charcot arthropathy

Charcot Arthropathy Mansoura 2nd International DF Training Course

Charcot Arthropathy.

Hanan El-Soutouhy Gawish.Prof Int Med, Diabetes Unit,Mansoura

UniversityInternational Working Group of Diabetic Foot

Egypt Representative


History

Mitchell,1831: The first association between joints and neurological diseases.

Charcot 1868: Arthropathy and tabes dorsalis.

Jordan 1936: Neuritic manifestation of DM


Charcot’s Foot A Neuropathic Arthropathy

Caused by repetitive trauma in the setting of:

• Diminished sensation & proprioception• Motor neuropathy results in muscle

imbalance & abnormal weight bearing.• “Rocker Bottom Deformity” a convex deformity of the foot’s plantar

aspect caused by the collapse of metatarsal bones


http://bjsm.bmjjournals.com/content/vol37/issue1/images/large/sm022279.f9.jpeg


Aetiopathogenesis

Peripheral sensory neuropathy is always present +/- motor.

Autonomic neuropathy leads to increased blood flow.( plethysmography & uptake of isotopes).

Trauma may be an important precipitating factor, although 2/3rd of patients don’t remember any injury.

Bone metabolism both osteoblastic and osteoclastic activities are increased.


Epidemiology

Incidence : 0.1 – 0.5 % . Increased in patients with neuropathy.Common in the 4th or 5th decades of life.Bilateral in 30 % of patients. Sex difference : NoType 1 or type 2: Both are at risk.Majority: in the mid foot but any bone or

joint in the foot or ankle can be affected.


Clinical Features and Diagnosis

Acute Charcot Warm, inflamed and swollen. Misdiagnosed as cellulitis, osteomyelitis or

inflammatory arthropathy as gouty or septic.Although sensory neuropathy, pain is

common feature followed by discomfort.Diagnosis by exclusion as investigations in

early stages are negative.



High index of suspicion is necessary so that appropriate treatment is immediately instituted to prevent severe deformity!



Chronic Charcot, may be months, painless, without temperature difference and deformed.

Reactivation by further trauma is frequent.Patients are at high risk of ulceration and

amputation, so long term follow up is recommended.


Investigations

X-ray : Early; absent or subtle finding. Late; bone and joint destruction, fragmentation.

Tc bisphosphonate bone scan: Increased bone uptake.

In labeled leucocytes scan to differentiate from osteomyelitis.

MRI: Bone marrow oedema is the earliest sign.


Treatment

1. Immobilization

2. Radiotherapy and Ultrasound.

3. Pharmacological Treatment.

4. Surgical Treatment.


Treatment

1. Immobilization:

Total Contact Cast (TCC), Removable Cast Walker (RCW).


Removable Cast Walker


Treatment

1. Immobilization:

Almost 16 weeks (3-6 months) but may be more. (temp gradient less than 1 on 2 occasions or radiology).


Treatment

2. Radiotherapy and Ultrasound:

May be useful in conjunction to offloading but only few small studies.


Treatment

3. Pharmacological Treatment.

Pilot study first using pamidronate,1994. Other Bisphosphonates were used to decrease

disease activity and bone turnover markers. Calcitonin were also used. Given for 12 weeks or till temp gradient is less than

2 on 2 consecutive visits.


Treatment

4. Surgical treatment: No role in acute. Later may be to remove bony deformities or

constructive surgeries to achieve a stable shape. Techniques include; Arthrodesis, exostectomies, reconstruction and Achilles tendon lengthening.


Conclusion

High degree of suspicion to diagnose acute Charcot arthropathy.

High risk categorization.Immobilization and Bisphosphonate.


Thank You

charcot arthropathy

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