Radiological imaging of diabetic and Charcot Foot.

Dr. Abd Allah Nazeer. MD.

A diabetic foot is a foot that exhibits any pathology that results directly from diabetes mellitus or any long-term (or "chronic") complication of diabetes mellitus. Presence of several characteristic diabetic foot pathologies such as infection, diabetic foot ulcer and neuropathic osteoarthropathy is called diabetic foot syndrome.Due to the peripheral nerve dysfunction associated with diabetes (diabetic neuropathy), patients have a reduced ability to feel pain. This means that minor injuries may remain undiscovered for a long while. People with diabetes are also at risk of developing a diabetic foot ulcer. Research estimates that the lifetime incidence of foot ulcers within the diabetic community is around 15% and may become as high as 25%.In diabetes, peripheral nerve dysfunction can be combined with peripheral artery disease (PAD) causing poor blood circulation to the extremities (diabetic angiopathy). Around half of patients with a diabetic foot ulcer have co-existing PAD.Where wounds take a long time to heal, infection may set in and lower limb amputation may be necessary. Foot infection is the most common cause of non-traumatic amputation in people with diabetes

Plain radiographyThe sensitivity of plain films in the diagnosis of OM has shown variable results. It is related to the chronicity of the infection and at least 30–50% bone loss is required to show visible changes on plain radiographs and such changes take at least 2–3 weeks to manifest. The specificity of radiographs is also lowered due to difficulty in distinguishing OM from Charcot neuroathropathy joint disease. The most common OM changes that may be seen on radiographs include osteopenia, periosteal thickening, cortical erosions, and new bone formation. Overall, the sensitivity and specificity are 54 and 68% respectively according to one meta-analysis. Nevertheless, plain radiographs should be performed initially as a baseline to assess the development and presentation of OM in a bone.

Magnetic resonance imagingMagnetic resonance imaging (MRI) is presently considered the investigation of choice for diagnosing diabetic foot OM. In OM, the loss of signal in T1-weighted images and higher intensity on T2-weighted images can reveal the pathology as early as 3 days after infection. However, this bone edema can sometimes be difficult to differentiate from non-infectious causes of edema. The accuracy of MRI is challenged when Charcot neuroarthropathy joint disease or recent surgical change is present. Meta-analyses and reviews show that MRI is probably the most useful imaging modality for assessing OM with a sensitivity of about 90% and a specificity of about 80%. MRI provides a good anatomical correlation but it is limited in terms of functional correlation

Bone scintigraphyThe three-phase bone scan using Technetium-99m-Medronic Acid Bisphosphonate provides a two-dimensional image of areas in bone with active bone turnover. For diabetic foot OM, bone scans have a sensitivity of 80–90% but a specificity of less than 50%. The poor specificity relates to inability of the bone scan to distinguish OM from other inflammatory or traumatic conditions involving the bone, such as Charcot neuroarthropathy joint disease, bone metastasis, gout, fracture, or even recent surgery. It must also be noted that it is difficult to delineate the exact anatomical location or extent of infection with a bone scan Single photon emission computerized tomographySingle photon emission computerized tomography (SPECT) combines bone scan with computerized tomography to improve the anatomical–functional correlation since it provides three-dimensional images of the foot. However, the technology is still not widely available and its diagnostic potential for diabetic foot OM is still being researched.

