MRI of Diabetic foot - appearances and mimics, a pictorial review Poster No.: C-0526 Congress: ECR 2012 Type: Educational Exhibit Authors: R. Dutta, M. George; Singapore/SG Keywords: Musculoskeletal joint, Musculoskeletal system, MR, Imaging sequences, Infection, Inflammation DOI: 10.1594/ecr2012/C-0526 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. www.myesr.org Page 1 of 22
Learning objectives 1. Identifying osteomyelitis in diabetic foot. 2. Differentiation between neuropathic joint and mimics. 3. Treatment planning, conservative vs surgical. Page 2 of 22
Background Approximately 15% diabetics develop diabetic foot. Diabetic foot infections originate from a foot ulcer. Patients with long standing diabetes have peripheral vascular disease and neuropathy. These eventually lead to ischaemia and sensory loss resulting in ulcerations, cellulites, abcesses, osteomyelitis and neuropathic joints. Long standing hyperglycemia results in degeneration of the sensory nerves, further resulting in hypertrophic neuroarthropathy. Degeneration of the sympathetic nerve causes loss of vasoconstrictive impulses leading to hyperemia and atrophic neuroarthropathy. Early and accurate diagnosis of infection or neuropathy of the diabetic foot is pertinent to successful management. Plain X-rays, US, CT, MRI, nuclear medicine and biopsy are the commonly used modalities for the work up of diabetic foot. MRI is the modality of choice for the early detection of osteomyelitis with or without neuropathic joints and other conditions. It helps in treatment planning immensely and also prevents spread of disease which may sometimes result in severe sepsis and may be fatal. Page 3 of 22
Imaging findings OR Procedure details MRI is increasingly being performed for the early detection of bone infection for diagnosis of osteomyelitis which can be complicated by signal changes from reactive osteitis in neuropathic joints, fractures, and post-operative residues and may mimic infection. The primary diagnostic challenges are to distinguish osteomyelitis from reactive bone marrow edema, neuroarthropathy, and the sterile from florid infected neuropathic joint. Differentiation of osteomyelitis from the rest requires careful analysis of the location of bone signal, their distribution, and pattern. MRI Sequences used Sagittal T1, STIR, Coronal PD STIR, Axial T2 Fat sat. Post contrast series in saggital, coronal and axial planes. Hyperintense marrow on T2w images with contrast enhancement is non specific and can be seen with most conditions enumerated above. The following 2 signs are most important signs for the diagnosis of osteomyelitis. (1) dark marrow signal on T1," Ghost sign" and (2) contiguous involvement of the underlying bone from pressure sores. The diagnosis of osteomyelitis in our study was established by the above mentioned MR criterion and correlated with pathologic specimen i.e. tissue/bone culture, or successful response to medical management. Cellulitis Page 4 of 22
Fig. 1: T1 image. Subcutaneous fat replacement. Fig. 26: T2 Fatsat. Hyperintense subcutaneous tissue on the dorsum of foot. Fig. 27: Post contrast enhancement seen with cellulitis unlike oedema. Pressure points. Contiguous spread with focus of abnormal bone marrow signal from the subchondral surface, adjacent to a skin ulcer, cellulitis, abscess, or sinus tract would be indicative of osteomyelitis. Page 5 of 22
Commonly at 1, 5th toes, MTP and calcaneus ulcerations at pressure points Fig. 2: T1 Saggital. healed pressure sore with scarring. No active infection. Fig. 3: T2 fat sat.pressure sore with scarring. No active infection. Fig. 4: Coronal T1image with pressure sore.. Page 6 of 22
Sinus tract/ abscess soft tissue/ intraosseous abscess. Fig. 5: Post contrast. Sinus tract. Fig. 6: Post- contrast T1 fat sat.abcess formation with tenosynovitis. Fig. 7: Intraosseous abcess.t2 Fat sat image. Cortical erosions Page 7 of 22
Fig. 8: Periarticular erosions at pressure points. Fig. 10: Periarticular erosions. Also fracture in Fig. 9: "Ghost sign" on T1 the proximal phalanx of at MTP of 2nd to 4th joints. great toe. Marrow replacement: Osteomyelitis and reactive marrow edema share increased T2w signal, osteomyelitis is confirmed by T1 hypointensity in the bone marrow as compared to reactive edema which demonstrates isolated T2 signal hyperintensity. Page 8 of 22
