Monoarticular Joint Disease.ppt

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  • 1. Acute Monoarticular Arthritis Rebecca L. Burns PGY3 September 15, 2008
  • 2. Or…
  • 3. Joints: Hot and Single
  • 4. Case: Mr. C
    • Mr. C is a 56 y.o. WM with PMH gout, DM, HTN who presented to the wade park ED with a 2 week history of increasing pain and swelling in his right elbow. The pt. denied any h/o trauma to the joint. Mr. C. reported 2 prior visits to the ED of an OSH where he was first given a 5 day prednisone burst for suspected gouty flare, and later a 7 day course of keflex for presumed cellulitis. His elbow continued to worsen to the point that he could no longer move the joint because of pain; he also noted a fever of 102 o . He returned to the ED where he was given IV vancomycin and admitted to a gen med service with the diagnosis of cellulitis.
  • 5. Mr. C (continued)
    • Upon arrival to the floor, the pt. remained febrile and examination of RUE revealed a diffusely swollen, erythematous R elbow with exquisite pain on palpation and active and passive ROM. Ortho was consulted for evaluation; arthrocentesis revealed 30 mls of cloudy, purulent fluid with >120,000 wbcs/mm3 and 90% PMNs; there were no crystals, culture later grew MSSA. Xrays revealed a large joint effusion and subtle erosions. He was taken to the OR the following morning and underwent extensive drainage and surgical debridement.
  • 6. Learning Objectives
    • Determine which patients require arthrocentesis, and when it is crucial to do so vs. proceeding with therapy without analysis of joint fluid
    • Know the key components of the initial evaluation of a patient with a single joint effusion, including history, physical exam, imaging, joint aspiration.
    • Be able to distinguish between intraarticular and periarticular joint disease
    • Demonstrate appropriate methods for aspirating joint and preparing synovial fluid for analysis
    • Obtain appropriate information / diagnosis from synovial fluid analysis
  • 7. Learning Objectives (cont.)
    • Distinguish b/n inflammatory and non-inflammatory causes of joint effusions
    • Provide differential diagnosis for both inflammatory/non inflammatory joint effusions
    • Describe key features of different types of joint effusions
      • Special emphasis on septic arthritis and crystal-induced arthropathies
  • 8. Evaluation of the Patient: The Rheumatologic History
    • Location of affected joint, other joints involved
    • Severity/nature of pain
    • Onset and chronology
      • Trauma?
      • Acute vs indolent
    • What aggravates/relieves pain
      • Associated with use vs. rest
      • Prior joint injections?
    • Waxing/waning? Constant? Progressively worsening?
      • OA: waxes and wanes in response to activity/joint use
      • Septic arthritis: worsens progressively until treated
  • 9. Evaluation of the Patient: The Rheumatologic History
    • Other characteristics of joint:
      • Hot/red/tender/swollen
      • Joint stiffness/duration
      • Limited ROM, joint instability, joint deformity
      • Functional losses associated with joint disease
    • Associated weakness/paresthesias/neurologic symptoms
  • 10. Evaluation of the Patient: The Rheumatologic History
    • Systemic/extra-articular features:
      • Constitutional symptoms (fatigue, weight loss, anorexia, fever) –malignancy or systemic inflammatory disease
      • Rash, diarrhea, urethritis, uveitis—reactive arthritis
      • Skin changes, photosensitivity, raynauds
      • Mouth/nasal/genital ulcers
      • Dryness of eyes/mouth/skin
  • 11. Evaluation of the Patient: The Rheumatologic History
    • Family history of rheumatic diseases
    • Sexual history
    • Social history (IVDA, travel, alcohol, smoking)
  • 12. Evaluation of the Patient: The Rheumatologic History
    • When to worry: (think infection!)
      • Acute/sudden onset
      • Progressively worsening in severity
      • New joint swelling/pain (no prior history of arthritis)
      • Established h/o arthritis (RA, OA)– acute flare of single joint, or joint inflammation out of proportion to other joints
      • Prior joint disease or surgery—infection until proven otherwise
      • Joint trauma
      • Hx of fever/chills, tick bites, risky sexual behaviors, IVDA, travel
  • 13. Evaluation of the Patient: Physical Exam
    • Distinguish articular (within joint) from periarticular disease (bursitis, tendinitis, cellulitis)
    • Articular: swelling/tenderness surrounding joint; warm, tense, swollen; limited ROM in all planes
    • Periarticular: Pain in one plane of movement; tenderness on one side of joint; pain with active ROM > passive ROM
  • 14. Physical Exam (cont.)
