The differential diagnosis of a unilaterally swollen lower limb is broad. It is important to reach a positive diagnosis so that appropriate treatment is offered—particularly where the integrity of the limb is threatened by delay in treatment. Deep vein thrombosis, ankle sprain, cellulitis or simple fracture are all possible diagnoses, but the finding of metatarsal fractures is key in ensuring that an acute (Charcot) neuroarthropathic joint is considered.

Jean-Marie Charcot described the neuroarthropathic joint in syphilis in 1883. In 1936, Jordan described similar changes as a 'neuritic manifestation [of] diabetes mellitus'. The (Charcot) neuroarthropathic joint of diabetes is now recognized as a potentially devastating late complication that affects 1 in 700 patients, though this is probably an underestimate.

The pathophysiology of neuroarthropathy is imperfectly understood but involves synergistic abnormalities of both the joints and vascular supply of the limb.

• Sensorimotor neuropathy in the affected limb is universal. Proprioceptive loss puts abnormal stresses through joints made lax by motor neuropathy. Inappropriate signalling of pain means that chronic low-grade trauma is under-recognized.

• Glycation of connective tissues may reduce flexibility of the foot and also induce abnormal stresses through small joints.

• Autonomic neuropathy causes abnormal shunting of blood resulting in osteopaenia, bounding foot pulses and inadequate resolution of chronic minor trauma.

• These factors increase the risk of low-trauma fracture and impair normal healing. The consequences of a minor fracture can then be potentially devastating: instability, further fracture, subluxation/dislocation of the tarsus/ankle, permanent deformity, plantar ulceration, infection and amputation are all recognized.

A long history of diabetes (usually >15 years) and profound peripheral neuropathy are universal, though pain is often a feature of acute neuroarthropathy. In a non-ulcerated foot, the diagnosis is frequently missed on first presentation and late diagnosis can be responsible for permanent disability. A high index of suspicion is needed. Plain X-ray may demonstrate only minimal changes of osteopaenia or loss of joint space. Vascular calcification is a frequent finding, but is not specific to neuroarthropathy. A stress fracture may be invisible on plain X-ray and a careful history, supported by bone scintigraphy or magnetic resonance imaging (MRI), may be needed. Resorption of phalanges, subluxation/ dislocation, bone fragmentation and sclerosis are characteristic late changes of neuro-arthropathy, but can be indistinguishable from changes associated with osteomyelitis. If there is ulceration/infection, then bone scintigraphy and MRI are often unhelpful in differentiating between neuroarthropathy and osteomyelitis. In this case it is pragmatic to treat both—though using a bisphosphonate would be unusual.

There are three potential treatments for the non-infected, acutely neuroarthropathic foot: offloading, bisphosphonates and surgery (Figure 44.1).


If acute neuroarthropathy is suspected, the limb should be promptly offloaded and immobilized. This will usually require a removable, non-weight-bearing cast with crutches/ wheelchair for mobility. This limits further disruption of the architecture of the foot and allows healing to commence. This is the mainstay of treatment and may require immobilization for many weeks or months until there is radiological evidence of stabilization and repair and the foot is cool.

Once the initial episode has resolved, considerable care should be taken to find appropriate footwear. Residual deformity should be accommodated in bespoke orthotic footwear. Where there is no or minimal residual deformity, precautions should be taken to protect the neuropathic foot from future trauma.


The objective, clinical evidence of benefit from bisphosphonates is modest. One prospective, randomized study of 39 patients has been published.1 This studied the effects of 90 mg pamidronate or placebo on clinical and biochemical measures of activity in a 'hot' neuroarthropathic foot. Symptom score, foot temperature and markers of bone turnover were lower in the foot treated with pamidronate during the initial weeks of treatment, though longer-term outcomes were not different between the two groups. Bisphosphonates are now used as adjunctive treatment. Oral bisphosphonates are likely to take the place of intravenous bisphosphonates.


There are many small studies of primary surgical treatment—particularly where the ankle is involved or there has been substantial subluxation/dislocation at the talo-navicular joint or of the whole tarso-metatarsal complex (the Lisfranc dislocation). Surgery should generally be avoided in the acute phase, unless late presentation means that limb salvage cannot be achieved in any other way.2 Surgery also has a role in selected patients following resolution of the acute episode. Collapse of the arch can cause deformities such as a 'rocker-bottom' foot or medial bony protuberance, which may cause skin ulceration due to abnormal pressure loading. Surgical intervention to realign the affected joint can be helpful, but usually only if there is no associated infection.

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