Dark on T1 ( ghost sign), bright on T2w and enhancement after the adminstration of intravenous contrast. Contiguous involvement. Fig. 11: T1 image.contiguity seen with osteomyelitis. Dark marrow signal on T1" Ghost Sign". Fig. 12: Non specific hyperintensity on T2 fat sat. Fig. 13: Enhancing ulceration with contiguous involvement of the calcaneus. Page 9 of 22
Treatment includes: 1. Medical - Control of blood pressure, cholesterol, stop smoking. - Measures to improve circulation. -Wound/ ulcer care. 2. Surgical -Angioplasty/ stenting. - Bypass surgery. - Debridement - amputations. Amputation options: Page 10 of 22
Fig. 36: Ray amputation of 5th metatarsal bone with mild osteitis. Fig. 37: Mid foot amputation with no residual infection. Fig. 38: Above knee amputation with surrounding inflammatory/ infective change. Patient also had a femoral-femoral bypass graft and above knee amputation on the left for severe ascending fascitis of left leg and foot. Page 11 of 22
Mimics and differentials: Reactive osteitis Marrow: iso on T1 and bright on T2 with enhancement.. Fig. 14: Talus marrow signal-isointense on T1. Fig. 15: Non specific Fig. 16: Isointense hyperintensity on T2 fat sat marrow signal from talus on T1. Page 12 of 22
is reactive osteitis since isointense on T1. Neuropathic joint. Midfoot.- hypertrophic/ atrophic or mixed types Fig. 18: T1 images. Normal marrow signal. Fig. 19: T2 Fatsat. Normal marrow signal. Page 13 of 22
Fig. 17: Neuropathic foot in a diabetic foot- mixed type Singapore Singapore Singapore Neuopathic foot Midfoot, subchondral, periarticular/polyarticular distribution of findings in the absence of a contiguous focus on skin disruptions would strongly support neuroarthropathy. Midfoot Periarticular erosions with abnormal signal. Page 14 of 22
Fig. 20: T1- Isointense marrow on T1. Fig. 21: T2 fat satperiarticular erosions with hyperintensity in the midfoot. Fig. 22: T1-Periarticular erosions. Altered marrow at the neuropathic joints due to superadded infection and Cellulitis Page 15 of 22
Fig. 28: T2 fat sat images.-subcutaneous oedema with abcess formation and osteomyelitis. Fig. 29: Subcutaneous infective tissue due to cellulitis and abcess formation which needed debridement. Fig. 30: Enhancing subcutaneous infective tissue due to cellulitis.. Stress fractures Dark on T1 and bright on T2 with no enhancement. Page 16 of 22
Fig. 23: Periosteal reaction at the distal shaft of 2nd metatarsal bone. Fig. 24: T1- Faint linear fracture line. Fig. 25: T2 Fat sat. Stress fracture with periosteal reaction. Long standing pain Other mimics: Insufficiency fractures in inflammatory joint disease. Page 17 of 22
Fig. 33: Rheumatoid arthritis on long term steroids and methotrexate. Periarticular erosions with flat foot. Fig. 31: T1-Insufficiency fractures in the distal tibia. References: TTSH. Singapore Fig. 32: T2w -Fat sat. Hyperintensity due to marrow oedema and insufficiency fracture of distal tibia.. Also cellulitis due to venous ulcer at the lateral aspect. Long standing Rheumatoid arthritis with fractures. Venous ulcer also at the lateral aspect of dorsum of foot. Page 18 of 22
Fig. 34: Periarticular erosions with synovitis due to rheumatoid arthritis. Venous ulcer on the lateral aspect. Fig. 35 Singapore Periarticular erosions in the mid foot due to synovitis in a case of long standing Rheumatoid arthritis. Page 19 of 22
Conclusion MRI is the modality of choice for distinguishing osteomyelitis from neuropathic joints, osteitis and stress fractures. It is of enormous help to guide patient management and to aid limited limb resection. Page 20 of 22
Personal Information 1. Dr Rupak Dutta, FRCR. Consultant in Dept of Radiology. Tan Tock Seng Hospital, 2, Dr Mathew George, FRCR. Associate consultant. Dept of Radiology. Tan Tock Hospital Page 21 of 22
References 1. Yuh WT, Corson JD, et al. AJR Am J Roentgenol. 1989 Apr;152(4):795-800. 2. Gold RH, Tong DJ et al. Skeletal Radiol. 1995 Nov;24(8):563-71. Review. 3. Semin in Musculoskelet Radiol. 2005 Sep;9(3):272-83 4. Donovan A, Schwitzer ME Radiol Clin North Am. 2008 Nov;46(6):1105-24, vii 5.Toledano TR et all Semin Musculoskelet Radiol.2011 Jul;15(3):257-68. Epub 2011 Jun 3 6.Andrea Donovan and,mark E. Schweitzer Use of MR Imaging in Diagnosing Diabetes-related Pedal Osteomyelitis. Radiographics May 2010 30:723-736 Page 22 of 22