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M. G. Hochman and C. Connolly

the neuropathic group (p = 0.027) [134]. Lin, Wu, et al. examined the foot musculature with 1H MRI at 3 T and quantitatively mapped the ratio of inorganic phosphate/ phosphocreatine (Pi/PCr) metabolic function with 31P imaging in diabetic and nondiabetic feet [142]. Muscle atrophy was signicantly more severe in diabetic feet compared to normal subjects in all regions (P< 0.01), and the Pi/PCr ratio in the exor hallucis and interosseous regions showed signicant differences between the diabetic and nondiabetic groups (P<0.0). Suzuki etal. measured fat/water and phosphocreatine/inorganic phosphate (PCr/Pi) ratios and calculated the intracellular pH of resting plantar muscles using a combined 1H-31P surface coil in 12 diabetic patients with supercial foot ulcers, 14 diabetic patients without foot ulcers, and 12 age- and sex- matched nondiabetic controls and found that motor nerve dysfunction in diabetic patients was closely associated with impaired energy metabolism, fatty inltration of muscles, increased intracellular pH of plantar muscles, and high frequency of foot ulcers [135]. Dinh etal. measured the phosphocreatinine/inorganic phosphate (PCr/Pi) ratio, total 31P concentration, and lipid/water ratio in the muscles in the metatarsal head region using MRI spectroscopy in healthy control subjects and in both nonneuropathic and neuropathic diabetic patients [133]. They found signicant differences in the muscle energy reserves among the three groups. Thus, the PCr/Pi ratio was highest in the control group, followed by the nonneuropathic group, and was lowest in the neuropathic group. In addition, the total 31P concentration, an indication of the muscle volume, was decreased in the neuropathic group but was comparable in the control and nonneuropathic groups. Similarly, the lipid/water ratio, an indication of muscle atrophy, was increased in the neuropathic group, but there was no lipid/ water ratio difference between the control and nonneuropathic groups. Their ndings supported the presence of an adverse effect on foot muscle energy reserves even before the development of clinical neuropathy, with a more pronounced degradation of energy reserves observed following the onset of clinical neuropathy. A series of studies have measured the rate of phosphocreatine resynthesis after exercise—considered an index of mitochondrial oxidative metabolism in muscle—and have observed differences in the rate of resynthesis between normal and pathological states, a tool that can be employed to track disease progression or response to treatment to evaluate the impact of different interventions [143–146]. Recently, Bolacchi et al. have turned their attention to the spectroscopy of marrow fat and have proposed the use of proton spectroscopy to follow changes in marrow lipids in the setting of stage 0 acute neuroarthropathy [147].

Dierentiating Osteomyelitis fromNeuroarthropathy

Differentiation between osteomyelitis and neuroarthropathy is often difcult. Certain neuroarthropathic changes resemble osteomyelitis on imaging. In order to better understand the similarities and differences, the imaging characteristics of neuroarthropathy will be presented here. A more complete discussion of neuro-osteoarthropathic changes are provided in another chapter of this book.

Neuroarthropathy

The loss of both pain and proprioceptive sensation is believed to predispose to repetitive trauma, leading to diabetic neuroarthropathy [16]. Though neuroarthropathy is potentially devastating, the reported incidence of neuropathic joints in the diabetic patient is surprisingly low, 0.1–7.5% [148]. The lifetime prevalence of Charcot neuroarthropathy in patients with diabetes has been reported to range from 0.1% to 10%, increasing to 29% to 35% if peripheral neuropathy is present [149]. The joints of the forefoot and midfoot are commonly involved. The distribution of neuroarthropathy in diabetic patients is 24% in the intertarsal region, 30% in the tarsometatarsal region (Fig.5.16), and 30% in the metatarsophalangeal joints [150]. Abnormalities of the ankle (11%) and interphalangeal (4%) joints are less frequent [150].

Two classic forms of neuroarthropathy, atrophic and hypertrophic, have been described [151]. The atrophic form, representing the acute resorptive or hyperemic phase, is characterized by osseous resorption and osteopenia. This form frequently appears in the forefoot and the metatarsophalangeal joints, leading to the partial or complete disappearance of the metatarsal heads and proximal phalanges. Osteolytic changes produce the tapering or “pencil-pointing” of phalangeal and metatarsal shafts. Marrow changes in the atrophic or hyperemic form show hypointense T1 (low T1) and hyperintense STIR (bright STIR) signal and mimic the changes seen in osteomyelitis. The hypertrophic form, representing the healing or reparative phase, is characterized by sclerosis, osteophytosis, and radiographic appearance of extreme degenerative change (Fig.5.16). In its early phase, the hypertrophic form of neuroarthropathy may be confused with osteoarthritis. Concurrent osseous fragmentation, subluxation, or dislocation predominates in the intertarsal and tarsometatarsal joints. Ruptured ligaments in the mid- and forefoot cause the dorso-lateral displacement of the metatarsal bones in relation to the tarsal bones. This classic nding resembles an acute Lisfranc fracture dislocation (Fig.5.17).

