Arthritis

Educational Objectives

The goal of this program is to increase the knowledge and understanding of the diagnosis and management of osteoarthritis, other commonly encountered types of arthritis, and prosthetic joint infections. After hearing and assimilating this program, the clinician will be better able to:

1. Discuss the incidence, pathophysiology, diagnostic techniques, and management of osteoarthritis.
2. Identify the subtypes of osteoarthritis.
3. Characterize other types of arthritis encountered by clinicians.
4. Describe the incidence, diagnostic considerations, and management of patients with prosthetic joint infections.

Summary

PDF of all summaries for this board review course

Osteoarthritis (OA): most common type of arthritis out of >100 types; affects 240 million people worldwide (30 million Americans); more prevalent in developed countries and prevalence increases with age; most common sites hands and knees but can affect any joint; associated with significant morbidity; one of leading contributors to yrs lived with disability

Pathophysiology: previously considered “wear-and-tear” condition, natural part of aging; cause not fully understood, but has been shown to result from combination of biomechanical factors and proinflammatory mediators and proteases; proinflammatory factors drive production of proteolytic enzymes, resulting in progression of OA; pathologic changes include fraying and fibrillation of articular cartilage, thickening of subchondral bone, and formation of osteophytes

Contributing factors: age — 14% of adults aged ≥25 yrs and 34% of adults aged ≥65 yrs have symptomatic osteoarthritis; seen on x-ray in persons as early as age 25 yrs; sex — more prevalent in females; Framingham Osteoarthritis Study showed 1.7-fold higher incidence of OA of knee in women; gender difference in prevalence less pronounced than in rheumatoid arthritis (RA); genetics — influence of genetic factors associated with 30% to 50% of risk of OA, but no clear gene or pathway identified to explain link; previous injury — joints with previous injury more likely to develop OA, especially in knee; biomechanical stresses — also cause OA; anatomic abnormalities — study showed knee OA progressed faster if varus alignment compared with those with valgus alignment; if OA in 1 knee, contralateral knee has higher rate of development of OA partly because of abnormal biomechanical factors from OA in other knee; obesity — associated with higher risk of OA, especially in lower-extremity joints; hand joints also increased risk of OA in obese persons; activities with repetitive motion and heavy physical workload — associated with increased risk of OA

Types of OA: primary OA- occurs in absence of other forms of arthritis; secondary OA- develops in presence of another form of arthritis (eg, inflammatory arthritis, gout, hemochromatosis, Ehlers-Danlos syndrome, ochronosis, hemoglobinopathy); patients with inflammatory arthritis (eg, rheumatoid arthritis [RA] and psoriatic arthritis [PsA]) have higher risk for OA in same joints as those with inflammatory arthritis; inflammatory changes in joints can accelerate development of concomitant OA

Diffuse idiopathic skeletal hyperostosis (DISH): noninflammatory process; development of flowing osteophytes in anterolateral aspect of ≥4 contiguous vertebrae, peripheral enthesitis, and ossification of ligaments and nonvertebral locations on imaging; can be confused with ankylosing spondylitis (AS), but DISH develops in patients aged >50 yrs; more common in men than in women; treated in same way as OA; important to differentiate DISH from AS

Erosive OA: aggressive subset of OA in hand; has inflammatory component; manifests in distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints; not seen in metacarpal phalangeal (MCP) joint or carpometacarpal (CMC) joints; possibility of joint fusion; can be confused on imaging with inflammatory arthritis; treated like OA, not like inflammatory arthritis

Presentation: pain, tenderness, decreased range of motion, bony swelling, joint deformity, joint instability, and morning stiffness <30 mins; starts as sharp and short-lived pain when contact made with joint; over time, more constant pain and stiffness develop; can become dull ache with periods of intense pain; tenderness along joint lines and decreased range of motion of joint; bony swelling can confuse patient, as bony swelling may be resemble swelling; Heberden nodes in DIP joint from osteophyte formation; Bouchard nodes from osteophyte formation at PIP joint; as disease progresses, joint deformity occurs; joint may become unstable; patient may complain of laxity of joint; most common in knees, joints of hands (eg, DIP, PIP, first CMC) and feet (eg, first MTP), hips, facet joints of cervical and lower lumbar spine; less-commonly affected joints include elbow, wrist, shoulder, and ankle; gelling phenomenon — stiffness occurring after period of immobility; after <5 mins, relief of pain long as joint moved