    • Extra-articular signs:
      • Oral/genital ulcers (behcet’s, reactive, SLE, sjogren’s)
      • Psoriatic rash
      • Erythema nodosum (sarcoid, IBD)
      • Heart murmur (bacterial endocarditis)
  • 15. Evaluation of the Patient: Labs
    • CBC/RFP/Coags
    • ESR/CRP
    • Blood cultures
    • Rheum labs: RF, ANA, specific serologies based on clinical suspicion
    • Uric acid
        • Increased does NOT mean gout
        • Normal level does not mean not gout
    • HIV
    • Lyme antibodies
  • 16. Evaluation of the Patient: Misc.
    • Imaging
      • Xray
      • MRI/CT
      • Arthroscopy
    • Malignancy workup
    • And of course….Arthrocentesis!!!
  • 17. Arthrocentesis: Indications
    • Any time there exists any uncertainty about the etiology of joint effusion
    • Any acute monoarticular arthritis should be considered infection until proven otherwise!
    • Patients with likely poor follow up (ED)
    • In patients with known h/o arthritis, any dramatically new or “different” presentation may be an indicator of superimposed infection and should be tapped.
  • 18. Arthrocentesis: Indications
    • Other indications:
      • Therapeutic procedure to drain large effusions or hemarthroses
      • To instill corticosteroids or local anesthetic
  • 19. Arthrocentesis: Contraindications
    • Cellulitis overlying site of needle entry
    • Suspected bacteremia (relative contraindication—if septic arthritis is suspected, should be tapped)
    • Other relative contraindications: coagulopathy/anticoagulant meds
      • Consider reversal agents or FFP/plts
      • H/o multiple repetitive injxns of same joint may lead to cartilaginous damage (this is controversial, see below)
  • 20. Arthrocentesis: Contraindications
    • Some studies in humans with RA show lack of long-term deleterious effects of repetitive injections
    • Roberts et al 1996:
    • Study of bilateral pairs of joints in pts with RA who received 4 or more kenalog injxns of knee in single year
      • Suppression of inflammation by intraarticular corticosteriods may slow cartilage degradation from RA
      • The injected joint lost cartilage at a rate equal to or lower than that of the contralateral joint (average 7.4 yr f/u)
  • 21. Arthrocentesis: Complications
    • Rare
    • Iatrogenic infection
    • Localized trauma/bleeding
    • Post-injection flare
      • Should begin within and last less than 48 hrs after procedure (Roberts et al. 1996)
    • Pain
    • Reaccumulation of fluid
  • 22. Arthrocentesis: Complications
    • Dry tap
    • Flushing reaction (Kenalog); occurs in up to 10% of patients
    • Leakage of joint fluid
  • 23. Arthrocentesis: Prep
    • Explain risks and benefits/informed consent
    • Need for u/s or other imaging modalities (hip)
    • Appropriate positioning
      • Knee: Extended (or flexed at 15 to 20 degrees)
      • Elbow: flexed to 90 degrees
      • Shoulder: Neutral position, or external rotation
    • Identify anatomical landmarks
    • Demarcate site of entry
  • 24. Arthrocentesis: Prep
    • Sterilize (iodine prep, chloraprep)
    • Anesthetize:25 gauge needle
      • Skin wheal
      • Deeper tissues in anticipated trajectory of arthrocentesis needle
      • Ethyl chloride spray
    • Arthrocentesis: 18-20 gauge needle; 22 gauge for smaller joints
  • 25. Arthrocentesis: Technique
    • Approach
      • Based on 2 principles: ease of access to joint capsule, and avoidance of neurovascular bundles
      • Knee: medial or lateral approach
      • Elbow: Just under lateral epicondyle
      • Shoulder
        • Anterior: inferolateral to coracoid
        • Posterior: under acromion
      • Use a hemostat to steady needle when switching syringes
  • 26. Source: Textbook of Rheumatology, 4 th ed, Kelley, WN, Harris, ED Jr, Ruddy, S, et al, WB Saunders, Phil. 1993. P.545
  • 27. Source: Textbook of Rheumatology, 4 th ed, Kelley, WN, Harris, ED Jr, Ruddy, S, et al, WB Saunders, Phil. 1993. P.545
  • 28. Source: UpToDate, courtesy Bruce C. Anderson, MD.
