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Topic Review :
How to Approach Arthritis
             Ext.สรวิศ / พ.อภิญญา
                 8 พฤษภาคม 2555
What’s Heading in Topic

Clinical Approach to patients with Arthritis ?

Common Disease in Rheumatology
• Rheumatoid Arthritis
• Crystal induced arthritis (Gout and CPPD)

Case study
CLINICAL APPROACH
TO PATIENT WITH ARTHRITIS ?
Importance of History

Duration of Complaints


    Number of Joints Involved


      Distribution of Joints Involved


    Pattern of Involvement


Duration of Early Morning Stiffness
Importance of History

History of Joint Swelling


     Extra-articular Complaints


      Associated Medical Illness


     Significant Past History


Family History of Rheumatic Disease
Importance of Physical Examination

       Presence of Swelling of Joint

       Local Warmth

       Redness

       Range of Motion

       Any Deformity
Diagnostic Approach to
 Musculoskeletal Pain
Diagnostic Approach to
            Patient with Arthritis

                                     Arthritis



                 Acute                                   Chronic


   Mono /                                      Mono /
                         Polyarthritis                         Polyarthritis
Oligoarthritis                              Oligoarthritis
Differential Diagnosis

      Acute                    Acute                  Chronic                   Chronic
   Monoarthritis            Polyarthritis           Monoarthritis             Polyarthritis
Pyogenic                Acute rheumatic fever    Chronic infection (TB,   Rheumatoid
Gout                    Pyogenic (2-3 ข้อ)          pyogenic, fungus)     Gout
Pseudogout                esp. GC, salmonella    Osteoarthritis           Pseudogout
Acute rheumatic fever   SLE                      Gout                     Osteoarthritis
Traumatic arthritis     Serum sickness           Pseudogout               Psoraitic
Reiter’s disease        Reiter’s disease         Avascular necrosis       Ankylosing spodylitis
Psoriasis               Psoriatic arthritis      Tumor                    SLE
Rheumatoid arthritis    Ankylosing spondylitis   Neuropathic              Other connective
Hemophilic arthritis    Viral                                                 tissue diseases
                        Leukemia                                          Hypertrophic
                        Hemophilic                                            osteoarthropathy
                                                                          Neuopathic
Examination of Synovial Fluid

                    Normal      Noninflammatory     Inflammatory         Septic
   Clarity        Transparent      Transparent         Cloudy            Cloudy
    Color            Clear            Yellow           Yellow            Yellow
WBC*/microliter      <200          <200–2000         200–50,000         >25,000
 PMNs (%)*            <25              <25              >50                >90
   Culture         Negative         Negative          Negative        >50% positive
                                                                          None
   Crystals          None             None         Multiple or none

                                                  Gout, pseudogout,
                                  Osteoarthritis,                   Nongonococcal or
  Associated                                      spondyloarthropat
                      -         trauma, rheumatic                   gonococcal septic
  conditions                                       hy, rheumatoid
                                      fever                             arthritis
                                                    arthritis, SLE
COMMON DISEASE
IN RHEUMATOLOGY
RHEUMATOID ARTHRITIS
Rheumatoid Arthritis
• The most common form, autoimmune
  inflammatory arthritis
• Characterized by symmetric arthritis of
  the small joints of the hands and feet
• Chronic erosive arthritis need early and
  aggressive management
• Prevalence 0.5 – 1 %
Pathogenesis
• Characterized by
   – synovial inflammation and hyperplasia
     (“swelling”),
   – autoantibody production (rheumatoid factor
     and anti–citrullinated protein antibody
     [ACPA]),
   – cartilage and bone destruction
     (“deformity”),
   – systemic features, including
      • cardiovascular, pulmonary, psychological, and
        skeletal disorders.
Pathophysiology
Criteria Diagnosis
   • At least 4 of these 7 criteria
         – criteria 1 to 4 must have been present for ≥6 weeks
                           Morning stiffness
                  Arthritis of 3 or more joint areas
                           Arthritis of hands
                         Symmetric arthritis
                         Rheumatoid nodules
                      Serum rheumatoid factor
                       Radiographic changes
Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987
                          revised criteria for the classification of rheumatoid arthritis.
                                                   Arthritis Rheum. 1988;31:315-324.
Criteria Diagnosis
Criteria Diagnosis
Criteria Diagnosis
Criteria Diagnosis
Criteria Diagnosis
American College of Rheumatology (ACR)/European League
                              Against Rheumatism (EULAR) collaborative initiative 2010
                                       rheumatoid arthritis classification criteria
                                                                                    Score
Joint involvement 1 large joint (shoulder, elbow, hip, knee, ankle)                   0
                  2–10 large joints                                                   1
                  1–3 small joints (MCP, PIP, Thumb IP, MTP, wrists)                  2
                  4–10 small joints                                                   3
                  >10 joints (at least 1 small joint)                                 5
     Serology     Negative RF and negative ACPA                                       0
                  Low-positive RF or low-positive anti-CCP antibodies                 2
                  (3 times ULN)
                  High-positive RF or high-positive anti-CCP antibodies               3
                  (>3 times ULN)
  Acute-phase Normal CRP and normal ESR                                               0
    reactants     Abnormal CRP or abnormal ESR                                        1
   Duration of    <6 weeks                                                            0
    symptoms      6 weeks                                                             1
Extraarticular manifestations of
      rheumatoid arthritis
Management
Management
              For Primary care Physicians
Establish Diagnosis of Rheumatoid Arthritis Early
Document Baseline Disease Activity and Damage
Estimate Prognosis


        Start Treatment
         Patient Education
         Start DMARD(s) within 3 months
         Consider NSAIDs
         Consider Local / Low-dose Steroid
         Physical / Occupational Therapy