Diagnosis: imaging- x-rays most common test; show joint-space narrowing, subchondral sclerosis, cysts; radiographic changes in early OA do not reliably correlate with symptoms; autoantibody testing to rule out RA not necessary if patient has signs and symptoms based on clinical criteria and x-ray findings; role of musculoskeletal ultrasound and magnetic resonance imaging (MRI) in diagnosing OA not defined; laboratory tests- synovial fluid analysis not usually needed for diagnosis of OA (if done, expect noninflammatory or mildly inflammatory synovial fluid; <2000 white blood cells [WBCs]/mm³)

Differential diagnosis:

Inflammatory arthritis: differentiated from OA based on pattern of joints involved, lack of symmetry in OA, lack of associated findings in OA, and presence of morning stiffness such as in RA and PsA not found in OA

Crystal arthropathy: smoldering polyarticular crystal arthropathy can mimic OA; if suspected by history, synovial fluid analysis, blood tests, and x-rays can help differentiate crystal arthropathy from OA

Hemochromatosis: iron overload arthropathy; most common in MCP and wrists; distinct findings on radiographs include squared-off bone ends and hooklike osteophytes; if suspected, get x-rays and blood tests to determine if iron overload

Infectious arthritis: presents with red, warm, swollen joint; if unsure whether infectious arthritis or OA, joint aspiration needed to help determine process causing symptoms

Management: nonpharmacologic therapy — first-line treatment for OA; includes exercise, physical therapy (PT), assessment for correctable biomechanical abnormalities, weight loss when applicable; pharmacologic therapy — nonsteroidal anti-inflammatory drugs (NSAIDs); topical and oral available; use cautiously in patients with comorbidities such as hypertension, diabetes, or history of or increased risk of gastrointestinal (GI) bleeding; cannot be used in patients taking blood thinners or who have kidney impairment; duloxetine can be used in patients with intolerance to or inadequate response to NSAIDs; prior to starting duloxetine, assess for depression (duloxetine antidepressant medication); if no success with oral or topical medications, intraarticular injections with corticosteroids (almost any joint) or hyaluronic acid (only in the knee) preparations; surgery — reserved for patients not successfully treated with medical therapies; total joint replacement most common surgical treatment for OA; most commonly done in knees and hips; arthroscopic debridement of knee not helpful

Spondyloarthritis: group of disorders including AS, PsA, inflammatory bowel disease (IBD)-related arthritis, reactive arthritis, and undifferentiated spondyloarthritis; features include inflammation of axial skeleton, inflammation of tendons and entheses, calcification of tendon can occur; some diseases also include mucocutaneous, GI, and ocular inflammation

Genetic factors: HLA-B27 — present in 90% of patients with AS; 60% to 70% of patients with reactive arthritis, IBD-associated arthritis, and axial PsA; 25% of patients with PsA without axial involvement; helpful clue, but most people with HLA-B27 do not have spondyloarthropathies, and negative results seen in those with spondyloarthropathies; physical exam and clinical presentation more important than genetic marker

Ankylosing spondylitis: can affect axial skeleton and peripheral joints; also extraarticular manifestations; more common in men than in women (3:1 ratio); peak age of onset in second and third decades; male sex and early age of onset portend poor prognosis

Presentation: inflammatory low-back pain of insidious onset; pain and stiffness worse after immobility, better with use; pain and morning stiffness >1 hr; skeletal manifestations — axial involvement, symmetric involvement of sacroiliac (SI) joints progressing up spine (does not skip areas of spine); peripheral involvement — enthesitis and asymmetric large-joint oligoarthritis; increased risk of spine fracture because of spinal fragility caused by ankylosing changes; extraarticular manifestations — uveitis (typically anterior, unilateral, and recurrent); asymptomatic intestinal ulcerations; urethritis; cardiac manifestations including aortitis, aortic valve disease, conduction abnormalities, coronary artery disease; pulmonary manifestations including apical fibrosis and restrictive lung disease

Physical exam: spine tenderness, SI joint tenderness, limited range of motion of spine, enthesopathy, synovitis

Diagnosis: laboratory — complete blood count(CBC), comprehensive panel, sedimentation rate (ESR), and HLA-B27 when applicable; radiology — x-rays of SI joints, spine, and peripheral joints; may show erosions, new bone formation, and enthesitis; vertebral changes may include sclerosis at attachment of annulus fibrosis to anterior corner of vertebral endplate and squared vertebral bodies; late x-ray findings include calcification of anterior longitudinal ligament, bridging syndesmophytes (bamboo spine appearance), and new bone formation and changes; at enthesis in SI joint, bilateral and symmetric sacroiliitis; early SI corrosion appears as irregular widening of joint space; sclerotic changes over time lead to fusion and narrowing of SI joints; if x-rays of SI joints and spine negative but suspicious for ankylosing spondylitis, MRI of SI joints warranted

