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Inflammatory arthritis
1. Inflammatory Arthritis
Michael Aref, MD, PhD
Hospitalist, Carle Physician Group
Department of Nuclear, Plasma, and Radiological Engineering, UIUC
Department of Medicine, UICOM-UC
2. Objectives
• Review the history and physical examination
findings of inflammatory arthritis
• Define and categorize inflammatory arthritis
• Understand the initial laboratory and radiological
evaluation of suspected rheumatological disease
• Increase clinical sensitivity and specificity to
rheumatological disease
3. Chest pain rule-out
• 45 y/o WM
• Persistent, bilateral shoulder, elbow, and hand pain,
worse with activity. Associated fatigue.
• Smoker, mother has history of rheumatoid
arthritis.
• VSS, decreased ROM of shoulders, with bilateral
finger, elbow, and shoulder synovitis.
• Mild normochromic, normocytic anemia and
hypokalemia; EKG and chest x-ray benign.
• What test(s) would you like to order next?
4. Objectives
• Review the history and physical examination
findings of inflammatory arthritis
• Define and categorize inflammatory arthritis
• Understand the initial laboratory and radiological
evaluation of suspected rheumatological disease
• Increase clinical sensitivity and specificity to
rheumatological disease
5. History
Aggravating and alleviating factors
Severity
Character
Location
Associated symptoms
Setting
Timing
• Does activity make your symptoms better or worse?
• Probably pretty bad, or they wouldn’t be in the hospital.
• Are the same joints affected persistently or are different joints affected?
• How many joints are affected? 1 (monoarticular), 2-4 (oligoarticular), or more (polyarticular)?
• Any association with your back, particularly your spine?
• Joint swelling? Low grade temperature? Rash? Fatigue?
• When you wake up in the morning, how long do your symptoms last?
• How long have you been noticing these symptoms?
6. Physical Examination
• Main signs of active inflammation include
Erythema (Rubor)
Warmth (Calor)
Swelling (Tumor)
Tenderness (Dolor)
Loss of Function
• Enthesopathy
Pathology or lesions of enthesis (the site where ligament or tendon inserts into bone) Examples include: plantar
fasciitis,Achilles tendonitis.
• Dislocation
Articulating surfaces are displaced and no longer in contact
• Subluxation
Partial dislocation
• Synovitis
Inflammation of the synovial membrane
• Valgus
Lower limb deformity whereby distal part is directed away from the midline e.g. hallux valgus
• Varus
Lower limb deformity whereby distal part is directed towards the midline e.g. varus knee with medial
compartment OA
GALS Screen Basic Rheumatologic Examination
9. Objectives
• Review the history and physical examination
findings of inflammatory arthritis
• Define and categorize inflammatory arthritis
• Understand the initial laboratory and radiological
evaluation of suspected rheumatological disease
• Increase clinical sensitivity and specificity to
rheumatological disease
10. Inflammatory vs. Non-
inflammatory
FeaturesFeatures InflammatoryInflammatory Non-inflammatoryNon-inflammatory
Hx
Morning stiffness > 1 hour
Low-grade temperature
Fatigue
Rash
Morning stiffness < 1 hour
Px Erythema (Rubor) • Warmth (Calor) • Swelling (Tumor)
• Tenderness (Dolor) • Loss of Function
Bony proliferation in osteoarthritis
Labs
(+)ve ESR ± CRP
Anemia of chronic disease
(+)ve rheumatoid factor or anti-CCP antibodies
Within normal limits
Radiographs
Erosions
Periostitis
Joint-space narrowing
Joint-space narrowing
Osteophytes
Subchondral sclerosis
Synovial Fluid
Non-infectious Infectious
Leukocyte count < 2,000/uL
< 50% neutrophilsLeukocyte count >
2,000 /uL
Predominantly neutrophils
Leukocyte count > 50,000
/uL
MKSAP 15 Rheumatology
15. Objectives
• Review the history and physical examination
findings of inflammatory arthritis
• Define and categorize inflammatory arthritis
• Understand the initial laboratory and radiological
evaluation of suspected rheumatological disease
• Increase clinical sensitivity and specificity to
rheumatological disease
16. Erythrocyte Sedimentation Rate (ESR)
• Conditions with increased immunoglobulins
• Age
• Normal males = age/2
• Normal females = (age + 10)/2
• Myeloma,Waldenström’s, 1° amyloid
• SLE, Sjogren’s
• Chronic liver disease/cirrhosis
Miller ML, The Little Black Book of Rheumatology
17. “C-Reactive Protein”
Cytokine Response Protein (CRP)
Cytokine Response Protein (CRP)
• ESR and CRP both elevated:
• Infection
• Inflammatory States
• Trauma
• Cancer
Miller ML, The Little Black Book of Rheumatology
18. Serology
• Rheumatoid Factor (RF)
• Titer of IgM against IgG
• Present in 80% of rheumatoid arthritis
• Sensitivity 69% / Specificity 85%
• Anti-citrulline-containing peptide antibody (Anti-
CCP Ab)
• Associated the development of erosive disease
• Sensitivity 67% / Specificity 95%
Miller ML, The Little Black Book of Rheumatology
Ann Int Med, 2007; 146:797
20. Objectives
• Review the history and physical examination
findings of inflammatory arthritis
• Define and categorize inflammatory arthritis
• Understand the initial laboratory and radiological
evaluation of suspected rheumatological disease
• Increase clinical sensitivity and specificity to
rheumatological disease
23. Ankylosing Spondylitis
Modified NewYork Criteria (1984)
• Definite ankylosing spondylitis is present if
• Radiologic criterion is present in addition to at least one clinical criterion.
