaria, sickle cell disease, liver disease, and in those using salicylates.

CRP
C-reactive protein is a protein not normally found in blood. It can be detected in the serum during the active phases of many inflammatory and non-inflammatory conditions (such as active tissue destruction). It has its greatest usefulness in the management of rheumatic fever since it is a sensitive indicator of disease activity.

CBC
A normochromic, normocytic anemia may be associated with chronic disease and therefore present in patients with systemic arthritides. Leukocytosis may be found in serum sickness, rheumatic fever, and many cases of active rheumatoid arthritis, infectious arthritides, polyarteritis nodosa, leukemia, and acute gout. Leukopenia may be found in tuberculous arthritis, systemic lupus erythematosus (SLE), sarcoidosis, and Feltys syndrome (rheumatoid arthritis with splenomegaly, anemia, and leukopenia).

Rheumatoid Factors
Rheumatoid factors are antiglobulin antibodies (against IgG). They may be IgG, IgA, or IgM, with IgM being the one most commonly measured. Rheumatoid factors are not diagnostic of rheumatoid arthritis. They may not be detectable in patients with recent onset of disease, tend to be present in those with subcutaneous nodules, increase with severity of disease, and are usually not present in children with juvenile rheumatoid arthritis. Low titers may be found in up to 5% of the population, with frequency increasing in the elderly. It is felt that titers below 1:160 are insignificant. Rheumatoid factor may be found in patients with rheumatoid arthritis, SLE, scleroderma, polymyositis, dermatomyositis, polyarteritis nodosa, sarcoidosis, and Sjgrens syndrome. Other conditions in which rheumatoid factors may be present include tuberculosis, syphilis, infectious hepatitis, infectious mononucleosis, subacute bacterial endocarditid, leismaniasis, trypanosomiasis, larva migrans, schistosomiasis, bacterial bronchitis, pneumoconiasis,

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asbestosis, silicosis, idiopathic pulmonary fibrosis. Leprosy, leukemia, multiple myeloma, macroglobulinemia, hyperglobulinemias, repeated transfusions, post irradiation, and post chemotherapy.

LE Cell Prep
The lupus erythematosus (LE) cell is a polymorphonuclear leukocyte that has ingested a large inclusion body so that its nucleus is pushed to one side. LE cell formation is an in vitro phenomenon. The factor responsible for formation of LE cells is an antinucleoprotein antibody, which cannot penetrate intact cells. It is for this reason that LE cells do not form in vivo but only under laboratory conditions. False positives are found in patients with penicillin allergy, taking hydralazine, and in collagen vascular diseases. Because the test was found to be difficult to perform, and because it had to be performed three times on three different occasions before being considered negative this test has been replaced by the antinuclear antibody test which tests for LE factor directly.

ANA
The antinuclear antibody test (ANA) is easily performed and reproducible. Characteristic patterns of fluorescence result from differences in location of the antigen: Homogenous (diffuse)- produced by the binding of antinuclear protein antibody to nucleoprotein. This is the most common pattern and may be found in SLE, rheumatoid arthritis, Sjgrens syndrome, and scleroderma Peripheral (shaggy) - due to binding of an anti-DNA antibody and seen almost exclusively in SLE, especially in patients with active nephritis Speckled- due to an anti-nucleoglycoprotein antibody. Seen in rheumatoid arthritis, liver disease, ulcerative colitis, Sjgrens, scleroderma, and normal elderly Nucleolar- rare, seen in scleroderma and Sjgrens syndrome

STS
The importance of serologic tests for syphilis (STS) in an arthritis profile lies in the fact that chronic biologic false positive tests, which may precede the onset of clinical symptoms, are associated with many connective tissue diseases. Chronic biologic false positive non-treponemal antigen tests are seen in patients with connective tissue disease, malaria, and leprosy. False positive treponemal antigen tests may be found in patients with rheumatoid factor and antinuclear factors.