Management: nonpharmacologic — initial conservative therapy with exercise and localized glucocorticoid injection; medications usually, if not always, required; pharmacologic — NSAIDs for pain control; conventional disease-modifying drugs (DMARDS; eg, methotrexate) not helpful in axial disease but can be helpful in peripheral disease; anti-tumor necrosis factor (TNF) agents and secukinumab (targets interleukin [IL]-17A); helpful for both peripheral and axial joint pain

Psoriatic arthritis: arthritis occurring in conjunction with psoriasis; peak age of onset 40 yrs to 60 yrs; prevalence ~1% of general population; 15% to 20% of people with psoriasis develop PsA; axial involvement in PsA can occur at any level of spine and may skip regions of spine; extraaxial involvement can include peripheral arthritis, dactylitis, tenosynovitis, enthesitis, and, if untreated or nonresponsive to therapy, can result in arthritis mutilans; conjunctivitis and uveitis may occur; in majority of cases, psoriasis precedes joint involvement, but sometimes joint involvement precedes skin involvement by ≤2 yrs; additional cutaneous manifestations include nail pitting and onycholysis

Presentation: 2 patterns of joint involvement — 1. oligoarticular, asymmetric lower-extremity arthritis; 2. symmetric polyarthritis at DIP, PIP, MCP, and MTP joints; in either pattern, patients may have dactylitis, SI joint involvement, asymmetric spondylitis with skip lesions

Diagnosis:

ClASsification criteria for Psoriatic ARthritis (CASPAR criteria): patient must have inflammatory articular disease as well as 3 of 5 following criteria: 1. personal or family history of psoriasis; 2. psoriatic nail dystrophy; 3. negative rheumatoid factor (RF); 4. dactylitis; 5. Radiographic evidence of juxtaarticular new bone formation

Other: negative RF part of CASPAR criteria, but small percentage of patients have positive RF; physical exam — spine tenderness, SI joint tenderness, peripheral joint arthritis, dactylitis, enthesitis, psoriasis, nail dystrophy, or onycholysis; laboratory- CBC, comprehensive metabolic panel, HLA-B27, ESR, C-reactive protein, RF, and anti-cyclic citrullinated peptide (CCP) blood test; if expecting to use biologic DMARD, test for tuberculosis (TB) and hepatitis; imaging — x-ray of affected joints if peripheral arthritis; x-ray of SI joints or spine if axial involvement

Management: collaboration between rheumatologist and dermatologist; conservative management — exercise, localized corticosteroid injections into joints or skin; medications- topical creams for skin disease, NSAIDs for joint pain, conventional DMARDs for peripheral arthritis, biologic DMARDs (including anti-TNF agents, ustekinumab, secukinumab, tofacitinib, and apremilast)

Inflammatory bowel disease–related arthritis: associated with IBD; involve axial and peripheral skeleton; 20% to 30% of individuals with IBD will develop IBD-related arthritis; axial involvement in IBD-related arthritis does not parallel bowel disease activity; SI joint involvement often present in axial disease of IBD arthritis, frequently asymmetric; peripheral involvement has 3 different patterns — 1. monoarticular large-joint involvement of lower extremity, parallels IBD activity; 2. polyarticular small-joint arthritis in upper extremities; does not parallel IBD; possibly enthesitis or dactylitis; 3. skin disease that manifests as pyoderma gangrenosum or erythema nodosum, uveitis (insidious or chronic, usually anterior and bilateral), episcleritis or conjunctivitis; increased risk of thromboembolism in patients with IBD; also increased risk of nephrolithiasis and renal disease

Diagnosis: based on history of IBD (eg, Crohn disease or ulcerative colitis) and presence of axial or peripheral arthritis meeting above patterns; imaging — to demonstrate changes related to IBD arthritis; x-rays of involved joints important

Management: glucocorticoids; biologic DMARDs may help control both IBD and arthritis

Reactive arthritis: noninfectious inflammatory arthritis; occurs after GI or genitourinary (GU) infection; autoimmune process, not infectious; usually 3 wks to 6 wks after infection, but latency can be anywhere from 2 wks to 6 mos after infection; 50% of cases resolve within 6 mos; 20% become chronic; once patient has episode reactive arthritis, increased risk for repeated episodes thereafter; associated GI pathogens include Yersinia, Salmonella, Shigella, Campylobacter, Escherichia coli, and C difficile; associated GU pathogens include Chlamydia and Ureaplasma urealyticum

