Approach to the Patient with Arthritis John B. Imboden, MD ‘When evaluating a patient with arthritis, itis important to determine whether the process is acute (presenting within days) or chronic (persisting for weeks or more) and whether it is monarticular, oligoarticular (two to four joints involved), or polyarticular (five or more af- fected joints). If more than one joint is involved, the arthritis should be characterized as symmetric or asym- metric and as additive or migratory. The distinction be- tween inflammatory and noninflammatory arthritis is ctical for accurate diagnosis. The presence of constitu tional signs or symptoms and the involvement of other organ systems can be important clues to the correct di- agnosis. INFLAMMATORY VERSUS NONINFLAMMATORY ARTHRITIS The most reliable means for distinguishing between in- flammatory and noninflammatory arthritis is analyzing the white blood cell (WBC) count in the synovial fluid. In inflammatory arthritis, che WBC count is > 2000/ UL; in noninflammatory arthritis, the WBC count is < 2000/j1L. Arthrocentesis should be performed when- ever feasible because, although clinical features and other laboratory investigations also help distinguish in- flammatory from noninflammatory arthritis, no single finding is definitive. Patients with an inflammatory arthritis usually complain of pain and stiffness in in- volved joints; typically these symptoms are worse in the morning or after periods of inactivity (the so-called “gel phenomenon”) and improve with mild to moderate ac- tivity. On examination, the larger joints can be warm and, when severely inflamed, can have erythema of the overlying skin. Laboratory studies often reveal an cle- vated erythrocyte sedimentation rate (ESR) and a high C-reactive protein (CRP) level. In contrast, patients 2 with noninflammatory arthritis have pain that worsens with activity and improves with rest. Stiffness is gener- ally mild and usually not a prominent symptom. The ESR and CRP are usually normal. ACUTE MONOARTHRITIS E> ESSENTIAL FEATURES + Bacterial infection, crystat-induced arthritis, and trauma are leading causes of acute monoarthrits. + Septic arthritis is a major concern and must be ruled out. + Arthrocentesis is the most important diagnostic test. I Clinical Evaluation ‘The history and physical examination should determine whether the process is acute (onset over hours to days), involves the joint rather than surrounding tissues or bone, and is truly monarticular. The most common causes of acute monoartht infection, crystal-induced arthritis, and trauma (Table 4-1), In cases of suspected trauma, itis important to as- certain whether the reported crauma is sufficiently se- vere to account for the joine findings. (Patients with new-onset joint effusions often attribute the joint ab- normality to incidental bumps, turns, or other minor trauma.) The foremost concern in evaluating a patient with acute pain and swelling in a single joint that is noc28 | CHAPTER4 Table 4-1. Common causes of acute monoarthritis. Bacterial infection of the joint space Nongonacoccal: Especially, Staphylococcus aureus F hemolytic streptococci Streptococcus pneumoniae gram-negative organisms Gonococcal: Often preceded by a migra vitis or oligoarthrits associated with characte! story tenosyno- ristic skin lesions + Crystalinduced arthritis Gout (monosodium urate crystals) Pseudogout (calcium pyrophosphate “Trauma e dihydrate crystals) clearly due to trauma is the possiblity of a joint space infection. ‘A. LABORATORY EVALUATION “Arthrocentesis is indicated forall cases of unexplained cute monoarthrits. Synovial fluid should be sene for culture (bacterial, mycobacterial, and fungal), WBC count, and Gram stain and examined for crystals by po- Iarized light microscopy. Determining whether the syn- vial uid is inflammatory, noninflammatory, or bloody guides the intial differential diagnosis. Polarized light microscopy is a sensitive test for urate cxystls. Calcium pyrophosphate dihydrate crystals are Somewhat more difficule co visualize because of their weaker birefringence, but