The document discusses crystal deposition disorders affecting joints, primarily focusing on gout and pseudogout. It outlines the causes, clinical features, diagnostic methods, and treatment options for both conditions, emphasizing the differences between them in terms of joint involvement and crystal types. Additionally, it highlights the importance of understanding hyperuricemia and its role in gout pathogenesis, as well as the treatment strategies for managing acute and chronic symptoms.

1. ORTHOPAEDICS NOTES
CRYSTAL DEPOSITION DISORDERS
Crystal deposition disorders around joints, bursae or tendons.

2. Outlines
• Gout
• Pseudogout (Calcium Pyrophosphate Dihydrate Arthropathy, CPPD)
• Calcium hydroxyapatite (HA) deposition disorder

3. GOUT

4. Introduction
• A disorder of purine metabolism
• Characterized by:
• Hyperuricemia
• Deposition of monosodium urate monohydrate crystals in joints and periarticular
tissues
• Recurrent attacks of acute synovitis
• Late changes:
• Cartilage degeneration
• Renal dysfunction
• Uric acid urolithiasis

5. Pathology
Hyperuricemia
• Serum urate concentration
which is significantly higher
than that of the population to
which they belong.

6. Gout
• Urate crystals are deposited in minute clumps in connective tissue (articular
cartilage – commonly small joints of the hands and feet)
• Remain inert until local trauma  the crystals dispersed into the joints and
surrounding tissues  acute inflammatory reactions
• The urate may deposits in periarticular tissues, tendons, bursae, joints as
‘tophi’ (chalky materials in appearance). Common sites:
• Metatarsophalangeal joints of the big toes
• Achilles tendons
• Olecranon bursae
• Pinnae of the ears

7. Classification
• Primary vs Secondary
Primary Gout Secondary Gout
Epidemiology 95% 5%
Etiology • No obvious cause
• Under-excretion of urate
• Over-production of urate
• Prolonged hyperuricemia d/t
acquired disorders (eg
myeloproliferative disease,
diuretics administration, renal
failure)

8. Clinical Features
Risk factors of hyperuricemia

9. Acute Attack
• Signs and symptoms:
• Sudden onset of severe joint pain for weeks – may be precipitated by local
trauma, operation, intercurrent illness, unaccustomed exercise, alcohol
consumption
• Skin redness, shiny, swelling
• Tender, warm joints
• Common sites: (usually >1 site)
• Metatarsophalangeal joints of the big toes
• Ankle
• Finger joints
• Olecranon bursa
• Uric acid level may be normal! (hyperuricemia is not diagnostic)
• So, examine the synovial fluid by using polarizing microscopy:
• Negatively birefringent urate crystals (needle-like shape)

10. Chronic gout
• Polyarticular
• Joint erosion  chronic pain, stiffness, deformity (may be mistakenly as RA)
• Tophi (may ulcerate through the skin with chalky discharge)
• Renal lesions
• Calculi: due to uric acid deposition
• Parenchymal disease: due to monosodium urate deposition from the blood

11. Imaging
Acute attack
Soft-tissue swelling
Chronic gout
Joint space narrowing
Secondary OA
Tophi appeared as ‘punched-out cyst’ or deep
erosions in the para-articular bone ends
Bone destruction (may resembles neoplastic
disease)
X-rays

12. Differential Diagnoses
• Infections
• Cellulitis
• Septic bursitis
• Infected bunion
• Septic arthritis
• Reiter’s disease
• Pseudogout
• Rheumatoid arthritis

13. Treatment
Acute attack
Joint resting, ice-
pack
NSAIDs or oral
corticosteroid in pt
who unable to
tolerate NSAIDs
Cholcicine – SE:
Nausea, vomiting,
diarrhoea
Corticosteroid
intra-articular
injection – for
tense joint effusion

14. Losing weight Cutting alcohols Eliminate diuretics
Urate-lowering drug therapy –
recurrent attacks, tophi, renal
complication, do not start
before acute attack symptoms
subside (may prolong or
precipitate acute attck)
Uricosuric drugs
(probenecid,
sulfinpyrazone) – if no
renal complication
Xanthine oxidase
inhibitor (allopurinol) –
preferred in pt with
renal complication +
chronic tophaceous
gout allopurinol
Interval therapy
Surgery
• In ulcerating tophi

15. PSEUDOGOUT
(Calcium Pyrophosphate Dihydrate Arthropathy, CPPD)

16. Introduction
• Encompasses 3 overlapping conditions:
• Chondrocalcinosis – the appearance of calcific material in articular cartilage and
menisci
• Pseudogout – crystal-induced synovitis
• Chronic pyrophosphate arthropathy – a type of degenerative joint disease

17. Pathogenesis
• Rises with increasing age
• W = M
• Family history
• Pyrophosphate is probably generated in abnormal cartilage by enzyme
activity at chondrocyte surfaces  combines with calcium ions in the matrix
where crystal nucleation occurs on collagen fibres  crystals grow into
microscopic ‘tophi’, which appear as nests of amorphous material in the
cartilage matrix.
• CPPD crystals are extruded into the joints  inflammatory reactions

18. Clinical Features
Asymptomatic chondrocalcinosis
• Elderly
• Calcification of the menisci, usually asymptomatic
• If seen <50y, suggest the possibility of underlying metabolic disease or familial disorder.
Acute synovitis (pseudogout)
• Middle-aged women
• Acute pain and swelling in large joints – usually the knee
• Sometimes attack is precipitated by minor illness or operation
• Tense, inflamed joint but not as acute as gout
• Lasts for few weeks, subsides spontaneously
• X-rays: Chondrocalcinosis
• Synovial fluid aspiration: positive biferingent crystals

19. Chronic pyrophosphate arthropathy
• Elderly women
• Polyarticular OA affecting large joints (hip, knees)
• Pain, stiffness, swelling, joint crepitus, loss of movement
• Often diagnosed as ‘generalized OA’

20. Imaging
X-rays
• Intra-articular & peri-articular calcification
• Knees, wrists, shoulders, hips, pubic symphysis, intervertebral discs
• Less common sites: joint synovium, capsules, ligaments, tendon, bursae
• Bilateral, symmetrical
• In articular cartilage: appeared as thin line parallel to the joint
• In fibrocartilagenous menisci and discs: appeared cloudy, irregular opacities
• Degenerative arthritis in distinctive sites
• Same as osteoarthritis BUT in distinctive uncommon sites – in non-weightbearing
joints
• Eg: isolated patellofemoral compartment, talonavicular joint
• Loose bodies might be seen as well

21. Treatment
Pseudogout
• Treatment is the same as acute gout – rest, high dose anti-inflammatory
therapy
• Joint aspiration & intra-articular steroid – in elderly to reduce the side effects
of NSAIDs
Chronic chondrocalcinosis
• Irreversible but few symptoms
• Treat as advanced OA

22. Gout vs Pseudogout
Gout Pseudogout
Joint involvement Smaller joints Larger joints
Pain Intense Moderate
Joint characteristic Inflammed Swollen
Typical
characteristic
Hyperuricemia Chondrocalcinosis
Synovial fluid Uric acid crystals
(negative birefringent crystals,
needle-like shape)
Calcium pyrophosphate crystals
(positive brefringent crystals,
rhomboid-shaped)