GOUTY ARTHRITIS,

Dr.T.Upendra, ortho
 GOUT

Defenition

• Gout is a hereditary condition of disturbed uric acid

metabolism in which urate salts gets deposited in articular,

periarticular and subcutaneous tissues.

• Also know as RICH MAN diseases.

• Also know as PODAGRA

• Clinically it is characterised by reccurring attacks
of acute arthritis by interval of freedom from pain
&
• In late stages by deforming arthritis, nephritis,
urinary calculi.
Predisposing factors:
• Alcohol abuse
• High consumption of Red meat
&Beans
• Obesity
• Diabetes
• Hypertension
• Hyperlipidemia
• Chronic inflammatory diseases
• Long term use of diuretics or aspirin
• Hyper parathyroidism
• Myeloprolifrative disorders
Etiology
• Idiopathic
• Hereditory :family members have hyperuricemia without
gout .

• Race : Whites> Blacks

• Sex : Males >Females

• Age :2nd to 4th decade common at 40years.

• Adrenal cortex isufficiency: an adequate amount of
coticosteroids counteracts the gouty attack.

• Disturbed electrolyte equilibrium: Marked diuresis that

preceeds acute attacks of gout.
 Purine nucleotides

hypoxanthine

xanthine
Xanthine oxidase
Uric acid

Urinary Alimentary Tissue deposition in

excretion excretion excess

Urate crystal microtophi

Phagocytosis with acute

inflammation and arthritis
7
Dr.Sandeep Agrawal,Agrasen Hospital,Gondia M S
Pathology
• Sodium urate is deposited as crystals on
the surface of articular cartilage.

• Then articular cartilage is eroded

• The subchondral bone is replaced by
crystaline deposit.(tophii)

• A pannus of granulation tissue grows

over the articular surface, invades and
replaces the cartilage .

• Then granulation tissue bridges the joint

to the opposite articular surface and
producing fibrous ankylosis
Microscopically
The deposites are
surronded by an
inflamatory
reaction,fibrous tissue
and giant cells
Common sites
Smaller joints:
First metatarsophalyngeal
joints
Interphalyngeal joints of
foot
Interphalyngeal joints of
the hands
Knee joint
Elbow joint
 Classification

• Primary gout (95%)

• Secondary gout (5%)

 Primary gout
• Common type (95%)
• Idiopathic
• Due to under excretion or overproduction of
monosodium urate (MSU).
 Secondary gout
• Comprises 5%
• Prolonged hyperuricaemia
• Administration of diuretics
• Renal failure
.
 Gout staging
• Typical sequence involves progression
through:

– Asymptomatic Hyperuricemia

– Acute gouty arthritis

– Interval or Intercritical gout

– Chronic or tophaceous gout

pathogenesis
Hyperuricaemia
⇩
May be asymptomatic
⇩
Deposition of monosodium urate crystals in
synovial tissue
(contain various Ig’s, complement,
fibrinogen, fibronectin)
⇩
Complement activated
⇩
Neutrophils phagocytose & lyse crystals
⇩
Release chemical mediators (e.g. TNF-α; IL-
1)
⇩
ACUTE GOUTYARTHRITIS
⇩
May resolve & become asymptomatic
(INTERCRITICAL GOUT)
 Recurrent episodes of Gout
⇩
Large deposits of chalky white
urate  tophi
⇩
Chronic granulomatous
inflammatory condition
⇩
Fibrosis of synovium
⇩
Erosion of articular cartilage
⇩
CHRONIC TOPHACEOUS
ARTHRITIS
⇩
ankylosis
⇩
Tophi may be deposited in soft
tissue
⇩
Can ulcerate if sub-cutaneous
 Clinical features
Acute gout:
 Precipitated by local trauma
unaccustomed excercise and alcohol
consumption
 Acute arthritis is the most common
manifestation
 Excruciating pain over hours
frequently nocturnal
 Swelling, redness and tenderness
 Monoarticular and lower
extremities(MetatarsoPhalyngeal
joint, ankle and knee).
• 1st MTP classicpresentation
• May affect knees, wrist, elbow,
and rarely SI and hips.
 Pain appears last,
disappears first
 Mimic septic arthritis,
cellulitis or
thromboplebitis
 Nocturnal attacks are
common.
• Attacks subside in 3 to 10
days.
• Recurrent attacks involve
more joints and usually
persist longer.
• Systemic reaction like
malaise,fever.
Intercritical gout:
• Asymptomatic period
between crises
• Duration varies, but
untreated patients may have
a second episode within two
years.
• Some patients evolve to
chronic polyarticular gout
without pain free
intercritical episodes.
Chronic tophaceus Gout:
• The clinical characteristic is the
deposition of solid urate in the
connective tissue.
• It is associated with early age of
onset