their detection should not present difficulties for the experienced clinician. On the other hand, Gram staining for bacteria is relatively in- sensitive (false-negative rates range from 25% to 50% for nongonococcal septic arthritis and are substantially higher for gonococcal infections), Thus, the absence of crystals is a strong argument against microcrystalline disease, but a negative Gram stain does not exclude in. fection. Occasionally, infection and microcrystalline dias coe, therefore, the finding of costs in the ic sym Muid does nor exhde the posit of infec Properly performed cultures of synovial fui in up t0 90% of cases). However, synovial fluid eae are positive in only 20-50% of cases of eseueures arthritis. The diagnosis often depends on Soceec2! Neiseria gonorrueae on culture from the nin urethra, cervix, or rectum (in apprenee =, PeayX: 80-90%) or, in some cases, on the nate Postive in sppropie aio theapy Patient's response to urine laboratory tests, count, serum elecuolytesand seat, blood el and urinalysis) ide helpful ancillary information. Blog io ul ovis informatic rel abrained if septic arthritis is suspeges tures should be B, IMAGING STUDIES Radiographs can demonstrate fractures in cases of yay, paeeally contribute lide co the diagnosis oe nontraumatic monoarthritis. Occasionally, imaging sug noneipe misleading. In cass of septic arth, org. ample, radiographs may show evidence of osteoantr, am Fer chronic conditions chat predispose to inn but are not the cause of the acute joint inflammation, Differential Diagnosis ‘A. INFLAMMATORY. Differentiating between arthritis caused by infecion iced arthritis can be difficult without and crystal-induced arth 1 dults fom synovial fluid analysis and culture, Pains ‘with septic arthritis may be afebrile and may not mai festa peripheral leukocytosis. Conversely, patens wih crystal-induced arthritis can have fever and an elevated peripheral blood WBC count. An elevated serum uc acid level does not establish a diagnosis of gout, and pu tients with gout can have a normal serum uric acid lewd at the time of an acute attack. Septic arthritis indicates the presence of a potentaly life-threatening infection. Delaying treatment of nor gonococcal septic arthritis can cause substantial mor bidity due to the rapid destruction of articular catlag Therefore, acute inflammatory monoarthritis should be considered septic arthritis until there is compelling & dence either against bacterial infection or in favor of alternative diagnosis. When the synovial fluid is high! inflammatory (WBC count > 50,000/HL) but ti Gram stain and the polarized light microscopy fins axe negative, empiric treatment with antibiotics i P dent until the results of synovial fluid and othe emake known. Depending on the clinical con" sans antibiodc coverage also may be indicat! 8 eed ay geute inflammatory monoartrits aes aaocacs eas count < 50,000/ML. Altho Srna eaca septic arthritis often generaes vr! ception nd AZBC counts (+ 100,000/uL), che synced gs le. Septic arthritis ean presen luid WBC counts as low as 3000/1 sear ‘ that are typically oligoarticular 0:Table 4-2. Differential diagnosis of chronic inflammatory monoarthritis. + Infection Nongonococeal septic arthritis Gonococcal Chronic Lyme disease and other spirochetal infections Mycobacterial Fungal Viral + Crystal-induced arthritis Gout Pseudogout Calcium apatite crystals? + Monarticular presentation of an oligoarthritis or polyarthritis Spondyloarthropathy Rheumatoid arthritis Lupus and other systemic autoimmune diseases + Sarcoidosis* + Uncommon or rare Familial Mediterranean fever ‘Amyloidosis* Foreign-body synovitis due to plant thorns, sea urchin spikes, wood fragments, ete Pigmented villonodular synovitis: *Also can cause noninflammatory synovial fluid. Not detected by polarized light microscopy. Commonly associated with bloody, or blood:-tinged brown, syn- vial fluid. yarticular, such as the spondyloarthropathies and adult- ‘onset Still disease, occasionally begin as an inflammato- ry monoarthritis. B. NONINFLAMMATORY. Noninflammatory synovial fluid can