5% population

Risk factors

• increasing age

  • after \~ 50yo risk double every decade

• Prior joint injury / sugery

• histoyr of gout

  • 20% with CPPD also hyperuricaemia

  • 25% of these develop gout

• Family history

  • present younger age

  • more likely have polyarticular involvement

• History of endocrine/metabolic condition

  • haemachromatosis

  • primary hyperparathyroidism

  • hypophosphatasia

  • hypomagnesaemia

• association between CPPD and OA complex

Clincal presentation

• can be asymptomatic - changes seen on XR incidentally

• may present similar to other forms of arthritis

• CPPD may also coexist with gout, OA and joint infection

• deposition of crystals results in infalammatory reaction

• may also present with:

  • nec pain

  • headahce

  • fever

  • occur up to 50%

• often affects large joints

• polyarticular in 2/3 patients

• asymmetric pattern

Clinical syndromes

asymptomatic

• incidental XR

• no apparent clinical consequence

• although many have history of joint symptoms

Acute CPP crystal arthritis

• acute onset of painful swollen joint(s)

• self limiting synovitis

• compared to gout:

  • more ommon in knee compared to MTPJ

  • less painful

  • slower to reach peak intensity

  • slower to resolve even with sympotmatic treatment

    • 3/12

OA with CPPD

• occurs in a joint with pre-existing degenerative changes

• OA and CPPD isloated conditions

  • often involve knee

  • but CPPD with OA

    • pain more intense

    • tendnerss

    • systemic symptoms

    • atypical distribution

      • doesn’t usually involve wrist, elbow, shoulder, ankle alone

Chronic CPP cystal inflammatory arthritis

• symmetrical distrivution to affected joints

• younger \<50yo

Chondrocalcinosis

• calcification of articular cartilage ID on XR

• usually caused by CPPD

• reserved fro decibing radiologic changes of cartilage calcification compared to clinical situation

History

• number/site of affected joints

• speed of onset and severity of pain

• presence of systemic symptoms

• acute injury

• past history of pain, truama, surgery

• histoyr of recent severe illness or surgery (especially parathyroidectomy)

  • rapid decrease in serum calcium which may ppt. attack

• family history

• co-morbiditieis

  • haemochromatosis

  • parathyroid disease

investigations

exclude septic arthritis

• identification of CPP crystold from synovial fluid = gold standard

  • rectangular, square, rhoboid, rod shaped using polarised light microscopy

• bloods

  • FBC

  • CRP

  • urate

    • normal result reduces likelihood of gout

    • normal in some patients with acute gout

    • Cr and electrolytes

• if \<55yo underlying metabolic disease

  • hypomagnesemia

  • hyperparathryoidism

  • haemochromatosis

• XR

  • may help

  • chondrocacinosis

    • linear or puctate calcification of hyaline and fibrocartilage

  • Knees, wrists, AP view of pelvis

Treatment

• no effective treatment to lower CPPD

• Acute attack

  • Ice/cool packs

  • rest

  • joint aspiration

  • oral NSAIDS

  • low dose cochicine

    • 0.5mg up to 3-4times daily

    • optional loading dose =- 1mg

    • 0.5 od or bd may be effective in reducing number of attacks iwth frequent recurent episdoes

  • corticosteroids