  • 29. Synovial Fluid: Analysis
      • Only need 1-2 ml (1 drop may be sufficient for crystals)
      • Gross appearance: clarity, color, viscosity
        • Clarity:
          • Increased opacity usually indicates large number of WBCs or RBCs (inflammatory effusions, hemarthroses)
          • May also be due to influx of acellular material, such as lipids (fat necrosis, fracture), cholesterol crystals (chylous effusions), monosodium urate crystals (gout)
        • Color:
          • Clear, colorless (normal)
          • Yellow/yellow-green: inflammatory or septic fluids
          • Bright red, rusty, chocolate brown: fresh or old blood
  • 30. Synovial Fluid: Analysis (cont.)
    • Viscosity:
      • Normal fluid produces long, string-like extension as it falls and is highly viscous
      • Release of proteolytic enzymes into inflamed synovial fluid causes decrease in viscosity
      • Frankly purulent (septic) effusions may also be viscous
  • 31. Synovial Fluid: Analysis (cont.)
      • Cell count/diff
      • Culture and Gram’s stain
        • Nongonococcal septic arthritis: sensitivity 50-75% for gram’s stain and 75-95% for culture
        • Gonococcal: <10% gram’s stain and 10-50% for culture (Thomsen et al. 2006)
      • Crystal analysis
  • 32. Synovial Fluid: Analysis (cont.)
    • Other tests:
      • Glucose, protein, LDH are often performed, but have little diagnostic utility
      • Specific stains/cultures for atypical infectious agents
      • Cytology for suspected malignant effusions
  • 33. Synovial Fluid: Analysis
    • Normal:
      • Highly viscous
      • Clear
      • Nearly acellular
      • Protein concentration = 1/3 that of plasma
      • Glucose concentration similar to that of plasma
  • 34. Synovial Fluid: Analysis
    • Cell Count/Diff:
      • Normal: <180 wbcs/mm3 (mostly monos)
      • Non-inflammatory: <2000 cells/mm3; <75% PMNs
      • Definitely inflammatory: >2000 cells/mm3, >75% PMNs
      • >100,000 cells/mm3 = SEPTIC
  • 35. Synovial Fluid: Analysis
    • Eosinophilia:
      • Parasitic infxn
      • Allergy
      • Neoplasm
      • Lyme disease
    • May also see phagocytosis of nuclear material, malignant cells, etc.
  • 36. Synovial Fluid: misc.
    • Fat droplets in fluid
      • Bone fracture involving marrow space
      • Pancreatic fat necrosis
  • 37. Synovial fluid: Crystal analysis
    • Crystal analysis:
      • Polarizing light microscopy to identify monosodium urate crystals (gout) or calcium pyrophosphate dihydrate (pseudogout)
      • Birefringence: describes optical property of crystals
      • Background appears dark; birefringent materials (MSU and CPPD crystals) appear brighter than background
  • 38. Synovial fluid: Crystal analysis
    • Sensitivity is high (Shmerling, RH. 1994)
      • 80-95% (gout)
      • 65-80% (pseudogout)
    • Presence of crystals does NOT exclude possibility of septic arthritis
  • 39. Synovial fluid: Crystal analysis
    • MSU crystals: Brightly birefringent, needle shaped
      • Yellow when aligned parallel to axis of analyzer
      • =negatively birefringent
    • CPPD crystals: weakly birefringent; rhomboidal or rectangular shaped
      • Blue when long axis is parallel to analyzer
      • =positively birefringent
  • 40. Source: UpToDate, Courtesy of Ralph SchumacherMD .
  • 41. Synovial fluid: Crystal analysis
    • Other types of crystals:
      • Cholesterol/lipid crystals
        • Cholesterol: notched polygonal plates
        • Lipids: Maltese cross
          • Suspect fracture
      • Hydroxyapatite
      • Calcium phosphate
      • Monoclonal proteins
  • 42. Source: UpToDate, Courtesy of Harvard Medical School.