be seen with inter- nal derangements (eg, torn meniscus of the knee). Os- teoarthritis ofa single joint usually presents as a chronic condition, but occasionally, the onset of pain may be acute. Similarly, neuropathic arthropathy, amyloidosis, and osteonecrosis usually cause chronic noninflamma- tory arthritis of one or several joints, but acute symp- toms are sometimes present. C. HEMARTHROSIS Frank blood on arthrocentesis can be indicative of a fracture or other joint trauma and should prompt ap- propriate imaging studies and referral to an orthopedic surgeon. Hemarthrosis also occurs in patients receiving anticoagulant therapy or who have a clotting factor defi- ciency such as hemophilia. Bloody synovial fluid can be seen in pigmented villonodular synovitis, a rare prolifer- ———er 5 ative disorder of the synovium th, moc py i hi CHRONIC MONOARTHRITIS R> ESSENTIAL FEATURES * Chronic. inflammatory monoarthrtis may be ‘caused by infection, crystal-induced arthritis sor. coidosis, or a monarticular presentation of an oligoarthritis or polyarthritis, * Chronic noninflammatory monoarthritis may be caused by osteoarthritis, internal derangements, chondromalacia patellae, and osteonecrosis. + Arthrocentesis and imaging studies are important diagnostic tests. Initial Clinical Evaluation Infections, particularly indolent infections, ate a con- cern with inflammatory monoarthritis that lasts ftom weeks to months. The particular joint involved influ- ences the differential diagnosis. A. LABORATORY EVALUATION A ceitical step is to determine whether the monoarthti- tis is inflammatory or noninflammatory, preferably by analyzing synovial fluid. Synovial fluid should be sent for culture (bacterial, mycobacterial, and fungal), WBC count, and Gram stain and examined for crystals by po- larized light microscopy. Routine laboratory studies (eg, complete blood cell count, serum electrolytes and creatinine, and urinalysis) and determinations of the ESR or CRP level can pro- vide helpful information, Patients with inflammatory monoarthritis and negative bacterial cultures should be tested for reactivity to purified protein derivative (PPD). B. IMAGING StuDiES —_—— Unlike in acute monoarthritis, radiographs can be help- ful in evaluating chronic monoarthritis and can point to the correct diagnosis in cases of infection, ostcoarthts ‘osteonecrosis, neuropathic joints, and other disorders. Differential gnosis ‘Ac IevaMMAaToRY ‘A wide range of diseases can cause inlay BS i tis in a single joint for several weeks or longer (Tel 4-2). Most patients with septic arthritis and gono — ‘APPROACH TO THE PATIENT WITH ARTHRITIS 7 2930 = / CHAPTER4 arthritis experience significant pain in the infected joint and seek medical attention within hours to days of the onset of symptoms. However, some patients may delay in seeking treatment for several weeks, particularly if symptoms have been partially masked by the use of nonsteroidal anti-inflammatory drugs, antibiotics, or corticosteroids (systemic or intra-articular). Patients with untreated indolent infections com- monly have sympcoms for weeks or longer before seeking medical attention. In these types of infections, synovial fluid culture is negative for bacteria, and additional di- agnostic rests and cultures are required to establish the correct diagnosis. Chronic Lyme disease can cause an inflammatory monoarthritis, often of the knee, with synovial fluid WBC count typically in the 10,000 25,000/tiL range. Tuberculous infection of a joint can present after days, weeks, or months of symptoms. Smears for acid-fast bacilli are positive in only 20% of cases; cultures for mycobacteria are positive in 80%, but test results take weeks. Synovial biopsy can expedite the diagnosis of tuberculous arthritis and is also indi- cated in suspected cases of fungal arthritis. B. NONINFLAMMATORY Osteoarthritis is the leading cause of chronic noni flammatory monoarthritis, particularly when the hip, knee, first carpometacarpal joint, or acromioclavicular joint is involved (Table 4-3). Internal derangements, such as a torn meniscus in