Gout is a form of inflammatory arthritis caused by crystallization of uric acid in the joints. It is associated with conditions like hypertension, alcohol abuse, and disorders with increased cell turnover. Gout typically presents as an acute monoarthritis of the big toe. The underlying cause is hyperuricemia, defined as a serum urate level over 6.8 mg/dl. Gout occurs more in men and postmenopausal women, with prevalence rising with age to 9% in men over 80 years old. Acute gout causes sudden severe pain, swelling and redness in one joint. Without treatment, it can progress to chronic tophaceous gout with persistent joint discomfort and visible urate deposits called to

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