Board tutorial for ASCE 2018 rheumatologyreviews.berlinpharm.com/20180505/Board_tutorial... · Board tutorial for ASCE 2018 Rheumatology (gout, OA, RA) Asst. Prof. Boonjing Siripaitoon,

Board tutorial for ASCE 2018 Rheumatology (gout, OA, RA)

Asst. Prof. Boonjing Siripaitoon, MD. MSc.

Division of Rheumatology

Prince of Songkla UniversityContact: [email protected]

Please download handout for your reference!

12 stations, 10-15 minutes each

Type of questions

1. OPD setting (management of common complaints, preoperative, consultation)-5 stations

2. Emergency management, including ACLS -2 stations

3. Rational use of investigations and drugs-2 stations

4. Communication and counseling-2 stations

5. CPD and quality improvement of patient care-1 station

(not more than 2 stations in each specialty)

Domains of competencies

A. Physical examination and identifying physical signsB. Clinical communication including history taking relevant to patient’s

complaint, patient and family education, counseling, breaking bad news, written communication and certification, referral process

C. problem identification and DDxD. Interpretation of clinical data including laboratory and radiographic

investigationsE. Clinical reasoning and judgement for management planF. Humanistic qualities/professionalism- manner, managing patient’s

concern and welfare, cost-conscious careG. 21st century skill: information technology, evidence-based medicine and

continuous professional development

OPD setting (management of common complaints that can be done within 15 min)

• Gout and Hyperuricemia

• RA

• SLE

• OA

• Osteoporosis

• back pain

Rational use of drugs

• NSAID, GI risk, CVS risk

• Gout-ULT, colchicine, HLA-B 5801

• OP drugs- bisphosphonate, cacium, vit D2

• OA drugs

Communication and counseling

• Gout & hyperuricemia

• OA

• OP

• SLE

Emergency management

• Acute monoarthritis (septic a, gout, pseudogout)

• Arthrocentesis: knee (mannequin), ankle

• SF analysis

GOUT

GOUT

• OPD setting (management of common complaints, consultation)

• Rational use of investigations and drugs

• Communication and counseling

• Emergency management

ตวัอย่างสถานการณ์ชาย 50 ปี ความดนัโลหติสงู โรคไตเสือ่มระยะ 3 มขีอ้เทา้ปวดบวมเป็นพกัๆ มาหลายปี ซือ้ยาแกป้วดกนิเวลามอีาการขอ้อกัเสบ วนัน้ีไมป่วดขอ้

ค าสัง่ประเมนิอาการขอ้ ใหก้ารวนิิจฉยัโรค ใหค้ าแนะน าและสัง่การรกัษา

ลกัษณะสถานี OPD setting (โต๊ะ เกา้อี ้เตยีงตรวจ)ผูป่้วย tophaceous goutอปุกรณ์1. ชุดเครือ่งมอืตรวจมาตรฐาน2. ผลเลอืด และ film x ray

Tested Domain

• Physical examination (15)

• Clinical communication• history taking (20)

• Advice non-pharmacological treatment (20)

• Problem identification and DDx (15)

• Management plan (25)

• Professionalism- manner, management of patient’s concern(10)

Gout

• Diagnosis

• Management

• Education

Diagnosis of Gout

Diagnosis: Clinical - acute gout flare

• symptoms : pain, swelling, heat, redness, and difficulty moving the affected joint.

• severe pain usually peaks within 24 h

•The most common site of involvement is the first metatarsophalangeal joint, other sites in the foot and ankle are also commonly affected

•Triggers for flares include acute medical or surgical illness, dehydration, or dietary factors such as alcohol intake and purine-rich foods

Diagnosis: Clinical – chronic gout

Tophaceous Gout

Diagnosis: The gold standard

• Aspirate joint/tophi

• MSU crystal

sometimes >50 000 cells per mm3

Serum urate testing

• is useful to assist with clinical diagnosis of gout in symptomatic individuals

• But hyperuricaemia alone is NOT sufficient for diagnosis (most people with hyperuricaemiado not have gout.)

