Gout arthritis - comprehensive ppt

GOUT
Dr.RAJASEKHAR YALAMANCHI
M.D (GENERAL MEDICINE)

INTRODUCTION
• Gout is a metabolic disease
• Results from an increased body pool of urate with hyperuricemia.
• It is characterized by episodic acute arthritis or chronic arthritis caused by
deposition of MSU crystals in joints and connective tissue tophi.
• There is a risk for deposition in kidney interstitium or uric acid
nephrolithiasis.

• Hyperuricaemia is defined as an SUA level greater than 2
standard deviations above the mean for the population.
• Normal serum uric acid levels –
male – 3.4 to 7 mg/dl
female – 2.4 to 6 mg/dl

EPIDEMIOLOGY
• Prevalence is approximately 1-2% with a strong male
predominance (>5:1).
• Affects middle-aged to elderly men and postmenopausal
women.

Factors that predispose to chronic
hyperuricaemia and gout
Diminished renal excretion (common) :
- Inherited isolated renal tubular defect (under-excretors)
- Renal failure
- Chronic drug therapy
Thiazide and loop diuretics
low – dose aspirin
ciclosporin
pyrazinamide
- Lead toxicity (in moonshine drinkers)
- Lactic acidosis (alcohol)

Increased production of uric acid (uncommon):
- Increased purine turnover
chronic myeloproliferative or lymphoproliferative disorders
(e.g. polycythaemia,chonic lymphatic leukaemia)
- Increased de novo synthesis (over producers)
unidentified abnormality (most common)
specific enzyme defect (rare)
hypoxanthine – guanine phosphoribosyl transferase
deficiency(lesch-nyhan syndrome)
phosphoribosyl pyrophosphate synthetase over – activity
glucose-6-phosphatase deficiency

ACUTE ARTHRITIS
• Acute arthritis is the most common early clinical manifestations of gout
• Only one joint is affected initially , but polyarticular acute gout can occur
in subsequent episodes.
• The metatarsophalangeal joint of the first toe often is involved, but tarsal
joints, ankles, and knees also are affected commonly.
• Especially in elderly patients or in advanced disease, finger joints may be
involved.
• Inflamed Heberden’s or Bouchard’s nodes may be a first manifestation of
gouty arthritis.

Gout arthritis - comprehensive ppt

• The first episode of acute gouty arthritis frequently begins at night
with dramatic joint pain and swelling.
• Joints rapidly become warm, red, and tender, with a clinical
appearance that often mimics that of cellulitis.
• Early attacks tend to subside spontaneously within 3–10 days, and
most patients have intervals of varying length with no residual
symptoms until the next episode.

• events precipitate acute gouty arthritis:
dietary excess
trauma
surgery
excessive ethanol ingestion
hypouricemic therapy and
serious medical illnesses such as myocardial
infarction and stroke.

CHRONIC ARTHRITIS
• After many acute mono- or oligoarticular attacks, a proportion of
gouty patients may present with a chronic nonsymmetric synovitis,
causing potential confusion with rheumatoid arthritis .
• chronic gouty arthritis will be the only manifestation
• Rarely the disease will manifest only as periarticular tophaceous
deposits in the absence of synovitis.

symptoms
• Podagra (initial joint manifestation in 50% of gout cases and
eventually involved in 90%)
• Arthritis in other sites
• Monoarticular involvement most commonly, though polyarticular
acute flares are not rare and many different joints may be involved
simultaneously or in rapid succession
• Attacks that begin abruptly and typically reach maximum intensity
within 8-12 hours
• Without treatment , symptom patterns that change over time attacks
can become more polyarticular involve more proximal and upper
extremity joints

Physical findings:
• Involvement of single or multiple joints
• Signs of inflammation – swelling, warmth,erythema
(sometimes resembling cellulitis) and tenderness
• Fever (consider infectious arthritis)
• Tophi in soft tissues (helix of ear, fingers, toes, prepatellar
bursa, olecranon)

