You are on page 1of 56

Gouty Arthritis

Diagnosis and Treatment


dr Budi Liem, M.Med
Subbagian Reumatologi
Bagian Penyakit Dalam
FK Universitas Kristen Maranatha
RS Immanuel

DEFINITION OF GOUT
An acute arthritis caused by the
inflammatory response to
monosodium urate crystals in the
joint.
Neutrophils phagocytose the crystals
and degranulate. The enzymes
released cause the clinical
manifestations of
inflammation.

Epidemiology
mean age of onset
incidence (age 32-64)

men
49
2.8%

women
60
1.5%

the lower incidence and later onset of gout in women


is attributed to more efficient urate excretion
attack before the age of 30 is rare and suggest a
genetic metabolic disorder

Pathophysiology
Gout is caused by disorders of purine
metabolism resulting in elevated levels of
uric acid
> 7 mg/dl in men
> 6 mg/dl in women

prolonged hyperuricemia leads to


formation of monosodium urate
monohydrate crystals

The 4 stages of gout


Asymptomatic hyperuricemic (but many
hyperuricemic people do not develop
gout)
Acute gouty arthritis (the usual
presentation)
Intercritical gout (variable symptom-free
periods between acute attacks may last
weeks or years)
Chronic tophaceous gout.

Serum Urate Level


any sudden change in serum urate
concentration can provoke an acute gouty
attack
sudden increase favors formation of new
crystals
sudden decrease promotes shedding of
previously formed crystals from the synovial
membrane

Serum Urate Level


during a gouty attack, serum urate levels
are normal in about 20% of cases
repeat blood tests eventually detect
hyperuricemia

Manifestations of Hyperuricemia
subcutaneous tophaceous deposits
urolithiasis
nephrolithiasis
renal diseases involving the tubules,
interstitium, or glomeruli

CLASSIFICATION OF HYPERURICEMIA
OVERPRODUCTION (METABOLIC)
(10%)
PRIMARY
SECONDARY
RENAL UNDEREXCRETION (90%)
PRIMARY
SECONDARY

OVERPRODUCTION
PRIMARY
1. IDIOPATHIC
2. SPECIFIC ENZYME DEFECTS

(<1% of Primary Gout)


a. PRPP synthetase overactivity
b. Partial deficiency of HGPRTase
c. Complete deficiency of HGPRTase

OVERPRODUCTION cont.

SECONDARY
INCREASED NUCLEIC ACID TURNOVER
a. Lymphoproliferative or myeloproliferative
disorders or their chemotherapy
b. Chronic hemolysis
c. Psoriasis

Underexcretion (Renal Handling of urate)


PRIMARY
1. Idiopathic
SECONDARY
1. Acute or chronic renal failure
2. Volume depletion
3. Altered renal tubular handling of uric
acid due to drugs, volume status or
endogenous metabolic products

A. Filtration
B. Reabsorption
C. Secretion

Underexcretion- Filtration

Almost 100% urate is filtered.


Decreased filtration causes
increased serum uric acid such as
in:
Renal failure
Volume depletion

Underexcretion- Reabsorption
Increased reabsorption causes increased
serum uric acid as in:
Volume depletion

Decreased reabsorption causes decreased


uric acid = uricosuria.
Medications which cause uricosuria are:
Probenecid
Sulfinpyrazone
High-dose salicylate

Underexcretion- Secretion
Decreased secretion causes increased
serum uric acid.
Conditions which contribute to this:
Diuretic therapy
Low-dose salicylate therapy
Lactic acid
Ketoacidosis
Ethanol

Acute gouty arthritis.


Acute onset of severely painful arthritis usually
in lower extremities. Often early attacks in 1st
MTP joint (podagra). May be precipitated by
trauma, surgery or major medical illness,
alcohol ingestion, or systemic infections. Initial
attacks self-limited but may become chronic.
Synovial fluid is inflammatory with needleshaped monosodium urate crystals with strong
negative birefringence.

1. Arthritis (Joint

inflammation):
redness
warmth
tenderness
swelling
2. Surrounding soft tissue
inflammation

Source: WebPath

Gouty arthritis results from deposition of sodium urate crystals in


joints. The joint most often affected is the first MP joint (big toe) as
seen here. Acute attacks are characterized by severe pain, swelling,
and erythema of the joint.

Chronic tophaceous gout.

If untreated, mono- sodium urate may


deposit in cartilage, tendons, bursae, soft
tissue and synovium in deposits called
tophi. These are commonly found in
olecranon bursae, Achilles tendon, around
joints and ear. May extrude white pasty
material and can limit joint mobility.

Chronic tophaceous gout


persistent gout chronic tophaceous
gout produces tophi,
solid deposits of of monosodium urate
crystals
form in the joints, cartilage, bones,
and elsewhere in the body.
develop on average about 10 years
after the onset

Gouty tophi project from the fingers as rubbery nodules. Below:


A section from a tophus shows extracellular masses of urate
crystals with accompanying foreign body giant cells.

What are the typical


laboratory findings in gout?