  • 43. Inflammatory vs. Non-inflammatory causes of monoarthritis
    • Inflammatory:
      • Crystal-induced
        • Gout (monosodium urate)
        • Calcium pyrophosphate (pseudogout)
        • Calcium oxalate
        • Liquid lipid microspherules
  • 44. Inflammatory Causes of Monoarthritis
    • Infectious:
      • Bacterial
      • Fungal
      • Lyme/spirochetes
      • Mycobacterial
      • Viral (HIV, other)
  • 45. Inflammatory Causes of Monoarthritis
    • “ pseudoseptic arthritis”(Krey PR et al. 1979)
      • May cause leukocytosis >100,000/mm3
      • Sterile
      • Caused by reactions to intraarticular injxns, RA flares, leukemic infiltration, gout
  • 46. Inflammatory Causes of Monoarthritis
    • Monoarthritis associated with systemic disease:
      • Psoriatic
      • Reactive
      • RA
      • SLE
      • Ankylosing spondylitis
      • IBD
      • Systemic sclerosis
  • 47. Non-inflammatory causes of Monoarthritis
    • Fracture
    • Hemarthrosis
    • Internal derangement, including ligamentous or meniscal injuries
    • Malignancy
    • OA
    • Neuropathic arthropathy
  • 48. Non-inflammatory causes of Monoarthritis
    • Storage and deposition diseases:
      • Hemochromatosis
      • Wilson’s disease
      • Gaucher’s disease
      • Fabry’s disease
      • Farber’s Disease
      • Amyloid arthropathy
    • Mostly occur as a result of deposition of excess/abnormal molecule in cartilage and other joint tissues  erosion of cartilage, bony destruction, synovial inflammation
  • 49. Non-inflammatory causes of Monoarthritis
    • Osteonecrosis
    • Benign tumors
      • Osteochondroma
      • Synovial chondromatosis
      • Pigmented villonodular synovitis
    • Malignant joint tumors: either originate within joint, or penetrate/metastasize into it
  • 50.
    • Septic Arthritis
  • 51. Septic Arthritis
    • Can occur in:
      • Normal joint
      • Diseased joint
      • Prosthetic joint
    • Mortality up to 50% in non-gonococcal arthritis
  • 52. Source: Anwar et al.: Bilateral Hip Septic Arthritis. J.Orthopaedics 2007;4(2)e14.
  • 53. Septic Arthritis
    • Risk factors:
      • Any diseased/prosthetic joint
      • Age >80y.o.
      • DM
      • RA/chronic arthritis
      • Recent joint surgery
      • Skin infection
      • Immunocompromised state
      • Chronic illnesses: liver cirrosis, CRF, malignancy, HIV, transplanted organs
  • 54. Septic Arthritis: Etiology
    • Usually from bacteremic seeding of joint from extra-articular source
      • Staph aureus (cellulitis)
      • E. coli (pyelonephritis)
    • Orthopedic surgical procedures or trauma
    • Direct inoculation of pathogen into joint
      • Pasteurella multocida (animal bite)
      • Pseudomonas (nail puncture thru shoe)
      • Sporotrichosis (thorn)
  • 55. Septic Arthritis: Etiology
    • Rare causes:
      • Infxn resulting from arthrocentesis/joint injection that introduces bacteria from skin
        • Estimated to occur at rate of 0.0002% (Esterhai JL. 1991)
      • Injection of contaminated solution
  • 56. Septic Arthritis: Etiology
    • Bacteria
    • Mycobacteria
    • Fungi
    • Viral
    • Parasitic
  • 57. Septic Arthritis: Diagnosis
    • Synovial fluid: purulent, wbc counts ranging from few thousand to >150,000 cells/mm3, >90% PMNs
    • Margaretten et al, 2007:
      • Likelihood of septic arthritis increases with observed synovial fluid WBC count
      • As the synovial leukocyte count increased from 25,000  50,000  100,000/mm3, the +LR increased from 2.9  7.7  28 respectively
  • 58. Septic Arthritis: Diagnosis
      • Likelihood of septic arthritis was reduced in setting of synovial leukocyte count <25,000
        • However, low counts may be observed in IC pts with septic arthritis, and in infections 2/2 mycobacterial, Neisserial, gram + organisms
  • 59. Septic Arthritis: Diagnosis
    • Gram’s stain: + in 60-80%
    • Glucose, protein levels in fluid not sensitive or specific
    • Bacterial cultures should always be sent
    • If slow-growing organism, PCR to detect DNA (Neisseria, mycoplasma)
  • 60. Septic Arthritis: Diagnosis
    • When should cultures be sent for unusual organisms?
      • H/o tuberculosis exposure
      • H/o trauma or animal bite
      • Travel to/living in area endemic with fungal infxns or Lyme disease
      • Immunosuppressed
      • Monoarthritis refractory to conventional therapy
  • 61.  