Complications of gout
• Severe degenerative arthritis
• Secondary infections
• Urate or uric acid nephropathy
• Increased susceptibility to infection
• Urate nephropathy
• Renal stones
• Nerve or spinal cord impingement
• Fractures in joints with tophaceous gout

Acute uratenephropathy
• Urate crystals  renal tubules  obstructiveARF
• Dehydration,low urine pH are precipitating factors
Chronic uratenephropathy
• Urate crystals  interstitium and renal medulla
inflammation +surrounding fibrosis  irreversible
CRF
• Renal impairment can occur in ~40%in chronic gout

Urate nephrolithiasis :
– Stones  flank pain/ureteric colic/hematuria
– Urate (radiolucent) / mixt. Calcium oxalate and/or calcium
phosphate (radio-opaque)
– Contributing factors : hyperuricosuria, low urine output,
acidicurine
– Urinary alkalinization (pot. Citrate or NaHCO3) 
dissolution of existing stones and prevention of
recurrence

Gout in women
• Women represent only 5–20% of all patients with gout.
• Most women with gouty arthritis are postmenopausal and
elderly, have osteoarthritis and arterial hypertension that
causes mild renal insufficiency, and usually are receiving
diuretics.
• precocious gout in young women caused by decreased renal
urate clearance and renal insufficiency have been described.

Gout in old age
• Aetiology : predominantly primary gout, but a higher
proportion of secondary gout (chronic diuretic therapy or
chronic kidney disease) than in middle aged patients.
• Nodal generalised OA :an additional risk factor for gout
• Presentation: painful tophi and chronic symptoms,rather than
as classic acute attacks ,presentation in upper rather than
lower limbs.

Continued:
• Treatment of acute attacks: by aspiration and intra-
articular injection of long acting corticosteroid
followed by early mobilisation.
• oral NSAID and colchicine are best avoided because of
increased toxicity.
• Allopurinol: because of increased toxicity ,should be
started at the low dose of 50-100 mg/day.

Diagnostic criteria
 Two ofthefollowingcriteriaarerequiredfor clinical diagnosis:
1. Clearh/oatleast2attacksofpainfuljoint swellingwithcomplete
resolutionwithin2 weeks
2. Clearhistoryorobservationofpodagra
3. Presenceoftophus
4. Rapidresponseto colchicinewithin48hoursof treatmentinitiation
 Definitive diagnosis: presenceof monosodiumuratecrystalsseenin
synovial fluid/tissues

Laboratory investigations
• Joint aspiration and synovial fluid analysis.
• Serum uric acid measurement .
• 24 – hour urinary uric acid evaluation
• Blood studies (including white blood cells(WBCs) , triglyceride,
high density lipoprotein, glucose, and renal and liver function
tests.

Synovial fluid analysis
• During acute gouty attacks, needle-shaped MSU crystals
typically are seen both intracellularly and extracellularly
• With compensated polarized light, these crystals are brightly
birefringent with negative elongation.

 Skeletalx-rays
 Acutegouty arthritis :normal;soft tissueswelling
 Chronic tophaceous gout : tophi, erosive bone lesions (punched
out lesions), joint spaceis preserveduntil late stage,
pathognomonicin foot and bigtoe

X-ray findings typical of gout
• Maintenance of the joint space
• Absence of periarticular osteopenia
• Location outside the joint capsule
• Sclerotic (cookie – cutter,punched out )borders
• Asymmetric distribution among the joints with a strong
predilection for distal joints especially the lower extremities

 Renalimaging
 PlainabdXRdetectsonly 10%of all uratestones
 USKUB: investigations of choice for nephrocalcinosis,
significantrenalstones(>3mm) whetherradio-opaqueor
radiolucent,obstructive nephropathy
 PlainCTU:mostsensitiveto detectanystone