                  Periodically Assess Disease Activity
Baseline Evaluation
• Subjective
   –   Degree of joint pain
   –   Duration of morning stiffness
   –   Duration of fatigue
   –   Limitation of function
• Physical examination
   – Actively inflamed joints (tender and swollen joint
     counts)
   – Mechanical joint problems: loss of motion, crepitus,
     instability,
   – malalignment, and/or deformity
   – Extraarticular manifestations
Baseline Evaluation
• Laboratory
   –   Erythrocyte sedimentation rate/C-reactive protein level
   –   Rheumatoid factor
   –   Complete blood cell count
   –   Electrolyte levels and Creatinine level
   –   Hepatic enzyme levels (AST, ALT, and albumin)
   –   Urinalysis
   –   Synovial fluid analysis
   –   Stool guaiac
• Radiography
   – Radiographs of selected involved joints
• Other
   – Functional status or quality of life assessments using
     standardized
DMARDs Used for the Treatment of
                                 Rheumatoid Arthritis
                                                           Other Common
    Drug           Dosage           Serious Toxicities                       Monitoring
                                                            Side Effects
  Hydroxy 200–400 mg/d           Irreversible retinal    Nausea            Funduscopic
chloroquine orally               damage                  Diarrhea          and visual
            ( 6.5 mg/kg)         Cardiotoxicity          Headache          field testing
                                 Blood dyscrasia         Rash              every 12
                                                                           months
Sulfasalazine Initial:            Granulocytopenia       Nausea            CBC every 2–4
              500 mg orally       Hemolytic anemia       Diarrhea          weeks for first
              twice daily         (with G6PD deficiency) Headache          3 months, then
              Maintenance:                                                 every 3
              1–1.5 g twice daily                                          months
DMARDs Used for the Treatment of
                                 Rheumatoid Arthritis
                                                           Other Common
    Drug           Dosage          Serious Toxicities                        Monitoring
                                                            Side Effects
Methotrexate 10–25 mg/week      Hepatotoxicity           Nausea             CBC,
             orally             Myelosuppression         Diarrhea           creatinine,
             or SQ              Infection                Stomatitis/mouth   LFTs every 2–
             Folic acid :       Interstitial pneumonitis ulcers             3 months
             1 mg/d to reduce   Pregnancy category X Alopecia
             toxicities                                  Fatigue
Leflunomide 10–20 mg/d          Hepatotoxicity           Alopecia           CBC,
                                Myelosuppression         Diarrhea           creatinine,
                                Infection                                   LFTs every 2–
                                Pregnancy category X                        3 months
approximate time to benefit of disease-
modifying antirheumatic drugs used in the
    treatment of rheumatoid arthritis
Physical Therapy
Management
by Rheumatologist
CRYSTAL - INDUCED ARTHRITIS
Type of Crystal                                     Disease
Monosodium urate (MSU)                      Gout, tophaceous gout
Calcium pyrophosphate dihydrate (CPPD)      Pseudogout, pyrophosphate arthropathy,
                                            calcium pyrophosphate dihydrate deposition
                                            disease, tophaceous pseudogout
Basic calcium phosphate; calcium carbonate Acute periarthritis, acute arthritis,
(CC), hydroxy apatite (HA), octacalcium     destructive
phosphate (OCP), tricalcium phosphate (TCP) arthropathy, Milwaukee shoulder/knee
                                            syndrome
Calcium oxalate                             Acute and subacute arthritis
Cholesterol                                 Asymptomatic, chronic effusion
Lipid liquid                                Acute arthritis
Cryoglobulin                                Acute arthritis
Charcot-Leyden                              Acute arthritis, eosinophilic synovitis
Corticosteroid                              extrinsic crystal Post intra-articular injection
                                            synovitis
GOUT
Gout
• Gout is a type of inflammatory arthritis
  induced by the deposition of monosodium
  urate crystals in synovial fluid and other
  tissues.
• It is associated with hyperuricemia, which
  is defined as a serum urate level of 6.8
  mg per deciliter or more.
• In Population, 0.5% prevalence of gout
  overall
Risk Factor
• Hyperuricemia
   – thiazide diuretics, cyclosporine, and low-dose
     aspirin (<1 g per day)
• Triggers for recurrent flares include
   – recent diuretic use, alcohol intake,
     hospitalization, and surgery.
• Urate-lowering therapy
   – which reduces the risk of gout attacks in the
     long term, can trigger attacks in the early
     period after its initiation
Pathophysiology
Classification of Gout
      Clinical category                       Cause                        Metabolic defect
 Primary gout (90% of cases) Enzyme defects unknown (85%-90% - Overproduction of uric acid
                              of primary gout)                   - Normal excretion (majority)
                                                                 - Increased excretion (minority)
                                                                 - Normal production of uric acid
                                                                 - Under-excretion
                              Known enzyme defects, e.g. partial - Overproduction of uric acid
                              HGPRT deficiency
Secondary gout (10% of cases) Associated with increased nucleic - Over production of uric acid with
                              acid turnover, e.g. leukemia       increased urinary excretion
                              Chronic renal failure              - Reduced excretion of uric acid
                                                                 with normal production
                              Inborn errors of metabolism, e.g. - Overproduction of uric acid with
                              complete HGPRT deficiency (Lesh- increased urinary excretion
                              Nyhan syndrome)
Clinical Phase