US is another widely available and noninvasive imaging modality, although its role in the evaluation of diabetes-related foot complications is limited. It is especially useful for the detection of infectious/inflammatory soft tissue changes and localization of foreign bodies, diagnosis of tenosynovitis and joint effusion, and differentiation of infected/reactive collection. This modality is also important in providing guidance for the aspiration of abscesses, cystic lesions, and sterile collections PET/CT with 18F-fluoro-2-deoxy-d-glucose an indicator of increased intracellular glucose metabolism that accumulates at the sites of infection, is associated with high sensitivity (80–95%) and specificity rates (90–100%) in the diagnosis of diabetes-related osteomyelitis and neuroarthropathy. A precise diagnosis of osteomyelitis versus soft tissue infection with better anatomic localization is possible with PET/CT.Although the presence of an underlying neuroarthropathy makes the diagnosis of osteomyelitis difficult, high accuracy and specificity rates have been achieved using PET/CT for the differentiation of osteomyelitis from neuroarthropathy. Furthermore, PET/CT has been found to be superior to leukocyte-labeled and antigranulocyte monoclonal antibody fragment techniques in the diagnosis of chronic osteomyelitis . In patients with medical implants, which can cause distortion in MRI, PET/CT is a good alternative. This technique might also be preferred in the postoperative assessment of these patients.

Diabetic foot with soft tissue swelling and bone destruction at first metatarsophalangeal joint.

Known diabetic patient on oral hypoglycemic agents initially presented with erythema and swelling of the foot, with no recent history of any trauma to the region. There was also no other systemic signs or symptoms present. MRI performed after the initial screening radiographs demonstrates increased osseous edema at the region of the mid foot (as illustrated), suspicious for early neuroarthropathic changes. The patient was however eventually lost to follow up. (a) Oblique radiographic projections of the foot demonstrates diffuse periosteal reaction along the shaft of the 4th metatarsal, likely secondary to previous fracture/trauma. No other significant structural changes are however noted. (b) T2-weighted fat suppressed axial MRI image demonstrates marrow edema at all the metatarsophalangeal joints (arrows)

(a) Radiographic projection of the foot demonstrates diffuse soft tissue swelling over the right forefoot. Subtle bony erosions and ill defined lucencies seen over the 4th and 5th metatarsal heads, suspicious for osteomyelitis. There are flexion deformities at the metatarsophalangeal joints, possibly related to underlying neuropathy. (b) T1-weighted sagittal (c) STIR sagittal (d) gadolinium enhanced T1-weighted fat suppressed MRI images demonstrate marrow edema, with low signal intensity on T1-weighted image, high signal on STIR image and consequently enhancement of the marrow post contrast administration of the 4th and 5th (not demonstrated) metatarsals. Features are in keeping with osteomyelitis of the 4th and 5th metatarsal heads, with likely septic arthritis of corresponding metatarsophalangeal joints. (e) Axial gadolinium-enhanced T1-weighted fat-suppressed MR image shows a central plantar ulcer (#, with discontinuity of the skin)and a partially imaged lateral dorsal ulcer. The dorsally located ulcer is noted to be associated with a deep seated collection/abscess (*), with additional ramifications/extensions in keeping with sinus tract formation and adjacent cellulites.

(a) Frontal and oblique radiographic projection of the foot shows extensive bony erosions involving the base of the 1st and 2nd metatarsals, navicular as well as the medial, middle and lateral cuneiform bones. Findings are compatible with osteomyelitis. There is also likely bony fusion of the first metatarsal, medial cuneiform and navicular bones. Soft tissue swelling of the mid-foot is noted. (b) Axial T1-weighted, (c) T2-weighted fat suppressed and (d) gadolinium-enhanced T1-weighted fat-suppressed MR images show intraosseous rim enhancing abscesses involving predominantly the medial and middle cuneiform bones (*). A discharging tract was also noted medially (not demonstrated on available images) with surrounding adjacent cellulitis, small dorsal abscesses and soft tissue edema noted. Osteomyelitis of the 1st metatarsal, base of the second metatarsal, medial and middle cuneiform and navicular bones were also demonstrated. There is also synovial thickening and fluid distension of the flexor hallucis longus tendon (arrows), in keeping with tenosynovitis.

Heel ulcer and calcaneal osteomyelitis. MRI from the same patient as Fig 1. (A) Sagittal T1-weighted image and (B) T2-weighted fat-suppresed image showing bone marrow edema underlying a skin ulcer. (C)T1-weighted image with fat suppression showing enhancement of bone marrow, findings indicative of osteomyelitis. Hyperintense area on (B) with intense enhancement on (C) at the base of the ulcer indicate the presence of granulation tissue (arrow).