Uric Acid
Elevation of serum uric acid level (hyperuricemia) occurs in patients with gout but may be normal during an acute attack. Hyperuricemia may be best detected 10 days after the attack subsides.

Synovianalysis
The process of joint aspiration (arthrocentesis) must follow strict aseptic technique. The fluid withdrawn is evaluated for the following: Clarity Normal synovial fluid is clear (print can be read through it). Clarity is lost in the presence of inflammation and the fluid becomes turbid. The more turbid the fluid the higher the leukocyte count Color Normal synovial fluid is colorless to straw color. Degenerative joint disease: yellow-amber color RA: yellow to greenish Gout: yellow to white or milky Septic: creamy or grayish Traumatic: sanguineous Red streaks in the fluid are usually an indication of puncture of a small vessel during the procedure

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Viscosity Normal synovial fluid is of high viscosity, the viscosity decreasing with inflammation. The viscosity will be decreased in RA but normal in osteoarthritis. Under normal conditions, synovial fluid allowed to form a drop from the syringe will form a string 1.5 inches long before falling free (drop test). If a drop of normal synovial fluid is held between the gloved fingers of the examiners hand the fingers can be spread 1.5inches before the string of fluid breaks (stringing test) Crystals View under a polarizing microscope Urate- negative birefringence Calcium pyrophosphate- weak positive birefringence Cell Count Culture and Sensitivity Bacterial Aerobic Anaerobic Fungal

Degenerative Joint Disease

Degenerative joint disease, also known as osteoarthritis, osteoarthrosis, hypertrophic arthritis, and senescent arthritis, is a slowly evolving non-inflammatory disorder of the diarthrodial joints. Whether primary or secondary, the condition is characterized by deterioration and abrasion of the articular cartilage, formation of new bone (osteophytes) at the joint surfaces, and capsular fibrosis. Joint pain, stiffness, and limitation of motion gradually develop. Osteoarthritis is the most common form of arthritis and is the second most common cause of long term disability in the United States. The cardinal symptom of osteoarthritis is pain. This pain at first occurs after the joint is used and is relieved by rest. With progression of the condition, the pain may occur with minimal motion or even at rest and may awaken the patient from sleep (likely due to loss of conscious splinting when awake). This pain is reported to increase with changes in the weather, probably the result of increased capsular distension associated with the falling barometric pressure. Although there have been many explanations as to the source of the pain (elevation of periosteum following marginal bony proliferation, pressure on exposed subchondral bone, trabecular microfractures, capsular distension, pinching or abrasion of synovial villi, synovitis or capsulitis, muscle spasm, abnormal joint motion resulting from cartilage degeneration and/or osteophyte production) it is agreed that the joint cartilage itself is not the direct source of pain since cartilage is aneural. Other features of osteoarthritis are morning stiffness (and stiffness after a period of inactivity), limitation of motion, and deformity. The stiffness is of short duration (usually less than fifteen minutes). Limitation of joint motion is the result of joint surface incongruity, muscle spasms/contracture, and mechanical block due to osteophytes or loose bodies (joint mice) in the joint. Deformity in osteoarthritis is caused by cartilage loss, subchondral collapse, and osteophyte production. The joints most commonly affected by deformity in osteoarthritis are the distal and proximal interphalangeal joints (where Heberdens and Bouchards nodes develop), the hip (typically in flexion, adduction, and external rotation resulting is an apparent shortening of the leg), and knee. Heberdens and Bouchards nodes are bony and cartilaginous growths at the dorsomedial and dorsolateral aspects of the distal and proximal finger interphalangeal joints respectively. Localized areas of softening of the articular cartilage develop and are associated with a velvety appearance. It is in these areas that there is a dehiscence of the cartilage along the collagen fibrils of the matrix with resulting flaking and fibrillation leading to denuding of the subchondral bone. Non-uniform joint space narrowing is the result of this process. Secondary changes then develop. Fibroblast proliferation occurs where the articular cartilage is thinned,