Asymptomatic hyperuricemia


   Acute gouty arthritis


     Intercritical gout


 Chronic tophaceous gout
Chronic tophaceous gout




Adapted from BMJ Case Reports 2009 [doi:10.1136/bcr.03.2009.1668]
                 Copyright © 2009 by the BMJ Publishing Group Ltd
Diagnosis
              (Definite Dx)
• synovial fluid or tophus aspiration
  with identification of
      • light microscopy ; needle shape crystal
      • compensated polarized light microscopy
        ; positive birefringence with negative
        elongation
Diagnosis
                (Presumptive Dx)
• Medical Treatment with Colchicine improve within 12 - 24 hr
• Criteria Diagnosis from American college of Rheumatology (6 in
  12)
   – More than one attack of acute arthritis
   – Maximum inflammation developed within 1 day
   – Monoarthritis attack, redness observed over joints
   – First metatarsophalangeal joint painful or swollen
   – Unilateral first metatarsophalangeal joint attack
   – Unilateral tarsal joint attack
   – Tophus (confirmed or suspected)
   – Hyperuricaemia
   – Asymmetric swelling within a joint on x-ray film
   – Subcortical cyst without erosions on x-ray film
   – Joint culture negative for organism during attack.
Complication
• Acute uric acid nephropathy
   – most commonly in patients treated with
     cytotoxic agents, especially for
     lymphoproliferative disorders and large tumour
     burdens
• Chronic urate or gouty nephropathy
   – Accumulated in medullary interstitium induced
     inflammation process
• Uric acid stone
   – Uric acid calculi constitute 10% of the renal
     stones
Management
             Acute gout attack
• Aim of therapy for acute gout
   – rapid relief of pain and disability caused by
     intense inflammation.
• Drug used
   – nonsteroidal antiinflammatory drugs (NSAIDs),
     colchicine, glucocorticoids, and possibly
     corticotropin.
• Adjunctive treatment include
   – applying ice to and resting the affected joint.
• NSAIDs and colchicine are first-line agents
  for acute attacks
What if treatment fails
          in acute gout ?
• If there is no improvement in symptoms
  after 2–3 days:
   – Review the diagnosis, check compliance with
     medication, and encourage self-care
     strategies.
   – Increase the dose of medication to maximum
     and add paracetamol, with or without codeine.
• If there is still no improvement in symptoms,
  try an alternative drug or consider
  combining treatment, or seek specialist
  advice.
What follow up is recommended
    after an acute attack of gout?
• Follow up the person 4–6 weeks after an acute
  attack of gout has resolved, and:
   – Check the serum uric acid level.
   – Measure their blood pressure and take blood for
     fasting glucose, renal function, and lipid profile.
   – Identify underlying conditions such as hypertension,
     diabetes, or renal impairment, and assess the person's
     overall cardiovascular risk.
   – Assess and provide advice on risk factors such as
     obesity, diet, excessive alcohol consumption, and
     exercise.
   – Consider the need to start prophylactic medication if
     the person is having two or more attacks of gout in a
     year.
Management
Patient with Hyperuricemia
Management
      Patient with Hyperuricemia
• The purpose of lowering serum urate levels
   – To prevent acute flares and development of tophi
• When treatment
   – Severity and frequency of flares, the presence of
     coexisting illnesses (including nephrolithiasis), and
     patient preference are additional considerations
• Urate-lowering therapy
   – should not be initiated during acute attacks
   – started 2 to 4 weeks after flare resolution
• The dose should be adjusted as necessary
   – maintain a serum urate level below 6 mg per
     deciliter which is associated with a reduced risk of
     recurrent attacks and tophi.
Management
     Patient with Hyperuricemia
• How long for used Urate – lowering
  therapy
   – Suggest patient can keep uric acid level
     below 6.0 mg/dl and no attack at least 4-5
     years
   – In Chronic tophaceous stage should stop
     when tophaceous gout resolve and continue
     for 4-5 years after resolution
Management
     Patient with Hyperuricemia
• Flare Prophylaxis during Initiation
  of Urate-Lowering Therapy
   – general recommendation for flare
     prophylaxis is to use colchicine at a dose of
     0.6 mg once or twice daily, with dose
     adjustments as needed for renal impairment
   – Diarrhea was common, resulting in a once-
     daily regimen of colchicine for many
     patients
CALCIUM PYROPHOSPHATE DEPOSITION DISEASE
                                  (CPPD)
Calcium pyrophosphate deposition
         disease (CPPD)
• metabolic arthropathy caused by the
  deposition of calcium pyrophosphate
  dihydrate in and around joints,
   – especially in articular cartilage and
     fibrocartilage.
• Although CPDD is often asymptomatic, with
  only radiographic changes seen
   – (ie, chondrocalcinosis)
• various clinical manifestations may occur,
  including
   – acute (pseudogout) and chronic arthritis
Risk Factor
• Age is most important risk factor
• Osteoarthritis (OA) - threefold increased risk
  if CPPD present
• Previous joint trauma/injury
• Joint surgery/lavage promotes crystal
  shedding4
• Metabolic disease
   – Hemochromatosis, 1˚Hyperparathroidism,
     Hypomagnesemia, Malabsorption syndromes
   – Consider in age <50-60 yo, especially if
     polyarticular chondrocalcinosis (CC)
• Familial predisposition to CPPD
Clinical Presentation
• Associated with both acute and chronic arthritis
• Acute CPP crystal arthritis
    – inflammatory arthritis of one or more joints. Knees,
      wrists, shoulders, ankles, elbows, or hands can be
      affected.
• chronic form of CPP arthritis
    – mimics osteoarthritis or rheumatoid arthritis and is
      associated with variable degrees of inflammation.
• Typically occurs in older patients but can occur in
  younger patients with associated metabolic
  conditions, such as hyperparathyroidism and
  haemochromatosis.
Most common presentations
             of CPDD
Type A. Pseudogout
Type B. Pseudorheumatoid arthritis
Type C and D. Pseudoosteoarthritis
Type E. Lanthenic or asymptomatic
Type F. Pseudoneuropathic joint
Other :
• ankylosing spondylytis or diffuse idiopathic skeletal
  hyperostosis (DISH)
• pseudotophaceous disease
Diagnostic Criteria
         (Definite & Probable)
• I. Demonstration of CPP crystals in tissues
  or synovial fluid
   – IIA. Identification of CPP crystals by
     morphological analysis using compensated
     polarising light microscopy.
   – IIB. Typical calcifications on x-rays
     (cartilage calcification); heavy punctuate or
     linear calcifications in fibro-cartilage,
     articular (hyaline) cartilage, or joint
     capsules.
Chrondocalcinosis
Chrondocalcinosis
Diagnostic Criteria
                     (Possible)
• IIIA. Acute arthritis, especially of the knee or other large
  joints.
• IIIB. Chronic arthritis of the knee, hip, wrist, elbow, shoulder,
  or MCPs, particularly if accompanied by acute
  exacerbations, and if characterised by:
     – Involvement of uncommon sites for primary osteoarthritis
     – Radiographical appearance, including severe patellofemoral
       involvement
     – Subchondral cyst formation
     – Severe progressive joint degeneration with bony collapse
     – Variable and inconsistent osteophyte formation
     – Tendon calcifications, particularly of the Achilles, triceps, and
       obturator tendons
     – Axial skeletal involvement with subchondral cysts, disc
       calcification, and vacuum disc phenomena, as well as
       sacroiliac joint involvement.
Management
     (Acute attack)
Ice and Rest