Osteomyelitis of first metatarsal with cellulitis and fluid tracking around flexor hallucis longus tendon.

Ulcer on big toe. Region of interest is therefore zone 1, the forefoot.

 Heel ulcer. Zone 3 scan to assess ulceration and calcaneum.

Osteomyelitis of first metatarsal. Note bone cortex destruction, marrow enhancement and contiguous soft tissue infection.

The use of gadolinium in delineating abscess formation.

Osteomyelitis of first metatarsal with cellulitis and fluid tracking around flexor hallucis longus tendon.

MRI of the whole foot, sagittal (a) T2W FS, (b &c) T1W FSE pre- and (d) post- contrast images; show a big heal ulcer (long open white arrow on a,b & d) with calcaneal bone marrow edema (a). No significant enhancement of the marrow was seen on post-contrast image (d) ruling out osteomyelitis. There is retraction of the frayed Achilles tendon ( thin white arrow on a, b & d) with bulbous high-signal distal end consistent with degenerative atritic tendinopathy. Note the callus (short open arrow on c) developed under the head of M5 due to gait imbalance and diabetic myopathy (black dotted oval on a &b).

MRI of the hind foot/Ankle region, sequential sagittal (a) pre-contrast T1W FSE, (b) T2W FS and short-axis/coronal (c) T2W FS, (d) post-contrast T1W FS images, show a big heel ulcer (open white arrows on a & c) with tumefactive edematous soft-tissue replacement of the underlying heel fat pad and remarkable bone marrow edema of the calcaneous (Black dotted circle in b). There is FHL tenosynovitis under the sustanaculum tali (black arrow in c). Note the enhancing tram-track like sinus tract (short black arrow on d) and multiple linear and rounded signal void air loculi (white stars on d) leaking from the open sinus.

MRI of the fore-foot; short-axis (a) T2 FS, sagittal (b) non-contrast as well as (c) post-contrast T1W FSE, and short-axis (d) T1W FS as well as long-axis (e) T1W FS images; show large dorsal ulcer overlying the 5th MTP articulation (long white arrow on d). There is marked enhancing (black arrow on e) bone marrow edema (black arrow on b) of the M5 indicating presence of osteomyelitis. Note also remarkable dorsal skin and soft-tissue edema (twin short white arrows on a through d) as well as edema of the deep short foot muscles and its fatty infiltration on (black dotted oval on a & c) due to associated diabetic neuropathy and myopathy; respectively.

Images of a patient with a small cutaneous defect and subcutaneous edema at the metatarsals.A secondary sign, an abscess, is shown in the forefoot, with high signal intensity on STIR, low or intermediate

signal on intensity T1W, and ring-enhancement of the borders showing high signal intensity on T1+Gd.

The right foot (plantar and lateral views) of a 59-year-old man with diabetic neuropathy showing collapse of the internal arch (arrow) and a large neuropathic ulcer on the mid plantar surface. (B) Computed tomographic images (dorsoplantar and lateral views) of the patient’s right foot showing a subchondral cyst (arrow), fragmentation, disorganization, and loss of normal architecture of the talus, calcaneous, tarsal bones and bases of the metatarsals.

Isotope bone scan of feet. Areas of increased uptake are present in both feet. Further investigation required to determine cause of increased uptake e.g. osteomyelitis, degenerative joint disease.

Bone scan. Bone scan showing increased uptake localized to the base of the fifth metatarsal, indicating osteomyelitis.

Diabetic man who presented with fever and swollen, tender right foot. 18F-FDG PET/CT was performed because of clinical suspicion of diabetic foot osteomyelitis. Serum glucose level at time of study was 290 mg/dL. Trans-axial 18F-FDG PET (left), PET/CT (center), and CT (right) slices show 18F-FDG uptake at medial aspect of right forefoot, involving only soft tissues with sparing of metatarsal bones (arrow). Extensive soft-tissue infection involving muscles and planter fascia and no osteomyelitis were found at surgery.