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Fig. 5.16 Hypertrophic form of neuroarthropathy. (a) AP and (b) lat- eral radiographs show hypertrophic changes in the medial midfoot (arrows), centered about the tarso-metatarsal joint. There is bony proliferative change, increased density, and nonaggressive periosteal new

The disruption of the talonavicular and calcaneocuboid

bone formation (arrowheads) in the rst and second metatarsal bones and increased density in the corresponding cuneiforms. In its early phase, this form of neuroarthropathy may be confused with osteoarthritis. Note soft tissue swelling, with effacement of fat planes

Radiography

joints causes the collapse of the longitudinal arch, with the subsequent plantar displacement of the talus. These changes produce the classic “rocker-bottom” deformity [152]. The recognition of this deformity is important because it creates new pressure points that lead to callus formation and ulceration (Fig.5.18). Attempts to classify neuropathic joints into the two classic forms may be difcult as a mixed pattern, composed of both forms, occurs in 40% of neuropathic joints [153]. Traditionally, the classication of the natural history of the clinical and radiographic features of neuropathic osteoarthropathy has been based on the Eichenholtz classication, though many updated and alternative systems have also been proposed [148, 154, 155]. Notably, the Eichenholtz classication has been modied to include stage 0, which is characterized by swelling, erythema, and warmth, but with normal-appearing radiographs [156–158]. In stage 0, even though radiographs are negative, MRI and nuclear medicine exams can reveal abnormal ndings of early neuroarthropathy, such as bone marrow edema on MRI and increased activity on scintigraphic exams. By facilitating early treatment, the recognition of early changes of neuroarthropathy may help forestall disease progression and foot deformity [149, 159–164].

Radiography is the rst-line imaging modality for the assessment of suspected neuropathic osteoarthropathy [25, 26,

149]. However, sensitivity for the diagnosis of acute neuroar-

thropathy is relatively low (60%), with specicity of around 80% [148, 165]. Initial radiographs may be negative but can serve as a baseline for comparison [149]. Early radiographic ndings include soft tissue swelling (which can be minimal), focal demineralization, subchondral fracture (e.g., head of second metatarsal), and small ecks of bone suggesting ligamentous avulsion, periarticular bone resorption [149, 155,

166]. Radiographic ndings in chronic Charcot osteoar-

thropathy are more readily appreciated and include subluxation, dislocation, fractures, bone fragmentation with debris formation, and evidence of “healing” or recrudescence, such as sclerosis at bone edges, osteophyte formation, and areas of bone fusion, with resultant overall deformity [155]. Weight-bearing radiographs are helpful in assessing alignment, including pes planus and “rocker bottom” deformity, plantar and dorsal subluxation of metatarsal bases, and Lisfranc subluxation and dislocation, and are helpful for preoperative planning, with comparison between bilateral weight-bearing radiographs helping to highlight subtle early

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M. G. Hochman and C. Connolly

Fig. 5.17 Midfoot deformity related to neuroarthropathy. (a) Lateral radiograph demonstrates the collapse of the usual longitudinal arch of the foot. Progression can result in extreme “rocker bottom deformity”

changes in alignment [149, 167, 168]. Alignment abnormalities demonstrated on standing lms have been associated with the prediction of ulceration [154, 155, 169, 170].

(b). AP view shows Lis-Franc malalignment (arrow) as well as disruption of the navicular-cuneiform articulations

ent without soft tissue ulceration [25]. CT is particularly helpful in the evaluation of the mid-foot where a bony overlap limits visualization on radiographs. In chronic neuroarthropathy, CT may be useful for preoperative planning [25, 155, 171, 172].

CT has limited sensitivity for the detection of bone marrow edema, which limits its utility in the early stage of neuroosteoarthropathy. However, CT—with or without IV contrast—can be more sensitive for the detection of early fracture and subluxation than radiographs and therefore may help in demonstrating early structural changes of neuroarthropathy, to help in distinguishing it from osteomyelitis, as a cause of soft tissue swelling in diabetic patients who pres-

Ultrasound

Ultrasound has very limited value in assessing the bone and joint changes of neuroarthropathy. However, a pilot study describing the use of ultrasound to detect soft tissue changes of neuroarthropathy in grade-0-modied Eichenholz classication patients with negative radiographs has been described [173].