Joint aspiration


Oral Non steroidal Anti-inflammatory Drugs


Colchicine


Intraarticular glucocorticosteroids (GCS)


IV/IM/PO corticosteroid
Management
          (Long term / Chronic)
• Prophylaxis against frequent recurrent acute
  attacks
   – Colchicine 0.6 mg twice daily
   – Low dose oral NSAIDs
• Chronic CPP crystal inflammatory arthritis
   – Correct metabolic disease
   – Oral NSAIDs with gastro-protective treatment
   – Colchicine 0.5-1.0 mg daily
   – Daily low dose corticosteroids
   – Magnesium –a cofactor for enzymes that break
     down pyrophosphate
   – MTX / Hydroxychloroquine
CASE STUDY
Case #1
• A 72-year-old woman presents with polyarticular
  joint pain.
• She has long-standing mild joint pain, but over the
  last 10 years notes increasing discomfort in her
  wrists, shoulders, knees, and ankles. She has had
  several recent episodes of severe pain in 1 or 2
  joints, with swelling and warmth of the affected
  areas. These episodes often last 3 to 4 weeks.
• Her examination shows severe bony changes
  consistent with osteoarthritis in many joints, and
  slight swelling, warmth, and tenderness without
  erythema in the second and third MCP joints, left
  shoulder, and the right wrist.
Case #2
• A 52-year-old woman presents with a 2-month
  history of bilateral hand and wrist pain, and
  swelling in her fingers.
• She has also recently noted similar pain in the
  balls of her feet. She finds it hard to get going in
  the morning and feels stiff for hours after waking
  up. She also complains of increasing fatigue and
  is unable to turn on and off taps or use a
  keyboard at work without a significant amount of
  pain in her hands.
• She denies any infections before or since her
  symptoms started.
Case #3
• A 54-year-old man complains of severe pain and
  swelling in his right first toe that developed
  overnight. He is limping because of the pain and
  states that this is the most severe pain he has
  ever had ('even covering my foot with the bed
  sheet hurts'). He has had no previous episodes.
  His only medication is hydrochlorothiazide for
  hypertension. He drinks 2 to 3 beers a day. On
  examination, he is obese. There is swelling,
  erythema, warmth, and tenderness of the right
  first toe. There is also tenderness and warmth
  with mild swelling over the mid foot.
REFERENCE
Reference
• American College of Rheumatoogy Ad Iloe Committee
  on Clinical Guidelines. Guidelines for the initial
  evaluation of the adult patient with musculoskeletal
  symptoms, /Irth,.itis Rheum 1996; 39: 1-8.
• Ellrodt AG. Cho M. Cush J el. af. An evidence-based
  medicine approach to the diagnosis and management
  of musculoskeletal complaints. lIm J Med 1997:
  103(45 ): 3-6.
• Ashok Kumar. ; Clinical Guide : Approach to Arthritis.
  Vol. 4 No.1, January-March 2002; p.51-54
• William P. Arend AND George V. Lawry; Chapter 264
  Approach to the Patient with Rheumatic Disease in
  Goldman’s Cecil medicine. Rev. ed. of: Cecil
  medicine. 23rd ed. c2008. p.1648-1651
Reference
• Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL,
  Loscalzo J: Chapter 321. Rheumatoid Arthritis in Harrison's
  Principles of Internal Medicine, 18th edition: McGraw-Hill
  Companies,2012.
• Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL,
  Loscalzo J: Chapter 331. Approach to Articular and
  Musculoskeletal Disorders in Harrison's Principles of Internal
  Medicine, 18th edition: McGraw-Hill Companies,2012.
• Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL,
  Loscalzo J: Chapter 333. Gout and Other Crystal-Associated
  Arthropathies in Harrison's Principles of Internal Medicine,
  18th edition: McGraw-Hill Companies,2012.
• Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK,
  Meckler GD: Chapter 281. Acute Disorders of the Joints and
  Bursae in Tintinalli's Emergency Medicine : A Comprehensive
  Study Guide, 7th Edition. McGraw-Hill. 2010
Reference
• Arnett FC, Edworthy SM, Block DA, et al. The ARA
  1987 revised criteria for the classification of
  rheumatoid arthritis. Arthritis Rheum 1988, 31: 315-
  24
• American College of Rheumatology Subcommittee on
  Rheumatoid Arthritis Guidelines. Guidelines for the
  management of rheumatoid arthritis 2002 update.
  Arthritis Rheum 2002;46:328-46
• Aletaha D, Neogi T, Silman AJ, et al. 2010
  Rheumatoid arthritis classification criteria: an
  American College of Rheumatology/European League
  Against Rheumatism collaborative initiative. Arthritis
  Rheum. 2010;62:2569-2581
• แนวทางเวชปฏิบัติโรคข้ออักเสบรูมาตอยด์ (rheumatoid
  arthritis) โดยสมาคมรูมาติสซั่มแห่งประเทศไทย. วารสาร
  โรคข้อและรูมาติสซั่ม, 2545;13:25-31
Reference
• Iain B. McInnes, F.R.C.P., Ph.D., and Georg Schett,
  M.D. The Pathogenesis of Rheumatoid Arthritis. N
  Engl J Med 2011; 365:2205-2219
• Tuhina Neogi, M.D., Ph.D. ;Clinical Practice : Gout. N
  Engl J Med 2011; 364:443-452February 3, 2011
• Emilio B. Gonzalez ; An update on the pathology and
  clinical management of gouty arthritis.Clin Rheumatol
  (2012) 31:13–21
• Newsome G. ;Guidelines for the management of
  rheumatoid arthritis: 2002 update.J Am Acad Nurse
  Pract. 2002 Oct;14(10):432-7.
• C. Ferrone, R. Andracco, M.A. Cimmino ; Calcium
  pyrophosphate deposition disease: clinical
  manifestations.Reumatismo, 2011; 63 (4): 246-252
Reference
• Iain B. McInnes, F.R.C.P., Ph.D., and Georg
  Schett, M.D. The Pathogenesis of
  Rheumatoid Arthritis. N Engl J Med 2011;
  365:2205-2219
• Tuhina Neogi, M.D., Ph.D. ;Clinical Practice :
  Gout. N Engl J Med 2011; 364:443-
  452February 3, 2011
• Emilio B. Gonzalez ; An update on the
  pathology and clinical management of gouty
  arthritis.Clin Rheumatol (2012) 31:13–21
• Choi HK, Mount DB, Reginato AM.
  Pathogenesis of gout. Ann Intern Med.
  2005;143:499-516.
Reference
• Zhang W, Doherty M, Bardin T, et al. European League
  Against Rheumatism recommendations for calcium
  pyrophosphate deposition. Part I: terminology and
  diagnosis. Ann Rheum Dis 2011; 70: 563-70.
• Zhang W, Doherty M, Pascual E, et al. EULAR
  recommendations for calcium pyrophosphate deposition.
  Part II: management. Ann Rheum Dis 2011; 70: 571-75.
• Rosenthal A, Ryan LM. Calcium pyrophosphate crystal
  deposition diseases, pseudogout, and articular
  chondrocalcinosis. In: Koopman WJ, Moreland LW, eds.
  Arthritis and allied conditions. 15th ed. Philadelphia, PA:
  Lippincott Williams & Wilkins; 2004:2373-2396.
• McCarty DJ. Crystal identification in human synovial
  fluids. Methods and interpretation. Rheum Dis Clin North
  Am 1988;14:253-67.
Thank you for your kind attention