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new bone is produced, subcortical trabecular thicken, and subchondral cysts filled with fibrous tissue may appear at the points of maximum pressure and trauma. Periosteal bone proliferation occurs at the joint margins and at the enthesis (site of ligament and tendon insertion) forming osteophytes that may limit or stop motion. True bony ankylosis does not occur in osteoarthritis although the joint may behave as if fused (as in hallux rigidus). The ESR and CBC are normal; latex fixation and ANA are negative. Cartilage debris may be found in joint fluid. The presence of a normal x-ray does not necessarily rule out the presence of osteoarthritis as clinical symptoms may be produced by minimal changes that cannot be detected. Characteristic x-ray changes include irregular (non-uniform) joint space narrowing, sub-chondral bone sclerosis (eburnation), marginal osteophyte production, and periarticular subchondral bone cysts. These cysts are surrounded by a rim of dense bone and do not break through. Primary osteoarthritis has no definitive etiology. In general, males and females are equally affected by primary osteoarthritis. The joints most commonly affected are the distal interphalangeal joints of the fingers, first carpometacarpal joint, hips, knees, first metatarsophalangeal joint, and lower lumbar and cervical vertebrae. Four types of primary osteoarthritis have been described: Involving a single or a few joints (primary localized osteoarthritis) Diffuse, polyarticular (primary generalized osteoarthritis) Erosive inflammatory osteoarthritis (an inflammatory synovitis of the interphalangeal joints of the hands in association with juxta-articular bone erosions) DISH disease (diffuse idiopathic skeletal hyperostosis; also known as ankylosing hyperostosis and Forestiers disease)- characterized by flowing ossification along the anterolateral aspect of at least four consecutive vertebral bodies along with the preservation of disc height and the absence of marginal sclerosis of the vertebral body. Extra-spinal manifestations include the formation of large bone spurs, especially on the calcaneus where there may be several, and calcification of the sacrotuberous, iliolumbar, and patellar ligaments Among the underlying causes of secondary osteoarthritis are trauma (acute, such as fracture, and chronic, such as occupational and biomechanical), other joint disorders (old fracture, aseptic necrosis, acute/chronic infection, rheumatoid arthritis, hemarthrosis), neuropathic disorder (tabes dorsalis, diabetes, syringomyelia, meningomyelocele, peripheral nerve section), and metabolic disorders (alkaptonuria, gout) Treatment of osteoarthritis is generally symptomatic and includes adequate periods of rest to avoid excessive use. Weight reduction, physical therapy, use of assistive devices (such as canes and crutches), and orthoses all may be of help. Topical application of counterirritants and capsacin containing preparations and oral analgesics may also provide relief. Local injection of anesthetic and corticosteroid can also help in the reduction of pain and increase range of motion. The anesthetic will permit the patient to put the joint through a greater range of motion thereby reducing adhesions and fibrosis while the corticosteroid reduces local inflammation already present or resulting from the mobilization. The anesthetic may also break existing muscle spasm resulting from the pain. Recently there has been much interest in the use of chondroitin sulfate and glucosamine in the treatment of osteoarthritis. These agents are, by some, believed to block the progression of osteoarthritis and stimulate cartilage repair. Glucosamine is a three amino sugar precursor of glycosaminoglycans and is believed to stimulate chondrocyte collagen and proteoglycan production, stimulate synoviocytes, and provide mild anti-inflammatory action. It should be use with care in diabetics. Chondroitin sulfate is believed to inhibit enzymes responsible for cartilage degradation, add to the glycosaminoglycan pool, and prevent synovial thrombi. Its structure is similar to heparin and therefore should be used with caution in patients on anticoagulants or with bleeding disorders.