• Importantly, serum urate concentrations can fall into the normal range during an acute flare (40%, ACTH –uricosuric effect), and if gout diagnosis is uncertain, serum urate should be retested after the flare has resolved.

Imagings

•Plain film: insensitive

(tophi, punch-out with overhanging edge in chronic tophaceous gout)

Two Key Ultrasound Features

Ultrasound – tophusSensitivity: 0.65Specificity: 0.80

Ultrasound – double contour signSensitivity: 0.80Specificity: 0.76

hyperechoic enhancement overthe surface of the hyaline cartilage

hyperechoic inhomogeneousmaterial surrounded by a small anechoic rim

snowstorm signof crystals within synovial fl uid

Dual energy CT –Advanced imaging

• a method of CT imaging that, by analysing the difference in attenuation in a material exposed to two different x-ray spectrums, can identify and colour-code urate deposits in patients with gout

Tophi in green color

Comparison with Existing CriteriaCriteria AUC Sensitivity Specificity

2015 ACR/EULAR Criteria 0.95 0.92 0.89Clinical only (no synovial fluid or imaging information) 0.89 0.85 0.78

ARA 1977 (full) 0.83 1.00* 0.51ARA 1977 (survey) 0.83 0.84 0.62Rome 0.95 0.97 0.78Rome (clinical) NA 0.77 0.78New York 0.83 1.00* 0.79New York (clinical) NA 0.79 0.78Mexico 0.84 1.00* 0.44Mexico (clinical) NA 0.95 0.44Netherlands 0.87 0.95 0.59

*100% sensitive by definition with MSU positivity; such individuals would meet sufficient criterion for 2015 ACR/EULAR criteria

ENTRY CRITERION: Has the patient/subject had at least one episode of swelling, pain, or tenderness in a peripheral joint or bursa?

SUFFICIENT CRITERION:MSU+?

Do not score

YES NO

YES

SUBJECT CAN BE CLASSIFIED AS

GOUT

NO (UNKNOWN)

PROCEED TO CLASSIFICATION

CRITERIA SCORING

2015 ACR-EULAR Gout Classification Criteria (1)

2015 ACR-EULAR Gout Classification Criteria (2)

Maximum score is 23. Threshold to classify as gout is ≥8.

Principles of gout management

Emergency management

• Acute monoarthritis (septic a, gout, pseudogout)

• Arthrocentesis: knee (mannequin), ankle

• SF analysis

Synovial fluid analysis

Management of acute gout flares

• Option1- monotherapy

– NSAID- inflammatory dose, shortest period, beware of renal/GI effect

– Colchicine –if attack<12 hr,

• 1-2 tab stat and then 1 tab 1 hour later (evidence B), or

• 1 tab q 6-8 hr (if normal GFR) (high dose is not recommended)

– Medium dose glucocorticoid- 30-35 mg/d split 5 days and then taper within 1 wk(beware of rebound effect, hyperglycemia)

– (intraarticular steroid injection-selected case)

• Option2- combination therapy eg. Colchicine +NSAID, colchicine + steroid

• High dose: 2 tab po stat, 1 tab q hr for 6 hr (4.8 mg over 6 hr)

• Low dose: 2 tab po stat, 1 tab 1 hr later, followed by placebo doses every hour for 5 hours (1.8 mg over 1 hour)

• Placebo

The AGREE study(Acute Gout Flare Receiving Colchicine Evaluation)

Terkeltaub RA, et al. ARTHRITIS & RHEUMATISM 2010

RDU- therapeutic dose of colchicine for gout flare

Richette P, et al. EULAR recommendation 2016

Combination therapy- gout flare (evidence C)

• Initial combination is appropriate for an acute , severe gout attack, particularly with involvement of multiple large joints or polyarticular arthritis Acceptable combination therapy

1. Colchicine and NSAID

2. Colchicine and oral steroid

3. IA steroid with all other modalities

• For patients not responding adequately to initial monotherapy, adding a second agents is acceptable

