Topic review approach_arthritis

Topic Review :How to Approach Arthritis

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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

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• 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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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

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• แนวทางเวชปฏิบัติโรคข้ออักเสบรูมาตอยด์ (rheumatoid arthritis) โดยสมาคมรูมาติสซ่ัมแห่งประเทศไทย. วารสารโรคข้อและรูมาติสซั่ม, 2545;13:25-31

Reference

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Reference

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• Emilio B. Gonzalez ; An update on the pathology and clinical management of gouty arthritis.Clin Rheumatol (2012) 31:13–21

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Reference

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