GOUT:
DIAGNOSIS AND
MANAGEMENT
Gout
Metabolic disorder due to excessive
accumulation of uric acid in tissues
leading to acute and chronic arthritis
and soft tissue and bone deposition of
uric acid (tophi).
Acute Gouty Arthritis
Abrupt
75%
onset often at night
of initial attacks in first MTP
joint
Usually
monoarticular, may be
polyarticular
Attack
Na+
subsides in 3-10 days
urate crystals in synovial
fluid
Hyperuricemia
present
may or may not be
The victim goes to bed and sleeps
in good health. About 2 o’clock
in the morning he is awakened by
a severe pain in the great toe;
more rarely in the heel, ankle or
instep.
The pain is like that of a
dislocation, and yet the parts feel
as if cold water were poured over
them…Now it is a violent
stretching and tearing of the
ligaments – now it is a gnawing
pain, and now a pressure and
tightening.
So exquisite and lively
meanwhile is the feeling of the
part affected, that it cannot bear
the weight of the bedclothes nor
the jar of person walking in the
room. The night is spent in
torture.
- Thomas Sydenham (1624-1689)
QUESTION: Who gets gout?
ANSWER: Individuals with
prolonged hyperuricemia
So who gets hyperuricemia?
Hyperuricemia
Overproduction (10%)
(80 % idiopathic)
Ethanol
HGPRT or
G6PD
deficiency
PRPP synthetase
overactivity
Myeloproliferative
disorders
Hyperuricemia
Underexcretion (90%)
(80% idiopathic)
Renal
insufficiency
Drugs
and toxins
–Diuretics
–Ethanol
–Cyclosporine A
–Pyrazinamide
–Lead nephropathy
–Low dose aspirin
Ketosis
So who gets gout?
Young and middle-aged men
 Individuals with hypertension, obesity,renal
insufficiency, metabolic syndrome, organ
transplants
 Patients on diuretics
 Beer drinkers

Who doesn’t get gout?

Women
 Unless
 Post-menopausal
 Renal insufficiency
 Chronic diuretic use
 Myeloproliferative disorder
The prevalence of gout is
increasing
Patients with CHF and renal disease are
surviving longer
 Obesity/metabolic syndrome epidemic
 More organ transplants
 Less estrogen used
 Low dose aspirin use

GOUT: DIAGNOSIS




Presentation
Patient demographics
Physical findings
Differentiate from:
 Sepsis
 RA
 Spondyloarthropathy(psoriasis, reactive)
 Lyme
GOUT: DIAGNOSIS
Arthrocentesis and crystal identification
 Serum uric acid may be misleading and is
not a good diagnostic test for acute gout.

TREATMENT OF ACUTE GOUT
NSAIDS
 Intra-articular steroids
 Prednisone
 Colchicine
 PO – no fun
 IV – be careful (limited availability)

TREATMENT OF RECURRENT GOUT
PO daily low-dose colchicine
 Colchicine neuromypathy
 Lower serum uric acid level

TREATMENT OF HYPERURICEMIA:
INDICATIONS
Repeated or severe acute gout attacks
 Patient preference
 Tophaceous/erosive gout
 Chemotherapy of hematologic
malignancies
 Nephrolithiasis

Treatment of Hyperuricemia
Decrease uric acid production
 Allopurinol
 Febuxostat (Uloric)
 Uricosuric agents
 Probenecid
 Sulfinpyrazone

TREATMENT OF HYPERURICEMIA:
ALLOPURINOL/FEBUXOSTAT
Marked hyperuricemia
 Increased urinary uric acid excretion
 Tophaceous or erosive gout
 Renal insufficiency
 Nephrolithiasis

TREATMENT OF HYPERURICEMIA:
URICOSURICS
Low urinary uric acid excretion
 Mild renal insufficiency

(Probenecid, sulfinpyrazone)
TREATMENT PEARLS
Aspirin makes gout worse.
 Allopurinol/febuxostat is a treatment for
hyperuricemia and not acute gout.
 Giving allopurinol or febuxostat during an
acute attack will prolong the attack.
 Starting allopurinol/febuxostat may provoke
attacks.
 Therefore add colchicine for 6-12 mos.