USG:
• A ‘double contour’ sign consisting of a hyperechoic
,irregular line of MSU crystals on the surface of articular
cartilage overlying an adjacent hyperechoic bony contour.
• ‘Wet clumps of sugar’ representing tophaceous material
described as hyperechoic and hypoechoic heterogeneous
material with an anechoic rim.
• bony erosions adjacent to tophaceous deposists

Gout vs CPPD
• Similar Acute attacks
• Different crystals under Microscope:
Rhomboid, irregular in CPPD

Gout vs RA
• Both have polyarticular, symmetric arthritis
• Tophi can be mistaken for RA nodules

Management
 Lifestyle modification anddietary advice
 Management ofcomorbidities
 Nonessential prescriptions thatinduce hyperuricaemia
 Main aim:
- Toachive idealBW
- Prevent acute goutyattacks
- Reduceserum uratelevel
 Strict purine-freediet reducedonly 15–20%of serum urate, thus is
considered an adjunct therapy to medication.

Treatment
 Contributing factorseg.thiazide/loop diuretics;low doseaspirin may be
discontinued or substituted, if appropriate
 Pharmacotherapyof asymptomatichyperuricemia
is NOTnecessary,except:-
 Persistent severehyperuricemia
- >13mg/dLinmale
- >10mg/dLinfemale
 Persistent elevated urinaryexcretion of urate
->11mg/day , a/w50%increasedrisk of urate calculi
 Tumor lysissyndrome
- chemotherapy/radiotherapy  extensive tumorcytolysis
=>require pre-hydration andallopurinol to preventacute urate
nephropathy

Treatmentofacutegoutyarthritis
 Initiation within 24 hoursof onset
 If onAllopurinol, continue without interruption
NSAIDs
Effective in 90% of patients and resolution of signs and
symptoms usually occurs in 5-8days
 Caution in h/o PUD,HPT,renal impairment, IHD, liver impairment
 COX-2inhibitors (celecoxib,etoricoxib, parecoxib) =alternative for
above risk factors
 Studieshave shown that etoxicoxib (Arcoxia) has equal
efficacy to indomethacin
Indomethacin – 25-50mg tid , naproxen 500mg bd , ibuprofen
800mg tid , diclofenac 50mg tid.

 COLCHICINE
 Inhibitingmitosisandneutrophilsmotility andactivity, leadingto a
net anti-inflammatoryeffect.
 Alternative drugifcontraindicationsto nsaids,but ispoorlytolerated by
elderly
 Therapeutic index isnarrow and slower onset ofaction
 Evidencebasefor prophylaxisisstrongerthanfor nsaids
 Sideeffects:nausea,vomiting ,abdominalpain,profusediarrhoea
 Dosage:0.5mg–0.6mgBD-QID

 Steroids
 Can be considered in elderly people and patients with
renal/liver impairment, IHD, PUD, hypersensitivity to
NSAIDs
 IM steroids eg.Triamcinolone (20-40mg)or
methylprednisolone (25-50mg) canbe given .
 Short courseof oral prednisolone up to 30-50mg/day can
be given and tapered offover 4 -10 days

Treatment : chronic
gouty
arthritis

Urate lowering therapy
(hypouricaemic therapy)
 Allopurinolshouldnot bestarteduntil acuteattack hasresolved
 Mayprolongattackor leadto reboundflaresif started duringattack
 Shouldbestarted2weeksafter attackiswell- controlled
 Indications forULT:
1. Frequentanddisabling attacksof gouty arthritis (3or more
attacks/year)
2. Clinicalor radiographic signsof erosive gouty arthritis
3. The presenceof tophaceousdeposits
4. Uratenephropathy
5. Uratenephrolithiasis
6. Impending cytotoxic chemo-/radiotherapy for lymphoma or leukemia

Xanthine oxidase i n h i b i t o r
 ALLOPURINOL
 More superior thanprobenecid
 Primarily excretedbykidneys,thusneedrenal adjustment
 Aim:reduceto <6mg/dl andmaintainwith minimal doseofallopurinol
 Duringinitiation ofallopurinol therapy, colchicine (0.5mg BD)canbe usedas prophylaxis
to reducefrequencyof attacks.Can becontinued until patient isattack free for 6
months or target serumurate level isachieved for 1month.
 Forpatientwho can’ttolerate colchicine,low doseNSAIDscanbeused.used
 Dosage:singlemorningdoseof100mginitiallyandincreasingupto800mgifneeded.

