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Imaging of the Diabetic Foot


Jan Gielen ,

Universitair Ziekenhuis Antwerpen, Edegem; University of Antwerp, BE
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Leo Vael

Universitair Ziekenhuis Antwerpen, Edegem, BE
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Osteomyelitis in the diabetic foot is located in continuity with skin ulcers. The exact location of skin ulcers is essential to discriminate osteomyelitis per continuitatem from active Charcot osteoarthropathy.

How to Cite: Gielen J, Vael L. Imaging of the Diabetic Foot. Journal of the Belgian Society of Radiology. 2021;105(1):73. DOI:
  Published on 19 Nov 2021
 Accepted on 27 Sep 2021            Submitted on 15 Sep 2021

Presence and location of a skin ulcer is the most important consideration for the clinician and radiologist to determine whether a red-hot swollen foot is from acute Charcot neuro- osteoarthropathy or surinfection [1].

Diabetic foot ulcers result from peripheral neuropathy and ischemia (peripheral arterial disease) [2]. Surinfected foot ulcer is the most common antecedent to limb loss in diabetes [2, 5].

Direct inoculation by contiguous spread from a skin ulcer, accounts for most diabetic foot infections. Contrary to other patient groups, bone infection in diabetics rarely arises from hematogeneous spread, a foreign body or iatrogenic cause.

Diabetic foot ulcers, develop at pressure points, either from weight bearing or constrictive shoes in ambulatory patients, or at dorsal and lateral points of the externally rotated foot in bed ridden patients. In diabetic claw feet pressure points are located at the dorsal aspect of the proximal interphalangeal joint and the plantar aspect of the metatarsal head. In chronic Charcot, the foot is no longer warm and red. The related rocker bottom malformation is a specific site of pressure, with development of a neuropathic ulcer typically located at the plantar midfoot.

In early stages of osteomyelitis plain films may remain normal [2]. Computed Tomography (CT) and MRI can define osseous anatomy as well as small intraosseous abscesses and sinus tracts that are diagnostic for infection. Radionuclide imaging can be combined with morphologic imaging (most often CT) for a better accuracy. The most performed radionuclide tests in diabetic foot are Single-Photon Emission Computed Tomography (SPECT) and labeled leukocyte imaging. As both techniques are sensitive but not specific, SPECT can be used as a screening test or to facilitate localization of activity on labeled leukocyte imaging [2, 3, 4]. However, because of the high sensitivity and prevalence of positive results on SPECT, its value as a screening test is questionable, and investigations comparing labeled leukocyte imaging alone to labeled leukocyte plus SPECT, demonstrate only marginal improvement for the combined study [4]. There are few data available using Positron Emission Tomography (PET) [4].

MRI is thus the modality of choice in diabetic patients to rule out infection in the presence of an ulcer [2, 3]. MRI accurately demonstrates neuropathic ulcer complicated with cellulitis/osteomyelitis in chronic Charcot neuro-osteoarthropathy.

The most reliable way to diagnose osteomyelitis on Magnetic Resonance Imaging (MRI) is to track the ulcer or sinus tract to the underlying bone and evaluate for the presence of bone marrow edema (Figures 1 and 3) [1]. If no ulcer is present, a red swollen foot represents an acute Charcot neuro- osteoarthropathy (Figure 4). This is typically located periarticular at tarso-metatarsal and metatarsophalangeal joints. In these circumstances acute Charcot neuro-osteoarthropathy is a confident clinical diagnosis. Contrast medium uptake rate obtained at D-MRI represents a reproducible parameter that is reliable for predicting and monitoring treatment outcome in acute Charcot foot [6].

Figure 1 

MRI demonstration of osteomyelitis in a 48y old male with ulcus at the distal phalanx of the first toe.

