Approach to Joint pain QUIZ - PowerPoint Presentation

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Approach to Joint pain

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QUIZ

https://tinyurl.com/yakeqhj5

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78 yo Chi MaleNKDAADL-I, comm ambulantNon-smoker non-drinkerPMHxHTNHL Gastric Diffuse large B cell lymphoma- CHOP chemotherapy 9 yrs ago, CHOP-R x 6 cycles-In complete remissionCardiomyopathy post chemotherapy- EF 21% in 2009, multiple adm for fluid overload- Echo 2017 jan: LVEF 32% w RWMAIHD - PCI: DES to prox and mLAD 28/2/17R inguinal hernia s/p repairGout- Adm for flare in Jan 2017: gout vs OABPHAdmitted from ED to DIM for Bilateral LL weakness 2. Fever x 1/73. Right knee and ankle pain x 3/7

What other history would you like to obtain?

What pertinent physical examination findings will you look out for?

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78

yo

Chi Male

NKDA

ADL-I,

comm

ambulant

Non-smoker non-drinker

PMHx

HTN

HL

Gastric Diffuse large B cell lymphoma

- CHOP chemotherapy 9

yrs

ago, CHOP-R x 6 cycles

-In complete remission

Cardiomyopathy post chemotherapy

- EF 21% in 2009, multiple

adm

for fluid overload

- Echo 2017

jan

: LVEF 32% w RWMA

IHD

- PCI: DES to

prox

and

mLAD

28/2/17

R inguinal hernia s/p repair

Gout

Diagnosed by GP, initially big toe and ankle swelling

Has on and off right knee swelling and pain 1-2x/year, take pain meds from GP

not been on

urate

lowering therapy before.

-

Adm

for flare in Jan 2017: gout vs OA

BPH

Admitted from ED to NEM for

Bilat

LL weakness

-

nil facial weakness, slurring of speech

nil hearing impairment/visual impairment/diplopia

Nil bowel/bladder incontinence

Nil focal neurological

sx

2. Fever x 1/7

a/w

runny nose and productive cough 3-4/7(yellowish sputum), sore throat

Nil chills/rigors

nil SOB/CP/palpitation

BO/PU NAD

Nil recent travel/sick contacts

3. Right knee and ankle pain x 3/7

- associated with knee swelling

pain limiting ambulation, pain score 8/10

No other joints are involved.

Nil recent trauma/fall

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On examinationWell non toxicHydration goodVitals T: 38.5, BP : 133/81, HR: 96 RR: 14, SpO2 100% on RAH S1S2L clearA soft no masses.No cervical LNsDRE: brown stools nil massesRight knee: mild-mod effusion, active ROM to 45deg. Warmth +Left knee: no effusion. Right & left ankles no effusion nor warmth.Right MTPJ no swelling or warmth. Other joints no swellingNo tophi seenPower 4/5 in right proximal LL, limited by knee pain in LLPower 5/5 in left LL

What are your differentials?What investigations would you like to order?

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Differentials

Septic arthritisCrystal arthropathiesGoutPseudogoutBasic calcium phosphateTraumaticOASystemic rheumatic diseases (RA/psoriasis)Cellulitis

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Will you tap the joint in the middle of the night?

Your seniors are not free, ask you to tap.

How will you tap it?

What investigations to send for?

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Right knee aspiration revealed: Synovial Fluid, Knee Joint:- Inflammatory exudate.- Urate crystals are present. GROSS DESCRIPTION - Specimen container received with patient's data, labeled as "Fine Needle Aspiration Knee joint aspiration". 4ml of yellowish fluid was received. MICROSCOPIC DESCRIPTION - 2 Pap,1 Diff-Quick stained smears and 1 wet mount smear are examined. Smears show severe, acute inflammatory exudate. Numerous, extracellular, negatively birefringent crystals are seen.Gram stain Smear MICROSCOPY EXAM Polymorphs 1+ Organisms not seen Joint fluid culture : nil BG

