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Topic Review :How to Approach Arthritis
Ext.สรวิศ / พ.อภิญญา8 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 toPatient with Arthritis
Arthritis
Acute
Mono /
OligoarthritisPolyarthritis
Chronic
Mono /
OligoarthritisPolyarthritis
Differential Diagnosis
Acute Monoarthritis
Acute Polyarthritis
Chronic Monoarthritis
Chronic Polyarthritis
PyogenicGoutPseudogoutAcute rheumatic feverTraumatic arthritisReiter’s diseasePsoriasisRheumatoid arthritisHemophilic arthritis
Acute rheumatic feverPyogenic (2-3 ข้อ)
esp. GC, salmonellaSLESerum sicknessReiter’s diseasePsoriatic arthritis Ankylosing spondylitisViralLeukemiaHemophilic
Chronic infection (TB, pyogenic, fungus)
OsteoarthritisGoutPseudogoutAvascular necrosisTumorNeuropathic
RheumatoidGoutPseudogoutOsteoarthritisPsoraiticAnkylosing spodylitisSLEOther connective
tissue diseasesHypertrophic
osteoarthropathyNeuopathic
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
Crystals None None Multiple or noneNone
Associated conditions
-Osteoarthritis,
trauma, rheumatic fever
Gout, pseudogout, spondyloarthropat
hy, rheumatoid arthritis, SLE
Nongonococcal or gonococcal septic
arthritis
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
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.
Morning stiffness
Arthritis of 3 or more joint areas
Arthritis of hands
Symmetric arthritis
Rheumatoid nodules
Serum rheumatoid factor
Radiographic changes
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 criteriaScore
Joint involvement 1 large joint (shoulder, elbow, hip, knee, ankle) 02–10 large joints 11–3 small joints (MCP, PIP, Thumb IP, MTP, wrists) 24–10 small joints 3>10 joints (at least 1 small joint) 5
Serology Negative RF and negative ACPA 0Low-positive RF or low-positive anti-CCP antibodies(3 times ULN)
2
High-positive RF or high-positive anti-CCP antibodies(>3 times ULN)
3
Acute-phase reactants
Normal CRP and normal ESR 0Abnormal CRP or abnormal ESR 1
Duration of symptoms
<6 weeks 06 weeks 1
Extraarticular manifestations of rheumatoid arthritis
Management
ManagementFor 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
Drug Dosage Serious ToxicitiesOther Common
Side EffectsMonitoring
Hydroxy
chloroquine
200–400 mg/d
orally
( 6.5 mg/kg)
Irreversible retinal
damage
Cardiotoxicity
Blood dyscrasia
Nausea
Diarrhea
Headache
Rash
Funduscopic
and visual
field testing
every 12
months
Sulfasalazine Initial:
500 mg orally
twice daily
Maintenance:
1–1.5 g twice daily
Granulocytopenia
Hemolytic anemia
(with G6PD deficiency)
Nausea
Diarrhea
Headache
CBC every 2–4
weeks for first
3 months, then
every 3
months
DMARDs Used for the Treatment of Rheumatoid Arthritis
Drug Dosage Serious ToxicitiesOther Common
Side EffectsMonitoring
Methotrexate 10–25 mg/week
orally
or SQ
Folic acid :
1 mg/d to reduce
toxicities
Hepatotoxicity
Myelosuppression
Infection
Interstitial pneumonitis
Pregnancy category X
Nausea
Diarrhea
Stomatitis/mouth
ulcers
Alopecia
Fatigue
CBC,
creatinine,
LFTs every 2–
3 months
Leflunomide 10–20 mg/d Hepatotoxicity
Myelosuppression
Infection
Pregnancy category X
Alopecia
Diarrhea
CBC,
creatinine,
LFTs every 2–
3 months
approximate time to benefit of disease-modifying antirheumatic drugs used in the
treatment of rheumatoid arthritis
Physical Therapy
Managementby Rheumatologist
CRYSTAL - INDUCED ARTHRITIS
Type of Crystal DiseaseMonosodium urate (MSU) Gout, tophaceous gout
Calcium pyrophosphate dihydrate (CPPD) Pseudogout, pyrophosphate arthropathy,calcium pyrophosphate dihydrate depositiondisease, tophaceous pseudogout
Basic calcium phosphate; calcium carbonate(CC), hydroxy apatite (HA), octacalciumphosphate (OCP), tricalcium phosphate (TCP)
Acute periarthritis, acute arthritis, destructivearthropathy, Milwaukee shoulder/kneesyndrome
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%
of primary gout)
- Overproduction of uric acid
- Normal excretion (majority)
- Increased excretion (minority)
- Normal production of uric acid
- Under-excretion
Known enzyme defects, e.g. partial
HGPRT deficiency
- Overproduction of uric acid
Secondary gout (10% of cases) Associated with increased nucleic
acid turnover, e.g. leukemia
- Over production of uric acid with
increased urinary excretion
Chronic renal failure - Reduced excretion of uric acid
with normal production
Inborn errors of metabolism, e.g.
complete HGPRT deficiency (Lesh-
Nyhan syndrome)
- Overproduction of uric acid with
increased urinary excretion
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 tumourburdens
• Chronic urate or gouty nephropathy– Accumulated in medullary interstitium induced
inflammation process
• Uric acid stone– Uric acid calculi constitute 10% of the renal
stones
ManagementAcute 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.
ManagementPatient with Hyperuricemia
ManagementPatient 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.
ManagementPatient 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
ManagementPatient 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 polyarticularjoint 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.
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