A 51-year-old white man with a medical history signiﬁcant for Type I diabetes mellitus and peripheral vascular disease necessitating multiple prior distal amputations presented with increasing right foot pain. He reported no recent trauma or corticosteroid therapy. Physical examination revealed prior transmetatarsal amputation and a large nonhealing ulcer that penetrated deeply to the lateral aspect of the ankle. In addition, erythema, warmth, and edema of the leg and foot were noted, leading to a strong clinical suspicion of osteomyelitis.
Walter Silbert, MD
Maroun Karam, MD,
Department of Radiology, Albany Medical College, Albany, NY.
A 51-year-old white man with a medical history significant for
Type I diabetes mellitus and peripheral vascular disease
necessitating multiple prior distal amputations presented with
increasing right foot pain. He reported no recent trauma or
corticosteroid therapy. Physical examination revealed prior
transmetatarsal amputation and a large nonhealing ulcer that
penetrated deeply to the lateral aspect of the ankle. In addition,
erythema, warmth, and edema of the leg and foot were noted, leading
to a strong clinical suspicion of osteomyelitis.
Calcaneal bone osteomyelitis
Radiographic examination revealed a mildly dis-placed fracture
of the calcaneal tuberosity (Figure 1). Focal bone lysis and
periosteal reaction typical of osteomyelitis were not appreciated.
However, they may not be detected for 7 to 14 days. Given the
strong clinical suspicion of osteomyelitis, a technetium-99m
methylene disphosphonate three-phase bone scan was requested, which
revealed increased blood flow and soft-tissue uptake in the right
lower extremity and a photopenic focus in the region of the
calcaneal tuberosity on delayed imaging (Figure 2). A diagnosis of
lower extremity cellulitis and aseptic necrosis of the calcaneus
was suggested. Subsequent magnetic resonance imaging (MRI) revealed
mild diffuse marrow signal abnormality within the posterior
calcaneal fracture fragment. However, there was no localized area
of intense marrow infiltration along the lateral aspect of the
calcaneus abutting the nonhealing ulcer to support the diagnosis of
osteomyelitis (Figure 3A). In addition, anterior to the fracture
line, a serpiginous region of low signal intensity was seen on both
T1- and T2-weighted images, corre-sponding to the photopenic area
on the bone scan, a specific characteristic of a bone infarct
(Figures 3B and 3C). A lower extremity angiogram revealed occluded
anterior and posterior tibial arteries with reconstitution of the
dorsal and plantar arches via collaterals.
Bone infarction is also known as osteonecrosis.
All forms of osteonecrosis result from ischemic death of cellular
constituents of bone and marrow. The mechanisms that produce
ischemia include mechanical vascular interruption, corticosteroids,
thrombosis and embolism, vessel injury due to vasculitis or
radiation injury, increased intraosseous pressure with vascular
compromise, and venous hypertension. Usual causes include trauma,
steroids, sickle cell anemia, dysbaric causes, systemic lupus
erythematosis, Gaucher's disease, alcoholism, and pancreatitis. The
pathologic features of osteonecrosis are the same regardless of the
A localized cold lesion on bone scan is nonspecific for bone
infarction and may also be seen with early osteomyelitis and marrow
involvement by primary or metastatic tumor. The earliest MRI
appearance of bone infarction, marrow edema, is also nonspecific.
However, there is rapid progression to a distinctive, well-defined
pattern that allows a specific diagnosis to be made. The
characteristic pattern is a low signal intensity serpentine rim at
the interface of living and dead bone on both T1- and T2-weighted
images. This corresponds to the margin of advancing new bone and
granulation tissue histologically. The early and specific diagnosis
of bone infarction by MRI allows early appropriate intervention to
reduce the risk of potential complications, including bone collapse
and secondary degenerative joint disease.
Given the finding of perfusion of the dorsal and plantar arches
via collaterals on angiography, and a negative history for steroid
treatment, the bone infarct in this case may be a consequence of
spontaneous calcaneus fracture with resulting mechanical vascular
interruption. Spontaneous fracture in this patient is not
surprising. In addition to bone resorption, resulting from
hyperemia secondary to the adjacent nonhealing ulcer, diabetes
mellitus results in decreased bone mineralization via multiple
pathological processes. Diabetes alone is known to be associated
with decreased bone density before other complications become
clinically evident. Neuropathic changes may also contribute to bone
loss in diabetic patients through altered weight bearing. In
addition, nephropathy and uremia are associated with abnormal or
decreased bone mineralization.
Diabetes mellitus, peripheral vascular disease, and hyperemia
secondary to soft-tissue infection predisposes to calcaneal
insufficiency fractures that may disrupt intraosseous vasculature
and result in bone infarction. To the best of our knowledge, few
cases of calcaneal bone infarction detected by bone scanning are
reported in the literature.
Although nonspecific, a cold defect on a bone scan is suggestive
of bone infarction in this clinical setting. The diagnosis was
confirmed in this case by MRI. Early and accurate diagnosis of bone
infarction facilitates appropriate management, reducing the risk of
bone collapse and secondary degenerative disease.
- Diacam dual-head gamma camera (Siemens Medical Solutions,
Hoffman Estates, IL)
- Signa 1.5TMRI scanner (GE Healthcare, Waukesha, WI)
- 25 mCi of Tc-99m MDP