Colchicine: full dose or prophylactic dose

Khanna D, et al. ACR guidelines for gout (part2) 2012

Richette P, et al. EULAR guideline for GOUT 2016

RDU- gout


Prophylaxis of Gout Flare

Khanna D, et al. ACR guidelines 2012

With adjusted dose for GFR

RDU- colchicine prophylaxis of gout

Terkeltaub, R. Rheumatology.2015

Aware of drug interaction with colchicine

Urate lowering agent

Rees, F. et al. Nat. Rev. Rheumatol. 2014

= 6 mg/dl

severe gout-tophi, -chronic arthropathy, -frequent attacks



Lifestyle risk factors of hyperuricemia and gout

Choi HK. Current Opinion in Rheumatology 2010

Screening for comorbidity

• Obesity, dietary factors

• Excessive alcohol intake

• Metabolic syndrome, type 2 diabetes mellitus

• Hypertension

• Hyperlipidemia, modifiable risk factors for coronary artery disease or stroke

• Serum urate elevating medications

• History of urolithiasis

• Chronic kidney, glomerular, or interstitial renal disease

(e.g., analgesic nephropathy, polycystic kidney disease)

evidence C for all


Drug induced

Chaker Ben Salem et al. Rheumatology (oxford) 2016

Choi HK, et al. JAMA. 2010

ATP : adenosine triphosphateADP : adenosine diphosphateAMP: adenosine monophosphateIMP : inosine monophosphatePi : inorganic phosphate

Activate catabolic pathways

Choice of ULT

1. Lower uric producton-XO inh.• Allopurinol• Febuxostat

2. Increase uric excretion- uricosuric (no KUB stone)• Probenecid (GFR>60)• benzbromarone(GFR>25, no liver disease)

Nicola Dalbeth, et al. Lancet 2016


or HLA-B*5801 in Thai,Korean, Chinese HAN

Start low, go slow

Stamp LS et al. Rheumatology (Oxford). 2017

• Overall incidence 2% rash, Occurs in the first 180 days,

• Rare severe AHS

Clinical features of severe allopurinol adverse events

Stamp LS et al. Rheumatology (Oxford). 2017

Risks for Allopurinol hypersensitivity reaction

1. HLA-B*5801

2. CKD

3. Concomitant diuretic

4. Starting dose of allopurinol

HLA-B*5801, Odd ratio = 348 (27 AHS, 54 allopurinol tolerant, + 100% vs 13%)

-Tassaneeyakul W et al, Pharmacogenet Genomics. 2009

Avoidance of allopurinol in those individuals who are positive for HLA-B*5801 is currently recommended by the Clinical Pharmacogenomics Implementation Consortium

–Hershfield M et al. Clin Pharmacol Ther 2013

Stamp LK, et al. Arthritis & Rheumatism 2012

Starting Dose Is a Risk Factor forAllopurinol Hypersensitivity Syndrome

Stamp LK, et al. Arthritis & Rheumatism 2012

RDU- allopurinol for gout

RDU- ULT for gout

OA knee

ตวัอย่างสถานการณ์ชายสงูวยั 67 ปี โรคประจ าตวั เบาหวาน ความดนัโลหติสงู ควบคุมไดค้อ่นขา้งด ีกนิยาสม ่าเสมอ บ่นปวดเขา่ทัง้สองขา้ง ท ากจิวตัรประจ าวนัไดไ้มค่อ่ยสะดวก มาขอรบัค าแนะน าเรือ่งการรกัษาอาการปวดเขา่ค าสัง่จงตรวจประเมนิอาการปวดเขา่ บอกการวนิิจฉยั ใหค้ าแนะน าและสัง่การรกัษาผูป่้วย

ลกัษณะสถานี OPD setting (โต๊ะ เกา้อี ้เตยีงตรวจ)ผูป่้วย OA kneeอปุกรณ์1. ชุดเครือ่งมอืตรวจมาตรฐาน2. ผลเลอืด (abnormal-cr 1.7) และ film x ray (knee-KL grade 3)3. ยากลโูคซามนี

Tested Domain

• Physical examination (15)