  • 62. Septic Arthritis: Treatment
    • Appropriate antibiotics
      • Broad  narrow spectrum
      • Depends on results of gram stain
      • Ceftriaxone if suspect gonococcus
    • Immobilization of joint
    • Analgesia
    • Ortho consult
      • Surgical drainage and irrigation
      • Removal of infected synovium
      • Debridement of bone
  • 63. Nongonococcal Bacterial Arthritis
    • Most common non-gonococcal culprits: staphylococci, streptococci, gram negative bacteria
      • S. epidermidis: prosthetic joint infections
    • 80% gram positive aerobes
      • Staph aureus accounts for 60%
    • 18% Gram negative bacteria
      • IVDA and IC patients
    • Spirochetes
      • Lyme
      • Treponema pallidum
  • 64. Nongonococcal Bacterial Arthritis
    • 80-90% are monoarticular
    • Usually result from hematogenous spread; may also result from direct extension from overlying cellulitis or other soft tissue infection, or from adjacent osteomyelitis
  • 65. Gonococcal Arthritis
    • Typical presentation: fever, chills, skin lesions, polyarthralgia which evolves into persistent mono- or oligoarthritis
    • Sexually active adults
    • Gonococcal arthritis: only ~25% have + culture
      • Culture and gram stain of blood/skin lesions/ulcers/cervix/urethral swabs/urine if infectious arthritis is suspected
  • 66. Gonococcal Arthritis
    • Organism often cannot be cultured on routine culture media
      • Increased yield with Thayer-Martin medium or chocolate agar plates
      • PCR to detect gonococcal DNA in synovial fluid
  • 67. Lyme Disease
    • Caused by tick-borne spirochete Borrelia burgdorferi
    • 15,000 cases reported each year
      • Most common vector-borne disease in U.S.
      • Primarily in NE (Maine  Maryland), Midwest, West to northern California and Oregon
    • Early localized disease: erythema migrans, fever, fatigue, LAD, HSM, myalgias, arthralgias
    • Early disseminated disease: cardiac and neuro manifestations
  • 68. Lyme Disease (cont.)
    • Lyme arthritis:
      • usually occurs in Late phase of disease
      • 60% of untreated pts will develop joint sx’s
      • Months to years after initial infection
      • Usually monoarticular—knee
      • Causes erosion of cartilage and bone
      • Chronic arthritis usually lasts 5-8 years
  • 69. Lyme Arthritis
    • Pts usually strongly seropositive by the time arthritis develops
    • Diagnosis:
      • Suggested by history/PE findings: tick bite, characteristic rash
      • Organism usually cannot be cultured from synovial fluid
      • Synovial tissue biopsy shows synovial hypertrophy, vascular proliferation, marked infiltration of mononuclear cells
      • Serologic testing: ELISA/western blot for detection of B. burgdorferi DNA
  • 70. Lyme Arthritis
    • Treatment:
      • Antibiotics early in disease usually prevents progression to arthritis
      • Early localized or disseminated phases: doxycycline 14-21 days
      • Oral doxy (30-60 days) or IV ceftriaxone (14-28 days) usually effective for treatment of Lyme arthritis (Steere, AC 2001)
  • 71. Mycobacterial Arthritis
    • Usually in IC patients or immigrants from endemic countries
    • Also associated with repetitive joint injxns with corticosteroids
    • Consider in pt. with persistent culture-negative oligo- or monoarthritis
    • H/o exposure to TB or positive ppd
  • 72. Copyright ©Radiological Society of North America, 2000 Engin, G. et al. Radiographics 2000;20:471-488 Figure 4b. Tuberculous osteomyelitis in a 52-year-old woman with pain
  • 73. Mycobacterial Arthritis
    • Bone infxn occurs from hematogenous seeding (primary or latent TB)
      • Osteoarticular involvement occurs in 1-5% of TB pts
    • Classic presentation is Pott’s disease, but may occur in peripheral joints
      • Mainly in hips and knees
