Teaching Case

A 56-year-old male with a history of type 2 Diabetes Mellitus presented to our institution with a painless “mass” in the left foot, associated with local swollenness, developing in the previous 2 months.

For radiological evaluation, Left Foot Radiographs and MRI were requested.

Left Foot Radiographs revealed articular bone erosions/destruction and joint distension and dislocation involving the tarsometatarsal joints (Fig. 1).

Left Foot MRI confirmed the abovementioned radiographic findings and revealed extensive bone marrow oedema involving the midfoot and metatarsals, as well as inflammatory changes in the surrounding soft tissues, including a necroinflammatory collection; the plantar subcutaneous tissue was preserved and there was no ulcer or other signs of infection. (Fig. 2).

In the context of the patient’s Diabetes Mellitus, these Imaging findings suggested Charcot neuroarthropathy of the foot.

Charcot neuroarthropathy represents a spectrum of severely destructive osteoarticular processes associated with neurosensory deficit. [1] The most common cause of Charcot neuroarthropathy worldwide is Diabetes Mellitus; other common causes are tabes dorsalis, syringomyelia and spinal cord injury. The main pathophysiology hypothesis suggests that Charcot neuroarthropathy results from progressive inflammatory damage after a minor injury, in the context of absence of normal protective sensory feedback. [2]

One of the segments most commonly affected by Charcot neuroarthropathy is the foot, which classically occurs in the setting of Diabetes Mellitus. [1]

Charcot neuroarthropathy of the foot manifests as distortion of the articular architecture with deformity of the foot, which can lead to recurrent ulceration, cellulitis, osteomyelitis and, ultimately, amputation [2]; these features are characteristically painless [3]. Lisfranc joint is the most frequently affected joint in Charcot neuroarthropathy; involvement of the second toe with subluxation results in collapse of the foot’s longitudinal arch with “rocker-bottom” deformity, leading to increased load bearing on the cuboid and predisposing to the abovementioned consequences. [4]

Charcot neuroarthropathy may present in an atrophic - the most frequent - or a hypertrophic pattern. Both variants share joint disorganization and effusion as common Imaging features; the atrophic pattern is distinctively characterized by severe bone reabsorption and absence of/ minimal osteosclerosis, osteophytosis and bony debris; the hypertrophic pattern is distinctively characterized by osteosclerosis, osteophytosis and bony debris and absence of/ minimal bone reabsorption. [1]

Radiography is usually the first Imaging modality performed for the evaluation of Charcot neuroarthropathy, allowing overall assessment of the abovementioned imaging features. [4]

MRI plays a complementary role and allows a more sensible assessment and the detection of potential complications such as osteomyelitis and soft tissue infection. T1-weighted images reveal decreased signal intensity in the involved segments. In the initial stages, T2-weighted images depict increased signal intensity in the involved bones due to bone marrow oedema, initially in subarticular locations. In later stages, loss of demarcation of cortical outline and cortical destruction will be present. [3,4] Contrast material intravenous administration is used to better evaluate sinus tracts, abscesses, devitalized tissues, and joint or tendon involvement.

CT may be used in later-stage Charcot neuroarthropathy for better visualization of bony proliferation or for surgical planning and follow-up of immobilisation therapy. [3]

Radiologists should be familiar with the radiologic spectrum of Charcot neuroarthropathy of the foot, in order to ensure a prompt and timely diagnosis, so that the devastating consequences of a late diagnosis may be avoided. [2]

Written informed patient consent for publication has been obtained.