Charcot’s Joint

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Introduction

Charcot’s Joint (aka Charcot’s osteoarthropathy or Charcot’s neuroarthropathy) is most commonly seen as a complication of diabetes, but is also sometimes seen with syphilis. It is the result of peripheral neuropathy.

It results in swelling, redness and pain, typically the ankle, and sometimes involving other joints of the feet.

It can cause gross structural deformities, skin ulceration and may result in lower limb amputation. The onset of often insidious, and diagnosis frequently missed. It may be mistaken for cellulitis, gout or DVT or any other cause of lower limb pain, welling and redness.

It was first described by French Physician Jean Martin Charcot in around 1880.

It is a medical emergency. Delay to diagnosis and misdiagnosis can significantly impact the outcome.

Epidemiology

  • Estimates vary widely, from 0.1% – 13% of patients with diabetes
  • Frequently misdiagnosed
    • Delay in diagnosis often leads to much worse prognosis

Presentation

  • Usually a history of diabetes, with established peripheral neuropathy
  • Pain (75%)
  • Swelling of the foot
  • Redness
  • Increased skin temperature

It may be difficult to differentiate from osteomyelitis both clinically and radiologically.

Charcot Arthopathy Presentation in left foot
Charcot Arthopathy Presentation in left foot

Pathophysiology

  • Monoarthritis
  • This is a neuropathic arthropathy
  • it is a progressive degeneration of a weight bearing joint – usually in the ankle. There is usually bone destruction, remodelling and resorption, with ultimately results in deformity
    • Initially acute inflammation, which subsequently leads to fracture of the bone, joint instability +/- dislocation, and ultimately causing large deformities
  • Usually gradual slow onset
  • Can also result in ulceration – usually due to severe deformity causing abrasions of the skin against footwear which develop into ulcers

It is believed that loss of proprioception due to peripheral neuropathy induces recurrent micro trauma at the affected joint. This damage is not noticed, due to another effect of peripheral neuropathy: loss of sensation. It is also believed that the microvascular effects of diabetes lead to alteration of blood flow to the damaged foot (increased blood flow: hyperaemia) which causes increased osteoclast activity, thus further weakening the bone and contributing to bony destruction.

In syphilis, the knee is atypical affected.

Staging

  • Stage – 0
    • No x-ray changes, but signs of inflammation may be apparent on MRi or bone scan
  • Fragmentation stage
    • Bony fragments are apparent on x-ray as bones break down
    • Often there is joint disruption with bony fragments around joints
  • Coalescence
    • The bony fragments may coalesce and attempt to heal

Investigation

If the diagnosis is a possibility, consider:

  • X-ray
    • May miss early disease
    • May show fractures or other bone deformities in later disease
  • MRI
    • Can detect early disease
    • Often shows bone marrow oedema, as well as bone deformities
  • Bone scan
    • Can also detect early disease
    • Shows up areas of rapid bone turnover (i.e. inflammation in this instance)
Charcot arthropathy X-ray
Charcot arthropathy X-ray

Management

  • Treatment is limited; early identification allows for modifications to minimise deformity
    • If diagnosed in Stage 0 the risk of long-term deformity and future ulceration is very low
  • Non-weight bearing
    • Usually for several weeks, with gradual introduction of weight bearing as the inflammation settles
  • Strict diabetic control
  • Total contact casting (TCC)
    • A type of cast that completely covers the foot and the lower leg
    • It redistributes weight from the foot into the leg, allowing the foot to heal
    • After a period of weight bearing, patients can mobilise with their TCC
    • It may take up to 9 months for symptoms to settle, the average healing time is about 2-3 months
  • In the long term, after the inflammatory process has settled, any deformity may require the use of custom made footwear, to redistribute weight in a similar manner to the TCC
  • Amputation may be required in severe cases where there is complete bony destruction of the foot and severe ulceration

References

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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