Used PET and MRI of a patient with diabetic foot and suspected bone infection.

A) Osteomyelitis of the right great toe is shown. Three-phase bone scan is true positive. (B) Labeled leukocyte study is true positive. (C) Reactive bone (same patient illustrated in Fig. 3). Three-phase bone scan is false positive. (D) Labeled leukocyte study is false positive. In these 2 cases, the bone scan did not alter the interpretation of the labeled leukocyte scan.

Positive three-phase hydroxymethanediphosphonate (99mTc-HDP) bone scan in a male with a clinical suspicion of osteomyelitis. First phase (angiographic) (A) bone scan demonstrating asymmetric blood flow with markedly increased tracer delivery to the region of the right toe (black arrow). Second phase (blood pool) (B), and third phase (delayed) (C) bone scan images illustrating marked increase in tracer activity (black arrows) in the same region consistent with osteomyelitis. Bone marrow changes in sagittal T1-weighted (D) and T2-weighted fat-suppressed (E) images also indicate presence of osteomyelitis in the first metatarsal head (white arrows).

WBC scintigraphy, which was positive for osteomyelitis (T/B ratio > 2.0 and increasing over time), and 18F-FDG PET/CT, which was negative for osteomyelitis (SUVmax < 2.0): clinical image of diabetic foot (A); anterior and posterior WBC scintigraphy images after 30 min, 3 h, and 20 h (B); transaxial 18F-FDG PET/CT images after 1 h (C). Ant = anterior; Post = posterior.

Osteomyelitis may be associated with soft tissue collections which can be seen on ultrasound. (A) Transverse section ultrasound image demonstrating a well-defined complex fluid collection which has an irregular thick wall (white arrowheads) and a hyperechoic septation (white arrow); (B) percutaneous needle aspiration of the fluid collection was performed (black arrowheads). Culture of the aspirate grew Staphylococcus aureus.

Charcot joint, also known as a neuropathic or neurotrophic joint, refers to a progressive degenerative/destructive joint disorder in patients with abnormal pain sensation and proprioception.EpidemiologyIn modern Western societies by far the most common cause of Charcot joints is diabetes, and therefore, the demographics of patients matches those of older diabetics. Prevalence differs depending on the severity of diabetes:~0.1% in general diabetic population~15% in high-risk diabetic population~30% in patients with peripheral neuropathyClinical presentationPatients present insidiously or are identified incidentally, or as a result of investigation for deformities. Unlike septic arthritis, Charcot joints although swollen are normal temperature without elevated inflammatory markers. Importantly they are painless. PathologyThere are two forms of Charcot joint: atrophic and hypertrophic. Charcot joints are typically unilateral but are bilateral in ~20% (range 5.9-39.3%) of cases.The pathogenesis of a Charcot joint is thought to be an inflammatory response from a minor injury that results in osteolysis. In the setting of peripheral neuropathy both the initial insult and inflammatory response is not well appreciated, allowing ongoing inflammation and injury .

Atrophic formmost common formoccurs earlierhas an acute progressioncharacterized by reabsorption of the ends of the affected bonejoint destruction with resorption of fragmentsabsence of osteosclerosis and osteophytesmainly occurs in non-weight bearing joints of the upper limb.

Hypertrophic formonly sensory nerves affectedslow progressionjoint destruction with periarticular debris/bone fragmentationinitially widened then narrowed joint spacepresence of osteosclerosis and osteophytes.absence of osteoporosis (unless joint is infected).