Diagnosis: based upon clinical presentation and history of antecedent infection; other manifestations include skin findings (eg, keratoderma blenorrhagicum, circinate balanitis), enthesitis, and asymmetric large-joint oligoarthritis; nonerosive arthritis, so x-rays not helpful(but can distinguish reactive arthritis from another suspected process)

Treatment: conservative; localized glucocorticoid injections, NSAIDs; rarely, conventional or biologic DMARDs

Gout: painful joint inflammation caused by monosodium urate crystals; prevalence 4% in US; risk factors include genetic factors, age, chronic kidney disease; men and postmenopausal women have higher risk; comorbidities include diabetes, kidney disease, obesity, vascular disease, and dyslipidemia

Pathophysiology: uric acid end product of purine metabolism in humans; other animals (eg, birds) have uricase (enzyme that breaks down uric acids), humans do not; xanthine oxidase breaks down products of purine metabolism into uric acid; uric acid can accumulate; monosodium urate crystals form when uric acid concentration >6.8 mg/dL; uric acid cleared from kidney via glomerular filtration, secretion, and resorption; causes of elevated uric acid (hyperuricemia) — primary renal uric acid underexcretion, chronic kidney disease, uric acid overproduction resulting from defect in purine metabolism, conditions with increased cell turnover (leading to increased purines), drug-induced hyperuricemia, and diet-induced hyperuricemia; drugs that commonly cause hyperuricemia — thiazide diuretics, loop diuretics, low-dose salicylates, ethambutol, pyrazinamide, lead; dietary factors that can cause hyperuricemia — increased consumption of meat, shellfish, alcohol, high-fructose–sweetened beverages and foods; dehydration increases serum uric acid; once uric acid at level where crystals can form, monosodium uric crystals phagocytosed by macrophages, initiating inflammatory cascade 3. types of clinical presentations: acute gouty arthritis — red, swollen, tender joint; quick onset (occurs over 12-24 hrs); majority of first attacks monoarticular, beginning at night and in lower extremity; low-grade fever, peripheral leukocytosis, elevated inflammatory markers; associated inflammatory changes in surrounding soft tissues that may mimic cellulitis; uric acid may be normal at time of attack, probably from increased uric acid excretion caused by circulating cytokines; intercritical gout — period between gout attacks; tophi may be forming, but no acutely red, swollen, or tender joint; chronic recurrent tophaceous gout — also called pseudorheumatoid arthritis; frequent attacks so close in timing that seem contiguous or chronic arthritis with synovitis-like presentation; possible to confuse chronic recurrent gout with rheumatoid arthritis

Tophus: stone-like deposit of monosodium urate surrounded by inflammatory fibrous rind outside of joint; hallmark of gout; typical on tendons (eg, Achilles tendon), tips of ears

Diagnosis: consider gout with acute monoarticular or polyarticular inflammation; laboratory — serum urate levels may be elevated in acute attack, but may also be normal, so not used as diagnostic criterion (poor negative and positive predictive value); joint aspiration gold standard for diagnosis; inflammatory synovial fluid with elevated WBC count, neutrophilic predominance; negative culture; polarized microscopy analysis of joint fluid shows needle-shaped, negatively birefringent crystals; imaging — not useful in diagnosing acute gout, but can help rule out other conditions; monitors for gout-related changes in chronic gout; gouty erosions seen on x-ray appear as punched-out lesions or “rat-bite” lesions, characterized by overhanging edges

Differential diagnosis: infectious arthritis, acute pseudogout, basic calcium phosphate deposition, inflammatory arthritis (RA, PsA); joint aspiration gold standard for differential diagnosis

Management: acute (gout flare) management — colchicine, NSAIDs, oral or intraarticular steroids; colchicine first-line therapy if patient seeks medical attention within first 36 hrs of flare (dosed at 1.2 mg at time 0, 0.6 mg at time 1 hr, 0.6 mg daily thereafter; dosage based on renal function); chronic management — eliminate or limit foods and beverages that increase risk of gout (eg, alcohol, meat, shellfish, foods and beverages containing high-fructose sweeteners); urate-lowering therapy for patients with ≥2 gout flares in 1-yr period, or 1 gout flare in 1-year period in setting of chronic kidney disease Stage 2 or worse, kidney stones; patients with gouty erosions on x-ray or tophi should be offered urate-lowering treatment; target uric acid ≤6 mg/dL, ≤5 mg/dL if tophi present; medications that lower uric acid — xanthine oxidase inhibitors, allopurinol and febuxosat; probenecid, uricosuric agent, blocks renal uric acid resorption; increases risk of kidney stones, so not helpful in patients with chronic kidney disease; pegloticase, uricase that can be given intravenously (IV); high rate of allergic reactions; in patient with hyperuricemia treated with urate-lowering therapy, flare prophylaxis with colchicine, steroids, or NSAIDs while lowering uric acid until goal reached