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Fig. 5.18 Rocker bottom deformity and ulceration at the focus of high plantar pressure on MRI. (a) Sagittal T1-weighted and (b) STIR images show the disruption of the talonavicular joint, causing the collapse of the longitudinal arch. These changes produce the classic “rocker-

MRI

bottom” deformity. This deformity is important because it creates new pressure points that lead to callus and ulcer formation (arrow). The diffuse marrow edema associated with neuroarthropathy of the tarsal bones mimics osteomyelitis. T talus, CU cuboid, C calcaneus, TIB tibia

neus, and malleoli and is associated with focal cortical lesions and close proximity to the ulcer. Marrow changes in

In the acute phase, MRI ndings in neuroarthropathy include soft tissue edema, joint effusion, subchondral marrow edema, disruption of the Lisfranc ligament, and osseous and/or articular disorganization, patchy intraosseous bone marrow on uid-sensitive sequences, and enhancement of subchondral marrow on postcontrast sequences [154, 174–176]. In chronic neuroarthropathy, soft tissue edema may persist. However, marrow edema and enhancement decreases [154,

174–176]. Subchondral cysts (rounded low T1/high T2 foci)

and linear areas of low T1 signal as well as subluxation, dislocation, and bone fragmentation and hypertrophy are seen [154, 174, 175]. Other than the characteristic ndings of diffuse dark marrow signal on T1-weighted, STIR, and T2-weighted MR images associated with hypertrophic neuroarthropathy (as opposed to high T2 and high STIR signal seen in osteomyelitis), there is no easy method of distinguishing between osteomyelitis and neuroarthropathy [165,

166, 174, 177]. Secondary ndings such as involvement of

the midfoot and of multiple joints, absence of cortical destruction, presence of small subchondral cyst-like lesions, and distance between soft tissue infection and bone changes favor a diagnosis of neuroarthropathy (Table 5.6). In contrast, osteomyelitis favors the toes or metatarsal heads, calca-

osteomyelitis tend to occur on one side of the joint (unless associated with septic arthritis), while neuroarthopathic changes tend to occur on both sides of a joint [154, 166,

174]. When assessing for potential superinfection of a neuro-

arthropathic joint, signs include sinus tracts, total effacement of the adjacent soft tissue fat signal, larger than expected uid collections in soft tissues, diffuse marrow edema throughout a bone, and interval disappearance of the subchondral cysts and/or intra-articular loose bodies. When cortical margins are indistinct on T1-weighted images but appear distinct on T2-weighted or contrast-enhanced images (ghost sign), that is also suggestive of superimposed osteomyelitis [126, 127]. Findings supporting an absence of superimposed infection are a thin rim of enhancement surrounding a joint effusion, the presence of subchondral cysts, or the presence of intra-articular bodies [126, 127].

The use of advanced MR imaging techniques—such as dynamic (rapid sequential) contrast enhancement and diffusion- weighted imaging—for the distinction between neuroarthropathy and osteomyelitis is currently being explored [178]. One recent study in a group of 30 patients suggests the potential utility of dynamic-contrast-enhanced MRI for differentiating between osteomyelitis and neuroar-

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Table 5.6 Osteomyelitis vs. neuroarthropathy

Favors osteomyelitis Favors neuroarthropathy

Radiography

Location Forefoot, metatarsal heads, and toes, calcaneus, malleoli Midfoot

One side of joint Both sides of joint Extent Single bone Multiple bones Cortical destruction Discrete cortical lesion No discrete cortical lesion Proximity to soft tissue ulcer

MRI

Signal characteristics of the abnormal marrow

Cysts Not common in osteomyelitis Well marginated cyst-like lesions

Fluid collections Abscess, which demonstrates thicker peripheral rim of contrast

Osteomyelitis superimposed on neuroarthropathy

Beneath or close to the ulcer or soft tissue infection Some distance from soft tissue infection

or ulcer

Hyperintense STIR, T2, or fat-saturated T2 marrow signal. (this signal

pattern is nonspecic and overlaps both the hyperemic form of

neuroarthropathy and acute fracture)