• Clinical communication• history taking (20)

• Advice non-pharmacological treatment (20)

• Problem identification and DDx (15)

• Management plan (25)

• Professionalism- manner, management of patient’s concern(10)

Diagnosis

Symptoms in OA

• Non-inflammatory joint pain: ปวดตือ้ๆ ทัว่ๆ ไปบรเิวณขอ้ ระบตุ ำแหน่งไมไ่ด ้ชดัเจน มกัเป็นเรือ้รังและปวดมำกขึน้เมือ่ใชง้ำนในทำ่งอเขำ่ กำรขึน้ลงบนัได หรอืลงน ้ำหนักบนขอ้นัน้ๆ และทเุลำลงเมือ่พักกำรใชง้ำน หำกกำรด ำเนนิโรครนุแรงขึน้อำจปวดตลอดเวลำ แมเ้วลำกลำงคนืหรอืขณะพักได ้บำงรำยมอีำกำรปวดตงึบรเิวณพับเขำ่ดว้ย

• Stiffness < 30 min, gel phenomenon

• Bony enlargement: มขีอ้บวมใหญซ่ึง่เกดิจำกกระดกูทีง่อกโปนบรเิวณขอ้ และเมือ่โรครนุแรงมำกขึน้อำจพบขำโกง่ (bow leg)

• Crepitus: มเีสยีงดงักรอบแกรบในขอ้เขำ่ขณะเคลือ่นไหว

• Reduced function: มคีวำมล ำบำกในกำรน่ัง ลกุ เดนิ หรอืขึน้ลงบนัได

• Restricted movement: เหยยีดตรงไดล้ ำบำก (flexion contracture) เมือ่มอีำกำรมำกขึน้จะท ำใหง้อเขำ่ไดล้ดลง

Primary vs secondary OA

Secondary OA

•Atypical age < 40 yr

•Atypical location: uncommon site

•Atypical character• Moderate-severe

inflammation• Uniform jt space narrowing• Hypertrophic osteophyte• Marginal erosion

Non-pharmacological therapy

1. Education

• ปัจจัยเสีย่งกำรเกดิโรค ไดแ้ก ่ควำมอว้น อำชพี อบุัตเิหตกุำรใชง้ำนขอ้ผดิวธิ ีและประวัตโิรคขอ้เสือ่มในครอบครัว

• ผูป่้วยแตล่ะรำยมกีำรด ำเนนิโรคแตกตำ่งกนั บำงรำยอำจไมม่อีำกำร บำงรำยมอีำกำรเพยีงชัว่ครำว แตส่ว่นใหญม่ักมอีำกำรเรือ้รัง และบำง

• รำยมกีำรด ำเนนิโรคแยล่งอยำ่งรวดเร็ว

• วัตถปุระสงคก์ำรรักษำ

• กำรปรับเปลีย่นพฤตกิรรม กำรออกก ำลงักำย กำรท ำกจิกรรม กำรลดน ้ำหนัก และกำรลดแรงกระท ำทีข่อ้

2. Weight reduction in case of BMI >23, reduce to standard weight or at least 5% of wt.

3. rehabilitation and exercise

• Assess ADL

• Strengthening quadriceps exercise, ROM exercise, low–impact aerobic exercise

Treatment

NSAID

Recommendations for Prevention of NSAID-related Ulcer Complications

LowGl Risk

Moderate High*Low CV risk(NO aspirin)

NSAID NSAID + PPI/misoprostol

(COXIB)

COXIB + PPI/misoprostol

* High risk: Complicated ulcer and 2+ risks

Risk: age >65, uncomplicated ulcer, high-dose NSAID, aspirin, steroid, anticoagulant

Lanza et al. Am J Gastroenterol 2009

Recommendations for Prevention of NSAID-related Ulcer Complications

LowGl Risk

Moderate High*Low CV risk(NO aspirin)

NSAID NSAID + PPI/misoprostol

(COXIB)

COXIB + PPI/misoprostol

High CV risk(ON aspirin)

Naproxen + PPI/misoprostol

Naproxen + PPI/misoprostol

Avoid NSAIDs or COXIBs.