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Glucosamine and chondroitin sulfate are given together, the dose being weight dependent: Patients < 120 pounds 1000 mg glucosamine 800 mg chondroitin sulfate Patients between 120-200 pounds 1500 mg glucosamine 1200 mg chondroitin sulfate Patients > 200 pounds 2000 mg glucosamine 1600 mg chondroitin sulfate

Juvenile Rheumatoid Arthritis

Juvenile rheumatoid arthritis (JRA), also called Stills disease, is a systemic rheumatologic disorder beginning before puberty having many clinical manifestations. There is often a history of upper respiratory infection, trauma, or stress preceding onset of the disease. In most cases there is a polyarticular onset (involving four or more joints). In another large percentage of cases onset is monarticular or oligoarticular (less than four joints) and may be symmetric or asymmetric in nature with or without systemic features. In a smaller number of instances the disease begins acutely with systemic manifestations and often without joint symptoms. These systemic features include: High fever which may be intermittent in nature Rash- evanescent macular or maculopapular eruption demonstrating the Koebner phenomenon (may be brought out by scratching, rubbing, or heat) Pericarditis Pneumonitis Splenomegaly Joint involvement may be recognized by swelling, guarding, limping, or refusing to walk. The joints initially affected tend to be the knees, wrists, ankles, and neck, with older children showing initial involvement of the smaller joints (symmetrical proximal interphalangeal joints and metacarpophalangeal joints). Pedal involvement includes bunion and hammertoe deformities, rheumatoid achillobursitis, calcaneal erosions, calcaneal spurs, and early apophyseal closure. The hand tends to show radial deviation rather than the ulnar deviation characteristic of adult rheumatoid arthritis. There is premature appearance and closure of epiphyses leading to deformity. Among the conditions to be considered in a differential diagnosis for JRA are: Tuberculous arthritis- especially when the presentation is monarticular Rheumatic fever- since both may present with Asymmetric polyarthritis Low-grade fever Pneumonitis and pleuritis Abdominal pain Elevated antistreptolysin O titers Pericarditis Pyarthrosis Childhood SLE Dermatomyositis/polymyositis Polyarteritis Scleroderma

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Gout
Gout is a disorder characterized by hyperuricemia and a characteristic acute onset arthritis (usually monarticular) caused by the deposition of monosodium urate monohydrate crystals in the joint. Addition deposition of these crystals may occur in the soft tissue (tophi) or kidney (urolithiasis). The condition may be primary or secondary. Primary gout may be inherited as idiopathic (responsible for 99% of primary gout) or as a disorder in which there is a specific metabolic defect in purine metabolism leading to the overproduction of uric acid. Secondary gout results from either an inherited disorder (as in Lesch-Nyhan syndrome and glycogen storage disease type I- Von Gierke) or the result of overproduction due to increased cellular turnover as in psoriasis, polycythemia, and malignancy or under excretion as in kidney disease or effects of drugs. Since primary gout is rare among premenopausal women, it is vital to look for underlying conditions responsible for the hyperuricemia. Attacks of the arthritis develop acutely with severe pain and swelling, often beginning at night and awakening the patient. Often a factor responsible for initiating the attack can be identified. These factors include dietary indiscretion (ingestion of foods high in purines, such as shellfish, beans, peas, lentils, organ meats, and anchovies). Ingestion of alcohol, which interferes with renal excretion of the urate, can also provoke an attack as can trauma, including surgery (leads to increased tissue destruction). It must be remembered that these factors increase urate load and are significant only in the already hyperuricemic patient. Thiazide diuretics interfere with urate excretion and can cause hyperuricemia or provoke an attack in a hyperuricemic patient. Doses of aspirin of less than 2 gm/day can increase uric acid level while higher doses are uricosuric. The first metatarsophalangeal joint is frequently affected. It has been postulated that this is the result of several factors: The trauma of walking causes a low-grade inflammation in the area resulting in a lowering of the local pH, which decreases the solubility of the urate crystals This area tends to be cool, which also decreases the solubility of the urate material The cooling of the extremities and slowing of heart rate during sleep further adds to making this environment more prone to deposition While the diagnosis of acute gouty arthritis is often made based on the history and clinical appearance (acute onset inflammatory arthritis with a history of previous attacks and/or a family history of gout and/or a history of a known provocative factor), it is only by arthrocentesis and the identification of the urate crystals (rod- or needleshaped crystals demonstrating negative birefringence under polarized light) in synovial fluid leukocytes that the diagnosis of acute gout can definitively be made. Blood tests performed during the attack may not be helpful. At this time the urate level may be normal since it is being deposited in the joint. Leukocytosis and elevated ESR may occur with gout as well as in infection. Among the conditions to be considered in the differential diagnosis are other crystal arthropathies, infection, sarcoidosis, and trauma. Except for soft tissue swelling, x-ray findings in acute gout may be unremarkable in the early stages of the disease. Later bone erosions with the characteristic overhanging cortex may develop. These erosions, unlike the erosions in RA, tend to be somewhat distant from the joint. The presence of tophaceous deposits may not be visible unless there is some degree of calcification. Treatment of the patient with gout involves not only treating the acute arthritis but also the underlying hyperuricemia. The acute arthritis may be treated with anti-inflammatory medications and local corticosteroid injection. The use of colchicine for acute attacks is based upon its ability to prevent leukocyte migration and therefore must be started within the first 24 hours of the attack. Colchicine for acute attacks has largely been replaced anti-inflammatory medications because of the frequency of gastrointestinal side effects and the time constraints on its use. Colchicine is used on a once or twice a day dose to prevent attacks in hyperuricemic patients and may be used to prevent attacks following surgery.