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Topic review approach_arthritis

  • 1. Topic Review : How to Approach Arthritis Ext.สรวิศ / พ.อภิญญา 8 พฤษภาคม 2555
  • 2. What’s Heading in Topic Clinical Approach to patients with Arthritis ? Common Disease in Rheumatology • Rheumatoid Arthritis • Crystal induced arthritis (Gout and CPPD) Case study
  • 3. CLINICAL APPROACH TO PATIENT WITH ARTHRITIS ?
  • 4. Importance of History Duration of Complaints Number of Joints Involved Distribution of Joints Involved Pattern of Involvement Duration of Early Morning Stiffness
  • 5. Importance of History History of Joint Swelling Extra-articular Complaints Associated Medical Illness Significant Past History Family History of Rheumatic Disease
  • 6. Importance of Physical Examination Presence of Swelling of Joint Local Warmth Redness Range of Motion Any Deformity
  • 7. Diagnostic Approach to Musculoskeletal Pain
  • 8. Diagnostic Approach to Patient with Arthritis Arthritis Acute Chronic Mono / Mono / Polyarthritis Polyarthritis Oligoarthritis Oligoarthritis
  • 9. Differential Diagnosis Acute Acute Chronic Chronic Monoarthritis Polyarthritis Monoarthritis Polyarthritis Pyogenic Acute rheumatic fever Chronic infection (TB, Rheumatoid Gout Pyogenic (2-3 ข้อ) pyogenic, fungus) Gout Pseudogout esp. GC, salmonella Osteoarthritis Pseudogout Acute rheumatic fever SLE Gout Osteoarthritis Traumatic arthritis Serum sickness Pseudogout Psoraitic Reiter’s disease Reiter’s disease Avascular necrosis Ankylosing spodylitis Psoriasis Psoriatic arthritis Tumor SLE Rheumatoid arthritis Ankylosing spondylitis Neuropathic Other connective Hemophilic arthritis Viral tissue diseases Leukemia Hypertrophic Hemophilic osteoarthropathy Neuopathic
  • 10. Examination of Synovial Fluid Normal Noninflammatory Inflammatory Septic Clarity Transparent Transparent Cloudy Cloudy Color Clear Yellow Yellow Yellow WBC*/microliter <200 <200–2000 200–50,000 >25,000 PMNs (%)* <25 <25 >50 >90 Culture Negative Negative Negative >50% positive None Crystals None None Multiple or none Gout, pseudogout, Osteoarthritis, Nongonococcal or Associated spondyloarthropat - trauma, rheumatic gonococcal septic conditions hy, rheumatoid fever arthritis arthritis, SLE
  • 13. Rheumatoid Arthritis • The most common form, autoimmune inflammatory arthritis • Characterized by symmetric arthritis of the small joints of the hands and feet • Chronic erosive arthritis need early and aggressive management • Prevalence 0.5 – 1 %
  • 14. Pathogenesis • Characterized by – synovial inflammation and hyperplasia (“swelling”), – autoantibody production (rheumatoid factor and anti–citrullinated protein antibody [ACPA]), – cartilage and bone destruction (“deformity”), – systemic features, including • cardiovascular, pulmonary, psychological, and skeletal disorders.
  • 16. Criteria Diagnosis • At least 4 of these 7 criteria – criteria 1 to 4 must have been present for ≥6 weeks Morning stiffness Arthritis of 3 or more joint areas Arthritis of hands Symmetric arthritis Rheumatoid nodules Serum rheumatoid factor Radiographic changes Arnett FC, Edworthy SM, Bloch DA, et al. The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum. 1988;31:315-324.
  • 22. American College of Rheumatology (ACR)/European League Against Rheumatism (EULAR) collaborative initiative 2010 rheumatoid arthritis classification criteria Score Joint involvement 1 large joint (shoulder, elbow, hip, knee, ankle) 0 2–10 large joints 1 1–3 small joints (MCP, PIP, Thumb IP, MTP, wrists) 2 4–10 small joints 3 >10 joints (at least 1 small joint) 5 Serology Negative RF and negative ACPA 0 Low-positive RF or low-positive anti-CCP antibodies 2 (3 times ULN) High-positive RF or high-positive anti-CCP antibodies 3 (>3 times ULN) Acute-phase Normal CRP and normal ESR 0 reactants Abnormal CRP or abnormal ESR 1 Duration of <6 weeks 0 symptoms 6 weeks 1
  • 23. Extraarticular manifestations of rheumatoid arthritis
  • 25. Management For Primary care Physicians Establish Diagnosis of Rheumatoid Arthritis Early Document Baseline Disease Activity and Damage Estimate Prognosis Start Treatment Patient Education Start DMARD(s) within 3 months Consider NSAIDs Consider Local / Low-dose Steroid Physical / Occupational Therapy Periodically Assess Disease Activity
  • 26. Baseline Evaluation • Subjective – Degree of joint pain – Duration of morning stiffness – Duration of fatigue – Limitation of function • Physical examination – Actively inflamed joints (tender and swollen joint counts) – Mechanical joint problems: loss of motion, crepitus, instability, – malalignment, and/or deformity – Extraarticular manifestations
  • 27. Baseline Evaluation • Laboratory – Erythrocyte sedimentation rate/C-reactive protein level – Rheumatoid factor – Complete blood cell count – Electrolyte levels and Creatinine level – Hepatic enzyme levels (AST, ALT, and albumin) – Urinalysis – Synovial fluid analysis – Stool guaiac • Radiography – Radiographs of selected involved joints • Other – Functional status or quality of life assessments using standardized
  • 28. DMARDs Used for the Treatment of Rheumatoid Arthritis Other Common Drug Dosage Serious Toxicities Monitoring Side Effects Hydroxy 200–400 mg/d Irreversible retinal Nausea Funduscopic chloroquine orally damage Diarrhea and visual ( 6.5 mg/kg) Cardiotoxicity Headache field testing Blood dyscrasia Rash every 12 months Sulfasalazine Initial: Granulocytopenia Nausea CBC every 2–4 500 mg orally Hemolytic anemia Diarrhea weeks for first twice daily (with G6PD deficiency) Headache 3 months, then Maintenance: every 3 1–1.5 g twice daily months
