introduction , clinical manifestation, diagnosis and treatment of gout ,,,,, differentiation with pseudogout...

1. Gout
Dr. Sunil pahari
3rd Year Resident
Department of Orthopedic surgery, Yangtze University
jingzhou , hubei , P.R. China

2. Definition
• Acute inflammatory monoarthritis
caused by precipitation of monosodium
urate (MSU) crystals in joints
• Uric acid is the normal end product of
the degradation of purine compounds.
– Major route of disposal is renal excretion
– Humans lack the enzyme uricase to break
down uric acid into more soluble form.

3. Epidemiology
• Most common of microcrystalline arthropathy
• Affects about 2.1million worldwide
• Gout is 5 times more common in males
• Acute attack tend to occur after a large meal or
alcohol consumption ( alcohol metabolites
compete for same excretion sites in kidney as
uric acid, causing decrease uric acid secretion
and subsequent build up in blood )

4. Classification of Hyperuricemia
• Uric acid overproduction
– Accounts for 10% of hyperuricemia
– Acquired disorders
• Excessive cell turnover rates such as myleoproliferative
disorders, Paget’s disease, hemolytic anemias
• Uric acid underexcretion
– Accounts for >90% of hyperuricemia
– Diminished tubular secretory rate, increased tubular
reabsorption, diminished uric acid filtration
– Can be exacerbated by certain medication ( thiazide diuretics)

5. Stages of Classic Gout
• Asymptomatic hyperuricemia
– Very common biochemical abnormality
– Majority of people with hyperuricemia never develop symptoms of uric acid
excess
• Acute Intermittent Gout (Gouty Arthritis)
– Episodes of acute attacks. Symptoms may be confined to a single joint or patient
may have systemic symptoms.
• Intercritical Gout
– Symptom free period interval between attacks. May have hyperuricemia and
MSU crystals in synovial fluid
• Chronic Tophaceous Gout
– Results from established disease and refers to stage of deposition of urate,
inflammatory cells and foreign body giant cells in the tissues. Deposits may be in
tendons or ligaments.
– Usually develops after 10 or more years of acute intermittent gout.

8. Presenting Symptoms
• Systemic: may have fever,
chills and malaise
• Musculoskeletal:
• Asymmetric joint distribution
• Joint is swollen ,red and painful.
• Classic manifestation is painful
MTP joint of the big toe
(podagra)
Tophus formation (often on
external ear,olecranon bursa ,
Achilles tendon )
Tophi achilles

9. Differential Diagnosis
• Trauma
• Infections
– septic arthritis, gonococcal arthritis, cellulitis
• Inflammatory
– Rheumatic arthritis, Reiter’s syndrome, Psoriatic
arthritis
• Metabolic
– pseudogout ( calcium pyrophosphate crystal )
• Miscellaneous
– Osteoarthrtis

10. Diagnosis
• Definitive diagnosis
only possible by
aspirating and
inspecting synovial
fluid or tophaceous
material and
demonstrating MSU
crystals.
• yellow crystals

11. Synovial Fluid Findings
• Needle shaped
crystals of
monosodium urate
monohydrate that
have been engulfed
by neutrophils

12. Diagnostic Studies
• Uric Acid
– Rise
• CBC
– Mild leukocytosis in acute attacks, but may be higher than 25,000/mm
• ESR
– mild elevation or may be 2-3x normal
• 24hr urine uric acid
– Only useful in patients being considered for uricosuric therapy or if
cause of marked hyperuricemia needs investigation .

13. Treatment Goals
• Gout can be treated without
complications.
• Therapeutic goals include
– terminating attacks
– providing control of pain and inflammation
– preventing future attacks
– preventing complications such as renal
stones, tophi, and destructive arthropathy

14. Treatment mechanism

15. Acute Gout Treatment
• NSAIDs
– Most commonly used.
– No NSAID found to work better than others
– Regimens:
• Indocin 50mg po bid-tid for 2-3 days and then taper
• Ibuprofen 400mg po q4-6 hr max 3.2g/day
• Ketorolac 60mg IM or 30mg IV X1 dose in patients<65
– 30mg IM or 15mg IV in single dose in patients >65yo, or with
patients who are renally impaired
• Continue meds until pain and inflammation have resolved for
48hr

16. Acute Treatment
• Colchicine
– Inhibits microtubule aggregation which disrupts
chemotaxis and phagocytosis
– Inhibts crystal-induced production of chemotatic
factors
– Administered orally in hourly doses of 0.5 to 0.6mg
until pain and inflammation have resolved or until GI
side effects prevent further use. Max dose 6mg/24hr
– 2mg IV then 0.5mg q6 until cumulative dose of 4mg
over 24hr

17. Acute treatment cont’d
• Corticosteriods
– Patients who cannot tolerate NSAIDs, or failed NSAID/colchicine
therapy
– Daily doses of prednisone 40-60mg a day for 3-5 days then
taper 1-2 weeks
– Improvement seen in 12-24hr
• Intra-articular injection with steroids
– Beneficial in patient with one or two large joints affected
– Good option for elderly patient with renal or PUD or other illness
– Triamcinolone 10-40mg or Dexamethasone 2-10mg alone or in
combination with Lidocaine

18. Chronic gout drugs (preventive)
• Allopurinol- MoA – inhibit xanthine
oxidase, decrease conversion of xanthine
to uric acid .
• Febuxostat- inhibit xanthine oxidase
• Probenecid (uricosuric drug )- inhibit
reabsortion of uric acid in PCT.

19. Non- Pharmacologic Treatments
• Immobilization of Joint
• Ice Packs
• Abstinence of Alcohol
– Consumption can increase serum urate levels by
increasing uric acid . When used in excess it can be
converted to lactic acid which inhibits uric acid
excretion in the kidney
• Dietary modification
– Low carbohydrates
– Decrease in dietary purine-meat and seafood
– Dairy and vegetables do not seem to affect uric acid

20. Newer Therapies
• Uricase
– Enzyme that oxidizes uric acid to a more soluble form
– Natural Uricase from Aspergillus flavus and Candida utilis under
investigation
• Febuxostat
– New class of Xanthine Oxidase inhibitor
– More selective than allopurinol
– Little dependence on renal excretion
• Losartan
• Fenofibrate

21. Complications
• Renal Failure
– ARF can be caused by
hyperuricemia, chronic
urate nephropathy
• Nephrolithiasis
• Joint deformity
• Recurrent Gout

22. Pseudo gout