Dr.Angelo Smith M.D
WHPL

"Be temperate in wine, in
eating, girls, and sloth, or the
Gout will seize you and
plague you…"
-- Franklin

 History:
 Galen (129-199 AD), an ex-gladiatorial
surgeon in the Pergamon arena in Asia
Minor who moved to Rome, described gout
as a discharge of the four humors of the
body in unbalanced amounts into the joints
(hence gout = gutta, a drop).
 The first radiological description of gout
was made by Huber in 1896, a few months
after Röentgen described the x-ray.

 Monosodium urate
 Calcium pyrophosphate dihydratte
 Hydroxyapatite
 Corticosteroid esters
 Calcium oxalate

GOUT (monosodium
urate)
PSEUDOGOUT (calcium
pyrophosphate)
HYDROXYAPATITE

 Inflammatory arthritis mediated by the
crystallization of uric acid within joints, tophi
 Often associated with hyperuricemia
 Incidence: 62.3 /100,000 (2-fold increase)
 Associations: DM, HTN, metabolic syndrome,
obesity, CVD, renal stones, CPPD
 Risk Factors: genetics, age, CRF, serum uric
acid, diet, alcohol, medications

Uric Acid
Balance

 Uric acid: overproduction vs.
underexcretion
 Mechanisms of urate “production”
 cellular nucleoproteins/nucleotides (~ 66%)
 diet (~33%)
 Mechanisms of urate excretion
 kidney (~66%)
 gut (~33%)

 Completely filtered by the glomerulus
 Completely (essentially) reabsorbed in the
proximal tubule
 Approximately 50% is secreted back into the
tubule in the descending loop
 Approximately 80% (of the 50% now in the
loop) is reabsorbed in the ascending loop
 Net excretion = 10% of filtered load

 Hyperuricemia alone does NOT make a
diagnosis of gout
-only a subset of people with hyperuricemia will
develop gout
-probability of gout increases with higher uric
acid levels
 Asymptomatic hyperuricemia generally
requires no treatment

 Hyperuricemia (>7.0 mg/dl) in 5% - 8% of
male population.
 Most (about ⅔) are forever asymptomatic.
 80% of gouty patients have uric acid < 9
mg/dl.
 Above 10 mg/dl, risk rises rapidly.
 Gout is the most common cause of
monarthritis in middle-aged and elderly men
(8% yearly prevalence).

 Lymphomas (esp. Hodgkin’s disease)
 Myeloproliferative disorders
 Diabetes
 Psoriasis
 Sarcoid
 Glycogen storage disease

 Urate precipitation leads to acute gouty
arthritis
 Local factors – temperature, pH, trauma, joint
hydration
 Systemic factors – hydration state, fevers, meds,
alcohol, co-morbid conditions
 Attack resolves spontaneously 10-15 days

 Lasts several days to several weeks.
 May spread from joint to joint.
 Often accompanied by fever,
leukocytosis.
 Gets worse as the years go on.
 Pain appears last, disappears first.
 Petite attacks occur (lasting hours).

 ACUTE GOUT
 First attack 4th-6th decade for men
 Women almost always postmenopausal
 Classically monoarticular LE– podagra
(50%), (vs pseudopodogra) >ankle
>gonagra >upper extremity.
 Proximal joint, central arthropathy
uncommon

 MSU
 CPPD
 Hydroxyapatite
 Septic
 Psoriatic, Reiter’s
 Rheumatoid

 Evidence-based medicine based on EULAR
(ESCISIT) – 10 key points
 Acute attack 6-12 peak intensity with S/W/E/T
 Aspiration always recommended if possible
 Prompt polarized microscopic analysis performed
 Definitive Dx – requires crystal confirmation
 Gout and Sepsis can coexist – fluid should be sent Gram’s
stain, culture
 Serum uric acid levels neither confirm nor exclude gout
 Radiographs not necessary
 Risk factor assessment

 Hyperuricemia
 biochemical hallmark of gout, but not by itself
diagnostic for gout
 Leukocytosis
 Increased ESR
 Synovial Fluid
 leukocyte counts = septic arthritis
 viscosity is < septic or inflammatory arthritis
 MSU needle - like intracellular & extracellular
crystals
 Negatively birefringent crystals under polarized light
microscopy