  • 29. DMARDs Used for the Treatment of Rheumatoid Arthritis Other Common Drug Dosage Serious Toxicities Monitoring Side Effects Methotrexate 10–25 mg/week Hepatotoxicity Nausea CBC, orally Myelosuppression Diarrhea creatinine, or SQ Infection Stomatitis/mouth LFTs every 2– Folic acid : Interstitial pneumonitis ulcers 3 months 1 mg/d to reduce Pregnancy category X Alopecia toxicities Fatigue Leflunomide 10–20 mg/d Hepatotoxicity Alopecia CBC, Myelosuppression Diarrhea creatinine, Infection LFTs every 2– Pregnancy category X 3 months
  • 30. approximate time to benefit of disease- modifying antirheumatic drugs used in the treatment of rheumatoid arthritis
  • 33. CRYSTAL - INDUCED ARTHRITIS
  • 34. Type of Crystal Disease Monosodium urate (MSU) Gout, tophaceous gout Calcium pyrophosphate dihydrate (CPPD) Pseudogout, pyrophosphate arthropathy, calcium pyrophosphate dihydrate deposition disease, tophaceous pseudogout Basic calcium phosphate; calcium carbonate Acute periarthritis, acute arthritis, (CC), hydroxy apatite (HA), octacalcium destructive phosphate (OCP), tricalcium phosphate (TCP) arthropathy, Milwaukee shoulder/knee syndrome Calcium oxalate Acute and subacute arthritis Cholesterol Asymptomatic, chronic effusion Lipid liquid Acute arthritis Cryoglobulin Acute arthritis Charcot-Leyden Acute arthritis, eosinophilic synovitis Corticosteroid extrinsic crystal Post intra-articular injection synovitis
  • 35. GOUT
  • 36. Gout • Gout is a type of inflammatory arthritis induced by the deposition of monosodium urate crystals in synovial fluid and other tissues. • It is associated with hyperuricemia, which is defined as a serum urate level of 6.8 mg per deciliter or more. • In Population, 0.5% prevalence of gout overall
  • 37. Risk Factor • Hyperuricemia – thiazide diuretics, cyclosporine, and low-dose aspirin (<1 g per day) • Triggers for recurrent flares include – recent diuretic use, alcohol intake, hospitalization, and surgery. • Urate-lowering therapy – which reduces the risk of gout attacks in the long term, can trigger attacks in the early period after its initiation
  • 39. Classification of Gout Clinical category Cause Metabolic defect Primary gout (90% of cases) Enzyme defects unknown (85%-90% - Overproduction of uric acid of primary gout) - Normal excretion (majority) - Increased excretion (minority) - Normal production of uric acid - Under-excretion Known enzyme defects, e.g. partial - Overproduction of uric acid HGPRT deficiency Secondary gout (10% of cases) Associated with increased nucleic - Over production of uric acid with acid turnover, e.g. leukemia increased urinary excretion Chronic renal failure - Reduced excretion of uric acid with normal production Inborn errors of metabolism, e.g. - Overproduction of uric acid with complete HGPRT deficiency (Lesh- increased urinary excretion Nyhan syndrome)
  • 40. Clinical Phase Asymptomatic hyperuricemia Acute gouty arthritis Intercritical gout Chronic tophaceous gout
  • 41. Chronic tophaceous gout Adapted from BMJ Case Reports 2009 [doi:10.1136/bcr.03.2009.1668] Copyright © 2009 by the BMJ Publishing Group Ltd
  • 42. Diagnosis (Definite Dx) • synovial fluid or tophus aspiration with identification of • light microscopy ; needle shape crystal • compensated polarized light microscopy ; positive birefringence with negative elongation
  • 43.
  • 44. Diagnosis (Presumptive Dx) • Medical Treatment with Colchicine improve within 12 - 24 hr • Criteria Diagnosis from American college of Rheumatology (6 in 12) – More than one attack of acute arthritis – Maximum inflammation developed within 1 day – Monoarthritis attack, redness observed over joints – First metatarsophalangeal joint painful or swollen – Unilateral first metatarsophalangeal joint attack – Unilateral tarsal joint attack – Tophus (confirmed or suspected) – Hyperuricaemia – Asymmetric swelling within a joint on x-ray film – Subcortical cyst without erosions on x-ray film – Joint culture negative for organism during attack.
  • 45. Complication • Acute uric acid nephropathy – most commonly in patients treated with cytotoxic agents, especially for lymphoproliferative disorders and large tumour burdens • Chronic urate or gouty nephropathy – Accumulated in medullary interstitium induced inflammation process • Uric acid stone – Uric acid calculi constitute 10% of the renal stones
  • 46. Management Acute gout attack • Aim of therapy for acute gout – rapid relief of pain and disability caused by intense inflammation. • Drug used – nonsteroidal antiinflammatory drugs (NSAIDs), colchicine, glucocorticoids, and possibly corticotropin. • Adjunctive treatment include – applying ice to and resting the affected joint. • NSAIDs and colchicine are first-line agents for acute attacks
  • 47.
  • 48. What if treatment fails in acute gout ? • If there is no improvement in symptoms after 2–3 days: – Review the diagnosis, check compliance with medication, and encourage self-care strategies. – Increase the dose of medication to maximum and add paracetamol, with or without codeine. • If there is still no improvement in symptoms, try an alternative drug or consider combining treatment, or seek specialist advice.