Uricosuri c agent
PROBENECID
 Analternativeto allopurinolinpatientswithNORMALRENAL FUNCTION
 Dosage:250mgtwicedailyandincreseadgraduallyasneededupto3g/daytoachieveserumuricacidlevel<6mg/dl.
 Sideeffects:
 GIdisturbance
 Hypersensitiverash
 Contraindications:
- uricacidoverproductionandoverexcretion(24hrsurinaryurate
excretion more than800mg/day)
- uratenephropathy
-- uratenephrolithiasis
 Losartanhasmodesturicosuriceffect
 Fenofibrate too
Riskofcrystal
precipitation

PEGLOTICASE
• Biological treatment in which the enzyme uricase has been
conjugated to monomethoxy-polyethylene glycol.
• Indicated for the treatment of tophaceous gout resistant to
standard therapy
• Administered as an intravenous infusion every 2 weeks for
upto 6months
• It is highly effective at controlling hyperuricaemia and causes
regression of tophi.
• Adverese effects – infusion reactions (can be treated with
antihistamines or steroids

Treatment o f urate nephropathy
 Increaseurineoutput
 3Lof H2O/daywith urine output >2.5Lif not ESRF
 IncreaseurinepH
 Preventurate stoneformation andpromote dissolution of
stone
 Targeturine pH:6.5–7
 Potassiumcitrate 40–50mmol/day(max100mmol/day)
 Sodiumsalt :Uralsachet(with analgesic properties)
Dosage: 1–2 sachetsQID
CIin renalimpairment/hypernatraemia
 Decreaseurateexcretion
 Dietary purine intakerestriction
 Treat withallopurinol

Treatment o f urate nephrolithiasis
 Intrarenalstones<5mmcanbeobservedunless causingpain
 Intrarenalstone5–15mmorcomplexstaghorn calculi referto urologistfor ESWLor
PCNL
 Uretericstones:conservativemanagement
 If uncomplicated (min obstruction/nosepsis),andsize
<5mm,at lower ureter  maypassspontaneously
 If fail to passafter 2weeks  refer for removal
 Pureuratestonescanbechemolysedbypot.Cit.or Ural (oral/directirrigation)
 Longterm chemoprophylaxisusingpot.Cit.has shownto behighly effective

SURGICAL I N T E R V E N T I O N
 Lastresortfor gouty arthritis
 Removal oftophi
 Joint fusion
 Joint replacement
 Ulcerationof tophi : debridement,dressingwith sodium bicarbonate
solution
 Indicationsfor chronictophaceousgout :
 Advancedtophi deposition resulting in major joint destruction
 Lossof involved joint movementsa/wseverepain
 Tophicollection causingpressuresymptoms, egcarpal tunnel syndrome of
wrist
 Tophaceousulcer
 Cosmetic eg: ear lobetophi

when to reduce urate lowering agents
 If serumurate <6mg/dl, andhavebeenno gouty attacks
for 1year  canreduce T. allopurinol by100mg.
 Checkserumurate 6monthly, if still
<6mg/dl  canfurther reduce
 Patientsthat havetophi aremost likely to require
lifelongULT

REFERENCES
• Harrisons principles of internal medicine 20th edition
: pg 2631 to 2633
• Davidson principles and practice of medicine

Gout arthritis - comprehensive ppt

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