Figure 19.3 An accessory ossicle (normal variant) is present on the medial side of the great toe, adjacent to the interphalangeal joint. In people with diabetes, such bony prominences can predispose to ulceration
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226 RADIOLOGY AND MAGNETIC RESONANCE IMAGING OF THE DIABETIC FOOT
ossicles.
Although two sesamoid bones are usually present under the great toe, these can be bi- or tripartite and sesamoids can also occur under other toes.
Recognition of normal variants of radiographic appearances in the foot and ankle by reference to relevant texts is recommended.5 Accessory ossicles or variations in the morphology or alignment of the metatarsals and pha- langes are clearly demonstrated on plain radiographs.
Whilst usually considered to be normal variants, and of no clinical significance, these features may predispose to ulceration in diabetic feet, for example an interphalangeal accessory sesamoid in the great toe was present in 13 of 29 people with diabetes with great toe ulcers.6 Such normal variants are, however, no more common in people with diabetes than in the rest of the population.7
TRAUMA Plain radiography is fundamental to the diagnosis and management of fracture and dislocation in the foot and ankle.
Recent fractures and dislocations, bone deformities from healed previous fractures and progressing neuropathic fracture/dislocations will all be demonstrated on radio- graphs (Figure 19.4).
Although foot deformity will be clinically apparent, the radiographs can draw attention to underlying bone deformities that may predispose to soft tissue ulceration by forming pressure points.
Metallic or glass radio-opaque foreign bodies may be identified in the foot8,9 and may predispose to infection.
Bone regrowth after surgical partial resection of metatarsal bone may also form pressure points and predispose to ulceration (Figure 19.5).
Plain film demonstration of regrowth exceeding 3 mm was seen in 45% of such patients between 1 and 3 years after surgery.10 Evidence of traumatic fractures, often previously unrecognised, in neuropathic diabetic feet is common, being found in 22% of neuropathic diabetic feet in one study.7
VASCULAR DISEASE
Peripheral vascular disease is common in diabetes.
In the foot and ankle, relative sparing of the dorsalis pedis but involvement of the posterior tibial and peroneal arteries is often seen.
On plain radiographs, small vessel calcification is seen throughout the foot (Figure 19.6).
When completely avascular, such as in dry gangrene of the foot, the affected bones will remain unchanged, whilst the bone that is still vascularised and viable becomes demineralised, resulting in a demarcation on the plain radiograph between viable (osteopaenic) and dead (normal density) bone.
Proper assessment of the vascular supply requires angiography, though contrast enhanced MR may replace conventional catheter angiography for this.
The presence of radiographically demonstrated medial arterial calcinosis in diabetic feet is associated with neuropathy, ulceration, amputation and excess mortality.11
NEUROPATHY AND NEUROARTHROPATHY Although originally described as the changes in the lower limb in Charcot, Marie, Tooth syn- drome, neuropathic changes in the foot are most commonly caused by diabetes and are of- ten described as Charcot neuroarthropathy. Neuroarthropathic changes in the skeleton are
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Figure 19.4 Recent intra-articular fracture of the great toe proximal phalanx. There is also a healed fracture of the fifth metatarsal
believed to be due to unnoticed repeated minor trauma, resulting in progressive joint de- struction.
This is superimposed on bones rendered osteopaenic from increased osteoclastic activity, driven by hyperaemia from sympathetic denervation of small blood vessels.12 Re- duced bone density directly predisposes to fracture, as bone density is a major determinant of bone strength.
Consequently, neuropathic changes may manifest as arthropathy, dislocation, fracture or a combination of these features.
Study of bone mineral density in diabetic feet has demonstrated peripheral osteopaenia in those patients with a fracture pattern of neuropathy,
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Figure 19.5 Lateral view of the foot demonstrates a bone spike projecting from the amputation stump of the great toe metatarsal; this may predispose to ulceration
Figure 19.6 Extensive vascular calcification in the foot. There is also a soft tissue ulcer crater and underlying osteomyelitis in the great toe
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INFECTION 229
Figure 19.7 Chronic stable neuropathic foot
but relatively normal bone density in those with a dislocation pattern13 and in those with neuropathy but no arthropathy.14 The fracture pattern of neuropathy was commonest in the ankle and forefoot, whilst dislocations were commonest in the midfoot.13 The Charcot foot commonly goes unrecognised until severe complications have occurred.15 The mean delay between first clinical presentation and diagnosis of a Charcot foot in diabetes was 29 weeks in one study.16 The changes in the Charcot foot have been divided into five stages17 : Stage 0 is a clinical stage with a swollen, warm and often painful foot.
