Charcot Arthropathy: A Case Study

Charcot foot is a well-documented complication of diabetic neuropathy. The mechanism of this is not fully understood but two theories exist – namely, the neurovascular and neurotraumatic theories. In the neurovascular theory, an underlying autonomic neuropathy leads to hypervascularity, osteolytic changes and demineralization. However, the neurotraumatic hypothesis indicates that unperceived trauma to an insensate extremity leads to continued bony destruction on ambulation, which worsens and progresses. These theories imply that a sufficient time frame is required for established Charcot foot destruction to develop.

Typical progression of Charcot foot occurs over months to years, although rare acute onsets have been reported. However, the progression seen in our patient, from normal X-Ray appearances to established, acute Charcot foot with considerable mid-foot destruction over a period of just 10 days is a rarely described progression of Charcot arthropathy. The combination of local skin warmth with decreased sensation in the left foot and feeling of a bony lump on the left arch raised the suspicion of a bone tumor, but X-Rays as well as CT Scan of the foot beside the uncontrolled diabetes in this patient made Charcot foot a more possible diagnosis.

Early recognition of Charcot Arthropathy is a mandatory to ensure improved outcomes. It is important to differentiate between acute Charcot foot, infection and bone tumors through clinical investigations as well as patient medical history. The presence of ulcers should raise the suspicion of infection or osteomyelitis, and therefore, the importance of early imaging cannot be overstated. Modestly raised inflammatory markers (CRP-68) in this diabetic patient along with left foot deformities suggest an acute Charcot foot than an infectious process. The latter frequently presents with high laboratory values.

The initial management of the patient was fixation with a total contact leg cast, followed by open reduction and internal fixation (ORIF) with locking plates, combined with lengthening of Achilles tendon to permit full dorsiflexion and subsequent re-casting.

Due to osteodegenerative nature of CN, all attempts at pharmacological treatment have focused on anti-osteoporotic drugs so we started the patient on an Alindronate beside a more strict control of his diabetes. His post-operative progress was satisfactory and he is currently non-weight bearing for 6 months post-ORIF.