 THERAPY (for all crystal diseases):
 Corticosteroids: intrarticular > systemic
 NSAIDs – fast acting full dose if no
contraindications
 Colchicine (PO,IV route dangerous)
▪ narrow therapeutic window
▪ Bone marrow suppression, myopathy, neuropathy
▪ purgative effects – “Pt often run before they walk”
 ACTH
 NEVER ALLOPURINOL

 70% prevelance of MSU crystals remain in the
joint
 Lasts months to years for 75-80%, 20% never
have another attack

 Lifestyle, dietary modification
 Diet high in vegetables, dairy, water
beneficial
 Initiate uric acid lowering therapy after 1(?)
or 2 episodes of acute gouty arthritis
 Always prophylaxis for first 6 months with
low dose steroids, NSAIDs, or colchicine

 USUALLY PRESENT AFTER 10YEARS OF
ACUTE INTERMITTANTGOUT
 TOPHI DEPOSITION
 CHRONIC SWOLLEN JOINTS
 JOINT DESTRUCTION
 ABSOLUTELY REQUIRES ALLOPURINOL

 Overhanging edges
 Punched out lesions with sclerotic borders.
 Preservation of joint space (till late)
 Degenerative changes

The “Double Contour Sign” of Gout.
Filippucci E, Grassi W
Department of Rheumatology, University of Ancona, Italy

 Gout
 hallux, ankle, knee, hand
 younger, male
 Pseudogout
 knee, wrist, ankle
 older, female
 Almost any joint can be affected by either
disease!

 Aging
 Previous joint surgery
 Previous joint trauma
 Familial types
 Gout
 Amyloidosis
 Hyperpara
 Hemochromatosis
 Hypomagnesemia
 Familial hypocalciuric
hypercalcemia
 Hypophosphatasia
 Wilson’s disease
 Ochronosis

CHONDROCALCINOSIS
 Acute arthritis caused by Calcium pyrophosphate
dihydrate (CPPD) crystal-induced inflammation
 May perfectly mimic gout during acute flare
 Attacks occurring before age 50 are uncommon
Clinical:
 Most often affects the knee and the wrists
Radiology:
 Calcification densities in hyaline or fibrocartilage,
which are found in knee menisci, acetabular labrum,
& TFCC

 Fluid analysis:
 CPPD crystals are visualized under compensated polarized
light microscopy
 crystals may be more difficult to detect than MSU crystals
because of their smaller size, more intralysosomal
location, & less brilliant colors
 CPPD crystals show weak positive birefringency and have
squared or rhomboidal shaped ends
 alizarin red stain, can confirm that these clumps are
masses of calcium crystals
Treatment:
 aspiration of the involved joint and steroid injection,
once diagnosis of infection has been excluded, will
usually control symptoms

 Hydroxyapatite
 Calcium carbonate
 Octacalcium phosphate
 Tricalcium phosphate (whitlockite)
 Hydroxyapatite is non-
birefringent.

 Acute monoarthritis (pseudopseudogout)
 Acute calcific tendinitis, bursitis
 Scleroderma, dermatomyositis
 Heterotopic calcification
 Milwaukee shoulder
 Crowned Dens Syndrome

 Is usually a peri-arthritis.
 Intense inflammation (looks septic)
 Synovial fluid often non-inflammatory.
 Often causes podagra (especially in
younger women).
 Look for the telltale calcifications on
radiographs.

 Severe, destructive shoulder arthropathy.
 Seen in elderly females with DJD of
shoulder.
 High-riding humeral head on radiographs
(large rotator cuff tear).
 Non-inflammatory fluid with BCP crystals.

 Is an association of acute cervical pain and
calcifications in the peri-odontoid space.
 This disease affects only adult females.
 Patients present with inflammatory signs,
can be treated with non-steroid anti-
inflammatory drugs and recover without
sequela.
 CPPD deposition can also lead to this
syndrome.
 Radiologically - crowned dens.