• Probable ankylosing spondylitis is present if
• Three clinical criterion are present alone or if
• The radiologic criterion is present but no clinical criteria are present.
Clinical criteria
• Low back pain: present for more than 3 months, improved by exercise but not relieved by rest.
• Limitation of lumbar spine motion in sagittal and frontal planes.
• Limitation of chest expansion relative to normal values for age and sex.
Radiologic criterion
• Sacroiliitis on radiographs
http://emedicine.medscape.com/article/386639-overview
25. Genetic Predisposition for Development
of Ankylosing Spondylitis (AS)
HLA-B27
positive
AS and HLA-
B27 positive
Western European
Whites
8% 90%
African Americans 2% to 4% 48%
Guidelines in Rheumatology: Ankylosing Spondylitis
31. Infectious Arthritis
• Septic arthritis is the presumed diagnosis in any
patient with acute monoarthritis and fever.
• Synovial fluid analysis is the diagnostic test
• White cell count with differential
• Gram stain (sensitivity 29-50%)
• Crystal search using polarized light microscopy
• Culture (positive in the majority of patients with
nongonococcal bacterial arthritis)
Guidelines for the initial evaluation of the adult patient with acute musculoskeletal symptoms. American College of Rheumatology Ad Hoc Committee on Clinical Guidelines. Arthritis Rheum 1996; 39:1
35. Lyme Arthritis
Characterized by intermittent or persistent arthritis. Monoarthritis of the knee is
most common, but can also present as asymmetric oligoarthritis, usually including
the knee.
•Knee > shoulder > ankle > elbow > temporomandibular joint > wrist
•≤ 5 joints, large joints > small joints
•Abrupt presentation, lasts from several weeks to months
•Large joint effusions are common in the knees and elsewhere and often recur after
aspiration
•Affected joints are usually very swollen and warm
Ann Intern Med 1987 Nov;107(5):725-31
37. Reactive Arthritis
Willkens RF et al. Arthritis Rheum 1981;24:844-9
SensitivitySensitivity SpecificitySpecificity
Episode of arthritis of more than 1 month with
urethritis and/or cervicitis
84.3%
(70/83)
98.2%
(163/166)
Episode of arthritis of more than 1 month and
either urethritis or cervicitis, or bilateral
conjunctivitis
85.5%
(71/83)
96.4%
(160/166)
Episode of arthritis, conjunctivitis, and urethritis 50.6%
(42/83)
98.8%
(164/166)
Episode of arthritis of more than 1 month,
conjunctivitis, and urethritis
48.2%
(40/83)
98.8%
(164/166)
38. Reactive Arthritis
• Preceding enteric infection (i.e. diarrhea)
• Salmonella of various serovars
• Shigella, especially Shigella flexneri, but also
Shigella dysenteriae and sonnei
• Yersinia includingYersinia enterocolitica 0:3 and
0:9 andYersinia pseudotuberculosis
• Campylobacter especially Campylobacter jejuni
• Clostridium difficile
• Preceding genitourinary infection (i.e. urethritis)
• Chlamydia trachomatis
Up-To-Date
40. Gout
1977 American College of1977 American College of
Rheumatology CriteriaRheumatology Criteria
New York CriteriaNew York Criteria Rome CriteriaRome Criteria
Monosodium urate monohydrate microcrystals in joint
fluid during attack or ≥ 6 of the following
MSU microcrystals in joint fluid or tissue or tophus or
≥ 2 of the following
≥ 2 of the following
> 1 attack of acute arthritis 2 attacks of painful limb joint swelling
Maximum inflammation developed within 1 day Abrupt onset and remission in 1-2 weeks initially
Abrupt, painful joint swelling, clearing in 1-2 weeks
initially
Monoarthritis attack
Redness observed over joints
First metatarsophalangeal joint painful or swollen First metatarsophalangeal joint attack
Unilateral first metatarsophalangeal joint attack
Unilateral tarsal joint attack
Tophus (proven or suspected) Presence of a tophus Presence of tophi
Hyperuricemia Serum uric acid > 7 in males and > 6 in females
Asymmetric swelling within a joint on x-ray
Subcortical cysts without erosions on x-ray
Joint fluid culture negative for organisms during attack
Response to colchicine—major reduction in
inflammation within 48 hours MSU microcrystals in joint fluid or tissueWallace SL, et al. Arthritis Rheum 1977;20:895-900 and J Clin Rheumatol. 2009 Feb;15(1):22-4
41.