  • 49. What follow up is recommended after an acute attack of gout? • Follow up the person 4–6 weeks after an acute attack of gout has resolved, and: – Check the serum uric acid level. – Measure their blood pressure and take blood for fasting glucose, renal function, and lipid profile. – Identify underlying conditions such as hypertension, diabetes, or renal impairment, and assess the person's overall cardiovascular risk. – Assess and provide advice on risk factors such as obesity, diet, excessive alcohol consumption, and exercise. – Consider the need to start prophylactic medication if the person is having two or more attacks of gout in a year.
  • 51. Management Patient with Hyperuricemia • The purpose of lowering serum urate levels – To prevent acute flares and development of tophi • When treatment – Severity and frequency of flares, the presence of coexisting illnesses (including nephrolithiasis), and patient preference are additional considerations • Urate-lowering therapy – should not be initiated during acute attacks – started 2 to 4 weeks after flare resolution • The dose should be adjusted as necessary – maintain a serum urate level below 6 mg per deciliter which is associated with a reduced risk of recurrent attacks and tophi.
  • 52. Management Patient with Hyperuricemia • How long for used Urate – lowering therapy – Suggest patient can keep uric acid level below 6.0 mg/dl and no attack at least 4-5 years – In Chronic tophaceous stage should stop when tophaceous gout resolve and continue for 4-5 years after resolution
  • 53. Management Patient with Hyperuricemia • Flare Prophylaxis during Initiation of Urate-Lowering Therapy – general recommendation for flare prophylaxis is to use colchicine at a dose of 0.6 mg once or twice daily, with dose adjustments as needed for renal impairment – Diarrhea was common, resulting in a once- daily regimen of colchicine for many patients
  • 55. Calcium pyrophosphate deposition disease (CPPD) • metabolic arthropathy caused by the deposition of calcium pyrophosphate dihydrate in and around joints, – especially in articular cartilage and fibrocartilage. • Although CPDD is often asymptomatic, with only radiographic changes seen – (ie, chondrocalcinosis) • various clinical manifestations may occur, including – acute (pseudogout) and chronic arthritis
  • 56. Risk Factor • Age is most important risk factor • Osteoarthritis (OA) - threefold increased risk if CPPD present • Previous joint trauma/injury • Joint surgery/lavage promotes crystal shedding4 • Metabolic disease – Hemochromatosis, 1˚Hyperparathroidism, Hypomagnesemia, Malabsorption syndromes – Consider in age <50-60 yo, especially if polyarticular chondrocalcinosis (CC) • Familial predisposition to CPPD
  • 57. Clinical Presentation • Associated with both acute and chronic arthritis • Acute CPP crystal arthritis – inflammatory arthritis of one or more joints. Knees, wrists, shoulders, ankles, elbows, or hands can be affected. • chronic form of CPP arthritis – mimics osteoarthritis or rheumatoid arthritis and is associated with variable degrees of inflammation. • Typically occurs in older patients but can occur in younger patients with associated metabolic conditions, such as hyperparathyroidism and haemochromatosis.
  • 58. Most common presentations of CPDD Type A. Pseudogout Type B. Pseudorheumatoid arthritis Type C and D. Pseudoosteoarthritis Type E. Lanthenic or asymptomatic Type F. Pseudoneuropathic joint Other : • ankylosing spondylytis or diffuse idiopathic skeletal hyperostosis (DISH) • pseudotophaceous disease
  • 59. Diagnostic Criteria (Definite & Probable) • I. Demonstration of CPP crystals in tissues or synovial fluid – IIA. Identification of CPP crystals by morphological analysis using compensated polarising light microscopy. – IIB. Typical calcifications on x-rays (cartilage calcification); heavy punctuate or linear calcifications in fibro-cartilage, articular (hyaline) cartilage, or joint capsules.
  • 62. Diagnostic Criteria (Possible) • IIIA. Acute arthritis, especially of the knee or other large joints. • IIIB. Chronic arthritis of the knee, hip, wrist, elbow, shoulder, or MCPs, particularly if accompanied by acute exacerbations, and if characterised by: – Involvement of uncommon sites for primary osteoarthritis – Radiographical appearance, including severe patellofemoral involvement – Subchondral cyst formation – Severe progressive joint degeneration with bony collapse – Variable and inconsistent osteophyte formation – Tendon calcifications, particularly of the Achilles, triceps, and obturator tendons – Axial skeletal involvement with subchondral cysts, disc calcification, and vacuum disc phenomena, as well as sacroiliac joint involvement.
  • 63. Management (Acute attack) Ice and Rest Joint aspiration Oral Non steroidal Anti-inflammatory Drugs Colchicine Intraarticular glucocorticosteroids (GCS) IV/IM/PO corticosteroid
  • 64. Management (Long term / Chronic) • Prophylaxis against frequent recurrent acute attacks – Colchicine 0.6 mg twice daily – Low dose oral NSAIDs • Chronic CPP crystal inflammatory arthritis – Correct metabolic disease – Oral NSAIDs with gastro-protective treatment – Colchicine 0.5-1.0 mg daily – Daily low dose corticosteroids – Magnesium –a cofactor for enzymes that break down pyrophosphate – MTX / Hydroxychloroquine