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Before the hyperuricemia can be treated it must be determined whether the patients hyperuricemia is due to overproduction or under excretion. This can be evaluated by determining the amount of urate excreted in the urine in a 24-hour period. Gouty patients excreting more than 600 mg of urate when on restricted purine intake are considered to be overproducers and are placed on a xanthine oxidase inhibitor (allopurinol) to decrease uric acid production (xanthine oxidase is responsible for the conversion of hypoxanthine to xanthine and xanthine to uric acid). Under excretors are placed on uricosuric medications such as probenecid. Because decreasing the urate level in the blood often leads to redissolving (mobilization) of tophaceous deposits with resulting acute gouty attacks these drugs are often initially given with colchicine to prevent an acute attack. The untreated hyperuricemic patient often goes through several stages. The first stage is that of asymptomatic hyperuricemia. This stage may last for many years before the patient enters the next stage, acute intermittent gout (it should be noted that many patients with hyperuricemia never pass into the second stage of acute gout). If untreated an acute attack will resolve, lasting from several hours to one to two weeks. This stage may last for many years, with the patient experiencing repeated attacks, each resolving and the patient becoming asymptomatic. It has been noted that these subsequent attacks eventually come closer together and are often more severe than previous attacks. At some point the patient remains uncomfortable even though the acute attack has passed. The patient has now entered the last stage, chronic tophaceous gout. In this stage tophaceous deposits become noticeable and attacks become polyarticular.

Psoriatic Arthritis
Psoriatic arthritis, the arthritis associated with psoriasis, has an incidence of approximately 0.1% in the United States, affecting 5-7% of the people with psoriasis. The condition has been divided into three categories: Polyarthritis- the most common form, symmetrically affecting the small joints of the hands and feet, wrists, ankles, knees, and elbows. Arthritis mutilans develops as a result of telescoping due to osteolysis of the phalanges and metacarpals or metatarsals Monarthritis or oligoarthritis Axial disease- presents with spondylitis, sacroiliitis, and/or arthritis of the hip and shoulder joints When the digits are affected they present with uniform swelling described as sausage swelling. Cutaneous signs of psoriasis (which may be limited to nail pitting) must be present in order to arrive at a diagnosis of psoriatic arthritis. The pencil-in-cup deformity (tapering of a phalangeal or metacarpal/metatarsal head with widening of the base of the articulating phalanx) and a fluffy periostitis are characteristic of psoriatic arthritis.