42. Pseudogout
Definite diagnosis of pseudogout requires either:
• The demonstration of CPPD crystals in tissue or synovial fluid by
definitive means (eg, x-ray diffraction, etc) or
• The presence of both positively (but weakly) birefringent crystals by
compensated polarized light microscopy and typical cartilage or joint
capsule calcification on x-ray examination
Probable diagnosis of pseudogout occurs with either:
• The identification of positively (but weakly) birefringent crystals by
compensated polarized light microscopy or
• The presence of typical cartilage or joint capsule calcification on
radiographic examination.
Up-To-Date
45. CODE SPEED
• 75 y/o WM
• Admitted for fever and malaise, back pain noted on ROS
• Obesity, HTN, HCL, DM, CAD, and CKD III
• “Social” drinker, family history noncontributory.
• Febrile, tachycardic, hypotensive, diaphoretic, examination otherwise
noncontributory
• Mild leukocytosis otherwise CBC and CMP benign, negative blood and urine
cultures, chest x-ray negative
• Patient intubated and started on vasopressors for shock
• What’s the differential diagnosis?
Notas del editor
Examination of the hand
Examination of the thumb
Examination of the wrist
Examination of the elbow
Examination of the shoulder joint
Examination of the rotator cuff
Examination of the acromioclavicular joint
Examination of the neck
Examination of the hip joint
Examination of the trochanteric bursa
Examination of the knee I
Examination of the knee II
Examination of the ankle
Subtalar examination
Examination of the tarsals
Plantar Fascia and Achilles heel examination
Examination of the metatarsals
Rheumatoid arthritis is an insidious polyarthritis
Ankylosing spondylitis typically presents with back and buttock pain
Psoriatic and inflammatory bowel disease associated arthritis are associated with autoimmune disease of the skin and gastrointestinal system respectively
Crystal arthropathies present like septic joints but don’t grow anything and don’t respond to antibiotics
Genetic Predisposition for Development of Ankylosing Spondylitis (AS)
Ankylosing spondylitis (AS) is a common, complex, and systemic inflammatory disease with the potential to cause severe debilitation.1-3 Although etiology remains unknown and pathogenesis is not fully understood, a strong association between AS and HLA-B27 (an allele of the major histocompatibility complex) suggests a genetic predisposition. Presence of allele and expression of the condition vary, however, among different ethnic/racial groups. For example, 8% of western European whites are positive for HLA-B27, and it is detected in over 90% of white patients with primary AS; but 2% of African Americans are positive for HLA-B27, and it is present in only 48% of African Americans with AS.4-6 Consequently prevalence rates vary between groups.
Khan MA. Clinical features of ankylosing spondylitis. In: Hochberg MC, Silman AJ, Smolen JS, Weinblatt ME, Weisman MH, eds. Rheumatology. vol 2, 3rd ed, New York, NY: Mosby; 2003:1161-1181.
Sieper J, Braun J, Rudwaleit M, Boonen A, Zink A. Ankylosing spondylitis: an overview. Ann Rheum Dis. 2002;61(suppl III):iii8-iii18.
Khan MA. Spondyloarthropathies. In: Hunder GG, ed. Atlas of Rheumatology. 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002.
Khan MA. Update on spondyloarthropathies. Ann Intern Med. 2002;136:896-907.
Khan MA. Thoughts concerning the early diagnosis of ankylosing spondylitis and related diseases. Clin Exp Rheumatol. 2002;20(suppl 28):S6-S10.
6. Khan MA, Braun WE, Kushner I, et al. HLA B27 in ankylosing spondylitis differences in frequency and relative risk in American Blacks and Caucasians. J Rheumatol. 1977;4(Suppl 3):39-43.