Etiologydiabetes (most common)leprosymultiple sclerosispoliomyelitisrheumatoid arthritistertiary syphilissteroid usesyringomyeliaspinal cord injuryspina bifidasclerodermaThese can be recalled with the "S" mnemonic.LocationThe involved joint is highly suggestive of the etiology:wrist: diabetes, syringomyeliahip: alcohol, tabes dorsalisknee: tabes dorsalis, congenital insensitivity to painankle and foot: diabetesspine: spinal cord injury, diabetes, tabes dorsalis

Radiographic features: Radiologic features of neuropathic arthropathy (Charcot joint) are the same irrespective of the etiology and distribution. Early stage radiographic findings include persistent or progressive joint effusion, narrowing of the joint space, soft-tissue calcification, minimal subluxation, preservation of bone density (unless infected), and fragmentation of eburnated subchondral bone. In the late stage, there is radiographic evidence of destruction of articular surfaces, subchondral sclerosis, osteophytosis, intra-articular loose bodies (bag of bones), subluxation, Lisfranc fracture/dislocation of midtarsal bones, and rapid bone resorption demonstrating pencil-in-a-cup deformity (see the images below). Complications of septic arthritis that are demonstrated on radiographs include osteomyelitis and bone ankylosis. Radiograph and CTGeneral characteristics include (six Ds mnemonic):dense bones (subchondral sclerosis)degenerationdestruction of articular cartilagedeformity (pencil-point deformity of metatarsal heads)debris (loose bodies)dislocation

Magnetic Resonance Imaging:On T1-weighted MRIs, joints involved in neuropathic arthropathy (Charcot joint) appear diffusely swollen and demonstrate low signal intensity. The fat plane adjacent to the skin ulceration appears hypointense; when the joints are infected with a gas-producing organism, areas showing a loss of signal intensity are seen. After the intravenous administration of a gadolinium-based contrast agent, the inflammatory mass enhances and demonstrates central nonenhancing necrotic debris.On short-tau inversion recovery (STIR) sequences, early bone infection may be evidenced by high-signal marrow edema. Later, loss of clarity of the cortical outline and cortical destruction can be identified.Features that help differentiate spinal neuroarthropathy from disk infection include joint disorganization; facet involvement; debris; a pattern of diffuse signal intensity in the vertebral bodies; spondylolisthesis; and rim enhancement of the disk on gadolinium-enhanced MRIs. Features that do not help in differentiation include endplate sclerosis, erosions, osteophytes, a reduction in disk height, and paraspinal soft-tissue masses.

Nuclear ImagingThe role of radioisotopic studies is to detect osteomyelitis in a neuropathic joint.[9]Three-phase phosphate scintigraphy has a high sensitivity (85%) but a low specificity (55%) because of bone remodeling of other causes. Studies using uptake of the gallium-67 (67 Ga) citrate have a high false-positive rate. Scanning using indium-111 (111 In)–labeled leukocytes has the highest sensitivity (87%) and specificity (81%) for detecting osteomyelitis in a neuropathic foot. The role of positron emission tomography (PET) scanning with fluorodeoxyglucose (FDG) is promising.One study has shown a valuable role of FDG-PET scanning in the setting of neuroarthropathic arthropathy (Charcot joint) by reliably differentiating it from osteomyelitis, both in general and when foot ulcer is present.[11] In diabetic patients in the setting of concomitant foot ulcer, FDG-PET scanning accurately rules out osteomyelitis. Basu and associates estimated a 100% sensitivity and 93.8% accuracy of FDG-PET scanning in the diagnosis of Charcot foot; by contrast, MRI had a sensitivity of 76.9% and an accuracy of 75%.

T1 and T1 fat sat post contrast sagittal images of mid foot. Note marrow edema and soft tissue edema. Normal bone alignment.

T1 and T1 fat sat sagittal images 4 weeks later than figure 19. Acute Charcot arthropathy with subluxation of the navicular. Note widespread soft tissue inflammatory change.

Chronic Charcot arthropathy at Lisfranc joint and Charcot joint. Note loss of normal alignment and bone loss.

Neuropathic arthropathy (Charcot joint). Neuropathic arthropathy in a patient with syringomyelia. Antero-posterior and lateral views of the elbow demonstrates resorption of the bone with opaque subchondral bone.