  • 66. Case #1 • A 72-year-old woman presents with polyarticular joint pain. • She has long-standing mild joint pain, but over the last 10 years notes increasing discomfort in her wrists, shoulders, knees, and ankles. She has had several recent episodes of severe pain in 1 or 2 joints, with swelling and warmth of the affected areas. These episodes often last 3 to 4 weeks. • Her examination shows severe bony changes consistent with osteoarthritis in many joints, and slight swelling, warmth, and tenderness without erythema in the second and third MCP joints, left shoulder, and the right wrist.
  • 67. Case #2 • A 52-year-old woman presents with a 2-month history of bilateral hand and wrist pain, and swelling in her fingers. • She has also recently noted similar pain in the balls of her feet. She finds it hard to get going in the morning and feels stiff for hours after waking up. She also complains of increasing fatigue and is unable to turn on and off taps or use a keyboard at work without a significant amount of pain in her hands. • She denies any infections before or since her symptoms started.
  • 68. Case #3 • A 54-year-old man complains of severe pain and swelling in his right first toe that developed overnight. He is limping because of the pain and states that this is the most severe pain he has ever had ('even covering my foot with the bed sheet hurts'). He has had no previous episodes. His only medication is hydrochlorothiazide for hypertension. He drinks 2 to 3 beers a day. On examination, he is obese. There is swelling, erythema, warmth, and tenderness of the right first toe. There is also tenderness and warmth with mild swelling over the mid foot.
  • 70. Reference • American College of Rheumatoogy Ad Iloe Committee on Clinical Guidelines. Guidelines for the initial evaluation of the adult patient with musculoskeletal symptoms, /Irth,.itis Rheum 1996; 39: 1-8. • Ellrodt AG. Cho M. Cush J el. af. An evidence-based medicine approach to the diagnosis and management of musculoskeletal complaints. lIm J Med 1997: 103(45 ): 3-6. • Ashok Kumar. ; Clinical Guide : Approach to Arthritis. Vol. 4 No.1, January-March 2002; p.51-54 • William P. Arend AND George V. Lawry; Chapter 264 Approach to the Patient with Rheumatic Disease in Goldman’s Cecil medicine. Rev. ed. of: Cecil medicine. 23rd ed. c2008. p.1648-1651
  • 71. Reference • Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Chapter 321. Rheumatoid Arthritis in Harrison's Principles of Internal Medicine, 18th edition: McGraw-Hill Companies,2012. • Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Chapter 331. Approach to Articular and Musculoskeletal Disorders in Harrison's Principles of Internal Medicine, 18th edition: McGraw-Hill Companies,2012. • Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J: Chapter 333. Gout and Other Crystal-Associated Arthropathies in Harrison's Principles of Internal Medicine, 18th edition: McGraw-Hill Companies,2012. • Tintinalli JE, Stapczynski JS, Ma OJ, Cline DM, Cydulka RK, Meckler GD: Chapter 281. Acute Disorders of the Joints and Bursae in Tintinalli's Emergency Medicine : A Comprehensive Study Guide, 7th Edition. McGraw-Hill. 2010
  • 72. Reference • Arnett FC, Edworthy SM, Block DA, et al. The ARA 1987 revised criteria for the classification of rheumatoid arthritis. Arthritis Rheum 1988, 31: 315- 24 • American College of Rheumatology Subcommittee on Rheumatoid Arthritis Guidelines. Guidelines for the management of rheumatoid arthritis 2002 update. Arthritis Rheum 2002;46:328-46 • Aletaha D, Neogi T, Silman AJ, et al. 2010 Rheumatoid arthritis classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Arthritis Rheum. 2010;62:2569-2581 • แนวทางเวชปฏิบัติโรคข้ออักเสบรูมาตอยด์ (rheumatoid arthritis) โดยสมาคมรูมาติสซั่มแห่งประเทศไทย. วารสาร โรคข้อและรูมาติสซั่ม, 2545;13:25-31
  • 73. Reference • Iain B. McInnes, F.R.C.P., Ph.D., and Georg Schett, M.D. The Pathogenesis of Rheumatoid Arthritis. N Engl J Med 2011; 365:2205-2219 • Tuhina Neogi, M.D., Ph.D. ;Clinical Practice : Gout. N Engl J Med 2011; 364:443-452February 3, 2011 • Emilio B. Gonzalez ; An update on the pathology and clinical management of gouty arthritis.Clin Rheumatol (2012) 31:13–21 • Newsome G. ;Guidelines for the management of rheumatoid arthritis: 2002 update.J Am Acad Nurse Pract. 2002 Oct;14(10):432-7. • C. Ferrone, R. Andracco, M.A. Cimmino ; Calcium pyrophosphate deposition disease: clinical manifestations.Reumatismo, 2011; 63 (4): 246-252
  • 74. Reference • Iain B. McInnes, F.R.C.P., Ph.D., and Georg Schett, M.D. The Pathogenesis of Rheumatoid Arthritis. N Engl J Med 2011; 365:2205-2219 • Tuhina Neogi, M.D., Ph.D. ;Clinical Practice : Gout. N Engl J Med 2011; 364:443- 452February 3, 2011 • Emilio B. Gonzalez ; An update on the pathology and clinical management of gouty arthritis.Clin Rheumatol (2012) 31:13–21 • Choi HK, Mount DB, Reginato AM. Pathogenesis of gout. Ann Intern Med. 2005;143:499-516.
  • 75. Reference • Zhang W, Doherty M, Bardin T, et al. European League Against Rheumatism recommendations for calcium pyrophosphate deposition. Part I: terminology and diagnosis. Ann Rheum Dis 2011; 70: 563-70. • Zhang W, Doherty M, Pascual E, et al. EULAR recommendations for calcium pyrophosphate deposition. Part II: management. Ann Rheum Dis 2011; 70: 571-75. • Rosenthal A, Ryan LM. Calcium pyrophosphate crystal deposition diseases, pseudogout, and articular chondrocalcinosis. In: Koopman WJ, Moreland LW, eds. Arthritis and allied conditions. 15th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004:2373-2396. • McCarty DJ. Crystal identification in human synovial fluids. Methods and interpretation. Rheum Dis Clin North Am 1988;14:253-67.
  • 76. Thank you for your kind attention