the knee, often produce me- chanical symptoms and characteristic findings on phys- ical examination (see Chapter 12). Pain is frequently a prominent feature of osteonecrosis, which can produce large knee effusions when the distal femur is involved. Radiographs are often normal early in the course of os- teonecrosis, and diagnosis may require magnetic reso- nance imaging. Hip pain with a normal radiograph should raise the possibilty of early osteonecrosis, partic- ularly if the patient is relatively young or has a risk Table 4-3. Differential diagnosis of chronic noninflammatory monoarthritis. — + Osteoarthritis * Internal derangements (eg, torn meniscus)* + Chondromalacia patellae* + Osteonecrosis# + Uncommon or rare Neuropathic (Charcot) arthropathy Sarcoidosist® Amyloidosis*® “Radiograph of the affected joint often normal at re Can also cause inflammatory synovial uid, P=Setation, factor for osteonecrosis (ee Chapt 54). Diab tus is the most common underlying cause of fa arthropathy, which should be considered Fretic patient with foot, ankle, or knee arth jvolved joint may be warm and painful, but rej fluid is ypically noninflammatory. Radiographs show characteristic neuropathic changes ee Ca ter 51). ACUTE OLIGOARTHRITIS g> ESSENTIAL FEATURES + Disseminated gonococcal infection, nongonococ. cal septic arthritis, and the spondyloarthropathies are leading causes of acute inflammatory oligoarthritis. + Arthrocentesis and appropriate cultures are im- portant diagnostic tests. al Evaluation ‘Acute oligoarthritis is usually due co an inflammatory process. Infectious causes of the arthritis need to be ruled out, Disseminated gonococcal infection is the most common cause of acute oligoarthritis in sexlly active young people. Nongonococcal septic arthritis usually monarticular but involves more than one joi in up to 20% of cases, __ Spondyloarthropathies typically cause an asymm fic eligoarehrics OF these, reactive arthritis is most el present with acute onser of arthritis and, Semminaedd be dficule to distinguish fom The ee as infection. oligoantn GU Joins as «dividing ine be and there i neopets is somewhat abi olgcarthri and eae, oeeween disorders that BID inochi Polacthrts. For example, par occasion od Usually causes a crue polyarchrit b Produces an oligoarthritis. Many of the di ders listed in T ted in Table 44 som 01 iw i re that ut joints \etimes involve mor A-Lasonsrony Evatuarion the evaluat Culture of the synovial fluid are critic! ‘on of acute oligoarthritis, The pharynx, rectum should be tested for NV goTable 4-4. Differential diagnosis of acute inflammatory oligoarthritis. Infection Disseminated gonococcal infection* Nongonococcal septic arthritis Bacterial endocarditis” Viral + Postinfection Reactive arthritis” Rheumatic fever (post-streptococcal arthritis)* + Spondyloarthropathy Reactive arthritis? ‘Ankylosing spondylitis? Psoriatic arthritis? Inflammatory bowel disease” + Oligoarticular presentation of rheumatoid arthritis, systemic lupus erythematosus,* adult-onset stil disease, or other polyarthritis + Gout and pseudogout “often migratory. "Can be associated with back pain. “Usually causes polyarthritis but occasionally oligoarticular and sometimes noninflammatory. Migratory in children but notin adults. performed for Chlamydia trachomatis. If bacterial endo- carditis is a possibility, at least three blood cultures should be obtained, and a transesophageal echocardio- gram may be indicated. Complete blood cell count, serum electrolytes and creatinine, and urinalysis should be obtained. B. IMaGinG Stupies Radiographs usually are of litle help if the onset of the oligoarthtritis is truly acute. Differential Diagnosis Disseminated gonococcal infection usually presents as a migratory tenosynovitis, often with characteristic skin lesions; meningococcemia can cause a similar syndrome bur is much less common, Bacterial endocarditis can cause an oligoarthritis with either septic joints (due to hematogenous spread) or sterile inflammatory synovial fluid (likely due to immune complex disease); back pain is common, particularly in