• long duration of untreated disease

• upper extremity involvement
• polyarticular disease and elevated
serum uric acid
• Cyclosporine and/or diuretics
increased risk for tophaceus gout
Most common sites for tophi

• olecranon,

• prepatellar bursa,

• ulnar surface

• Achilles tendon.
• Arthrocentesis:
Daignosis
Polarising Microscopy showing
Monosodium urate (MSU) : needle-shaped
negatively birefringent either free floating
or within neutrophils & macrophages.
Joint Fluid analysis:
Acute gout=
• Inflammatory (>2000 cells/ml);
• Monosodium urate (MSU) crystals do not
exclude the possibility of septic arthritis,
for this reason it is also recommended to
request a Gram smear.
Serum Uric Acid:
• Normal = 4.0 to 8.6 mg/dl in men
= 3.0 to 5.9 mg/dl in women.
• Urinary levels are normal below 750 mg/ 24h.

• Urinary levels above 750 mg/dl in 24h in gout

• > 1100 mg/dl in asymptomatic hyperuricemia
(indicates urate overproduction.)
24 urine collection for uric acid determination :

•Assessing the risk of renal stones and planning

for therapy.(uric acid stones=nephrolithiasis)
 Radiological examination
• To exclude other kinds
of arthritis.
• Tophi
• Normal mineralization
• Asymmetric polyarticular
distribution
• Juxta-articular bony erosion
associated with periarticular
tophi
• subchondral erosions with
overhanging bony edges .
 Differential Diagnosis of gout
Acute Gout:
• Septic arthritis.
• Pseudogout (calcium pyrophosphate crystals)
• Reactive arthritis.
• Acute rheumatic fever
• Other crystalline arthropathies.
Chronic tophaceus gout:
• Rheumatoid Arthritis
• Pseudogout
Treatment for gout
 Non pharmacological treatment

Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS

Non-drug Management:

Stop alcohol weight loss

Dietary changes
Stop diuretics

31
Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS
 Dietary advices:

Avoid:

Beer

Red meat/sea food.

32
Dr.Sandeep Agrawal,Agrasen Hospital,Gondia MS
 Pharmacotherapy
Uricosurics
• Non steroidal anti
• Probenecid,
inflamatory drugs
(NSAID’S) • Sulfinpyrazone.
• Colchicine,
• Corticosteroids Synthesis inhibitor
• Allopurinol,
• Febuxostat .
 Purine nucleotides

hypoxanthine Allopurinol
xanthine Xanthine
oxidase
Oxypurinol
Uric acid

Urinary Alimentary Tissue deposition in

excretion excretion excess

Urate crystal microtophi

uricosurics
Phagocytosis
colchicine with acute
NSAID
inflammation 34
Dr.Sandeep Agrawal,Agrasen Hospital,Gondia M S
and
For acute attack
• Absolute bed rest,
• Ice packs,
• Avoidance of alcohol
• Tab. Colchicine 0.5 mg 3rd hrly followed by maintenance dose of
0.5 – 1 mg/day. It has significant GI toxicity and delayed onset of
action.

• Tab.Phenylbutazone 200mg TDS for colchicine resistant patient

• Alternatively oral Prednisolone 20-40mg/day is also effective

For chronic gout,
Allopurinol
The first choice of drug in chronic gout started
with 100mg OD and gradually increased upto
300mg/day,

Febuxostat
It is a recently introduced nonpurine xanthain
oxidase inhibitor dosage is 40-80mg/day, it has
hepatotoxic side effect hence pt followed up with
liver function test.
• Intra-articular corticosteroids.

• Surgical treatment
Excision of gout trophy.

Arthrodesis of the joint in functional position,

Removal of lesion adjacent to the joint preserves joint
function.