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Neuro-osteoarthropathy

Introduction
Aetiology
Treatment
Further reading
Neuro-osteoarthropathy

Neuro-osteoarthropathy should be suspected in any patient with neuropathy if

they present with a hot, red, and swollen foot; they should be referred
immediately to a specialist diabetic foot care team.

Differentiation from infection is important to ensure correct management.

The aim of treatment is to limit weight bearing with effective offloading and rest
in order to prevent severe deformity.

Introduction

Neuro-osteoarthropathy, also referred to as acute Charcot foot, is among the most devastating
complications of the foot in people with diabetes. It is a rare condition, which complicates diabetic
neuropathy. Acute Charcot usually presents with a hot, inflamed, swollen and sometimes painful
foot, with no break in the skin. Clear differentiation from infection is important to ensure appropriate
management; infection may be suggested by an increase in CRP or ESR.

Although the X-ray may be normal in the acute Charcot foot at presentation, there is often rapid
progression, with bone fragmentation and destruction of joints, accompanied by exuberant
periosteal reaction. On either plain X-ray or MRI, there are no clear differences between acute
Charcot and osteomyelitis, and it can be impossible to exclude infection if the skin is ulcerated.
Collapse of the medial longitudinal arch of the foot is common, leading to the typical 'rocker
bottom' deformity, under which large ulcers tend to form. Approximately one third of cases are
complicated by secondary ulceration.

Aetiology

The aetiology of this process is not clearly understood. However, the combination of neuropathy
and intact large arterial flow results in foot pulses that typically are easy to feel. Precipitating
trauma - such as a twisted ankle or trip - is often reported by the patient; it is increasingly thought
that the condition may be triggered by any earlier event that causes inflammation in the foot, such
as an ulcer, injury, surgery or infection. The process eventually becomes quiescent, although this
may not occur for 6-12 months or more; surface skin temperature is sometimes used to monitor its
activity. However, even if the inflammation settles, any deformity of the foot will remain.
Involvement of the ankle has a less-favourable prognosis because the damage may leave the joint
critically unstable. In 20- 30% cases, the other (unaffected) foot is at risk of becoming involved,
and should be watched carefully.

Treatment

Treatment is empirical and relies on rest and strict limitation of weight bearing, usually with total
contact casting. Removable casts and walkers have also been recommended. Although conclusive
evidence is still lacking, controlled trials have suggested that treatment with bisphosphonates may
be beneficial. There may also be a place for calcitonin, or calcium and Vitamin D, but this is not
established. The duration of non-weight bearing may be protracted, but is continued until the lack
of temperature difference between the two feet suggests that the inflammatory phase of the
disease has gone into remission, and the patient can slowly start to return to full weight bearing. A
small number of surgeons recommend operative stabilization in the acute phase, but surgery is
usually reserved for reconstruction once the acute process has subsided. Cases of suspected

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neuroosteoarthropathy require immediate specialized assessment and should always be referred

to a specialist diabetic foot service, as delay in treatment may lead to progressive and severe
deformities of the foot.

Further reading

Armstrong DG, Todd WF, Harkless LB, Bushman TR. The natural history of acute Charcot's
arthropathy in a diabetic foot specialty clinic. Diabet Med 1997; 14: 357-63.

Schon LC, Easley ME, Weinfeld SB. Charcot neuroarthropathy of the foot and ankle. Clin Orthop
1998; 349: 116-31.

Jude EB, Selby PL, Burgess J, Lilleystone P, Mawer EB, Page SR, Donohoe M, Foster AV,
Edmonds ME, Boulton AJ. Bisphosphonates in the treatment of Charcot neuroarthropathy: a
double-blind randomised controlled trial. Diabetologia 2001; 44: 2032-37.

Sanders LJ, Frykberg RG. Charcot neuroarthropathy of the foot. In: Levin ME, O'Neal LW, Bowker
JH, Pfeifer MA, eds. The Diabetic Foot, 6th edn. Mosby. St Louis, 2001: 439-65. Rajbhandari SM,
Jenkins RC, Davies C, Tesfaye S. Charcot neuroarthropathy in diabetes mellitus. Diabetologia
2002; 45: 1085-96.

Jeffcoate WJ. Vascular calcification and osteolysis in diabetic neuropathy - is RANK-L the missing
link? Diabetologia 2004; 47: 1488-92.

Jeffcoate WJ, Game F, Cavanagh PR. The role of proinflamatory cytokines in the cause of
neuropathic osteoarthropathy (acute Charcot foot) in diabetes. Lancet 2005; 366: 2058-61.

Bem R, Jirkovska A, Fejfarova V, Skibova J, Jude E. Intranasal calcitonin in the treatment of acute
Charcot neuro-osteoarthropathy. A randomized controlled trial. Diabetes Care 2006; 29: 1392-94.

Neuro-osteoarthropathy

Neuro-osteoarthropathy
24-year old female with a calcaneal fracture;
development of neuroosteoarthropathy
(Charcotfoot).

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Typical Charcot-foot; noninfectious destruction

of bone and joint associated with neuropathy

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