acute bacterial endocarditis (Table 4-4). Reactive arthritis classically follows within 1 to 4 weeks of enteric or genitourinary infections, but the triggering infection is sometimes subclinical. In its presenting phase, reactive arthritis can be associated with significant constitutional signs and symptoms in- cluding prominent weight loss and fever. Most patients with new-onset psoriatic arthritis either have, or have rr APPROACH TO THE PATIENT WITH ARTHRITIS I 31 had, psoriasis; however, disease in about 15% of ation produces 2 migratory anhvice i however, post-streprococcal arthritis gratory and is rarely associated with tive manifestations of rheu taneous nodules, carditis, the arthritis precedes the skin te theumatic fever hildren; in ada is usually noe ni. the other distinc. imatic fever (eg, ra aad ea Bh, subeae CHRONIC OLIGOARTHRITIS R> ESSENTIAL FEATURES. * Careful description of the arthritis and detection of extra-articular disease facilitate accurate diag- nosis. + Radiographs are often of diagnostic value, Initial Clinical Evaluation Spondyloarthropathies are the most common cause of chronic inflammatory oligoarthritis (Table 4-5). How- ever, distinguishing spondyloarchropathies from eatly- onset rheumatoid arthritis may be difficult, caking months or longer. Osteoarthritis commonly presents as a noninflammatory oligoarthritis of che hips or knees and usually does not present diagnostic difficulties. ‘A. Lasoratory EVALUATION Synovial fluid should be analyzed for crystals and cul- tured, The distinction between inflammatory and non- inflammatory chronic oligoarthritis often can be made ‘on clinical grounds but is confirmed by the synovi fluid WBC count. . ‘A postive tet for serum rheumatoid factors seen in 70-80% of patients with rheumatoid arthritis and, al- though not a specific test for this disease, can help e5- tablish the diagnosis in the proper clinical cones Testing for HLA-B27 is usually of limited value (6 Chapter 18). B. IMAGING Stupies —______-—__~ Radiographs can be of considerable value. Ae pet enced radiologist or rheumacologist can offen Cort guish among the erosions of the spondslarchropaics Theumacoid arthritis, and gout. Radiographic v4 of sacroiliitis indicates a spondyloarhropad y rows the differential diagnosis considerably.32 1 CHAPTER4 Table 4-5. Differential diagnosis of chronic oligoarthritis. ——— + Inflammatory causes Common ‘Spondyloarthropathy Reactive arthritis? Ankylosing spondy! Psoriatic arthritis Inflammatory bowel disease : Atypical presentation of rheumatoid arthritis Gout ‘Uncommon or rare Subacute bacterial endocarditis Sarcoidosis? Behget disease Relapsing polychondrtis Celia disease* + Noninflammatory causes Common Osteoarthritis Uncommon or rare Hypothyroidism Amyloidosis Can be associated with involvement ofthe axial skeleton. Can be a migratory arthritis and have either inflammatory or noninflammatory synovial fluid. Differential Diagnosis Although. spondyloarthropathies typically cause an asymmetric oligoarthrts and theumatoid arthritis is usually a symmetric polyarthritis, it can be difficult to differentiate these disorders in a subset of patients with relatively early disease. Several features are helpful in making this distinction. Inflammatory axial skeleton disease with sacroiliitis that causes pain and stiffness in the low back, particularly in the morning, is always seen in ankylosing spondylitis and often seen in other spondyloarthropathies (Table 4-5). Sacroilitis is not a feature of rheumatoid arthritis, which involves the cer- vical spine but no other part of the axial skeleton, The prominent tenosynovitis of the spondyloarthropathies can produce dactylitis ("sausage digits") of the toes or fingers. Dactyltis is not seen in rheumatoid arthr (Dacryliisis not specific forthe spondyloarthropathies; it may also occur in sarcoidosis and gout.) React. arthritis and the arthritis of inflammatory bowel freee have a predilection for the lower extremities Rhen a es. Rheuma- toid arthritis invariably involves the hands, and «9 of aesevenaly eve wiscanit a ‘Many of the