Conuent low T1 signal in a geographic medullary distribution is the

most suggestive of osteomyelitis

Ulcer connected to abnormal bone marrow via stulous tract,

highlighted by “tramtrack” contrast enhancement of stula walls

enhancement, supports osteomyelitis. While simple uid has

homogeneous low T1/high T2 and high STIR signal, pus present

within the abscess can cause somewhat higher T1/lower T2 and STIR

signal than simple uid

“Ghost sign”=cortical margins that are indistinct on T1W images but

distinct on T2W and contrast-enhanced images

Disappearance of previously seen subchondral cysts and loose bodies

Peri-articular low T1/high T2-high STIR signal (can be seen with acute neuroarthropathy) Hypointense marrow signal on all T1, T2, and STIR sequences (corresponds to the hypertrophic form of neuroarthropathy) No stulous communication between ulcer and abnormal bone

(hypointense on T1 and hyperintense on T2 or STIR sequences) Thin rim of peripheral enhancement can be seen around a joint effusion

Presence of subcortical cysts and intra-articular loose bodies

M. G. Hochman and C. Connolly

thropathy in the foot. Two parameters derived from the time course of dynamic contrast enhancement showed signicant correlation with C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) and, moreover, showed signicantly different values in the areas of osteomyelitis vs. neuropathic arthropathy [106]. In a prospective study of 31 patients with diabetic foot infection, MRI showed good accuracy in differentiating neuroarthropathy and osteomyelitis based on both ratios between pathologic and normal bone on diffusion-weighted images and on parameters derived from dynamic enhancement (AUC 0.814–0.830) when larger regions of interest were employed [179]. Ultimately, based on currently available techniques, differential diagnosis may require the aspiration of joint uid or percutaneous biopsy, though care should be taken to avoid introducing infection into a noninfected bone [155, 174].

Radionuclide Studies

A technetium 99m methylene diphosphonate bone scan will show increased activity in the areas of increased bone turnover, but this nding is nonspecic and can be seen with trauma, postsurgical change, and infection. As a result, changes of Charcot osteoarthropathy can result in increased activity on bone scan and can cause a false positive scan for osteomyelitis [25, 149].

While white blood cell scans are often negative in the setting of Charcot neuro-osteoarthropathy alone [149, 160], false positive WBC scans can occur in an uninfected foot, in the setting of recent-onset neuroarthropathy, due to WBC accumulation at the site of neuroarthropathy [25, 46]. This false positive uptake has been hypothesized to be secondary to the presence of hematopoietically active marrow [45, 46,

180]. Combined WBC/sulfur colloid bone marrow scintigra-

phy has been proposed as a means to differentiate between marrow and infection as the cause of WBC accumulation in the neuropathic joint, and in a small series, this combined study was superior to both three-phase bone scan alone and combined bone-and-WBC scan [45, 46, 180].

Keidar etal. found that 18FDG uptake on PET scans was increased in both infection and osteoarthropathy [52]. However, several studies have suggested a potential future role for FDG-PET in distinguishing neuroarthropathy from osteomyelitis [59, 181, 182]. Garcia Deiz etal. compared diffusion-weighted and dynamic-contrast-enhanced MRI with 18F FDG PET/CT for the differentiation of osteomyelitis from neuroarthropathy in the foot in 31 diabetic patients and found that a visual assessment of FDG PET/CT images was the most accurate technique for differentiation, with a signicantly higher AUC (0.848–0.903) than with MRI performed with diffusion weighting and dynamic contrast enhancement [179]. A few early reports based on the use of novel radionuclides have also been proposed [183, 184].

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Imaging Algorithm: Approach totheDiagnosis ofPedal Osteomyelitis intheDiabetic Patient

A suggested algorithm for imaging pedal osteomyelitis in the diabetic patient is presented in Fig.5.19.

Soft Tissue Ulceration Exposing Bone

When a soft tissue ulcer exposes bone, there is a relatively high positive predictive value for osteomyelitis [1, 21]. Radiography is appropriate to provide a baseline and to document bone complications. MRI may be useful for preoperative planning as it provides detailed anatomic landmarks for bone and soft tissue pathology and has a high negative predictive value for osteomyelitis and soft tissue infection, thus demarcating normal bone and soft tissue.

Soft Tissue Inammation (Ulcers and/or Cellulitis) withNo Exposed Bone

Radiographic ndings are used to further separate patients into two groups—(i) those who have obvious changes of osteomyelitis on their foot radiographs, yielding a presumptive diagnosis of osteomyelitis, and (ii) those whose foot radiographs appear normal.

If radiographs show characteristic changes of osteomyelitis, an MRI may be performed for preoperative planning in order to map the extent of the abnormalities and localize any devitalized areas.

