Charcot Foot

Charcot neuro osteoarthropathy is a progressive, destructive disorder of bones and joints of the foot in patients with peripheral neuropathy. Diabetes is the commonest cause. Others are alcohol related neuropathy, syphilis, syringomyelia, leprosy, spinal cord injury and renal failure. It affects about 0.1 to 0.4% of people with diabetes, and up to 13% of those with severe neuropathy, usually after 10 or more years of disease.

Mechanisms: loss of protective sensation leaves repetitive microtrauma unnoticed, and autonomic neuropathy increases bone blood flow, which promotes inflammatory bone resorption through RANKL-driven osteoclast activity. Stages (Eichenholtz):

• 0: prodromal swelling with normal radiographs
• 1: development, with fragmentation and dislocation
• 2: coalescence, with absorption of debris
• 3: reconstruction, with consolidation and deformity

The midfoot (tarsometatarsal and naviculocuneiform) is involved in about 60%. The result is rocker bottom deformity, a plantar ulcer, infection and amputation. The contralateral foot is affected in 25 to 30%.

• A hot, swollen, mildly painful or painless foot in a neuropathic patient, often after minor trauma
• Skin temperature over 2 degrees Celsius higher than the contralateral foot
• Bounding pulses (distinguishing from ischemia), erythema, effusion, and later a rocker bottom deformity with a plantar ulcer
• Loss of protective sensation (10 g monofilament)
• Red flags: an open ulcer with a probe reaching bone, fever, rapid progression and spreading erythema, suggesting osteomyelitis

• Clinical diagnosis by temperature difference and neuropathy.
• Weight bearing radiographs: fragmentation, subluxation, bone debris, and loss of the arch (lateral talo first metatarsal angle reversed).
• MRI (stage 0 bone marrow edema, or to separate osteomyelitis from Charcot).
• Laboratory tests: white cell count, CRP, ESR (over 70 mm/h suggests osteomyelitis) and glucose control.
• Probe-to-bone test and bone biopsy with culture when osteomyelitis is suspected.
• Nuclear imaging (labelled white cell scan) when MRI is inconclusive.

Differentials: cellulitis, osteomyelitis, gout, acute deep vein thrombosis, rheumatoid arthritis, acute fracture.

• Immobilization and offloading: a non-removable total contact cast changed weekly for the first 4 weeks, then every 1 to 2 weeks, with crutches or a wheelchair to prevent weight bearing in the acute phase.
• Continue immobilization until the temperature difference is under 2 degrees Celsius at two consecutive visits and radiographs show consolidation, typically 8 to 12 weeks (up to 6 months for severe cases).
• Transition: a removable cast walker for 4 to 8 weeks, then custom depth shoes with rigid rocker soles and custom insoles, or a Charcot restraint orthotic walker for severe deformity, for life.
• Glycemic control (HbA1c under 7.5%), vitamin D replacement (cholecalciferol 1000 to 2000 IU orally daily if deficient) and smoking cessation. Bisphosphonates have no proven benefit.
• Ulcer and infection: debridement, offloading, culture guided antibiotics for 6 weeks for osteomyelitis (selected by bone culture), and vascular assessment.
• Surgery for unstable deformity, non-plantigrade foot, recurrent ulcer or infection: exostectomy for a plantar prominence, Achilles tendon lengthening or gastrocnemius recession for equinus, and reconstructive arthrodesis with beams, plates or a circular external fixator. Prophylactic cefazolin 2 g IV before incision. Postoperative non-weight-bearing for 8 to 12 weeks.
• Complications: non-union, hardware failure, infection, amputation (the risk is higher with ulcer and osteomyelitis).

Follow up every 1 to 2 weeks during casting, then every 3 months with daily foot checks by the patient. Counsel on foot protection and early reporting of heat and swelling.