disorders that cause chroni tis have exra-articular manifestations that poe ee correct diagnosis but chat are easly overlooked foe ample, psoriasis may be subtle; the patient may be ie 7 jatic lesions, particularly in the umbil aa OE eridiory canals the sap, and the ana <4 the enema! i of reactive arthris ae pines andy The orl ete unless specifically Looked for by ck Young physician. Patients with inflammatory boyg cgamining Pot volunteet that they have chronic dir dicts Te aly if bowel sympcoms ate item thea, Pace ancerior uveitis can bean important clu Antecedice of 2 spondylarthropathy, But pany Scealy do not associate ocular inflammation wit Lae ‘and may not mention a past episode of anterior tiveitis unless asked directly. ACUTE POLYARTHRITIS g> ESSENTIAL FEATURES + Viral infections and rheumatoid arthritis are the leading causes of acute polyarthritis. + Observation to distinguish persistent from self- limited polyarthritis is critical. Initial Clinical Evaluation Although rheumatoid arthritis often has an insidious onset and patients have symptoms for months before seeking medical attention, it begins abruptly in some patients. Acute-onset rheumatoid arthritis can be diff cult to distinguish from virally induced acute poly. thritis, and many rheumatologists are hesitant to make a diagnosis of rheumatoid arthritis in the acute setting Viral polyarthritis usually resolves over days to weeks (but can persist for months), Thus, the lon: the polyarthritis persists, theless likely viral pols ALLABORATORY EVALUATION. Routine laboratory studies (including complet bl on eet tim electrolytes and creatinine, liver fu Bok ees itd urinalysis) and determinations of Fee GRP loves should be done. Tests for s tai Raraaetesd ae caer p+ hepatitis B are indice antibodies (ANA); # ficity for the na 262" is_an autoantibody with spe spite ity naan (808 of immunoglobulin (Ig) G. ! for a sen, *heumatoid factor is neither a spee tens for aan {6st for theumatoid arthritis. Pos! Hous onde atatoid actor are seen in a vaiety of i cause are et Conditions, some of which See Chapter 3), Eventually, 70-80"patients with rheumatoid arthritis test positive for theumatoid factor, but this figure is substantially lower (about 50%) early in the course of the disease. Testing for ANA is essentially 100% sensitive for systemic lupus erythematosus (SLE) but has low speci- ficity. A positive assay for ANA should prompt a careful evaluation for other clinical signs of SLE and additional serologic tests (see Chapters 3 and 19). The likelihood of exposure and clinical features such as fever ot characteristic rash should guide the decision of whether to perform serologic tests for Lyme disease and parvovirus B19. The immunoglobulin class (IgM vs IgG) is crucial to interpret the antibody tests for par- vovirus B19. Patients with polyarthritis due to acute in- fection with parvovirus B19 have IgM antibodies that ‘wane in titer over several months. Detection of IgM an- tibodies to parvovirus B19, therefore, is indicative of re- cent infection and strongly suggests that the acute poly- arthritis is due to parvovirus B19. In the absence of an IgM response, IgG antibodies to parvovirus B19 simply reflect past infection with this common virus and are not likely to be a causative factor in acute polyarth Indeed, most healthy adults have detectable IgG to vovirus B19. B. ImacinG Stupies. Radiographs are rarely of value in acute polyarthritis and should be deferred until it is clear whether the polyarthritis is persistent. Differential Diagnosis ‘Many acute viral infections cause joint symptoms, with polyarthralgias being considerably more common than true polyarthritis. The prevalence of polyarthritis is high, however, in adults who have acute parvovirus B19, hepatitis B, or rubella infections (Table 4-6). The pactern of viral polyarthritis often mimics that of theu- matoid arthritis. Adults with acute parvovirus B19 i fection, the cause of “slapped cheek fever” in children, usually have only a faint rash on the trunk or no rash at all. IgM antibodies to parvovirus B19 are generally