Pseudogout (calcium pyrophosphate deposition disease [CPDD]): mostly idiopathic, increases with age, more common in women; risk factors include age, prior joint trauma, familial chondrocalcinosis and metabolic disorders, endocrine disorders; such disorders include hemochromatosis, hyperparathyroidism, gout, hypomagnesemia, hypophosphatasia, X-linked hypophosphatemic rickets, familial hypocalciuric hypercalcemia, acromegaly, Wilson disease, bisphosphonate use, and ???

Pathophysiology: excessive calcium or excessive calcium pyrophosphate; unclear mechanism

Presentation: acutely red, swollen, tender joint

Diagnosis: clinical presentation and joint aspiration; aspiration shows inflammatory joint fluid; crystal analysis shows rhomboid crystals with positive birefringence; x-ray may show chondrocalcinosis (cartilage calcification) in CPDD

Management: in acute CPDD, joint aspiration injection alleviates pain and relieves acute flare; medications — NSAIDs, colchicine, or glucocorticoids; if >3 attacks per yr, consider prophylaxis with colchicine, NSAIDs, or low-dose glucocorticoids

Infectious (septic) arthritis: bacterial, fungal, viral, or mycobacterial infection within joint; usually results from hematogenous spread, direct inoculation of joint, or contiguous spread; risk factors include age >80 yrs or <5 yrs, alcoholism, skin breakdown, end-stage renal disease, diabetes, history of instrumentation within region, injection drug use, low socioeconomic status, immunosuppression, sickle cell disease, and underlying malignancy; immunosuppressed patients or those who travel to or live in area where specific fungus endemic have increased risk of fungal septic arthritis

Presentation: warm, red, painful joint, decreased range of motion; bacterial infections develop over few days, while viral and fungal infections have more insidious onset; ~80% of septic arthritis cases monoarticular

Pathophysiology: gram-positive organisms — most common causes in adults; Staphylococcus aureus most common cause; toxin and local inflammatory response cause damage to joints; joint damage may develop within 48 hrs of development of septic arthritis; gram-negative organisms — nongonococcal gram-negative organisms such as E coli, Pseudomonas, and Salmonella (more prevalent in patients with sickle cell disease); 3% of patients with systemic gonorrhea develop disseminated gonococcal arthritis; 2 types of gonococcal arthritis — 1. purulent arthritis; no rash; no bacteremia; usually monoarticular or oligoarticular; positive cultures; localized septic arthritis, direct infection of joint; knee most common but seen in wrists, ankles, and elbow; 2. disseminated gonococcal disease with arthritis; does not involve direct infection of joint; bacteremia but negative synovial culture (synovial WBC <25,000); arthritis dermatitis, vesiculopustular or hemorrhagic macular lesions; polyarthralgia, tenosynovitis, fever and chills

Diagnosis: laboratory — joint aspiration for culture, cell count, gram stain, and crystal analysis; cultures 80% sensitive to identify bacterial cause; WBC count usually >50,000, with neutrophil predominance; important to aspirate joint before starting antibiotic treatment; if gonococcal arthritis suspected, get GU and pharyngeal culture, both traditional culture media and chocolate agar; imaging — x-ray to identify early osteomyelitis or erosions caused by aggressive septic arthritis

Lyme arthritis: infection with Borrelia species; 3 phases of Lyme disease

Presentation: arthralgia can be seen in early localized or early disseminated Lyme disease; arthritis seen in late Lyme disease, causes frank inflammation of joints, large effusions, and usually monoarticular or oligoarticular pattern with stiffness; prominent stiffness, little pain

Diagnosis: serologic diagnosis with positive ELISA test and Western blot test; joint aspiration shows moderately elevated WBC count (20,000-25,000) with high percentage of neutrophils and negative cultures; Borrelia burgdorferi DNA can be tested on synovial fluid

Mycobacterial arthritis: TB — 20% of TB infections extrapulmonary; joint or bone involvement seen in 2% of TB infections

