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 .
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 . 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 . There are few data available using Positron Emission Tomography (PET) .
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) . 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 .
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).
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].
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.
The authors have no competing interests to declare.
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