pre- sent at the onset of joint symptoms and persist for ap- proximately 2 months. Acute hepatitis B causes an im- mune complex-mediated arthritis, often with urticaria cor maculopapular rash, during the preicteric phase of infection; tests for hepatitis B surface antigen are posi- tive. Joint symptoms with rubella generally precede the onset of rash. Polyarthtitis due to rubella vaccination is less common with the currently used strain of attent- ated virus Fever can be an important diagnostic clue, Patients with virally induced polyarthritis often have a flu-like illness; fever is common and may precede the onset of sl APPROACH TO THE PATIENT WITH, ARTHRITIS 7 33 Table 4-6. Differential diagnosis of acute polyarthritis eal, ‘Acute viral infections, especial ts Byrbel and belavocches Early disseminated Lyme disease Rheumatoid arthritis Systemic lupus erythematosus + Uncommon or rare Paraneoplastic polyarthritis Remitting seronegative symmetric ting edema (RS3PE) Acute sarcoidosis, usually with erythema nodosum and hilar adenopathy Adult-onset stil disease Secondary syphilis Systemic autoimmune diseases and vascultides Whipple disease Vitus B19, hepa Polyarthrits with pit. the arthritis. Rheumatoid arthritis, in contrast, rarely causes fever higher than 38 °C. SLE can cause fever of up to 40 °C, but fever is unusual when polyarthritis is the major manifestation of the disease, Intermittent high fever is a common feature of adult-onset Still di ease. Fever can accompany polyarthritis due to drug-in- duced lupus, secondary syphilis, acute sarcoidosis, and systemic vasculitis. CHRONIC POLYARTHRITIS R> ESSENTIAL FEATURES + Rheumatoid arthritis and osteoarthritis are the leading causes of chronic polyarthritis * Careful delineation of the joints involved, particu- larly in the hands, can help point tothe correct d- agnosis. Initial Clinical Evaluat Rheumatoid arthritis is the leading cause of ‘chronic in- flammatory polyarthritis, and osteoarthritis is the —_ ‘common cause of chronic noninflammatory polyarhe tis, Nonetheless, polyarthritis chac persists for ea aa more has many possible causes and warrants care! agnostic evaluation (Table 4-7). As is the caseDe .. 34 1 CHAPTER4 Table 4-7. Differential diagnosis of chronic polyarthritis. + Inflammatory Common Rheumatoid arthritis Systemic lupus erythematosus as Spondyloarthropathies (especially psoriatic a Chronic hepatitis C infection Gout Drug-induced lupus syndromes Uncommon or rare Paraneoplastic polyarthritis Remitting seronegative symmetric ting edema (RS3PE) Adult-onset Still disease ‘Systemic autoimmune diseases an ‘Sjégren syndrome Viral infections other than hepatitis C Whipple disease + Noninflammatory Primary generalized osteoathritis, Hemochromatosis Calcium pyrophosphate deposition disease arthritis) polyarthritis with pit- 1d vasculitides other forms of arthritis, the distinction between inflam- matory and noninflammatory processes is critical. ‘A. LABORATORY EVALUATION If arthrocentess is feasible, synovial fluid should be ob- tained and tested for cell count and analyzed for crys- tals. Routine laboratory investigations (complete blood fell count, serum electrolytes and creatinine, and uri- nalysis) should be done, When the process appears in- flammatory, the ESR or CRP level should be deter- mined and tests for serum rheumatoid factor, ANA, and hepatitis B and C should be done. B. IMAGING SruDiEs Radiographs are indicated in most cases of chronic polyarthritis of the hand. Radiographs of the hand usu- ally show characteristic changes at the time of presenta tion of primary generalized osteoarthritis, hemochro- ‘matoss, calcium pyrophosphate deposition disease, and chronic tophaceous gout. In cases of sheumatoid arth tis and the spondyloarthropathies, however, the likeli hood of radiographic joint erosions and other charac. teristic findings increases with the duration of the polyarthritis; hand radiographs may be normal o¢ Remonstrate nonspecific changes only for mente longer. The polyarthritis of SLE, drug-induced lume and chronic hepatitis Cis usually nonerocive and