Presentation: joint involvement in initial infection or reactivation of latent TB; chronic, indolent infection; patient may or may not have other signs of TB; usually monoarticular; synovial fluid may be bland

Diagnosis: synovial fluid, specific culture for acid-fast bacilli; if strong suspicion for mycobacterial arthritis, synovial biopsy superior to acid-fast bacilli culture on synovial fluid (synovial fluid acid-fast bacilli cultures have high false-negative rate)

Mycobacteria marinum — fresh- and saltwater organism that enters through breaks in the skin; presents with red or purple plaque, nodules, abscesses under skin

Fungal arthritis: more common in immunosuppressed persons and in endemic areas; common causative fungi include Coccidioides, Sporothrix, Cryptococcus, Blastomyces, and Candida; fungal arthritis usually monoarticular; diagnosis by fungal culture and/or synovial biopsy

Viral arthritis: hepatitis B — can cause symmetric polyarthritis in prodrome stage of disease; associated with rash; can be transient or persistent; hepatitis C — causes arthralgia or arthritis; can be oligoarticular or polyarticular; parvovirus — symmetric swelling and stiffness of small joints of hands, feet, wrists, and knees; consider in adult population; can last for wks or mos; usually positive parvovirus IgM; can be managed with NSAIDs and steroids; consider parvovirus in patient with abrupt, symmetric inflammatory arthritis; rubella — rash, fever, lymphadenopathy, polyarthritis; positive IgM serology at time of arthritis; resolves in 2 wks; chikungunya and Zika virus- self-limited; supportive care required

Diagnosis: travel history; serology to help guide and diagnose

Prosthetic joint infections: rare complication of joint replacement; occurs in 2% of patients who have had joint replacement; most common, Staphylococcus within 2 yrs of surgery; risks include superficial skin infection or surgical-site infection, immunosuppression, and chronic illness; 3 types of prosthetic joint infections- 1. early-onset (within 3 mos after surgery); joint swelling, erythema, wound drainage, fever; 2. delayed-onset (within 3-12 mos after surgery); insidious and prolonged joint pain, may be confused with prosthetic failure; 3. late-onset (12 mos after surgery); acute pain and swelling

Management: aspiration of joint, prompt orthopedic evaluation; if suspicion of gram-positive cocci, administer vancomycin, linezolid, clindamycin, or daptomycin if methicillin-resistant S aureus (MRSA) suspected; but if methicillin-susceptible S aureus (MSSA) suspected, oxacillin, nafcillin or cephazolin; for gram-negative bacilli, third-generation cephalosporin or fluoroquinolone; Pseudomonas requires treatment with ceftazidime, aminoglycoside, carbapenem, piperacillin, cefepime, tazobactam, or fluoroquinolone; Neisseria gonorrhoeae requires treatment with IV ceftriaxone or fluoroquinolone; if gram stain unclear or unavailable, broad-spectrum treatment with vancomycin plus third-generation cephalosporin recommended; for suspected Lyme disease, oral doxycycline or amoxicillin; Mycobacterium tuberculosis treated with anti-TB therapy(isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin); for fungal infection, amphotericin or azoles; regardless of antibiotic, must drain purulent fluid from joint with bacterial infection

Readings

Chen D et al: Osteoarthritis: toward a comprehensive understanding of pathological mechanism. Bone Res. 2017;5(16044):1-13; Mease PJ et al: Characterization of patients with ankylosing spondylitis and nonradiographic axial spondyloarthritis in the US-Based Corrona Registry. Arth Care Res (Hoboken). 2018;70(11):1661-70; Mitra SP: Arthritis: classification, nature and cause — a review. American Journal of Biopharmacology, Biochemistry and Life Sciences. 2013;2(3):1-25; Singh JA et al: 2018 American College of Rheumatology/National Psoriasis Foundation Guideline for the Treatment of Psoriatic Arthritis. Arth Care Res (Hoboken). 2019;71(1):2-29.

Disclosures

For this activity, the faculty and planning committee reported nothing to disclose.

Acknowledgements

CME/CE INFO

Accreditation:

The Audio- Digest Foundation is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians.

The Audio- Digest Foundation designates this enduring material for a maximum of 0 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

Audio Digest Foundation is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's (ANCC's) Commission on Accreditation. Audio Digest Foundation designates this activity for 0 CE contact hours.

Lecture ID:

IMBR190142

Expiration:

This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.

Instructions:

To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.

Estimated time to complete this CME/CE course:

Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.