Gout presentation lecture jsmu

2. GOUT
DR. SHAFIQUE REHMAN ARAIN
Head Department of Rheumatology
Medical Ward-6
JPMC/JSMU

3. GOUT
Gout is a form of inflammatory
arthritis triggered by the
crystallization of uric acid within the
joints.

4. GOUT
The disease is associated with important
medical conditions including
The insulin resistance syndrome,
Hypertension,
Nephropathy,
Alcohol abuse,
Disorders associated with increased
cell turnover.

5. GOUT
Gout is a common metabolic disorder,
typically presenting as an acute
monoarthritis, most commonly of the 1st
metatarso-phalangeal joint.
The underlying basis for gout is an
increased total urate pool.
This is generally manifest as
hyperuricemia, which is defined as a
serum urate level > 6.8 mg/dl.

6. EPIDEMIOLOGY
Gout occurs predominantly among men
and postmenopausal women.
Peak age of onset is 5th decade.
The disease rarely occurs in men before
adolescence or in women before
menopause.

7. EPIDEMIOLOGY
The prevalence is approximately 2.7%.
The prevalence rises with advancing age,
Reaching a level of 9% in men older than
80 years of age, and 6% in women.

8. NATURAL HISTORY
Hyperuricemia can result from,
Increased urate production.
Decreased uric acid excretion by the
kidneys.
Combination of both.

11. PATHOGENESIS
Hyperuricemia, define as a serum urate level
of >6.8 mg/dl.
When individuals are hyperuricemic,
conditions exist such that urate crystal can
precipitate in and around joint tissue.

12. PATHOGENESIS
Without intervention crystal precipitation
continues forming larger and larger
aggregates of crystals, termed “tophi”.
An attack of acute gout follows the
ingestion of urate crystals by monocytes
and synoviocytes.

13. CLINICAL FEATURES
Natural history of gout can be divided into
three distinct stages.
Asymptomatic Hyperuricemia.
Acute and intermittent gout.
Chronic tophaceous gout.

16. CLINICAL FEATURES CONT….
Most un-treated cases of gout progress to
chronic tophaceous gout.
The course varies from one patient to
another.
Some pts experience only one or two
attacks during their life time.

17. ACUTE GOUT
Initial episode usually follows 10-30 yrs
of asymptomatic hyperuricemia.
Some pts experience prodromal episodes
of mild discomfort.
Rapid onset of severe pain, associated
with,
Warmth.
Swelling.
Erythema of the affected joint.

18. ACUTE GOUT CONT….
Pain escalated to its intense level over an 8-10
hour period.
Initial attacks usually affect only one joint.
Other joints frequently involved in the early
stage of gout include,
Midfoot.
Ankle.
Heel.
Knee.

19. ACUTE GOUT CONT….
The intensity of pain is such that pt cannot
stand even the weight of a bed sheet.
Most find it difficult or impossible to walk
when lower extremities are involved.
May be accompanied by,
Fever.
Chills.
Malaise.

20. ACUTE GOUT CONT….
Cutaneous erythema associated with attack may
extend beyond the involved joint and resemble
cellulitis.
Desquamation of skin may occur.
Symptoms resolves quickly with appropriate Tx.
Untreated acute attacks resolves spontaneously
over 1-2 weeks.
Patient enter into the “intercritical period”.

21. INTERCRITICAL PERIOD
Involved joints are free of symptoms.
Despite this, monosodium urate crystals
deposition continues and tophi increase in size.
Erosive changes indicative of bony tophi begin to
appear on x-ray.

23. CHRONIC GOUT
Usually develops after 10 yrs of acute
intermittent gout.
The involved joints are now persistently
uncomfortable and may be swollen.
Pt report stiffness.
Involved joint are persistently
uncomfortable and may be swollen.
Visible or palpable tophi may be detected
on examination.

24. LABORATORY FINDINGS
Leukocytosis.
High ESR.
Raised CRP.
Serum Uric Acid levels >6.8 mg/dl.

25. SYNOVIAL FLUID ANALYSIS
• During an acute attack synovial fluid shows
high leukocyte count ranges b/w 2000–80000.
• Definitive diagnosis is made by examination of
fluid with polarized light microscopy.
• Identifying the characteristics monosodium
urate crystals.

26. MONOSODIUM URATE CRYSTALS

27. IMAGNIG
• Normal x-ray at early stage.
• Soft tissue swelling in the involved joint
in acute gout.
• Advanced disease may show erosions
called overhanging edge.

30. COMPLICATIONS
• Destructive arthropathy.
• Nephrolithiasis.
• Renal failure.

31. TREATMENT
Management includes,
Providing rapid and safe pain relief.
Preventing further attacks.
Preventing formation of tophi and
destructive arthritis.
Addressing associated medical
conditions.

32. TREATMENT CONT….
The aim of treating the acute gout attack is to
eliminate the pain and other symptoms caused
by the intense inflammation as rapidly as
possible.
The choice in this situation include,
NSAIDs.
Colchicine.
Glucocorticoids.

33. NSAIDs
NSAIDs have become the most frequently
used agents to treat gout.
Selective NSAIDs should be started at its
recommended maximal dose.
NSAIDs should be avoided with active or
recent peptic ulcer disease.

34. CHOLCHICINE
Effective but less well tolerated then
NSAIDs.

35. GLUCOCORTICOIDS
Usually reserved for pts in whom colchicine
or NSAIDs are contraindicated or ineffective.
Usual dose is 20-40 mg/day.

36. PROPHYLAXIS
The goal of treatment is to maintain the
serum urate level at 6.0 mg/dl.
Xanthine oxidase inhibitor Allopurinol is
the agent of choice.
Used in pts with tophi, nephrolithiasis
and renal insufficiency.

37. PROPHYLAXIS CONT….
Febuxostat is also potent xanthine oxidase
inhibitor.
It has certain benefits compared with
Allopurinol,
Metabolized in Kidneys,
Used in liver insufficiency.

38. KEY POINTS
 Gout is due to deposition of urate crystals in joints
leading to inflammation.
 Diagnosis is by history and polarized microscopy of
synovial fluid.
 High serum uric acid does not mean the patient has
Gout.
 Gout is one of the most treatable arthritis.
 Treat acute attack and then consider prophylaxis of
future episodes.
 If untreated, can develop into chronic tophaceous Gout.

39. THANKS