    • Acutely may be associated with podagra
      • Difficult to distinguish from crystal-induced arthropathies
    • Involve the synovium
  • 74. Mycobacterial Arthritis
    • Ziehl-nelsen stain of synovial fluid to detect acid-fast bacilli often negative
    • Cultures may take 6-8 weeks to become +
    • Often need histologic exam from synovial membrane biopsy
      • Caseating or noncaseating granulomas
  • 75. Mycobacterial Arthritis
    • Characteristic xray findings: juxta-articular osteoporosis, erosions, joint space narrowing, soft-tissue swelling, subchondral cysts, periostitis, calcifications
    • Atypical mycobacterial causes:
      • M. bovis
      • M. marinum
      • M. kansasii
      • M. avium complex
  • 76. Copyright ©Radiological Society of North America, 2007 Burrill, J. et al. Radiographics 2007;27:1255-1273 Figure 24. Chronic tuberculous arthritis
  • 77. Copyright ©Radiological Society of North America, 2007 Burrill, J. et al. Radiographics 2007;27:1255-1273 Figure 22. Ankylosis secondary to tuberculous arthritis
  • 78. Copyright ©Radiological Society of North America, 2007 Burrill, J. et al. Radiographics 2007;27:1255-1273 Figure 20. Tuberculous dactylitis
  • 79. Fungal Arthritis
    • Insidious onset, indolent course
    • Generally mild inflammation
    • Pattern similar to TB arthritis
    • Causative agents:
      • Blastomycosis
      • Candida
      • Coccidiomycosis
      • Sporotrichosis
      • Cryptococcosis
      • Histoplasmosis
  • 80. Fungal Arthritis
    • Clues to diagnosis: trauma with possible sporotrichosis inoculation, recent surgical procedure, prosthetic joint, travel to specific regions in U.S. or endemic countries, immune deficiency (predisposes to candidal arthritis in particular)
    • Cause only 1% of infected prosthetic joints
    • Diagnosis is made by culture of synovial fluid or tissue biopsy
  • 81. Fungal Arthritis
    • Candida Arthritis:
      • Most common fungal arthritis
      • Arthritis arises from direct inoculation or hematogenous dissemination
      • Clinical course may be acute with marked synovitis, or indolent/milder
      • Monoarticular in 75% of cases—usually knee
      • Associated with IVDA, IC state, ICU patients, hospitalized infants, prosthetic/post-op joints, injected joints
  • 82. Candida Arthritis (cont.)
    • Infection related to joint injxn or surgery:
      • Chronic, monoarticular, indolent course
      • Often caused by species other than C. albicans
      • Symptoms may not develop until 2 yrs after surgery
    • Infxn from hematogenous spread:
      • Occurs with disseminated candidiasis
      • Clinical course acute, marked synovitis vs. indolent/mild
      • Monoarticular
  • 83. Fungal Arthritis
    • Coccidioidomycosis:
      • SW U.S., Central and South America
      • “ Valley fever”: arthritis, erythema nodosum/multiforme
      • Usually knee is involved
      • Pathology: villous hypertrophy, pannus formation, bony erosions
      • Rice bodies
  • 84. Source: LearningRadiology.com
  • 85. Parasitic Arthritis
    • Giardia lamblia
      • Acute onset, mild, recurrent arthritis
    • Entamoeba histolytica
    • Trichomona vaginalis
    • Toxoplasma gondii
    • Helminths (Strongyloides, beef tapeworm, schistosomiasis, filariasis)
  • 86. Viral Arthritis
    • Acute monoarthritis associated with:
      • Herpes simplex
      • Coxsackie B
      • HIV
      • Parvovirus B19
      • Hepatitis B
      • Rubella
  • 87. Case #2
    • A 70 y.o. WM with h/o HTN, PUD, CRI, and DM presents with an acutely swollen and painful L knee. Vital signs and PE are unremarkable. The knee has an obvious effusion and is warm, swollen, and red. Arthrocentesis reveals a WBC count of 20K/mm3, and a negative Gram stain.
    • What is your DDx?
    • What is the next step in diagnosis?
    • How do you want to treat it?
