Charcot’s Foot

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Progressive and destructive condition almost always due to diabetes mellitus, but can occur in those with chronic alcoholism, syringomyelia, spina bifada, Hansen’s disease/leprosy, congenital insensitivity to pain, injuries to the peripheral nerves, meningomyelocele, tabes dorsalis. First described by Charcot in 1868 in tabes dorsalis.
It is characterised by progressive deterioration of weight bearing joint with pathological fractures and/or dislocations resulting in varying degrees of deformity and functional changes.

Prevalence varies, depending on sensitivity of method of diagnosis – varies from 0.15% to 30% (changes on bone scans). Prevalence depends on denominator population (eg community diabetes population or tertiary referral clinic population)

Bilateral in 5 to 40% of cases. No gender predilection.

Almost always has an underlying neurological deficit – many have history of trauma (patient may not recollect). Many have had poorly controlled diabetes for >15 years.

Two key theories have been advanced to explain the pathogenesis:
Neurotraumatic theory:
repeated trauma in those with neuropathy produces the joint destruction (gross or microscopic)  continued ambulation progressives the bone and joint destruction
does not explain all aspects of Charcot’s neuroarthropathy

Neurovascular theory:
increased peripheral blood flow (from autonomic neuropathy)  hyperaemic bone resorption  weakening of bone (osteopenia)

Probably a combination of both theories is responsible for pathogenesis.

Chuter & Payne (2001) showed a high correlation between the presence of midfoot Charcot’s and dysfunction of the plantar fascia. Also LJM of first MPJ

Tendo achilles tightness

Eichenholtz (1966) stages:
Stage 1 (stage of development) – acute destruction of joint; debris formation; capsular distension; ligamentous laxity; subluxation
Stage 2 (stage of coalescence) – absorption of debris; fusion of fragments to adjacent bone
Stage 3 (stage of reconstruction) – remodelling of bone ends and fragments

Acute stage – active or destructive phase of the disease
Chronic/quiescent stage – coalescence and reconstruction

Clinical features:
Early acute stages – usually unilateral, areas of erythema, increased skin temperature, bounding pulses, deformity, instability, often markedly swollen ( shoe fitting difficulty). Anhidrotic skin, due to presence of autonomic neuropathy. Ulcer may be present in areas of high pressure due to deformity. Local temperature of affected foot is elevated compared to contralateral limbs – generally 3-7 degrees difference (unless bilateral)
Usually have history of >10 years of diabetes (may have been poorly controlled); most aged 50-60 years, but can affect any age.
Usually have history of trauma, but may not recollect it due to neuropathy.
Neuropathy almost always present (absent LOPS, deep tendon reflexes, proprioception) – but pain and discomfort often is present (but not as much as would be expected given extent of tissue damage).
Often hypermobile in early stages
Up to 40% may have concurrent ulcer (problem with differentiating from osteomyelitis)
Progression of deformity over time

Differential diagnosis – osteomyelitis; cellulitis; deep vein thrombosis; arthritic process; pronated foot

Radiographic changes:
X-rays may initially be normal in the early acute phases.
Characterised as atrophic (tend to occur early) or hypertrophic (tend to occur late):
Atrophic changes – phalangeal “hour glassing”; metatarsal head osteolysis; ‘mortar and pestle’ deformities; aggressive osteolysis; osteopenia/bone loss
Hypertrophic changes – osteochondral fragmentation; intra-articular debris; marginal osteophytes; periosteal new bone formation; absorption of debris; ankylosis; healed fractures with callus formation
Other changes – soft tissue oedema; joint effusions; fractures, subluxations; deformity

Patterns of foot involvement:
Appears to be five characteristic patterns :

• seen in up to a third of those with CN
• on x-ray usually atrophic or osteolysis of metatarsophalangeal joints and destructive
• can mimic osteomyelitis; medial joints more commonly involved
• plantar ulcers common

most common pattern seen in foot
characterised by collapse of midfoot with a dorsiflexion and abduction deformity
first sign on x-ray is usually a lateral deviation of the base of the second metatarsal
creates the classic ‘rocker bottom’ foot; plantar ulcer common at apex of rocker in what was the medial longitudinal arch

Naviculocuneiform, talonavicular and calcaneocuboid joint:
• characterised by dislocation/disruption of these joints
• early findings are often subtle – osteolytic changes
• calcaneocuboid joint (if involved) can drop plantarly  ulceration

• occurs in 1-2%
characterised by avulsion fracture of posterior aspect of calcaneus

• in up to 10% of cases of CN; less common than other types
• results in severe deformity  may need amputation
• subtalar joint may be involved

Accurate diagnosis (differentiate from osteomyelitis)
Nonweightbearing (bed rest; crutches; wheelchair)
Immobilisation (cast, brace, posterior splint) – especially total contact casts (replaced weekly and skin temperature measured and compared to contralateral limb as guide to healing; continue to use casts until temperature normalised) – x-rays also used to monitor healing progress. Can be up to 4-6 months. Alternative to total contact cast is prefabricated pneumatic walking brace.
Bisphosphonates (inhibit osteoclastic activity) has been used in those with CN with a change in clinical outcomes, but improvements in biochemical markers
Protected ambulation following healing (therapeutic footwear; orthoses – especially total contact orthoses; patella tendon bearing brace)

When conservative care has failed.
Indicated if there is gross deformity, instability and destruction is progressive despite immobilisation. Surgical resection of a bony prominence (exostosis) causing ulcers in a healed CN is common indication.
Tendo achilles lengthening

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