CRYSTAL-INDUCED

ARTHRITIS
GOUTY ARTHRITIS

CRYSTAL-INDUCED ARTHRITIS
A variety of crystals can deposit in and around
joints and cause an acute inflammatory arthritis ,
as well as a more chronic arthritis associated with
progressive joint damage.
Crystals can be the primary pathogenic agent, as in gout,
or an accessory factor, as in calcium pyrophosphate
deposition disease, in which crystals are deposited in
joints that are already abnormal.
Examples :
Monosodium urate monohydrate -Acute gout
-Chronic trophaceous gout
Calcium pryophosphate- Acute pseudogout
-Chronic (pyrophosphate) arthropathy
Basic calcium phosphates- Calcific periarthritis, Calcinosis

GOUTY ARTHRITIS
Inflammatory
disease
caused
by
deposition of monosodium urate
monohydrate crystals in and around
synovial joints.
Most common inflammatory arthritis
in men and in older women.
Risk increases with age and associated
with serum uric acid levels.
HYPERURICAEMIA GOUT

PURINE METABOLISM REVIEW

CLINICAL MANIFESTATIONS
Gout progresses through several clinical
phases, namely:
Acute gout
Intercritical gout- periods between
attack when patient is asymptomatic
Chronic gout

ACUTE GOUT
Rapid onset, reaching maximum severity in 2-6 hours,
and often waking the patient in the early morning
Severe pain
Extreme tenderness
Marked swelling with overlying red, shiny skin
Self-limiting, monoarticular over 5-14 days, with
complete resolution
+ fever, malaise, skin desquamation
Joints commonly affected:

1st MTP joint

Instep
Ankle joint
Knee joint
Wrist joint
Elbow joint
Finger joint

CHRONIC GOUT

acid crystal
deposition
subcutaneousl
y.

Polyarticular arthritis and the formation of tophi.

Sites of tophi: 1. Digits of the hands and feet
2. Pinna of the ear
3. Around elbows and knees
4. Achilles tendon
Chronic pain and joint damage, and occasionally
severe deformity and functional impairment
Tophaceous disease likely to occur in:
a) Polyarticular
b) Serum urate level > 9mg/dL (535mmol/L)
c) Younger age at disease onset (<40years)

TYPICAL GOUT VS. ELDERLY

ONSET

COMPLICATIONS

Severe degenerative
arthritis

Secondary infections

COMPLICATIONS

Urate
nephropathy

Urate
nephrolithia
sis

DIAGNOSTIC CRITERIA
Two of the following criteria are required for a clinical
diagnosis:
1. Presence of a clear history of at least two attacks of a
painful joint swelling with complete resolution within 2
weeks.
2. A clear history or observation of podagra
3. A presence of a tophus
4. Rapid response to colchicine within 48hours of starting
treatment
.A definitive diagnosis can be made if crystals of
monosodium urate are seen in the synovial fluid or in
the tissues.

INVESTIGATIONS

JOINT ASPIRATION & URATE

CRYSTAL IDENTIFICATION

X-RAY

MANAGEMENT
Weigh reduction- to achieve ideal BMI
Restriction of alcohol intake/elimination
Reduce intake of purine-rich food (adjunct
to medication only)
Control of co-morbidities
Contributing factors eg. Thiazide/loop
diuretics, low dose aspirin may be
discontinued or substituted, if appropriate

MANAGEMENT OF AN ACUTE GOUTY

ARTHRITIS

INITIATION WITHIN 24 HOURS OF

ONSET
If on allopurinol, continue without
interruption
NSAIDsAny except aspirin; diclofenac, indomethacin,
ketoprofen. **PUD, HTN, renal impairment,
cardiac failure
COX-2 inhibitor- alternative to NSAID if
contraindicated or those requiring prolonged
NSAID; etoricoxib

MANAGEMENT OF AN ACUTE
GOUTY ARTHRITIS

COLCHICINE

Inhibits mitosis and neutrophils motility and activity,

leading to a net anti-inflammatory effect.
Slower onset of action
Alternative to both.
Side effects: nausea, vomiting, abdominal pain, profuse
diarrhoea.**renal/hepatic dysfunction, elderly

GLUCOCORTICOIDS
intraarticular injection/ intramuscular /oral.
Use in elderly and
in those all above is contraindicated.

MANAGEMENT OF CHRONIC GOUT

MANAGEMENT OF CHRONIC GOUT:

Urate Lowering Therapy
ALLOPURINOL- Xanthine Oxidase Inhibitor
More superior than probenecid
Primarily excreted by kidneys, thus need renal adjustment
Only start after acute attack is resolved, may prolong
attack/lead to rebound flares if started during attack.
Start 2 weeks after attack is well-controlled
Can use with colchine initially to reduce frequency of
attacks.
ADR: rash, bone marrow suppression, aplastic anemia,
agranulocytosis, granulomatous hepatitis and jaundice

MANAGEMENT OF CHRONIC
GOUT: Urate Lowering Therapy
PROBENECID
An alternative to allopurinol in patients with NORMAL
RENAL FUNCTION
RP before commencing
SE: GI disturbance,
hypersensitivity rash

SURGERY

-excision to remove the tophi