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REVISION - APPROACH

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Taken from

Dr

Stanley

Angkodjojo

slides on approach to

monoarthritis

on

Infonet

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Synovial fluid analysis

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Hyperuricemia

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Gout

Definition: derangement in purine metabolism resulting in hyperuricemia; monosodium urate crystal deposits in tissues (tophi) and synovium (microtophi) Etiology

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Gout

Clinical ManifestationsAsymptomatic hyperuricemiaAcute arthritisIntercritical illnessChronic tophaeous goutRenal DiagnosisBloods (± raised WBC/ESR/Uric acid)Radiograph (tophi appear as soft tissues welling, punched-out lesions, erosion with “over-hanging”)Joint aspiration (needle shaped negatively birefringent crystals) GOLD STANDARD

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Score ≥8

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Gout

Acute treatment

IL-1 inhibitors

Anakinra

(100mg SC qd x 3d) Canakinumab (150mg SC x 1)

Expensive (off label)

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Acute Tx

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Gout (chronic tx)

Non-pharmacological (avoid food and drugs precipitating high uric levels)

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Long term tx

Principles

Education and counselling (when starting allopurinol must be compliant to allopurinol + colchicine/NSAIDs as there can be flares in the acute phase), dietary modification, avoidance of alcohol, stop drugs causing hyperuricemia, avoid triggers, adequate fluid intake (can always try non-pharmacological methods first in gout)

Lifestyle modifications as above

DIET (refer dietician)

Healthy diet according to health pyramid

No alcohol

esp

beer and stout

Redue

animal purines

eg

red meat, seafood, liver and kidney, sardines/

ikan

bilis

Increase fruit and veg

Less sugary drinks

Avoid binge eating on special occasions and high consumption of animal protein

Avoid dehydration

Gradual weight loss

PT/OT if tophaceous gout for preservation of function

Manage associated conditions like HTN/HLN/DM/obesity (lose weight)

Pharmacological therapy for acute attack and urate lowering therapy if indicated

Surgery rarely-

eg

removal of tophi for

cosmesis

and to improve function

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Drugs (chronic tx)

Consider uric acid lowering therapy in Recurrent gouty attacks (>/=2 times a year)Arthropathy with x-ray changesChronic tophaceous gout (aim SUA <300 to help dissolve the tophi)Urolithiasis/ Uric acid nephropathyLower threshold to treat in patients with renal impairmentConditions that may predispose to gout? after first gouty attack in chronic renal failure Tumor lysis syndrome (treat prior to chemotherapy or radiotherapy)Polycythaemia, lymphoproliferative, myeloproliferativePsoriasis Inborn errors of metabolism IEMGoal of urate lowering therapy is serum uric acid SUA <360µmol/L. However, goal of SUA <300 micromol/L should be used in patients with tophi, in order to speed resolution of tophi.Life long commitment: 40% of pts have Recurrent flare after 5 yrs after discontinuation

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Drug options

Xanthine oxidase inhibitorUse colchicine as prophylaxis in initial phase of lowering SUA because allopurinol can cause increase in flares in the initial phase before serum urate target is reachedWhen starting allopurinol, keep patient on colchicine prophylaxis (500mcg daily) until flares are infrequent and SUA below target. If renal impaired, give 500mcg (1tab) 2-3 x a weekAllopurinol Principle is: if started don’t stop, if not started don’t startStart low and go slow- start on 100mg/day then review in 4-6 weeks, check SUA levels and increase by 100mg if neededSide effects (monitor FBC, U/E/Cr, LFTs)Allopurinol hypersensitivity reaction (rash, hypereosinophilia, hepatitis, renal failure)↑ risk if HLA B5801 +veUsu occurs 3-4/52 after startingRash, SJS/TENGI SE common: diarrhoea, dyspepsia, nausea, headacheDrug fever Oral ulcer Leucopenia, thrombocytopenia (marrow suppression

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Xanthine oxidase inhibitors cont’d

Febuxostat

– non purine xanthine oxidase inhibitor

Used as second line if allopurinol hypersensitivity and probenecid contraindicated

SE

Rash

Arthralgia

Nausea

LFT changes

Uricosuric

agents

Probenecid

Start on 250mg BD and

uptitrate

slowly up to max of 3g

Before starting probenecid, rule out renal insufficiency and ensure no history of renal stones

CI: renal stones, GFR < 30-40ml/min

If starting on this warn patient of risk of stones and advise them to drink more water and

avoi

dehydration

Benzbromarone

Sulfinpyrazone

Rasburicase

?