At this stage, radiographs are normal but bone scintigraphy is positive.
Stage 1 has radiographic abnormality including periarticular cysts, erosions, localised osteopaenia and diastases.
Stage 2 has joint subluxations, most commonly between the middle cuneiform and base of the second metatarsal, which then spread laterally.
Stage 3 has full dislocation and collapse of the longitudinal arch of the foot.
The case illustrated in Figure 19.2 demonstrates the rapid progression from stage 0 to stage 3 that can occur.
Stage 4 is the healed, stable end result (Figure 19.7).
This description applies to neuroarthropathy involving the midfoot.
Metatarso-phalangeal joint involvement by neuroarthropathy is also common (Figure 19.8), as is multiple joint involvement.18 Neuropathic bone resorption of the phalanges can also occur, resulting in an appearance described as ‘sucked candy’ (Figure 19.9).
INFECTION Almost invariably, bone infection in the diabetic foot is acquired by direct spread from an adjacent infected cutaneous ulcer, though presumed haematogenous spread of tuberculosis (TB) to involve the tarsus in a diabetic patient with pulmonary TB has been described.19 When soft tissue infection extends to a bone, it should first affect the periosteum, causing periostitis, then the cortex of the bone, causing osteitis, and finally the marrow space, resulting in osteomyelitis.
The plain film features of bone infection are periosteal reaction, cortical bone destruction and medullary bone destruction.
Periosteal reaction is uncommon in osteomyelitis of tarsal bones but may be seen in metatarsal osteomyelitis (Figure 19.10).
The soft tissue ulcer may contain gas, which may extend down to the bone surface or into the osteomyelitic cavity within the bone.
Gas in the tissues may be in an ulcer cavity, ‘pumped’ into the soft tissues by the pressure of walking on an ulcer cavity or due to soft issue infection by a
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230 RADIOLOGY AND MAGNETIC RESONANCE IMAGING OF THE DIABETIC FOOT
Figure 19.8 Neuropathic great toe metatarso-phalangeal joint. There is also dislocation of the second toe metatarso-phalangeal joint and osteomyelitis of the third toe metatarsal head
gas-forming organism (Figure 19.11).
In necrotising fasciitis of the lower limb in diabetics, gas was seen in the soft tissues on plain radiographs in 44% of affected patients.20 In chronic osteomyelitis, dense foci of necrotic bone may be detached from the bone of origin to form sequestra.
In larger bones, these are usually within intra-osseous cavities with surrounding hypertrophic bone (the involucrum), but may be extruded through cloacae into sinus tracks or soft tissue cavities.
Involucrum formation is less common in the foot.
Sequestra may be extruded through the skin or removed during ulcer debridement.
As treatment of cutaneous ulcers may include the use of antibiotic-releasing pellets placed within the ulcer, the appearance of these pellets should be recognised on radiographs and not confused with sequestra, particularly when the pellets become smaller, irregular and fragmented with time (Figure 19.12).
Plain radiography, nuclear medicine scans, MR imaging and high-resolution ultrasound imaging of suspected osteomyelitis of the diabetic foot have all been compared.
Representative figures compared with histopathology in one study give sensitivities of 69, 79, 83 and 100% for plain
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MAGNETIC RESONANCE IMAGING 231
Figure 19.9 Neuropathic bone resorption resulting in a ‘sucked candy’ appearance to the residual phalanges of the third, fourth and fifth toes
films, ultrasound, bone scintigraphy and MR scanning respectively, with specificities of 80, 80, 75 and 75%.21 Higher specificity can be achieved in nuclear medicine with leucocyte- labelled scanning. A suggested imaging ‘cascade’ in suspected osteomyelitis is therefore plain radiography, and then three-phase bone scintigraphy or MRI. If clinically neuropathy is present then infection-specific radiopharmaceuticals may be needed.22