If the radiographs show normal bone and the clinical suspicion for osteomyelitis is high, then an MRI will help demonstrate the presence and distribution of bone and soft tissue infection [174]. Although the use of intravenous (IV) gadolinium contrast is generally preferred because it can help delineate stulous communication between an ulcer and areas of bony abnormality and also will outline soft tissue abscesses, if IV contrast is contraindicated, e.g., due to renal insufciency, MRI performed without IV contrast can still be very useful in demonstrating areas of bone and soft tissue abnormality. An MRI with classic ndings of osteomyelitis provides a presumptive diagnosis of osteomyelitis. A normal MRI has a high negative predictive value and effectively excludes osteomyelitis. Occasionally, an MRI may be indeterminate, particularly in cases when distinction between osteomyelitis and neuroarthropathy is difcult. While certain MR imaging features favor osteomyelitis vs. changes of osteoarthropathy, in some cases, the distinction between osteomyelitis and osteoarthropathy may be difcult [174]

(Table5.6). In those cases, additional workup is required, as detailed below.

If MRI is contraindicated or not available, then a labelled leukocyte (white blood cell) scan can serve as an effective alternative [25]. In the complex anatomy of the mid- and hindfoot, SPECT/CT images may be a useful adjunct to labeled leukocyte scanning in order to help determine whether increased activity is located in the soft tissues or in the bone [30, 31]. Combined WBC scan and bone scan can also be considered. When changes of osteoarthropathy are present, then a technetium-99m sulfur colloid bone marrow scan, as a complement to the labeled leukocyte scan, may be helpful [25, 46, 180]. Labeled leukocytes can accumulate in an uninfected neuropathic foot [46], and a correlative technetium- 99 m sulfur colloid bone scan helps differentiate labeled leukocyte activity due to bone marrow displacement vs. osteomyelitis. A study is positive for osteomyelitis when uptake is greater in either intensity or distribution on the labelled leukocyte scan, compared with the bone marrow scan [46]. In practice, an indium-111-labeled leukocyte (WBC) scan and a technetium-99m sulfur colloid bone marrow scan can both be performed in a single “sitting” rather than as sequential studies. FDG PET/CT is often not reimbursed for this indication, but evidence for the utility of FDG PET/CT in this setting is growing [179,

181, 182]. Nuclear medicine bone scan studies have long

been the mainstay for the imaging of osteomyelitis. While three-phase bone scans—as a stand-alone study—are no longer formally considered a rst-line nuclear medicine for the evaluation of osteomyelitis [25, 29], in practice, they are often employed as a rst-line alternative, when MRI is contraindicated or not available, because they are relatively easy and rapid to obtain.

Although CT has a limited role in the imaging workup of osteomyelitis, if radiographs are normal and suspicion for osteomyelitis is low, then CT may help demonstrate early changes of osteoarthropathy [25].

Equivocal MRI

If MRI is equivocal for osteomyelitis, then further imaging workup could include a labeled leukocyte scan, with SPECT or SPECT/CT, if required [25, 26, 30, 31]. Combined WBC scan and bone scan can also be considered. If there are changes of osteoarthropathy, a comparative technetium-99m sulfur colloid bone marrow scan could be considered [25,

180]. As noted above, in practice, three phase bone scans are

often employed as the next imaging study after an equivocal MRI because of their ready feasibility, even though they are not formally recommended as a next-line exam.

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M. G. Hochman and C. Connolly

Fig. 5.19 Suggested approach to the diagnosis of osteomyelitis in diabetic foot infection

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Conclusion

Imaging plays an important role in the assessment of a diabetic patient with foot problems. Nuclear medicine and MRI techniques detect osteomyelitis, characterize various soft tissue abnormalities, and depict the extent of bone involvement. Distinguishing osteomyelitis from coincident neuropathic change remains a challenge, but newer techniques such as dynamic contrast enhanced MRI, diffusionweighted MRI, combined WBC scans and bone marrow scans, and FDG PET/CT may come to play a role in making this distinction. Recent advances in MR spectroscopy provide tools to assess metabolic changes in the infected or neuropathic foot. Only with an understanding of the specic strengths and weaknesses of each modality, as they apply to the particular clinical problem in question, can this wide variety of imaging studies be utilized in an effective and efcient manner.

Acknowledgments Sincere thanks to Drs. Yvonne Cheung, J.Anthony Parker, Kevin Donohoe, David Brophy, Yuri Shif, Darlene Metter, and Kevin Banks for their contributions. Heartfelt thanks, as well, to Ms. Clotell Forde for her assistance in the preparation of this manuscript.

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