get tor produce characteristic radiographic Endings pifferential Diagnosis d rheumatoid arthritis have differen, in the hand. Osteoarth;. Osteoarthritis an halangeal (DIP) and proxi, patterns of joint i pas seal incerp paris che dsl nee v joints and the first cq. mal incerphalangeal (rT acid arthritis, in conta poms its the _metacarpophalangeal (MCp) involves © joints, and the ‘Osteoarthritis. @ certain joints. he Wests eumatoid arthritis ypcaly ne ccoarthritis usually does notin joins ee, wrists, elbows, glenohumea vale the ees degenerative arthritis of these joins ty of antecedent caus, cm py on disease, underlying osteonecto raphosphate deposition nderying oxo ‘ posit ropathy. Rheumatoid arth Sis oF neuropathic ee racic and lumbosacral tisualy spares the DIP joints, ne, and sacroiliac joints. 2 spine, ane ized osteoarthrics, intesphalangea joins, i to be inflamed (“in- artieuarly the DIPs, may appear t0 b ey, osteoarthritis"), thus causing some unce tainty about the diagnosis. Radiographs, however, uss ‘ily show typical degenerative changes (irregular jin Space narrowing, sclerosis, and osteophytes). Psoriatic sPanritis also commonly involves the DIP joints, usually ‘with radiographic changes distinct from those of os Teoarthritis, Psoriatic changes of the fingernail on the Same digit usually occur concomitantly with psoriatic involvement of a DIP joint. ‘Many diseases can mimic rheumatoid arthritis, but several warrant particular emphasis (Table 48). Features that distinguish rheumatoid arthritis and the spondy loarthropathies are discussed above. Chronic infection Table 4-8. Some mimics of chronic rheumatoid arthritis. Sa re ‘Arthritis with radiographic ero: sions SPondyloarthropathies, ‘especially psoriatic arthritis Arthritis with positive rheumatoid factor Chri hepatitis C infection mic lupus erythet Sarcodesis OSU Systemic vasculitid Polymyosits/dermat atomyositis esate bacterial endocarditis hrs with nodules {onic tophaceous gout 'yperlipoproteinemia (rare) Multicentric r i en reticulohistiocytosis (rare) Hemochromatosig? Phalangeal joints or wrists, or be Calcium, Pyrophosphate deposition disease eeeTe pe with hepatitis C is associated with a symmetric polyar- thritis and a positive test for rheumatoid factor. ‘The polyarthritis of SLE is nonerosive but can lead to re- ducible “swan neck” deformities of the fingers. On occa sion, chronic tophaceous gout is a remarkable mimic of theumatoid arthritis, with tophi mistaken for theuma- toid nodules. Gout is not associated with rheumatoid factor (virtually all cases of nodular rheumatoid arthritis are seropositive), and the erosions of gout and rheuma- toid arthritis have different radiographic character Analysis of synovial fluid for urate crystals is the defi tive diagnostic test. Hemochromatosis and other causes of calcium pyrophosphate deposition disease lead to arthtitis of the MCPs (especially the second and third) and wrists; radiographs often reveal “hook-like” osteo- phytes of the MCPs and degenerative changes, usually with chondrocalcinosis, of the wrist. Although theumatoid archi isthe leading cause of chronic inflammatory polyarthritis, physicians must be certain that theumatoid arthritis accounts for the full clinical picture, Rheumatoid arthritis is not a plausible APPROACH TO THE PATIENT: WITH ARTHRITIS I 35 explanation for the fo substantial weight los Capare from subcutancout neds proteinuria. Failure to account forthe ical findings can lead toa faure ee hee cases as SLE, Sill disease, subacue baceee act tis, paraneoplastic syndromes, and vast cms oraedi- culitides. REFERENCES Baker DG, Schumacher HR. Acute monoarthritis. NV 1993;329:1013. [PMID: 8366902] Tomah Be cof the differential diagnosis and evaluation of acute pa arthritis.) e lowing: fever Breater than 38 ° 8, Significant adenopathy, wate Pinals RS. Polyarchrits and fever. N Engl J Med. 1994:330769, (PMID: 810744) (Clinically useful guide to the imporane problem of fever in the setting of arthritis) Relevant World Wide Web Sites Uohns Hopkins Arthritis Center] hheep://www-hopkins-archritissom.jhmi.edul