1. Inflammatory synovial fluid


a. Cloudy
b. 20,000 to 100, 000 WBC/mm
c. Predominately PMN
2. Monosodium urate crystals in synovial fluid
a. Needle-shaped
b. Strong, negative birefringence with
compensated polarized light
3. Serum uric acid is elevated at some time in almost
all
patients. However it is NOT
DIAGNOSTIC.
4. Urine uric acid >750 to 1000 mg/day suggests
overproduction of uric acid.
5. May have leukocytosis, high ESR, increased Creactive protein during acute attack.

If synovial fluid is aspirated from a patient with gout, the


fluid can be examined for
the presence of sodium urate crystals, which are seen here
to be needle shaped.

Differential Diagnosis
Septic Arthritis
Septic and gouty arthritis present with
many of the same signs and symptoms
fever and monoarthritis

Beware: both septic and gouty arthritis


may present in the same joint

What are the typical radiographic


findings in gout?

1. Soft tissue swelling during

acute attack.
2. Soft tissue density if tophi

are present.
3. Oval bone erosions with
overhanging edge
is
classic abnormality.

Chronic gout leads to deposion of urates into a chalky mass known


as a "tophus". Such tophi can destroy the joint and adjacent bone as
seen in these sequential radiographs of the same foot.

Treatment

Acute Gout
(1) Nonsteroidal antiinflammatory drugs
(2) Corticosteroids if resistant to NSAID
and colchicine, of if they are contraindicated
(3) Colchicine generally outmoded for
acute attack. Often used as maintenance
antiinflammatory agent
(4)Allopurinol and uricosuric drugs are of
no benefit in acute gout and may make acute
attack more difficult to control.

Treatment of Acute gouty arthritis


Colchicine-- inhibits neutrophil activation,
effective, less frequently because of its side
effects.
Colchicine -- 0.5-mg dose every hour until :
improvement, GI adverse effects (abdominal
pain, diarrhea, and nausea), or a total of 10
doses without relief.

Treatment of Acute gouty arthritis


Indomethacin and other NSAID -- drugs of
choice
NSAIDs -a 7-10 day course or until 3-4 days
after all signs of inflammation have resolved.
Use NSAIDs with caution -- in edematous
states, such as heart failure, peptic ulcer
disease or renal insufficiency.

Treatment of Chronic Gouty


Arthritis
The choice of urate-lowering medications:
uricosuric drugs (which promote uric
acid excretion)
xanthine oxidase inhibitors (which
inhibit uric acid production).

Treatment of Chronic Gouty


Arthritis
uricosuric drug
Probenecid, benzbromazone
inhibits the tubular reabsorption of
filtered and secreted urate, thereby
increasing urate excretion.

Treatment of Chronic Gouty


Arthritis
Allopurinol is competitive inhibitors of
the enzyme xanthine oxidase
Treatment principle: lower the plasma
urate concentration to such a degree, as
to allow urate to be resorbed from the
surface of the tophi.

Treatment of Chronic Gouty


Arthritis
The ideal candidates for allopurinol treatment
are
uric acid overproducers
renal insufficiency
nephrolithiasis
tophaceous gout
at risk for developing uric acid nephropathy

Treatment of Chronic Gouty


Arthritis
allopurinol can be used in almost any
hyperuricemic state
the usual maintenance dose for adults is
between 200 and 300 mg/d
long half-life of oxypurinol makes once
daily dosing possible.

Treatment of Chronic Gouty


Arthritis
skin rash may proceed into severe
hypersensitivity reactions
patients who develop a skin rash should
discontinue allopurinol.
hepatotoxicity, bone marrow depression,
and interstitial nephritis are rare but
serious adverse effects of allopurinol.

Treatment of Tophi
Colchicine and most NSAIDs, while
controlling acute attacks, will not
prevent the formation of tophi and may,
by preventing the inflammatory
response, actually increase the
development of tophi unless
hyperuricemia is controlled at the same
time.

Treatment of Tophi
allopurinol is the treatment of choice.
dose of allopurinol serum uric acid
response checked after 3 months
adjust the dose (allopurinol 300mg
tablet)
treatment will be life-long
at the start of therapy acute attacks may
occur

Treatment of Tophi
The concomittant use of a NSAID or a
prophylactic dose of colchicine for the
first month of treatment with allopurinol
is therefore recommended
allopurinol should likewise not be
started within 1 month of an acute
attack of gout, as it may precipitate
another attack

Treatment of Tophi
The activity of allopurinol and
uricosurics is additive
when administered concomitantly,
smaller doses of each drug can be used
Combined use of the 2 types of drugs is
especially effective in the presence of
tophaceous deposits.

Treatment of Tophi
Dose of allopurinol
adult dose: initially 100mg daily in a
single dose
maintenance: 100-300mg daily is usually
adequate
maximum 900 mg/day in divided doses
renal impairment: low dose of
allopurinol (50mg daily)

Treatment of Tophi
Surgery is rarely used to treat gout.
Surgical indication: draining, infected,
or are interfering with the movement of
your joints
It is sometimes necessary to replace
joints.

Treatment of Tophi
non-drug methods
encourage controlled weight loss
avoidance of alcohol, salicylates and
food which may trigger an acute attack

Prognosis of Gout
Current therapy permits most patients
to live a normal life if the disease is
diagnosed early and medical advice is
followed.
Complications include urolithiasis,
urinary tract obstruction and infection,
with secondary tubulointerstitial disease.

You might also like