  • 88. Crystal-Induced Arthropathies
  • 89. Gout: epidemiology
    • Occurs predominantly in adult men; peak incidence in 5 th decade
    • Male: female ratio 7:1 to 9:1 (Terkeltaub, RA 2003)
  • 90. Gout: risk factors
    • Risk factors (other than uric acid):
      • HTN
      • Thiazide and loop diuretics
      • Obesity
      • High alcohol intake
        • Promotes hyperuricemia by increasing urate production and decreasing excretion
        • High purine content in etoh is another factor
      • Diet: meat, seafood
      • Gender, Age
  • 91. Gout: Risk factors
      • Post-menopausal women (diuretic-treated HTN, renal insufficiency)
      • Organ transplant recipients treated with cyclosporine
      • Hereditary disorders of purine metabolism
  • 92. Gout: Pathogenesis
    • Uric acid
      • End product of purine nucleotide catabolism
      • Lack of expression of enzyme uricase in humans leads to inability to degrade it
      • Normal uric acid levels in humans (6-7 mg/dL) approach limits of urate solubility
    • Results from overproduction or underexcretion of uric acid, or both
    • Urate crystal deposition as a monosodium salt in oversaturated joint tissues
  • 93. Gout: Pathogenesis
    • Urate crystals stimulate release of numerous inflammatory mediators
    • Induce phagocytes and synovial cells to generate and release mediators of inflammation and joint destruction
    • Neutrophil influx
    • COX, lysosomal proteases, TNF-a, IL-1, -6, -8 are involved
    • Systemic release of these mediators of inflammation cause systemic manifestations of gout (fever, leukocystosis, etc)
  • 94. Gout: clinical presentation
    • Classic symptoms: recurrent acute attacks painful mono- or oligoarticular inflammation
      • 1 st MTP involved in >50% of the time
      • Other commonly affected joints: midfoot, ankle, knees, wrists, elbow
    • Polyarthritis and chronic arthritis may also occur
  • 95. Gout: clinical presentation
    • Extra-articular manifestations:
      • Systemic manifestations (fever, leukocytosis, malaise)
      • Accumulation of articular, osseous, soft tissue, and cartilaginous crystalline deposits (tophi)
      • May be associated uric acid calculi in urinary tract (interstitial nephropathy)
  • 96. Gout: Diagnosis
    • Definitive diagnosis requires direct identification of urate crystals in joint
    • Serum urate levels are often normal during attacks of acute gout
    • Radiographic features:
      • Unremarkable initially
      • Acutely, may be soft tissue swelling around joint
      • Bone and joint abnormalities develop after years of urate crystal deposition—produce bony erosions, “overhanging edge”
  • 97. Source: LearningRadiology.com. 2006. Gout.
  • 98. Source: LearningRadiology.com. 2006. Gout.
  • 99. Gout: Pathology
    • Tophus: foreign-body granuloma surrounding a core of MSU crystals; surrounded by fibrous capsule
    • Inflammatory rxn consists of PMNs and giant cells
    • Erosion of cartilage and cortical bone occurs at sites of tophi
    • SubQ tophi occur most commonly in fingers, wrists, ears, knees, olecranon bursa, pressue points (ulnar aspect of forearm, achilles tendon)
  • 100. Source: Llauger, MD et al., 2000: Nonseptic Monoarthritis: Imaging Features with Clinical and Histopathologic Correlation .
  • 101. Gout: Pathology
    • Source: Eullaran, MD. et al. 2008. Images in Rheumatology.
  • 102. Source: Llauger, MD et al., 2000: Nonseptic Monoarthritis: Imaging Features with Clinical and Histopathologic Correlation .
  • 103. Gout: Treatment
    • Goals:
      • Treat acute inflammation and urolithiasis
      • Lower urate levels/prevent recurrent attacks
    • Treatment of Acute flares:
      • First-line: NSAIDs (ibuprofen, naproxen, indomethacin)
        • Can use selective COX-2 inhibitors in pts with GI problems
      • Intrarticular or subQ steroid injection
      • Prednisone taper
      • Colchicine
  • 104. Gout: Treatment
    • Colchicine:
      • Acute gout flares
      • Effective pain relief usually within 48 hrs
      • Disrupts chemotaxis/phagocytosis of cells involved in inflammatory pathway
      • Can be administed orally in hourly doses of 0.5-0.6mg up to 3 doses until pain/inflammation are alleviated
        • Give pts supply so they can self treat at first signs of flare
  • 105. Gout: Treatment
    • May also be used chronically as prophylaxis against future attacks, or until uric-acid lowering agent (allopurinol) can be initiated—should not be used for >6 months
    • IV colchicine rarely used (BM suppression, RF, DIC, seizures, death)
  • 106. Gout: Treatment
    • Uric acid lowering therapy:
      • Indications for long-term use: large tophi, frequent attacks (3 or more yearly), documented state of uric acid overproduction
      • Don’t initiate during acute flare—can worsen arthritis by destabilizing micro-tophi, causing them to break apart into synovial fluid and thereby precipitating attack
  • 107. Uric Acid Lowering Therapy
    • Allopurinol:
      • Xanthine oxidase inhibitor—inhibits uric acid synthesis
      • Minor rxns: hypersensitivity, pruritus, dermatitis
      • Serious rxns: rare,but can be life-threatening
    • Uricosuric agents (probenicid, sulfinpyrazone, etc)
  • 108. Pseudogout
    • CPPD crystals deposit in synovial lining, ligaments, tendons, periarticular soft tissue
    • Phagocytosis of crystals by neutrophils  release of proteases, PGs, cytokines  inflammatory rxn  degradation of cartilage
    • Acute monoarthritis clinically indistinguishable from gout
    • Can be hereditary, idiopathic, or associated with metabolic disease or trauma
  • 109. Pseudogout
    • Most commonly affects: wrist, knee
      • Less common: 1 st MTP
    • Radiologic features: chondrocalcinosis
      • Crystal deposition in articular cartilage, ligaments, tendons, fibrocartilaginous structures (menisci, intervertebral discs, etc.)