* High risk: Complicated ulcer and 2+ risks

Risk: age >65, uncomplicated ulcer, high-dose NSAID, aspirin, steroid, anticoagulant

Lanza et al. Am J Gastroenterol 2009

Treatment

Osteoarthritis of Hands

•Physical findings: •Deformity: radial/lateral deviation/subluxation , Squaring sign,

•Bony enlargement: Bouchard’s nodes, Heberden’s nodes•Joint : DIPs, PIPs, 1st CMC

Osteoarthritis

1. Subluxations

2. Nonuniform loss of joint space

3. Absence of erosions, central erosion

4. Subchondral sclerosis

5. Osteophyte

6. Gull wings sign

Contrasting radiographic features at interphalangeal joints (IPJs) of (A) osteoarthritis (OA): focal

narrowing, marginal osteophyte, sclerosis, osteochondral bodies; (B) erosive OA: subchondral

erosion; (C) psoriasis: proliferative marginal erosion, retained or increased bone density; and

(D) rheumatoid arthritis: non-proliferative marginal erosion, osteopoenia.

W Zhang et al. Ann Rheum Dis 2009;68:8-17

86

87

Osteoarthritis of 1st CMC joint

Rheumatoid Arthritis (RA)

• A chronic progressive disease causing inflammation in the joints and resulting in painful deformity and immobility, especially in the fingers, wrists, feet, and ankles.

This inflammation usually affects the lining of the joints (synovial membrane), but can also affect other organs.

88

hands : Deformity : Swan Neck, Boutonniere, Ulnar Deviation Complete joint exam at wrists, MCP, PIP :Swollen joint, tender joint ROM: handgrips, wrist flex/extend

subcutaneous nodule : rheumatoid nodule at ..(extensor tendon of elbow, extensor tendon of hands and feet)

Rheumatoid arthritis

Swan Neck deformity

Boutonniere Deformity

Ulnar Deviation

HEENTeye : pale, episcleritis, scleritismouth : salivary poolneck : LN

Heart : loud P2 Lung; crackle both basilar lung (ILD) Abd : splenomegaly neuromuscular:

Carpal tunnel syndrome : phalen’s, Tinel’s, thenar atrophyMononeuritis multiplex: foot drop/impaired sensationExtensor tendon rupture: finger drop

Extra-articular RA

Katchamart W et al. Int J Rheum Dis. 2016

Diagnosis

2016 Thai RA recommendation for non rheumatologistsKatchamart W et al. Int J Rheum Dis. 2016

Diagnosis

Both ACR revised criteria for the classification of RA 1987 and 2010 ACR/EULAR classification criteria for RA can be used to diagnose RA.

Rheumatoid arthritis

1. Peri-articular soft tissue swelling

2. Juxta-articular osteoporosis progressing to generalized osteoporosis

3. Uniform joint space narrowing

4. Marginal erosions progressing to severe erosions

5. Bilateral symmetrical distribution

6. Lack of bone formation

7. Subluxations/deformity

Treatment- Analgesics and anti-inflammatory agents


Treatment- DMARDs


Investigations prior to initiation of disease-modifying anti-rheumatic drugs, non-steroidal anti-inflammatory drugs and glucocorticoids


Follow-up


Investigations for monitoring treatment related toxicity


Indications for referral to rheumatologists

1) Uncertain diagnosis

2) Patients who have complications or extra-articular manifestations

3) Patients with comorbid diseases or conditions

4) Patients who do not respond or have inadequate response to high-dose DMARDs for at least 3–6 months

5) Patients who cannot stop glucocorticoids within 6–12 months of treatments

6) Patients who develop complications related to the treatments

7) Patients who are pregnant or in the lactation period


Documents

Board tutorial for ASCE 2018 rheumatologyreviews.berlinpharm.com/20180505/Board_tutorial... · Board tutorial for ASCE 2018 Rheumatology (gout, OA, RA) Asst. Prof. Boonjing Siripaitoon,