Bone marrow edema (thick arrow) at the distal phalanx in continuity with the skin ulcer. Edema with low SI on T1, increased signal on T2 with FS and marked enhancement after intravenous gadolinium DTPA administration documented on T1 WI with FS and subtracted series. Neuropathic soft tissue edema with unenhancing increased SI area on T2 WI at the dorsum of the foot (thin arrow).

Edema related to cellulitis/osteomyelitis is evidenced by low signal intensity (SI) on T1-weighted imaging (WI) and high SI on T2-WI with spectral fat saturation; or enhancement after intravenous gadolinium administration (Figures 1 and 3) [1, 3], that is most accurately demonstrated on subtraction imaging.

Subtraction contrast-enhanced series are most sensitive in demonstrating devitalization, active bone remodeling, abscesses, sinus tracts and joint or tendon involvement related to infectious osteitis or osteomyelitis. DIXON chemical shift series are preferred over (Turbo) Spin-Echo series to reduce magnetic field inhomogeneities (Figure 4). Subtraction nulls the artifacts of magnetic field inhomogeneities at the extremities (Figures 1 and 2).

Figure 2 

Radiographic and MRI demonstration of osteomyelitis and Charcot neuro-osteo-arthropathy of the third toe in a 67y old male with marked sausage toe and skin ulcer located at the lateroplantar aspect of the DIP joint of the third toe.

MRI demonstration of bone marrow and soft tissue edema with marked enhancement after intraveneous gadolinium DTPA administration at the whole toe, at the metatarsal head (thick arrow), proximal, middle and distal phalanx. Fragmentation of the distal metatarsal head (thick arrow) and proximal phalanx with increased signal and enhancement related to Charcot neuro-osteoarthropathy. No continuity with the skin ulceration at this level. No enhancement of the neuropathic edema at the dorsal aspect of the midfoot (thin arrow).

Radiography shows general osteopenia of the phalanges of the third toe, erosion at the lateral aspect of the DIP joint and of the diaphysis of the phalanx media (thin arrow) in continuity with the skin ulcer related to osteomyelitis. Fragmentation without marked osteopenia of the bony structures at the MTP joint related to Charcot neuro-osteo-arthropathy (thick arrow).

Abnormally decreased SI on plain T1-WI is a more specific indicator of marrow edema related to osteomyelitis than increased SI on T2-WI alone that may indicate either osteitis or non-infectious reactive bone marrow changes (Figures 1 and 3) [1, 3].

Figure 3 

MRI demonstration of osteomyelitis in a 53y old male with skin ulcer at the plantar aspect of the heel. Probing demonstrates bone contact.

Sagittal T2 FS and T1 FS images after intravenous gadolinium DTPA administration show high SI respectively marked enhancement at the calcanear corticalis and spongious bone (arrow) in continuity with the ulcus.

Neuropathic soft tissue edema does not enhance after contrast administration (Figures 1 and 4).

Figure 4 

MRI demonstration of active Charcot neuro-osteo-arthropathy at the Lisfranc joints in a 74y old female. No skin ulcer.

Erosions with destruction of the subchondral bone lamella of the tarsometatarsal joints with and bone marrow edema with low SI on T1 WI and high SI on DIXON T2 WI and marked enhancement after IV gadolinium DTPA administration. Homogeneous signal on DIXON T2 series that do not demonstrate increased signal at the dorsum of the foot. The increased signal on T1 WI with FS at the dorsum of the foot is an artifact related to magnetic field non-homogeneity and not to be interpreted as enhancement or cellulitis.

Key points

Osteomyelitis in the diabetic foot is located in continuity with skin ulcers. The exact location of skin ulcers is essential to discriminate osteomyelitis per continuitatem from active Charcot osteoarthropathy.

Competing Interests

The authors have no competing interests to declare.


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  6. Zampa V, Bargellini I, et al. Role of Dynamic MRI in the follow-up of acute Charcot foot in patients with diabetes mellitus. Skeletal Radiology. 2011; 40: 991–999. DOI: 

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