Not really used in

tx

of gout. More used in

tmour

lysis syndrome.

Side effect of concern is that of hypersensitivity

rxn

that can be as serious as anaphylaxis

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Others drugs- use losartan/CCBs to treat HTN and fenofibrate to treat HLD in patients with gout as these have uric acid lowering properties)

Losartan can help however that is the only ARB that helps

Fenofibrate

CCBs

The angiotensin receptor blocker (ARB) losartan is the most appropriate antihypertensive drug for this patient with hyperuricemia who is at increased risk for acute gout. Hypertension is a common comorbidity of gout and is found in approximately 74% of patients with gout. Antihypertensive drugs have variable effects on serum urate levels and risk of acute gout. A population-based, nested-case control study compared nearly 25,000 patients with a new diagnosis of gout with 50,000 control patients. The risk of gout was assessed according to antihypertensive drug class.

Losartan, but not other ARBs, and calcium channel blockers were associated with a reduced risk of gout (

relative risk for losartan: 0.81 [95% CI, 0.7-0.84]; relative risk for calcium channel blockers: 0.87 [95% CI, 0.82-0.93]). Both losartan and calcium channel blockers lower serum urate. Losartan, like probenecid, interferes with the urate-reabsorbing transporter, thereby promoting kidney urate excretion. The mechanism by which calcium channel blockers lower urate levels is unclear but may be mediated through increased glomerular filtration rate and increased urate clearance. Based upon these data, losartan and calcium channel blockers are the preferred antihypertensive agents if reducing the risk of gout is clinically relevant.

In this same study, ACE inhibitors, non-losartan ARBs, β-blockers, and diuretics were all associated with an increased risk of gout. The absolute risk of gout was greatest with diuretics, with an estimated risk of six events per 1000 person-years.

Choi HK, Soriano LC, Zhang Y, Rodríguez LA. Antihypertensive drugs and risk of incident gout among patients with hypertension: population based case-control study. BMJ. 2012 Jan 12;344:d8190.

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Prophylatic tx for urate lowering therapy

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Allopurinol hypersensitivity syndrome

HLA- B*5801 Allele

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Knee aspiration/injection

Diagnostic indicationTRO Septic arthritisTo aid diagnosis: gout vs CPPD, inflammatory vs non-inflammatory, haemarthrosis Therapeutic indicationPain relief (draining large effusions)Source control (draining septic effusion)Injection of medications to relief inflammation/painContraindications (relative)Overlying skin infectionCoagulopathyProsthetic jointAltered anatomy (fracture/ unaccesible joint)

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Knee aspiration video

NEJM Knee aspiration videohttp://www.nejm.org/doi/full/10.1056/NEJMvcm051914

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How to perform a knee aspiration

Obtain informed consent: small risk of post injection flare, bleed, infection, to avoid strenuous activity for 24-48h post procedureLateral and Medial Mid-Patellar and Patello-Femoral ApproachesThe traditional approach to knee injection accesses the patellofemoral joint1) (Fig. 1). This technique is performed with the knee in extension. The patella is pulled medially or laterally and a needle is advanced under the patella. The lateral midpatellar (LMP) approach is the most commonly used2). The patellofemoral joint, via the LMP and MMP approaches can then be used for joint aspiration and/or injection. When performing a procedure via the LMP approach, the needle is directed at a 45° angle towards the middle of the medial aspect of the joint. Injection via the MMP approach is undertaken with the needle entering the medial aspect of the knee joint under the middle of the patella (midpole), and is directed towards the lateral patellar midpole

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3953519/

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References

www.uptodate.comPocket medicineToronto NotesNEJMUptodateDr Stanley Angkodjojo slides on approach to monoarthritis on Infonet