This document discusses radiological imaging techniques for evaluating diabetic foot complications such as infection and Charcot foot. It provides examples of MRI, CT, ultrasound, bone scintigraphy, and PET/CT images showing osteomyelitis, soft tissue infections, and Charcot arthropathy in diabetic feet. MRI is highlighted as the most useful imaging method for diagnosing osteomyelitis, while PET/CT can help distinguish osteomyelitis from Charcot disease.

1. Radiological imaging of diabetic and Charcot Foot.
Dr. Abd Allah Nazeer. MD.

2. 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

3. Plain radiography
The 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.

4. Magnetic resonance imaging
Magnetic 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

5. Bone scintigraphy
The 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 tomography
Single 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.

6. 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.

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

8. 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)

9. (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.

11. (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.

12. 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).

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

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

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

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

17. The use of gadolinium in delineating abscess formation.

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

19. 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).

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.

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

26. 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.

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

28. 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.

29. 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).

30. 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.

31. 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.

32. 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.
Epidemiology
In 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 neuropathy
Clinical presentation
Patients 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.
Pathology
There 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 .

33. Atrophic form
most common form
occurs earlier
has an acute progression
characterized by reabsorption of the ends of the affected bone
joint destruction with resorption of fragments
absence of osteosclerosis and osteophytes
mainly occurs in non-weight bearing joints of the upper limb.
Hypertrophic form
only sensory nerves affected
slow progression
joint destruction with periarticular debris/bone fragmentation
initially widened then narrowed joint space
presence of osteosclerosis and osteophytes.
absence of osteoporosis (unless joint is infected).

34. Etiology
diabetes (most common)
leprosy
multiple sclerosis
poliomyelitis
rheumatoid arthritis
tertiary syphilis
steroid use
syringomyelia
spinal cord injury
spina bifida
scleroderma
These can be recalled with the "S" mnemonic.
Location
The involved joint is highly suggestive of the etiology:
wrist: diabetes, syringomyelia
hip: alcohol, tabes dorsalis
knee: tabes dorsalis, congenital insensitivity to pain
ankle and foot: diabetes
spine: spinal cord injury, diabetes, tabes dorsalis

35. 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 CT
General characteristics include (six Ds mnemonic):
dense bones (subchondral sclerosis)
degeneration
destruction of articular cartilage
deformity (pencil-point deformity of metatarsal heads)
debris (loose bodies)
dislocation

36. 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.

37. Nuclear Imaging
The 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%.

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

39. 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.

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

41. 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.

42. 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.

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

44. 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.

45. Charcot foot
with rocker-
bottom
deformity and
ulceration
beneath the
bony
protuberance
of the cuboid
STIR and T1W
images in
Charcot
neuro-
osteoarthrop
athy with a
plantar ulcer
(asterix) and
osteomyelitis
of the cuboid.

46. Osteomyelitis in chronic Charcot neuro-osteoarthropathy.

47. No osteomyelitis in chronic Charcot neuro-osteoarthropathy.

48. 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.

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

50. 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.

51. 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)

52. 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.

53. 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.

54. 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.

55. Thank You.