Systemic Lupus Erythematosus

SLE is an autoimmune disorder, tending to affect young women, having many clinical signs and symptoms. Among its manifestations are: Malar rash (butterfly rash)- erythematous, flat or raised, sparing the nasolabial folds Photosensitivity Alopecia Oro-phalangeal ulcerations Genital ulcerations Palpable purpura Splinter hemorrhages Skin infarcts Teleangiectasis Raynauds phenomenon

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 Mesenteric vasculitis Arthralgia Arthritis- symmetrical, commonly affecting the small joints of the hand, wrists, knees Muscle pain and weakness Kidney disease- nephrotic syndrome; renal failure Neuropathy- cranial, peripheral Seizures Headaches Psychosis Organic brain syndrome Serositis- pleurisy, pericarditis, peritonitis Cardiac disease- pericarditis, myocarditis, endocarditis, coronary artery disease It should be noted that certain drugs (chlorpromazine, methyldopa, hydrazaline, procainamide, and isoniazide) are known to induce lupus.

Scleroderma
Scleroderma, characterized by hardening of the skin, may be limited to the skin (localized scleroderma) or may also involve internal organs (systemic sclerosis). Systemic sclerosis usually initially resents with Raynauds phenomenon, fatigue, and musculoskeletal symptoms. Subsequently (weeks to months later), puffiness of the skin of the hands and fingers develops, followed by further skin changes and visceral disease. Many patients develop CREST syndrome: Subcutaneous calcinosis Raynauds phenomenon Esophageal dysmotility (lead pipe esophagus seen on barium swallow Sclerodactyly Teleangiectasis

Reiters Syndrome
Reiters syndrome is characterized by the trial of non-Gonococcal urethritis, conjunctivitis, and arthritis. A fourth finding, oral and genital ulceration (balanitis circinata), is considered to complete a tetrad of symptoms. Reiters syndrome tends to affect young males and has been tied to a preceding infection, either venereal or gastrointestinal. It has also been linked to the presence of HLA B-27 (as has ankylosing spondylitis). Additionally, the finger and toenails may become thickened, resembling psoriatic or mycotic nails. Keratotic lesions affecting the soles, keratoderma blennorrhagicum have also been described. These keratoses may begin as small papules, which coalesce forming larger keratotic plaques. These keratoses spontaneously resolve, leaving normal skin. The arthritis appears as additive, asymmetric, and oligoarticular and most commonly affects the knees, ankles, and small joints of the feet. The affected joints appear swollen, warm, and are very tender upon palpation and motion. Digits take on a sausage type swelling (dactylitis). Enthesitis may also be present, most commonly affecting the insertion of the Achilles tendon and plantar fascia with erosions visible on x-ray and the patient complaining of heel pain (lovers heel).

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Ankylosing Spondylitis
Ankylosing spondylitis is a chronic inflammatory disorder of the axial skeleton, affecting the spine and sacroiliac joints. The condition has been linked to the presence of HLA B-27. Symptoms usually appear in late adolescence or early adulthood with back pain the earliest complaint. A patient presenting with back pain and showing radiographic evidence of sacroiliitis is generally considered to have ankylosing spondylitis. Late in the disease, spinal ankylosis results in the classic bamboo spine seen on x-ray.

Sources
1. Klippel, John H., editor: Primer on the Rheumatic Diseases, 11th edition, Arthritis Foundation, 1997. 2. Wyngaarden, Jamed B. and Smith, Lloyd H. Jr., editors: Cecil Textbook of Medicine 18th edition, W.B. Saunders Company, 1988.

418 The 2005 Podiatry Study Guide