      • Appear as radiodensities on xray
  • 110. Llauger, MD et al., 2000: Nonseptic Monoarthritis: Imaging Features with Clinical and Histopathologic Correlation.
  • 111. Source: UpToDate, Courtesy of Ralph SchumacherMD .
  • 112. Pseudogout
    • Treatment: NSAIDs, colchicine, joint aspiration and injection of steroids
  • 113. Board Questions:
    • In a patient with acute bacterial arthritis, all of the following are portals of entry for bacteria into the joint except :
    • Direct inoculation during surgery
    • Lymphangitic spread
    • Inoculation from bloodstream
    • Contiguous infxn from bone or soft tissue
    • Traumatic injury
  • 114. Board Questions
    • Answer:
    • B. Lymphangitic spread
    • (There is no direct mechanism for lymphatic drainage to enter the joint space)
  • 115. Board Questions
    • You are working in urgent care. A female patient presents to you with complaints of L knee pain. Temp is 38.3, and her L knee is swollen with warmth and overlying erythema. Which of the following associated medical conditions puts this pt. at highest risk of developing nongonococcal bacterial arthritis?
    • HTN
    • ESRD
    • Diabetes
    • Rheumatoid arthritis
    • Osteoarthritis
  • 116. Board Questions
    • Answer:
    • D. Rheumatoid Arthritis
    • Pts. with RA have the highest incidence of infective arthritis (most commonly staph aureus), because of chronically inflamed joints, chronic steroid use, and breakdown of skin overlying joint deformities. The DMARDs such as etanercept and infliximab also predispose to mycobacterial infectious arthritis.
  • 117. References
    • Klippel, JH. Et al. Primer on the Rheumatic Diseases. Edition 12. Copyright 2001 by Arthritis Foundation. Atlanta, Georgia.
    • Roberts, WN, Babcock, EA, Breitbach, SA, et al. Corticosteroid injection in rheumatoid arthritis does not increase rate of total joint arthroplasty. J Rheumatol 1996; 23:1001.
    • Textbook of Rheumatology, 4 th ed, Kelley, WN, Harris, ED Jr, Ruddy, S, et al, WB Saunders, Phil. 1993. P.545
    • Thomsen, TW. Et al. Arthrocentesis of the Knee. NEJM 2006; 354:19.
    • Schmerling, RH. Synovial analysis. A critical reappraisal. Rheum Dis Clin North Am 1994; 20:503.
    • Krey, PR, Bailen, DA. Synovial fluid leukocytosis. A study of extremes. Am J Med 1979; 67:436.
  • 118. References
    • Anwar et al.: Bilateral Hip Septic Arthritis. J.Orthopaedics 2007;4(2)e14
    • Esterhai JL Jr, Gelb I. Adult septic arthritis. Orthop Clin North Am 1991; 22:503-514.
    • Margaretten, ME, Kohlwes, J, et al. Does this adult patient have septic arthritis? JAMA 2007; 297:1478.
    • Steere, AC. Lyme Disease. NEJM 2001; 345, no. 2:115.
    • Terkeltaub, RA. Gout. NEJM 2003; 349;17.
    • Llauger, MD et al., 2000: Nonseptic Monoarthritis: Imaging Features with Clinical and Histopathologic Correlation.
    • McDonnell SM, Preston BL, et al. A survey of 2,851 patients with hemochromatosis: symptoms and response to treatment. Am J Med 1999;106:619-624.
    • UptoDate.com
    • LearningRadiology.com
  • 119. Questions???