CRYSTAL ARTHRITIS Dr. Angelo Smith M.D WHPL
CRYSTAL ARTHRITISDr. Angelo Smith M.DWHPL
Ben Franklin (1706 -1790)
"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.
MAJOR ARTHRITOGENIC CRYSTALS
Monosodium urateCalcium pyrophosphate dihydratte
HydroxyapatiteCorticosteroid estersCalcium oxalate
CRYSTAL ARTHRITIS
GOUT (monosodium urate)
PSEUDOGOUT (calcium pyrophosphate)
HYDROXYAPATITE
GOUT
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
Gout: Pathophysiology
Uric acid: overproduction vs. underexcretion
Mechanisms of urate “production” cellular nucleoproteins/nucleotides (~ 66%) diet (~33%)
Mechanisms of urate excretion kidney (~66%) gut (~33%)
Renal Excretion of Uric Acid
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
Diet
Diet
Asymptomatic Hyperuricemia
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 – Preclinical Period
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).
Conditions AssociatedWith Hyperuricemia
Lymphomas (esp. Hodgkin’s disease) Myeloproliferative disorders Diabetes Psoriasis Sarcoid Glycogen storage disease
GOUT
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
A Typical Attack of Gout
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).
GOUT
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
Causes of Podagra
MSUCPPDHydroxyapatiteSepticPsoriatic, Reiter’sRheumatoid
Diagnosis
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
Laboratory
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
ACUTE GOUT
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
Intercritical Period
70% prevelance of MSU crystals remain in the joint
Lasts months to years for 75-80%, 20% never have another attack
Uric Acid Lowering Therapy
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
CHRONIC GOUT
USUALLY PRESENT AFTER 10 YEARS OF ACUTE INTERMITTANT GOUT
TOPHI DEPOSITION CHRONIC SWOLLEN JOINTS JOINT DESTRUCTION ABSOLUTELY REQUIRES
ALLOPURINOL
CHRONIC GOUT
Radiographic Hallmarks of Gout
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 vs. Pseudogout
Gout hallux, ankle, knee, hand younger, male
Pseudogout knee, wrist, ankle older, female
Almost any joint can be affected by either disease!
Clinical Associations with Psuedogout
Aging Previous joint surgery Previous joint trauma Familial types Gout Amyloidosis
Hyperpara Hemochromatosis Hypomagnesemia Familial
hypocalciuric hypercalcemia
Hypophosphatasia Wilson’s disease Ochronosis
PSEUDOGOUT
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
Laboratory
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
The Basic (Non-Acidic) Calcium Phosphates
HydroxyapatiteCalcium carbonateOctacalcium phosphateTricalcium phosphate (whitlockite)
Hydroxyapatite is non-birefringent.
Syndromes Associated with Hydroxyapatite
Acute monoarthritis (pseudopseudogout)
Acute calcific tendinitis, bursitis Scleroderma, dermatomyositis Heterotopic calcification Milwaukee shoulder Crowned Dens Syndrome
Acute Apatite Monoarthritis(Pseudopseudogout)
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.
Milwaukee Shoulder
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.
Crowned dens syndrome
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.