Neuropathic arthropathy (Charcot joint). Charcot joint in a patient with tabes dorsalis who has dislocation, osseous fragmentation, and sclerosis. The opacities projected over the iliac blades represent intramuscular bismuth-containing injections.

Neuropathic arthropathy (Charcot joint). Gross disorganization of the hip joints in a patient with tabes dorsalis.

Neuropathic arthropathy (Charcot joint). Fragmentation and collapse of the chondral and osseous structures of both knee joints in a patient with tabes dorsalis.

Neuropathic arthropathy (Charcot joint). Oblique view of the foot in a patient with diabetes and neuropathic arthropathy shows destruction of the articular surface of the intertarsal joints with subchondral sclerosis.

Charcot foot with rocker-bottom deformity and ulceration beneath the bony protuberance of the cuboid

STIR and T1W images in Charcot neuro-osteoarthropathy with a plantar ulcer (asterix) and osteomyelitis of the cuboid.

Osteomyelitis in chronic Charcot neuro-osteoarthropathy.

No osteomyelitis in chronic Charcot neuro-osteoarthropathy.

Neuropathic arthropathy (Charcot joint). Computed tomography scan of the ankle in a patient with neuropathic arthropathy. Note the destruction of the articular surface, disorganization of the joint, and fragmentation.

T1 sagittal and axial and T1 fat sat post contrast sagittal images. Chronic Charcot arthropathy with joint fluid and marrow edema.

Neuroarthropathy with superimposed osteomyelitis. (a) Sagittal T1-weighted MR image shows a rocker-bottom deformity, a plantar ulcer (arrowhead), and fragmentation and subluxation at the midfoot (black arrows). The osseous structures of the midfoot appear to be absent, and an extensive, diffuse area of hypointensity is seen. White arrows = fluid collections. (b) Sagittal T2-weighted fat-suppressed MR image shows the osseous structures of the midfoot, which appear more regular and better defined than in a. This appearance, which is known as the ghost sign, is indicative of neuroarthropathy with superimposed osteomyelitis. Arrowhead = plantar ulcer, black arrows = midfoot fragmentation, white arrows = fluid collections. (c) Sagittal gadolinium-enhanced T1-weighted fat-suppressed MR image shows diffuse marrow enhancement; multiple fluid collections, mostly in the mid foot articulations and the ankle joint; and thick synovial enhancement (white arrows). Arrowhead = plantar ulcer, black arrows,= midfoot fragmentation.

Sagittal (a) T1-W, (b) T2-W FS and (c) contrast-enhanced T1-W FS MR images of the right foot show extensive bony destruction centered around the midfoot joints, consistent with chronic neuroarthropathy. This is well demonstrated on the accompanying (d) oblique radiograph of the right foot. On the MR images, abnormal marrow signal is seen diffusely in the bones of the midfoot, extending beyond the subchondral bone; the affected bones show marked low T1-W signal and corresponding high T2-W signal as well as enhancement (arrows)

Chronic neuropathic osteoarthropathy (A–E). Anteroposterior (A), and lateral (B) plain radiographs of the foot and ankle illustrate fragmentation and subluxation (arrowheads) at the midfoot with dorsal soft tissue swelling. There is an extensive edematous bone marrow changes (black arrows) in the midfoot in T1 (C), and T2-weighted fat-suppressed images (D). Multiple fluid collections (black arrows) mostly in the midfoot articulations were also demonstrated. Diffuse bone marrow enhancement and associated periarticular subchondral cysts (white arrows) in post-contrast long axis T1 weighted fat-suppressed (E) images are all suggestive for neuroarthropathy only. Note there is no associated ulcer, sinus tract or abscess formation. Clinical evaluation revealed no signs of infection.

The SUVmax values were found to vary from 1.4 in chronic Charcot s ′to a maximum of 03 in acutely inflamed Charcot s arthropathy.′

 A : CT scan; B : PET scan; C : PET/CT scan in acute Charcot foot. Note the enhanced 18 F-FDG uptake observed at the midtarsal area ( B and C ) before treatment.

Thank You.